Zoonotic Diseases — F–L

DIPYLIDIASIS

Synonyms and scope

Dog and cat flea tapeworm infection; Dipylidium caninum infection. This is a genuine but uncommon zoonosis, most often recognized in young children. People and vertebrate animals acquire infection by swallowing an infected flea or, less often, the dog chewing louse; infection is not acquired by direct contact with eggs in feces.

Etiologic agent

Dipylidium caninum, a cyclophyllidean cestode. Molecular work has identified dog-associated and cat-associated genotypes, but the clinical and control implications are still being defined.

Animals involved and epidemiologic roles

• Dogs: Common definitive hosts; infected animals shed motile proglottids containing egg packets.
• Cats: Common definitive hosts and household sources of infected fleas.
• Wild canids and felids: Additional definitive hosts.
• Fleas: Larvae of Ctenocephalides felis, C. canis, and occasionally other fleas ingest eggs and develop infective cysticercoids; adult fleas transmit infection when swallowed.
• Dog chewing lice: Trichodectes canis can serve as an intermediate host.
• People: Accidental definitive hosts, especially toddlers with close pet contact.

Geographic distribution and occurrence

Worldwide wherever dogs, cats, and fleas coexist. Veterinary infection is common and underdiagnosed; documented human disease is uncommon and probably underrecognized.

Reservoir, life cycle, and transmission

Adult tapeworms live in the small intestine of dogs, cats, wild carnivores, or people. Proglottids pass in feces or crawl from the anus and release egg packets. Flea larvae or chewing lice ingest eggs; cysticercoids become infective as the arthropod matures. Grooming animals and young children become infected by swallowing the arthropod. The approximately three-week flea life cycle and continual environmental emergence can cause rapid reinfection unless flea control accompanies cestocide treatment.

Incubation period

Proglottids may appear approximately 2–3 weeks after an infected flea is swallowed, although recognition may be delayed. Clinical signs, when present, are nonspecific and do not define an incubation period.

Disease in humans

Most infections are asymptomatic. Motile, rice-grain-like proglottids in diapers, stool, or the perianal area are the usual finding. Mild abdominal discomfort, diarrhea, irritability, anorexia, perianal pruritus, or urticaria can occur.

Disease in animals—by species

• Dogs and cats: Usually asymptomatic; visible proglottids, perianal irritation, scooting, or mild gastrointestinal signs may occur. Heavy burdens are more consequential in young, debilitated, or heavily flea-infested animals.
• Wild carnivores: Usually subclinical intestinal infection.
• Fleas and lice: Intermediate-host infection is not generally recognized as clinical disease.

Pathology

Adult worms attach to the small-intestinal mucosa and usually cause little tissue injury. Mild catarrhal enteritis may occur with a large burden. Human and animal disease is generally caused more by irritation and parasite movement than by invasive pathology.

Human diagnosis

Identify proglottids or characteristic egg packets from stool or the perianal area. Routine ova-and-parasite microscopy can miss infection because eggs are retained in packets and released intermittently. Species confirmation may require a parasitology laboratory.

Animal diagnosis

Identify fresh motile proglottids on the animal, bedding, or feces, or demonstrate egg packets microscopically. Centrifugal fecal flotation has low sensitivity. Examine every affected animal for fleas and, in dogs, chewing lice.

Differential diagnoses

Other cestodes, pinworm in children, fly larvae or food material mistaken for segments, anal-sac disease, allergic dermatitis, flea-allergy dermatitis, and other causes of diarrhea or scooting.

Treatment in humans

Clinician-prescribed praziquantel is highly effective, generally as a single oral dose. Niclosamide is an alternative in some countries but is not available for human use in the United States. Continued passage of proglottids after treatment suggests reinfection, inadequate treatment, or need for diagnostic reassessment.

Treatment in animals—by species

• Dogs: Use a labeled cestocide containing praziquantel or epsiprantel at the veterinary product dose; treat concurrent flea or chewing-louse infestation.
• Cats: Use a feline-labeled praziquantel or epsiprantel product and institute cat-safe flea control. Never apply canine permethrin products to cats.
• Young, pregnant, debilitated, or food-producing animals: Select only a product specifically approved or appropriately prescribed for that species and status.

Animal and environmental control

Treat all infected pets and implement sustained flea control on every dog and cat in the household. Vacuum floors and furniture, launder bedding, manage premises according to the flea product label, and prevent hunting or scavenging. Treat canine chewing lice when present. Deworming without arthropod control permits rapid reinfection.

Prevention in humans

Maintain year-round veterinary flea prevention, wash hands after animal and fecal contact, discourage face licking, promptly dispose of feces, and supervise young children's pet contact. Finding proglottids in a child warrants medical evaluation and coordinated treatment of household pets and fleas.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Excellent after appropriate cestocide treatment plus elimination of infected fleas or lice. Recurrence almost always reflects continued arthropod exposure rather than drug resistance.

Reporting, legal, and regulatory considerations

Usually not reportable in people or animals. Childcare, shelter, kennel, and multi-animal outbreaks may justify public-health or veterinary investigation of flea control and sanitation. Pesticides and veterinary drugs must be used according to species-specific labels and local law.

Selected current sources

• CDC—About Dog and Cat Tapeworm
• CDC—Clinical Care of Dipylidium
• Companion Animal Parasite Council—Dipylidium caninum

FATAL HUMAN INFECTION WITH RABIES-RELATED DUVENHAGE VIRUS, SOUTH AFRICA

Synonyms and scope

Duvenhage virus infection; DUVV encephalitis. This retained title originated as a 2006 case report. The monograph addresses the disease represented by that report rather than reproducing the article. DUVV infection is a rare bat-associated lyssavirus zoonosis that is clinically indistinguishable from rabies.

Etiologic agent

Duvenhage lyssavirus (DUVV), a phylogroup I member of genus Lyssavirus, family Rhabdoviridae. It is distinct from classical rabies lyssavirus but causes the same progressive encephalitic syndrome.

Animals involved and epidemiologic roles

• Insectivorous bats: Presumed maintenance hosts and the source of recognized human infections; virus has been isolated from African bats.
• People: Accidental dead-end hosts after bat bites or scratches.
• Other mammals: Biologically susceptible to lyssaviruses, but no established terrestrial DUVV reservoir or transmission cycle has been demonstrated.
• Dogs and cats: Not recognized DUVV reservoirs; nevertheless, any mammal with compatible neurologic disease requires rabies risk assessment.

Geographic distribution and occurrence

Confirmed detections are exceptionally rare and have been associated with sub-Saharan Africa, particularly southern Africa. Sparse recognition does not define the full bat distribution. Travelers and animal workers can be exposed outside their home country.

Reservoir, life cycle, and transmission

Bats are the reservoir. Infectious saliva is inoculated through a bite, scratch, or contact with mucosa or broken skin. A scratch may be unnoticed or may be contaminated with saliva. Casual contact, intact-skin contact, urine, or feces has not been established as transmission. Human-to-human DUVV transmission has not been reported.

Incubation period

The 2006 South African patient became ill 27 days after a bat scratch. As with rabies, incubation can vary from days to months and occasionally longer depending on inoculum, wound site, innervation, and host factors.

Disease in humans

Initial fever, headache, malaise, or paresthesia progresses to encephalitis with agitation or altered behavior, dysphagia, hypersalivation, muscle spasms, seizures, autonomic instability, paralysis, coma, and death. Hydrophobia need not be present. Once neurologic disease begins, fatality is expected.

Disease in animals—by species

• Bats: Infection may be inapparent or cause abnormal flight, daytime activity, weakness, paralysis, or death; normal behavior does not exclude infection.
• Other mammals: Natural DUVV disease is not well characterized. Exposure should be managed as a potentially fatal lyssavirus infection rather than inferred from appearance.

Pathology

Fatal human infection produces nonsuppurative polioencephalitis, neuronopathy, neuronal loss, gliosis, and perivascular mononuclear inflammation, often involving brainstem and diencephalon. Viral antigen or inclusion bodies may be sparse, so a negative single test or brain region is insufficient.

Human diagnosis

Immediately involve public health and a specialized rabies reference laboratory. Antemortem testing uses multiple specimen types—saliva RT-PCR, nuchal skin biopsy, serum, and cerebrospinal fluid—because sensitivity varies. Postmortem brain testing and virus characterization confirm the agent. Standard assays must be able to recognize divergent lyssaviruses.

Animal diagnosis

Do not handle or necropsy suspect bats or mammals routinely. Submit the intact animal or designated brain tissues through animal-health or public-health authorities. Direct fluorescent-antibody testing, immunohistochemistry, RT-PCR, sequencing, and virus isolation may be used; molecular typing distinguishes DUVV from other lyssaviruses.

Differential diagnoses

Classical rabies, other lyssaviruses, herpes simplex encephalitis, arboviral encephalitis, tetanus, bacterial meningoencephalitis, autoimmune encephalitis, toxic exposure, acute psychosis, and in animals distemper or other neurologic diseases.

