Dr. Bob's All Creatures Site
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Please note: This is an informative page only. It is not meant to recommend treatment for either animal or human disease. If you have health concerns for your pet contact your Veterinarian. If you have health concerns for yourself contact your physician.
Much of the information on this site is based on text modified from a document created by Michael S. Rand DVM, ACLAM
ACARIASIS
AGENT:
Sarcoptes scabeii, Notoedres cati, and other species of mites.
MEANS OF TRANSMISSION TO HUMANS:
Contact.
MOST COMMON SPECIES ASSOCIATED WITH TRANSMISSION TO HUMANS:
Dogs, cats, horses, goats, sheep, swine, birds
ASCARIASIS
(Roundworm infection, ascaridiasis) A common, but usually mild, roundworm infection of bothhumans and animals, occurring worldwide. There is doubt whether the worms cross between species. The causative agent in humans is usually Ascaris lumbricoides. Ascaris suum in pigs is considered occasionally a zoonotic infection (Nematoda). There is no vaccine.
RESERVOIR AND MODE OF TRANSMISSION:
A. lumbricoides has its reservoir in humans and in contaminated soil. A. suum occurs in pigs. Eggs are passed in feces and become infective after two weeks. Infection is by the ingestion of eggs in soil or undercooked food. Eggs hatch in the gut, penetrate its wall and reach the lungs via the bloodstream. Larvae develop in the lungs, ascend the trachea and are swallowed and mature in the gut. Egg-laying begins 45-60 days after initial infection.INCUBATION PERIOD:
Humans. About two months. Animals. Development of A. suum in the pig is said to be quicker than in the human.CLINICAL FEATURES:
Humans. The condition is usually asymptomatic but there may be fever with asthma, spasmodic coughing and possibly pneumonitis. Abdominal pain, and even bowel or bile duct obstruction, is possible. Occasionally migrating larvae cause symptoms referable to the brain, eyes, kidneys and liver. Animals. Migrating larvae cause irregular breathing and coughing. Heavy infection gives abdominal pain with diarrhoea. Suckling pigs are most affected.PATHOLOGY:
Humans. Eosinophilia and pulmonary eosinophilic infiltration occur. Liver abscesses and cholangitis are sometimes seen. Animals. Larvae migrating through the lung cause pneumonia. Worms in the intestine give enteritis.DIAGNOSIS:
Humans. Identify eggs or adult worms in feces. Larvae in sputum or gastric washings are diagnostic. Animals. Examine feces for eggs, or monitor worms passed rectally or via mouth and nose. An egg count of more than 1OOO/g of feces indicates clinical disease.PROGNOSIS:
: Humans. The condition is rarely fatal. Aberrant larvae in brain, eyes and kidney can give severe symptoms. Animals.Rarely fatal.PREVENTION:
Humans. Sanitary disposal of feces coupled with good personal and food hygiene are essential. Animals. Worm and wash sows before farrowing. Rear pigs on concrete or avoid close confinement on soil.TREATMENT:
Humans and animals. Pyrantel pamoate is the treatment of choice. Stools should be rechecked at 2 weeks and patients retreated until all ascarids are removed.LEGISLATION:
Humans and animals. None.AGENT:
Actinobacillus lignieresii, Actinobacillus equuli, and Actinobacillus suis
RESERVOIR AND INCIDENCE:
These bacteria belong to the oropharyngeal resident microbiota of horses, cattle, sheep, and pigs. Persons at risk are butchers and individuals having intensive contact with farm animals.
TRANSMISSION:
Human infections are mostly due to animal bites but may result from direct contact (skin lesions) with the animals mentioned above.
DISEASE IN HUMANS:
Wound infections with abscess formation are observed mainly on the hands and forearms. Septicemia may occur.
DIAGNOSIS:
Diagnosis is performed by culture and biochemical reactions.
DIFERENTIAL DIAGNOSIS:
Other bacterial agents causing purulent infections such as Staphylococci, Streptococci, Pasteurella, Streptobacillus moniliformis, and Capnocytophaga spp. must be ruled out.
THERAPY:
β-Lactam antibiotics or fluoroquinolones are recommended.
PREVENTION:
Proper hand cleaning and veterinary hygiene.
Afipia felis - See Cat Scratch Disease
AFRICAN TRYPANOSOMIASIS
(African Sleeping Sickness, Gambian Trypanosomiasis, Rhodesian Trypanosomiasis)AGENT:
Trypanosoma brucei gambiense and rhodesiense.RESERVOIR AND INCIDENCE
Many wild and domestic animals harbor infection. In Gambian trypanosomiasis, humans are the main reservoir and source of infection for the vector tsetse fly (Glossina palpalis, tachinoides, or fuscipes). In Rhodesian trypanosomiasis, animals, especially domestic cattle and pigs, play an important role as reservoirs.TRANSMISSION:
The tsetse fly is infected when it bites during the parasitemic phases and the trypanosome develops in the vector, culminating in infection of its saliva. Transmission is by the tsetse fly bite. In humans, intrauterine infection has been recorded.DISEASE IN ANIMALS:
Occasionally mild disease occurs in domestic animals with chronic nervous sequela in T. gambiense infection.DISEASE IN HUMANS:
The trypanosomal chancre: This a local pruritic, painful inflammatory reaction with regional lymphadenopathy that appears about 48 hours after the tsetse bite and lasts 2-4 weeks. The hemolymphatic stage: Usually absent or unnoticed in T. b. gambiense infections. Irregular fevers, headaches, joint pains, malaise, pruritus, papular skin rash, edemas. Patients may succumb to myocarditis before signs of central nervous system invasion appear. The meningoencephalitic stage: Insomnia, motor and sensory disorders, abnormal reflexes, somnolence to coma. Trypanosomes and increased white cells and protein in cerebrospinal fluid.DIAGNOSIS:
Definitive diagnosis requires identifying the organism in the bite lesion, blood, lymph node aspirate, or CSF. Serologic tests become positive after 12 days.TREATMENT:
Hemolymphatic stage: Suramin, eflornithine or pentamidine. Late disease: melarsoprol or eflornithine or tryparsamide plus suramin.PREVENTION/CONTROL:
Wear long sleeves and trousers in endemic areas. Avoid wearing dark-colored clothing, and use mosquito nets while sleeping. Repellents do not work on tsetse flies. Pentamidine is used as a chemoprophylaxis against the Gambian type.AMERICAN TRYPANOSOMIASIS
(Chagas's Disease, Chagas-Mazza Disease, South American Trypanosomiasis)AGENT:
Trypanosoma cruziRESERVOIR AND INCIDENCE
Dogs, cats, and guinea pigs are the main reservoirs for human infection. T. cruzi occurs only in the Americas; it is found from southern South America to northern Mexico, Texas, and the southwestern U.S. An estimated 12 million people are infected, mostly in rural areas, resulting in about 60,000 deaths yearly.TRANSMISSION:
Humans are infected when the insect's feces become rubbed into the wound caused by the bite of an infected bloodsucking insect (triatomid) or when the conjunctiva, mucous membranes or abrasions become contaminated. After invading local reticuloendothelial cells, the trypanosome multiplies in the blood. Adaption of triatomid vector to the human domestic environment allows transfer of infection between animals, from animals to humans or from human to human. Transmission by blood transfusions from infected persons, congenital infection, breast milk and laboratory accidents are possible.DISEASE IN ANIMALS:
Acute and inapparent infection occur in wild animals and chronic disease is seen in dogs. The acute form, which includes fever, enlarged liver and lymph nodes and heart irregularities, lasts 10-30 days before becoming chronic without further clinical signs, though sometimes myocarditis occurs. Lesions in dogs resemble those in humans.DISEASE IN HUMANS:
Acute illness usually occurs in children with a furuncle at the site of infection. Signs include fever, malaise, enlarged lymph nodes, liver and spleen. If the primary site of infection is the eye there is unilateral edema of eyelids and conjunctivitis. Rarely myocarditis and meningoencephalitis occur. Chronic symptoms in adults result from arrhythmias and dilation of the heart, esophagus and colon. Furuncles (chagoma) appear at the point of entry of the infection. Enlarged liver and spleen, myocarditis, grossly dilated heart, intestines, esophagus, ureter and bladder and meningoencephalitis occur.DIAGNOSIS:
Several serologic tests are available and are of presumptive value; when possible, more than one test should be used. In the acute stage, trypanosomes should be looked for by examination of anticoagulated fresh blood for motile organisms. In the chronic stage, the parasite can only be detected by culture or xenodiagnosis.TREATMENT:
Therapy is unsatisfactory; the drugs are toxic and often ineffective. In the acute phase, however, cure is usually possible. In the chronic phase, although parasitemia and xenodiagnosis become negative, treatment does not alter the serologic reaction, cardiac function, or progression of the disease. Nifurtimox or benznidazole is used. Ketoconazole shows promise also.PREVENTION/CONTROL:
Destroy the vector by insecticides. Use insect nets to prevent bites. Screen blood donors.
ALLERGIC SENSITIVITIES
Allergic skin and respiratory reactions are quite common in personnel working with laboratory animals. Many animals are implicated including the cat, dog, horse, rabbit, rat, mouse, hamster, gerbil, guinea pig, and NHP. Up to 8% of clients with budgies are affected. Hypersensitivity reactions include: 1. Nasal congestion 2. Runny nose 3. Sneezing 4. Itching of eyes 5. Angioedema 6. Asthma 7. A variety of skin manifestations (localized urticaria and eczema) Maximal allergenic activity in humans resulted from the albumin fraction of pelt extracts from rats, mice, and rabbits. The fraction of G. pig extract with maximum allergic activity seems to be a prealbumin. Two major allergens in mouse serum, skin, and urine have been identified. *THE MAJOR URINARY PROTEIN COMPLEX IS ONE OF THE MOST RECENT ALLERGENS TO BE IDENTIFIED FROM MOUSE PELTS AND SKIN. Suggests that a possible cause of sensitization in lab personnel is dispersal of urinary protein from litter in mouse cages.DIAGNOSIS:
History Physical Exam Pulmonary Function Tests Skin Testing Laboratory Tests a. CBC b. Immunoglobulins and IgE antibody specific to one allergen as measured by the RAST (Radioallergosorbent Test) c. Nasal smears for eosinophilia d. Serum precipitants to specific allergensTREATMENT AND PREVENTION:
Pharmacologic treatment Allergen Immunotherapy Complete avoidance of the antigen Reducing exposure to offending antigen a. Reduction of direct animal contact time b. Increasing room ventilation c. Exhaust hoods d. Filter caps on cages e. Protective clothing, masks, and respirators
AMEBIASIS
(Amebic Dysentery, Amebiosis)AGENT:
Entamoeba histolytica.RESERVOIR AND INCIDENCE
The reservoir of E. histolytica is man. The infections is present worldwide but is most prevalent and severe in tropical areas, where rates may exceed 40% under conditions of crowding, poor sanitation, and poor nutrition. It is estimated that there are about 50 million case of invasive amebiasis and 40,000-100,000 deaths annually worldwide. In temperate areas, however, amebiasis tends to be asymptomatic or a mild, chronic infection that often remains undiagnosed. In the USA, seropositive rates up to 2-5% have been reported in some populations. Reported incidence of 0-31% in the feces of clinically normal Rhesus monkeys, 2-67% in Chimps, and up to 30% in other NHP.TRANSMISSION:
Transmission may be by ingestion of infective cysts, contaminated water or food, by flies, or fomites. Exists as resistant cysts or more fragile trophozoites CYSTS are the INFECTIOUS form found in the stool of asymptomatic carriers or patients with mild disease. The cysts remain viable, if moist and cool for 12 days. Remain viable for 30 days in water. Laboratory animal personnel are usually infected from fecal matter transferred to the skin or clothing.DISEASE IN ANIMALS:
In dogs, infection by E. histolytica is generally asymptomatic and frequently localized in the cecum. Occasionally, it can invade tissues and cause acute or chronic amebiasis. Rhesus monkeys are generally resistant and usually experience asymptomatic infection, but chronic, mild colitis can occur. In chimpanzees, the infection can persist for a long time, in most cases subclinically, but sometimes it invades the tissues causing ulcerative colitis and hepatic abscesses. New World monkeys are considered more susceptible to the disease than Asian or African monkeys. Wild rats can also harbor E. histolytica; the protozoan can be found in the large intestine as a commensal or it can invade the mucosa and cause amebic dysentery.DISEASE IN HUMANS:
Mild to moderate colitis: recurrent diarrhea and abdominal cramps, sometimes alternating with constipation; mucus may be present; blood is usually absent. Severe colitis: semiformed to liquid stools streaked with blood and mucus, fever, colic, prostration. In fulminant cases, ileus, perforation, peritonitis, and hemorrhage occur. Hepatic amebiasis: fever, hepatomegaly, pain, localized tenderness.DIAGNOSIS:
Use fresh fecal specimen to identify cysts or trophozoites. Sedimentation. Must measure to distinguish from other nonpathogenic amoebae. Indirect HI For hepatic amebiasis, ultrasonography can locate the cyst and fine needle aspiration is performed to find the organism.TREATMENT:
May require the concurrent or sequential use of several drugs. The tissue amebicides dehydroemetine and emetine act on organisms in the bowel wall and in other tissue but not in gut lumen. Chloroquine is active principally against amebas in the liver. The luminal amebicides diloxanide furoate, iodoquinol, and paromomycin act on organisms in the bowel lumen but are ineffective against amebas in the bowel wall or other tissue. Metronidazole is unique in that it is effective both in the lumen and in the wall and in other tissue. However, when used alone, it only cures 50% of the cases.PREVENTION/CONTROL:
Strict sanitation & personal hygiene, protective clothing and gloves. Fecal screening of NHP. Protect water supply from fecal contamination. Usual chlorine levels don't destroy cysts. *10ppm chlorine residual necessary to destroy cysts Heat to 50oC (122oF) kills cysts. Adequate cooking to destroy cysts. Protect food from fly contamination.
ANCYLOSTOMIASIS
(Uncinariasis, Necatoriasis, Hookworm Disease)AGENT:
The causative agents are mainly Necator americanus and Ancylostoma duodenale; occasionally A. ceylanicum and A. caninum.RESERVOIR AND INCIDENCE
A common worm infection of humans and domestic dogs and cats in various tropical and subtropical countries where disposal of human feces is inadequate. The reservoirs are humans, dogs, and cats.TRANSMISSION:
Adult worms, living in the small intestines of humans, produce eggs which pass on to the ground in feces. The eggs hatch and go through three larval stages. Human infection results from the third-stage larvae which survive in soil for several weeks in moist and warm conditions. Animals and man become infected by contact with infected soil, the larvae penetrating through skin or mucosa of the digestive tract. The parasites then migrate through the blood capillaries to the lung, eventually to be coughed up and swallowed. They reach maturity and complete their cycle in the intestines.DISEASE IN ANIMALS:
Factors such as the weight of infection and nutritional state of the animal are important. Loss of blood together with malnutrition produce anemia. Severe enteritis causes hemorrhagic diarrhea and weight loss from intestinal malabsorption. Prenatal infection of the dog causes death of the fetal pups. Mild infections generally cause no clinical signs.DISEASE IN MAN:
The condition is often asymptomatic. Self-limiting vesicular/pustular skin eruptions may appear at the site of larval entry. A. caninum does not penetrate human skin beyond the epidermis. With other species chronic symptoms due to iron deficiency anemia may occur. Rarely there is tracheitis and coughing due to lung infiltration with parasites.DIAGNOSIS:
Fecal flotationTREATMENT:
Pyrantel pamoate, mebendazole, albendazole, levamisole, or tetrachloroethylene.PREVENTION/CONTROL:
Educate the public to the dangers of soil contamination by feces. Wear shoes! Screen feces from persons and animals from endemic areas. Keep kennel floors dry and avoid feeding animals on the ground.
ANGIOSTRONGYLIASIS
SYNONYMS:
Angiostrongylosis, eosinophilic meningitis or meningoencephalitis (A. cantonensis), abdominal angiostrongylosis (A. costaricensis).ETIOLOGY:
Two metastrongylids, Angiostrongylus (Morerastrongylus) costaricensis and A. cantonensis, are the etiologic agents. The first species is responsible for abdominal angiostrongyliasis, and the second one for eosinophilic meningitis or meningoencephalitis.The definitive hosts of both species are rodents; man is an accidental host. Both species require mollusks as intermediate hosts for the completion of their life cycle. The main definitive host of A. costaricensis is the cotton rat, Sigmondon hispidus, in which the adult nematode lodges in the mesenteric arteries and their branches on the intestinal wall. The first-stage larva emerges from eggs laid in the arteries, penetrates the intestinal wall, and is then carried with the fecal matter to the exterior. In order to continue their development, the first-stage larvae have to be ingested by a slug. Vaginulus ameghini, in which they change successively into second- and third-stage larvae. When the infective third-stage larva is ingested by a rodent, it seeks the ileocecal region, where it penetrates the intestinal wall and locates in the lymphatic vessels (both inside and outside the abdominal lymph nodes). In this location the larvae undergo two molts before migrating to their final habitat, the mesenteric arteries of the cecal region. Oviposition begins after about 18 days. and the first-stage larvae appear in the feces 24 days after infection (prepatent period). In man, an accidental host. the parasite can reach sexual maturity and produce eggs, but the eggs usually degenerate, causing a granulomatous tissue reaction. The development cycle of A. cantonensis is similar to that of A. costaricensis. The intermediate hosts are various species of land snails, slugs, and freshwater snails. The definitive hosts can become infected by ingesting infected snails, or plants and water contaminated by them with the third larvae. In addition, infection can occur as a result of consuming transfer hosts (paratenic hosts), such as crustaceans, fish, amphibians, and reptiles, which in turn have eaten infected mollusks (primary intermediate hosts). The definitive hosts of A. cantonensis are primarily various species of the genus Rattus. When they enter a rat's body, the third-stage larvae (which developed in a mollusk) penetrate the intestine and are carried by the circulatory system to the brain, where they undergo two more molts and become young adult parasites. From the cerebral parenchyma they migrate to the surface of the brain. They remain for a time in the subarachnoid space and later migrate to the pulmonary arteries, where they reach sexual maturity and begin oviposition. The eggs hatch in the pulmonary arterioles, releasing the first larva, which migrates up the trachea, is swallowed, and is eliminated with the feces. Mollusks are infected by ingesting fecal matter of infected rodents. In man, who is an accidental host, the larvae and young adults of A. cantonensis generally die in the brain, meninges, or medulla oblongata. The nematode can occasionally be found in the lungs.GEOGRAPHIC DISTRIBUTION AND OCCURRENCE:
Abdominal angiostrongyliasis, caused by A. costaricensis, is a parasitosis described a few years ago in Costa Rica; it is one of the most recently recognized zoonoses. Human disease has also been confirmed in Honduras, El Salvador, and Brazil. Suspected clinical cases have occurred in Nicaragua and Venezuela. In Panama, the adult parasite was found in five species of rodents belonging to three different families. In the past few years, the parasite has been found in several specimens of Sigmodon hispidus in Texas, USA. Ozyomys caliginosus in Colombia; and slugs in Guayaquil, Ecuador. The parasitosis is probably much more widespread than is currently recognized. A. costaricensis has not been recorded outside the Americas. Human cases of parasitism by A. cantonensis have occurred in Thailand, Vietnam, Kampuchea, the Philippines, Indonesia, Taiwan, Japan, Australia, and several Pacific islands. The parasite is much more widely distributed, and its existence in rats has been confirmed in southern China, India, Malaysia, Sri Lanka, Madagascar, Mauritius, and Egypt. Until recently, the geographic distribution of A. cantonensis was thought to be limited to Asia, Australia, the Pacific islands, and Africa. However, in recent years its presence has been confirmed in Cuba, where infected rats (Rattus norvegicus) and mollusks have been found; likewise, five human cases of meningoencephalitis have been attributed to A. cantonensis in that country. It is believed that the parasite was introduced to the island some years ago by rats from a ship from Asia. In a study carried out on rat species (R. norvegicus, R. rattus, and R. exulans) on the Hawaiian and Society Islands, the parasite was found in more than 40% of the specimens captured. In Egypt, 32.7% of 55 specimens of R. norvegicus harbored the parasite. In the province of Havana, Cuba, 12 out of 30 captured R. norvegicus were infected. In view of the worldwide distribution of R. norvegicus and R. rattus, these rodents were examined for the parasite in Puerto Rico, London, and New Orleans, but the results were negative. Eosinophilic meningitis associated with infection by A. cantonensis has been recorded in several hundred patients in endemic areas.THE DISEASE IN MAN:
The clinical manifestations of abdominal angiostrongyliasis caused by A. cantonensis are moderate but prolonged fever, abdominal pain on the right side. and, frequently, anorexia, diarrhea, and vomiting. Leukocytosis is characteristic (20,000 to 50,000 per mm3), with marked eosinophilia (11 to 82%). Palpation sometimes reveals tumoral masses or abscesses. Rectal examination is painful, and a tumor can occasionally be palpated. Lesions are located primarily in the ileocecal region, the ascending colon. appendix, and regional lymph nodes, but they are also found in the small intestine. Granulomatous inflammation of the intestinal wall can cause partial or complete obstruction. Appendicitis was the preoperativeDIAGNOSIS:
in 34 cases. All but two of the children survived and recovered. The highest prevalence (53%) was found in children 6 to 13 years old, and twice as many boys as girls were affected. Ectopic localizations may occur; when the liver was affected in some Costa Rican patients, the syndrome resembled visceral larva migrans. Serologic studies carried out in Australia, in human populations living in localities where the infection occurs in rats and those living in other places where it does not, indicate that many human infections are asymptomatic.THE DISEASE IN ANIMALS:
In rodents, A. costaricensis produces lesions that are located primarily in the cecum, as well as focal or diffuse edema of the subserosa, a reduction in mesenteric fat, and swelling of the regional lymph nodes. In highly parasitized animals, eggs and larvae may be found in various viscera of the body. No significant difference in weight between parasitized and nonparasitized animals has been confirmed. Rats infected by A. cantonensis may show consolidation and fibrosis in the lungs. However, the physical appearance of the animals does not reflect the degree of pathologic changes. For both parasites, the prevalence of the infection is greater in adult than in young rodents.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
Several species of rodents are known to serve as definitive hosts of A. costaricensis: Sigmodon hispidus, Rattus rattus, Zygodontomys microtinus, Liomys adspersus, 0ryzomys fulvescens, and 0. caliginosus; also, natural infection has been found in a coati (Nasua narica) and marmosets (Saguinus mystax). In a study carried out in Panama, the highest prevalence of the infection was found in the cotton rat S. hispidus, which was also the most abundant rodent in the six localities studied. The cotton rat inhabits areas close to dwellings in both tropical and temperate America. it is omnivorous, feeding on both plants and small vertebrate and invertebrate animals, including slugs (V. ameghini). All these facts indicate that the cotton rat is a prime reservoir and that it plays an important role in the epidemiology of the parasitosis. Rodents are infected by ingesting infected mollusks. Another probable source of infection is plants contaminated with mollusk secretions "slime") containing third-stage infective larvae of the parasite. The manner in which man contracts the infection is not well known. Infection probably occurs by ingestion of poorly washed vegetables containing small slugs or their secretions. It is believed that children can become infected while playing in areas where slugs are abundant by transferring snail secretions found on vegetation to their mouths. An increase in cases in children occurs in Costa Rica during the rainy season, when slugs are most plentiful. Humidity is an important factor in the survival of both the first- and third-stage larvae in the environment, since they are susceptible to desiccation. The parasite species in the Far East (A. cantonensis) has been found in at least ten different species of the genus Rattus and in Bandicota indica and Melomys littoralis. These rodents, natural definitive hosts, are infected by consuming mollusks or paratenic hosts that harbor third-stage larvae. The infection rate of the mollusks is usually high; both the prevalence and the number of larvae an individual mollusk can harbor vary according to the species. Man, who is an accidental host, is infected by consuming raw mollusks and also paratenic hosts such as crustaceans or fish. The ecology of angiostrongyliasis is closely related to the plant community, since it ultimately supports the appropriate mollusks and rodents. The frequency of the human parasitosis depends on the abundance of these hosts and the degree to which they are infected, and, also, in the case of A. cantonensis, on eating habits (consumption of raw mollusks, crustaceans, and fish).DIAGNOSIS:
The spinal fluid characteristically shows elevated protein and an eosinophilic pleocytosis. Occasionally, the parasite can be recovered from spinal fluid. Peripheral eosinophilia with a low-grade leukocytosis is common. A serologic test is available from the Centers for Disease Control and Prevention; its sensitivity and specificity are not established. CT and MRI may show a central nervous system lesion.TREATMENT:
No specific treatment is available; however, levamisole, albendazole, thiabendazole (25 mg/kg three times daily for 3 days), or ivermectin can be tried. Symptomatic treatment with analgesics or corticosteroids may be necessary. The illness usually persists for weeks to months, the parasite dies, and the patient then recovers spontaneously, usually without sequelae. However, fatalities have been recorded.CONTROL:
At least theoretically, angiostrongyliasis could be controlled by reducing rodent and mollusk populations. Preventive measures at the individual level consist of washing vegetables thoroughly, washing hands after garden or field work, not eating raw or undercooked mollusks and crustaceans, and not drinking water that may be unhygienic.
ANISAKIASIS
(Herring worm disease) A common parasitic infection from fish. The parasites are widely distributed. Human disease occurs where people eat raw or lightly smoked or salted saltwater fish or squid (e.g., in Japan, the Netherlands, Scandinavia and Central America). The causative agents are Anisakis, Phocanema and Contracaecum (Nematoda). There is no vaccine.RESERVOIR AND MODE OF TRANSMISSION:
Definitive hosts are marine mammals such as dolphins or seals. These pass the parasite's eggs in their feces. The eggs hatch and produce larvae which infect the first intermediate host, usually a crustacean. A fish may be the second intermediate host. Humans are aberrant hosts infected by eating fish.INCUBATION PERIOD:
Humans and animals. A few hours to a few weeks.CLINICAL FEATURES:
Humans. There may be fever, abdominal pain, vomiting, hematemesis, coughing, pseudoappendicitis, and possibly symptoms associated with intestinal perforation. Animals. Fish fail to thrive if heavily infected.PATHOLOGY:
Humans.The larvae usually remain in the intestine causing few lesions. However, they sometimes invade the stomach wall causing hematemesis and may lodge in the mesenteric veins or in the viscera where they induce eosinophilic granulomas and abscesses. Larvae may migrate up the esophagus to the oropharynx. There is a low grade eosinophilia. Animals. In fish, atrophy of the liver occurs and sometimes fatal infection of the heart. Visceral adhesions and muscle damage can be severe.DIAGNOSIS:
: Humans. Stools may show occult blood. Mild leukocytosis and eosinophilia may be present. ELISA and RAST serologic tests may be tried but are not reliable in chronic disease. In acute infection, the larvae sometimes can be seen and removed endoscopically from the stomach. X-rays of the stomach may show a localized edematous, ulcerated area with an irregularly thickened wall, decreased peristalsis, and rigidity. Double contrast technique may show the threadlike larvae. Small bowel x-rays may show thickened mucosa and segments of stenosis with proximal dilation. Ultrasound examination of gastric and intestinal lesions may also be useful. In the chronic stage, x-rays and endoscopy of the stomach-but not of the bowels-may be helpful. The diagnosis is often made only at laparotomy with surgical removal of the parasite. Animals. Demonstrate the parasite in tissues of fish.PROGNOSIS:
Humans. The condition is rarely fatal. Animals. Wide distribution of the parasites and consequent disease results in difficulty in maintaining marine vertebrates in laboratories.PREVENTION:
Humans. Avoid raw or undercooked fish. Freezing fish kills larvae. Eviscerate fish immediately after catching. Animals. Impractical.TREATMENT:
Humans. Physical removal of larvae by gastroscopy or surgery. Animals. Not appropriate. Legislation Humans and animals. None.ANTHRAX
(Malignant pustule, wool-sorters' disease, charbon, malignant edema, splenic fever) An acute bacterial infection of humans and animals which may be rapidly fatal. The disease occurs worldwide and is enzootic in certain African and Asian countries. It is an occupational hazard of persons such as wool-sorters, fellmongers, knackermen, farm workers and veterinarians in contact with infected animals or their products (e.g., blood, wool, hides and bones). The causative agent is Bacillus anthracis (bacterium).
RESERVOIR AND MODE OF TRANSMISSION:
All domestic, zoo and wild animals are potentially at risk of infection. Anthrax bacilli are released from infected carcasses and form resistant spores on exposure to air. These spores contaminate soil for many years. Humans are usually infected by inoculation from direct contact with infected animals, carcasses or animal products and contaminated soil. Inhalation or ingestion of spores may occur. Animals are infected from contaminated feed, forage, water or carcasses. Laboratory accidents have occurred.INCUBATION PERIOD:
Humans. Cutaneous 3-10 days inhalation 1-5 days gastrointestinal 2-5 days. Animals. 1-5 days.CLINICAL FEATURES:
Humans. Various forms include: 1. Cutaneous anthrax; localized ulceration and scab with fever and headache which may be followed within a few days by septicemia and meningitis. 2. Inhalation anthrax; fulminating pneumonia. 3. Intestinal anthrax; acute gastroenteritis with bloody diarrhoea. Animals. Peracute cases are found dead or moribund. Acute cases show fever, excitation followed by depression, incoordination, convulsion and death. Chronic cases show edema of throat, pharynx and brisket, especially in pigs.PATHOLOGY:
Humans. Features include black scab (eschar) with edema, enlargement of regional lymph nodes and possibly septicemia; pneumonia and generalized hemorrhages. Animals. Carcasses should not be opened, hence necropsy is rarely carried out. Main features include failure of the blood to clot and hemorrhages throughout the body. The spleen is enlarged and softened. The subcutaneous swelling, mainly about the neck and throat of affected pigs and horses, contains gelatinous fluid. The blood contains very large numbers of B. anthracis.DIAGNOSIS:
Humans. Identify B. anthracis in stained blood smears or by inoculation of laboratory animals. Culture swabs from wounds. Animals. As for humans. Specific antigen for anthrax may be found in animal products (e.g. hides) using a precipitin (Ascoli) test.PROGNOSIS:
: Humans. Untreated cutaneous anthrax has a fatality rate of 5-20 Per cent and gastrointestinal anthrax of 25-75 per cent. Pulmonary anthrax is usually fatal. Animals. The condition is usually fatal in cattle unless treated early. Pigs and horses are more resistant.PREVENTION:
Humans. Prohibit contact with infected animals and their products. Establish environmental and personal hygiene (e.g., ventilation and protective clothing) where a special risk exists. Treat wounds promptly and disinfect imports of hairs and wool. Vaccination may protect those occupationally exposed to risk. Apply strict laboratory safety measures. Isolate infected patients, with concurrent disinfection. Animals. Sterilize, or avoid using, meat and bone meal from high-risk countries for animal feed. Vaccinate livestock grazing in enzootic area. Dispose of infected carcasses safely and fence off areas contaminated by inadequately buried carcasses.TREATMENT:
Humans. The mortality rate is high despite proper therapy, especially in pulmonary disease. Penicillin G, 2 million units IV every 4 hours, is the therapy of choice. tetracycline, 500 mg orally every 6 hours, may be used for mild, localized cutaneous infection. Animals. Penicillin injection of all animals showing fever after the first case is confirmed. This involves checking temperatures twice daily.VACCINATION:
Humans. Offered to workers at risk. Animals. Non-encapsulated Stern strain vaccine can be used in all species of domestic animal. Annual vaccination of grazing animals using spore or alum precipitated antigen vaccine in areas of high risk is recommended.LEGISLATION:
Humans. The disease is notifiable in most countries. It is a recognized occupational disease in some countries, including the UK. Animals. Notifiable in many countries with mandatory disposal of infected carcasses by burning or deep burial under lime. Opening of moving suspect carcasses is prohibited.ARTHROPOD INFESTATIONS
In addition to the mite that causes sarcoptic scabies, there are several other species that occasionally infest human skin and cause a temporary dermatitis, although they are incapable of establishing themselves on this aberrant host. These mites belong to the families Cheyletidae, Dermanyssidae, and Macronyssidae. Animals play an essential role in the life cycle of the flies whose larvae cause specific myiases. Man is only an accidental host of these larvae, and in some myiases, such as those due to Oestrus ovis or Gasterophilus spp., an aberrant host in which the larvae cannot complete their development. Larval invasions of human skin or natural cavities occur when there is a high incidence of animal myiasis. Pentasomes (Armillifer sp.) are wormlike arthropods that are almost exclusively parasites of the reptilian respiratory system. Snakes are the definitive hosts and many wild rodents, on which snakes feed are the intermediate hosts. The female parasite deposits eggs in the respiratory cavities of the reptiles. The eggs are expectorated or swallowed and then eliminated with the feces. Humans can be accidental hosts, by handling infected reptiles and placing contaminated hands to the mouth. In humans the infection is usually asymptomatic. The encapsulated larvae might be found during laparotomies or can be diagnosed by radiographic examination.PREVENTION/CONTROL:
Fleas, ticks, and mites should be controlled. Gloves and protective clothing should be worn when handling lab animals.Arthropod borne ARBOVIRUSES:
GENERAL:
In most man is an accidental host infected when arthropods feed on him. Therefore quarantine of wild caught animals and elimination of ectoparasites should prevent:EXAMPLES:
TICK BORNE viruses:1. Russian-Spring-Summer Encephalitis
2. Louping Ill
MOSQUITO BORNE viruses, ie
1. DENGUE (Breakbone Fever, Dengue Hemorrhagic Fever)
AGENT: Flavivirus, Flavidviridae
RESERVOIR:nonhuman primates,occurs in Asia, Africa, Australia, the Caribbean
including Puerto Rico, the Pacific Islands, S. Europe, S. America
TRANSMISSION: mosquito vector (Aedes)
DISEASE IN NONHUMAN PRIMATES: subclinical
DISEASE IN HUMANS: The first phase of illness is usually mild fever, headache, myalgia,
lymphadenitis, pharyngitis, rhinitis and cough lasting 1-5 days and is followed by 1-2 days of
remission. The second peak of fever is accompanied by a morbilliform maculopapular rash.
Severe hemorrhagic manifestations occur during the second phase especially in children.
DIAGNOSIS:> HI, CF, ELISA, or virus isolation.
TREATMENT: Treat shock by expanding circulating blood volume. Acetaminophen given for
discomfort. Prolonged convalescence.
PREVENTION/CONTROL: Mosquito control by screening and insect repellents. Others, in
addition to spread by vector, have presented problems in the laboratory as a result of contact
with tissues or secretions of lab animals experimentally infected with virus.
Examples:
1. EQUINE ENCEPHALITIDES (EASTERN, WESTERN, AND VENEZUELAN). These are diseases
of horses, mules, birds, humans, and other animals caused by the neurotropic viruses,
Alphavirus and Flavivirus. Wild birds serve as a reservoir, and the virus requires an arthropod
vector to transfer from reservoir host to other susceptible species. Mosquitoes, chicken mites
and lice, ticks, and any other bloodsucking insects can serve as vectors. This group of
encephalitis viruses is unique to the New World. Prevention is accomplished by adequate
vector control and vaccination of horses. Pigeons, chickens, pheasants, prairie chickens,
ducks, and geese are susceptible and, if infected when suitable vectors are present, may
pose a potential source of disease for humans. There is a high mortality in humans infected
with these viruses.
2. CRIMEAN CONGO HEMORRHAGIC FEVER. Nairovirus, Bunyaviridae family. Causes
epidemics in Bulgaria, USSR, and sporadic cases in Iraq, Pakistan and East Africa. Associated
with tick bites, primarily Hyalomma genus. Also nosocomial outbreaks among hospital personnel.
3. OMSK HEMORRHAGIC FEVER (rodents)
4. KYASANUR FOREST DISEASE (monkeys) Togaviridae occurs in bonnet macaques,
languors, and rodents in India spread by ticks lab workers in the US affected while working
with infected primates (no vector) NHP exhibit fever, vomiting, diarrhea, epistaxis, and death.
In humans, there is a sudden onset of fever which may be biphasic, with headache,
generalized pains, prostration, conjunctivitis, diarrhea, and vomiting. Vesicles occur on the
soft palate. Hemorrhagic manifestations may follow. Case fatality rate is 2-50%.
Diagnosed thru serology or viral isolation.
Treatment is supportive. Convalescent plasma with a high neutralizing antibody titer has
been reported to be useful. Prevention is thru tick control.
5. CHIKUNGUNYA: Maintained by vervets and baboons in Southern Africa. Transmitted by
biting flies and mosquitoes
6. RIFT VALLEY FEVER (Enzootic Hepatitis)
AGENT:
Phlebovirus, BunyaviridaeRESERVOIR AND INCIDENCE
endemic in Africa and Egypt. Affects nonhuman primates, and man. Cattle, bats, and sheep may be reservoir hosts.TRANSMISSION:
mosquito vector highly contagious among laboratory workers where transmission does not require vector.DISEASE IN ANIMALS:
Rapid death after fever occurs in lambs. In cattle abortion and diarrhea occur. Liver lesions predominate histologically, with areas of necrosis. Widespread hemorrhages occur.DISEASE IN MAN:
Fever (which may be biphasic) has a sudden onset, with severe headache, muscle and joint pains and photophobia. In a small proportion of cases there are hemorrhages, liver necrosis, encephalitis and retinitis.DIAGNOSIS:
Serology and virus isolation.PREVENTION/CONTROL:
Control mosquitos. Precaution in handling necropsy specimens. Arbovirus where the natural cycle of transmission DOES involve man:
BABESIOSIS
(Piroplasmosis)AGENT:
Babesiosis in humans is a rare intraerythrocytic infection caused by Babesia divergens and microti.RESERVOIR AND INCIDENCE
Natural hosts for B. microti are various wild and domestic animals, particularly the white-footed mouse and white-tailed deer. With extensions of the deer's habitat, the range of human infection appears to be increasing. In the USA, the parasite has been found in coastal and island areas of the northeast and mid-Atlantic states as well as Wisconsin, Minnesota, and California. B. divergens occurs in Europe.TRANSMISSION:
Humans are infected as a result of Ixodes tick bites, but transmission from blood transfusion has also been reported. Splenectomized, elderly, or immunosuppressed persons are the most likely to have severe manifestations.DISEASE IN ANIMALS:
Many animals show only mild fever and recover spontaneously. Deaths, which occur commonly in cattle, are due to either anemic anoxia or pulmonary thrombosis. Other lesions stem from the hemolysis and include enlarged spleen, liver, and hemoglobinuric nephrosis.DISEASE IN HUMANS:
B. microti infection lasts a few weeks to a month; the illness is characterized by irregular fever, chills, headache, diaphoresis, myalgia, and fatigue but is without malaria-like periodicity of symptoms. Most patients have a moderate hemolytic anemia, and some have hepatosplenomegaly. The disease is self-limited and most patents recover without sequelae. Infection with B. divergens has only been reported in splenectomized patients and progresses rapidly with high fever, severe hemolytic anemia, jaundice, hemoglobinuria, and renal failure; death usually follows.DIAGNOSIS:
ID of the intraerythrocytic parasite on Giemsa-stained blood smears or serology.TREATMENT:
B. divergens: blood transfusions, renal dialysis, pentamidine plus trimethoprim-sulfa. B. microti: Treat symptomatically since most case are self-limiting. In splenectomized patients, quinine plus clindamycin and transfusions.PREVENTION/CONTROL:
Control rodents and ticks. Vaccinate livestock.