Treatment in humans

No treatment has reliably cured symptomatic DUVV encephalitis. Provide intensive supportive and palliative care, protect staff from saliva exposure, and seek immediate national/international rabies-expert consultation. Experimental coma or antiviral protocols have not established dependable benefit.

Treatment in animals—by species

No curative treatment is established. Suspect bats and other mammals must be managed under official rabies/lyssavirus protocols, with safe confinement or humane euthanasia and diagnostic testing as directed. Do not attempt unprotected clinical treatment or rehabilitation.

Animal and environmental control

Exclude bats from occupied buildings using humane, legally permitted methods after confirming no dependent young are trapped; secure animal housing; vaccinate domestic animals against classical rabies as required; train wildlife staff; and submit suspect animals safely. Do not handle grounded or strangely behaving bats bare-handed.

Prevention in humans

After any bat bite, scratch, or credible saliva exposure in an endemic or uncertain region, immediately wash and irrigate the wound for at least 15 minutes and contact public health urgently. Do not wait for symptoms. Rabies postexposure prophylaxis with wound care, vaccine, and rabies immunoglobulin or an approved monoclonal product is generally used for phylogroup I exposures, but DUVV-specific risk and biologic advice should come from rabies experts.

Human vaccination

No DUVV-specific vaccine is licensed. Modern rabies vaccines are used for pre-exposure and postexposure protection against phylogroup I lyssaviruses under WHO/national guidance; exposure to a non-classical lyssavirus warrants expert consultation because cross-protection is not uniform across the genus.

Animal vaccination

No animal vaccine is licensed specifically for DUVV. Routine rabies vaccination remains essential for domestic mammals but must not be represented as proven or licensed DUVV protection.

Prognosis

Essentially fatal after neurologic signs develop. Prompt, correctly administered postexposure prophylaxis before illness is the critical life-saving intervention.

Reporting, legal, and regulatory considerations

Human and animal suspect lyssavirus infections are immediately notifiable in most jurisdictions. Bat capture, euthanasia, specimen shipment, occupational exposure, quarantine, and animal disposition are governed by public-health, animal-health, wildlife, and dangerous-goods rules.

Selected current sources

• Emerging Infectious Diseases—Fatal Human DUVV Infection, South Africa
• WHO Expert Consultation on Rabies, Third Report
• CDC—Rabies Postexposure Prophylaxis

LYSSAVIRUS

Synonyms and scope

Rabies and rabies-related lyssavirus infection. This umbrella entry includes classical rabies lyssavirus and recognized non-rabies lyssaviruses. Taxonomy and detected host ranges continue to evolve; not every lyssavirus has caused confirmed human disease.

Etiologic agent

Genus Lyssavirus, family Rhabdoviridae, including rabies lyssavirus (RABV), Australian bat lyssavirus, European bat lyssaviruses, Duvenhage lyssavirus, Mokola lyssavirus, Irkut lyssavirus, and other bat-associated species. Antigenic phylogroups matter because standard rabies vaccines and immunoglobulins do not provide equivalent cross-neutralization of all species.

Animals involved and epidemiologic roles

• Dogs: Principal source of human RABV deaths globally.
• Bats: Reservoirs of RABV in the Americas and of diverse non-RABV lyssaviruses worldwide.
• Wild carnivores: Foxes, raccoons, skunks, mongooses, jackals, and other region-specific reservoirs of RABV.
• Cats: Susceptible spillover hosts and important sources of human exposure where vaccination is incomplete.
• Livestock and horses: Dead-end spillover hosts that can expose handlers through saliva and neural tissue.
• Ferrets and other mammals: Susceptible; management depends on species, vaccination status, and jurisdiction.
• Small rodents and lagomorphs: Rarely infected with RABV and seldom sources of human rabies, but circumstances require public-health assessment; some African lyssaviruses have been detected in shrews or rodents.
• People: Accidental hosts; human-to-human transmission is extraordinarily rare and has occurred mainly through transplanted tissues or organs.

Geographic distribution and occurrence

Lyssaviruses occur on every inhabited continent except Antarctica. Canine RABV remains concentrated in parts of Asia and Africa; wildlife variants predominate in the Americas and parts of Europe. Bat lyssaviruses have broad but incompletely mapped ranges. National freedom from terrestrial rabies does not imply absence of bat lyssaviruses.

Reservoir, life cycle, and transmission

Virus is maintained in reservoir mammal populations and shed mainly in saliva. Transmission follows bites, scratches contaminated by saliva, or saliva contact with mucosa or broken skin. After local replication, virus travels through peripheral nerves to the central nervous system and then centrifugal nerves to salivary glands. Blood, urine, feces, and intact-skin contact are not routine transmission routes.

Incubation period

Humans usually develop disease within 1–3 months, but intervals from days to more than a year occur. In animals the interval is commonly weeks to months and varies with virus, species, inoculum, wound site, and innervation.

Disease in humans

Prodromal fever, malaise, pain or paresthesia at the exposure site progresses to furious encephalitic disease with hydrophobia, aerophobia, agitation, and autonomic instability, or to paralytic rabies with ascending weakness. Both forms progress to coma and death once symptoms begin.

Disease in animals—by species

• Dogs/cats/ferrets: Behavior change, unexplained aggression or friendliness, dysphagia, hypersalivation, altered bark/meow, ataxia, paralysis, seizures, and death.
• Livestock/horses: Subtle behavioral change, colic-like signs, dysphagia, lameness, ataxia, recumbency, or paralysis; furious behavior is not required.
• Wild carnivores: Loss of fear, abnormal activity, aggression, ataxia, or paralysis.
• Bats: Grounding, inability to fly, daytime activity, weakness, or no obvious signs.

Pathology

Acute nonsuppurative encephalomyelitis with neuronal degeneration, gliosis, perivascular inflammation, and sometimes intracytoplasmic Negri bodies. Lesions and inclusions can be mild or absent; laboratory antigen or nucleic-acid detection is required.

Human diagnosis

Urgently notify public health. Antemortem diagnosis requires coordinated testing of saliva, nuchal skin biopsy, serum, and cerebrospinal fluid using RT-PCR, antigen detection, and antibody assays. Multiple samples may be necessary. Postmortem brain testing remains definitive.

Animal diagnosis

There is no validated routine live-animal rule-out test. Authorized laboratories examine brainstem and cerebellar tissue with direct fluorescent-antibody or rapid immunohistochemical testing and may use RT-PCR and sequencing. Personnel must avoid aerosol-generating necropsy and follow official submission protocols.

Differential diagnoses

Canine distemper, pseudorabies where present, tetanus, botulism, listeriosis, equine or other viral encephalitides, toxicities, trauma, metabolic encephalopathy, autoimmune encephalitis, bacterial meningitis, and acute psychiatric or paralytic syndromes.

Treatment in humans

Once clinical disease begins, no therapy is reliably effective; intensive supportive and palliative care and specialist infection-control management are required. Postexposure prophylaxis prevents disease but is not treatment for established neurologic rabies.

Treatment in animals—by species

No curative treatment is available or appropriate for clinically suspect domestic animals or wildlife. Isolate the animal, prevent saliva exposure, and contact public-health/animal-health authorities immediately. Observation, quarantine, euthanasia, and testing depend on the exposing species, vaccination history, and jurisdiction.

Animal and environmental control

Maintain high vaccination coverage in dogs, cats, ferrets, and at-risk livestock; conduct mass dog vaccination in canine-rabies regions; use oral wildlife vaccination where authorized; control stray-dog populations humanely; prevent wildlife contact; and maintain exposure-response plans for clinics, shelters, farms, and laboratories.

Prevention in humans

Avoid contact with wildlife and unknown animals, teach children not to handle bats, vaccinate pets, and use appropriate PPE for suspect animals and neural tissue. Immediately wash any potential exposure for at least 15 minutes and obtain public-health assessment. PEP must be based on agent, animal, geography, exposure type, testing, and prior vaccination.

Human vaccination

Modern inactivated rabies vaccines are used for risk-based pre-exposure vaccination and, with wound care and rabies immunoglobulin or an approved monoclonal antibody when indicated, for postexposure prophylaxis. They protect well against RABV and are expected to cover several phylogroup I lyssaviruses, but protection against phylogroup II/III viruses is inadequate or uncertain; expert consultation is essential.

Animal vaccination

Licensed RABV vaccines are available for dogs, cats, ferrets, horses, cattle, sheep, and selected wildlife applications depending on country. Follow the exact species label and legal booster schedule. These products are not licensed as universal vaccines against every lyssavirus.

Prognosis

Clinical disease is almost invariably fatal in people and animals. Correctly administered prophylaxis before symptom onset is highly effective.

Reporting, legal, and regulatory considerations

Rabies and suspect lyssavirus infections are urgently notifiable. Quarantine, observation periods, testing, vaccination, animal movement, occupational exposure, and specimen transport are legally controlled and vary by jurisdiction. Contact authorities before euthanasia or specimen collection when feasible.

Selected current sources

• WHO—Rabies Fact Sheet
• CDC—Information for Veterinarians
• World Organisation for Animal Health—Rabies
• WHO Expert Consultation on Rabies, Third Report

FILARIASIS

Synonyms and scope

Zoonotic filarial infection; zoonotic filariasis; dirofilariasis; zoonotic brugiasis; zoonotic onchocerciasis. This retained umbrella entry must not imply that human lymphatic filariasis due to Wuchereria bancrofti is animal-borne; it is maintained among people. The principal veterinary zoonotic concerns are Dirofilaria species and Onchocerca lupi, with occasional zoonotic Brugia and other filarioids.

Etiologic agent

Dirofilaria immitis, D. repens, D. tenuis, D. ursi-like worms, and rarer Dirofilaria; Onchocerca lupi; zoonotic Brugia species; and rare animal filarioids. Agent identity determines host, vector, geography, syndrome, and therapy.

Animals involved and epidemiologic roles

• Dogs and wild canids: Principal definitive hosts and reservoirs for D. immitis and D. repens; dogs are the best-recognized reservoir for O. lupi.
• Cats: Susceptible to D. immitis and sometimes D. repens, but usually have low or absent microfilaremia and are inefficient reservoirs.
• Ferrets: Highly susceptible to heartworm disease.
• Raccoons: Definitive hosts for D. tenuis.
• Bears: Hosts for D. ursi; black flies transmit infection.
• Wild felids and porcupines: Hosts for selected subcutaneous Dirofilaria species.
• Nonhuman primates and some domestic/wild carnivores: Reservoirs for certain zoonotic Brugia cycles.
• Mosquitoes, black flies, and other biting arthropods: Required biological vectors; people do not acquire infection directly from dogs or cats.

Geographic distribution and occurrence

D. immitis occurs widely in warm and temperate regions worldwide and is endemic across much of the Americas. D. repens occurs in Europe, Africa, and Asia and is expanding northward in Europe. D. tenuis is associated with raccoons in North America. O. lupi has been recognized in Europe, the Middle East, and North America. Zoonotic Brugia occurs focally in Asia and elsewhere.

Reservoir, life cycle, and transmission

Adult female worms in definitive animal hosts release microfilariae. A competent arthropod ingests them, supports development to third-stage larvae, and deposits larvae during a later blood meal. Humans are usually aberrant hosts in whom worms fail to become fully patent. Vector season, climate, animal movement, reservoir prevalence, and preventive-drug coverage determine risk.

Incubation period

Human nodules may appear months after vector exposure and the interval is often unknown. In dogs, D. immitis patency generally requires about 6–7 months and D. repens approximately 6–9 months. Clinical heartworm disease can emerge later. Development varies by species, host, and temperature.

Disease in humans

D. immitis usually causes a solitary pulmonary infarct or “coin lesion,” often found incidentally and confused with neoplasia. D. repens, D. tenuis, and related species cause subcutaneous, migratory, ocular, periocular, or other nodules. O. lupi can cause ocular disease or spinal-canal masses with neurologic deficits. Zoonotic Brugia usually produces lymph-node or subcutaneous lesions; patent microfilaremia is rare.

Disease in animals—by species

• Dogs—D. immitis: Cough, exercise intolerance, pulmonary hypertension, right-sided heart failure, caval syndrome, collapse, and death; many early infections are subclinical.
• Dogs—D. repens: Often subclinical microfilaremia; pruritic dermatitis, nodules, or ocular/subcutaneous worms may occur.
• Dogs—O. lupi: Episcleral or subconjunctival granulomas, ocular pain, discharge, uveitis, or other nodules.
• Cats: Heartworm-associated respiratory disease, vomiting, cough, dyspnea, neurologic signs, or sudden death may result from very few worms.
• Ferrets: Severe cardiopulmonary disease can occur with a small worm burden.
• Wildlife/reservoir hosts: Infection ranges from subclinical microfilaremia to nodular or cardiopulmonary disease, depending on agent.

Pathology

Human disease usually reflects a dead or degenerating worm with eosinophilic granulomatous inflammation, thrombosis, pulmonary infarction, or a subcutaneous/ocular mass. In canine heartworm disease, endarteritis, pulmonary vascular remodeling, thrombosis, and right-heart strain dominate; dying worms can precipitate embolic inflammation.

Human diagnosis

Diagnosis commonly follows surgical or biopsy removal with histopathology and, when available, PCR or sequencing. Imaging defines pulmonary, ocular, or spinal lesions but is nonspecific. Routine human serology is not reliably diagnostic for zoonotic Dirofilaria; circulating microfilariae are unusual.

Animal diagnosis

For canine heartworm, combine antigen testing with a microfilaria test and repeat or resolve discordant results; thoracic imaging, CBC/chemistry, urinalysis, and echocardiography stage disease. In cats, use antigen and antibody tests plus imaging because antigen tests miss many infections. Modified Knott testing, morphology, PCR, biopsy, or worm recovery distinguishes subcutaneous filarioids and O. lupi.

Differential diagnoses

Pulmonary neoplasia, fungal granuloma, tuberculosis, foreign body, other helminth nodules, lymphadenopathy, allergic or eosinophilic disease, bacterial endocarditis, chronic bronchitis, feline asthma, pulmonary thromboembolism, and other causes of ocular or spinal masses.

Treatment in humans

Complete surgical or endoscopic removal is generally curative for solitary pulmonary, subcutaneous, or ocular Dirofilaria and often avoids unnecessary major surgery when recognized. O. lupi or zoonotic Brugia may require removal plus specialist-directed antiparasitic therapy; spinal disease needs neurosurgical and infectious-disease input. No single drug regimen applies to all zoonotic filariae.

Treatment in animals—by species

• Dogs with D. immitis: Restrict exercise; stabilize severe disease; use an American Heartworm Society/CAPC adulticide protocol centered on melarsomine with a macrocyclic lactone and doxycycline, plus indicated anti-inflammatory care. Caval syndrome requires urgent extraction.
• Dogs with D. repens: Use regionally licensed macrocyclic-lactone or moxidectin-based therapy and manage nodules; monitor microfilariae. Regimens and approvals vary by country.
• Dogs with O. lupi: Surgically remove accessible worms/granulomas and use specialist-directed macrocyclic-lactone and/or doxycycline protocols; recurrence can occur.
• Cats: No approved safe adulticide regimen for heartworm. Manage respiratory inflammation and complications; surgical removal is reserved for selected visible worms. Prevent new infection.
• Ferrets: Specialist adulticide or extraction and stabilization are required because cardiopulmonary reserve is limited.
• Food-producing or wild animals: Treatment is case-specific and constrained by residue, wildlife, and product-approval rules.

Animal and environmental control

Give dogs year-round heartworm prevention according to veterinary guidelines, test dogs at recommended intervals, prevent lapses, and use mosquito reduction without ecological harm. Test before initiating or changing prevention as directed. In D. repens and O. lupi areas, diagnose and treat reservoir dogs and use effective vector control. Pet travel or importation requires local risk assessment.

Prevention in humans

Use EPA- or nationally registered repellents, protective clothing, window screens, and community mosquito/black-fly control. Keep pets on veterinary parasite prevention. Direct isolation of an infected pet does not prevent human infection because a vector is required.

Human vaccination

No vaccine is available for zoonotic filarial infections.

Animal vaccination

No licensed vaccine is available. Continuous chemoprophylaxis, testing, reservoir management, and vector reduction are the preventive tools.

Prognosis

Human solitary lesions generally have an excellent prognosis after removal; ocular and spinal O. lupi disease can cause permanent damage. Canine heartworm prognosis ranges from good in early disease to guarded or grave with pulmonary hypertension or caval syndrome. Feline infection can be fatal even with a low burden.

Reporting, legal, and regulatory considerations

Most human and animal filarial infections are not routinely notifiable, but emerging autochthonous cases may warrant public-health, veterinary, and vector-surveillance notification. Follow prescription, extralabel-use, importation, and food-animal drug rules. Regional heartworm and D. repens surveillance supports One Health risk assessment.

Selected current sources

• CDC DPDx—Dirofilariasis
• Companion Animal Parasite Council—Heartworm
• American Heartworm Society—Current Canine and Feline Guidelines
• ESCCAP—Control of Vector-Borne Diseases in Dogs and Cats

FLAVOBACTERIUM GROUP IIB-LIKE BACTERIA

Synonyms and scope

Flavobacterium group IIb-like organism associated with a pig bite. This legacy entry is retained because a 1990 report described recovery of an unusual organism from an infected human hand after a pig bite. Evidence for a reproducible zoonosis is very limited: the isolate was incompletely classified, no characteristic disease in pigs was established, and modern taxonomy cannot be assigned retrospectively with confidence.