BALANTIDIASIS
(Balantidial dysentery)AGENT:
large ciliated protozoan, Balantidium coli. Trophozoite 50-70 microns by 40-50 microns.RESERVOIR AND INCIDENCE
Distributed worldwide especially in the tropics. Swine and possibly rats and NHP's are the reservoir hosts. Humans, great apes, & several monkey species may carry it. Incidence in NHP colonies - 0 to 63% Usually asymptomatic, but may see diarrhea.TRANSMISSION:
Ingestion of cysts or trophozoites from infected animal or human feces. Cyst is the infectious form. Contaminated water or food.DISEASE IN ANIMALS AND MAN:
Many infections are asymptomatic and probably need not be treated. Chronic recurrent diarrhea, alternating with constipation, is most common, but severe dysentery with bloody mucoid stools, tenesmus, and colic may occur intermittently.DIAGNOSIS:
Use fresh fecal samples to identify trophozoites or cysts Trophozoites in scrapings or biopsy of ulcers of the large bowel.TREATMENT:
tetracycline or iodoquinolPREVENTION/CONTROL:
Good sanitation & personal hygiene practices in NHP & Swine colonies. Protect water & food from fecal contamination Identify positive lab animals and treat.
Bartonella - See Cat Scratch Disease
BAYLISASCARIASIS
AGENT: Baylisascaris procyonis
Means of transmission to humans:
Contact
Most common species associated with transmission to humans:
Raccoon.
BORDETELLA BRONCHISEPTICA INFECTION
AGENT:
Bordetella bronchiseptica
Means of transmission to humans:
Aerosol
Most common species associated with transmission to humans:
Dogs, swine, rabbits, guinea pigs
Bergeyella (Weeksella) zoohelcum
Species associated with infection - B. zoohelcumReported infections - wound infection, septicaemia, meningitis
Reported susceptibilities and treatments - cefotaxime, penicillins, ciprofloxacin, tetracycline
Notes - associated with cat and dog bites - previously classified as Weeksella zoohelcom
References - Reina, J., Borrell, N. (1992). Leg abscess caused by Weeksella zoohelcum following a dog bite. Clin. infect. Dis. 14, 1162-1163.
BERTIELLIASIS
AGENT:
o Bertiella studeri and mucronanta, anoplocephalid tapeworms. o 260-300mm length tapeworm with 10mm width. o Gravid segments shed off in groups of about 20.RESERVOIRS AND INCIDENCE:
NHP's.TRANSMISSION:
NHP's acquire the parasitosis by ingesting mites infected with cysticercoid larvae. Man can become infected accidentally by ingesting food containing the mites.DISEASE IN NHP'S:
asymptomatic.DISEASE IN HUMANS:
The infection is usually asymptomatic, but cases with recurrent abdominal pain, vomiting, anorexia, constipation, and intermittent diarrhea have been observed.DIAGNOSIS:
Diagnosis is based on microscopic observation of the proglottids eliminated in the feces. The egg possesses a characteristic pyriform apparatus.TREATMENT:
DichlorophenPREVENTION/CONTROL:
Control mites.BITES AND SCRATCHES
One to two million Americans are bitten by animals annually, and bites are responsible for 1% of emergency department visits. The estimated annual incidence of animal bites is as follows: dog bites, 1-2 million; cat bites, 400,000; snake bites, 45,000; and rats and mice, 43,000. An increased risk of infection in patients more than 50 years of age, those with wounds of the upper extremities, and those with puncture wounds has been noted. Prior splenectomy or mastectomy may increase the risk of severe infection. Wild rat bites present public health problems. Bites cause pain, anxiety, wound disfigurement, and wound infections. Many organisms are capable of infecting animal bite wounds including Pasteurella spp., Capnocytophaga canimorsus, Afipia felis, Rochalimaea henselae and quintana, Clostridium tetani, Streptobacillus moniliformis, Spirillum minus, Tularemia, and Rabies. Bites from NHP's infected with Herpes B-Virus could pose a serious threat to humans. Pit Bulls were reported to be responsible for 20% of dog bite-related fatalities in 1979/80. By 1987-88, the breed was responsible for 62% of such deaths.TREATMENT OF BITE WOUNDS:
Maintain records of all bites and scratches in the animal facility. Notify physician. A lab animal program should have an occupational medicine service available that understands the problems associated with animal handling and is informed about zoonotic diseases. Cultures should be taken and clean wound properly. * All wounds should be liberally irrigated. * Edematous body parts should be elevated. * Apply antiseptic. * Tetanus must be current. * Assess Rabies or Herpes B risk (notify public health personnel). * Antibiotic therapy should be based on the wound culture.BLASTOMYCOSIS
SYNONYMS:
North American blastomycosis, Chicago disease, Gilchrist's disease.ETIOLOGY:
Blastomyces dermatitidis, a dimorphic fungus existing in mycelial form in cultures and as a budding yeast in the tissues of infected mammals.GEOGRAPHIC DISTRIBUTION:
The disease has been observed in the United States, eastern Canada, Zaire, Tanzania, South Africa, and Tunisia. Autochthonous cases may have occurred in some Latin American countries.THE DISEASE IN MAN:
The incubation period is not well known; it possibly extends to several weeks or months. Blastomycosis is a chronic disease that principally affects the lungs. The respiratory symptomatology initially resembles influenzas purulent or bloody expectoration, weight loss, and cachexia, in addition to fever and cough, may develop later. If the infection remains localized, it can become asymptomatic. When it disseminates, it can cause subcutaneous abscesses as well as localized infections in several organs. Death frequently results in cases of untreated disseminated infection. The cutaneous form is commonly secondary to the pulmo-nary and is characterized by an irregular-shaped, scabby ulcer that has raised borders and contains minute abscesses. Lesions develop on exposed parts of the body.THE DISEASE IN ANIMALS:
The highest incidence is observed in dogs around 2 years of age. The symptoms consist of weight loss, chronic cough, dyspnea, cutaneous abscesses, fever, anorexia, and sometimes blindness. The lesions localize in the lungs, lymph nodes, eyes, skin, and joints and bones. Of 47 clinical cases recently described, 72% occurred in large males. There were lesions of the respiratory tract in 85% of the cases.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
The reservoir is environmental, probably the soil, but the ecologic biotope has not been determined. Transmission to man and to animals is effected by aerosols; the fungal conidia are the infecting element. Persons at highest risk are those having the most contact with the soil. Dogs most frequently infected are sporting and hunting breeds.ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
None. It is a disease common to man and animals. Cases of transmission from individual to individual (man or animal) are not known.DIAGNOSIS:
Diagnosis is based on direct microscopic examination of sputum and material from lesions, on isolation of the agent in culture media, and on examination of histologic preparations. B. dermatitidis grows well in Sabouraud's culture medium or other adequate median it is most distinctive in its sprouting yeast form, and therefore the inoculated medium should be incubated at 37oC, since at ambient temperature the mycelial form of the fungus is obtained. B. dermatitidis in its yeast form (in tissues or cultures at 37oC) is characterized by a single bud attached to the parent cell by a wide base, from which it detaches when it has reached a size similar to the parent cell. In contrast, Paracoccidioides brasiliensis, the agent of paracoccidioidomycosis ("South American blastomycosis"), has multiple buds in the yeast phase. Serologic tests in use are complement fixation and gel immunodiffusion; the latter gives better results. It should be borne in mind that cross-reactions with Histoplasma and Coccidioides may occur. At present, the intradermal test is considered to have no diagnostic value.TREATMENT:
Humans. Itraconazole, 100-200 mg/d orally, is now the therapy of choice for nonmeningeal disease, with a response rate of over 70%. Amphotericin B is given for treatment failures or cases with central nervous system involvement. Follow-up for relapse should be regularly made for several years so that therapy may be resumed or another drug instituted. Animals. Rare primary cutaneous disease may persist for months; these lesions should be removed surgically since blastomycosis responds poorly to therapy. Amphotericin B is considered the drug of choice, but treatment is of little avail once the disease is disseminated. The combination of amphotericin B and ketoconazole has been suggested to reduce the rate of relapse.CONTROL:
As long as the ecologic biotope remains poorly defined, practical prevention methods cannot be established.
BORRELIOSIS -- also see Lyme disease
(Relapsing fever, tick-borne relapsing fever, spirochetal fever, vagabond fever, famine fever) A widely distributed bacterial infection spread from wild rodents by ticks or lice, with high fatality Tick-borne relapsing fever occurs in Africa, the Americas, Asia and possibly parts of Europe. The causative agents are Borrelia recurrentis and several other borrelia strains (bacterium). There is no vaccine.RESERVOIR AND MODE OF TRANSMISSION:
Epidemic louse-borne infection is not considered zoonotic. Endemic tick-borne relapsing fever is transmitted from the natural wild rodent reservoir by tick bites to humans and dogs. Transovarial transmission in ticks occurs. Blood-borne person-to-person and intrauterine transmission have been reported.INCUBATION PERIOD:
Humans: 1-15 days. Animals.Unknown.CLINICAL FEATURES:
Humans. Sudden onset of fever lasting for 3-5 days ends with a crisis. Then a febrile period of 2-4 days is followed by one to ten or more recurrences of fever accompanied by severe headaches, nausea, vomiting, diarrhoea, jaundice and sometimes a macular rash with bleeding due to thrombocytopenia. Meningitis and cranial nerve involvement are possible. Animals. Arthritis and fever predominate in infected dogs. The arthritis recurs and may progress to chronic deformity.PATHOLOGY:
Humans. Many lesions occur, including enlarged, soft, infarcted spleen, hepatomegaly, hemorrhages in bone marrow and skin, myocarditis, bronchopneumonia, and meningitis. Animals. Arthritis, especially of the phalangeal joints, occurs with the possibility of progression to fibrosis of the joint capsule and ankylosis.DIAGNOSIS:
Humans. Identify borrelia in thick blood smears. Otherwise isolate the pathogen by inoculation of blood into susceptible animals if possible. Animals. Inoculate blood or tissues into rats or mice.PROGNOSIS:
Humans. The fatality rate is up to 40 per cent. Animals. Although fatality is uncommon, the lesions tend to be progressive.PREVENTION:
Humans and animals. Control tick vectors and prevent tick bites.TREATMENT:
Humans. A single dose of tetracycline or erythromycin, 0.5 g orally, or a single dose of procaine penicillin G, 600,000 units intramuscularly, probably constitutes adequate treatment for louse-borne relapsing fevers. Because of higher relapse rates, tick-borne disease is treated with 0.5 g of tetracycline or erythromycin given 4 times daily for 5-10 days. Jarisch-Herxheimer reactions may occur and respond to aspirin given every 4 hours. Pretreatment with steroids is not effective in preventing this reaction. Animals. Tetracycline, penicillin, erythromycin, and ceftriaxone at standard dosages for 21-28 days.LEGISLATION:
Humans.Louse-borne relapsing fever is notifiable to the World Health organization. Tick-borne infection may be notifiable in some countries (e.g. the UK). Animals.None.(In humans: Mediterranean fever, undulant fever, Malta fever. In animals: contagious abortion, epizootic abortion, Bang's disease)
AGENT:
Brucella abortus: cattle, sheep Brucella canis: dogs Brucella melitensis: sheep, goats Brucella suis: swineRESERVOIR AND INCIDENCE
Of the above species, Brucella canis is most likely zoonotic agent in the lab animal facility due to the extensive use of random source and lab bred dogs, in contrast to use of large domestic animals. Prevalence: 1 to 10% in dogs, throughout the U.S. B. canis is well adapted to dogs, and is not the subject of a large scale eradication program in the general dog population, as Brucella has been in other animals. Human brucellosis due to B. canis is uncommon but can be acquired from dogs; most cases resulted from contact with aborting bitches. In 1988, the CDC noted 96 cases of brucellosis reported in the U.S.: 22 from Texas and 20 from Calif.TRANSMISSION:
Ingestion of unpasteurized milk Lab accidents Poorly defined transmission cycle in zoonotic diseases: contact with infected animals especially aborted fetuses, fluids or membranes, or urine. Possibly airborne.DISEASE IN ANIMALS:
abortions are followed by immunity, though carrier state persists especially with secretions from the udder. infertility, testicular abnormalities, poor semen quality in dogs. inapparent infection may be common, as indicated by seropositivity.DISEASE IN MAN:
Lymphadenopathy, splenomegaly, fever, headache, chills, orchitis, weakness, nausea, weight loss. The chronic form may assume an undulant nature, with periods of normal temperature between acute attacks; symptoms may persist for years, either continuously or intermittently. Antibiotics can effect a cure within one year in about 80% of cases. Case fatality if untreated is less than 2%.DIAGNOSIS:
Rapid slide agglutination test is available. Blood culture and additional serologic tests used to confirm slide test results.TREATMENT:
Single-drug regimens are not recommended because the relapse rate may be as high as 50%. Combination regimens of two or three drugs are more effective. Either (1) doxycycline plus rifampin or streptomycin (or both) (2) trimethoprim-sulfamethoxazole plus rifampin or streptomycin (or both) are effective in doses for 21 days. Longer courses of therapy may be required to cure relapses, osteomyelitis, or meningitis.PREVENTION\CONTROL:
Quarantine and test Disposable gloves Chlorine, organic iodine, quaternary ammonium compounds are rapid bactericidal agents.CALIFORNIA ENCEPHALITIS/LA CROSSE ENCEPHALITIS
(USA) (Tahyna virus [Europe]) A mild, febrile, viral disease which occasionally causes severe encephalitis. It is transmitted by mosquitoes from small wild mammals, mainly in summer, to persons frequenting woodland areas of the USA and Canada, and certain European countries such as Yugoslavia and the USSR. The causative agents are the California encephalitis group of viruses (Bunyaviridae). There is no vaccine.RESERVOIR AND MODE OF TRANSMISSION:
The virus cycles amongst small wild animals (e. chipmunks, squirrels, rabbits and hares) and a variety of mosquito species. The infection can be maintained independently over several years by transovarial transmission in the mosquito. Humans are accidental hosts infected by mosquito bite during occupational or recreational activities in wooded areas. Accidental infections from laboratory accidents have occurred.INCUBATION PERIOD:
Humans. 5-15 days. Animals. Unknown.CLINICAL FEATURES:
Humans. Symptoms lasting about 5-10 days range from fever and headache with nausea and vomiting to fits and signs of aseptic meningitis, encephalitis and neurological sequelae. Animals. Unknown but assumed subclinical.PATHOLOGY:
Humans. Encephalitis. Animals. Unknown.DIAGNOSIS:
:Humans. The virus may sometimes be isolated from blood or rarely, from cerebrospinal fluid. Serologic tests of blood or cerebrospinal fluid may be diagnostic in specific types of encephalitis (by demonstrating virus-specific IgM or a fourfold change in complement-fixing or neutralizing antibodies). Animals. Impracticable.PROGNOSIS:
: Humans. In humans, fatality is rare but neurological defects may persist. Animals. Thought to be subclinical.PREVENTION:
Humans. Prevent mosquito bites. Control the mosquito vector. Apply laboratory safety procedures. Animals. Impracticable.TREATMENT:
Humans. Vigorous symptomatic therapy. Such measures include reduction of intracranial pressure (Mannitol), monitoring of intraventricular pressure, the control of convulsions, maintenance of the airway, administration of oxygen, and attention to adequate nutrition during periods of prolonged coma. Animals. Not applicable.LEGISLATION:
Humans. Acute encephalitis is notifiable in many countries, including the USA and the UK. Animals.None.(Vibriosis, vibrionic abortion)
AGENT:
Campylobacter (Vibrio) fetus ss. jejuni, a gram negative, microaerophilic, curved, motile rod that is worldwide in distribution.RESERVOIR AND INCIDENCE
Isolated from laboratory animals including dog, cat, hamsters, ferrets (>60 % in one study), nonhuman primates, rabbits, swine, sheep, cattle, and birds Although most cases of human campylobacteriosis are of unknown origin, infection after contact with sick animals has been well documented. *In most reports of pet to human transmission of C. jejuni, diarrheic puppies or kittens from pounds have been the source of infection. Pet birds, chickens, and kittens are implicated in other reports. A lab animal technician developed Campylobacter enteritis after feeding and cleaning up after a recently imported nonhuman primate. The organism was first isolated from nonhuman primates from Macaca fascicularis in 1979 and has since been reported in baboons, rhesus, patas, and marmosets. Can be shed for long periods of time in stool by asymptomatic carriers. Younger animals seem more likely to acquire the infection and hence may more commonly shed the organism.TRANSMISSION:
Transmission is thought to occur by the fecal-oral route, through contamination of food or water, or by direct contact with infected fecal material. The organism has also been isolated from houseflies. At 40 C the organism is viable for three weeks in feces and milk, four weeks in water, and five weeks in urine. Campylobacter is shed in the feces for at least six weeks after infection. Infected children may transmit infection to puppies or kittens, which may then expose other children. Poultry and cattle are the main reservoirs for human infection, which is acquired by ingesting contaminated raw milk, undercooked chicken or other food contaminated in the kitchen.DISEASE IN NONHUMAN PRIMATES:
Variable. the majority are asymptomatic carriers. Mild to severe enteritis may be seen accompanied by fever, vomiting, and mucus and blood in the feces. Bacteremia may occur complicated by meningitis or abortion. Most signs appear 1 to 7 days after exposure and affect primarily the jejunum, ileum, and colon.DISEASE IN FERRETS:
Asymptomatic to proliferative colitis. Shed organisms for long period of time (> 16 weeks).DISEASE IN OTHER ANIMALS:
Has also been shown to cause hepatitis in poultry, proliferative ileitis in hamsters, and abortion in ruminants. In all animals, it may be associated with diarrhea, especially when acting secondarily to virus infection.DISEASE IN MAN:
Acute gastrointestinal illness, diarrhea with or without blood, abdominal pain, and fever. It may cause pseudoappendicitis and, rarely, septicemia and arthritis. Usually a brief, self-limiting disease. In humans the asymptomatic carrier state is rare. Reinfection is possible in both animals and man.DIAGNOSIS:
1. Rapid diagnosis is done with dark field or phase contrast microscopy of fecal material.2. This is confirmed by stool culture which requires a special selective growth media(CAMPY-BAP) and incubation at 43oC with 10% CO2, 5% O2 and 85% Nitrogen.
3. Warthin Starry stain and histo
4. Various techniques are being used to detect seroconversion to the antigens of Campylobacter.
TREATMENT:
Animals can be treated based on culture and sensitivity. Currently erythromycin is the drug of choice, but does not eliminate the carrier state. Tetracycline or ciprofloxacin are alternatives.PREVENTION\CONTROL:
Vaccines provide partial protection of short duration and routine use is not recommended. Control is aimed at isolation of affected individuals and personal hygiene. An increased awareness of the potential of infection due to Campylobacter is of primary importance. Thoroughly cook all foodstuffs derived from animal sources, particularly poultry. Recognize, prevent, and control Campylobacter infections among domestic animals and pets. Wash hands after handling poultry and animal feces.CAPILLARIASIS
AGENT:
The causative agents are Capillaria hepatica (hepatic form), C. philippinensis (intestinal form) and C. aerophila (respiratory form).RESERVOIR AND INCIDENCE
C. hepatica and C. aerophila are very rare infections with isolated cases reported from North, Central and South America, Asia, and Europe. C. philippinensis is endemic in certain areas of the Philippines and cases have been reported from Thailand and Japan. Humans are the reservoir for C. philippinensis. With C. hepatica, rodents are the reservoirs. Cats and dogs are the reservoir for C. aerophila. Peromyscus maniculatus and Cletheronomys gapperi are the major hosts in North America.TRANSMISSION:
Humans are infected by eating raw fish containing infective larvae. The worm parasite lives in the intestines of humans and autoinfection occurs. Human feces contain large numbers of ova which contaminate watercourses and infect freshwater fish. Humans may be infected by the ingestion of ova in the soil also.DISEASE IN ANIMALS:
Infection with C. aerophila causes coughing, sneezing, and nasal discharge in dogs, cats, and foxes. Worms of C. hepatica mature and deposit eggs in liver tissue causing a local chronic inflammatory response in mice and rats.DISEASE IN MAN:
C. hepatica: acute and subacute hepatitis. The liver lesions consist of enlargements with foci of granulation tissue containing worms and ova. C. philippinensis: progressive weight and protein loss due to diarrhea and malabsorption. The jejunal villi are obliterated with massive accumulations of worms and ova. C. aerophila: fever and coughing. Worms present in epithelial lining of respiratory tract causing pneumonitis.DIAGNOSIS:
Liver or intestinal biopsy, necropsy, clinical signs & symptoms. Fecal exam for ova, larva, or adults.TREATMENT:
Albendazole, Thiabendazole, Mebendazole.PREVENTION/CONTROL:
Do not eat uncooked fish and other aquatic animal life in endemic areas. Control rodents and improve hygiene. Prevent pica. Sanitary disposal of feces.AGENT:
Capnocytophaga canimorsus (formerly Dysgonic fermenter-2), a recently described aerobic, gram negative bacillus with unusual fermentation pattern.RESERVOIR AND INCIDENCE
Found as part of oral flora of normal dogs and cats. C. canimorsus has been isolated from the mouths of 24% and 17% of normal dogs and cats respectively. Serious infections in man are most commonly reported in splenectomized or immunocompromised people, alcoholics, or persons who have chronic respiratory disease. More than 40 cases reported, many fatal, since first reported in 1976.TRANSMISSION:
Contact, bite or scratch from dog or catDISEASE IN MAN:
Can lead to cellulitis and overwhelming bacteremia, meningitis, endocarditis, septic arthritis, and DIC. The organism appears to have an affinity for the eye, causing angular blepharitis and severe keratitis. Accidental corneal inoculation occurred during a tooth extraction in a Poodle causing severe refractory keratitis in a veterinarian. The predisposition of the cornea to infection may be due to its avascularity and to the low concentrations of immunoglobulins and complement components in the tissue. Most serious disease and fatalities have occurred in splenectomized people. Case fatality rates of 4-27% have been reported.DIAGNOSIS:
History, clinical signs, and culture. ORGANISM IS SLOW GROWING. May require 8 days of incubation. Micro exam of blood smear or buffy coat with gram stain to detect organisms.PREVENTION/CONTROL:
Awareness, especially of high risk individuals Treatment of bite wounds, Penicillin G. (Treatment of high risk people even without sign of infection recommended.)
CAT SCRATCH DISEASE
(Cat Scratch Fever, Benign Lymphoreticulosis, Benign nonbacterial Lymphadenitis, Bacillary Angiomatosis, Bacillary Peliosis Hepatis)AGENT:
Controversial, it is not currently possible to definitively name the causative agent responsible for CSD. Felt to be either Afipia felis, a gram-negative rod or Rochalimaea henselae and Rochalimaea quintana. Both are members of class Proteobacteria and both are intracellular parasitic bacteria.RESERVOIR AND INCIDENCE
Associated with domestic cats throughout the USA, and worldwide. Over 6000 cases annually. Seen more often in men than in women . Have seen clusters of infection within families within a 2 to 3 week period, suggesting that shedding by cats may occur periodically. Other sources of infection have included scratches from other species including dogs, squirrels, and goats and from wounds induced by crab claws, barbed wire, and plant material.TRANSMISSION:
90% of patients have been exposed to a cat. 75% of these have been bitten, scratched, or licked. Most affected individuals are <20 years of age. 75-80% of the cases of CSD are diagnosed between September and February with a peak incidence in December. 4 to 6% of the general population and 20% of veterinarians have positive skin test reactions to CSD antigen.DISEASE IN ANIMALS:
SubclinicalDISEASE IN MAN:
Different distinct syndromes exist:Typical CSD
A primary lesion, most common on neck or extremities, will develop in 50% of the cases and appear approximately 10 days after a bite or scratch. A pustule persists for 1-2 weeks. 10-14 days after the lesion appears, lymphadenopathy develops and usually regresses within 6 weeks. 30-50% of the enlarged nodes become suppurative. Of the approximately 65% who develop systemic illness, fever and malaise are the symptoms most often noted. The disease is usually benign and most patients recover spontaneously without sequelae within 2-4 months. Many unrecognized cases probably occur. Disease appears to confer lifelong immunity.Atypical CSD
The atypical forms of CSD, which constitute 11% of all cases, are extremely varied. The most common, representing 6% of all cases, is Parinaud's oculoglandular syndrome (POGS), or granulomatous conjunctivitis with preauricular adenopathy. Other, atypical presentations include tonsillitis, encephalitis, cerebral arteritis, transverse myelitis, radiculitis, granulomatous hepatitis and/or splenitis, osteolysis, atypical pneumonia, hilar adenopathy, pleural effusion, erythema nodosum, erythema annulare, maculopapular rash, thrombocytopenic purpura, and breast tumor. Bacillary Angiomatosis Dermal BA presents in several ways. The commonest form is an enlarging red papule with some resemblance to a cranberry, often with a collarette of scale and sometimes with a suggestion of surrounding erythema. This type of lesion may be mistaken for pyogenic granuloma, unless fairly deep biopsy specimens are examined. These lesions begin as small papules and enlarge, occasionally becoming several centimeters in diameter and rarely ulcerating. They may be single or quite numerous. Another form of dermal BA is a deeper, subcutaneous nodule that appears flesh-colored and may be either fixed to subcutaneous tissues or freely mobile. Rarely BA may present as a dermal plaque. BA has been reported to occur in every organ system, including the brain, and is often difficult to differentiate from mycobacterial and fungal infections or malignancy without the use of biopsy. It is unclear if the personality changes, ranging from frank psychosis to depression, that have been described in association with BA represent CNS involvement or a neurotoxic product of this infection. Bacillary Peliosis Hepatis BPH, a vasoproliferative condition involving the liver of HIV-infected patients, is characterized by a proliferation of cystic blood-filled spaces surrounded by fibromyxoid stroma in which one can see bacteria similar to those seen in BA. Clinically these patients may or may not have visible bacillary angiomas. Their symptoms usually include fever, weight loss, and abdominal pain or fullness. Physical exam may reveal organomegaly. Laboratory studies usually demonstrate elevation of alkaline phosphatase and -glutamyltransferase levels out of proportion to those of aminotransferase and bilirubin.DIAGNOSIS:
The sedimentation rate is elevated, the white blood cell count normal, and the pus from the nodes is sterile. ID skin testing with antigen prepared from the pus is positive. Excisional biopsy, usually performed to exclude lymphoma, confirms the diagnosis.TREATMENT:
For CSD: Rifampin, ciprofloxacin, gentamycin, and trimethoprim-sulfa. Aspiration of suppurating nodes is recommended for relief of pain. Symptoms resolve without treatment in 2-4 months. BA and BPH respond to erythromycin, rifampin, or doxycycline. Therapy must be continue for 4-6 weeks to avoid relapse.PREVENTION/CONTROL:
Education. Wash hands after handling cat. Wash cuts and scratches promptly and don't allow cat to lick open wound.Cheyletiella Cheyletiella spp mites (Cheyletiellosis, Cheyletosis, "Walking Dandruff")
This article is taken from the Boxer Parade Magazine, Summer 1979 Vol 2 Issue 1
Although 5 different species
of Cheyletiella have been differentiated on the basis of minute morphological
detail, the species most often referred to as C. parasitivorax (the rabbit fur
mite). Cheyletiella spp have been reported from: rabbits, squirrels,
birds, dogs, cats and man. Cheyletiella dermatitis is a mild, nonsuppurative
mite-induced dermatitis produced by Cheyletiella spp. living on the surface of
the skin. Significant Facts easily identified by 3 characteristics
- very heavy thick pedipalps, each armed with a heavy "claw". (gives the appearance of an extra pair of legs)
- comb-like appendage on the end of each foot (not claw)
- prominent peritremes (of respiratory function, look like "fish gills")
LIFE CYCLE:
| EGG | LARVA | NYMPH I | NYMPH II | ADULT |
| white, attached by fine
cocoon to base of hair Hatches in 4 days |
(6 legs) Whire, 7 1/2 days |
(8 legs) White, 4 1/2 days |
(8 legs) White to Yellow, 5 days |
(8 legs) Yellowish, moves rapidly 14 days |
- all stages occur on the host
- adult female mite fastens eggs to hair (like louse nits)
- egg hatches in about 4 days (six legged larva)
- after moulting larva becomes eight-legged nymph
- nymph moults again to adult form
- complete cycle takes 3 to 4 weeks
BEHAVIOR OF THE MITES:
- non burrowing obligatory mite
- live in the keratin layer of the dermis
- not associated with hair follicles
- very active movement in dermal debris
- when feeding, attaches firmly at 30" angle and engorges on a clear colourless fluid
- thought at one time to feed on other mites leg. Demodex) and hence the name C. parasitivorax
- repeated attempts to demonstrate this have failed and there is no indication that Demodex sp, or any other ectoparasite is attacked
- off host survival is poor
The mites do not burrow but live in the keratin layer of the epidermis and are not associated with hair follicles. They move about rapidly in pseudotunnels in dermal debris, but periodically attach firmly to the epidermis, pierce the skin with their styletlike chelicerae and become engorged with a clear colourless fluid (Foxx and Ewing, 1969).
CLINICAL SIGNS:
- usually subclinical in rabbits and cats
- extremely irritating to dogs and man
- persistant pruritis with scurfiness
- trauma of scratching may result in denuded lesions all over the body
- one case reported excessive surfy dandruff but an otherwise normal appearing coat in a litter of five Sealyham terriers
On puppies it is usually found in the rump region. Infestation spreads over the back and head but eventually much of the body is affected. Cats tend to have milder, more diffuse lesions and are remarkably free of pruritus. The cat's daily licking and washing probably remove many mites. Affected animals have excessively scurfy, slightly oily coats. The white (or yellowish) mites and eggs together with the keratin scales produced by the epidermal reaction produce an appearance of severe "dandruff'. Except for the scaling there is remarkably little skin reaction per se.
DIAGNOSIS:
- routine skin scraping
- mites clear well and preserve in Berlese medium
- sometimes find mites during routine microscopic examination of sodium nitrate fecal floatations, especially in cats where there may be many mites with no obvious clinical signs closer skin examination in these cases may reveal many characteristic Cheyletiella sp mites.
TREATMENT:
Since all available references indicate success with a variety of insecticide treatments it appears as if the mite is highly susceptible to many chemicals. Removal of the mites has been reported with the topical use of Led-O-Sen, sulphur, benzyl benzoatelindone solutions, and organo phosphate dips.Thorough treatment of all animals on the premises is necessary. Malathion, ronnel, lindane or carbaryl will be effective for dogs Pyrethrins, rotenone powder or limi-sulfur dips may be used safely on cats or rabbits. Treatment should be repeated three times at weekly intervals.
Although mites do not live very long off the host, a strong effort should be made to physically clean the premises, improve sanitation practices and spray the area thoroughly at least once with a good residual insecticide.
Promising results in control have been obtained by hanging appropriate numbers of dichlorvos fly strips in the general kennel area of pet shops with severe infestations.
All new animals should be carefully inspected and dusted or sprayed with an insecticide before being added to colony housed animal facilities.
CHEYLETIELLA SP INFECTION IN MAN:
- mite commonly transmits from animal to man
- human infestation may occur either by direct skin contact between man and animal or through clothing
- most common site of infection is arms and torso
- causes a very irritating itchy dermatitis
- any insecticidal preparation for external parasites of man is likely effective in treatment leg. Lindane lotion- "Kwellada")
REFERENCES:
Carroll, H. F.: Cheyletiella dermatitis. In Kirk, R. W. (ed.): Current Veterinary Therapy V. W. B. SaundersCompany, Philadelphia, 1974. Soulsby, E. I. L.: Helminths, Arthropods and Protozoa of Domesticated Animals. The Williams 6. Wilkins Company, Baltimore, 1968.
(Ornithosis, Parrot Fever, Chlamydiosis, Psitticosis)
AGENT:
Obligate,intracellular organism with a unique development cycle and worldwide distribution Genus Chlamydia has only four species, many strains 1. Chlamydia trachomatis- humans, mice (Zoonotic potential not known) 2. Chlamydia psittaci- BIRDS, Mice, g. pig, rabbits, cats, frogs, ruminants 3. Chlamydia pneumoniae- humans 4. Chlamydia pecorum- ruminantsRESERVOIR AND INCIDENCE
The mammalian strains appear to be a zoonotic problem only rarely. 2 cases of human conjunctivitis reported from close association with cats with chlamydial pneumonitis and conjunctivitis. Birds are the main reservoir of human infection, however, 25% of human cases have no history of avian contact. Ovine strains may infect pregnant women.TRANSMISSION:
Inhalation; dry feces produce highly infective aerosols Direct contact with feces or respiratory secretions May survive in dust for several months.DISEASE IN ANIMALS:
There are many strains of C. psittaci which produce a diverse disease spectrum in animals, e.g., conjunctivitis, air sacculitis, pericarditis, hepatitis, meningoencephalitis, enteritis, urethritis, arthritis, and endometritis with abortion. G.I. infection results in enteric shedding of the organism. Latency - Well recognized feature of Chlamydia infection, i.e., the organism can cause inapparent infection or fulminant infection in the same host. In clinically healthy birds, stress can precipitate clinical signs and shedding of the organism.DISEASE IN MAN:
Asymptomatic or clinical disease after 1-2 week incubation period. Fever, chills, myalgia, anorexia, headache, nonproductive cough. Pneumonitis or atypical pneumonia may be present. May see a toxic or septic form with hepatosplenomegaly, hepatitis, meningoencephalitis and cardiac involvement with endocarditis. Ovine chlamydial infection in pregnant women is life-threatening, causing late abortion and neonatal death and disseminated intravascular coagulation in the mother.DIAGNOSIS:
Fecal culture (rarely successful) serology (CF, IFA) [Note: African Grey Parrot, cockatiel, and budgie may remain serologically negative despite active infection.] ELISA-based tests for antigen in feces has proven reliable.TREATMENT:
Tetracycline or Erythromycin.PREVENTION/CONTROL:
Treatment with tetracycline Introduce birds into colony from psittacosis-free flocks or use chlortetracycline chemoprophylaxis. Protective clothing (masks, gowns, gloves). Wild caught birds should be placed on chlortetracycline during quarantine. In sheep, keep flocks closed or vaccinate annually. Isolate aborting ewes until discharges cease.
CLOSTRIDIAL INFECTIONS
(Clostridial myositis: black leg, malignant edema, gas gangrene. Enterotoxemia: pulpy kidney, struck, lamb dysentery, braxy. Tetanus: lockjaw)AGENT:
Clostridium tetani (horses)--tetanus Clostridium perfringens (cattle, sheep)--gas gangrene Clostridium septicum (cattle) malignant edemaRESERVOIR AND INCIDENCE
Clostridia are normal intestinal flora and also survive by spores in the soil.TRANSMISSION:
Infection may be by contamination of deep, penetrating wounds to cause tetanus, by ingestion of preformed toxin or spores which vegetate in the digestive tract to cause enterotoxemia, or by ingestion of spores which are carried by the blood to muscles where they remain dormant until activated by trauma to produce necrotizing myositis. C. perfringens food poisoning is due to spore contamination of foods which survive heating to vegetate in unrefrigerated conditions. Neonatal tetanus in humans is frequently caused by contamination of the umbilicus.DISEASE IN ANIMALS:
Tetanus: as in humans. In myositis (black leg) cases a limb is still and painful with crepitus on palpation. Signs of toxemia. Rapidly fatal. C. chauvoei, novyi, and septicum toxins produce massive muscle necrosis, often with edema and SC gas formation. C. perfringens causes a variety of profound toxemias with cloudy swelling of parenchymatous organs and excess fluids, often bloodstained in serous cavities.DISEASE IN MAN:
Tetanus: painful toxic contractions of muscles and trismus. The case fatality rate for tetanus is 30-90% even when treated. Gas gangrene: fever, toxemia, painful edema spreading from the edges of wounds, interstitial emphysema, neck stiffness. Food poisoning: vomiting and diarrhea of a few days' duration.TREATMENT:
Myositis: penicillin, adequate surgical debridement and exposure of infected areas. Tetanus: immune globulin, penicillin, mechanical ventilation. Spasms are controlled with chlorpromazine or diazepam combined with a sedative.PREVENTION/CONTROL:
immunization with toxoids (good for 10 years), proper treatment of wounds. Good food hygiene is essential. In animals, prevent wound contamination during lambing, shearing, castration and docking.COLIBACILLOSIS
(Colibacteriosis, colitoxemia, white scours, gut edema of swine)AGENT:
Escherichia coli are gram-negative, aerobic, and facultatively anaerobic medium-sized rods.RESERVOIR AND INCIDENCE
Worldwide; some endemic areas exist in developing countries.TRANSMISSION:
Some serotypes are species-specific, others are not. Milk, milk products, and meat products can contain pathogenic serotypes. Foods of animal origin and contact with dogs and cats have been indicated as sources of infection for children.DISEASE IN ANIMALS:
Calf diarrhea (white scours) is an acute disease causing mortality in calves less than 10 days old. It manifests itself as serious diarrhea, with whitish feces and rapid dehydration. Mastitis caused by E. coli appears especially in older cows with dilated milk ducts. A long-term study of horse fetuses and newborn colts found that close to 1% of abortions and 5% of deaths of newborns were due to E. coli. Neonatal enteritis caused by E. coli in suckling pigs begins 12 hours after birth with a profuse watery diarrhea, and may end with fatal dehydration. Edema in suckling pigs (gut edema) is an acute disease that generally attacks between 6 and 14 weeks of age. It is characterized by sudden onset, incoordination, and edema of the eyelids, the cardiac region of the stomach, and sometimes other parts of the body. During septicemic diseases of fowl, such as cases of salpingitis and pericarditis, pathogenic serotypes of E. coli have been isolated. A colibacillary etiology has also been attributed to Hjarre's disease (coligranuloma), which is a condition in adult fowl characterized by granulomatous lesions in the liver, cecum, spleen, bone marrow, and lungs.DISEASE IN HUMANS:
The enterotoxigenic stains (ETEC) cause profuse and watery diarrhea, abdominal colic, vomiting, acidosis, and dehydration. Enteroinvasive strains cause a dysenteric syndrome with mucoid diarrhea, at times tinged with blood. E. coli is also an important agent of urogenital infections.DIAGNOSIS:
Stool culture or immunoassays for enterotoxins.TREATMENT:
Ciprofloxacin or trimethoprim-sulfa.PREVENTION/CONTROL:
With respect to man, control measures include: a) personal cleanliness and hygienic practices, sanitary waste removal and b) protection of food products. Vaccines for swine and bovine have been developed.CONTAGIOUS ECTHYMA
(Orf, Contagious pustular dermatitis, Contagious Pustular Stomatitis, Ecthyma Contagiosum)AGENT:
Genus Parapoxvirus of Family Poxviridae.RESERVOIR AND INCIDENCE
- Sheep and goats worldwide.TRANSMISSION:
- crusted areas on muzzle, eyelids, oral cavity, feet, or external genitalia are laden with virus. Transmitted easily from animals to man by contact. The virus is highly resistant to adverse environments and persists for many years.DISEASE IN ANIMALS:
necrosis in the skin and mucous membranes of the gastrointestinal and urogenital tracts. Intense pain can interfere with eating.DISEASE IN MAN:
Large painful nodules usually distributed on the hands. Weeping red surfaces. These resolve with minimum scarring 1-2 months later.DIAGNOSIS:
Diagnosis is made by a history of contact with sheep, goats, or wild ungulates; by EM demonstration of the poxvirus in the lesion; cell culture; or serologically.PREVENTION/CONTROL:
Wear rubber gloves when handling infected sheep and when working in an environment near infected sheep.DESCRIPTION:
The contagious virus responsible for Cowpox in cattle can also affect other species including humans, small wild mammals and cats. There is only one reported case of cowpox affecting a dog. Signs of the disease include skin lesions (nodules, scabs and ulcers), eye problems (conjunctivitis) and respiratory signs (pneumonia). Cowpox in cats occurs mainly in Europe and Asia.
CAUSE:
The cause of Cowpox is an orthopoxvirus. It is transmitted through a bite or skin wound and usually causes skin lesions, although respiratory and ocular signs may occur following viraemia. Cats are usually infected having caught infected rodents but direct transmission from cat to cat, or human to human can occur. In cattle transmission is via milkers hands or teat clusters on automated milking machines.The virus is resistant in the environment surviving many months under dry conditions.
BREED OCCURRENCE:
Dairy cattle are at greater risk than others.In cats there is no breed predisposition to infection, but predators (eg cats) that catch infected small wild animals (especially gerbils, ground squirrels, voles, wood mice) which act as a reservoir for the disease are at greater risk of contracting the disease.
SIGNS:
Typical signs of cowpox virus infection include :- Cattle
- Incubation period about 3-6 days
- Scabby pox lesions (1-2 cm) and ulcers on the teats and udder
- Most cows in a herd will be infected
- Secondary mastitis develops in some cases
- Calves - get lesions in the mouth
- Bulls - get lesions on the scrotum
- Cats
- Many infected cats may not show any signs.
- Widespread scabby skin lesions
- Sometimes a single scabby skin lesion
- Conjunctivitis occurs in some cats
- Mouth ulcers and vesicles occur in some cats
- Usual site of the skin lesions initially is the head, neck and foreleg, but generalised secondary nodules, ulcers and scabs form over a 4-5 day period and dry leaving bald patches which may or may not regrow hair.
- If viraemia occurs the cat may develop:
- Depression
- High body temperature
- Inappetance
- Diarrhoea
- Pneumonia if cat is immune-compromised - grave prognosis
- Painful skin - with scabby lesions - usually on the hands or face
- General malaise - if they are viraemic
- Fever
- Death - very rare
COMPLICATIONS:
Secondary bacterial infections can occur, and viraemia causes generalised disease.DIAGNOSIS:
Diagnosis can be made by :- Isolating Cowpox virus from scabs collected from skin lesions.
- Measuring blood antibodies (fluorescent antibody test)
TREATMENT:
Most cats and cattle recover without treatment.- There is no specific treatment for Cowpox virus, and no vaccine.
- Antibiotics may help to control secondary bacterial infections.
- The environment should be disinfected with hypochlorite solution (bleach)
PROGNOSIS:
In cattle the prognosis is good because it produces a mild, localized infection in most individuals.Good in cats with skin lesions and no viraemia, but poor if severely affected and pneumonia develops.
CRYPTOCOCCOSIS AND HISTOPLASMOSIS
Cryptococcosis and histoplasmosis are systemic fungal infections caused by the organisms Cryptococcus neoformans and Histoplasma capsulatum. Cases of infection are worldwide and sporadic. These organisms are found in soil, pigeons, and starlings and are spread in bird feces. These systemic fungi have a predilection for the lung and central nervous system. There is an increased susceptibility in humans on steroid therapy and with disorders of the reticuloendothelial system.AGENT:
Extracellular protozoal organisms - similar to coccidia. Genus: Cryptosporidium, it remains unsettled whether more than one species exists. Taxonomy of species somewhat controversial but considered to be infective across species lines.RESERVOIR AND INCIDENCE
Rodents, birds (particularly turkeys and chickens), ruminants, fish, reptiles, cats, dogs, rabbits, NHP's. Children over 2 years of age, animal handlers, travelers, homosexual men, and close personal contacts of infected individuals (families, health care and day-care workers) may be particularly likely to be infected. More than a dozen outbreaks have been reported in day-care centers around the world. Two major waterborne outbreaks have been documented. Cryptosporidium antibodies were detected in the serum of 20 of 23 cats (87%) suggesting that the exposure rate may be high.TRANSMISSION:
Fecal-oral transmission is from animals to humans or humans to humans; waterborne transmission is also important. Oocysts passed in stool are fully sporulated and infectious; infection occurs as a result of their ingestion. In humans and animals, the full life cycle occurs within a single host. The organisms attach to the microvillous borders of enterocytes of the small bowel and also are found free in mucosal crypts. The host cell membrane deteriorates, leaving the parasitic membrane in direct contact with epithelial cell cytoplasm. The organisms do not, however, invade the tissues.DISEASE IN ANIMALS:
Severe watery diarrhea in neonatal calves and lambs. In turkeys and chickens, the parasites are reported to occur in the sinuses, trachea, bronchi, cloaca, and bursa of Fabricius. The respiratory disease causes coughing, gasping, and airsacculitis. In reptiles, cryptosporidiosis is frequently reported in association with postprandial regurgitation. The organism affects the GI mucosa, resulting in marked thickening of the rugae and loss of segmented motility.DISEASE IN MAN:
In immunocompetent persons, infection varies from no symptoms to mild enteritis to marked watery diarrhea (up to 10 stools daily) without mucus or gross or microscopic blood. Low-grade fever, malaise, nausea, vomiting, abdominal cramps, anorexia and weight loss may occur. The infection is generally self-limited and lasts a few days to about 2 weeks. In immunologically deficient patients, the illness is characterized by profuse (up to 15L daily), cholera-like diarrhea and by fever, severe malabsorption, marked weight loss, and lymphadenopathy. In AIDS, infection may involve any part of the GI tract, and multisystemic involvement has been described, especially involving the respiratory tract.DIAGNOSIS:
Diagnosis is by detection of oocysts in stool by a variety of flotation or concentration methods or by mucosal biopsy, followed by special staining methods that use modifications of an acid-fast stain (routine fecal staining methods do not detect the organisms). Three stools should be examined over 5 days. A fluorescein-labeled IgG monoclonal antibody test has recently become available to detect oocysts.TREATMENT:
No successful treatment has been developed so far. Generally, no treatment other than supportive is needed in immunocompetent persons since it is self-limiting. In immunoincompetent persons, spiramycin, zidovudine (AZT), paromomycin, octreotide, and eflornithine have been reported of value.PREVENTION/CONTROL:
Personal hygiene. Careful handwashing by those in contact with any animals with scours.
(Creeping Eruption)
AGENT:
Caused by the larvae of the dog and cat hookworms, Ancylostoma braziliense and Ancylostoma caninum. A number of other animal hookworms, gnathostomiasis, and strongyloidiasis are rarely also causative agents.RESERVOIR AND INCIDENCE
Cutaneous Larval Migrans is prevalent throughout the tropic and subtropics. Human infection is common in SE U.S., particularly where people come in contact with moist sandy soil (e.g., beaches, children's sand piles) contaminated by dog or cat feces.TRANSMISSION:
Direct skin contact with larvae. soil to skin contact. contamination with animal feces.DISEASE IN ANIMALS:
Same as Ancylostomiasis.DISEASE IN MAN:
At the site of larval entry, particularly on the hands or feet, up to several hundred minute, intensely pruritic erythematous papules appear. Two to 3 days later, serpiginous eruptions appear as the larvae migrate at a rate of several millimeters a day; the parasite lies slightly ahead of the advancing border. The process continues for weeks or up to a year, and the lesions may remain severely pruritic, vesiculate, and become encrusted and secondarily infected. Without treatment, the larvae eventually die and are absorbed.DIAGNOSIS:
Presumptive - Characteristic clinical manifestations. Etiologic - ID of agent by biopsy in skin section but this is usually very difficult to achieve. Most cases are really not confirmed. No valid serodiagnostic tests currently available.TREATMENT:
Simple transient cases require no treatment. Albendazole or thiabendazole. Antihistamines and antibiotic ointments.PREVENTION/CONTROL:
Minimize contact (e.g., wear shoes!). Decontaminate environment: 10 lbs/ 100 sq ft. sodium borate - gravel/clay dog run; 1% sodium hypochlorite solution - cement dog run. Prevent environmental contamination. Public health education.CYTOMEGALOVIRUS DISEASE
Most cytomegalovirus infections in healthy individuals are asymptomatic, with the virus remaining (exact cells of latency are not known). However the virus is isolable from up to 25% of salivary glands, 10% of uterine cervices, and 1% of neonatal urine samples. Seroprevalence increases with age and the number of sexual partners; detectable antibody is present in the serum of most homosexual men. Transmission is sexual, congenital, through or transplantation, and person-to-person (e.g., day care centers). Severe disease occurs primarily in the immunocompromised, especially those with AIDS and transplant patients.DISEASE IN MAN:
A. Classification: There are three recognizable syndromes.1. Perinatal disease and cytomegalovirus inclusion disease-Intrauterine infection of infants whose mothers had a primary infection during pregnancy results in a neonatal syndrome of jaundice, hepatosplenomegaly, thrombocytopenia, periventricular central nervous system calcifications, mental retardation, motor disability, and purpura.
DIAGNOSIS:
confirmed by viruria within the first week after birth or serum IgM antibodies to cytomegalovirus. Hearing deficits occur in over 15% and mental retardation in up to 30%. Neonatally acquired disease may resemble mononucleosis; while it is often asymptomatic, neurologic deficits may ensue later in life.
2. Acute acquired cytomegalovirus infection--This syndrome, akin to EBV-associated infectious mononucleosis, is characterized by fever, malaise, myalgias and arthralgias (but not pharyngitis or respiratory symptoms), atypical lymphocytes, and abnormal liver function tests. Unlike EBV-associated infectious mononucleosis, the heterophil antibody is not found. Transmission can be by sexual contact, by milk, by respiratory droplets (probably) among nursery or day care center attendants, and by (usually massive) transfusions of blood.
3. Disease in immunocompromised hosts-Tissue and bone marrow transplant patients are at increased risk for CMV infection, especially in the first I 00 days after allograft transplantation. HIV-infected patients may have a variety of CMV manifestations. Cytomegalovirus is itself immunosuppressive and may worsen manifestations of HIV infection, including Pneumocystis carinii pneumonia. a. CMV retinitis-Retinitis due to CMV infection occurs primarily in AIDS patients. Screening for visual symptoms may be helpful, but ophthalmologic documentation of neovascular, proliferative lesions ("pizza-pie" retinopathy) is required for diagnosis. b. Gastrointestinal and hepatobiliary CMV-Serious gastrointestinal CMV disease occurs in AIDS and after organ transplantation, cancer chemotherapy, or steroid therapy. Esophagitis presents with odynophagia; small bowel disease may mimic inflammatory bowel disease or may present as ulceration or perforation. Colonic CMV disease causes diarrhea, hematochezia. abdominal pain, fever, and weight loss. Pancreatitis, when not due to pentamidine, didanosine, or (less often) zalcitabine is often due to cytomegalovirus; hepatobiliary involvement often includes other pathogens, including Cryptosporidium. Diagnosis is by mucosal biopsy that shows characteristic CMV histopathologic findings of intranuclear ("owl's eye") and intracytoplasmic inclusions. c. Pulmonary CMV-Pulmonary CMV infection occurs in about 15% of bone marrow transplant recipients: the mortality rate is 80-90% in this group. CMV seronegative blood products should be used in seronegative recipients of seronegative transplants. High-titer CMV immunoglobulins may be effective in preventing CMV pneumonia in the seronegative recipients. d. Neurologic CMV-Polyradiculopathy and encephalitis have been reported but are not common. When they do occur, there is often concomitant retinitis, which may be subclinical. Prolonged ganciclovir may be helpful, and treatment should be continued indefinitely.
DIAGNOSIS:
Cytomegalovirus is isolable from urine, cervical secretions, semen, saliva, blood, and other tissues, but virus isolation is most useful when combined with pathologic findings, including large cells with intranuclear and intracytoplasmic inclusions that resemble owl's eyes: cultures alone are of little use in diagnosing AIDS-related cytomegalovirus infections. Retinitis among aids patients is diagnosed clinically. The acute mononucleosis syndrome is associated with a lymphocytosis, often 2 weeks after the fever. Serologic tests (IFA and the anticomplement immunofluorescent antibody [ACIF]) are useful primarily in seroepidemiologic studies. In AIDS patients, titers may be depressed, and seroconversions are seldom documented, with most seroconversions having occurred in the past. Antigen detection by virus technology (including the polymerase chain reaction technique) must be interpreted in the context of clinical and pathologic findings.TREATMENT:
Two antiviral agents with efficacy against cytomegalovirus are ganciclovir, given in a dosage of 5 mg/kg IV every 12 hours for 14-21 days (maintenance: 5-7 mg/kg/day for 5 days each week, with dose reduction for renal impairment); and foscarnet, given as a loading dose of 20 mg/kg IV and then 60 mg/kg every 8 hours over 2 weeks (maintenance: 120 mg/kg/day). The induction phase is essential for AIDS patients with cytomegalovirus disease involving critical parts of the retina; for less critical areas, maintenance therapy can be used from the outset. Both agents are effective in preventing progression of retinitis, and ganciclovir is useful in cytomegalovirus colitis; treatment is usually lifelong in patients with AIDS. Complications include neutropenia with ganciclovir (preventing concomitant zidovudine therapy) and renal impairment with foscarnet (often manageable with hydration).CONTROL:
Cytomegalovirus hyperimmune globulin given to seronegative bone marrow or renal transplant recipients may be prophylactic. Limiting transfusions, using products filtered to remove leukocytes, and selecting cytomegalovirus-seronegative donors are all important in reducing the rate of cytomegalovirus transmission.(Ringworm, Dermatophytosis, Tinea, Trichophytosis, Microsporosis, Jock Itch, Athlete's Foot)
AGENT:
Organisms are subclassified into: 1. Geophilic - inhabit soil 2. Zoophilic - parasitic on animals 3. Anthropophilic - Primarily infects humans All can produce disease in humans. Grouped in three genera 1. Microsporum 2. Trichophyton 3. EpidermophytonRESERVOIR AND INCIDENCE
Fungal spores remain viable for long periods on carrier animals and fomites. Exposure to reservoir hosts harboring different dermatophytes determines the type and incidence of infection in humans. Microsporum canis can be carried by up to 89% of nonsymptomatic cats. Up to 50% of people exposed to infected cats, both symptomatic and asymptomatic, have acquired infection. Pets may also acquire disease from humans. **T. mentagrophytes is most commonly transmitted to man from rodents, M. canis from dogs and cats, and T. verrucosum from cattle and horses.TRANSMISSION:
Direct or indirect contact with asymptomatic animals or with skin lesions of infected animals Contaminated bedding Equipment Fungi in air, dust, or on surfaces of room (spores persist on contaminated surfaces)DISEASE IN ANIMALS:
In rodents is often asymptomatic and not recognized until people are affected. In cats is often asymptomatic. Dogs often show classic skin lesions. Varying severity of dermatitis occurs with local loss of hair. Deeper invasion produces a mild inflammatory reaction which increases in severity with the development of hypersensitivity.DISEASE IN MAN:
Often mild, self limiting; scaling, redness, and occasionally vesicles or fissures. Thickening & discoloring of nails. May show circular lesions which clear in the center forming a ring. Fungal infections in man are categorized as to the location on the body: 1. Tinea capitis - Scalp & hair 2. Tinea corporis - Body (extremities, arm and hand, are most often affected in infections acquired from lab animals.) 3. Tinea pedis - foot 4. Tinea unguium - NailsDIAGNOSIS:
KOH mount of skin scrapings, Fungal cultureTREATMENT:
Macerated (moist softening and fissuring) stage- aluminum subacetate ("Domeboro") solution soaks with potassium permanganate for secondary infections. Athlete's feet may respond better to 30% aqueous aluminum chloride or the carbol-fuchsin paint than to antifungal agents. Broad spectrum antifungal creams and solutions containing imidazoles or ciclopirox) instead of tolnaftate and haloprogin help to combat diphtheroids and other gram-positive organisms present at this stage and alone may be adequate therapy. Dry and scaly stage- several topical creams, liquids, or lotions are recommended (miconazole, clotrimazole, ketoconazole, econazole, sulconazole, oxiconazole, ciclopirox or naftifine. Betamethasone dipropionate with clotrimazole is recommended for acutely inflamed tinea lesions. For severe cutaneous infections, griseofulvin or ketoconazole is recommended.PREVENTION/CONTROL:
Screen newly received animals. Routine sanitization of contaminated environment, equipment, and caging. Gloves, protective clothing, wash hands after exposure.DERMATOPHILOSIS
(Streptotrichosis, Mycotic Dermatitis of Sheep)AGENT:
Dermatophilus congolensis. An aerobic actinomycete with gram positive long branching filaments and coccoid bodies.RESERVOIR AND INCIDENCE
Occurs in temperate regions worldwide. Natural disease described in horses, cattle, sheep, goats, cottontail rabbits, owl monkeys, lizards & humans.TRANSMISSION:
The etiologic agent is an obligate parasite that has been isolated only from lesions in animals. Human cases have arisen from direct contact with infected animals. The most common means of transmission between animals is mechanical thru arthropod vectors. The infection may also be transmitted by means of objects, such as plant thorns or shears.DISEASE IN ANIMALS:
Circumscribed areas of alopecia, elevated crusty papillomatous lesions, and exudative dermatitis. **Owl monkeys may have relapsing Dermatophilosis after apparently appropriate antibiotic regimens. Therefore organism may persist on pelage of animals after resolution of lesions. In cats, the lesions differ from those of other domestic animals by affecting deeper tissues. In cats, granulomatous lesions have been found on the tongue, bladder, and popliteal lymph nodes.DISEASE IN MAN:
pustular desquamative dermatitisDIAGNOSIS:
Microscopic exam of stained material from lesions and culture.PREVENTION\CONTROL:
1. Treatment with antibiotics2. Isolate affected animals
3. Protective clothing, gloves, personal hygiene
4. Tick control
DIPHYLLOBOTHRIASIS
(Fish tapeworm infection) A benign tapeworm infection of the small intestines caused by eating raw fish. The causative agents are Diphyllobothrium latum and D. pacificum (Cestoda). There is no vaccine. D. latum is common in northern temperate regions where the fish are eaten raw (e.g., in the Baltic countries, Finland and Canada/Alaska). D. pacificum is common in coastal South America, especially Peru.RESERVOIR AND MODE OF TRANSMISSION:
The definitive hosts of D. latum include humans, dogs and cats. For D. pacificum the natural reservoir is seals. Two intermediate hosts include a plankton crustacean and a freshwater fish. Gravid proglottids pass in the feces of the definitive host. The eggs hatch in lakes and waterways and then infect the crustacean. Freshwater fish consume these and the larvae encyst in the musculature. The fish, in their turn, may be eaten by larger fish which can still transmit the infection. Humans acquire the parasite by eating raw infected fish.INCUBATION PERIOD:
Humans. 3-6 weeks from ingestion to adult tapeworm. Animals. Unknown but presumably as for humans, in dogs and cats.CLINICAL FEATURES:
Humans. The condition is usually asymptomatic. Some patients develop vitamin B12 deficiency anemia. Massive infection may cause diarrhoea and intestinal obstruction. Animals. No clinical signs are seen in dogs and cats. Heavy infection with larvae can kill the fish intermediate host.PATHOLOGY:
Humans. The presence of the large tapeworm, 3 to 10 meters long, in the intestine can cause mechanical obstruction. Megaloblastic anemia occurs owing to vitamin B12 deficiency. Animals. Subclinical. In fish, myositis and possibly even death occur in heavy infestation.DIAGNOSIS:
Humans and animals. Identify characteristic eggs in feces.PROGNOSIS:
: Humans. Usually benign. Animals. Usually benign, but heavy infection may be fatal to fish.PREVENTION:
Humans and animals. Dispose of feces hygienically. Educate for proper cooking of fish. Freeze fish or salt cure before marketing.TREATMENT:
Humans and animals. Anthelmintics, especially niclosamide and praziquantel.LEGISLATION:
Humans and animals. None.AGENT:
Dipylidium caninum - common intestinal cestode of dogs. Gravid proglottids are "pumpkinseed" shaped.RESERVOIRS AND INCIDENCE:
Dogs, cats, and their wild counterparts. Arthropods serve as intermediate hosts. These include the dog flea (Ctenocephalides canis), the cat flea (C. felis), and dog louse (Trichodectes canis). Cosmopolitan including the U.S.TRANSMISSION:
Humans, dogs, and cats are infected by ingestion of arthropod intermediate hosts which harbor the cysticercoid larvae.DISEASE IN ANIMALS:
Usually no severe pathology. Possibly mild digestive problems or perianal pruritus.DISEASE IN MAN:
Slight symptoms, if any. Mild weight loss, perianal itching, diarrhea, vague abdominal pain.DIAGNOSIS:
Recovery of gravid proglottids that are passed in the feces or that crawl out of the anus.TREATMENT:
Niclosamide or praziquantel.PREVENTION/CONTROL:
Screen animals. Treat infected animals. Eliminate ectoparasites. Teach proper handling of pets to children.Volume 12, Number 12December 2006
Dispatch
Fatal Human Infection with Rabies-related Duvenhage Virus, South Africa
Janusz T. Paweska,* Lucille H. Blumberg,* Charl
Liebenberg, Richard H. Hewlett, Antoinette A. Grobbelaar,* Patricia A. Leman,*
Janice E. Croft,* Louis H. Nel, Louise Nutt, and Robert Swanepoel*
*National Institute for Communicable Diseases, Sandringham, South Africa; Durbanville
Mediclinic, Cape Town, South Africa; University of Stellenbosch, Tygerberg,
South Africa; and University of Pretoria, Pretoria, South Africa
Abstract
Duvenhage virus was isolated
from a patient who died of a rabieslike disease after being scratched by a
bat early in 2006. This occurred ≈80 km from the site where the only other
known human infection with the virus had occurred 36 years earlier.
The genus Lyssavirus within the family Rhabdoviridae currently includes rabies virus (RABV) (genotype 1) and 6 rabies-related viruses: 3 from Africa, Lagos bat virus (LBV) (genotype 2), Mokola virus (MOKV) (genotype 3), and Duvenhage virus (DUVV) (genotype 4); European bat lyssaviruses 1 and 2 (EBLV1 and 2) (genotypes 5 and 6); and Australian bat lyssavirus (ABLV) (genotype 7). Strains of RABV (genotype 1) undergo genetic adaptation to particular animal hosts so that within specific areas the disease is manifested and transmitted predominantly by 1 host species. The canid, or dog, biotype of RABV is the most widely distributed in the world. In South Africa, RABV is transmitted by dogs and jackals in the northern region of the country, by dogs in the eastern region where most cases of human rabies occur, and by bat-eared foxes in the western region. In addition, an indigenous herpestid biotype of RABV (genotype 1) is transmitted by mongooses (Herpestidae) on the interior plateau of South Africa. This biotype does not spread readily to dogs but causes occasional cases of rabies in dogs, cats, humans, and more frequently, cattle and sheep.
RABV (genotype 1) has never been isolated from bats outside North and South America, but rabies-related viruses have been isolated from bats elsewhere. In Africa, LBV and DUVV are associated with bats, but MOKV is uniquely associated with shrews and rodents, not bats. Fifteen isolations of LBV have been reported, including 8 from fruit bats and a cat in KwaZulu-Natal Province of South Africa, but the virus has never been associated with human disease. MOKV has been isolated from shrews, rodents, cats, and a dog in Africa and from 7 cats with rabies-like disease in KwaZulu-Natal and Eastern Cape provinces of South Africa. The virus is believed to have caused rabieslike disease in 2 persons in Nigeria in 1969 and 1971, shortly after its initial discovery in shrews in 1968, but no cases of human infection have subsequently been recognized. DUVV was discovered in 1970 when it caused fatal rabieslike disease in a person bitten by an unidentified insectivorous bat ≈150 km northwest of Johannesburg, South Africa. In 1981, the virus was isolated from what is believed to have been a Miniopterus schreibersi insectivorous bat caught in daylight by a cat in Makhado town (formerly Louis Trichardt) in Limpopo Province, South Africa, and in 1986 the virus was recovered from an insectivorous bat, Nycteris thebaica, trapped in a survey in Zimbabwe.
The Study
DUVV infection was recently confirmed in a 77-year-old man with type 2 diabetes who was scratched on the face by what appears to have been an insectivorous bat in February 2006 in North West Province, South Africa, ≈80 km from the location where the first DUVV infection occurred 36 years earlier. The bat flew into a room at night, landed on the man's spectacles while he was attempting to chase it out, and scratched his face as he brushed it off. The bat did not appear to have bitten him, and it escaped after the incident. He did not seek medical care, and thus no postexposure treatment was given. He became ill at home in Cape Town 27 days later and received treatment for influenzalike illness. He slept most of the following day, had hallucinations that night, and was admitted to a hospital on the third day of illness. On admission, he had a fever (40C), tachycardia, neck and general limb rigidity, hyperreflexia, facial fasciculation, and involuntary grimacing. Within 24 hours generalized tonic-clonic seizures had developed with status epilepticus supervening. These necessitated intubation, sedation, and mechanical ventilation. He died on day 14 of his illness.
Heminested reverse transcriptionPCR was performed as previously described with modified forward primer JW12. This procedure detected lyssavirus nucleic acid in saliva taken on day 10 of illness and in brain tissue collected postmortem. Nucleotide sequencing of the PCR products and phylogenetic analysis performed as previously described confirmed the identity of the agent as DUVV, and live virus was isolated from saliva and brain tissue by mouse inoculation. Immunofluorescence tests with antirabies conjugate prepared to be cross-reactive with the African rabiesrelated viruses (Onderstepoort Veterinary Institute, Pretoria, South Africa) showed small and sparse inclusion bodies in impression smears of the cortex, hippocampus, thalamus, medulla, and cerebellum. Histopathologic examination of sections from the cortex, hippocampus, thalamus, hypothalamus, midbrain, pons, medulla, and cerebellum showed polioencephalitis affecting predominantly the diencephalon and brainstem and involving varying degrees of neuronopathy, neuronal loss, astrocytosis, parenchymal and perivascular lymphocytic infiltration with CD45 immunopositivity, sparse macrophage activation, and axonal spheroid formation. No nuclear or cytoplasmic inclusions were observed.
Conclusions
The ability to distinguish between various lyssaviruses and monitor their relative distribution and prevalence has important implications for implementation of control measures. It was recognized in 1932 that mongoose-associated rabies in South Africa differs from classic dog rabies. Although an inadequately characterized lyssavirus was isolated from a bat trapped in a survey in 1963, before the existence of rabies-related viruses was known, awareness of lyssaviruses other than rabies viruses dates from the identification of DUVV in 1970 and was followed by detection of LBV and MOKV in South Africa. Routine differentiation of diagnostic isolates became feasible with the availability of monoclonal antibodies during the 1980s and the subsequent introduction of molecular epidemiology techniques. Although instances of persons seeking rabies prophylaxis after exposure to bats have been reported, the recent case of DUVV infection constitutes only the second known instance of a person in South Africa with lyssavirus infection after such an encounter. Nevertheless, it is clear that rabies-related viruses are widely endemic in South Africa and that active investigation of the bat-associated lyssaviruses is warranted.Dr Paweska is head of the Special Pathogens Unit, National Institute for Communicable Diseases, South Africa. His research interests include viral hemorrhagic fevers, rabies, and rabies-related viruses.
References
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Suggested Citation for this Article
Paweska JT, Blumberg LH, Liebenberg C, Hewlett RH, Grobbelaar AA, Leman PA, et al. Fatal human infection with rabies-related Duvenhage virus, South Africa. Emerg Infect Dis [serial on the Internet]. 2006 Dec [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol12no12/06-0764.htm
EBOLA
(African Hemorrhagic Fever)AGENT:
similar to Marburg morphologically similar but antigenically distinct. Both are RNA Filoviruses and have bizarre branching and filamentous or tubular forms shared with no other known virus group.RESERVOIR AND INCIDENCE
Reservoirs unknown. Monkeys are probably accidental hosts, along with humans. First recognized in 1976 in Northern Zaire and Southern Sudan, 500 cases with 350 deaths reported.TRANSMISSION:
Person-to-person transmission occurs by direct contact with infected blood, secretions, organs or semen. Nosocomial infections have been frequent; all Zaire cases acquired from contaminated syringes and needles died.DISEASE IN MAN:
Fever, headache, malaise, followed by chest discomfort, diarrhea, and vomiting. Case fatality rate is 50-90%.DIAGNOSIS:
IFA, ELISA, Western blot, EM, or virus isolation.TREATMENT:
Supportive Possibly immune serumPREVENTION/CONTROL:
Strict quarantine on newly imported, wild-caught primates. Naturally infected monkeys should become ill or die within several weeks. Hygiene ,sanitation, and protective clothing Isolation of human patients with prevention of sexual intercourse until semen is free of virus.ECHINOCOCCOSIS
(Hydatidosis, Hydatid Disease)AGENT:
Echinococcus granulosis - causes "cystic" disease. Echinococcus multilocularis - causes "alveolar" disease. E. vogeli - causes polycystic disease.RESERVOIR AND INCIDENCE
The definitive host for E. granulosis is a carnivore (all of which, except for the lion, are Canidae) that harbors the adult tapeworm in the small intestine. Human infection with E. granulosus occurs principally where dogs are used to herd grazing animals, particularly sheep. The disease is common throughout southern S. America, the Mediterranean and Middle East, central Asia, and East Africa. Foci of endemicity are in eastern Europe, Russia, Australasia, India, and the UK. In North America, endemic foci have been reported from the western USA, the lower Mississippi Valley, Alaska, and northwestern Canada. The life cycle for E. multilocularis involves foxes as definitive host and microtine (e.g., voles and meadow mice) rodents as intermediate host. Domestic dogs and cats can also become infected with the adult tapeworm when they eat infected wild rodents. The disease in humans has been reported in parts of central Europe, much of Siberia, northwestern Canada, and western Alaska. One case has been reported in Minnesota. The principle definitive host for E. vogeli is the bush dog; the main intermediate hosts are the paca and spiny rat. Domestic hunting dogs are also definitive hosts, and serve as an important source of human infection. Cases have been reported in South America.TRANSMISSION:
E. granulosis: Human infection occurs when eggs passed in dog feces are accidentally swallowed. E. multilocularis: Human infection is by accidental ingestion of tapeworm eggs passed in fox or dog feces.DISEASE IN ANIMALS:
Usually no clinical signs except for enteritis in heavy infestations. In sheep, hydatid cysts cause considerable condemnation of meat and loss of production.DISEASE IN MAN:
E. granulosis - Cystic hydatid disease A liver cyst may remain silent for 10-20 years or more until it becomes large enough to be palpable, to be visible as an abdominal swelling, to produce pressure effects, or to produce symptoms due to leakage or rupture. There may be right upper quadrant pain, nausea, and vomiting. The effects of pressure may result in biliary obstruction. If a cyst ruptures, anaphylaxis and death may result. If fluid and hydatid particles escape slowly, allergic manifestations may result. Rupture can occur into the pleural, pericardial, or peritoneal space or into the duodenum, colon, or renal pelvis. Dissemination of germinal elements may be followed by the development of multiple secondary cysts. Pulmonary cysts cause no symptoms until they leak; become large enough to obstruct a bronchus, or erode a bronchus and rupture. Brain cysts produce symptoms earlier and may cause seizures. Cysts in the bone marrow may present as pain or spontaneous fracture. The bones most often affected are the vertebrae and paraplegia may develop due to compression of the spinal cord. 20% of patients have multiple cysts. 15% of untreated patients eventually die. E. multilocularis - Alveolar disease The primary localization of alveolar cysts is in the liver, where they may extend locally or metastasize to other tissues. The larval mass has poorly defined borders and behaves like a neoplasm; it infiltrates and proliferates indefinitely by exogenous budding of the germinative membrane, producing an alveolus-like pattern of microvesicles. 90% of untreated cases die within 10 years. E. vogeli - Polycystic form of human hydatid disease. Symptoms are variable according to cyst size and location. The polycystic hydatid is unique in that the germinal membrane proliferates externally to form new cysts and internally to form septi that divide the cavity into numerous microcysts. Brood capsules containing many protoscolices develop in the microcysts.DIAGNOSIS:
Immunoblot assay.TREATMENT:
Currently the definitive treatment is surgical removal of cysts. Newly available chemotherapy (albendazole or mebendazole) may alter this position.PREVENTION/CONTROL:
In endemic areas, prevention is by prophylactic treatment of pet dogs with praziquantel and prevention of feeding dogs offal.(Tick-borne fever)
AGENT:
An intraleukocytic rickettsia, E. canis (many species of Ehrlichia exist. Previously only E. sennetsu was known to infect man). Occurs intracytoplasmically, singly or in compact clusters (morulae) in circulating leukocytes.RESERVOIR AND INCIDENCE
First recognized in dogs in 1935. Epizootic occurred in military working dogs in Vietnam 1968-1970. Now known to have worldwide distribution. 11 to 58% of dogs in U.S. are serologically positive. First reported case of E. canis in man in 1987. Several cases since then.TRANSMISSION:
tick vector, Rhipicephalus sanguineus, Brown Dog Tick. It is presumably transmitted to humans by tick bite.DISEASE IN DOGS:
Incubation period 10 to 14 days. Fever, lymphadenopathy, edema of legs and scrotum, epistaxis. Acute disease followed by a subclinical carrier stage.DISEASE IN MAN:
Similar to Rocky mountain spotted fever, but no rash. 12 to 14 day incubation period and prodrome consisting of malaise, back pain and nausea, the patient develops sudden fever, bradycardia, and headache. Leukopenia and absolute lymphopenia as well as thrombocytopenia occur frequently.DIAGNOSIS:
Not easy to identify in peripheral blood smears but can attempt to identify organisms in leukocytes. An IFA assay that may be used to diagnose infection is available thru CDC and requires acute and convalescent sera.TREATMENT:
TetracyclinePREVENTION/CONTROL:
Control ticksERYSIPELOID
(Rosenbach's erysipeloid, erythema migrans, erysipelotrichosis, rose disease in swine, diamond skin disease in swine, fish-handler's disease or fish rose in man)AGENT:
Erysipelothrix rhusiopathiae (insidiosa). 22 different serotypes are recognized. *Discovered by ROBERT KOCH==He called it the Bacillus of Mouse SepticemiaRESERVOIR AND INCIDENCE
Saprophyte in soil, water, and decaying organic matter. Pathogen in swine, lambs, calves, poultry, fish, & wild and lab mice. *Pigs probably represent the most likely source of exposure in the laboratory environment. (Natural disease or zoonotic transmission from lab rodents has NOT been reported.)TRANSMISSION:
contamination of wounds while handling infected tissuesDISEASE IN ANIMALS:
Diamond skin disease in pigs. Arthritis in sheep and swine. Cyanosis and hemorrhages in turkeys. Can be septicemic disease in many species.DISEASE IN MAN:
Disease in humans is called Erysipeloid, and is primarily occupation related. Inflammatory lesions of the skin, with elevated erythematous edge; spreads circumferentially. Septicemia is an infrequent complication.DIAGNOSIS:
Culture from lesion or bloodPREVENTION\CONTROL:
Treatment with Penicillin Gloves when handling animals Vaccine for swine and turkeysFILARIASIS
(Brugiasis)AGENT:
The commonest causative agent is Wuchereria bancrofti, which is not zoonotic. Brugia malayi is zoonotic. Dirofilaria immitis may occasionally infect humans.RESERVOIR AND INCIDENCE
B. malayi has been identified in Malaya and the Philippines. D. immitis occurs in dogs in North and South America, Australia, India, the Far East and Europe. Wild monkeys and felines are the reservoir for B. malayi.TRANSMISSION:
Transmission to humans is via the bite of a mosquito vector (Mansonia and Anopheles). These, on biting humans, release microfilariae on to skin which enter the body through the puncture wound and pass via the lymphatics to lymph nodes. The worms are viviparous, producing microfilaria. These appear in the blood and reinfect the biting insect.DISEASE IN ANIMALS:
D. immitis is found in the right ventricle of dogs and in the pulmonary artery. Mild infection causes no signs, but long continued infection leads to cardiac insufficiency with ascites and passive congestion.DISEASE IN MAN:
B. malayi: Repeated bouts of fever, lymphadenopathy, lymphangitis and abscesses occur. This leads to lymphatic obstruction and massive lymphedema followed by fibrosis (so-called elephantiasis) especially in the legs. D. immitis: Initial symptoms include cough, chest pain, or hemoptysis. However, the filariae die in the human pulmonary vasculature and consequently nodules have been found in the skin or as solitary 1-2 cm "coin" lesions in the periphery of the lungs.DIAGNOSIS:
Diagnosis is established by finding microfilariae in the blood. Serologic testing is available but false-positive and false-negative reactions occur.TREATMENT:
DiethylcarbamazinePREVENTION/CONTROL:
Diethylcarbamazine or Ivermectin can be given as a prophylaxis. Control vectors and avoid their bites. Prophylactic treatment of dogs.GIARDIASIS
Most common intestinal protozoan parasite of people in the U.S.AGENT:
Giardia lamblia Has both a cyst (infective) and trophozoite formRESERVOIR AND INCIDENCE
The parasite occurs worldwide and is nearly universal in children in developing countries. Humans are the reservoir for Giardia, but dogs and beavers have been implicated as a zoonotic source of infection. In psittacines, the disease is commonly found in cockatiels and budgerigars. Giardiasis is a well-recognized problem in special groups including travelers, campers, male homosexuals, and persons with impaired immune states. However, Giardiasis does not appear to be an opportunistic infection in AIDS.TRANSMISSION:
Only the cyst form is infectious by the oral route; trophozoites are destroyed by gastric acidity. Most infections are sporadic, resulting from cysts transmitted as a result of fecal contamination of water or food, by person-to-person contact, or by anal-oral sexual contact. After the cysts are ingested, trophozoites emerge in the duodenum and jejunum. They can cause epithelial damage, atrophy of villi, hypertrophic crypts, and extensive cellular infiltration of the lamina propria by lymphocytes, plasma cells, and neutrophils.DISEASE IN ANIMALS:
Giardia infections in dogs and cats may be inapparent or produce weight loss and chronic diarrhea or steatorrhea, which can be continuous or intermittent, particularly in puppies and kittens. Calves with clinical giardiasis have been reported. Feces are usually soft, poorly formed, pale, and contain mucus. Gross intestinal lesions are seldom evident, although microscopic lesions, consisting of villous atrophy and cuboidal enterocytes, may be present.DISEASE IN MAN:
Most infections are asymptomatic. In some cases, acute or chronic diarrhea, mild to severe, with bulky, greasy, frothy, malodorous stools, free of pus and blood. Upper abdominal discomfort, cramps, distention, excessive flatus, and lassitude.DIAGNOSIS:
Diagnosis is by identifying cysts or trophozoites in feces or duodenal fluid. Unless they can be examined with an hour, specimens should be preserved immediately in a fixative. Three stool specimens should be examined at intervals of 2 days or longer. A stool ELISA test or IgM serology are available.TREATMENT:
Tinidazole, Metronidazole (FLAGYL), quinacrine, or furazolidone. Alternative drugs are Tinidazole or albendazole.PREVENTION/CONTROL:
Fecals to screen dogs and NHP's. Hygiene, protective clothing, when handling animals. Prevention requires safe water supplies, sanitary disposal of human feces, adequate cooking of foods to destroy cysts, protection of foods from fly contamination, washing hands after defecation and before preparing or eating foods, and, in endemic areas, avoidance of foods that cannot be cooked or peeled.GLANDERS
(Farcy)AGENT:
Pseudomonas mallei (Actinobacillus mallei) NONMOTILE, gram negative rodRESERVOIR AND INCIDENCE
disease of equidae and rarely man. Occasionally reported in dogs, cats, sheep, and goats. Mostly seen in Asia and Mediterranean areas, rare in North America.TRANSMISSION:
spread by contamination by infectious discharges of wounds and mucus membranes and by ingestion.DISEASE IN ANIMALS AND MAN:
pulmonary form: cough, nasal discharge. cutaneous form: multiple, purulent, cutaneous eruptions, often following lymphatics. Usually affects hind legs of horses. May have long periods of remission. The fatality rate in humans is 95% if left untreated. Horses usually suffer chronic and sometimes fatal illness. Asses and mules usually suffer acute disease which is often fatal.DIAGNOSIS:
Cannot be differentiated from P. pseudomallei serologically. Specific diagnosis can be made only by characterization of the isolated organism.TREATMENT:
Streptomycin + tetracycline or chloramphenicol + streptomycinPREVENTION/CONTROL:
1. Treatment with antibiotics2. Elimination of carrier animals
3. Gloves, protective clothing when handling infected animals.
HANTAVIRUS PULMONARY SYNDROME
INTRODUCTION:
On May 14, 1993, the New Mexico Department of Health was notified of 2 persons who had died within 5 days of each other. Their illnesses were characterized by abrupt onset of fever, myalgia, headache, and cough, followed by the rapid development of respiratory failure. Tests for Yersinia pestis and other bacterial and viral pathogens were negative. After additional persons who had recently died following a similar clinical course were reported by the Indian Health Service, the health services of Arizona, Colorado and Utah were contacted to seek other possible cases. Blood and tissue specimens were sent to the Centers for Disease Control and Prevention (CDC). The results were negative except for signals for the Puumala hantavirus. Relying on molecular and immunological research performed by the Army, the National Institutes of Health, and the CDC itself, by June 9th, the CDC was able to prove that a new hantavirus was the culprit (1). As of November 5th, laboratory evidence of acute hantavirus infection had been confirmed in 42 persons. Twenty-six (62%) of these persons have died. Most cases were in the Southwest but some have been reported as far afield as North Dakota and California (1). This paper presents a brief overview of hantavirus infections with primary focus on Hantavirus Pulmonary Syndrome (HPS) and recommended laboratory precautions to reduce the risk of accidental exposure. Other detailed reviews are available elsewhere (2-7).AGENT:
Isolation of the first recognized hantavirus (Hantaan virus) was reported from the Republic of Korea in 1978. The genus Hantavirus is a member of the family Bunyaviridae. Hantaviruses are further divided into genotypes. Representative viruses in each genotype are the Hantaan virus, the Seoul virus, the Puumala virus, and the Prospect Hill virus. Additional groups exist. Hantaan, Puumala, and Seoul viruses are known human pathogens; Prospect Hill has not been associated with disease. The causative agent of HPS represents a previously unidentified genotype. Since the 1930s, epidemic and sporadic hantavirus-associated disease has been described throughout Eurasia, especially in Scandinavia and Northeastern Asia. In the 1950s, thousands of United Nations military personnel were infected with hantavirus during the Korean conflict; more recently, transmission has been documented among United States military personnel training in the Republic of Korea. Hantaviruses have been isolated from rodents in the United States, and serological studies have documented human infections with hantaviruses. However, acute disease associated with infection by pathogenic hantaviruses has not previously been reported in the Western Hemisphere (8). Previously called the Four Corners Virus and Muerto Canyon Virus, the causative genotype for HPS is now called Sin Nombre Virus.DISEASE IN HUMANS:
The clinical manifestations previously associated with hantavirus infections have been characterized by hemorrhagic features and by renal involvement. In HPS, however, onset of illness has been characterized by a prodrome consisting of fever, myalgia, and variable respiratory symptoms followed by the abrupt onset of acute respiratory distress. Other symptoms reported during the early phase of illness have included headache and gastrointestinal complaints. Hemoconcentration and thrombocytopenia have developed in a majority of the cases. The hospital course has been characterized by bilateral pulmonary infiltration, fever, hypoxia, and hypotension; recovery in survivors has been without sequelae. It is important to note that no defined set of symptoms and signs reliably distinguishes HPS from other forms of noncardiogenic pulmonary edema or adult respiratory distress syndrome (9). Postmortem examination has routinely revealed serous pleural effusions and heavy edematous lungs. Microscopic findings have included interstitial infiltrates of mononuclear cells in the alveolar septa, congestion, septal and alveolar edema with or without mononuclear cell exudate, focal hyaline membranes, and occasional alveolar hemorrhage. Large mononuclear cells with the appearance of immunoblasts have been found in red and periarteriolar white pulp of the spleen, hepatic portal triads, and other sites. Hantavirus antigens, localized primarily in endothelial cells, have been detected in most organs, with marked accumulations in the lungs (9). The incubation period for the known pathogenic hantaviruses, although highly variable, generally range from 2 to 4 weeks (8). Based on reported cases, the incubation period for HPS appears to be one to three weeks (10).RESERVOIRS:
Rodents are the primary reservoir hosts with each hantavirus appearing to have a preferential rodent host. The epidemiological characteristics of outbreaks of human disease and the severity for the infection are determined mainly by the rodent host. Available data strongly supports the deer mouse (Peromyscus maniculatus) as the primary reservoir of the newly recognized hantavirus (11). Serologic evidence of infection has also been found in pion mice (P. truei) and the brush mice (P. boylii). Other rodent species that have tested positive so far include the house mouse (Mus musculus), the harvest mouse (Reithrodontomys sp.), the rock squirrel (Spermophalus variegatus), the white-throated wood rat (Neotoma albigula), and the western chipmunk (Tamias spp.). P. maniculatus is highly adaptable and is found in different habitats, including human residences in rural and semirural areas, but generally not in urban centers (12). The wood mouse or striped field mouse (Apodemus sp.) associated hantaviruses also cause severe human disease with mortality rates between 3 and 7%. Rattus associated disease is less severe and asymptomatic infections may be more common. The most benign form of hantaviral disease (HVD), also called Nephropathia epidemica and first described in Scandinavia, is caused by a hantavirus that infects voles (Clethrionomys species). Infected voles and human disease occur throughout western Europe (13). The hantaviruses have been identified in other animals. At the International Symposium on Hemorrhagic Fever with Renal Syndrome (HFRS), Leningrad, 5-10 May 1991, the presence of hantaviral antigen was reported in 13 species of birds in eastern parts of the former U.S.S.R. (13). The CDC is also investigating whether other animals, particularly those that prey on rodents, may carry the virus. The impetus for this research is a 1987 study suggesting that cats, which tested positive for two other hantaviruses-the Hantaan and Seoul types-may help transmit the virus to humans in China. As for the HPS virus, so far CDC scientists have identified one infected nonrodent species (aside from humans): the desert cottontail (Sylvilagus auduboni). But virologists think most nonrodents are "dead-end" hosts that shed little virus and are unlikely to infect people (14). Laboratory rats, which were a reservoir of hantavirus, have been responsible for several outbreaks of HVD among animal caretakers and laboratory workers at research institutions in Korea, China, the former Soviet Union, Japan, Scandinavia, the U.K., France, the Netherlands and Belgium (13). Transmission of Hantavirus from laboratory reared mice and rats has not been documented in the United States.TRANSMISSION:
Susceptibility of rodents may vary depending on the combination of rodent species and virus strains; however, Hantaviruses do not cause apparent illness in their reservoir hosts (15). In rodents, the virus is detected primarily in the lung and kidney, where it persists despite the presence of serum antibodies. Infected rodents shed large quantities of virus in saliva, urine, and feces for many weeks, but the duration and period of maximum infectivity are unknown. Although the main route of transmission is aerosolization, the demonstrated presence of infectious virus in saliva of infected rodents and the marked sensitivity of these animals to hantaviruses following inoculation suggests that biting may also be an important mode of transmission among rodents (12). Arthropod vectors are not known to have a role in the transmission of hantaviruses. Domestic animals may bring infected rodents into contact with humans (12). Human infection may occur when infective saliva or excreta are inhaled as aerosols produced directly from the animal. Transmission may also occur when dried materials contaminated by rodent excreta are disturbed, directly introduced into broken skin, introduced onto the conjunctivae, or, possibly, ingested in contaminated food or water. Persons have also become infected after being bitten by rodents (12). Person-to-person transmission has not been associated with any of the previously identified hantaviruses nor with the recent outbreak in the Southwest (16). In the current epidemic, known hantavirus infections of humans have occurred primarily in adults and are associated with domestic, occupational, or leisure activities that bring humans into contact with infected rodents, usually in a rural setting. Cases have been epidemiologically associated with the following situations: Planting or harvesting field crops Occupying previously vacant cabins or other dwellings Cleaning barns and other outbuildings Disturbing rodent-infested areas while hiking or camping Inhabiting dwellings with indoor rodent populations Residing in or visiting areas in which the rodent population has shown an increase in density (12). In Europe, isolation of hantaviruses from immunocytomas and ascites tumors has highlighted additional risks from working with persistently infected rodents. Tumors, passaged over the years in hantavirus-infected laboratory rats, transfer the virus when implanted in hantavirus-free rats. Since, in rodents, hantaviruses are not transmitted vertically but horizontally, the use of caesarian section and foster mother techniques have been recommended for laboratories breeding rodent colonies. Before implantation, tumors should be checked for the presence of the hantaviruses (this precaution should be followed by laboratory workers in the U.S. importing tumors, organs, or live rodents from hantavirus endemic areas) (12).DIAGNOSIS:
The CDC in consultation with the Council of State and Territorial Epidemiologists has developed screening criteria for HPS (9). Cases meeting the screening criteria should be reported to the CDC through state health departments. These criteria are: Potential case-patients must have one of the following: a febrile illness (temperature 101 oF [38.3 oC]) occurring in a previously healthy person characterized by unexplained adult respiratory distress syndrome, or bilateral interstitial pulmonary infiltrates developing within 1 week of hospitalization with respiratory compromise requiring supplemental oxygen, OR an unexplained respiratory illness resulting in death in conjunction with an autopsy examination demonstrating noncardiogenic pulmonary edema without an identifiable specific cause of death. Potential case-patients are to be excluded if they have any of the following: a predisposing underlying medical condition (e.g., severe underlying pulmonary disease, solid tumors or hematologic malignancies, congenital or acquired immunodeficiency disorders, or medical conditions [e.g., rheumatoid arthritis or organ transplant recipients] requiring immunosuppressive drug therapy [e.g., steroids or cytotoxic chemotherapy]). an acute illness that provides a likely explanation for the respiratory illness (e.g., recent major trauma, burn, or surgery; recent seizures or history of aspiration; bacterial sepsis; another respiratory disorder such as respiratory syncytial virus in young children; influenza; or legionella pneumonia). Confirmed case-patients must have the following: at least one specimen (i.e., serum and/or tissue) available for laboratory testing for evidence of hantavirus infection. AND in a patient with a compatible clinical illness, diagnosis is confirmed when any of the following criteria are met: IgM antibodies to hantavirus antigens, fourfold or greater increase in immunoglobulin G titers to hantavirus antigens in paired serum specimens, a positive immunohistochemical stain for hantavirus antigen in tissues, or positive polymerase chain reaction (PCR) for hantavirus ribonucleic acid. Currently, diagnosis of the HPS strain of Hantavirus in animals is in its infancy. IFA based tests offered by national research laboratories may be used for screening; however, false negatives can occur depending on the antigen used. PCR remains the method of choice for strain identification. Presently, one laboratory (Rockefeller University Laboratory Animal Research Center, [212]327-8522) offers this service with more, hopefully, coming on line in the future (17).TREATMENT:
Supportive care and meticulous monitoring of vital signs and fluid balance are the basis for therapy. Severe hypoxia and overhydration should be avoided or prevented. Pressors or cardiotonic drugs should be employed to maintain perfusion without excessive fluid administration (9). In one controlled study involving HFRS, intravenous administration of the antiviral drug ribavirin was effective in treating severe cases of hantavirus infection when administered early in the course of illness (8). The effectiveness of using ribavirin to treat HPS has not been established, yet.PREVENTION AND CONTROL:
Hantaviruses have lipid envelopes that are susceptible to most disinfectants (e.g., dilute hypochlorite solutions, detergents, ethyl alcohol (70%), or most general-purpose household disinfectants). How long these viruses survive after being shed in the environment is uncertain (12). The reservoir hosts of the hantavirus in the southwestern United States also act as hosts for the bacterium Yersinia pestis, the etiology agent of plague. Although fleas and other ectoparasites are not known to play a role in hantavirus epidemiology, rodent fleas transmit plague. Control of rodents without concurrent control of fleas may increase the risk of human plague as the rodent fleas seek an alternative food source. Thus, eradicating the reservoir hosts of hantaviruses is neither feasible nor desirable. Once the virus has been cultured, it might be possible to develop a vaccine against the HPS strain. However, currently, the best available approach for disease control and prevention is risk reduction through environmental hygiene practices that deter rodents from colonizing the home and work environment (12). No restriction of travel to areas affected by this outbreak is considered necessary; however, activities that may disrupt rodent burrows or result in contact with rodents or aerosolization or rodent excreta should be avoided. Laboratory workers practicing universal precautions while processing routine clinical materials (such as blood, urine, and respiratory specimens) are not considered to be at increased risk for hantavirus infection. However, laboratory-acquired infections have occurred among persons who handled infected wild or laboratory rodents. Therefore, laboratory work that may result in propagation of hantaviruses should be conducted in a special facility (biosafety level 3) (8). Recommendations for laboratory animal facilities housing wild-caught rodents include: Access to rooms should be restricted to only those individuals who have a legitimate need to be in the room. Colony should be serologically screened for the agent. Animals should be housed and handled under standard microisolation techniques. Biological safety cabinets should be used and not laminar flow workbenches. Until the status of the colony can be ascertained, individuals working with the rodent should: a. Obtain a baseline serum sample. The serum should be stored at -20oC. b. Insure that all persons involved are informed of the symptoms of the disease and given detailed guidance on prevention measures. c. Seek immediate medical attention if a febrile or respiratory illness develops within 45 days of the last potential exposure. The attending physician should be informed of the potential occupational risk of hantavirus infection. d. Wear an half-face air-purifying (or negative-pressure) respirator or powered air-purifying respirator with HEPA filter when handling rodents or their cages. Respirators are not considered protective if facial hair interferes with the face seal. Respirators should be fitted by trained personnel in accordance with OSHA standards. e. Wear rubber or plastic gloves when handling rodents or cages. Gloves should be washed and disinfected before removing them. f. Wear dedicated outer garments (disposable, if possible), rubber boots or disposable shoe covers and protective goggles. Personal protective gear should be decontaminated upon removal. If not disposable, they should be laundered on site using hot water and detergent. Machine-dry using a high setting. If no laundry facilities are available, non-disposable items should be immersed in liquid disinfectant until they can be washed. All potentially infective waste material (including respirator filters, bedding, caging, disposable protective garments, and used disposables such as syringes, gauze, etc.) should be placed in autoclavable plastic bags and sterilized. Needles, scalpels, pipettes, and other sharp materials should be placed in puncture proof containers and sterilized. Spread from feral rodents was postulated as the cause of one source of contamination (18). Therefore, facilities and individual rooms should be vermin-proof to prevent accidental egress and ingress of rodents. All openings greater than inch should be screened or sealed. Carcasses should be placed in a plastic bag and disposed as biohazard waste or incinerated. Since feral rodents may transmit the disease, it is recommended that Hantavirus testing be included in animal health monitoring programs. Why the Current Epidemic? Because of the rodent connection with this disease, medical investigators and public health officials sought ecological information on the deer mouse and other native rodent species. Anecdotal information from residents in the afflicted areas suggested that rodents were exceptionally abundant last winter, and scientists speculated that, if true, the increased potential for rodent-human contact and disease transmission might account for the sudden epidemic. Biologists with the Sevilleta, New Mexico Long-Term Ecological Research (LTER) site have long-term data on rodent communities in the region. At the request of the CDC and the New Mexico Health Department, LTER researchers provided detailed demographic analyses from 1989-1993 for the 22 rodent species inhabiting the area. The LTER data showed tenfold population increases in various Peromyscus species and wood rats (Neotoma spp.) during the spring of 1993. Population increases occurred simultaneously in grasslands, desert-shrublands, and woodlands. Comparisons of the rodent data to the region's climatological data indicated that rodent population dynamics is associated with above-average precipitation during the winter of 1992-93, in turn leading to abundant food sources (19).References
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Spiral Bacteria in the Human Stomach: The Gastric Helicobacters
Andre Dubois, M.D., Ph.D.Digestive Diseases Division, Department of Medicine,
Uniformed Services University of the Health Sciences Bethesda, Maryland, USA
During the past decade, Helicobacter pylori has become recognized as one of the most common human pathogens, colonizing the gastric mucosa of almost all persons exposed to poor hygienic conditions from childhood. It also is often found, albeit with a lower frequency, in groups of high socioeconomic status. H. pylori causes chronic active gastritis and is a major factor in the pathogenesis of duodenal ulcers and, to a lesser extent, gastric ulcers. In addition, the presence of this bacterium is now recognized as a risk factor for gastric adenocarcinoma and lymphoma. Nevertheless, most infections appear without clinical consequences. In this second decade of intensive research, it is important to understand why H. pylori is sometimes a dangerous pathogen, and to determine how it can be eradicated in those at highest risk for severe disease.
At the end of the 19th century, several types of spirochetes and spirilla were observed for the first time in the stomach of animals (1,2). Beginning at the turn of the 20th century, similar spiral bacteria were found in gastrectomy specimens from patients with gastric cancer and peptic ulcer disease (3,4). In addition, gastroenterologists and surgeons noted but could not explain the almost universal presence of antral gastritis in patients with duodenal ulcers and the frequent presence of atrophic gastritis in patients with gastric ulcer and cancer. Nevertheless, the possibility that peptic ulcer disease or gastric cancer might be caused by an infectious agent was generally discounted. The observation made in 1975 that gram-negative bacteria were present in 80% of patients with gastric ulcer (5) was largely ignored by the scientific community which, at the time, was busily developing potent antiulcer agents (6). Skepticism remained the overwhelming reaction to the 1983 reports describing the frequent association between antral gastritis and the presence of Campylobacter-like bacteria (7), as well as of their culture and isolation from patients with gastritis (8). A similar reaction followed the subsequent demonstration that these Campylobacter-like bacteria were present in almost all patients with gastric and duodenal ulcers, and were generally associated with antral gastritis (9). In the past decade, however, a number of studies have confirmed and extended these early observations. A consensus regarding the major role of this bacterium, now named Helicobacter pylori, in causing gastroduodenal ulceration was formally presented in 1994 (10). Furthermore, in June 1994, the International Agency for Research on Cancer Working Group stated , "H. pylori plays a causal role in the chain of events leading to cancer," referring to adenocarcinoma and lymphoma of the stomach as well as to the more benign mucosal-associated lymphoid tissues (MALT) (11-13).
An important consequence of the considerable interest generated by these clinical observations is that extensive bacteriologic and molecular studies have been performed on this bacterium and similar organisms. 16S rRNA gene sequence analysis has revealed important differences between H. pylori and the closely related Campylobacter, Flexispira, and Wolinella genuses. These differences have necessitated the creation of the genus Helicobacter, which, to date, includes eight gastric, three intestinal, and two hepatic species (14). Each of these Helicobacter species colonizes different, or a spectrum of, mammalian species. This review summarizes our current knowledge of the two Helicobacter species that have been observed in the human stomach and reported on extensively in the literature: H. pylori, the type strain, and H. heilmannii, also known as Gastrospirillum hominis (15,16).
CHARACTERISTICS OF GASTRIC HELICOBACTERS OBSERVED IN HUMANS:
H. pylori, a gram-negative bacterium with a curved, spiral, or gull-wing shape, is 2.5 to 3.5 m long and 0.5 to 1.0 m in diameter and has a periodicity of 1 to 2m. It has smooth surfaces, and one to six polar-sheathed flagellae emerge from one of its rounded ends. Since it is morphologically similar to C. jejuni, it was initially named "pyloric Campylobacter" and subsequently C. pyloridis and C. pylori before finally being named H. pylori. This organism colonizes only the non-acid-secreting mucosa of the stomach and is not found where parietal cells are numerous. Thus, it may be observed in the gastric antrum and the cardia, but also in the corpus, when atrophic gastritis is present, and attached to the gastric epithelial cells found in the duodenum, when gastric metaplasia is present.G. hominis (H. heilmannii) is tightly spiraled, and is 3.5 to 7.5 m in length and 0.9m in diameter; it has a periodicity of 0.8 to 1 m and up to 12 flagellae at each pole. 16S rRNA indicates that this organism belongs to the genus Helicobacter, and is more closely related to a Helicobacter sp. isolated from the stomach of cats (H. felis) than to H. pylori (17). The name H. heilmannii was proposed in honor of the late German pathologist Heilmann. However, the subsequent examination of the rRNA of different clinical isolates indicates that there is enough heterogeneity among isolates tentatively identified as H. heilmannii that it is premature to propose an official name (17) . This bacterium colonizes only the parietal cell area of the gastric mucosa and may be found within parietal cells (18,19).
DIAGNOSIS:
H. pylori infection may be diagnosed by harvesting gastric biopsy specimens during endoscopy, by culturing and isolating the bacterium under microaerobic conditions (90% N2, 5% O2, and 5% CO2), and by characterizing the enzymes (urease, catalase, and oxidase) it produces. Visualization of the bacterium by light microscopy on slides stained with hematoxylin and eosin, Gram, Giemsa, Genta, or Warthin-Starry stain is also of great benefit since it allows the concurrent diagnosis of the extent of the antral chronic-active gastritis that H. pylori causes. However, because H. pylori colonization is focal, negative biopsy results do not exclude the possibility of infection in areas not sampled. Infection also may be diagnosed by determining plasma and salivary immunoglobulin (Ig) G or IgA levels with enzyme-linked immunosorbent assays (20,21). This latter technique is noninvasive, specific, and sensitive and is believed to reflect the mucosal and systemic immunity induced by H. pylori infection.Two other tests, which rely on the production of urease, also can be used to identify H. pylori. One is the CLO (for Campylobacter-like organisms) test, which is performed by placing a mucosal biopsy specimen in medium containing urea and a pH- sensitive dye that changes color in the presence of OH- ions. The second test is the noninvasive 14C or 13C breath test following the oral administration of 14C- or 13C-urea. Neither of these tests is specific for H. pylori since G. hominis, which generates urease, also gives a positive reaction. Until specific methods based on the polymerase chain reaction (PCR) amplification of 16S rRNA (17) become widely available, the diagnosis of G. hominis infection must rely on histologic morphologic characteristics; histologic identification must be confirmed by transmission electron microscopy since other spiral organisms, e.g., Flexispira rappini, also may be present in the stomach of humans (22).
EPIDEMIOLOGY:
The seroepidemiology of H. pylori has been extensively studied in the United States and in other countries (23). The high frequency of seropositivity (up to 100% in some age groups in Albania) and acquisition of the infection during infancy are characteristic of disadvantaged socioeconomic groups living in crowded or poor hygienic conditions and appears to be independent of gender and ethnic origin. In adults of higher socioeconomic groups, the rate of seroconversion is estimated at 0.5% per year, although the frequency of seropositivity increases with age and may be as high as 40%. A longitudinal study has indicated that the high frequency of seropositivity in older adults might be due to a higher rate of H. pylori infection in Western countries in the years between the two world wars than during recent years (cohort effect) (24). Alternatively, the increase in frequency of infection in older adults might be due to years of low but cumulative risk for infection. Although the route of transmission for this infection is not known, the contamination of drinking water may play a role in certain developing countries (25). In the United States and in other regions, direct contact and/or consumption of food or water contaminated by saliva (26), gastric contents, or feces (27) may be major factors. The recent observation that H. pylori can be isolated from cats (28) suggests that transmission from pets to humans (or humans to pets) is also possible.The epidemiology and route of transmission of G. hominis are largely unknown. The frequency of this infection appears to range from less than 1% of the population in industrialized countries (29) to 3% to 8% in developing countries (30). Although the detection of spirilla in the stomach of cats and dogs suggests possible transmission from pets, marked morphologic differences exist between these spirilla and the organism found in the stomach of humans.
PATHOGENICITY:
H. pylori is considered a pathogen because its presence is always associated with chronic active gastritis, and eradication of the bacterium is always followed by resolution of gastritis. In addition, nearly all patients with duodenal ulcer disease have H. pylori gastritis, and ulcer relapse is exceptional after H. pylori eradication. Thus, the presence of H. pylori seems necessary for the production of duodenal ulcers, with the exception of ulcers attributed to the use of nonsteroidal antiinflammatory agents or to the Zollinger-Ellison syndrome (10). The association with gastric ulcers is not as strong, although H. pylori infection is present in 80% of patients with gastric ulcers who do not consume nonsteroidal anti-inflammatory agents (10). However, most H. pylori-infected persons do not report any clinical symptoms. This may be because these persons are colonized by less virulent strains or because other host or bacterial cofactors are required for overt disease.In addition, three prospective cohort studies have demonstrated that H. pylori-infected persons have an increased risk of developing intestinal-type, but not undifferentiated, gastric adenocarcinoma (10). In fact, the association of H. pylori with either gastric ulcer or gastric cancer may be underestimated in these studies: the atrophic gastritis that follows long-term infection makes the gastric niche less hospitable for the bacterium, which may either eliminate H. pylori or make it difficult to detect. Nevertheless, atrophic gastritis per se is believed to be a precancerous lesion that leads to carcinogenesis without the presence of H. pylori.
The pathogenicity of G. hominis is unclear. The organism has been associated with upper gastrointestinal complaints, and its carriage is generally accompanied by gastritis, although the inflammation and gastric atrophy are less than noted with H. pylori (31,32). In addition, G. hominis was observed in gastric cancer patients (3) as well as in patients with only minimal gastritis (29). In this relatively small number of cases, the frequent concurrent infection with H. pylori makes interpreting the respective pathogenic role of either bacterium difficult. It is probable that G. hominis will turn out to be at least somewhat pathogenic, as it makes urease and products of urease action that have been implicated in inflammation.
COLONIZATION AND VIRULENCE FACTORS:
H. pylori multiplies with great efficiency in the hostile environment within the stomach but survives poorly in the gastric lumen; it is mainly found where the pH ranges between 4 and 7, i.e., under the mucous layer and in close proximity, or even attached, to gastric superficial epithelial cells. The virulence and the ecologic niche of G. hominis are unknown, although its presence within parietal cells of patients with gastrointestinal complaints (18,19) suggests that it is even more resistant to acid than H. pylori.The production of urease was the first putative colonization or virulence factor studied. The production of this enzyme is shared by the two organisms, and it may explain their extraordinary ability to survive in an environment previously considered sterile because of the presence of proteolytic enzymes, as well as the low pH of gastric contents. Because the ecologic niches of these bacteria are rich in urea, urease generates OH- ions that neutralize gastric acid. Although the neutralization of gastric acid benefits the two bacteria, the production of hydroxide ions also is toxic to gastric epithelial cells in vivo, as indicated by in vitro experiments (33).
Two other important virulence factors shared by H. pylori and G. hominis are their spiral shape and the motility of their flagellae, which render them resistant to peristaltic flushing of the gastric contents and enable them to persist in the mucous layer. Because G. hominis appears to infect fewer persons than H. pylori, a more important role might be attributable to characteristics that are unique to H. pylori; these include the production of other enzymes (catalase, oxidase, protease, and phospholipase), as well as the synthesis of specific adhesin proteins that enable them to adhere to mucous and epithelial cells, both in vivo and in vitro (34-36).
The putative virulence factor of H. pylori that has commanded the most attention during the past few years has been its vacuolating cytotoxin (vacA gene product). Intragastric administration of the toxin to mice causes some (but not all) of the tissue damage seen in H. pylori-infected persons (37). In addition, cytotoxin production is highly correlated with the production of a high molecular weight (120 to 128 kilodaltons) major protein antigen that is called cytotoxin-associated protein (cagA) and is not the toxin itself (38).
DIVERSITY OF H. PYLORI:
H. pylori isolates may differ with respect to each of the virulence factors described above; this diversity is likely to contribute to variation in colonization or disease. For example, urease-negative strains have been isolated, and the vacuolating cytoxin is produced by only a subset of H. pylori strains (vacA+ or tox+ strains)(39-41). This observation is probably clinically relevant because most or all strains from duodenal ulcer patients, and many strains from gastric cancer patients, produce cytotoxin, whereas only a fraction of strains from patients with gastritis alone produce the cytotoxin (42,43). This phenotypic diversity is mirrored in great diversity on the DNA level. Thus, only cytotoxin-producing strains contain the gene for this cytotoxin-associated protein (cagA)(38,42), although genetic tests have shown that cagA protein is not needed for toxin production (44). Strains that do not produce the 128-kDa cagA protein generally lack the entire cagA gene and additional neighboring genes. Although the function of the cagA region is unknown, its presence or absence is easily scored by hybridization or PCR and thus serves as an easy marker for probable cytotoxin production and possible virulence of H. pylori strains. Additional virulence factors are likely to be present. For example, another recently discovered region constitutes at least 21 kilobases of the H. pylori genome in hybridization experiments, and its presence is highly correlated with the presence of cagA: 39 of 40 strains lacking cagA also lacked this region, and 50 of 52 strains containing cagA contained this region. This newly discovered region is being called cagII, and the effort to sequence it is nearly complete (D. E. Berg, pers. comm.). Preliminary searches have identified several open reading frames with strong homologies to virulence functions from other microbes (45).In addition to these extensively studied genes, genetic diversity of various H. pylori strains can be demonstrated by the use of two sensitive, efficient, and reliable PCR-based methods (46,47). This approach is particularly useful because it allows tracing of strains in epidemiologic studies.
INFECTION AND IMMUNE RESPONSE:
One of the most puzzling aspects of gastric infection with H. pylori is its persistence despite intense local and systemic immune responses. These immune responses are extremely complex and vary among infected humans. The systemic response is characterized by a marked increase in plasma IgG, which remains present for months after the infection has been cured. The local response includes the production of IgA, which binds to the surface antigens of H. pylori in vitro and coats the bacterium in vivo. In addition, infection is consistently associated with an intense inflammatory response and the infiltration of cells into the gastric mucosa. Although polymorphonuclear cells are often present, most cells in such infiltrates are mononuclear cells. Both B and T cells are present, and recent studies have indicated that the natural killer activity of peripheral blood lymphocytes can be increased by H. pylori, possibly by its stimulating the production of interferon and other cytokines (48). Thus, the long-term carriage of the infection may be related to the ability of the bacterium to influence the T-cell response. Fragmentary evidence also suggests that this infection can be abortive and cure spontaneously without the use of antibiotics (A. Dubois and D. E. Berg, unpublished).On the other hand, the mucosal response may promote colonization, as indicated by the observation that patients with acquired immunodeficiency syndrome (AIDS) tend to have a lower rate of infection than aged-matched subjects who are negative for human immunodeficiency virus (49,50). The latter study (50) also demonstrated that AIDS patients had a different pattern of gastritis, characterized by greater mononuclear cell responses, fewer lymphoid follicles, and a greater prevalence of intestinal metaplasia. The immune response may also prevent the invasiveness of H. pylori, as suggested by the anecdotal but puzzling observation of invasive H. pylori infection in a patient with AIDS (51).
TREATMENT:
Although H. pylori is sensitive to many antimicrobial drugs in vitro, it is difficult to eradicate from the stomach. This may be ascribed to antibiotic breakdown by gastric acid, clearance by gastric emptying, and the difficult-to-penetrate mucous layer in which the bacterium resides. Resistance of H. pylori to specific antibiotics, especially metronidazole, is also frequent. Therefore, it is generally accepted that a combination of at least two, and possibly three, antimicrobial agents should be given for a minimum of 1 week. The regimen found to be most effective is the administration of amoxicillin (or tetracycline) plus metronidazole and bismuth subsalicylate 2 to 4 times a day for 2 to 3 weeks (52). The use of one antibiotic associated with an antisecretory agent, such as a histamine H2 receptor antagonist, has given disappointing results. In contrast, the combination of a proton pump inhibitor (H+-K+ ATPase antagonist) with amoxicillin or acid-stable macrolides (clarythromycin or roxithromycin) appears more promising; a number of studies are being conducted to determine the optimal dose, duration, concomitant therapy, and cost-effectiveness of these compounds (53,54). Recently, it was shown that at least a 7-day course of any of these regimens is required to obtain a high (90%) cure rate, but that continuing treatment for more than 10 days does not significantly improve its efficacy. Finally, topical therapy for 1 h was recently tried with excellent results, albeit in only one center at this time (55). This treatment involves a 2-day administration of a mucolytic agent to dissolve the mucous layer and of a proton pump inhibitor. On the third day, a balloon is introduced into the second portion of the duodenum under fluoroscopic control, and a solution of pronase, amoxicillin, metronidazole, and bismuth subsalicylate is injected into the stomach, where it is left for 1 h. The presence of the duodenal balloon appears to prevent emptying of the antibiotics and the mucolytic agent, thus ensuring maximum efficacy of the therapy.FUTURE RESEARCH:
The past 12 years have seen extensive progress in research on H. pylori as a cause of chronic active gastritis, duodenal ulcer disease, and gastric cancer. This has been largely due to an unusual collaboration among gastroenterologists, pathologists, molecular geneticists, bacteriologists, and immunologists. However, our understanding of how H. pylori colonizes and causes diseases is far from complete, and it will benefit from studies performed in animal models that can be experimentally infected with H. pylori (56-59). In addition, no easily administered treatment leading to eradication of this bacterium in all patients is yet available, although a better knowledge of its physiology may lead to the development of such a "silver bullet." Studies in animals that are not naturally infected with H. pylori suggest possibilities for vaccines (56,57), and ongoing trials in nonhuman primates are exploring the possibility of immunizing hosts that can be naturally infected with this organism. Although the elimination of peptic ulcer disease and of certain forms of gastric cancer will require extensive and coordinated efforts from public health authorities, this goal now appears to be within the reach of the scientific and medical community.ACKNOWLEDGEMENTS:
The author thanks Drs. P. Baker and D.E. Berg for their helpful comments and suggestions during the preparation of this review.Dr. Dubois is professor of medicine and surgery (research), assistant director, Digestive Diseases Division, and chief, Laboratory of Gastrointestinal and Liver Studies, F. Edward Hbert School of Medicine of the Uniformed Services University of the Health Sciences, Bethesda, Maryland. He studies the physiology and pathophysiology of gastric secretion and gastric emptying as well as the role of gastric infection with H. pylori in gastroduodenal diseases.
Address for correspondence: Andre Dubois
Department of Medicine
Uniformed Services University
4301 Jones Bridge Road
Bethesda, MD 20814-4799, USA
Fax: 301-295-3676 or -3557
E-mail: dubois@usuhsb.usuhs.mil.
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HEMORRHAGIC FEVER WITH RENAL SYNDROME [HFRS]
(Korean Hemorrhagic Fever, Nephropathia Epidemica, Epidemic Hemorrhagic Fever, Hemorrhagic Nephrosonephritis)AGENT:
Bunyaviridae family, Hantaan virus genusRESERVOIR AND INCIDENCE
Recognized originally in troops serving in the Korean war. Named Hantaan after river in endemic area of Korea. Isolated in 1978 in Apodemus agrarius, then adapted to tissue culture and laboratory rats. Serologic mapping indicates that Hantaviruses have infected large numbers of people in the region from Japan across central and north Asia to the Scandinavian Peninsula, and southward in Europe to the Balkans. Other Hantaviruses have been identified in urban rats captured in major Asian and Western cities, including the USA and Brazil. Hosts of hantavirus are wild Rodents Several antigenic subtypes exist, each associated with a single rodent species: Apodemus species - Striped field mouse - A. agrarius (Korea) associated with KHF. Domestic Rattus norvegicus and Rattus rattus in Korea and Domestic Rattus norvegicus in the U.S. had virus similar to prototype Hantaan virus yet distinct from it. Microtus pennsylvanicus: the meadow vole. Reservoir for Prospect Hill virus, most recently isolated Hantavirus. Isolated at NIH and named for Prospect Hill in Frederick, MD where the vole was captured that yielded the first isolate. No human disease associated with this so far but antibody has been identified among mammalogists in the U.S.(1982). Cletheronomys glareolus: the bank vole. Reservoir for Puumala virus, cause of Nephropathia epidemica (NE), a mild form of HFRS found in Scandinavia, Western Soviet Union and much of Europe.TRANSMISSION:
Aerosol transmission from rodent excreta is presumed. Virus is present in urine, feces and saliva of persistently infected asymptomatic rodents; highest virus concentration is found in the lungs. Human to human transmission does not occur.DISEASE IN RODENTS:
Chronic, ASYMPTOMATIC infection. Following infection, rodent is viremic for about 1 week when virus is disseminated throughout the body. After viremia antigen is usually abundant in the lungs, spleen and kidneys. Antibody is produced and persists but does not diminish the abundance of antigen expressed in organs.DISEASE IN MAN:
Symptoms begin with the sudden onset of fever which lasts 1-2 weeks, accompanied by prostration, anorexia, generalized pains, conjunctivitis, proteinuria and hypotension, possibly followed by hemorrhages and hematuria with renal failure. Case fatality rate is 7%.DIAGNOSIS:
Serology using indirect immunofluorescence or ELISA.TREATMENT:
IV ribavirinPREVENTION/CONTROL:
Although most US commercial animal breeders have eliminated these viruses through barrier breeding and caesarean derivation, small suppliers and producers of select inbred strains may be at risk of infection. Be aware of potentially infected animals when receiving shipments from Japan, Belgium or other countries which may have the agent present in lab. animals (where virus-free certification cannot be provided). Animals should be serologically tested in advance of shipment. Test all rodent tissues, tumors, cell lines received from source that cannot provide virus free certification. Education and awareness of potential problem. Exclude rodents from housing and other buildings in endemic areas.