Etiologic agent

An unnamed yellow-pigmented, nonfermenting gram-negative rod phenotypically described as “Flavobacterium group IIb-like.” Organisms historically placed in CDC group IIb were later distributed among genera including Chryseobacterium and Myroides; the original pig-bite isolate should not be relabeled as a modern species without preserved-isolate molecular testing.

Animals involved and epidemiologic roles

• Pigs: The only clearly documented animal association was traumatic inoculation during a pig bite; normal carriage prevalence and reservoir status are unknown.
• People: One published bite-associated hand infection established potential pathogenicity, not a common zoonotic cycle.
• Other animals: No defined epidemiologic role for this specific unclassified isolate.
• Environment: Related flavobacterial taxa occur in soil and water, but environmental occurrence does not prove identity with the pig-bite organism.

Geographic distribution and occurrence

The sentinel case was reported in the United States. There are no adequate surveillance data from which to define geographic range, incidence, swine carriage, or occupational prevalence. Modern reports of Chryseobacterium or Myroides infection should not automatically be counted as this animal-associated entity.

Reservoir, life cycle, and transmission

No reservoir has been established. The reported transmission circumstance was direct inoculation of a hand wound by a pig bite. Whether the organism was part of porcine oral flora, transient contamination, or an environmental contaminant is unresolved. Person-to-person, foodborne, airborne, and vector-borne transmission have not been demonstrated.

Incubation period

Not established. Bacterial bite-wound infections commonly become apparent within hours to several days, but that general observation cannot be assigned specifically to this unclassified organism.

Disease in humans

The historical case involved infection of the hand after a pig bite. No reliable syndrome beyond localized bite-wound infection can be defined. Related nonfermenting organisms can cause opportunistic wound, bloodstream, respiratory, or device-associated infections, mainly in medically vulnerable patients, but those infections are usually healthcare- or environment-associated rather than zoonotic.

Disease in animals—by species

• Pigs: No characteristic disease, lesion, or shedding state has been attributed to the historical group IIb-like isolate.
• Other animals: No disease association established for this exact organism. Fish diseases caused by currently recognized Flavobacterium species are separate conditions and should not be conflated with this entry.

Pathology

No organism-specific human or animal pathology is defined. Pig bites can produce crush injury, devitalized tissue, tendon or joint inoculation, polymicrobial cellulitis, abscess, tenosynovitis, septic arthritis, and osteomyelitis.

Human diagnosis

Obtain deep-tissue or aspirate cultures before antibiotics when clinically feasible; superficial swabs are less useful. Request aerobic and anaerobic culture, modern identification by MALDI-TOF or sequencing when an unusual nonfermenter is recovered, and antimicrobial susceptibility testing. Image and obtain surgical consultation for retained foreign body, fracture, tendon, joint, or deep-space involvement.

Animal diagnosis

No testing is recommended for healthy pigs after a human bite injury and no validated carriage assay exists. If a pig has oral disease or systemic illness, investigate on its own veterinary merits with lesion-directed culture and histopathology rather than testing for the historical label.

Differential diagnoses

Polymicrobial bite-wound infection involving streptococci, staphylococci, enteric gram-negative organisms, anaerobes, Pasteurella, Actinobacillus, Streptococcus suis, Erysipelothrix rhusiopathiae, and other unusual nonfermenters; sterile inflammatory reaction, tendon injury, foreign body, and fracture.

Treatment in humans

Immediately irrigate and debride as indicated; assess tendon, joint, bone, neurovascular injury, tetanus status, and need for surgical management. Initial antimicrobial therapy should cover ordinary polymicrobial animal-bite flora according to current clinical guidance. If a group IIb-like, Chryseobacterium, or Myroides-like organism is recovered, tailor treatment to definitive identification and susceptibility because intrinsic resistance to many beta-lactams and aminoglycosides is common and species-dependent.

Treatment in animals—by species

No treatment is indicated for a clinically normal biting pig solely because a person developed wound infection. Treat any porcine oral lesion, trauma, or systemic disease according to its established diagnosis, susceptibility results, and food-animal drug and withdrawal regulations.

Animal and environmental control

Prevent bites through trained handling, appropriate facilities, restraint planning, and attention to fearful, painful, maternal, or aggressive pigs. Maintain clean housing and equipment. There is no evidence-based rationale for herd screening, depopulation, isolation, or antimicrobial treatment directed at this historical organism.

Prevention in humans

Use barriers and safe restraint, cover skin breaks, wash hands, and promptly wash and irrigate every bite. Hand wounds, punctures, crush injuries, immunocompromised patients, or developing pain, erythema, swelling, drainage, fever, or reduced motion require urgent medical assessment. Evaluate tetanus and jurisdiction-specific rabies risk separately.

Human vaccination

No vaccine exists for this organism. Maintain routine tetanus vaccination for wound protection; tetanus vaccine does not prevent the bite-wound organism itself.

Animal vaccination

No vaccine exists and none is indicated.

Prognosis

The organism-specific prognosis cannot be estimated from a single report. Outcome of pig-bite infection depends on prompt irrigation, depth, hand-structure involvement, host factors, surgical care, and active antimicrobial selection.

Reporting, legal, and regulatory considerations

The organism is not routinely notifiable. Animal bites may be reportable locally and occupational injuries require workplace documentation. Public health should guide rabies assessment; clinicians should report unusual resistance or clusters through laboratory and infection-control channels as appropriate.

Selected current sources

• Journal of Clinical Microbiology—Historical Pig-Bite Group IIb-Like Isolate
• Clinical Microbiology Reviews—Microbiology of Animal Bite-Wound Infections
• Medicina—Clinical Features and Susceptibility of Chryseobacterium Species

FLEAS

Synonyms and scope

Flea infestation; pulicosis; flea-bite dermatitis. This animal-associated hazard includes direct bites, allergic disease, anemia in animals, and flea transmission of zoonotic agents. Individual infections such as plague, murine typhus, flea-borne spotted fever, bartonellosis, and dipylidiasis require their own diagnosis and treatment.

Etiologic agent

Medically important fleas include Ctenocephalides felis, C. canis, Pulex irritans, Xenopsylla cheopis, Oropsylla species, Echidnophaga gallinacea, and Tunga penetrans. The cat flea, C. felis, is the dominant flea of both dogs and cats in many regions.

Animals involved and epidemiologic roles

• Cats and dogs: Principal household hosts for C. felis; develop dermatitis and maintain environmental infestations.
• Rodents and lagomorphs: Hosts for fleas involved in plague and murine-typhus cycles; sudden host death can drive infected fleas to people or pets.
• Opossums and periurban wildlife: Important hosts in some flea-borne typhus and Rickettsia felis ecologies.
• Birds/poultry: Hosts for sticktight and other fleas that can bite people and other animals.
• Rabbits, ferrets, and small mammals: Susceptible to infestation, anemia, and species-specific drug toxicity.
• People: Incidental hosts for many animal fleas and definitive hosts for tungiasis lesions.

Geographic distribution and occurrence

Worldwide. Warmth and humidity accelerate development, while heated buildings permit year-round infestation in cooler climates. Vector-borne disease risk is focal: plague persists in wildlife foci, and murine typhus is concentrated in tropical/subtropical and selected periurban regions, including parts of California, Texas, and Hawaii.

Reservoir, life cycle, and transmission

Adults feed and reproduce on a host; eggs fall into bedding and resting sites; larvae consume organic debris and flea feces; pupae in protected cocoons can delay emergence. Heat, vibration, and carbon dioxide stimulate emergence. Pathogens are transmitted during feeding or when infected flea feces contaminate skin or wounds. Dipylidium caninum is acquired by swallowing an infected flea.

Incubation period

Bite reactions can begin within minutes to days. Under favorable conditions the egg-to-adult cycle may complete in several weeks, but pupal persistence can extend household emergence for months. Incubation of flea-borne infections varies by pathogen and is addressed in the relevant disease monograph.

Disease in humans

Pruritic clustered papules, commonly on ankles or legs, may develop central puncta, excoriation, urticaria, or secondary bacterial infection. Fleas can transmit plague, murine typhus, flea-borne spotted fever, and indirectly cat-scratch disease, and can transmit Dipylidium when swallowed. Tungiasis causes an embedded enlarging lesion, usually on the foot.

Disease in animals—by species

• Dogs: Pruritus, papules, flea-allergy dermatitis, lumbosacral alopecia, excoriation, hot spots, pyoderma, and rarely anemia.
• Cats: Miliary dermatitis, head/neck or lumbosacral pruritus, overgrooming, symmetric alopecia, eosinophilic lesions, and severe anemia in kittens.
• Rabbits/small mammals: Pruritus, crusting, alopecia, debility, and potentially life-threatening anemia.
• Poultry/birds: Irritation, anemia, reduced production, facial or comb lesions with sticktight fleas, and nestling losses.
• Wildlife/rodents: Often tolerant reservoirs, but heavy infestation and flea-borne infection may cause morbidity or death.