OTHER HEMORRHAGIC FEVERS
(Arenaviruses) All have natural persistent infection in rodents with humans being accidental hosts. Route of transmission to humans is generally thought to occur thru contamination of food, water, or air by rodent feces or urine or by inoculation of skin abrasions. Humans are infected primarily through infected rodents invading human habitats. Contact with infected rodent feces has produced disease in laboratory personnel.DIAGNOSIS:
is by serology or virus isolation. Control is to reduce opportunity for exposure to infected rodents. 1. JUNIN VIRUS: produces Argentinian hemorrhagic fever There is an illness of 1-2 weeks with insidious onset of fever, malaise, rigors, fatigue, headache, vomiting, constipation or diarrhea, conjunctival congestion, retro-orbital pain, epistaxis, petechial hemorrhages beneath skin, palate and gums. Edema of the upper body is possible. In severe cases hematemesis and melena, encephalopathy, bradycardia and hypertension occur. Case fatality rate 5-30%. Several hundred cases reported each year in Argentina. Associated with at least 3 different cricetine rodent species in Argentina 2. MACHUPO VIRUS: produces Bolivian Hemorrhagic fever Signs and case fatality rate like Junin virus. Case #s have been decreasing rapidly since initiation of rodent control programs in 1975. Associated with Calomys callosus (Bolivia). 3. LASSA FEVER: Serologically related to Lymphocytic Choriomeningitis, Machupo, and Junin virus. Fever has insidious onset over 2-3 days and may persist for up to 4 weeks, with malaise, headache and generalized aching and sore throat. Vomiting and diarrhea, possibly edema of face and neck, lymphadenopathy with hemorrhages and renal failure occurs in the second week. The prostration is out of proportion to fever. Often there is a maculopapular rash. Occurs in large areas in West Africa. Documented man to man transmission. Found in common rodent Mastomys natalensis, multimammate rat (West Africa).HEPATITIS A
(Infectious hepatitis, Epidemic hepatitis, Epidemic jaundice)AGENT:
Family Picornaviridae, Genus enterovirusRESERVOIR AND INCIDENCE
More than 200 cases of hepatitis A virus infection in humans have been associated with nonhuman primates, principally chimpanzees but also woolly and patas monkeys, Celebes apes, siamangs, and gorillas. Man, and, rarely captive chimpanzees are the reservoir host; less frequently, certain other nonhuman primates. An enzootic focus has been identified in Malaysia, but there is no suggestion of transmission to man.TRANSMISSION:
Although transmission of the virus may occur by contaminated needles, it is usually by the fecal-oral route. Nonhuman primates acquire the disease from man.DISEASE IN NONHUMAN PRIMATES:
Usually do not show clinical signs, although malaise, vomiting, and jaundice have been reported. Disease is detected by elevated liver enzymes or diagnostic liver biopsies. Usually a self-limiting disease.DISEASE IN MAN:
Fever, malaise, anorexia, headache, muscle pain, abdominal discomfort, and jaundice. Liver enzymes are elevated along with LDH, bilirubin, and alkaline phosphatase. Morbidity is variable and mortality is 0.6% Development of antibody confers lifelong immunity.DIAGNOSIS:
RIA or ELISATREATMENT:
Bed rest, IV fluids if dehydrated.PREVENTION/CONTROL:
Strictly quarantine newly arrived chimps and allow only limited human contact for at least 45-60 days. Protective clothing (gown, gloves, & mask) Routine disinfection of equipment and personal hygiene. Administer immune serum to handlers of newly imported chimpanzees (0.02ml/kg) every 3 mos. or 0.06 ml/kg every 4 months. Vaccine being developed.
HERPES B
(Herpesvirus simiae, Simian B Disease)AGENT:
Double-stranded DNA Virus. Direct zoonosis. For each Herpesvirus there exists a host for which the virus is almost uniformly fatal and reservoir hosts in which the virus exists in subclinical or latent infection. a. H. suis latent in swine, fatal in cattle. b. H. simplex I latent in man, fatal in Aotus, Gibbon, Marmoset (especially). c. H. saimiri I latent in Saimiri sciureus, fatal in Marmosets, Aotus (also known as Herpes T, Herpes M, Herpes Tamarinus). d. H. saimiri II latent in Saimiri sciureus, fatal in Marmosets, Aotus (this is an oncogenic virus, causing Malignant Melanoma of Reticulum Cell Type). e. H. simiae latent in rhesus and other macaques, fatal in man (also known as Herpes B Virus). f. Liverpool Vervet Monkey Virus: reservoir host ???, fatal in Cercopithecus aethiops. The Herpesviruses are serologically distinct but do share some antigenic properties. Herpes B Virus has been shown to have some antigenic relationship to Herpesvirus simplex by serum neutralization tests. However, antibody from Herpesvirus simplex does not confer immunity to Herpes B Virus.RESERVOIR AND INCIDENCE
Incidence of infection of the reservoir host is normally high but you rarely see clinical disease. Clinical disease is usually confined to the very young or to the immunologically compromised. On occasion lethal infection occurs in the reservoir host: in humans, generalized Herpes simplex is often fatal in infants; in swine, Herpes suis is fatal in piglets. Natural infection does not result in elimination of the virus or in immunity but produces a latent infection or carrier, which always makes vaccination of reservoirs impractical. Herpesvirus B was first described in 1934 by Sabin/Wright. The virus was recovered from a laboratory worker who had been bitten 18 days previously by an apparently healthy rhesus. Since 1934, there have been 24 reported cases, all fatal, except four. Of the four, only one is reasonably free of severe neurological deficits. (Patients have remained in coma for as long as 40 months prior to succumbing to the disease.) Incubation is considered to be 10-20 days from exposure to the virus; however, in the Pensacola cases, clinical disease occurred within 4-5 days of exposure. Contact with macaques does not constitute exposure. The susceptibility of man to clinical B infection is low although mortality is high.TRANSMISSION:
direct contact, including sexual transmission, aerosols, and fomites.THE DISEASE IN NHP:
The reservoir hosts for Herpesvirus simiae are monkeys of the genus Macaca. Monkeys incriminated include M. mulatta (rhesus), M. fascicularis (cyno), M. fuscata (Japanese macaque), and M. arctoides (Stump-tail macaque). B virus may produce mild cold-sore type lesions, primarily at mucocutaneous junctions, mucous membranes, and tongue. But, it has been demonstrated that infection is not confined to the mouth but can also be found in the genitalia. These lesions are similar to those caused by Herpesvirus simplex I in man. Two factors have been associated with antibody increases with age; 80-100% of imported adult rhesus may have antibody compared to 20% imported juveniles. The second factor was type of caging. Animals housed together had significantly higher titers than individually-caged animals. Clinical disease may develop at the time of primary infection but it is not known if lesions invariably follow infection. However, periodic shedding of the virus may occur without the presence of visible lesions. Once a monkey is infected with B Virus, it should be considered infective for life.THE DISEASE IN MAN:
Human infection is characterized by encephalitis with diplopia; nystagmus, patch paresthesia of head, neck and upper extremities. Acute abdominal pain, fever and diarrhea have also been observed prior to neurologic symptoms. Patients may also have a vesicular rash and/or keratoconjunctivitis. The histopathological changes resemble those of fatal, systemic Herpesvirus simplex in infants: encephalitis, myelitis and foci of necrosis in liver, spleen, lymph nodes and adrenals. The case fatality rate is 70%.DIAGNOSIS:
ELISA and viral isolation.TREATMENT:
acyclovir.PREVENTION/CONTROL:
Control includes personal hygiene, protective clothing and common sense in handling monkeys. The virus is susceptible to oxidizing agents, soap, and water. Guidelines for prevention and treatment have been developed. The reader is referred to the reference by Holmes, GP, et al for further details. Emphasis can not be too strong concerning the use of protective clothing when entering a room with macaques. A perfectly healthy monkey may be lethal to you.
(Rat Tapeworm Infection)
AGENT:
Hymenolepis diminuta is the common tapeworm of rodents. Size varies from 100-600 mm.RESERVOIR AND INCIDENCE
Rodents, many arthropods (fleas, beetles, and cockroaches) serve as intermediate hosts.TRANSMISSION:
Rodents and humans are infected by accidentally swallowing the infected arthropods, usually in cereals or stored products.DISEASE IN ANIMALS:
Mild catarrhal enteritis with diarrhea occurs if the infection is heavy.DISEASE IN MAN:
Light infections are generally asymptomatic. Heavy infections may cause diarrhea, abdominal pain, anorexia, vomiting, weight loss, and irritability, particularly in young children.DIAGNOSIS:
Infections are diagnosed by finding characteristic eggs in feces; proglottids are usually not seen.TREATMENT:
Niclosamide or praziquantel.PREVENTION/CONTROL:
Eliminate rodents and insects in facilities.AGENT:
Dwarf tapeworm, Hymenolepis nana - measures 5-90 mm long.RESERVOIRS AND INCIDENCE:
The animal reservoir is the house mouse, but humans can be both definitive and intermediate hosts. Worldwide occurrence in warm climates.TRANSMISSION:
Gravid proglottids disintegrate and eggs pass in the feces and may be ingested by another human. Larvae then develop in the intestinal villi and pass to the lumen of the gut to become the adult forms. Dogs, cats and their fleas can be infected as well as grain beetles which can serve as intermediate hosts.DISEASE IN ANIMALS:
Same as H. diminuta.DISEASE IN MAN:
Same as H. diminuta.DIAGNOSIS:
Same as H. diminuta.TREATMENT:
Same as H. diminuta.PREVENTION/CONTROL:
Personal hygiene, protective clothing and gloves Vermin control. Protect stored grains and feeds from grain beetles.INFLUENZA
(Swine and Equine Influenza, Fowl Plague)AGENT:
The causative agent is influenza type A (Orthomyxoviridae).RESERVOIR AND INCIDENCE
Humans, wild and domestic birds, horses and pigs are reservoirs of influenza viruses, which appear to be species specific. Convalescent carriers act as reservoir hosts between epidemics. Antigenic shift is probably required before animal virus becomes epidemic in humans. Sporadic human infections with swine and avian strains have been reported. Human cases of influenza have occurred from contamination by aerosols from infected ferrets and vice versa.TRANSMISSION:
Transmission is by inhalation of droplets produced by coughing and sneezing, especially in crowded, enclosed spaces.DISEASE IN ANIMALS:
Fever has a sudden onset followed by anorexia, coughing, respiratory distress and mucoid nasal discharge, with rapid recovery. There is consolidation in the lung. Copious mucopurulent exudate fills the bronchioles.DISEASE IN HUMANS:
Typical symptoms include fever, chills, headache, myalgia, malaise, coryza, pharyngitis and cough with full recovery within two weeks, although viral or secondary bacterial pneumonia may develop, especially in the elderly.DIAGNOSIS:
Virus isolation, CF or HI serology.TREATMENT:
Bed rest, analgesics, and cough mixtures. Amantadine decreases duration by 50%. Antibiotics are reserved for bacterial complications. Ribavirin aerosol has helped severely ill patients.PREVENTION/CONTROL:
Polyvalent human influenza vaccine provides partial immunity (about 85% efficacy) for a few months to one year. The vaccine's antigenic configuration changes yearly and is based on prevalent strains of the preceding year. Chemoprophylaxis with amantadine will markedly reduce the attack rate among exposed individuals if begun immediately and continued for 10 days. Vaccinate horses annually. Prohibit imports of live poultry and poultry meat from countries where fowl plague occurs.KASOKERO VIRUS
Am J Trop Med Hyg. 1986 Mar;35(2):387-92.
Kalunda M, Mukwaya LG, Mukuye A, Lule M, Sekyalo E, Wright J, Casals
J.
Two virus strains were isolated by mouse inoculation from blood of Rousettus aegyptiacus fruit-eating bats collected from Kasokero Cave in Uganda. Shortly after these strains were introduced in the laboratory, four additional strains were recovered from laboratory workers who had developed mild to severe illnesses presumably as a result of laboratory infection. Serological studies established that these six isolates are strains of the same virus. Serological tests showed also that this virus is related to Yogue, an unclassified virus.
PMID: 3082234 [PubMed - indexed for MEDLINE]
LEISHMANIASIS
[Cutaneous leishmaniasis: Chiclero ulcer, espundia, pianbols, uta, and buba (in the Americas); oriental sore, Aleppo boil (in the Old World); Bagdad boil, Delhi boil, Bauru ulcer (in the Middle East). Visceral leishmaniasis: kala-azar]AGENT:
The causative agents of cutaneous leishmaniasis are Leishmania mexicana and L. brasiliensis in the Americas, and L. tropica in the Old World; and of visceral leishmaniasis, L. donovani, L. infantum, and L. chagasi.RESERVOIRS AND INCIDENCE:
The geographic distribution of the cutaneous disease is Texas, Mexico, Central and South America, India, Pakistan, the Middle East, southern Russia, the Mediterranean coast and Africa. The distribution of visceral leishmaniasis is poorly reported, but foci probably occur in the Mediterranean basin, the Middle East, India, China, Mexico, Central and South America, and Africa. Wild animals, dogs and humans serve as reservoirs. Domestic dogs may be an important reservoir for humans. Humans are the only known reservoir in India.TRANSMISSION:
Sandfly vectors transmit cutaneous leishmaniasis. Person-to-person, congenital, and blood-borne transmission of visceral leishmaniasis are possible.DISEASE IN ANIMALS:
L. mexicana causes ulcers of the skin in rodents and other wild animals, usually at the base of the tail. L. braziliensis causes a systemic infection with few skin lesions in wild animals. No skin lesions have been found in dogs. Dogs infected by L. tropica may suffer form cutaneous lesions similar to those found in humans. L. donovani produces visceral lesions in dogs, with enlarged lymph nodes, liver and spleen.DISEASE IN HUMANS:
In the cutaneous disease, the primary lesion is a painful ulcer or nodule at the site of infection persisting for several months, with residual scarring. Further lesions may develop in skin and mucous membranes. Infiltration by inflammatory cells at the inoculation site supports the growth of the parasite. This progresses into a large area of chronically inflamed granulation tissue. The overlying skin undergoes hyperplasia and then necrosis with spreading ulceration. Metastatic lesions occur with a similar inflammatory reaction. The lesions may heal, become fibrosed or extend indefinitely to produce considerable disfigurement. In the visceral disease, intermittent irregular fever occurs with sweats, enlarged spleen, weight loss and anemia leading to ascites, edema, diarrhea and secondary infections. Dark pigmentation of the skin may occur. There is gross enlargement of liver and spleen. Without treatment, the case fatality rate is 90%.DIAGNOSIS:
Definitive diagnosis is achieved by finding the parasite-either the amastigote in stained smears or biopsies, or the motile promastigote in culture. Serologic and skin tests provide only indirect evidence of infection.TREATMENT:
Treatment remains inadequate because of drug toxicity, long courses required, and frequent need for hospitalization. The drug of choice is sodium antimony gluconate. Alternative drugs for some forms of infection are amphotericin B and pentamidine.PREVENTION/CONTROL:
Use insecticides in house and buildings to control the vector. Eliminate rubbish heaps which are breeding areas for sandflies. Avoid sandfly bites by using insect repellents and protective clothing. Keep dogs indoors after sundown and remove infected dogs.SYNONYM:
Hansen's disease.ETIOLOGY:
Mycobacterium leprae, a polymorphic acid-alcohol-fast bacillus. M. leprae is hard to distinguish from other unculturable mycobacteria naturally infecting animals. The failure of attempts to culture M. leprae in vitro constitutes a great barrier to better determining its biochemical characteristics for identification purposes as well as for therapeutic and immunologic studies. In part, this difficulty has been overcome, first, by in vivo culture on mouse foot pads and, lately, by the discovery that the leprosy organism can infect the nine-banded armadillo (Dasypus novemcinctus). At present, the latter serves as a model for lepromatous leprosy and provides a large number of bacilli for research.OCCURRENCE IN MAN:
An estimated 12 million people are affected by leprosy. The highest prevalence is in tropical and subtropical regions of Asia, Africa, Latin America, and Oceania. Leprosy is very prevalent in India, Southeast Asia, the Philippines, Korea, southern China, Papua New Guinea, and some pacific islands. Ninety percent of the cases reported in the Americas come from five countries: Argentina, Brazil, Colombia, Mexico, and Venezuela. Chile is the only South American country free of the infection. In the United States 2,500 cases are known, most of them in immigrants. Autochthonous cases arise in Hawaii, Puerto Rico, Texas, and Louisiana. The infection's prevalence is related to the socioeconomic level of the population. The fact that the disease has practically disappeared in Europe is attributed to the improved standard of living there. The proportion of total leprosy cases represented by lepromatous leprosy (see The Disease in Man) varies with the region. In Asia and the Americas this form makes up between 25 and 65% of all cases, while in Africa it accounts for only 6 to 20%.THE DISEASE IN MAN:
The incubation period is usually 3 to 5 years, but it can vary from 6 months to 10 years or more. Clinical forms of leprosy cover a wide spectrum, ranging from mild self-healing lesions to a progressive and destructive chronic disease. The polar form at one end of the spectrum is tuberculoid leprosy, and at the other, lepromatous leprosy. Intermediate forms are also found. Tuberculoid leprosy is characterized by localized lesions of the skin and nerves, often asymptomatic. Basically, the lesions consist of a granulomatous, paucibacillary, inflammatory process. The bacilli are difficult to detect, and can be observed most frequently in the nerve endings of the skin. This form results from active destruction of the bacilli by the cellular immunity of the patient. On the other hand, serum antibody titers are generally low. Nerve destruction causes lowered conduction; heat sensibility is the most affected, tactile sensibility less so. Trophic and autonomic changes are common, especially ulcers on the sole and mutilation of body members. Lepromatous leprosy is characterized by numerous symmetrical skin lesions consisting of macules and diffuse infiltrations, plaques, and nodules of varying sizes (lepromas). There is involvement of the mucosa of the upper respiratory tract, of lymph nodes, liver, spleen, and testicles. Infiltrates are basically histiocytes with a few lymphocytes. Cellular immunity is absent (negative reaction to lepromin) and antibody titers are high. In this form of the disease, as in the borderline, erythema nodosum leprosum (ENL) often appears. The indeterminate form of leprosy has still not been adequately characterized from the clinical point of view; it is considered to be the initial stage of the disease. The first cutaneous lesions are flat, hypopigmented, and have ill-defined borders. If this form is not treated, it may develop into tuberculoid, borderline, or lepromatous leprosy. Bacilli are few, and it is difficult to confirm their presence. Finally, the borderline form occupies a position intermediate between the two polar forms (tuberculoid and lepromatous), and shares properties of both; it is unstable and may progress in either direction. Destruction of nerve trunks may be extensive. Bacilli are observed in scrapings taken from skin lesions. An estimated one-third of clinical cases become incapacitated. half of them completely. Nevertheless, these proportions are now changing, due to both prevention/control programs and early implementation of effective treatments. There is evidence that inapparent infection may occur with a certain frequency among persons, especially family members, in contact with patients.THE DISEASE IN ANIMALS:
The disease in armadillos (Dasypus novemcinctus) is similar to the lepromatous form in man. Infection in these animals is characterized by macrophage infiltrates containing a large number of bacilli. Skin lesions vary from mild to severe. The small dermal nerves are invaded by the etiologic agent. Many bacilli are seen in the macrophages of the lymph tissue, in the pulp of the spleen, and in Kupffer's cells in the liver. M. leprae is known to prefer the coolish parts of the human or mouse body. For this reason, armadillos were used as experimental animals even before natural inaction was confirmed in them, since their body temperature is from 30 to 35oC. Experimental inoculation of armadillos with human leproma material reproduces the disease, characterized by broad dissemination of the agent, and involvement of lymph glands, liver, spleen, lungs, bone marrow, meninges, and other issues, in a more intense form than is usually observed in man. The disease in the chimpanzee appeared as a progressive chronic dermatitis with nodular thickening of the skin of the ears, eyebrow nose, and lips. Lesions of the nose, skin, and dermal nerves contained copious quantities of acid-fast bacteria. The case was histologically classified as borderline 12 months after the clinical symptoms were first observed, and as lepromatous after a later biopsy. In the case of the Cercocebus monkey, the initial lesion consisted of nodules on the face. Four months later, a massive infiltration and ulceration were seen on the face and nodules appeared on the car and the forearms. Sixteen months after cutaneous lesions were first observed. The animal began to suffer deformities and paralysis of the extremities. Histopathologic findings indicated the subpolar or intermediate lepromatous form. The disease was progressive, with neuropathic deformation of feet and hands. It seemed to regress when specific treatment was administered. The animal apparently contracted the disease from a patient with active leprosy. Experimental infections carried out to date have indicated that these animals may experience a spectrum of different forms similar to those in man.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
Man is the principal reservoir of M. leprae. The method of transmission is still not well known due to the extended incubation period. Nevertheless, the principal source of infection is believed to be lepromatous patients, in whom the infection is multibacillary, skin lesions are often ulcerous, and a great number of bacilli are shed through the nose similarly. Bacilli are found in the mouth and pharynx. Consequently, transmission might be effected by contact with infected skin, especially through wounds or abrasions, and by aerosols, as is the case in tuberculosis. Lately, more importance has been attributed to aerosol transmission. Oral transmission and transmission by hematophagous arthropods are not discounted, but they are assigned less epidemiologic importance. Until recently, leprosy was believed to be an exclusively human disease. But research in recent years has demonstrated that the infection and the disease also occur naturally in wild animals. Even though some researchers have expressed doubt that the animal infection is identical to the human, at present an accumulation of evidence indicates that the etiologic agent is the same. The origin of infection in animals is unknown. It is believed that armadillos contracted the infection from a human source, perhaps from multibacillary patients before the era of sulfones. In this regard, it should be pointed out that leprosy bacilli may remain viable for a week in dried nasal secretions and that armadillos are in close contact with the soil. The high disease prevalence in some localities would indicate armadillos can transmit the infection to one another, either by inhalation or direct contact. Another possible transmission vehicle is maternal milk, in which the agent has been detected. It is difficult to demonstrate that armadillos are a source infection for man because of the long incubation period in humans and the impossibility of excluding a human source in an endemic area. In Texas, a case of human leprosy was attributed to a patient's practice of capturing armadillos and eating their meat. Subsequently, another five cases with hand lesions were detected in natives of the same state who habitually hunted and cleaned armadillos but had no known contact with human cases. The prevalence of leprosy in armadillos in Louisiana and Texas suggests that these animals could serve as a reservoir of M. leprae; however, nothing is known about the frequency of infection in nonhuman primates and the role they may play in transmission of the disease. The sources of the cases of leprosy in these animals were probably people with lepromatous leprosy.DIAGNOSIS:
Laboratory confirmation of leprosy requires the demonstration of acid-fast bacilli in scrapings from slit skin smears or the nasal septum. Biopsy of skin or of a thickened involved nerve also gives a typical histologic picture. M. leprae does not grow in artificial media.CONTROL:
Control is based on early detection and chemotherapy. In the face of multiple confirmed cases of resistance to dapsone, combination of this medication with rifampicin is presently recommended for paucibacillary leprosy, and the same two medications in combination with clofazimine for multibacillary leprosy. Rifampicin has a rapid bactericidal effect and eliminates contagion in patients in 1 to 2 weeks. The isolation of patients in leprosariums is no longer necessary, since the chemotherapy effectively eliminates infectiousness and thereby interrupts transmission of the disease.[Weil's disease, Hemorrhagic jaundice (Leptospira icterohaemorrhagiae), canicola fever (L. canicola), dairy worker fever (L. hardjo)]
AGENT
: Spirochete, Leptospira. Pathogenic leptospires belong to the species Leptospira interrogans, which is subdivided into more than 200 serovars. The main natural reservoirs for human infection vary with serovar: L. canicola in dogs, L. hardjo in cattle, L. pomona in swine, and L. icterohaemorrhagiae in rats.RESERVOIR AND INCIDENCE
Rats, mice, field moles, guinea pigs, gerbils, squirrels, rabbits, hamsters, reptiles, nonhuman primates, livestock, and dogs. In one study, 40 % of stray dogs were seropositive. Rats and mice are common animal hosts for L. ballum. Infection in mice is inapparent and can persist for the animal's lifetime. *Rodents are the only major animal species that can shed leptospires throughout their life-span without clinical manifestations. Active shedding by lab animals can go unrecognized until personnel handling the animals become clinically ill.TRANSMISSION:
Handling affected animals, contaminating hands, or abrasions with urine, or aerosol exposure during cage cleaning are most common. The organism is often transmitted to humans by the urine of the reservoir host. The organism may also enter through minor skin lesions and probably via the conjunctiva. Many infections have followed bathing or swimming in infected waters.DISEASE IN ANIMALS:
In cattle, fever and anorexia occur with rapid decline in milk yield and atypical mastitis. Pregnant cows abort with retention of the placenta. Also, mild jaundice and severe anemia occurs with enlarged and friable liver and swollen kidneys. In pigs subclinical infection is common, though it can cause abortion and birth of weak piglets. In dogs and cats, gastroenteritis, jaundice, and nephritis may occur.DISEASE IN MAN:
Ranges from inapparent infection to severe infection and death. Biphasic Illness a. Weakness, headache, myalgia, malaise, chills, & fever. b. Leukocytosis, painful orchitis (testes not usually enlarged), conjunctival effusion, and rash. Icteric leptospirosis (Weil's syndrome-usually caused by L. icterohaemorrhagiae) is the most severe form of the disease, characterized by impaired renal and hepatic function, abnormal mental status, hypotension, and a 5-10% mortality rate. Signs and symptoms are continuous and not biphasic.DIAGNOSIS:
Early in the disease, the organism may be identified by darkfield examination of the patient's blood or by culture on a semisolid medium. Culture is difficult and requires several weeks. A rapid diagnosis is made with the DOT-ELISA test. *Leptospires can be recovered only from mature mice even though antibodies can be detected from infected mice of all ages.TREATMENT:
Penicillins or tetracyclines. Can eliminate L. ballum from a colony (mice) with 1000 gm chlortetracycline HCL/Ton of feed for ten days.PREVENTION\CONTROL:
Vaccination in cattle, swine, and dogs Avoid swimming in or drinking from potentially contaminated water. Protect workers by providing boots and gloves. Rodent control. Drain wet ground. Doxycycline chemoprophylaxis for persons at high exposure.LISTERIOSIS
(Circling disease)AGENT
- Listeria monocytogenes, gram positive, pleomorphic rodRESERVOIR AND INCIDENCE
Isolated from fish, birds, swine, horses, ruminants, guinea pigs, ferrets, gerbils, rabbits, and chinchillas. The principle reservoir of the organism is in forage, water, mud, and silage. The seasonal use of silage as fodder is frequently followed by an increased incidence of listeriosis in animals.TRANSMISSION:
outbreaks have been reported associated with ingestion of unpasteurized milk and cheese and contaminated vegetables; some sporadic cases may also be due to foodborne transmission. Refrigeration of foods may provide selective growth of Listeria. Papular lesions on hands and arms may occur from direct contact with infectious material or soil contaminated with infected animal feces. In neonatal infections, the organism may have been transmitted from mother to fetus in utero or during passage through the infected birth canal. Person-to-person transmission through venereal contact is possible, as is infection from inhalation of the organism.DISEASE IN ANIMALS:
Two forms exist, the meningoencephalitic and visceral. The former involves neurological signs with dullness and somnolence. Drooling and lack of interest in food and mastication soon follow. There is lateral deviation of the head with a tendency to circle. Paralysis then sets in with recumbency and death from respiratory failure. The visceral from involves abortion, with retained placenta. Microabscesses occur throughout the brain. Visceral lesions involve multiple foci of necrosis in the liver, spleen and heart. Placental lesions are characteristic with yellow necrotic foci and multiple granulomas in the fetal liver. Abscess formation in the eye can lead to blindness. Fatality is very high, approaching 3-30% in outbreaks.DISEASE IN MAN:
Symptomless fecal carriage is common. Fever, headache, nausea, vomiting, endocarditis, granulomatous lesions in multiple organs, cutaneous involvement, coryza, conjunctivitis, metritis with abortion, sepsis, & meningitis. Granulomatous lesions and abscesses occur in the liver and other organs and beneath the skin. Focal necrosis in the placenta with mononuclear infiltration is seen. Fatality rates may exceed 20%.DIAGNOSIS:
culture and isolation (special media required). Serologic tests are unreliable because of cross reactions with other bacterial species.TREATMENT:
ampicillin plus an aminoglycoside or Trimethoprim-sulfamethoxazole.PREVENTION\CONTROL:
caution and protective clothing when handling infected tissues. Pregnant women and immunocompromised individuals should avoid contact with potentially infective materials such as aborted animal fetuses and known infected persons; they should eat only properly cooked meats and pasteurized dairy products.(Lyme arthritis, Bannworth's syndrome, tick-borne meningopolyneuritis, erythema chronicum migrans [ECM], Steere's disease)
AGENT:
spirochete, Borrelia burgdorferiRESERVOIR AND INCIDENCE
First implicated in 1982 as agent in a 1975 epidemic of juvenile inflammatory arthropathy in Old Lyme Connecticut. Cases have been reported from 46 states and the annual number of Lyme disease cases has increased 18 fold from 497 to 8803. It is now the most common tick transmitted disease in the USA. Also seen in Europe, England, Soviet Union, China, Japan, Southeast Asia, South Africa, Australia, and Canada.TRANSMISSION:
Transmitted mostly by Ixodes dammini and other ixodid ticks (three host tick with a two to three year life cycle). Ixodes dammini has a broad range of hosts; adults prefer white tailed deer but will also parasitize dogs, horses, and humans. Larvae feed primarily on rodents, especially mice. Nymphs feed on all hosts and appears to be primarily responsible for transmission of the disease to people. Birds are an important reservoir and means of dispersal. Also found in Dermacentor, Rhipicephalus and Amblyomma and other ticks and biting insects, including mosquitoes, fleas, and biting flies. Because of lack of any proof to the contrary it is generally believed at this time that any potential increased risk to human beings from infected animals is attributable to animals bringing ticks into areas of human habitation rather than any pet transmission. Dogs appear to be at greater risk than humans.DISEASE IN ANIMALS:
Serologic evidence has been reported in the dog, cat, horse, and ruminants. However, correlation with disease is lacking except in the dog. The dog exhibits the same symptoms as noted below for humans. Expanding skin lesions have been noted in mice and rabbits.DISEASE IN MAN:
Multisystemic disease which may have chronic sequelae; an annular rash known as erythema chronicum migrans (ECM) develops in 60-80% of patients in the area of the tick bite and is considered pathognomonic. Also flu like symptoms, which resolve in about three weeks. 8-10% of people develop cardiac involvement several weeks later. Manifestations include atrioventricular block, cardiomyopathy, heart failure, myocarditis, and pancarditis. 15% develop neurologic disorders such as facial nerve palsies which usually resolve. Other manifestations include meningitis, cranial neuritis, radiculoneuritis, neuropathy, and encephalopathy. 60% develop the most common sequelae, arthritis. Disease may remain latent with symptoms developing 4 years after seroconversion.DIAGNOSIS:
Most common test is detecting antibody titers by IFA or ELISA (on blood, CSF or synovial fluid). Culture is definitive but is difficult and requires special media such as Barbour-Stoener-Kelly media. Histologically with Dieterle Silver Stain or immunoperoxidase stains, but is often unrewarding.TREATMENT:
A positive serology is no grounds for treatment when no clinical signs are present. Borrelia burgdorferi is sensitive to tetracycline and moderately sensitive to penicillin. amoxicillin, ceftriaxone, and imipenem are also highly active.PREVENTION\CONTROL:
Tick control care when removing ticks or when handling potentially infective materials a vaccine against Lyme Disease tested in hamsters has been found effective. More research is needed but in the future vaccination may be beneficial for those at constant risk of exposure.LYMPHOCYTIC CHORIOMENINGITIS - LCM
AGENT:
Arenavirus Of many latent viruses present in mice, only LCM naturally infects humans. LCM can easily be transmitted from animals to humans. Isolated by Armstrong and Lillie during investigation of a St. Louis Encephalitis outbreak in 1933.RESERVOIR AND INCIDENCE
Worldwide in wild mice (M. . musculus). This disease is principally confined to the eastern seaboard and northeastern states in the U.S. Wild mice infect the lab mouse. Mouse and hamster are the only species in which long term, asymptomatic infection is known to exist. *LCM virus is present in experimental mouse tumors which is a second source of infection for humans. This was first recognized in a transplantable leukemia of C58 mice. The disease can also be transmitted to laboratory animals via inoculation of infected tissue culture cells. The infection also occurs in guinea pigs, rabbits, rats, canines, swine, and primates.TRANSMISSION:
Infection in mice is maintained by congenital infection followed by lifelong carriage and excretion of virus in saliva, urine, and feces. Human infections are probably from contaminated food and dust, the handling of dead mice, and mouse bites. Bloodsucking arthropod vectors such as ticks, lice, and mosquitos may transmit the disease. Person to person transmission does not occur.DISEASE IN ANIMALS:
The clinical signs of LCM depend on the host's resistance and age when infected, although the various categories of the disease are not always clearly delineated. Animals infected in utero or during the first 48 hours postpartum may develop a transient viremia but recover completely within a few weeks. Other animals similarly infected may develop a persistent tolerant infection (PTI) that continues asymptomatically for 6 or more months. Animals infected after the first few days, when the virus will be recognized as foreign, often overcome the infection completely, but an acute, usually fatal syndrome can develop. Signs of acute infection in mice continue for 1-2 weeks and include decreased growth, rough hair coat, hunched posture, blepharitis, weakness, photophobia, tremors, and convulsions. The terminal stage of the PTI, which occurs over several weeks to 5 to 12 month old mice, is characterized by weight loss, blepharitis, and impaired reproductive performance and runted litters. The important necropsy signs are microscopic. Visceral organs, including the liver, kidneys, lungs, pancreas, blood vessels, and meninges, are infiltrated by lymphocytes. A glomerulonephritis of probable immune complex origin is a characteristic feature of terminal PTI.DISEASE IN MAN:
The features may include influenza-like illness for up to 2 weeks, possibly with orchitis. Sometimes meningitis, paralysis and coma follow. Joint pains occur during convalescence.DIAGNOSIS:
CF or virus isolation.PREVENTION/CONTROL:
serologic monitoring Infection can be eradicated by cesarean derivation prevent wild mice from entering facilities control ectoparasites and roaches Restrict flow of traffic into and out of LCM infected colonies Protective clothing and proper care when handling infected animals or tissues. Basic hygienic practices Screen tissue culture cell lines and murine tumor lines and animals periodic serologic testing of high risk personnelMARBURG VIRUS
(African Hemorrhagic Fever, Green or Vervet Monkey Disease)AGENT:
Agent is classified as a Filovirus. It is an RNA virus, superficially resembling rhabdoviruses but has bizarre branching and filamentous or tubular forms shared with no other known virus group on EM.RESERVOIR AND INCIDENCE
An acute highly fatal disease first described in Marburg, Germany in 1967. Brought to Marburg in a shipment of infected African Green Monkeys from Uganda. 31 people were affected and 7 died in 1967. Exposure to tissue and blood from African Green monkeys (Cercopithecus aethiops) or secondary contact with infected humans led to the disease. No disease occurred in people who handled only intact animals or those who wore gloves and protective clothing when handling tissues. A second outbreak was reported in Africa in 1975 involving three people with no verified contact with monkeys. Third and fourth outbreaks in Kenya 1980 and 1987. Natural reservoir is unknown. Monkeys thought to be accidental hosts along with man. Antibodies have been found in African Green monkeys, baboons, and chimpanzees. 100% fatal in experimentally infected African Green Monkeys, Rhesus, squirrel monkeys, guinea pigs, and hamsters.TRANSMISSION:
Direct contact with infected blood or tissues or close contact with infected patients. Virus has also been found in semen, saliva, and urine.DISEASE IN NONHUMAN PRIMATES:
No clinical signs occur in green monkeys, but the disease is usually fatal after experimental infection of other primate species. Leukopenia and petechial hemorrhages throughout the body of experimentally infected monkeys, sometimes with GI hemorrhages.DISEASE IN MAN:
5-7 day incubation period. Headache, fever, muscle pain, vomiting, diarrhea, hemorrhagic diathesis, Conjunctivitis, photophobia, skin rash, and jaundice. Leukopenia, thrombocytopenia, proteinuria. Shock and death in 25% of cases. Hemorrhages throughout the body on post mortem examination.DIAGNOSIS:
IFA, ELISA, Western blot, EM, or virus isolation.TREATMENT:
Supportive Possibly immune serumPREVENTION/CONTROL:
Strict quarantine on newly imported, wild-caught primates. Naturally infected monkeys should become ill or die within several weeks. Hygiene, sanitation, and protective clothing Isolation of human patients with prevention of sexual intercourse until semen is free of virus.MEASLES
(Rubeola, Morbilli)AGENT:
Family Paramyxoviridae, Genus Morbillivirus. The same genus contains the viruses of Canine Distemper and Bovine Rinderpest.RESERVOIR AND INCIDENCE
Man is the only known reservoir. New world monkeys are more resistant than old world monkeys but exhibit high mortality when infected.TRANSMISSION:
Virus is excreted from the mucous membranes of the eye and pharynx and later from the respiratory and urinary tracts. Virus is shed in the prodromal phase and continues through the exanthematous phase. Highly contagious! Can spread from man to monkey, monkey to monkey, man to man, and monkey to man.DISEASE IN NONHUMAN PRIMATES:
Many infections occur subclinically. Rash, fever, facial edema, giant cell pneumonia, conjunctivitis, nasal discharge.DISEASE IN MAN:
Incubation period 10-14 days. Conjunctivitis Koplik spots - bluish white spots on buccal mucosa 2-3 days after onset Leukopenia Rash in mouth, cheeks, neck, chest, and body. Can be complicated by middle ear infection, bronchopneumonia, encephalitis Fetal risk if contracted during pregnancy. The mortality rate in children in the U.S. is 0.2%, but may be as high as 10% in developing countries.DIAGNOSIS:
clinical signs, serology, histopath.TREATMENT:
Bed rest, acetaminophen, saline eye sponges, nose drops. Vitamin A (400,000 IU/day) has been shown to reduce pediatric morbidity and mortality.PREVENTION/CONTROL:
Vaccinate personnel working with nonhuman primates (Live attenuated measles vaccine) if they do not have: 1. a titer to rubeola (HI >1:4 protective) 2. confirmed history of previous vaccination 3. confirmed prior disease Live attenuated measles vaccine can be given to macaques but causes disease and death in marmosets and owl monkeys.MELIOIDOSIS
(Pseudoglanders, Whitmore's disease)AGENT:
Pseudomonas pseudomallei (Malleomyces pseudomallei, Actinobacillus pseudomallei ) --MOTILE, Gram negative rodRESERVOIR AND INCIDENCE
Normal inhabitant of surface soil and water in Southeast Asia, and tropical areas. Recent studies have shown that the water of tanks in which exotic aquarium fishes were imported was contaminated. Occurs in wild rodents, goats, pigs, sheep. Also identified in Chimps, orangutans, and macaques. There is no evidence that animals are important reservoirs, except in the transfer of the agent to new foci. Rare in the U.S. except in drug users.TRANSMISSION:
by inhalation from moist soil-water reservoir, by contact with contaminated soil or water thru overt or inapparent skin wounds, or by ingestion of contaminated feeds. Can be venereal in man.DISEASE IN ANIMALS:
Signs include loss of weight, swelling of joints, fever, cough, and chest pain. Skin lesions with fistulous tracks can develop. Emaciation and multiple abscesses in lung, bone, viscera. A chronic draining purulent skin lesion in a primate is suspect. Incubation period can be 6 months to three years. Sheep seem especially susceptible- over 25% mortality can occur in outbreaks.DISEASE IN MAN:
Clinical disease is not common in man but subclinical disease in endemic areas based on serology is common. It may simulate typhoid fever or TB including pulmonary cavitation, empyema, chronic abscesses and osteomyelitis. High case fatality rate (80%) in people who do develop clinical signs.DIAGNOSIS:
Culture and isolation from lesions, a rising serological titer is confirmatory.TREATMENT:
ceftazidime. Alternates: Chloramphenicol or Trimethoprim-sulfamethoxazole.CONTROL:
Safe disposal of sputum and wound discharges.MICROSPORIDIOSIS
Protozoa of the order Microsporidia (Phylum: Microspora) are represented by about 700 species parasitic in hosts of many invertebrate and vertebrate groups. These protozoa have only recently been recognized as "opportunistic" parasites in patients with AIDS. In veterinary medicine, Microsporidia are well known as causative agents of certain animal infections, such as nosemosis in bees, encephalitozoonosis in rabbits and of numerous fish diseases. Microsporidia are obligatory intracellular parasites (macrophages, histiocytes, endothelial cells, kidney tubular cells, etc.) with a characteristic spore stage and a unique mode of infecting host cells. Spores of Microsporidia species infecting mammals are ovoid or piriform, 1.5-5.0 m long with mostly a thick wall consisting of 2 main layers (exospore, endospore). The spore contains a coiled, minute tube (polar tube or polar filament) connected with a complex extrusion apparatus and a nucleated, infective sporoplasm. After ingestion by a suitable host, the physiological conditions of the digestive tract stimulate the spores to evert with force the coiled polar filament. The tip of the filament penetrates the host cell membrane, the sporoplasm migrates through the tube and enters the cytoplasm where asexual multiplication (merogony) and spore formation (sporogony) occur. Sporoplasms usually infect the gut epithelium either to develop there or to be transferred, probably by the action of phagocytic cells, to the circulation and their preferred site of development in various organs. The spores, released to the environment from the intestinal or urinary tract, are ingested by a new host. All Microsporidia examined so far have a direct developmental cycle. Up to now 5 genera of Microsporidia have been identified as causative agents of human infections. ENCEPHALITOZOON CUNICULI has a worldwide distribution and is a common parasite of wild and domesticated rabbits, laboratory rodents and a wide spectrum of other mammals such as carnivores, ruminants, pigs, monkeys and man. Encephalitozoon parasites found in birds may belong to other species. E. cuniculi, widespread in conventional rabbit colonies in up to 76% of the stock, mostly causes latent infections and only rarely disease. Focal granulomatous encephalitis and nephritis are the main pathological changes. Natural transmission in rabbits is possible by the oral, tracheal and transplacental routes, but oral infection appears to be the most important way. In rabbits, spores of E. cuniculi are excreted in the urine in concentrations up to 106 spores/ml. The human cases of E. cuniculi infections include two cases of encephalitis with a favorable evolution in two immunocompetent children. In a 35-year old man with AIDS the E. cuniculi infection resulted in a granulomatous hepatitis. Recently, another case in a 45-year old patient with AIDS (Greek nationality) was described in Switzerland. An unusual peritonitis with a large granulomatous mass, containing developmental stages of E. cuniculi, were found at autopsy. In Sweden (S) and Great Britain (GB) high prevalences of serum antibodies against E. cuniculi antigen have been detected in persons with malaria (S: 38%, GB: 7%), Chagas disease (S: 15%), schistosomiasis (GB: 12%), filariases (S: 9%), neurological disorders (GB: 6%) and in travellers after a stay in the tropics (S: 12%) while non-exposed persons, animal dealers and some other groups were seronegative. The question is open whether E. cuniculi is more common in the tropics or whether tropical parasites cause immunodepression which supports microsporidian infections. Besides a systemic infection in a immunodefective child with Nosema conori and two cases of keratitis caused by Microsporidian species, the recent description of a myositis in an AIDS patient due to Pleistophora sp. is of special interest as parasite transmission from fish was suspected. Another species of this group is Enterocytozoon bieneusi. This parasite was first described in 1984 in France in a 29-year old AIDS patient who had suffered from heavy diarrhea. Microsporidia were found in enterocytes of the duodenum, jejunum and ileum. This parasite or similar forms were subsequently detected in at least 9 other patients with AIDS in the USA, Uganda and the Netherlands. The origin of this parasite is unknown. An infection similar to E. bieneusi in the enterocytes of a Callicebus monkey has been described.DIAGNOSIS:
Diagnosis is based on the direct detection of Microsporidia by histology after hematoxylin-eosin, Giemsa, Gram or other staining (spores are Gram-positive!) or by electron microscopy in autopsy or biopsy material. Serum antibody detection provides another tool for the in vivo diagnosis of encephalitozoonosis.TREATMENT:
Information on chemotherapy of microsporidian infections is scanty. In experimental infections chloroquine and oxytetracycline reduced harvests of E. cuniculi spores only by 69% and 58%, respectively. Treatment of an AIDS patient suggested that either metronidazole or ganciclovir may have inhibited the microsporidian infection.MONKEY POX
AGENT:
Orthopoxvirus Disease in humans is indistinguishable from smallpox, (Variola) i.e., serologic & clinical syndrome.RESERVOIR AND INCIDENCE
Animals: Nine reported outbreaks in captive NHP's, primarily rhesus and cynomolgus. Has also been reported in languors, baboons, chimpanzees, orangutans, marmosets, gorillas, gibbons, and squirrel monkeys. The virus has been isolated from a wild squirrel. Man: The first human case of Monkey Pox was reported in 1970. Between 1970 and 1986, over 400 cases had been reported from tropical rain forested areas of West and Central Africa.TRANSMISSION:
Transmission can be via direct contact, aerosol, ingestion, or parenteral administration. Person to person transmission can occur.DISEASE IN NONHUMAN PRIMATES:
Usually exhibit a high morbidity and low mortality. Clinical signs may be inapparent or an animal may exhibit fever, lymphadenopathy, and cutaneous eruptions of the extremities, trunk, lips, or face. Cynos seem to be most severely affected. Death is uncommon except in infant monkeys.DISEASE IN MAN:
Signs in man include fever, sore throat, headache, and a vesiculopustular rash of peripheral distribution which clears up in 5 to 25 days. Severe complications include bronchopneumonia, vomiting, and diarrhea. Case fatality rate 10-15%. Although the disease is not common in man it is important from the standpoint of differentiating it from smallpox.DIAGNOSIS:
based on progression of lesions, histopathology and virus isolation. On histological examination epidermal cells contain eosinophilic cytoplasmic and intranuclear inclusions. ELISATREATMENT:
Symptomatic.PREVENTION/CONTROL:
Sanitation, isolation. Vaccination with vaccinia virus is protective in both man and nonhuman primates.(Flea-borne Typhus Fever, Endemic Typhus Fever, Urban Typhus)
AGENT:
Rickettsia typhiRESERVOIR AND INCIDENCE
Natural pathogen of rats and mice. Other mammals including cats, and their ectoparasites have been found infected. Outbreaks continue to occur in U.S., especially Texas. Natural lab infections have not been reported but lab acquired infections in people handling experimentally infected mice have been documented.TRANSMISSION:
Transmitted by flea or lice (Xenopsylla cheopis, Nosopsyllus fasciatus) to rodents or man. Humans are infected by contamination of flea bites, broken skin or conjunctiva by flea feces. Domestic animals may transport the flea vector to humans. Inhalation of contaminated dust may be a route of infection.DISEASE IN ANIMALS:
The agent localizes in the brain and various organs but with no known lesions.DISEASE IN MAN:
There is a gradual onset of fever with severe headache, rigors, generalized pains and dry cough (sometimes developing to bronchopneumonia) of about 2 weeks. A macular rash appears by about 5 days, first appearing on the trunk and lasting about six days. CNS manifestations are possible. Damage is caused to vascular endothelia by invasion of rickettsia, possibly leading to thrombosis and hemorrhage. In untreated case, the case fatality rate is 1-2%.DIAGNOSIS:
CF or IFA.TREATMENT:
Tetracycline or chloramphenicol.PREVENTION/CONTROL:
Control wild rodents. In endemic areas control fleas while exterminating rats.
Neisseria canis infection: a case report
Sandie Safton,1 Gavine Cooper,1 Michael Harrison,1 Lynne Wright1 and Paul Walsh2
Abstract
The third case report, which is the first in Australia, of human infection with Neisseria canis is documented. This is the first case report in which the pathogenicity of this organism for humans is unequivocally demonstrated. Commun Dis Intell 1999;23:221.
INTRODUCTION:
Neisseria canis (N. canis ) was first described by Berger in 1962.1 The bacteriums normal habitat is the throat of the cat and dog. It is regarded as a true Neisseria with phenotypic properties that allow its recognition as a distinct species.2,3 Only two previous case reports of human infection have been found by the authors.4,5 The first case of human infection with N. canis was published by Hoke and Vedros4 in 1982. This isolate came from a cat bite wound on a child. No other clinical details were described. In 1989 N. canis was reported in a mixed culture that included Pasturella multocida (P. multocida) and Eiknella corrodens from a cat bite wound on the arm of a previously healthy 36 year old woman. The wound was inflamed and the patient was successfully treated with amoxycillin. P. multocida was regarded as the primary pathogen in this case.5CLINICAL FEATURES:
The patient, a 50 year old male normally in good health, presented with a purulent wound to the sole of his foot, with surrounding cellulitis. The patient recalled having trod on a dog bone a few days previously. A swab for culture was taken and antibiotics commenced (metronidazole and amoxycillin/clavulanic acid). Seven days later he made a complete recovery apart from some residual induration.
METHODS:
LABORATORY DIAGNOSIS:
Standard bacteriologic techniques as outlined in the Manual of Clinical Microbiology 6 were used. The Gram stain showed moderate numbers of polymorphs. A moderate pure growth of a small gram negative coccus was obtained on aerobic blood agar, with the formation of yellowish non-haemolytic, 2 - 4 mm slightly flat topped colonies after 48 hours. It grew well on nutrient agar but did not grow on MacConkey agar. The organism was a facultative anaerobe, non-capnophilic and growth at 37oC was better than at 30oC or 42oC. The remainder of the diagnostic tests were consistent with the identification of N. canis, and it was sensitive to benzylpenicillin, erythromycin, and tetracycline but resistant to vancomycin.A conserved segment (441 base pairs) of the isolates RNA was subject to molecular studies, using BLAST analysis with the GeneBank7 data bank. A significant similarity was found with a sequence of 422 matching base pairs (95%) with GenBank Accession number L06170 - Neisseria canis ATCC 14687.
DISCUSSION:
It is considered without doubt that N. canis was pathogenic. Currently the organism is a very rare isolate associated with cat or dog contact, but it may be under reported. The laboratory diagnostic clues are the isolation of an oxidase positive, gram negative, non-fastidious coccus that is very strongly catalase positive and forms dull yellow flat-topped non-haemolytic colonies on Day 2. It is nitrate positive but otherwise essentially asaccharolytic and rather inert in its biochemical reactions. It is described in the literature as galactosidase negative, tributyrin hydrolysis negative, DNase negative, nitrite negative and polysaccharide synthesis negative.3,6 Currently there is no reason to suspect that the organism would not be covered by the current Australian Antibiotic Guidelines8 for the management of animal bites.REFERENCES:
1. Berger U. Uber das vorkommen von neissien bei einigen. Tieren. Z Hyg. 1962;148:445-57.
2. Weyant RS, et al. Identification of unusual pathogenic gram- negative aerobic and facultatively anaerobic bacteria. 2nd Edition. Baltimore: Williams and Wilkins, 1995.
3. Krieg NR, Hold JG (Eds). Bergeys manual of systematic bacteriology, Vol 1. Baltimore: Williams and Wilkins, 1984.
4. Hoke C, Vedros NA. Characterization of atypical aerobic gram-negative cocci isolated from humans. J Clin Microbiol 1982;15:906-14.
5. Guibourdenche M, Lambert T, Riou, JY. Isolation of Neisseria canis in a mixed culture from a patient after a cat bite. J Clin Microbiol 1982;27:1673-74.
6. Murray PR (ed). Manual of Clinical Microbiology. 6th Edition Washington: ASM Press, 1995.
7. Benson DA, et al Nucleic Acids Res.26(1)1-7.
8. Therapeutic Guidelines Antibiotic, 10th Edition 1998-1999. Therapeutic Guidelines Limited, Melbourne, 1998.Author references1. Sullivan and Nicolaides and Partners Pathology, Lismore, New South Wales2. General Practitioner, Evans Head, New South Wales
NEWCASTLE DISEASE
(Pseudo Fowl Pest)AGENT:
Newcastle disease virus, family ParamyxoviridaeRESERVOIR AND INCIDENCE
The natural reservoir is wild and domesticated birds.TRANSMISSION:
Transmission is by inhalation of infectious aerosols. Intensive conditions favor spread by contact, on inanimate objects and airborne between poultry houses. Human infections occur mainly amongst laboratory workers and those who work with infected chickens or who give live vaccine, especially by aerosol.DISEASE IN ANIMALS:
In poultry, respiratory and nervous signs occur, including gasping and coughing; also drooping of wings, twisting of the head and neck; inappetence and paralysis. Egg production ceases. Petechial hemorrhages are characteristic, especially in the preventricular mucosa. Necrosis of the intestinal mucosa give a "bran" like appearance. Congestion and mucoid exudate appears in the lungs and bronchi.DISEASE IN HUMANS:
Usually symptoms are confined to painful conjunctivitis lasting a few days, but fever and influenza-like symptoms for up to 3 weeks may follow.DIAGNOSIS:
Virus isolation or ELISA.TREATMENT:
Symptomatic.PREVENTION/CONTROL:
Hygienic precautions are needed when handling infected birds. Avoid inoculation injuries and ensure laboratory safety. Maintain strict hygiene in poultry sheds and quarantine of imported live birds, prohibit importation from infected countries, sterilization of, or prohibition on, waste food fed to poultry. Vaccination of poultry.OESOPHAGOSTOMIASIS
(Nodular Intestinal Worm Infection)AGENT:
The causative agents are Oesophagostomum stephanostomum, bifurcum, and aculeatum.RESERVOIR AND INCIDENCE
The parasite lives in the intestines of various primates and sometimes humans. These definitive hosts can sometimes serve as intermediate hosts. It occurs mainly in Africa, but occasionally in South America and Asia.TRANSMISSION:
Eggs passed in feces release larvae which infect the definitive host on ingestion. The parasite invades the intestinal wall to form nodules. The fourth stage larvae which develop in these nodules migrate to the lumen of the large intestine to form the adult worm and complete the life cycle.DISEASE IN ANIMALS:
Mild infection is subclinical. Abdominal pain follows more severe infection with diarrhea or even dysentery. Death in the NHP may ensue from perforation of the intestine and peritonitis.DISEASE IN HUMANS:
Mild infection goes unnoticed but sometimes abdominal pain, and GI bleeding and even peritonitis occur. Granulomatous nodules in the intestinal wall contain larvae and parasites. These may be secondarily infected and lead to abscesses.DIAGNOSIS:
Fecal flotation. Culture to obtain larvae for species ID.TREATMENT:
Anthelmintic therapy.PREVENTION/CONTROL:
Fecal screening of NHP's Wearing of protective clothing and gloves. Ensure good personal hygiene. Sanitary disposal of feces is important.(Shipping or transport fever, hemorrhagic septicemia)
AGENT:
Pasteurella multocida, small, nonmotile, polymorphic, gram-positive bacilliRESERVOIR AND INCIDENCE
Inhabits the oral cavity and upper respiratory tract of many animals (Rabbits, rodents, dogs, cats, mice, birds, swine). Dogs and cats are frequently healthy carriers.TRANSMISSION:
All animals and birds may be colonized by pasteurellas, and human infection occurs by wound infection from bites or scratches. Animal-to-animal transmission may occur by ingestion and inhalation. 1986 case report of meningitis in a woman who kissed her dog (cultured positive for organism) and also had dental caries which was considered to be the route of infection.DISEASE IN ANIMALS:
Can cause acute pneumonia or septicemic disease in many species. May cause chronic infection of upper respiratory and middle ear especially in the rabbit.DISEASE IN MAN:
Local inflammation occurs around the bite or scratch, possibly leading to abscess formation with systemic symptoms.TREATMENT:
Penicillin, tetracycline, or cephalosporinPREVENTION/CONTROL:
Proper treatment of bite Protective clothing (mask,gloves) Euthanize aggressive dogs and cats. Vaccinate cattle and sheep.Plague -See Yersinia Pestis
PLASMODIUM spp.
Cause of malaria. Both quartan and tertian types occur in NHP. There is a high incidence in newly imported animals. Requires anopheline mosquitoes for transmission. Therefore zoonotic potential exists anywhere mosquitoes have access to infected animals. Generally thought that these conditions prevail only in Southern climates where monkeys are housed outdoors, but mosquitoes are found in Northern as well as Southern U.S. In general, human malaria caused by plasmodia of simian origin resembles a mild and benign infection caused by human plasmodia. The disease is of short duration, parasitemias are low, and relapses are rare. Must control flying insects in all primate facilities.
POX VIRUSES
INTRODUCTION
A range of pox viruses cause febrile illnesses
in man and animals with a prominent vesicular rash. The most prominent of them
was smallpox virus (variola) which caused a severe disease in man but
which has now been eliminated by intensive international vaccination.
Current interest in poxviruses centers around their possible use as vaccine
vectors.
THE VIRUS
Smallpox belongs to the Orthopox virus genus. Poxviruses are very large, brick-shaped viruses about 300 x 200 nm (the size of small bacteria). They have a complex internal structure - a large double-stranded DNA genome (about 200 kbp in size) is enclosed within a "core" that is flanked by 2 "lateral bodies". The surface of the virus particle is covered with filamentous protein components, so that the particles have the appearance of a "ball of knitting wool". The entire particle is enclosed in an envelope derived from the host cell membranes. Most poxviruses are host-species specific, but vaccinia is a remarkable exception.True pox viruses are antigenically rather similar, so that infection by one elicits immune protection against the others.
Laboratory diagnosis of pox viruses may be undertaken by electron microscopy of negatively stained vesicle fluid or lesion material. Some pox viruses can be cultured on the chorio-allantoic membrane of chick embryos, where they form pocks, and some can be isolated by cell-culture.
HUMAN INFECTION
Vaccinia -
a virus strain which has been used for immunization against smallpox.
It's origins are not known but it seems to be a genetically distinct type of pox
virus which grows readily in a variety of hosts. In man it causes a localized
pustule with scar formation. In immunocompromised persons or eczematous persons
it sometimes caused a severe generalised vaccinia infection. Routine immunization
of all children in RSA stopped in about mid 1980's. (Last case of
smallpox in RSA was on Transvaal-Botswana border in 1971.)
Cowpox - is acquired by humans usually by milking cows; it then manifests as ulcerative lesions (sometimes called "milkers nodules") on the hands of dairy workers. It was noted to protect against smallpox and was used by Jenner as a vaccine strain to protect persons against smallpox. Despite its name, rodents are the main reservoir of cowpox; it spreads secondarily to cows and domestic cats.
Molluscum contagiosum
- is a minor infectious warty papule of the skin with a central
umbilication, transferred by direct contact, sometimes as a veneral disease.
Click here to see electron micrograph
Monkey pox - is a rare smallpox like disease of children in central Africa. It is acquired from monkeys or wild squirrels, but does occasionally spread from man to man in unvaccinated communities. Antigenically cross-reacts with other poxviruses. Sick monkeys have not been identified, but apparently healthy animals have antibodies.
Pseudocowpox - occurs worldwide and is a disease primarily of cattle. In humans it causes non-ulcerating "milker's nodes".
ORF - a worldwide occupational disease associated with handling sheep and goats afflicted with "scabby mouth". In humans it manifests as a single painless, papulo-vesicular lesion on the hand, forearm or face.
POX VIRUSES AS VACCINE VECTORS
Certain poxvirus strains which cause localised lesions or abortive infections in mammals (vaccinia) or birds (avipox) are currently being studied as possible recombinant vaccine vectors for use in man and domestic animals.
Genes coding for immunising antigens of a variety of pathogens may be inserted into the large poxvirus genome, and some undesirable genes of the pox virus may be excised. A vaccinia-based rabies vaccine has been successfully used on wild foxes (via bait) in Europe. Half-a-dozen others are in clinical trial.
GA Keen, (JULY 1998)
(Query fever, Balkan influenza, Balkan grippe, pneumorickettsiosis, abattoir fever)
AGENT:
Coxiella burnetii Multiplies only in living cells. Stains red with Gimenez & Macchiavello stains and purple with Giemsa. Infections in lab workers have been recognized for many years. Serious laboratory hazard in research facilities where infected "asymptomatic" ewes are used for projects.RESERVOIR AND INCIDENCE
Found worldwide in wild and domestic animals in two self perpetuating cycles: 1. Wild animals, with numerous tick hosts 2. Domestic animals - sheep, goats, cattle. Widespread in sheep in the U.S. Dogs, cats, and chickens can also be infected. Enzootic infection among domestic animals is the main reservoir of infection for humans.TRANSMISSION:
Organism shed in urine, feces, milk, and especially birth products of domestic ungulates that generally do not show clinical disease (usually sheep and goats). Organism is resistant to drying and can persist for months while providing extensive environmental contamination. Aerosol is a major means of transmission. Contact with infected tissues: placenta of the infected ewe contains 109 organisms per gram of tissue. Amniotic and fetal tissues are highly infective. Soiled linen may infect personnel in the laundry. One organism is considered to be enough to cause infection in humans. Ingestion.DISEASE IN MAN:
Two weeks to one month incubation. Febrile illness or subacute endocarditis. No skin eruption or rash, which distinguishes it from other Rickettsial species infections. Severe frontal headache with retro-orbital pain, profuse sweating, myalgia, and nausea. Pulmonary involvement in half the cases. Asymptomatic in many cases. Most cases resolve in two weeks but may be protracted or relapsing in the elderly. Chronic endocarditis, particularly in persons with preexisting valvular disease, is difficult to treat and the case fatality rate may be as high as 60%.DIAGNOSIS:
Leukopenia with a diagnostic rise in specific CF antibodies to Coxiella phase 2. The Weil-Felix test (a test specific for typhus and other rickettsial diseases) is negative. Liver function tests are often abnormal. In Q fever endocarditis, there is a titer of 1:200 or more by CF or IFA with phase 1 antigen. Isolation of the organism from blood or sputum is rarely attempted due to zoonotic concerns.TREATMENT:
Treatment with tetracyclines can suppress symptoms and shorten the clinical course but does not always eradicate the infection. Even in untreated patients, the mortality rate is usually low, except with endocarditis. Treatment of endocarditis consists of protracted (often for years) of antibiotic therapy; valves often need replacement.PREVENTION/CONTROL:
Use male or non pregnant female sheep for research, when possible. Q-Fever free sheep - limited practicality because requires intense surveillance program and frequent testing. Also, serologic status is not a useful indicator of whether the animal is shedding virus. Personnel education and control. Physical separation of infected animals from humans are current methods of control. Restrictions on movement of animals within the facility (with considerations of air handling). Label all potentially infected material and sterilize or disinfect it. Protective clothing, masks, gloves, & shoe covers. Intensive medical surveillance and health education program. Treatment of acute disease in humans with tetracycline. Experimental vaccine for sheep has shown promise. Delayed hypersensitivity skin test is available for high risk personnel.SUITABLE DISINFECTANTS FOR Q-FEVER:
1:100 dilution of chlorine bleach containing 5-25% hypochlorite. 5% hydrogen peroxide. 1:100 Lysol.
(Hydrophobia, Lyssa)
AGENT:
- Rhabdovirus which causes an acute almost invariably fatal disease.RESERVOIR AND INCIDENCE
Worldwide distribution (few countries are exceptions) Primary reservoirs vary geographically, eg. foxes, bats, raccoons, skunks, dogs, cats, cattle, and others. In the U.S. and Canada, wildlife rabies most frequently involves skunks, raccoons, and bats. There has been a progressive epizootic among raccoons in the eastern U.S. for over a decade. Involve wild and domestic species. Mostly wild species involved, only 10% of cases are in domestic animals 16 cases have been confirmed in nonhuman primates, including chimpanzees, cebus, cynos, and squirrel monkeys. All source countries of NHP's have endemic rabies. In Germany, Paarman described 25 Avian cases of Rabies involving 11 chickens, 2 geese, 1 duck, 1 sparrow, 1 owl, 1 crow, 3 hawks, 1 kite, 1 magpie, and 4 buzzards with Negri bodies observed in only three. In the U.S., the Great Horned Owl may shed the virus in its droppings after consuming an infected skunk. Rodents and lagomorphs are unlikely to have rabies. In the U.S., rabies has been reported 13 times in ferrets since 1958, most often in pet ferrets acquired from pet shops.TRANSMISSION:
Virus laden saliva via bite, scratch, or abrasion Tissues and fluids in the laboratory Rabid dogs shed virus in saliva 5-7 days before showing signs. Cat does so for only 3 days before signs. Aerosol transmission has been documented in the laboratory and in caves where bats roost (requires a high concentration of suspended viral particles). Animals showing signs of rabies are usually shedding large amounts of virus.DISEASE IN ANIMALS:
Rabid animals of all species exhibit typical signs of CNS disturbance, with minor variations peculiar to carnivores, ruminants, bats, and man. The clinical course, particularly in dogs, can be divided into 3 phases: the prodromal, the excitative, and the paralytic. The term "furious rabies" refers to animals in which the excitative phase is predominant, and "dumb or paralytic rabies" to those in which the excitative phase is extremely short or absent and the disease progresses quickly to the paralytic phase. In any animal, the first sign is a change in behavior, which may be indistinguishable from a GI disorder, injury, foreign body in the mouth, poisoning, or an early infectious disease. Temperature change is not significant, and driveling may or may not be noted. Animals usually stop eating and drinking and may seek solitude. Frequently, the urogenital tract is irritated or stimulated as evidenced by frequent urination, erection in the male, and sexual desire. After the prodromal period of 1-3 days, animals either show signs of paralysis or become vicious. Carnivora, pigs, and occasionally, horses and mules bite other animals or people at the slightest provocation. Cattle butt any moving object. The disease progresses rapidly after the onset of paralysis, and death is virtually certain within 10 days of the first signs. Rabid domestic cats and bobcats attack suddenly, biting and scratching viciously. Rabid foxes frequently invade yards or even houses, attacking dogs and people. The irrationality of behavior that can occur is demonstrated in the fox that attacks a porcupine; finding a fox with porcupine quills can, in most cases, support aDIAGNOSIS:
of rabies. Rabid foxes and skunks are responsible for most pasture cattle losses, and have attacked cattle in barns. The rabid raccoon is characterized by its loss of fear of man, its frequent aggression and incoordination, and its activity during the day, being predominantly a nocturnal animal. In urban areas, they often attack domestic dogs. Bats flying in the daytime are probably rabid.DISEASE IN MAN:
There is usually a history of animal bite. Pain appears at the site of the bite, followed by paresthesias. The skin is quite sensitive to changes of temperature, especially air currents. Attempts at drinking cause extremely painful laryngeal spasm, so that the patient refuses to drink (hydrophobia). The patient is restless and behaves in a peculiar manner. Muscle spasm, laryngospasm, and extreme excitability are present. Convulsions occur. Large amounts of thick tenacious saliva are present.DIAGNOSIS:
Consider Rabies as a possible problem in any wild caught or random-source laboratory animal of unknown vaccination history showing central nervous system signs or symptoms. Virus isolation from body fluid or tissue Fluorescent antibody (FA) staining of tissues, including cornea, frozen skin, mucosal scrapings, as well as brain. Highly specific & rapid. Can now detect different strains (ie skunk vs raccoon origin) via monoclonal antibody analysis which is specific for one antigenic focus on the viral particle. The identifiable strains correlate well with species and geographic distributions observed. This allows identification of source and is an important epidemiologic tool. (5 strains have been isolated from terrestrial animals; 2 skunk, 1 raccoon, 1 gray fox, 1 red fox, More than 5 have been isolated from bats.)TREATMENT:
This very severe illness with an almost universally fatal outcome requires skillful intensive care with attention to the airway, maintenance of oxygenation, and control of seizures.PREVENTION/CONTROL:
Virus is destroyed rapidly at greater than 50 C and survives no more than a few hours at room temperature (Can persist for years in frozen tissues) Vigorous first aid for bite wounds. Consult Health Authority if suspected exposure. Postexposure immunization: Up to 50% of human rabies immune globulin is infiltrated around the wound; the rest is administered IM. Human Diploid Cell Vaccine (HDCV) is given as 5 injections IM at days 0, 3, 7, 14, and 28. Control disease in domestic animals by vaccination and enforced animal control measures. Discourage keeping of wild animals as pets. Discourage the vaccination of wild animal pets for rabies. Vaccination of high risk personnelRAT BITE FEVER
(Streptobacillary fever, Haverhill fever, epidemic arthritic erythema, sodoku)AGENT:
Gram negative, pleomorphic bacillus. Two different agents can cause disease: 1. Streptobacillus moniliformis (Haverhill Fever) *Named after a 1926 outbreak in Haverhill, Mass. attributed to contaminated milk. 2. Spirillum minus (Sodoku)RESERVOIR AND INCIDENCE
Present in the oral and respiratory passages of a large number of asymptomatic rodents, including Rats and Mice. Incidence of disease appears to be low. Historically, wild rat bites and subsequent illness (usually small children) relate to poor sanitation and overcrowding.TRANSMISSION:
Man infected by bite of infected rodent or via contaminated milk or foodDISEASE IN ANIMALS:
Rats: inapparent infection Mice: acute, systemic, fatal disease in immunologically inexperienced mice. Surviving mice (or if endemic disease), exhibit suppurative polyarthritis, swelling and loss of digits or limbs.DISEASE IN MAN:
Acute febrile disease following bite from a rodent. Can see inflammation, lymphadenopathy, and nonspecific signs. May exhibit rash on extremities, often soles and palms. May see arthritis with S. moniliformis. Incubation period variable: S. moniliformis: hours to 1 to 3 days S. minus: 1 to 6 weeks Symptoms usually resolve spontaneously. Complications, if not treated promptly, lead to pneumonia, hepatitis, enteritis, endocarditis with a 10% fatality rate.DIAGNOSIS:
Culture: S. moniliformis requires 10 to 20% horse or rabbit serum and reduced oxygen tension. S. minus- won't grow in vitro. Must inoculate culture specimens into lab animals and use dark field microscopy.TREATMENT:
Treat with procaine penicillin G or tetracycline HCl. Give supportive and symptomatic measures as indicated.PREVENTION/CONTROL:
Bacteriologic monitoring Proper treatment of rodent bitesRETROVIRUSES:
The human immunodeficiency viruses (HIVs)-acquired immunodeficiency syndrome (AIDS) or HAIDS pandemic originated from lentiviruses of nonhuman primates (thus qualifying as a zoonosis) that moved into humans in Africa. The HAIDS patients eventually die of opportunistic infections, all potentially zoonotic. The HAIDS infection remained parochial, first endemically and then epidemically, until the African urbanization that occurred in each of the countries postindependence. The latter included wars and the massive movement of soldiers (virologically naive) from the American continent to Africa and back. The HAIDS viral ecology coincided with African swine fever (ASF) in the Americas. Haiti became the focal point for both infections. Some infected Haitians also became, together with some infected drug addicts in the United States, a source of contaminated human blood for transfusions and production of plasma derivatives.RHODOCOCCUS EQUI INFECTION
AGENT:
Rhodococcus equi
MEANS OF TRANSMISSION:
Aerosol, Contact
Most common species associated with transmission to humans:
Horses
RICKETTSIALPOX
(Vesicular Rickettsiosis, Kew Gardens Spotted Fever)AGENT:
R. akariRESERVOIR AND INCIDENCE
House mouse is reservoir host; most commonly seen in rodent infested urban dwellings ie New York City and other Eastern U.S. cities. Rats and moles can also harbor the organism. Not identified as a natural disease in laboratory rodents.TRANSMISSION:
Mite, Allodermanyssus sanguineus, transmits to mice or to man. Lab infections in humans via respiratory route have occurred but lab infections due to mite bite have not been reported.DISEASE IN ANIMALS:
Not known in wild animals. In experimental mice death follows pneumonia.DISEASE IN MAN:
Illness lasting about a week is associated with an eschar which develops at the site of the mite bite, regional lymphadenopathy and fever. A vesicular rash over the body and limbs develops within 1-4 days.DIAGNOSIS:
Leukopenia and a rise in antibody titer with rickettsial antigen in CF tests. However, the Weil-Felix test is negative.TREATMENT:
TetracyclinePREVENTION/CONTROL:
Eliminate wild mice from animal facilities Control mites.(American Tick Typhus, Tick-borne Typhus Fever)
AGENT:
Rickettsia rickettsii.RESERVOIR AND INCIDENCE
Dogs, wild rodents and rabbits. Reported from most of continental U.S., highest incidence in S. Atlantic and South Central States. 2/3 of human cases are reported in children.TRANSMISSION:
Ixodid ticks (especially Dermacentor) or their host species. Most rickettsias are obligate intracellular parasites of the gut cells of invertebrates and can only survive briefly outside living cells. Crushed ticks or mites and their feces may infect through broken skin. Transmission from tick bite occurs only after several hours of attachment.DISEASE IN ANIMALS:
Subclinical only.DISEASE IN MAN:
Fever has a sudden onset, with chills, headache, severe muscle pains, photophobia and meningism for four weeks. A red, morbilliform rash develops within 3-5 days of onset of fever and with hemorrhages spreading on limbs. Enlarged liver and spleen, myocarditis, renal tubular necrosis and bronchopneumonia occur. Damage to endothelial cells of blood vessels by invasion of rickettsias causes thrombi and hemorrhages. Focal liver necrosis, hemorrhages in genitalis and gangrene of the scrotum may occur. The case fatality rate in untreated cases is 15-20%, but with prompt treatment is about 5%.DIAGNOSIS:
Rickettsiae can sometimes be isolated in special laboratories from blood obtained in the first few days of illness. A rise in antibody titer during the second week of illness can be detected by specific CF, IFA, and microhemagglutination tests or by the Weil-Felix test. Antibody response may be suppressed if antimicrobial drugs are given very early.TREATMENT/PREVENTION/CONTROL:
Treatment of human disease with tetracycline or chloramphenicol. Control ticks on newly arrived animals.ROTAVIRUS:
Rotaviruses cause gastroenteritis in animals and humans. They are not strictly species-specific, and experimental cross-infections with human or animal rotaviruses in several animal species have been confirmed. The finding of serotypes common to man and various animal species might indicate that some serotypes can infect both. However, the natural occurrence of cross-infections between species and the possible role of animals in the epidemiology of the disease in humans are still unknown.ST. LOUIS ENCEPHALITIS
SYNONYMS:
Type C lethargic encephalitis.ETIOLOGY:
RNA virus belonging to the genus Flavivirus (formerly group B of the arboviruses) of the family Togaviridae; forms part of the virus complex including Murray Valley, West Nile, and Japanese B encephalitides. There are indications that strains of the virus isolated in different zones differ in their capacity to produce viremia in birds, virulence in 3-week-old mice, and neurovirulence in rhesus monkeys. By the technique of nucleotide mapping, considerable genetic variation among the strains of the virus was demonstrated, and it was proposed to name these geographic variants as topotypes.GEOGRAPHIC DISTRIBUTION
The agent is distributed from Argentina to Canada. The disease is unknown outside the Americas.THE DISEASE IN MAN:
The clinical infection presents a wide spectrum, from an undifferentiated febrile disease similar to influenza to severe encephalitis. Three syndromes can be distinguished: febrile disease, aseptic meningitis, and encephalitis. The febrile syndrome usually has a benign course, with fever and intense cephalalgia lasting several days, followed by complete recovery. The aseptic meningitis has a sudden onset, with fever, stiffness of the neck, and positive Kemig and Brudzinski signs, but without neurologic dysfunction. Pleocytosis is common. The disease characterized by encephalitis also begins suddenly, with fever and one or more signs of brain inflammation, such as personality changes, confusion. delirium, lethargy, paresis, convulsions, and others. The encephalitis syndrome is more frequent in elderly persons; its frequency increases from 56% in patients up to 20 years old to 87% in those over 60. Convalescence in these cases lasts several weeks. The incubation period is estimated at 4 to 21 days. In the United States, the case fatality rate in 2,261 confirmed clinical cases between 1955 and 1968 was 5 to 10%. The majority of deaths were in persons over 50 years old, among whom the fatality rate can be as high as 30% or more. During the 1962 epidemic in Tampa Bay, Florida, the highest fatality rate (36.3%) was recorded in patients 65 years of age and older in Pinellas County, where a large number of retired persons live. In that county the general mortality rate was 22.2%, while the rate was 9.8% in the remaining three counties in that area. In Central and South America, most of the small number of recorded patients did not exhibit impairment of the central nervous system.THE DISEASE IN ANIMALS:
The infection is subclinical in animals. Experimental peripheral inoculation of the virus produces viremia without clinical symptoms in domestic and wild fowl and in various species of insectivorous bats. When the disease occurs in man, antibodies for SLE are generally found in horses and in some other mammals. In contrast to western, eastern, and Venezuelan equine encephalitides, St. Louis encephalitis does not cause clinical illness in equines. Some equines inoculated experimentally develop viremia.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
The basic cycle of the infection involves wild birds and omithophilic mosquitoes. Culex salinarius, from which the SLE virus has been isolated, could be the vector in the wild enzootic cycle. In the United States, two different epidemiologic situations are known, depending on the habits of the primary vector and other ecologic conditions. West of the Rocky Mountains the disease is rural and sporadic because the vector, C. tarsalis, is sparse and the widely scattered human population has a high rate of subclinical infection, protecting it against reinfection. Though the vector and birds reach high concentrations in areas flooded by irrigation water, human cases are not numerous for the reasons given. In the south-central and north-central states of the country, by contrast, the disease is urban-suburban in character, primarily because the vectors are the peridomestic and domestic mosquitoes C. quinquefasciatus and C. pipiens. These vectors proliferate where water contaminated with organic wastes collects, that is, in poorer urban and suburban areas deficient in environmental sanitation. The same conditions favor the proliferation of sparrows, pigeons, and other birds that feed among household wastes. Peridomestic birds and domestic fowl serve as amplifiers of the virus: that fact, together with the increased density of the human population, creates the conditions necessary for epidemics. During the 1964 epidemic in Houston, the virus was isolated from geese, domestic pigeons, and various other species of birds. In addition, antibodies were found in 20% of the birds, especially house sparrows (Passer domesticus), and in almost all poultry examined. How the virus gets into urban areas is not yet established, but it is suspected that migratory wild birds may introduce it. As is true for many other arboviruses, the mechanism that allows the virus to overwinter in temperate climates is not fully known. The virus has been isolated from hibernating adult female C. pipiens, which indicates that the virus can persist in the vector during the winter in temperate climates. It also has been proven experimentally that low-level transovarial transmission occurs in C. pipiens.ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
Man is an accidental host of the virus and does not play any role in the natural maintenance cycle. The basic reservoir is wild birds and perhaps the vector mosquitoes; poultry and peridomestic and domestic birds act as amplifiers of the virus, which circulates from one host to another by means of mosquitoes. Wild and domestic mammals are not thought to play a role in the virus cycle because their viremia is low-level and transitory and virus strains isolated from them possess low virulence. In Panama, sloths inoculated with the SLE virus developed prolonged high-titer viremia, but the role of these animals under natural conditions has not been determined. Likewise, bats may be involved in the virus's overwintering within enzootic foci in temperate climates, as well as in its dissemination to epizootic foci, a subject that requires further study.DIAGNOSIS:
SLE may be confused clinically with other febrile diseases or with encephalitides and aseptic meningitis caused by different agents. Laboratory confirmation is essential. Laboratory diagnosis is based primarily on serology. only on a few occasions has it been possible to isolate the etiologic agent from the blood of viremic patients. Most successful isolations have been made from the brain of patients who died a short time after contracting the disease.DIAGNOSIS:
is based on demonstrating serologic conversion in the patient by comparing titers of serum samples taken during the acute phase with those taken during convalescence. The most widely used tests are complement fixation, neutralization (which is the most specific), and hemagglutination inhibition. Antibodies can be detected during the first week of the disease by the hemagglutination inhibition and neutralization tests, while the complement fixation antibodies appear during the second or third week. In Latin American and Caribbean countries, where infections due to several flaviviruses occur, tests must include all of the other viruses of the group known to be present in the area.TREATMENT:
Vigorous supportive therapy. Such measures include reduction of intracranial pressure (mannitol), monitoring of intraventricular pressure, the control of convulsions, maintenance of the airway, administration of oxygen, and attention to adequate nutrition during periods of prolonged coma. No antiviral agent is effective for arboviral encephalitis.CONTROL:
The only preventive measure available is control of the vector. Programs of epidemiologic surveillance and vector control have given satisfactory results in California against C. tarsalis, in Florida against C. nigripalpus, and in Texas against C. quinquefasciatus. An effective vaccine is not yet available.(Salmonella food poisoning, enteric paratyphosis) A common bacterial cause of food-poisoning worldwide. Over 1800 food-poisoning serotypes of salmonella (bacterium) exist. The prevalence of individual serotypes constantly changes. In the U.S., 5 million cases are diagnosed annually. S. typhi, the cause of Typhoid Fever, rarely occurs in the U.S. and is not discussed here.