Pathology

Blood feeding causes focal inflammation and, with heavy burdens, iron-loss anemia. Salivary hypersensitivity produces disproportionate pruritic dermatitis. Self-trauma disrupts the barrier and promotes secondary infection. Pathology of transmitted agents is organism-specific.

Human diagnosis

Use exposure history, lesion pattern, and identification of fleas from animals or premises. Bite morphology alone is not specific. Fever, lymphadenopathy, eschar, severe headache, or systemic illness after flea or wildlife exposure requires pathogen-directed testing and urgent clinical assessment.

Animal diagnosis

Flea-comb the entire animal, especially the dorsum and tail base; wet dark debris to demonstrate the reddish-brown dissolution of digested blood. Absence of visible fleas does not exclude flea allergy. Assess CBC/PCV in pale, young, or heavily infested animals and test for vector-borne or tapeworm infection when indicated.

Differential diagnoses

Bedbugs, mosquitoes, mites, lice, ticks, contact dermatitis, atopy, food allergy, bacterial or yeast dermatitis, dermatophytosis, cheyletiellosis, psychogenic overgrooming, and pathogen-specific febrile diseases.

Treatment in humans

Wash lesions and use clinician-directed antipruritic therapy; treat secondary infection when present. Eliminate the animal and environmental infestation. Suspected plague requires immediate emergency/public-health evaluation and antibiotics; rickettsial illness requires prompt clinician-directed therapy. Embedded Tunga lesions need careful extraction or procedural care and tetanus review.

Treatment in animals—by species

• Dogs: Use a licensed rapid adulticide and sustained preventive selected for age, weight, health, neurologic history, and local efficacy; isoxazolines carry a class warning for possible neurologic adverse reactions.
• Cats: Use only feline-labeled products. Concentrated canine pyrethroids/permethrin can be fatal; prevent contact with recently treated dogs as the label directs.
• Rabbits/small mammals: Obtain exotic-animal guidance; fipronil is contraindicated in rabbits and many dog/cat products lack safety data.
• Birds/poultry: Treat bird and premises with an approved product and observe egg/meat withdrawal times.
• All species: Treat anemia, secondary infection, and allergic inflammation while eliminating fleas.

Animal and environmental control

Treat every susceptible pet continuously for long enough to exhaust environmental stages; vacuum resting areas and furniture frequently; launder bedding hot; and use approved premises products or insect-growth regulators when necessary. Control rodents by exclusion and sanitation. In plague areas, do not kill rodents before flea control, because displaced infected fleas may seek new hosts.

Prevention in humans

Maintain year-round veterinary flea control, avoid handling sick/dead wildlife, wear gloves when handling infested animals, use registered repellents where appropriate, and reduce rodent harborage. Seek prompt care for fever or lymph-node swelling after flea/wildlife exposure.

Human vaccination

No vaccine prevents flea infestation. No routinely available U.S. vaccine prevents plague, murine typhus, flea-borne spotted fever, or cat-scratch disease.

Animal vaccination

No licensed vaccine prevents fleas. Vaccines do not replace ectoparasite control for flea-borne pathogens.

Prognosis

Excellent for uncomplicated infestation once all hosts and environmental stages are addressed. Severe anemia, pesticide toxicosis, plague, and delayed treatment of flea-borne rickettsiosis can be life-threatening.

Reporting, legal, and regulatory considerations

Flea infestation itself is generally not reportable. Plague and several flea-borne infections are reportable; animal cases or unusual flea activity may trigger public-health/vector-control action. Follow pesticide labels, food-animal residue restrictions, and wildlife regulations.

Selected current sources

• CDC—About Fleas
• CDC DPDx—Fleas
• Companion Animal Parasite Council—Fleas
• FDA—Isoxazoline Safety Information

FOOT-AND-MOUTH DISEASE

Synonyms and scope

FMD; hoof-and-mouth disease; aphthous fever. This legacy listing is retained, but contemporary authorities regard FMD as a devastating transboundary animal disease, not a meaningful human zoonosis. Historical human case reports are exceptionally rare and sometimes uncertain. It is unrelated to human hand, foot, and mouth disease.

Etiologic agent

Foot-and-mouth disease virus (FMDV), genus Aphthovirus, family Picornaviridae. Seven immunologically distinct serotypes—O, A, C, Asia 1, SAT 1, SAT 2, and SAT 3—have limited cross-protection; numerous lineages and strains complicate vaccine matching.

Animals involved and epidemiologic roles

• Cattle and water buffalo: Highly susceptible indicator hosts that develop prominent oral and foot lesions and produce substantial aerosols.
• Pigs: Highly susceptible amplifying hosts that excrete very large amounts of airborne virus.
• Sheep and goats: Susceptible; mild or inapparent disease can delay detection.
• Wild cloven-hoofed mammals: Deer, antelope, wild pigs, and many other artiodactyls are susceptible; African buffalo maintain SAT viruses in some ecosystems.
• Camelids: Susceptibility varies; Bactrian camels are more susceptible than South American camelids.
• Horses, dogs, cats, and birds: Do not develop ordinary FMD, although they can mechanically move contaminated material.
• People: Not considered an epidemiologically important host or source.

Geographic distribution and occurrence

Endemic in parts of Africa, Asia, and the Middle East, with changing virus pools. North America, much of Europe, Australia, and New Zealand are free of endemic FMD but remain at continual incursion risk. Outbreaks produce enormous animal-welfare and trade consequences.

Reservoir, life cycle, and transmission

Infected animals shed virus in breath, saliva, vesicular fluid, milk, semen, urine, and feces before and during clinical disease. Spread occurs by direct contact, aerosols, animal products, contaminated feed, people, clothing, vehicles, equipment, and other fomites. Some recovered ruminants can carry pharyngeal virus; pigs do not become long-term carriers.

Incubation period

Usually 2–14 days in susceptible livestock; WOAH uses a 14-day incubation period for regulatory purposes. High-dose exposure can shorten onset. Species, strain, route, and dose influence the interval.

Disease in humans

People do not ordinarily acquire FMD. Historical reports described mild fever and vesicles after intense exposure, but modern confirmed disease is extraordinarily rare. Common human hand, foot, and mouth disease is caused by enteroviruses such as coxsackieviruses and is completely unrelated.

Disease in animals—by species

• Cattle: Fever, salivation, tongue/dental-pad/muzzle vesicles, teat lesions, severe lameness, milk drop, weight loss, and abortion.
• Pigs: Marked foot vesicles, coronary-band separation, reluctance to move, snout lesions, and sudden death of piglets from myocarditis.
• Sheep/goats: Often subtle fever and lameness with small oral lesions; neonatal mortality and production loss can occur.
• Young stock: Fatal myocarditis may occur without obvious vesicles.
• Wild ungulates: Variable vesicular disease, lameness, or subclinical infection.

Pathology

Virus replicates in pharyngeal epithelium and disseminates to stratified squamous epithelium, producing intraepidermal vesicles and erosions. Myocarditis with pale “tiger-heart” streaking may occur in young animals. Secondary infection and hoof damage prolong disability.

Human diagnosis

Routine human testing is not indicated. A person with vesicular illness after FMD exposure should be evaluated for common human causes and referred through public health if true FMD is considered. Testing would require a specialized high-containment reference laboratory.

Animal diagnosis

Treat suspicion as an emergency: stop movement and notify authorities before sampling. Authorized laboratories use real-time RT-PCR, antigen ELISA, virus isolation, sequencing, and serology, including nonstructural-protein assays where appropriate. Lesions alone cannot distinguish FMD from other vesicular diseases.

Differential diagnoses

Vesicular stomatitis, swine vesicular disease, Senecavirus A, vesicular exanthema of swine, bovine viral diarrhea/mucosal disease, malignant catarrhal fever, bluetongue, contagious ecthyma, chemical/thermal injury, trauma, and foot rot.

Treatment in humans

No specific human FMD treatment is established because accepted human disease is essentially absent. Provide medical evaluation and supportive care while diagnosing more likely causes; notify public health if credible occupational exposure and compatible lesions coexist.

Treatment in animals—by species

No antiviral treatment eliminates FMDV. In endemic settings, authorities may permit supportive care—soft feed, water, pain control, wound protection, and treatment of secondary infection—under outbreak rules. In disease-free countries, suspect animals must not be treated or moved routinely; official quarantine, testing, vaccination, depopulation, and disposal policy controls management.

Animal and environmental control

Immediately stop animal, product, vehicle, equipment, and personnel movement; establish biosecurity zones; trace contacts; clean and disinfect after organic material removal; and follow official surveillance, quarantine, stamping-out, emergency vaccination, and disposal instructions. Virus can persist in chilled or frozen animal products and under favorable environmental conditions.

Prevention in humans

Human disease prevention is not the primary issue. Personnel must use outbreak PPE and decontamination to avoid mechanically spreading virus between animals or premises. Do not consume unpasteurized milk from affected herds, enter suspect farms unnecessarily, or remove contaminated clothing or equipment.