RESERVOIR AND MODE OF TRANSMISSION:
Salmonellas are common commensals of all animals and birds and are excreted in feces. Host-adapted strains may cause serious illness (e.g., S. dublin in cattle, S. pullorum in chickens), but most human food-poisoning salmonellas do not cause clinical signs in animals. The main reservoirs for human infection are poultry, cattle, sheep and pigs. Infection in animals is maintained by recycling slaughterhouse waste as animal feed, fecal oral spread and fecal contamination of hatching eggs. Transmission occurs when organisms, introduced into the kitchen in poultry carcasses, meat or unpasteurized milk, multiply in food owing to inadequate cooking, cross-contamination of cooked foods and inadequate storage. Person-to-person spread is common in institutions such as hospitals. The organism inhabits the intestinal tract of many animals including birds, cattle, sheep, pigs, lab. animals (rats, mice, hamsters, guinea pigs, nonhuman primates) and humans. Salmonella occurs worldwide. *The house mouse may also be a reservoir of the infection and may play a role in human and animal salmonellosis. Humans, rarely, and animals may be carriers and asymptomatic shedders of the organism. *Salmonella prevalence in the U.S. canine population may be 10% or more. *Prevalence data from 8 studies conducted worldwide indicated that a wide range (0.6-27%) of cats were culture-positive for Salmonella. *Salmonella carriers in newly imported Rhesus and Cynomolgus monkeys exceeded 20% in some shipments. *Birds, reptiles, and turtles are especially dangerous sources of Salmonellosis. 94% of all reptiles harbor Salmonella. Turtles alone in 1970 may have caused 280,000 human cases of Salmonellosis. *In 1975 the FDA ruled it illegal to sell a. Viable Turtle eggs b. Live turtles with a carapace length < 10.2cm (4 inches) c. Exceptions - Educational & scientific institutions and marine turtles. d. Marine turtles have not been shown to be a reservoir of SalmonellaTRANSMISSION:
Indirect transmission via contaminated food and water are the most common sources but transmission may also be by direct contact. It is a common contaminant of sewage. Found in many environmental water sources. Environmental contamination continues to be a potential source of infection for lab animals and secondarily for personnel handling those animals. *Animal feed containing animal by products continues to be a source of Salmonella contamination, especially if the diets consist of raw meal and have not undergone the pelleting process.INCUBATION PERIOD:
Humans. 12-72 hours. Animals. 1-5 days.CLINICAL FEATURES:
Humans.The presence and severity of symptoms depends on the infecting dose. Typically there is watery diarrhoea for about ten days, possibly leading to dehydration, with abdominal pain and low-grade fever. Septicemia and abscess formation are rare. Animals. Subclinical infection is common and many animals may be intermittent or persistent carriers. However, cows may suffer with fever, diarrhoea and abortion. Calves undergo epizootic outbreaks of diarrhoea with high mortality. In pigs, fever and diarrhoea are less common than in cattle. Infected sheep, goats and poultry usually show no signs of infection.PATHOLOGY:
Humans. Enteritis is a feature. Extraintestinal infection may cause abscesses. Animals. Penetration of the infection into the mucosa is followed by inflammation, especially ileitis, progressing to inflamed mesenteric lymph nodes in the mesentery, possibly progressing to septicemia and pneumonia especially in calves. Dehydration and rapid loss of weight are due to stimulation of chloride excretion and inhibition of sodium absorption. Abortion in cattle is caused by massive proliferation of salmonella in the placenta leading to placental necrosis.DIAGNOSIS:
Humans. Isolate salmonella from feces and suspected foods using selective media followed by serotyping and, if appropriate, phage typing. Animals. Culture feces, postmortem tissues and foods of animal origin. Serological tests are of limited value as many noninfected animals have titers from past infections. Humans. Usually only a self-limiting illness occurs. Deaths from dehydration or septicemia are rare and occur usually in infants, or debilitated or elderly patients. Animals.There is abortion in cattle and endometritis with temporary infertility. In calves, dehydration and septicemia may lead to death.PREVENTION:
Humans. Educate food handlers in good kitchen hygiene. Ensure thorough cooking of meat, refrigerate cooked foods and prevent cross-contamination. Pasteurize all milk. Ensure personal hygiene. Reduce contamination of poultry carcasses at abattoirs. Irradiation of meat and other foods before purchase will reduce contamination. Animals. This is difficult and often impractical because there are many sources of infection. Principles of control include the following: maintain closed herds and flocks; keep animals in small groups; purchase replacements direct from the farm of origin; avoid mixing animals from different sources; sterilize ingredients of animal feed; provide mains drinking water for grazing livestock; prevent access of wild birds and rodents to animal houses; completely destock animals and thoroughly cleanse and disinfect housing between batches; monitor poultry breeding stock and remove excreters; disinfect hatching eggs and fumigate incubators.TREATMENT:
Humans. Treatment of uncomplicated enterocolitis is symptomatic only. Young, malnourished, or immunocompromised infants, severely ill patients, those with sickle cell disease, and those with suspected bacteremia should be treated for 3-5 days with trimethoprim-sulfamethoxazole (one double-strength tablet twice a day), ampicillin (100 mg/kg IV or orally), or ciprofloxacin 9750 mg twice daily). Animals. Treatment with antibiotics and sulfonamides immediately diarrhoea and fever occur reduces mortality but is contraindicated in healthy carriers in which treatment may prolong the carrier state.VACCINATION:
Humans. None. Animals. Vaccines are available against S. dublin and S. typhimurium in calves. A live vaccine prepared from a rough strain of S. dublin gives good protection in calves against both S. dublin and S. typhimurium.LEGISLATION:
Humans. The disease is notifiable specifically in the USA, Australia, New Zealand and several European countries, or as food-poisoning as in the UK. Animals. Notification of infection in food animals is obligatory in some countries, including the UK, with statutory sampling of animal protein for animal feed. Heat treatment of waste food applies in the UK. A slaughter policy is claimed in Luxembourg, Germany and Czechoslovakia.Sarcoptes is a microscopic mite that burrows through the skin of dogs. In doing so, it causes tremendous irritation: sarcoptic mange is one of the itchiest conditions in dogs. Although it can affect any area of the skin, the itching is often most severe on the dog's abdomen, chest, legs, and ears.
Where Does the Mite Come From?
The mites can be transmitted when a dog is in contact with another infected pet dog or other member of the canine family (such as a fox). Although the mites spend their entire lives on the dog, some mites do fall off into the environment when the dog scratches. These mites can survive in the environment for up to 3 weeks, and provide a source of infection for other dogs. Also, because some dogs can harbor (and transmit) the mite without showing signs of skin disease, all the dogs in the home of an infected dog have the potential to be infected and to require treatment.
Can the Mite Infect Humans?
Yes. The mites prefer to live on dogs, but can also live for at least 6 days on humans. They cause an itchy, uncomfortable skin condition. If you are exhibiting any unusual symptoms, please see your physician or dermatologist.
How is it Diagnosed?
The mite infestation is usually diagnosed by a skin scraping, which is a simple in-clinic procedure performed by a veterinarian. Since the mites can be very difficult to find, we sometimes make the diagnosis based on the signs exhibited by the dog.
How is it Treated?
The likelihood of a cure with Sarcoptes is excellent. The mites can be killed with a series of medicated dips, sprays, injections, oral medications, or a topical medication. Most of these treatments are performed several times, over 3 to 8 weeks, in order to kill all the life stages of the mite. In some cases, the dog's immediate environment is also treated to reduce the risk of contagion. It is also a good idea to wash the dog's bedding after every treatment. Because the itching can be so intense, anti-inflammatory medications are also sometimes prescribed. Some dogs become more itchy a day or two after the first treatment, but the treatments should reduce the itching significantly within 2 weeks.
SCHISTOSOMIASIS
(Bilharzia, Bilharziasis)AGENT:
Schistosomiasis infects more than 200 million persons worldwide. The causative agents are Schistosoma mansoni, haematobium, and japonicum.RESERVOIRS AND INCIDENCE:
Humans are the reservoir for S. mansoni and haematobium. S. japonicum infects cattle, water buffalo, horses, dogs, cats, rodents and monkeys. Intermediate hosts are species of snails (Biomphalaria and Bulinus). S. mansoni occurs in Africa, South America and some Caribbean islands (including Puerto Rico); S. haematobium in Africa and the Middle East; and S. japonicum in China, Japan, the Philippines, and South East Asia.TRANSMISSION:
Cercariae in contaminated water penetrate human skin, especially in irrigated fields or rivers. In the body the parasite migrates via the liver to the superior mesenteric vein where maturation takes place in about 6 weeks. Eggs are disseminated throughout the body via the blood, released into the intestinal lumen and excreted. In water miracidia develop and penetrate the snail, which in turn excretes cercariae into the water.DISEASE IN ANIMALS:
Abdominal pain, diarrhea, anemia, and emaciation occur. Cattle have hematuria.DISEASE IN HUMANS:
Penetration of larvae through the skin causes an itchy rash. With heavy infection, penetration of the parasite through the skin gives rise to local dermatitis and pruritus followed by pneumonitis when the parasites reach the lung. The deposition of ova provokes the growth of small multiple granulomata throughout the body. Eventually intestinal and hepatic fibroses develop. With S. japonicum, acute symptoms include fever, abdominal pain, cough, weight loss, diarrhea and dysentery. Chronic infection may result in symptoms months to years later, with enlarged liver and spleen, cirrhosis, ascites, and fits due to cerebral involvement.DIAGNOSIS:
Definitive diagnosis is made by finding the characteristic eggs in excreta or by mucosal or liver biopsy. Screening for infection is possible by skin or serologic tests, but neither is sufficiently sensitive or specific to justify treatment.TREATMENT:
Praziquantel, metrifonate, or oxamniquine.PREVENTION/CONTROL:
Dispose of feces and urine so that viable eggs will not reach bodies of fresh water containing intermediate snail hosts. Reduce snail habitats by removing vegetation or by draining and filling. Treat snail-breeding sites with molluscicides. Prevent exposure to contaminated water (e.g., wear rubber boots and gloves). To minimize cercarial penetration, towel dry, vigorously and completely, skin surfaces wet with suspected water. Apply 70% alcohol immediately to the skin to kill surface cercariae. Provide water for drinking, bathing, and washing clothes from sources free of cercariae. Rapid treatment of patients to prevent disease progression and to reduce transmission by reducing egg passage.REFERENCES
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SYNONYM:
Bacillary dysentery.ETIOLOGY:
The type species is Shigella dysenteriae, other agents are S. flexneri, S. boydii, and S. sonnei. The first three species are subdivided into serotypes.GEOGRAPHIC DISTRIBUTION:
Worldwide.THE DISEASE IN MAN:
It is seen most often in preschool-age children. A new serotype introduced into tropical areas where the population is undernourished provokes disease in all age groups, particularly children, the elderly, and debilitated individuals. Generally, the incubation period is less than 4 days. The disease begins with fever and abdominal pains, followed by diarrhea and dehydration for 1 to 3 days. A second phase of the symptomatology can last for several weeks. The main symptom is tenesmus; in serious cases, stools contain blood, mucus, and pus. The symptomatology is usually variable. In many countries, strains of Shigella resistant to sulfonamides and to several antibiotics have been observed.THE DISEASE IN ANIMALS:
A clinical picture similar to that in man occurs in monkeys.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
The principal reservoir of the infection for man is other humans that are sick or carriers. The sources of the infection are feces and contaminated objects. The most common mode of transmission is the fecal-oral route. Outbreaks comprising numerous cases have had their origin in a common source of infection, such as foods contaminated by hands or feces of carrier individuals. Insects, particularly flies, can also play a role as mechanical vectors. Bacillary dysentery is a serious disease with high mortality in nonhuman primates in captivity, but there is doubt that monkeys can harbor the etiologic agent in their natural habitat. Monkeys probably contract the infection by contact with infected humans. The infection spreads rapidly in nonhuman primate colonies because the monkeys defecate on the cage floor and also often throw their food there.ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
Of little significance. Cases of human bacillary dysentery contracted from nonhuman primates are known. The victims are mainly children. In highly endemic areas, dogs may shed Shigella temporarily. The etiologic agent has also been isolated from horses, bats, and rattlesnakes. Nevertheless, animals other than nonhuman primates play an insignificant role.DIAGNOSIS:
Definitive diagnosis depends on isolation of the etiologic agent by culture of fecal material on selective media. Serologic identification and typing are important from the epidemiologic viewpoint.TREATMENT:
In humans, treatment of dehydration and hypotension is lifesaving in severe cases. The current antimicrobial treatment of choice is trimethoprim-sulfamethoxazole (one double-strength tablet twice a day), or ciprofloxacin (750 mg twice a day; contraindicated in children and pregnant women). Parental hydration and correction of acidosis and electrolyte disturbances are of primary importance.Antispasmodics (e.g., tincture of belladonna) are helpful when cramps are severe. Drugs that inhibit intestinal peristalsis (paregoric, diphenoxylate with atropine) may ameliorate symptoms but prolong fever, diarrhea, and excretion of Shigella in feces. Appropriate precautions should be taken both in the hospital and in the home to limit spread of infection.CONTROL:
In man, control methods include a) environmental hygiene, especially disposal of human waste and provision for potable water; b) personal hygiene; c) education of the public and of food handlers about the sources of infection and methods of transmission; d) sanitary supervision of the production, preparation, and preservation of foods: e) control of flies; f) reporting and isolation of cases and sanitary disposal of feces; and g) search for contacts and the source of infection. A live, streptomycin-dependent vaccine, administered orally in three or four doses has given good protection against the clinical disease for 6 to 12 months. Its use is indicated in institutions where shigellosis is endemic. Indiscriminate use of antibiotics must be avoided tn order to prevent the emergence of multiresistant strains and to ensure that these medications remain available for use in severe cases. In animals, control consists of a) isolation and treatment of sick or carrier monkeys: b) careful cleaning and sterilization of cages; c) prevention of crowding in cages: and d) prompt disposal of wastes and control of insects.SPARGANOSIS
SYNONYM:
Larval diphyllobothriasis.ETIOLOGY:
The second larval stage (plerocercoid or sparganum) of the pseudophyllidean cestode of the genus Spirometra (Diphyllobothrium, Lueheela). Several species of medical interest have been described: Spirometra mansoni, S. mansonoides, S. erinacei-europaei, S. theileri, and S. proliferum. These are the most commonly accepted species at the present time, but it should be noted that they are difficult to differentiate and that the taxonomy remains in doubt. The definitive hosts are mainly domestic and wild canids and felids. The development cycle requires two intermediate hosts. The first is a copepod (planktonic crustacean) of the genus Cyclops. which ingests coracidia (free, ciliated embryos) that develop from Spirometra eggs when they reach the water with the feces of dogs or cats (definitive hosts). In the tissues of the copepod, the coracidium turns into the first larva, or procercoid. When a second intermediate host ingests an infected copepod, the procercoid develops into a second larval form, the plerocercoid or sparganum. The plerocercoid larva can be harbored by many vertebrates, including amphibians, reptiles, birds, small mammals (rodents and insectivores), man, nonhuman primates, and swine. Fish do not become infected. Some researchers believe that the second intermediate host is usually an amphibian, but can vary according to region. Numerous species of vertebrates become infected with plerocercoids by feeding on amphibians, but they may also develop plerocercoids after ingesting water containing copepods infected by procercoids (first larva). Several animal species that are not definitive hosts function as paratenic or transport hosts, since the larvae they acquire by feeding on animals infected with plerocercoids encyst again after passing through the intestinal wall and migrating to other tissues. This transfer process is undoubtedly important in the life cycle; but the fact that many species of secondary hosts can be infected directly by ingestion of copepods containing procercoids is probably no less important. When the sparganum reaches the intestine of the definitive host, it attaches to the mucosa; in 10 to 30 days, it matures into an adult cestode, completing the cycle. The adult S. mansonoides reaches about 25 cm in length in the intestine of the definitive hosts (cat, dog). The sparganum found in the tissues of the secondary intermediate hosts and paratenic hosts, including man, varies from 4 to 10 cm in length.GEOGRAPHIC DISTRIBUTION AND OCCURRENCE:
Sparganosis is found throughout the world, but human infection is not common. Just over 450 cases are known, mostly from Japan, China, Korea, and Southeast Asia. In the United States, about 60 cases have been described# in Latin America and the Caribbean, the disease has been recorded in Uruguay, Ecuador, Colombia, Venezuela, Guyana, Belize, and Puerto Rico; about 30 cases have been diagnosed in Africa. Infections in the Far East are attributed to plerocercoid larvae of Spirometra mansoni: in the United States, to S. mansonoides; in Europe, to S. erinacei-europaei; and in Africa, to S. theileri. However, as has already been mentioned, species identification can be difficult and therefore uncertain.THE DISEASE IN MAN:
The incubation period, determined in a study of 10 patients who ate raw frog meat, lasts from 20 days to 14 months. The most common localizations of the sparganum are subcutaneous connective tissue and superficial muscles. The lesion is nodular, develops slowly, and can be found on any part of the body. The main symptom is pruritus, sometimes accompanied by urticaria. The lesion is painful when there is inflammation. The patient may feel discomfort when the larva migrates from one location to another. The subcutaneous lesion resembles a lipoma, fibroma, or sebaceous cyst. Ocular sparganosis occurs mainly in Vietnam, Thailand, and parts of China. Its main symptoms consist of a painful edema of the eyelids, with lacrimation and pruritus. A nodule measuring I to 3 cm forms after 3 to 5 months, usually on the upper eyelid. Migration of the sparganum to internal organs can give rise to the visceral form of the disease. The preferred localizations are the intestinal wall, perirenal fat, and mesentery; vital organs are rarely affected. When the plerocercoid invades the lymphatic system, it produces a clinical picture similar to that of Eosinophils are abundant in the was near the parasite; examination of blood samples reveals mild leukocytosis and increased eosinophilia. An infrequent but serious form is proliferative sparganosis caused by Spirometra proliferum. The sparganum of S. proliferum is pleomorphic, with irregular branches and proliferative buds that detach from the larva and migrate to different tissues in the host, where they repeat the process and invade other organs. The life cycle of S. proliferum is not known.THE DISEASE IN ANIMALS:
The adult cestode, which lodges in the intestine of the definitive host, generally does not affect the health of the animal. In cats, however, it may produce weight loss, irritability, and emaciation, together with an abnormal or exaggerated appetite. Infection by the larvae or spargana can be clinically apparent when their number is large and especially when they invade vital organs. In the intermediate host, the disease is almost always asymptomatic if the number of parasites is relatively small.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
Sparganosis is maintained in nature primarily by contamination of natural or artificial bodies of water (lagoons, marshes, lakes, and others) with feces from felids and canids infected with Spirometra spp. Contamination of water with eggs of Spirometra spp. leads to the infection of copepods and, consequently, of the second intermediate hosts that ingest these crustaceans. An important means of infection is the transfer of the second larva (sparganum, plerocercoid) from one secondary host to another, which increases the number of animal species and individuals infected. The common route of infection is ingestion; various mammal and bird species become infected by feeding on parasitized frogs or snakes. The high rate of infection in wild pigs in Australia may be due to this mechanism, although it may also stem from ingestion of copepods with drinking-water from lagoons. In any case, contamination of the water by wild canids (definitive hosts) that share the habitat assures that the cycle is perpetuated. The infection rate in man is low, compared to the rate in other animals. Man acquires sparganosis mainly by ingesting larvae contained in raw or undercooked meat of animals infected with spargana, such as amphibians, reptiles, birds, and wild mammals. Another mode of infection, also by larval transfer, is by contact. In Vietnam and Thailand, frogs are popularly believe to have an antiphlogistic effect, and their muscles are applied as poultices. This custom is responsible for ocular sparganosis. It is also probable that man can acquire sparganosis via drinking-water by ingesting copepods infected with procercoids (first larvae). Man is an accidental host and does not usually play any role in the life cycle of the parasite. However, under ecologic conditions in some regions of central Africa, it is suspected that man acts as an intermediate host. In this region, hyenas are the definitive hosts of Spirometra, and man is apparently the only host infected with spargana. In these circumstances, the infection cycle is maintained as a result of tribal custom of letting hyenas devour human corpses.DIAGNOSIS:
Specific diagnosis can be made only by removing the nodular lesion and confirming the presence of the plerocercoid. Attempts have been made to identify the species of Spirometra larvae by infecting dogs and cats via the digestive route. For reasons already mentioned, differentiation of species has proven difficult. Diagnosis in definitive hosts infected with adult cestodes can be made by coprologic examination or autopsy.CONTROL:
Human sparganosis can be prevented by avoiding ingestion of contaminated water that has not been treated, and by making sure that meat that might contain spargana is sufficiently cooked. In the Far East, public health education should emphasize the danger of using the tissue of frogs or other cold-blooded animals for medicinal purposes.AGENT:
Sporothrix schenckii, dimorphic fungusRESERVOIR AND INCIDENCE
distributed worldwide with sporadic outbreaks. Saprophyte that grows on soil or vegetation. Has been reported in horses, dogs, cats and many other species. 19 cases of Sporotrichosis have been reported in man following contact with feline abscesses or ulcers (12 of these were veterinarians).TRANSMISSION:
Penetrating injury, or contact with plant or soil. Transmission from feline to man by direct contact with lesions (penetrating injury NOT required). Inhalation can lead to pulmonic disease.DISEASE IN ANIMALS:
Lesions can be anywhere but are usually located on distal extremities, head, or base of tail. Appear as draining puncture wounds, cellulitis. Can ulcerate and become nodular with seropurulent exudate. May cavitate and expose muscle and bone. May lead to disseminated disease which is usually fatalDISEASE IN MAN:
The most common clinical form is cutaneolymphatic; it begins with a nodule or pustule at the point where broken skin allowed inoculation. The infection may remain confined or may eventually spread and produce SC nodules along the enlarged lymph ducts. These nodules may ulcerate, and a gray or yellowish pus appears. Disseminated forms, which are rare, may give rise to localizations in different organs, especially the bones and joints, as well as in the mouth, nose, kidneys, or the SC tissue. Pulmonary sporotrichosis can be confused with TB.DIAGNOSIS:
Biopsy and histo fungal culture cytology of impression smear of exudate. Organisms are numerous in cats but are difficult to detect in man, horses, and dogs. Organism can also be found in feces of infected cat. Antigen tests are used to diagnose disseminated disease.TREATMENT:
Potassium iodide, Amphotericin B, or itraconazole.PREVENTION/CONTROL:
Gloves when handling infected animals. Wash with iodine or chlorhexidine.STAPHYLOCOCCAL FOOD POISONING
(Staphylococcal Alimentary Toxicosis, Staphylococcal Gastroenteritis)ETIOLOGY:
Coagulase-positive strains of Staphylococcus aureus that produce enterotoxins. Very few coagulase-negative stains are enterotoxigenic. The toxin is preformed in the food involved. To date, six types of enterotoxins are known: A, B, C, D, E, and F; of these A is the most prevalent in outbreaks. Enterotoxin F is implicated in toxic shock syndrome (TSS). Some strains can produce two or even three different enterotoxins. The toxins are heat-resistant and can withstand a temperature of 100oC for 30 minutes.GEOGRAPHIC DISTRIBUTION:
Worldwide.THE DISEASE IN MAN:
The incubation period is short, generally 3 hours after ingestion of the food involved. The interval between consumption of the enterotoxin and the first symptoms can vary from 30 minutes to 8 hours, depending on the quantity of toxin ingested and the susceptibility of the individual. The major symptoms are nausea, vomiting, abdominal pains, and diarrhea. Some patients may show low pyrexia (up to 38oC). More serious cases manifest prostration, cephalalgia, abnormal temperature, and lowered blood pressure, as well as blood and mucus in the stool and vomit. The course of the disease is usually benign and the patient recovers without medication in 24 to 72 hours. Recently, a toxic shock syndrome has been described. Symptoms consist of vomiting, diarrhea, high fever, erythroderma, edema, renal insufficiency, and toxic shock. Most patients are women who become ill during their menstrual period. The above-described symptoms also are observed in association with abscesses and osteomyelitis caused by S. aureus. A staphylococcal enterotoxin designated F was isolated from 94% of these patients strains of S. aureus from nine patients with toxic shock were examined, and production of enterotoxin F was confirmed in eight of them; only 42% of 50 strains isolated from other hospitalized patients produced this toxin. Toxin F production was not found in 48 strains originating from animal clinical specimens. Of 24 strains from healthy human carriers, 25% produced the toxin.SOURCE OF INFECTION AND MODE OF TRANSMISSION:
The principal reservoir of is S. aureus is the human carrier. A high proportion (from 30 to 35%) of healthy humans have staphylococci in the nasopharynx and on the skin. A carrier with a respiratory disease can contaminate foods by sneezing coughing, or expectorating. Similarly, he may contaminate foods he handles if he has a staphylococcal skin lesion. However. even if not sick himself, the carrier may spread the agent by handling food ingredients. utensils, and equipment. or the finished food product. According to different authors, the proportion of enterotoxin-producing S. aureus strains of human origin varies between 18 and 75%. The proportion of toxigenic strains isolated from various sources (human, animal, and food) is very high. Strains of human origin predominate in epidemics, but animals are also reservoirs of the infection. Milk from cow udders infected with staphylococci can contaminate numerous milk products. Many outbreaks have been produced by consumption of inadequately refrigerated raw milk or cheeses from cows whose udders harbored staphylococci. The largest outbreak affected at least 500 students in California between 1977 and 1981 and was traced to chocolate milk. In developing countries, where refrigeration after milking is often inadequate, milk and milk products may be an important source of staphylococcal intoxication. According to recent investigations, a high proportion of strains isolated from staphylococcal mastitis produce enterotoxin A, which causes many outbreaks in humans. In several investigations it was possible to isolate from skin lesions and cow's milk the S. aureus phage type 80/81, which is related to epidemic infections in man. One of the studies proved that phage type 80/81 produced interstitial mastitis in cows. The same phage type was found among animal caretakers, which indicates that the bacterium is intertransmissible between man and animals and that the latter may reinfect man. Infected fowl and dogs may also give rise to and be a source of staphylococcal poisoning in man. One subject that deserves special attention is the appearance of antibiotic-resistant strains in animals whose food includes antibiotics. Concern exists over the possible transmission of these strains to man. On several occasions, resistant stains have been found both in animals (cows, swine, and fowl) and in their caretakers, with the same antibiotic resistance. Moreover, "human" strains (phage typed) have on occasion been isolated from the nostrils and lesions of other species of domestic animals. A variety of foods and dishes may be vehicles of the toxin. If environmental conditions are favorable, S. aureus multiplies in the food and produces enterotoxins. Once made, the toxin is not destroyed even if the food is subjected to boiling while being cooked. Consequently, the toxin may be found in the food whereas staphylococci are not. An important causal factor in food-borne intoxications is holding food at room temperature, which permits multiplication of staphylococci. Lack of hygiene in food handling is another notable factor. Frequently, outbreaks of food poisoning may be traced to a single dish.THE ROLE OF ANIMALS IN THE EPIDEMIOLOGY OF THE DISEASE:
Most outbreaks are caused by human strains, and to a lesser degree by strains from cattle and other domestic animals. Animal products -- such as meat, ham, milk, cheese, cream, and ice cream -usually constitute a good substrate for staphylococcal multiplication. Milk pasteurization offers no guarantee of safety if toxins were produced before heat treatment, as the toxins are heat-resistant. Outbreaks have been caused by reconstituted powdered milk, even when the dried product contained few or no staphylococci.DIAGNOSIS:
The short incubation period between ingestion of contaminated food and appearance of symptoms is the most important clinical criterion. Laboratory confirmation, when possible, is based above all on demonstration of the presence of enterotoxin in the food. Biological methods (inoculation of cats with cultures of the suspect food, or of rhesus monkeys with the foodstuffs or cultures) are expensive and not always reliable. As substitutes, serologic methods such as immunodiffusion, immunofluorescence, hemagglutination inhibition, and, recently, ELISA are increasingly used. In febrile patients, blood cultures are indicated. Isolation of enterotoxigenic staphylococcal strains from foods and typing by phage or, more recently, by immunofluorescence have epidemiologic value. Quantitative examination of staphylococci in processed or cooked foods serves as an indicator of hygienic conditions in the processing plant and of personnel supervision.TREATMENT:
In humans, treatment usually consists of replacement of fluids and electrolytes and, very rarely, management of hypovolemic shock and respiratory embarrassment. If botulism is suspected, polyvalent antitoxin must be administered. Historically, antimicrobial drugs have not been recommended unless a specific microbial agent producing progressive systemic involvement can be identified. Preliminary data now suggest that ciprofloxacin, 500 mg every 12 hours for 5 days, may shorten the duration of diarrhea and lead to a more rapid resolution of symptoms. Antimotility drugs may relieve cramping and decrease diarrhea in mild cases. Their use should be limited to patients without fever and without dysentery (bloody stools), and they should be used in low doses.CONTROL:
It includes the following measures: a) education of persons who prepare food at home or commercially in proper personal hygiene; b) exclusion from handling food of individuals with abscesses or other skin lesions; and c) refrigeration of all foods to prevent bacterial multiplication and formation of toxins. Foods should be kept at room temperature as little time as possible. The veterinary milk inspection service should supervise dairy installations, ensuring that refrigeration units function correctly and are used immediately after milking, and that milk is refrigerated during transport to pasteurization plants. The veterinary meat inspection service should be responsible for enforcing hygienic regulations before and after slaughter as well as during handling and production of meat products. Control of hygienic conditions in meat retail establishments ts also important.J Clin Microbiol 2000 Apr;38(4):1628-31
Molecular Phylogenetic Evidence for Noninvasive Zoonotic Transmission of Staphylococcus intermedius from a Canine Pet to a Human
Tanner M.A., Everett C.L., Youvan D.C.
Kairos Scientific Inc., Santa Clara, California 95054, USArRNA-based molecular phylogenetic techniques were used to identify the bacterial species present in the ear fluid from a female patient with otitis externa. We report the identification of Staphylococcus intermedius from the patient and a possible route of transmission. Analysis of 16S ribosomal DNA restriction fragment length polymorphisms indicated that the dominant species present was S. intermedius. A pet dog owned by the patient also was tested and found to harbor S. intermedius. In humans, the disease is rare and considered a zoonosis. Previously, S. intermedius has been associated with dog bite wounds, catheter-related injuries, and surgery. This study represents the first reported case of a noninvasive infection with S. intermedius.
STREPTOCOCCOSIS
AGENT:
The causative agents are various streptococci species, including Streptococcus suis and S. zooepidemicus.RESERVOIR AND INCIDENCE
Pigs are the reservoir of S. suis.TRANSMISSION:
Humans are infected with S. suis by handling infected meat. S. zooepidemicus has occurred in persons in direct contact with domestic animals and from drinking raw milk.DISEASE IN ANIMALS:
S. suis epizootics may occur in pigs with high mortality, heralded by signs of meningitis including depression, fever, incoordination and paralysis. Suppurative arthritis may occur. More usually the disease is subclinical. S. zooepidemicus may cause mastitis in cattle.DISEASE IN MAN:
S. suis causes fever and occasionally meningitis. S. zooepidemicus may cause upper respiratory tract symptoms, cervical adenitis, pneumonia, endocarditis and nephritis. A fatality rate of 8% has been reported for S. suis, with residual deafness in a high proportion of survivors.DIAGNOSIS:
isolation and cultureTREATMENT:
Benzathine Penicillin G. For persons allergic to penicillin, erythromycin is an effective alternative. However, increasing reports of resistance from Europe threatens its clinical utility.PREVENTION/CONTROL:
Exercise caution in handling pig meat. Dress all wounds to avoid contamination. Pasteurize milk.STRONGYLOIDIASIS
AGENT:
Strongyloidiasis is caused by infection with Strongyloides stercoralis.RESERVOIR AND INCIDENCE
The condition is an infection of humans, but dogs, cats, and primates have been found naturally infected. The disease is endemic in tropical and subtropical regions; although the prevalence is generally low, in some areas disease rates exceed 25%. In the USA, the disease is endemic in southern wet areas.TRANSMISSION:
The parasite is uniquely capable of maintaining its life cycle both within the human host and in soil. Infection occurs when filariform larvae in soil penetrate the skin, enter the bloodstream, and are carried to the lungs, where they escape from capillaries into alveoli and ascend the bronchial tree to the glottis. The larvae are then swallowed and carried to the duodenum and upper jejunum, where maturation to the adult stage takes place. The parasitic female, generally held to be parthenogenetic, matures and lives embedded in the mucosa, where its eggs are laid and hatch. Rhabditiform larvae, which are noninfective, emerge, and most migrate into the intestinal lumen to leave the host via the feces. The life span of the adult worm may be as long as 5 years. In the soil, the rhabditiform larva metamorphose into the infective (filariform) larvae. However, the parasite also has a free-living cycle in soil, in which some rhabditiform larvae develop into adults that produce eggs from which rhabditiform larvae emerge to continue the life cycle. Internal autoinfection takes place in the lower bowel when some rhabditiform larvae, instead of passing with the feces, develop into filariform larvae that penetrate the intestinal mucosa, enter the intestinal lymphatic and portal circulation, are carried to the lungs, and return to the small bowel to complete the cycle.DISEASE IN ANIMALS:
Young dogs and cats have thin skins which allow massive infection to penetrate, giving severe dermatitis, inappetence, coughing and even bronchopneumonia. Vomiting occurs, as does severe dermatitis during the period of larval penetration.DISEASE IN MAN:
Pruritic dermatitis is seen at sites of larval penetration. Diarrhea, epigastric pain, nausea, malaise, weight loss, coughing, rales, transient pulmonary infiltrates are also seen. In the hyperinfection syndrome, autoinfection is greatly increased, resulting in a marked increase in the intestinal worm burden and in massive dissemination of filariform larvae to the lungs and most other tissues, where they can cause local inflammatory reactions and granuloma formation. Severe diarrhea, bronchopneumonia, and ileus can result.DIAGNOSIS:
Diagnosis requires finding the larval stages in feces or duodenal fluid. ELISA and IFA serologic tests are being developed.TREATMENT:
Thiabendazole, albendazole, mebendazole, cambendazole, ivermectin, or levamisole.PREVENTION/CONTROL:
Rigid attention to hygienic habits, including use of footwear in endemic areas. Sanitary disposal of feces. Fecal exams of monkeys, dogs, and cats in quarantine.TANAPOX
(Benign Epidermal Monkeypox, BEMP)AGENT:
Tanapox virus.RESERVOIR AND INCIDENCE
Monkeys. In 1966 23 human cases were reported in the U.S. among personnel who worked with monkeys affected at 3 primate centers. A serologic study carried out on 263 monkeys of Asian origin (Macaca) revealed a 15% rate; in 55 African Green Monkeys, the rate was 76%.TRANSMISSION:
Aerosols or vectors. Human cases in the laboratory have resulted from contamination of abrasions or scratches.DISEASE IN NONHUMAN PRIMATES:
Lesions occur primarily on the face, consisting of raised areas with a central scab. Papules ulcerate, scab and heal.DISEASE IN HUMANS:
There is a fever for a few days, with headache and prostration and a single skin vesicle. Cytoplasmic inclusions are seen in skin lesions. Within 3 weeks of onset, the lesion spontaneously regresses.DIAGNOSIS:
EM of skin scrapings or viral isolation.TREATMENT:
Symptomatic.PREVENTION/CONTROL:
Mosquito control. Asian and African monkeys should be housed separately. Wear protective clothes.
TAPEWORMS(CESTODES) (segmented worms)
Two major clinical groups
1. Intestinal Tapeworms: T. Saginata, T. Soluim, Diphyllobothrium,
Hymenolepsis, Dipylidium Caninum -humans are the definitive hosts and adult tape
worms live in the gastrointestinal tract.
2. Somatic Tapeworms: T. Solium, Echinococcosis, sparganosis, coenurosis
-humans are intermediate hosts and larval stage parasites are present in the
tissues.
Taenia solium (Pork
Tapeworm)
-humans are the only definitive host. Pigs are the usual intermediate
hosts (although dogs, cats and sheep may harbor the larval forms.(cystercicosis)
-exist worldwide but most prevalent in Mexico, Africa, SE Asia, Eastern Europe
and South America
-Occurs in industrialized nations largely as result of immingration from above
Two distinct types of disease, depending on the stage of the parasite that is ingested.
1. Intestinal T. Solium: The adult tapeworm develops in the intestine, causing symptoms such as abdominal pain, weight loss, and weakness. Eggs of T. solium are also passed in the feces. Eggscan be detected with greater frequency by applying clear cellulose acetate tape to the perianal skin and examining the tape as for pinworm. (T. solium eggs are indistinguishable from eggs of T. saginata (beef tapeworm)); diagnostic differentiation between the two species requires recovery of mature proglottids from the stool.
2. Cysticercosisis(Somatic T.
solium)-ingestion of T. solium eggs.
A. Uninfected person- ingestion may occur by consumption of food
contaminated by egg-containing feces from an infected person.
B. Infecteded persons with an intestinal worm, ingestion may occur
by autoinfection
involving hand-to-mouth fecal carriage or by regurgitation of egg-laden
proglottids into the duodenum or stomach.
Most infections are encountered in developing countries, where intestinal T.
solium infections occur frequently. Experience in the United States has
demonstrated, however, that cysticercosis may develop in those who have never
traveled abroad if family members, domestic workers, or others infected with T.
solium are a source of infectious eggs.
The ingested eggs hatch in the stomach and upper intestine, and the resultant oncospheres circulate in the blood to various tissues. Cysticerci develop most often in subcutaneous tissue, skeletal muscle, and the brain, as well as in other organs, includi ng the eyes, heart, liver, and lungs. Developing cysticerci elicit little host reaction, but as the cysticerci begin to degenerate, usually after several years, inflammation develops. Ultimately, the cysts, which range from 0.5 to about 2.0 cm in diameter, undergo necrosis and may become calcified.
CLINICAL FEATURES:
Clinical signs and symptoms depend on the organ compromised by the cysticerci, the specific localization of a cysticercus within the organ, the state of inflammation surrounding the cysticerci, and the viability of the cestode. The most serious forms of cysticercosis are those with ocular, cardiac, and neurologic involvement. In endemic regions, cysticercosis is the most common cause of seizure disorders.
LABORATORY FINDINGS AND IMAGING STUDIES:
CT and MRI has facilitated the recognition of CNS cysticercosis, has helped
delineate the various forms of neurocysticercosis, and has provided a means for
assessing the adequacy of therapy. Cysticerci may be present in the brain
parenchyma, within the ventricles, at the surface or the base of the brain, or
within the subarachnoid space. The manifestations -variable, depending on the
site of lesions and the evolution of inflammatory reactions, include seizure
disorders and focal deficits, hydrocephalus, arachnoiditis, and intracranial
hypertension.
CT may miss early lesions,
which have the same x-ray density as the brain, but hypodensity and
contrast-enhancing ring lesions are seen with the development of inflammation
around
the cyst. As sclerosis occurs, a cystic lesion develops, and the cyst wall may
calcify. Ultimately, degenerated cysts are replaced by small (1 to 4 mm in
diameter) calcified lesions
within the brain [see Figure 4].
Definitive diagnosis of cysticercosis only by biopsy of a cyst. Cysts in subcutaneous tissue and muscle, which have a puffed-rice appearance on radiographs after calcification, should be sought. Neurocysticercois is supported by the finding of characteristic multiple cystic or calcified lesions on CT scans in a patient from an endemic area. Serum and CSF for antibody, is available through the Centers for Disease Control and Prevention (CDC). ELISA testing for antibody, however, may be negative in about 20 percent of patients with cysticercosis, falsely positive in those with echinococcosis. An enzyme-linked immunoelectrotransfer blot assay for antibody is highly sensitive in patients who have several enhancing intracranial lesions; it is less sensitive in those who have only one lesion or calcified lesions. Stool examination for Taenia eggs may detect concurrent infection with the tapeworm but is not directly pertinent to the diagnosis of cysticercosis.
TREATMENT:
1. Ingested Cysterci:
Therapy for adults infected with intestinal pork tapeworm consists of
praziquantel (5 to 10 mg/kg, given once).
2.Cysticercosis
A. Pts with calcified soft tissue or CNS lesions do not require medical therapy.
B. Viable Cysts. Some uncertainty regarding efficacy of medical treatment.
Albendazole 15 mg/kg/day in three divided doses for eight to 28 days, or
praziquantel 50 mg/kg/day in three divided doses for 15 days. Treatment
may cause inflammatory reactions to develop around cysticerci. For
patients with neurocysticercosis, corticosteroids (e.g., dexamethasone, 4 to 16
mg/day, or prednisone, 60 to 100 mg/day) are usually given one to two days
before and during treatment with albendazole or praziquantel to minimize
inflammatory reactions. Patients who take anticonvulsant medications should
continue to use them during treatment for cysticercosis, but many patients can
stop taking antiseizure medications after cysticercosis therapy. CT scanning
should be repeated three to six months after therapy to determine whether any of
the cysts are still viable, and therapy should be repeated if viable cysts
remain.
C. Surgical for ocular cysticercosis and spinal cysticercosis inflammation
from medical treatment can cause irreversible damage. These lesions best
managed surgically.
Ventricular obstruction may require V-P shunting/ventriculostomy
FISH TAPEWORM
Humans acquire fish tapeworm infection by ingestion of inadequately cooked fish
containing the infective plerocercoid stage of parasitic Diphyllobothrium
species, including D. atum.76 The growing popularity of raw fish dishes, such as
sushi, sashimi, seviche, and Dutch green herring, has increased the risk of
acquiring diphyllobothriasis or anisakiasis. Freshwater fish, including pike and
yellow perch caught in the United States, may harbor Diphyllobothrium species,
as may anadromous salmon. Diphyllobothrium species other than D. latum are found
in Pacific salmon and Alaskan blackfish. Human infections are often
asymptomatic, although some patients experience anorexia, nausea, or weight
loss. Because D. latum competes with the host for vitamin B12, megaloblastic
anemia and neuropathy from vitamin B12 deficiency may develop. Diagnosis is made
by finding the operculated eggs in the stool or by recovering proglottids in the
stool after a saline purge. Therapy is with praziquantel (5 to 10 mg/kg, given
once), which is investigational for this use.
BEEF TAPEWORM
T. saginata, or beef tapeworm, causes an intestinal infection in persons who
have eaten undercooked beef containing cysticerci. The infection is usually
asymptomatic, although abdominal pain, weight loss, increased appetite, or
passage of proglottids may be experienced. As noted, the detection of eggs in
the feces or on the perianal skin is diagnostic of tapeworm infection, but
differentiation between Taenia species requires identification of the
proglottids. Therapy consists of praziquantel, as given for T. solium intestinal
infection. Infection with T. saginata does not lead to cysticercosis in humans.
DWARF TAPEWORM
Hymenolepis nana, a tapeworm measuring 25 to 40 mm long and 1 mm wide, has a
broad geographic distribution.76 In the United States, it is most commonly
encountered in persons living in the southern states, in institutionalized
patients, and in children. Unlike the other tapeworms, the larval and adult
stages of H. nana develop in the same host. Infection is spread by the
fecal-oral route and occurs when eggs, which are immediately infectious, are
ingested. An oncosphere hatches from an egg and penetrates the intestinal villi,
where it develops into a cerocyst; the cerocyst reenters the lumen of the small
intestine and develops into an adult worm. Eggs are liberated from the distal
segments of the adult worm, which lives for about one year. The eggs may cause
internal reinfection. Light infection is usually asymptomatic; diarrhea and
abdominal pain may accompany heavy infection. Diagnosis is made by finding
eggs in feces. Therapy consists of praziquantel, which is given once in a dose
of 25 mg/kg.(investigational)
Prevention
Adequate cooking of beef, pork or fish (54-56 degrees C for 5 minutes) will
destroy cysterci. Refrigeration or salting for prolonged periods also
kills cysterci. General preventive measures include inspection, proper
disposal of human and animal waste.
AGENT:
Toxoplasma gondii - 4 to 7 microns long. 2-4 wide - Subphylum Apicomplexa, Family EimeriidaeRESERVOIR AND INCIDENCE
Infection in humans and lower animals is widespread. An estimated 500 million humans have been infected with the organism. Serologic surveys in the United States using the SABIN-FELDMAN DYE TEST have demonstrated T. gondii infection in 30-80% of cats. Significance - Presumably all serologically positive cats have shed toxoplasma oocysts and could re-shed organisms during reinfection or reactivation. Life cycle consists of: 1. Definitive host (felids: intestinal infection with shedding of oocysts; only host in which sexual form develops.) - Domestic cat predominates as reservoir for zoonotic transmission in the home and laboratory environment. 2. Intermediate hosts - *Mice, rats, hamsters, G. pigs, rodents, rabbits, dogs, sheep, cattle, & NHP's. - These have not proved to be important in zoonotic infection in the laboratory animal environment (organism replicates asexually in extraintestinal sites only).TRANSMISSION:
Fecal-Oral: Ingestion of meat containing cysts or tachyzoites or ingestion of oocysts Oocysts become infective after sporulation - occurs in 2 to 3 days. Transmission to man occurs via a. Eating raw or undercooked meat containing cysts. b. Ingesting sporulated oocysts from cat feces. c. Transplacentally. 1/3 of US human population has serologic evidence of past infection.DISEASE IN CATS:
Most postnatally acquired infections in cats are ASYMPTOMATIC. Prepatent period variable - 3 days to several weeks. Shedding occurs for 1-2 weeks - PUBLIC HEALTH HAZARD. Oocyst shedding reactivated by induction of hypercorticism or superinfection with other feline microorganisms.DISEASE IN MAN:
The infection is very common in humans, but clinical disease is of low incidence and occurs only sporadically. Postnatal infection - Less severe disease and commonly presents as a generalized lymphadenopathy that may resolve without treatment in a few weeks. Congenital infection results in systemic disease often with severe neuropathological changes. Rarely, serious ocular or systemic toxoplasmosis can be acquired by older individuals or reactivated in immunocompromised individuals. Clinical Signs include fever, skin eruption, malaise, myalgia, arthralgia, cervical lymphadenopathy, pneumonia, myocarditis, meningoencephalitis, and chorioretinitis.DIAGNOSIS:
Serology, isolation, microscopic demonstration of organisms in smear or section. Paired serum samples taken one or more weeks apart. a. IFA: serial titers of suspected infections. b. Sabin- Feldman Dye Test: most sensitive test, but rarely used. c. ELISA. The demonstration of cysts does not establish a causal relationship to clinical illness, since cysts may be found in both acute and chronic infections. However, only finding tachyzoites in blood or body fluids confirms active infection.TREATMENT IN MAN:
The treatment of choice is pyrimethamine plus either trisulfapyrimidines or sulfadiazine. Folinic acid is given to avoid the hematologic effects of pyrimethamine-induced folate deficiency.PREVENTION/CONTROL:
Freezing of meat to -20oC (-4oF) for 2 days or heating to 60oC (140oF) kills cysts. Under appropriate environmental conditions, oocysts passed in cat feces can remain infective for a year or more. Thus, children's play areas should be protected from cat and dog feces. Cats a. Daily cleaning of litter pans (since oocysts not infective for 2 to 3 days) b. Wear gloves c. Wash hands before eating d. Should only be fed dry, canned, or cooked meats Pregnant women should have their serum examined for Toxoplasma antibody. If the IgM test is negative but an IgG titer is present and less than 1:1000, no further evaluation is necessary. Those with negative titers should take measures to prevent infection by avoiding contact with cat feces and avoid working in soil or gardens that could be contaminated by cats, etc. and by thoroughly cooking meat. Hands should be washed after handling raw meat and before eating or touching the face.
AGENT:
Trichinella spiralis, an intestinal nematode.RESERVOIR AND INCIDENCE
Swine, dogs, cats, rats and many wild animals. Worldwide. In the U.S., there has been a marked reduction in the prevalence of trichinosis both in humans and pigs; prevalence in commercial pork now ranges from nil to 0.7%. Fewer than 100 human cases are reported annually and usually have been as a result of eating homemade sausage and other meat products using pork, horse meat, or arctic mammals.TRANSMISSION:
In the natural cycle, larvae develop into adult worms in the intestines when a carnivore ingests parasitized muscle. Pigs generally become infected by feeding on uncooked scraps or, less often, by eating infected rats. In humans, infection occurs by eating insufficiently cooked meat. In the epithelium of the small intestine, larvae develop into adults. Gravid female worms then produce larvae, which penetrate the lymphatics or venules and are disseminated via the bloodstream throughout the body. The larvae become encapsulated in skeletal muscle.DISEASE IN ANIMALS:
Usually subclinical.DISEASE IN HUMANS:
Clinical disease in humans is highly variable and can range from inapparent infection to a fulminating, fatal disease depending on the number of larvae ingested. Sudden appearance of muscle soreness and pain, together with edema of upper eyelids are common early and characteristic signs. These are sometimes followed by subconjunctival, subungual and retinal hemorrhages, pain and photophobia. Thirst, profuse sweating, chills, weakness, prostration and rapidly increasing eosinophilia may follow. GI symptoms may also occur. Remittent fever, cardiac and neurologic complications may appear. Lastly, death due to myocardial failure may occur.DIAGNOSIS:
Serologic testing and muscle biopsy.TREATMENT:
Treatment is principally supportive, since in most cases recovery is spontaneous. Mebendazole, thiabendazole, or albendazole can be given.PREVENTION/CONTROL:
Cooking (at 77oC [171oF] or above) destroys the parasite. Freezing meat up to 15 cm at 5oF for 30 days or -13oF for 10 days will destroy the parasite. Thicker pieces need to be frozen at the lower temperature for at least 20 days. These temperatures will not kill the cold-resistant Arctic strains, however. Gamma irradiation will kill the parasite. Prevent pigs from gaining access to rats or uncooked offal.TRICHOSTRONGYLOSIS
(Trichostrongyliasis, Trichostrongylosis)AGENT:
Several species of Trichostrongylus including Trichostrongylus axei, T. affinis, T. colubriformis, and many others. RESERVOIRS AND INCIDENCE: The reservoirs of most of the species of Trichostrongylus are domestic and wild herbivores. Trichostrongylids are very common parasites in domestic ruminants and their distribution is worldwide.TRANSMISSION:
The sources of infection are soil and vegetation, in which the eggs deposited with the animal host's feces develop in a few days to the infective larval stage. Man and animals are infected orally. Man acquires the infection mainly by consuming raw vegetables contaminated with the infective larvae. Another important factor in transmission is the preparation and use of animal manure as fuel.DISEASE IN ANIMALS:
In horses, these worms produce a chronic catarrhal gastritis and may result in weight loss. The lesions comprise nodular areas of thickened mucosa surrounded by a zone of congestion and covered with a variable amount of mucus. The lesions may be rather small and irregularly circumscribed, or may coalesce and involve most or all of the glandular portion of the stomach, and erosions and ulcerations may be seen. In ruminants, gastritis with superficial erosion of the mucosa, hyperemia, and diarrhea may result. Protein loss from the damaged mucosa and anorexia cause hypoproteinemia and weight loss.DISEASE IN MAN:
Most cases asymptomatic. Severe infections - diarrhea, blood in stool, abdominal cramps, and emaciation.DIAGNOSIS:
:Flotation and fecal culture (identification of larvae used to distinguish between species).TREATMENT:
Pyrantel pamoate, mebendazole, or levamisole.PREVENTION/CONTROL:
Regular deworming of animals. Preventive measures for humans consist of improved food, environmental, and personal hygiene. In endemic areas, raw vegetables or other foods should not be eaten. Pasture management is important. Most of the larvae die in a field left ungrazed for a month.TRICHURIASIS -(WHIPWORM INFECTION)
AGENT:
Trichuris suis, Trichuris trichiura, Trichuris vulpis
Means of transmission to humans:
Contact
Most common species associated with transmission to humans:
Dogs, swine
(Consumption)
AGENT, RESERVOIR AND INCIDENCE
TB is caused by the gram positive, acid fast, aerobic, bacillus of the Mycobacterium genera. The most common species of mycobacteria are: 1. M. bovis (cattle, dogs, swine) 2. M. avium (birds, swine, sheep) 3. M. tuberculosis (man, nonhuman primates, cattle, dogs, swine, psitticines). 4. M. marinum, fortuitum, platypolcitis (fish) Note: Atypical mycobacterium, M. scrofulaceum, M. kansasii, and M. intracellulare have been reported in NHP's and are also present in soil and water. They can cause pulmonary disease refractory to treatment in man, and are most often seen in immunocompromised people. Specific reagents can be used to skin test for these bacteria. TB continues to be a major cause of morbidity and mortality throughout the world. One billion people are infected with the tubercle bacillus, and there are 8 million new cases and 3 million deaths annually. Cases of active tuberculosis are increasing in the United States after years of decline. A provisional total of 23,720 cases was reported by the end of 1990. Case rates increased 4.4 percent between 1988 and 1989, and perhaps another 1 percent in 1990. Overall rate was 9.5 per 100,000 in 1989, with the Middle Atlantic and Pacific regions reporting the highest rates, 36 percent and 34 percent, respectively, above the U.S. total. The lowest rates were in the West, North, Central, and Mountain regions. Rates continue to be higher among urbanites, minorities, the poor, the homeless, substance abusers and persons infected with HIV. All three types are capable of causing disease in man although M. tuberculosis (variety hominis) is by far the most common. Nonhuman primates can carry all three types but most infections are caused by M. tuberculosis variety hominis. While most nonhuman primates are capable of contracting TB, Old World species appear to be more susceptible to the disease than New World species and great apes. Most cases of TB in monkeys are thought to arise from human contact. Animals may be imported from areas of the world where the incidence of the disease is high and where contact between humans and simians is frequent. In close confinement the disease can spread rapidly.TRANSMISSION:
Mycobacterium bacilli are transmitted from infected animals or infected tissue primarily via the aerosol route. May also be contracted via ingestion or cutaneous inoculation of the bacilli. Personnel caring for infected animals as well as those performing necropsies on infected animals are at risk for contracting the disease. Exposure to dusty bedding of infected animals, coughing of infected animals, and aerosolization of the organism during sanitation procedures may also be sources of the disease in the lab environment. Once within the body the organism may spread throughout the lungs, lymphatics, blood vascular system, and many visceral organs.DISEASE IN NONHUMAN PRIMATES:
The signs of TB may be insidious with only slight behavioral changes noticed, followed by anorexia and lethargy. Often animals die suddenly while appearing to be in good condition. Other signs which might be seen include diarrhea, suppuration of lymph nodes, ulceration of the skin, and palpable splenomegaly and hepatomegaly. The organ of predilection is the lung but lesions may also be seen in the pleura, intestines, lymph nodes, liver, kidney, spleen, and peritoneum. Under the surface of these tissues are yellowish-white to gray nodules filled with caseous material which may rupture and produce cavitation. Although skeletal involvement in primates is rare, tuberculosis of the spine may cause paralysis of the hindlimbs (Pott's disease).DISEASE IN FISH:
In infected fish, granulomatous lesions are usually observed.DISEASE IN MAN:
In humans the clinical signs depend on the organ system involved. The most familiar signs related to pulmonary TB are cough, sputum production, and hemoptysis. The patient may be asymptomatic for years. General signs may include anorexia, weight loss, lassitude, fatigue, fever, chills and cachexia. Skin lesions are characterized by ulcers or by papular lesions progressing to dark suppurative lesions. TB may affect virtually every other organ system with signs or symptoms relating to the individual system. Miliary TB is most often seen in the very young and old people.DIAGNOSIS:
The diagnosis of TB is often difficult. Four tests are commonly used for presumptive diagnosis: 1. Intradermal TB test - Mammalian tuberculin 2. Radiography 3. Acid fast stained sputum smear 4. ELISA Confirmation by culture, histopath, or animal inoculation.TREATMENT:
Regimens currently accepted in the USA include isoniazid combined with rifampin, with or without pyrazinamide.PREVENTION\CONTROL:
Multifaceted and includes: personnel education wearing of protective clothing when handling nonhuman primates a regular health surveillance program for humans and nonhuman primates isolation and quarantine of suspect animals rapid euthanasia and careful disposal of infected animals Vaccine - A vaccine, BCG, is available (Bacille Calmette-Guerin, strain of M. Bovis) a. Used in humans quite often in G. Britain b. Used in high risk groups c. Effective, but it causes the patient to have a positive TB test. Personnel working with NHP's who convert to a positive skin test should be referred for appropriate medical treatment and follow up and should not work with animals until shown to be noninfectious.TULAREMIA
(Francis' disease, deer-fly fever, rabbit fever, O'Hara disease)AGENT
- Francisella tularensis, a small pleomorphic, gram-negative, nonmotile rod or coccobacillus that can survive several weeks in the external environment.RESERVOIR AND INCIDENCE
Common often fatal septicemic disease of rabbits, squirrels, muskrats, deer, bull snakes, sheep, wild rodents, cats and dogs. Major reservoirs are RABBITS, TICKS, MUSKRATS. Has been reported in NHP's at an urban zoo. Natural infection in laboratory animals and zoonotic transmission from them has NOT been reported.TRANSMISSION:
handling tissue of infected animals (direct contact with UNBROKEN skin is sufficient). Reported human infections due to a cat bite and scratch and a NHP bite also reported. transmitted by biting insects inhalation, ingestionDISEASE IN ANIMALS:
Clinical signs usually occur alongside heavy infestation with ticks, and include sudden high fever, anorexia and stiffness, eventually leading to prostration and death. In sheep, pregnant ewes may abort. Affected dogs have soft nodular swellings under the skin. Miliary foci of necrosis occur in the liver, spleen and lymph nodes. Severe lesions in the lung involve widespread consolidation with edema and pleurisy.DISEASE IN MAN:
Fever, headache, and nausea begin suddenly, and a local lesion-a papule-develops and soon ulcerates. Regional lymph nodes may become enlarged and tender and may suppurate. The local lesion may be on the skin of an extremity (ulceroglandular disease) or in the eye. Pleuropulmonary disease may develop from hematogenous spread or may be primary after inhalation. Following ingestion of infected meat or water, an enteric (typhoidal) form may be manifested by enteritis, stupor, and delirium. In any type of involvement, the spleen may be enlarged and tender and there may be nonspecific rashes, myalgias, and prostration. A case fatality rate of 5-10% mainly from the typhoidal or pulmonary form exists.DIAGNOSIS:
Culture (requires specialized laboratory and dangerous, therefore, not recommended) A positive agglutination test (>1:80) develops in the second week after infection and may persist for several years.TREATMENT IN MAN:
streptomycin + tetracycline. Chloramphenicol may be substituted for tetracycline.PREVENTION\CONTROL:
wear impervious gloves while handling animals or tissues cook the meat of wild rabbits and rodents thoroughly vaccine available for high risk personnel avoid bites of flies, mosquitoes, and ticks and avoid drinking, bathing, swimming in untreated water in endemic areas.VESICULAR STOMATITIS
AGENT:
Vesicular stomatitis virus
Means of transmission to humans:
Vector, contact, aerosol
Most common species associated with transmission to humans:
Horses, cattle, swine, sheep, goats
Vibrios other than Vibrio cholerae that cause human disease are Vibrio parahaemolyticus, Vibrio vulnificus and Vibrio alginolyticus. All are halophilic marine organisms. Infection is acquired by exposure to organisms in contaminated, undercooked, or raw crustaceans or shellfish and warm ( 20o C) ocean waters and estuaries. Infections are more common during the summer months from regions along the Atlantic coast and the Gulf of Mexico in the United States and from tropical waters around the world. Oysters are implicated in up to 90% of food-related cases. V. parahaemolyticus causes an acute watery diarrhea with crampy abdominal pain and fever, typically occurring within 24 hours after ingestion of contaminated shellfish. The disease is self-limited, and antimicrobial therapy is usually not necessary. V. parahaemolyticus may also cause cellulitis and sepsis, though these findings are more characteristic of V. vulnificus infection. V. vulnificus and V. alginolyticus-neither of which is associated with diarrheal illness-are important causes of cellulitis and primary bacteremia, which may follow ingestion of contaminated shellfish or exposure to sea water. Cellulitis with or without sepsis may be accompanied by bulla formation and necrosis with extensive soft tissue destruction, at times requiring debridement and amputation. The infection can be rapidly progressive and is particularly severe in immunocompromised individuals-especially those with cirrhosis-with death rates as high as 50%. Patients with chronic liver disease and those who are immunocompromised should be cautioned to avoid eating raw oysters. Tetracycline at a dose of 500 mg four times a day is the drug of choice for treatment of suspected or documented primary bacteremia or cellulitis caused by Vibrio species. V. vulnificus is susceptible in vitro to penicillin, ampicillin, cephalosporins, chloramphenicol, aminoglycosides, and fluoroquinolones, and these agents may also be effective. V. parahaemolyticus and V. alginolyticus produce betalactamase and therefore are resistant to penicillin and ampicillin, but susceptibilities otherwise are similar to those listed for V. vulnificus.
(Toxocariasis)
AGENT:
Most cases of visceral larval migrans (VLM) are due to Toxocara canis, an ascarid of dogs and other canids, but in a few cases Toxocara cati in domestic cats has been implicated and rarely Baylisascaris procyonis of raccoons.RESERVOIR AND INCIDENCE
The reservoir mechanism for T. canis is latent infections in female dogs which are reactivated during pregnancy. Transmission from mother to puppies is via the placenta and milk. The life cycle of T. cati is similar, but transplacental transmission does not occur. Human infections are sporadic and occur worldwide.TRANSMISSION:
Infection is generally in dirt-eating young children who ingest T. canis or T. cati eggs from soil or sand contaminated with animal feces, most often from puppies. Direct contact with infected animals does not produce infection, as the eggs require a 3 to 4 week extrinsic incubation period to become infective; thereafter, eggs in soil remain infective for months to years. In humans, hatched larvae are unable to mature and continue to migrate through the tissues for up to 6 months. Eventually they lodge in various organs, particularly the lungs and liver and less often the brain, eyes, and other tissues, where they produce eosinophilic granulomas up to 1 cm in diameter.DISEASE IN ANIMALS:
The first indication of infection in young animals is lack of growth and loss of condition. Infected animals have a dull coat and often are "potbellied". Worms may be vomited and are often voided in the feces. In the early stages, pulmonary damage due to migrating larvae may occur; this may be complicated by bacterial pneumonitis, so that respiratory distress of variable severity may supervene. Diarrhea with mucus may be evident. In severe infections of puppies, verminous pneumonia, ascites, fatty degeneration of the liver, and mucoid enteritis are common. Cortical kidney granulomas containing larvae are frequent in young dogs.DISEASE IN MAN:
Migrating larvae induce fever, cough, wheezing; hepatomegaly, and sometimes splenomegaly and lymphadenopathy are present. The acute phase may last 2-3 weeks, but resolution of all physical and laboratory findings may take up to 18 months. Leukocytosis is marked due to eosinophils. Hyperglobulinemia occurs when the liver is extensively invaded. Ocular toxocariasis results in a eosinophilic granuloma of the retina that may be mistaken for retinoblastoma.DIAGNOSIS:
ELISA, no parasitic forms can be found by fecal exam.TREATMENT:
Thiabendazole, Mebendazole, or Ivermectin. Corticosteroids, antibiotics, antihistamines, and analgesics are given for symptomatic relief. Treatment for Ocular Toxocariasis includes the above plus vitrectomy and laser photocoagulation.PREVENTION/CONTROL:
Disease in humans is best prevented by periodic treatment of puppies, kittens, and nursing dogs and cats. Children should be supervised to prevent pica; their hands should be washed after playing in soil and sand; and play areas should be protected from animal feces.WEST NILE VIRUS
AGENT:
West Nile Virus
Means of transmission to humans:
Vector
Most common species associated with transmission to humans:
Wild birds
YABAPOX
AGENT:
PoxvirusRESERVOIR AND INCIDENCE
Affects mangabeys, rhesus, cynos, vervets, stumptails, and patas monkeys. Latent infection in African species that can infect Asian primates and U.S. born African primates.TRANSMISSION:
Need further clarification of the epidemiology of this disease. Role of insect vectors has not been determined. Aerosol transmission has been proven experimentally. *Transmission to humans from monkeys has not been recorded. The virus can affect man usually after accidental skin puncture.DISEASE IN NONHUMAN PRIMATES:
Subcutaneous benign tumors (Histiocytomas) that may reach several cm. in diameter. They usually regress spontaneously in 3 to 6 weeks.DISEASE IN MAN:
Lesions similar to those seen in monkeysPREVENTION/CONTROL:
Usual care should be exercised by animal handlers, including wearing of protective clothing.YELLOW FEVER
(Black Vomit)AGENT:
RNA virus, Family Togaviridae, (Group B Arbovirus)RESERVOIR AND INCIDENCE
all primates susceptible; major Public Health problem in Central and S. America and Africa.TRANSMISSION:
mosquito vector: Aedes and HemagoguesDISEASE IN NONHUMAN PRIMATES:
There is high fever and vomiting, with jaundice, oliguria, and generalized hemorrhages. Microglobular fatty degeneration of liver cells occurs with disruption of the hepatic lobule and necrosis of midzonal liver cells, producing so called "Councilman" bodies. Degeneration and necrosis of the kidney tubules occurs. There are hemorrhages in tissues.DISEASE IN MAN:
Most cases have fever, severe headache and backache, jaundice and albuminuria, followed by full recovery with a week, but in severe cases there is a second episode of fever, prostration, jaundice, renal failure and generalized hemorrhages. Microglobular fatty degeneration of liver cells occurs with disruption of the hepatic lobule and necrosis of midzonal liver cells, producing so called "Councilman" bodies. Degeneration and necrosis of the kidney tubules occurs. There are hemorrhages in tissues. The case fatality rate among indigenous populations of endemic regions is <5%, but may exceed 50% among nonindigenous groups and in epidemics.DIAGNOSIS:
Virus isolation or serology.TREATMENT:
Consists of limiting food to high-carbohydrate, high-protein liquids, IV glucose and saline, analgesics and sedatives, and saline enemas.PREVENTION/CONTROL:
Monkeys should originate from a yellow fever free area, or be maintained in a double-screened mosquito-proof enclosure, or have been immunized against yellow fever. For humans, mosquito control, vaccination, and adherence to PHS quarantine standards.(Plague, Pest, black death, pestilential fever) The second pandemic of plague, known then as the "Black Death," originated in Mesopotamia about the middle of the 11th century, attained its height in the 14th century and did not disappear until the close of the 17th century. It is thought that the Crusaders, returning from the Holy Land in the 12th and 13th centuries, were instrumental in hastening the spread of the disease. Again the land along trade routes was primarily involved and from them the infections spread east, west, and north. During the course of the disease, 25,000,000 people perished, a fourth of the population of the world.
AGENT:
a gram negative coccobacillusRESERVOIR AND INCIDENCE
Endemic in wild rodents in Southwestern U.S., as well as in Africa and Asia. Most important reservoirs worldwide are the domestic rat, Rattus rattus, and the urban rat, Rattus norvegicus. Human infections have increased since 1965 and usually result from contact with infected fleas or rodents. The disease is also associated with cats, goats, camels, rabbits, dogs and coyotes. Dogs and cats may serve as passive transporters of infected rodent fleas into the home or laboratory.TRANSMISSION:
Contact with infected rodent fleas or rodents. Fleas may remain infected for months. Note: a protein secreted by the Yersinia is a coagulase that causes blood ingested by the flea to clot in the proventriculus. The bacillus proliferates in the proventriculus, and thousands of organisms are regurgitated by obstructed fleas and inoculated intradermally into the skin. This coagulase is inactive at high temperatures and is thought to explain the cessation of plague transmission during very hot weather. Pulmonary form spread by airborne or droplet infection. Human infections from non-rodent species usually result from direct contact with infected tissues, by scratch or bite injuries, and handling of infected animals. Several recent reports have detailed human plague associated with exposure to domestic cats. Exposure can be from inhalation of respiratory secretions of cats with pneumonic plague or by contaminating mucous membranes or skin wounds with secretins or exudates.DISEASE IN ANIMALS:
dogs usually have a brief self-limiting illness cats usually exhibit severe and often fatal infection, with fever, lymphadenopathy, hemorrhagic pneumonia, and encephalitis. rodents may carry the disease asymptomatically or develop fatal disease. infected rats and squirrels frequently die unless they are from an enzootic area and have acquired immunity.DISEASE IN MAN:
Incubation period 2 to 6 days. In humans the disease is called Bubonic, Septicemic, or Pneumonic plague depending on the pattern of distribution of the infection. Bubonic is the most common form causing fever and swollen, tender lymph nodes (called Buboes). Pneumonic plague is systemic plague with lung involvement. Mortality may exceed 50%. Plague is also called the "black death" because disseminated intravascular coagulation takes place and areas of skin undergo necrosis.DIAGNOSIS:
Impression smears of aspirates or blood stained with gram or Giemsa. Organisms have a typical "safety pin" appearance culture of the organisms can be performed, by reference lab FA of smear is confirmatory. Serology via Complement fixation, passive hemagglutination, and immunofluorescence (IFA)TREATMENT:
streptomycin with tetracycline or chloramphenicol.PREVENTION\CONTROL:
Wild rodents should be controlled and fleas should be eliminated. It is important to control rodents and fleas for outdoor housed animals. Sentinel animal programs used in endemic areas. Endemic areas of the U.S. include California, Nevada, Arizona, and New Mexico. Masks gowns, and gloves should be worn when handling cats suspected to be infected and all contaminated surfaces disinfected. Notify Health Department of suspected cases Vaccines available for high risk personnel.YERSINIA PSEUDOTUBERCULOSIS AND ENTEROCOLITICA
(Pseudotuberculosis)RESERVOIR AND INCIDENCE
Ubiquitous in nature, isolated from dust, soil, water, milk. Natural infections occur in man, birds, rodents, rabbits , guinea pigs, mice, cats, nonhuman primates, sheep, swine, goats.TRANSMISSION:
direct contact, or fecal contaminated food or water cause most transmission from animals to man. Human cases of have been reported in association with disease in household pets, particularly sick puppies and kittens. The most important source of Y. enterocolitica infection may be pork, as the pharynx of pigs may be heavily colonized.DISEASE IN ANIMALS:
guinea pigs, rabbits, and hamsters exhibit poor condition and enlarged lymph nodes. Subacute clinical signs are common, with diarrhea and weight loss, possibly death within 2 weeks to 3 months. Chinchillas are very susceptible to infection with Y. enterocolitica. In sheep, abortions, epididymitis and orchitis occur with high mortality. In cattle, abortion and pneumonia occur. Nonhuman primates exhibit an ulcerative colitis. Histopathological lesions include acute inflammation of the terminal ileum with mesenteric lymphadenitis occurs. Sometimes abscesses develop in the liver, spleen, and lungs. Usually self-limiting, but there is a fatality rate of 5-7%.DISEASE IN MAN:
acute watery diarrhea, mesenteric lymphadenitis which can be confused with appendicitis, fever, headache, pharyngitis, anorexia, vomiting erythema nodosum (in about 10% of adults), post-infectious arthritis, iritis, cutaneous ulceration, hepatosplenic abscesses, osteomyelitis and septicemia.DIAGNOSIS:
fecal culture using cold enrichment technique. Serologic diagnosis can be made by an agglutination test or by ELISA.TREATMENT:
usually resistant to penicillin and its derivatives. Agents of choice are the aminoglycosides and cotrimoxazole. Both are usually sensitive to the tetracyclines.PREVENTION/CONTROL:
Control rodents and prevent contamination of food and water by rodents and birds. Pasteurize milk. Cook pork thoroughly. Personal hygiene is important.Acknowledgements
Boxer Parade Magazine, Summer 1979 Vol 2 Issue 1
Neisseria canis infection: a case report
Sandie Safton, Gavine Cooper, Michael Harrison, Lynne Wright and Paul Walsh
Resident Report -- University of North Carolina, Chapel Hill, Dept. Of Internal Medicine
Spiral Bacteria in the Human Stomach: The Gastric Helicobacters
Andre Dubois, M.D., Ph.D.
Digestive Diseases Division, Department of Medicine,
Uniformed Services University of the
Health Sciences
Bethesda, Maryland,USA
Zoonotic diseases -- Michael S. Rand, DVM, ACLAM; Brent Martin, DVM, ACLAM
UCSB Dept. of Research
YULI VIRUS
(Also known as European bat Lyssavirus type 1)
Bat lyssaviruses are of the particular significance. Bats maintain circulation of all lyssavirus genotypes except one (Mokola virus). In the Americas, after successful implementation of rabies control in the terrestrial mammals by regular vaccination of dogs and oral vaccination of wild canids and raccoons, bats are the main source of human rabies. In the New World bats maintain circulation of classic rabies virus only (lyssavirus genotype 1), but in the Old World bats harbor at least 9 genotypes, including 4 novel, recently discovered at the territory of the former Soviet Union (one isolated in the KR, and another was isolated in the neighboring province of Tajikistan). These lyssaviruses obviously circulate among bats, as was shown for other non-rabies bat lyssaviruses. Nevertheless, all studied bat lyssaviruses (such as European bat lyssaviruses type 1 and 2, Duvenhage virus and Australian bat lyssavirus) cause human rabies. In general, the number of human rabies cases after exposure to bats is underestimated more significantly than human rabies of carnivore origin.
Non-rabies bat lyssaviruses are antigenically distinct from rabies virus, which is the basis for all commercially available anti-rabies biologicals (vaccines and immune globulins). Consequently, these biologicals protect against non-rabies lyssaviruses incompletely. This fact increases the significance of the goal to study host range, distribution and circulation properties of such viruses. Additionally, there is the need to evaluate the protective effect of anti-rabies biologicals available in the KR against these non-rabies lyssaviruses.