Human vaccination

No human FMD vaccine is licensed or indicated. Childhood hand-foot-and-mouth disease vaccines used in some countries target enteroviruses, not FMDV.

Animal vaccination

Inactivated, adjuvanted vaccines are used in endemic regions and emergency programs. Protection is serotype- and strain-match dependent, requires boosters, and does not guarantee sterile immunity. Vaccine selection, deployment, movement status, and postvaccination surveillance are controlled by animal-health authorities.

Prognosis

Adult case fatality is usually low, but morbidity approaches 100% in naive herds and recovery can leave chronic lameness, mastitis, reproductive loss, and reduced production. Mortality can be high in neonates from myocarditis. Herd-level economic consequences are severe.

Reporting, legal, and regulatory considerations

FMD is immediately notifiable to national veterinary authorities and reportable internationally to WOAH. In the United States it is a foreign animal disease: contact the state veterinarian or USDA APHIS immediately and do not sample, move, or necropsy without direction. Trade, quarantine, vaccination, depopulation, compensation, and disposal are legally controlled.

Selected current sources

• USDA APHIS—Foot-and-Mouth Disease Emergency Response
• WOAH—Foot-and-Mouth Disease
• WOAH Terrestrial Code—FMD
• Iowa State CFSPH—Foot-and-Mouth Disease

GIARDIASIS

Synonyms and scope

Giardia infection; lambliasis. A fecal-oral intestinal protozoal disease of people and many animals. Zoonotic potential is assemblage-dependent: human infections are mainly assemblages A and B, while most dogs and cats carry host-adapted assemblages. Therefore, an infected pet and person in one household do not by themselves prove cross-species transmission.

Etiologic agent

Giardia duodenalis species complex, also called G. intestinalis or G. lamblia. Assemblages A and B have the broadest zoonotic potential; C/D are dog-associated, E livestock-associated, F cat-associated, G rodent-associated, and H pinniped-associated. Other Giardia species infect birds, rodents, and amphibians.

Animals involved and epidemiologic roles

• People: Major reservoirs for human assemblages and person-to-person/waterborne spread.
• Dogs: Commonly infected, principally with C/D; occasional A/B detection makes zoonotic risk low but not zero.
• Cats: Principally assemblage F; occasional A/B infection.
• Cattle, sheep, goats, pigs, and camelids: Mainly assemblage E, with some A/B; young stock can shed many cysts.
• Chinchillas: Frequently infected and may carry assemblage B, representing a more credible companion-animal zoonotic concern.
• Beavers, muskrats, cervids, opossums, rodents, and other wildlife: Carry host-adapted or zoonotic assemblages and can contaminate water.
• Nonhuman primates: Can carry human-associated assemblages; occupational relevance is greater than for most pets.
• Birds: Carry avian species and occasionally zoonotically relevant genotypes; role depends on molecular identity.

Geographic distribution and occurrence

Worldwide. Infection is common in children, daycare settings, travelers, untreated-water users, and crowded animal populations such as kennels, shelters, catteries, breeding colonies, calf units, and laboratory or zoological primate facilities. Young animals have the highest clinical risk.

Reservoir, life cycle, and transmission

Immediately infective cysts pass in feces and are swallowed in contaminated water, food, soil, hands, fur, fomites, or through direct fecal-oral contact. Excysted trophozoites attach to small-intestinal epithelium and multiply without tissue invasion; encystation occurs before fecal passage. Cysts survive for weeks to months in cool, moist conditions.

Incubation period

Humans usually develop symptoms 1–2 weeks after exposure. The animal prepatent period is generally 3–10 days. Intermittent shedding can continue for weeks or recur after apparent clinical recovery.

Disease in humans

Asymptomatic infection is common. Acute or chronic foul-smelling, greasy diarrhea, abdominal cramps, bloating, flatulence, nausea, fatigue, weight loss, and malabsorption may occur. Blood and high fever are atypical and suggest another or additional diagnosis. Postinfectious lactose intolerance or functional gastrointestinal symptoms can persist.

Disease in animals—by species

• Dogs/cats: Often asymptomatic; puppies and kittens may develop intermittent soft, pale, malodorous, mucus-coated or fatty stool, poor growth, and weight loss. Hematochezia is atypical.
• Calves/lambs/kids: Subclinical shedding is common; diarrhea, reduced feed efficiency, and poor weight gain occur in some young stock.
• Chinchillas: Kits can develop diarrhea, dehydration, weight loss, and debility; asymptomatic carriage also occurs.
• Other small mammals/wildlife: Usually subclinical or variable enteric disease.
• Birds: Species-dependent diarrhea, poor condition, or no signs; avian Giardia taxonomy differs from mammalian infection.

Pathology

Trophozoite attachment, epithelial barrier disruption, immune responses, shortened microvilli, villus blunting, and reduced brush-border enzymes produce maldigestion and malabsorption. Gross lesions are usually absent; microscopic villous atrophy and cuboidal enterocytes may be present.

Human diagnosis

Use stool antigen or nucleic-acid testing, direct fluorescent-antibody testing, or microscopy for cysts/trophozoites. Because shedding is intermittent, collect multiple stools when initial testing is negative but suspicion remains. Molecular assemblage typing is mainly epidemiologic and is not routinely available.

Animal diagnosis

Interpret results with signs and population context. Combine centrifuged zinc-sulfate flotation with fecal antigen testing or validated PCR; examine a fresh saline smear promptly for motile trophozoites in diarrhea. Multiple samples may be needed. PCR/antigen positivity after treatment may persist and does not alone establish treatment failure.

Differential diagnoses

Dietary diarrhea, coccidiosis, cryptosporidiosis, tritrichomonosis in cats, bacterial or viral enteritis, helminths, exocrine pancreatic insufficiency, inflammatory enteropathy, dysbiosis, hyperthyroidism, neoplasia, and noninfectious malabsorption.

Treatment in humans

Rehydrate and correct electrolyte or nutritional deficits. Clinician-selected options include tinidazole, nitazoxanide, or metronidazole; alternatives and refractory regimens depend on age, pregnancy, immune status, availability, adherence, reinfection, and confirmed diagnosis. Persistent symptoms require reassessment rather than repeated empirical courses alone.

Treatment in animals—by species

• Dogs: Treat symptomatic patients. Fenbendazole 50 mg/kg PO every 24 hours for 3–5 days is first-line in many guidelines; metronidazole 10–25 mg/kg PO every 12 hours for 5–8 days is another option, with an FDA-approved canine suspension labeled at 25 mg/kg every 12 hours for 5 days. Avoid prolonged/high-dose metronidazole neurotoxicity.
• Cats: Fenbendazole 50 mg/kg PO every 24 hours for 3–5 days is commonly used extralabel in the US; no drug is FDA-approved for feline giardiasis. Metronidazole use is also extralabel and requires feline-specific veterinary dosing.
• Chinchillas/rabbits/other small mammals: Treat only with species-experienced veterinary guidance; correct dehydration, husbandry, and concurrent disease.
• Livestock: No US-approved giardiasis treatment. Population therapy is often unrewarding; any extralabel drug requires a valid veterinary relationship, legal authority, and withdrawal interval.
• All animals: Aim to resolve clinical disease and prevent transmission rather than repeatedly treating an asymptomatic positive test.

Animal and environmental control

Remove feces at least daily; bathe dogs/cats near the final treatment day to remove cysts from fur; wash bowls, bedding, crates, and tools; steam or use an effective hard-surface disinfectant after cleaning; and dry thoroughly. Isolate diarrheic animals when feasible, avoid communal water, and prevent treated pets from drinking or contaminating ponds and streams. Soil and grass cannot be reliably disinfected.

Prevention in humans

Wash hands after feces, diapers, animals, and soil; use safe drinking water; avoid swallowing recreational water; wash produce; manage human cases carefully; and use gloves for high-risk animal care. Immunocompromised people should minimize contact with diarrheic animals and seek individualized medical advice.

Human vaccination

No human vaccine is available.

Animal vaccination

No currently recommended, routinely available vaccine reliably prevents giardiasis. Previously marketed canine vaccines are not a substitute for hygiene, diagnosis, and treatment and are no longer generally available.

Prognosis

Usually good with hydration, appropriate therapy, and reinfection control. Young, malnourished, or immunocompromised hosts can develop significant dehydration and poor growth. Persistent diarrhea often reflects reinfection, coinfection, or another enteropathy rather than antimicrobial resistance alone.

Reporting, legal, and regulatory considerations

Human giardiasis is nationally notifiable in the United States, although local requirements vary. Animal infection is generally not reportable. Waterborne, childcare, institutional, foodborne, or linked human-animal clusters warrant public-health investigation and, when useful, molecular typing.

Selected current sources

• CDC—Giardia and Pets
• CDC—Treatment of Giardia Infection
• Companion Animal Parasite Council—Giardia
• Merck Veterinary Manual—Giardiasis in Animals

GNATHOSTOMA SPINIGERUM

Synonyms and scope

Gnathostomiasis; gnathostomosis; cutaneous or visceral larva migrans caused by Gnathostoma. The legacy title names G. spinigerum, but several congeners cause zoonotic disease. People are accidental hosts and do not transmit infection onward.

Etiologic agent

Gnathostoma spinigerum causes most recognized Asian cases. Other confirmed zoonotic species include G. binucleatum, G. hispidum, G. doloresi, and G. nipponicum. Species attribution requires morphology plus molecular confirmation where possible.

Animals involved and epidemiologic roles

• Dogs and cats: Definitive hosts for G. spinigerum and G. binucleatum; adults develop in gastric-wall nodules and eggs pass in feces.
• Pigs and wild boar: Definitive hosts for G. hispidum and G. doloresi and potential food sources.
• Weasels: Definitive hosts for G. nipponicum.
• Freshwater copepods: Required first intermediate hosts.
• Freshwater fish, eels, amphibians, and reptiles: Second intermediate or paratenic hosts carrying advanced third-stage larvae.
• Birds and other mammals: Paratenic hosts; raw poultry has occasionally been implicated.
• People: Accidental hosts after ingesting larvae; worms remain immature and migrate through tissues.

Geographic distribution and occurrence

Endemic foci occur in East and Southeast Asia, Japan, Mexico, and parts of Central and South America, with occasional cases linked to Africa and Australia. G. binucleatum accounts for many Latin American cases historically attributed to G. spinigerum. Imported disease occurs wherever raw endemic freshwater foods are consumed.

Reservoir, life cycle, and transmission

Eggs from definitive hosts embryonate in freshwater. Copepods ingest larvae; fish or other aquatic animals ingest copepods; predators accumulate infective larvae as paratenic hosts. Dogs, cats, pigs, wildlife, or people acquire infection by eating raw or inadequately cooked intermediate/paratenic hosts. Direct transmission from an infected pet, pig, or person does not occur. Infection from water containing copepods is possible but not firmly established in people.

Incubation period

Early gastrointestinal symptoms can begin within 24–48 hours, while migratory swellings usually appear weeks later and can recur for years. In definitive animal hosts, adult maturation and egg shedding generally require months; timing varies by species and host.

Disease in humans

Cutaneous disease causes intermittent, pruritic, painful, migratory subcutaneous swellings. Visceral migration may involve gastrointestinal, pulmonary, genitourinary, or other tissues. Ocular infection can impair vision. Neurognathostomiasis can cause radiculomyelitis, eosinophilic meningitis, myeloencephalitis, intracranial or subarachnoid hemorrhage, paralysis, and death.

Disease in animals—by species

• Dogs/cats: Often subclinical; gastric nodules can cause vomiting, anorexia, hematemesis, weight loss, anemia, or perforation/peritonitis.
• Pigs/wild boar: Gastric nodules and gastritis are often incidental but may cause poor condition or digestive signs.
• Fish/amphibians/reptiles/birds: Encysted larvae are commonly subclinical; migration can produce focal hemorrhage, inflammation, or tissue damage.
• Aberrant animal hosts: Migrating larvae can produce cutaneous, ocular, neurologic, or visceral lesions analogous to human disease.

Pathology

In definitive hosts, adult worms occupy a thick-walled gastric mass with a tract to the lumen. In accidental or paratenic hosts, spined larvae mechanically migrate through tissues, causing hemorrhagic tracks, eosinophilic inflammation, necrosis, and granulomas. Central nervous system injury is largely mechanical and may be irreversible.

Human diagnosis

Combine compatible food/travel exposure, recurrent migratory swelling, eosinophilia, and imaging. Definitive diagnosis follows extraction or biopsy identification of a larva, supported by PCR when available. Serology is available only through selected international laboratories and cross-reactions occur. Stool examination is not useful because human infection is not patent.

Animal diagnosis

Detect characteristic eggs by centrifugal fecal examination in patent definitive-host infection, recognizing intermittent shedding. Endoscopy, ultrasonography, surgery, or necropsy may identify gastric nodules or worms. Histopathology and molecular testing distinguish species. Negative fecal testing does not exclude immature, single-sex, or ectopic infection.

Differential diagnoses

Cutaneous larva migrans, sparganosis, dirofilariasis, toxocariasis, strongyloidiasis, fascioliasis, paragonimiasis, angiostrongyliasis, allergic urticaria, cellulitis, neoplasia, eosinophilic meningitis of other causes, and in animals foreign body, ulcer, gastric tumor, or other helminth disease.

Treatment in humans

Remove a visible cutaneous or ocular worm when safely possible. For cutaneous disease, specialist-directed albendazole or ivermectin regimens are used; relapse can occur for more than two years. Anthelmintic treatment of ocular or central nervous system disease is controversial because migration or inflammatory worsening may increase injury; such cases require urgent infectious-disease, ophthalmology, neurology, and surgical consultation with supportive management.

Treatment in animals—by species

• Dogs/cats: Endoscopic or surgical removal of gastric or accessible ectopic worms may be required. Anthelmintic protocols are not well standardized; use specialist-directed therapy and manage ulceration, anemia, obstruction, or peritonitis.
• Pigs: Routine individual treatment is uncommon; any anthelmintic use must follow food-animal approvals and withdrawal requirements.
• Fish and paratenic hosts: No practical treatment reliably removes encysted larvae from food animals; exclude affected raw tissues from consumption or feeding.

Animal and environmental control

Do not feed dogs, cats, pigs, zoo animals, or rehabilitation patients raw freshwater fish, eels, frogs, snakes, poultry, or wild-game tissues from endemic areas. Prevent scavenging and dispose of fish offal safely. Treating pets alone cannot eliminate an established aquatic wildlife cycle.

Prevention in humans

Thoroughly cook freshwater fish, eels, frogs, reptiles, poultry, and wild boar from endemic areas; prevent raw-food cross-contamination. Marinating, ceviche preparation, smoking, pickling, or visual inspection cannot be assumed to kill all larvae. Drink safely treated water and avoid using raw meat as a poultice.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Cutaneous disease usually resolves with removal or treatment but can relapse. Ocular prognosis depends on location and extraction injury. Neurologic disease can cause permanent deficits or death. Animal prognosis is good for uncomplicated gastric disease but guarded with perforation, major hemorrhage, or central nervous system migration.

Reporting, legal, and regulatory considerations

Usually not routinely notifiable. Human cases and food-associated clusters merit public-health and food-safety investigation. Imported animal foods, wildlife harvest, aquaculture inspection, and food-animal medication are governed by jurisdiction-specific rules.

Selected current sources

• CDC DPDx—Gnathostomiasis
• CDC—Clinical Care of Gnathostomiasis
• Clinical Microbiology Reviews—Gnathostomiasis as an Emerging Imported Disease

GLANDERS

Synonyms and scope

Farcy; equine glanders; Burkholderia mallei infection. Glanders is a serious zoonotic disease principally of horses, donkeys, and mules. Human disease is rare but can be severe or fatal. Because glanders is a regulated transboundary animal disease, suspected equine cases require immediate involvement of veterinary authorities rather than routine outpatient treatment.

Etiologic agent

Burkholderia mallei, a nonmotile gram-negative bacterium closely related to Burkholderia pseudomallei, the agent of melioidosis. Historical names include Pseudomonas mallei and Actinobacillus mallei.

Animals involved and epidemiologic roles

• Horses: Principal maintenance hosts; infection is often chronic and can include inapparent carriers.
• Donkeys and mules: Highly susceptible; disease is often acute and severe.
• Other equids: Zebras and related species are susceptible.
• Camels: Natural infection has been documented in endemic regions.
• Wild and domestic carnivores: Felines, dogs, and other carnivores can become infected, including after consuming infected animal tissues; they are not the principal maintenance reservoir.
• People: Accidental hosts, historically including veterinarians, horse handlers, animal-care workers, and laboratory personnel.

Geographic distribution and occurrence

Glanders has been eliminated from many countries through testing, movement control, and removal of infected equids. It remains endemic or sporadically reported in parts of Asia, the Middle East, Africa, and South America. North America, Australia, and most of Europe are free of endemic glanders, but importation remains a concern and suspect cases are treated as animal-health emergencies.

Reservoir, life cycle, and transmission

Equids are the principal reservoir. Infected animals shed organisms in nasal and respiratory secretions and in exudate from cutaneous lesions. Transmission among animals occurs through close contact, contaminated feed or water, and contaminated tack, grooming equipment, housing, or other fomites. Organisms can enter through mucous membranes or damaged skin. Human infection is associated with direct exposure of broken skin or mucous membranes to infectious animal material and, less commonly, inhalational exposure in high-risk settings. Person-to-person transmission is exceedingly rare.

Incubation period

The interval can range from a few days to several months, depending on exposure intensity, route, and host factors. Human cases after recognized exposure have often developed within approximately 1–2 weeks, but longer intervals can occur.

Disease in humans

Clinical presentations include localized cutaneous infection with nodules, ulcers, abscesses, or regional lymphadenitis; pulmonary disease with fever, cough, chest pain, pneumonia, or abscess formation; septicemic or disseminated disease with multiple organ involvement; and chronic relapsing infection. Nasal or mucosal disease can occur. Untreated systemic infection has historically carried a very high fatality rate.

Disease in animals—by species

• Horses: Often chronic disease with intermittent fever, weight loss, cough, nasal discharge, nasal ulcers, enlarged submaxillary lymph nodes, pulmonary nodules, and cutaneous lymphangitis with nodules and draining tracts known as farcy.
• Donkeys and mules: More commonly develop acute fever, severe respiratory disease, rapidly progressive septicemia, and death.
• Camels: May develop respiratory, nodal, and cutaneous disease resembling equine glanders.
• Carnivores: Infection can cause fever, respiratory disease, abscesses, nodules, lymphadenitis, and systemic illness; cases are uncommon.

Pathology

Characteristic lesions include granulomatous or suppurative nodules, ulcers, and abscesses in the nasal passages, respiratory tract, lungs, skin, and lymphatics. Pulmonary nodules can cavitate or become caseous. Cutaneous disease produces chains of nodules and ulcerated draining tracts along lymphatic vessels. Disseminated infection can involve liver, spleen, and other organs.

Human diagnosis

Glanders should be considered in a compatible febrile, pulmonary, cutaneous, or septic illness after exposure to equids from an affected region or another credible source. Immediately notify public health and the clinical laboratory before specimen handling. Diagnosis is confirmed in specialized reference laboratories using validated molecular and other organism-specific methods. Routine automated identification systems can misidentify unusual Burkholderia species, so unexpected results require reference-laboratory confirmation.

Animal diagnosis

Clinical signs alone are not diagnostic. Suspect equids should be isolated from unnecessary contact and reported immediately to the appropriate state, federal, or national veterinary authority before testing or movement. Official programs use validated serologic testing, including complement-fixation and other approved assays, with confirmatory testing as required by jurisdiction; molecular methods can support confirmation in authorized laboratories. The mallein hypersensitivity test is retained in some settings but is not generally preferred where validated laboratory testing is available.

Differential diagnoses

Melioidosis, strangles, ulcerative lymphangitis, epizootic lymphangitis, sporotrichosis, tuberculosis or other granulomatous disease, bacterial pneumonia, equine influenza or herpesvirus-associated respiratory disease, purpura or vasculitic lesions, and other causes of nasal ulcers, lymphangitis, abscesses, or chronic wasting.

Treatment in humans

Human glanders requires urgent infectious-disease and public-health consultation. Because controlled treatment trials are lacking, current therapy is based largely on clinical experience with glanders and melioidosis: an initial intensive phase with an active intravenous agent such as ceftazidime or a carbapenem is followed by a prolonged oral eradication phase, commonly using trimethoprim-sulfamethoxazole or another specialist-selected active regimen. Severe, disseminated, neurologic, bone, joint, or deep-organ disease generally requires longer therapy and close monitoring. Drainage or other source control may be needed for accessible abscesses.

Treatment in animals—by species

Veterinary treatment is not considered a reliable means of eliminating infection and is not an accepted control strategy for infected equids. In glanders-free or eradication programs, confirmed positive equids are typically humanely euthanized under official authority, with quarantine and disposition of exposed animals determined by regulation. Suspected cases should not be empirically treated in a way that delays diagnosis, obscures surveillance, or permits movement of potentially infected animals.

Animal and environmental control

Immediately restrict movement of suspect animals, people, tack, equipment, and potentially contaminated materials until veterinary authorities provide direction. Control programs rely on surveillance, testing of exposed equids, quarantine, identification and removal of infected animals, tracing of animal movements and contacts, and thorough cleaning and disinfection of affected premises and equipment. Import controls and health certification are important for preventing reintroduction into glanders-free regions.

Prevention in humans

Avoid unprotected contact with nasal discharge, respiratory secretions, draining skin lesions, blood, tissues, or contaminated equipment from suspect animals. Veterinary personnel should use gloves, protective clothing, eye and face protection when splash is possible, and appropriate respiratory protection when an exposure could generate infectious droplets or aerosols. Cover skin breaks, perform hand hygiene, and obtain prompt medical and public-health assessment after a credible occupational exposure or if compatible illness develops.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

No licensed animal vaccine is available. Vaccination is not part of current glanders control programs.

Prognosis

Human prognosis depends on disease form, speed of recognition, and timely effective antimicrobial treatment. Localized disease can be curable, whereas untreated septicemic or disseminated infection may be rapidly fatal. In equids, chronic infection can persist for months to years, while acute disease in donkeys and mules is often fatal; because infected equids remain an important transmission risk, regulatory control rather than clinical recovery determines their disposition.

Reporting, legal, and regulatory considerations

Glanders is a WOAH-listed disease and is immediately reportable to veterinary authorities in many countries. In the United States it is treated as a foreign animal disease: veterinarians should contact state and federal animal-health officials immediately and should not move, ship, or routinely sample suspect equids without official guidance. Human cases or credible exposures require prompt public-health notification. Animal movement, testing, quarantine, euthanasia, disposal, and import/export certification are governed by jurisdiction-specific law.

Selected current sources

• World Organisation for Animal Health—Glanders
• WOAH Terrestrial Manual—Glanders and Melioidosis
• USDA APHIS—Glanders Etiology and Ecology
• CDC Emerging Infectious Diseases—Treatment and Postexposure Prophylaxis for B. pseudomallei and B. mallei
• CDC Emerging Infectious Diseases—Human Burkholderia mallei Infection, Brazil

HANTAVIRUS PULMONARY SYNDROME

Synonyms and scope

Hantavirus pulmonary syndrome (HPS); hantavirus cardiopulmonary syndrome (HCPS). This entry focuses on New World orthohantaviruses that cause severe cardiopulmonary disease. Hemorrhagic fever with renal syndrome (HFRS), caused mainly by Old World hantaviruses and Seoul virus, is retained as a separate entry on this page.

Etiologic agent

Several rodent-associated orthohantaviruses can cause HPS. In the United States, Sin Nombre virus is the most common cause. Other New World hantaviruses occur in the Americas. Andes virus is notable because, unlike other recognized hantaviruses, it can rarely spread from person to person during close contact.

Animals involved and epidemiologic roles

• Deer mice and related sigmodontine rodents: Important reservoirs of Sin Nombre and other HPS-associated viruses; infected rodents usually remain clinically normal while shedding virus.
• Cotton rats, rice rats, white-footed mice, and other region-specific rodents: Reservoirs for particular hantaviruses.
• People: Accidental hosts after exposure to infected rodents or contaminated environments.
• Dogs, cats, livestock, and horses: Not recognized maintenance reservoirs for HPS-associated hantaviruses and are not considered routine sources of human HPS.

Geographic distribution and occurrence

HPS occurs throughout the Americas wherever competent reservoir rodents and their viruses occur. U.S. cases have been reported in many states, with the greatest historical concentration in western states. Risk is linked to rodent exposure rather than to a particular type of building or occupation.

Reservoir, life cycle, and transmission

Reservoir rodents acquire persistent infection and shed virus in urine, feces, and saliva. People are infected mainly when contaminated rodent excreta or nesting material is disturbed and infectious particles are inhaled, or when contaminated material contacts mucous membranes or broken skin. Rodent bites are an uncommon possible route. Person-to-person spread is not expected for U.S. hantaviruses; Andes virus is the important exception.

Incubation period

Symptoms of HPS generally begin about 1–8 weeks after exposure. Andes-virus illness may begin approximately 4–42 days after exposure. A compatible exposure history during the preceding several weeks is therefore important even when the patient does not recall direct rodent contact.

Disease in humans

Early illness typically includes fever, profound fatigue, myalgia, headache, dizziness, chills, and gastrointestinal signs. Several days later, cough and rapidly progressive dyspnea may develop as capillary leakage causes noncardiogenic pulmonary edema. Hypotension, myocardial depression, shock, and respiratory failure can follow. HPS is a medical emergency and can be fatal.

Disease in animals—by species

• Reservoir rodents: Usually persistent, asymptomatic infection despite shedding virus.
• Pet rats: More relevant to Seoul virus and HFRS than to classic U.S. HPS; apparently healthy rats can carry Seoul virus.
• Domestic animals: No recognized clinical HPS syndrome or important transmission role has been established in dogs, cats, horses, or livestock.

Pathology

The hallmark is widespread capillary leak, especially in the lungs, producing interstitial edema and pleural effusions without the pattern of primary bacterial pneumonia. Severe disease can include myocardial depression and shock. Thrombocytopenia and hemoconcentration are characteristic laboratory findings.

Human diagnosis

Suspect HPS in a patient with compatible febrile illness, thrombocytopenia, pulmonary edema or respiratory compromise, and recent rodent exposure. Diagnosis is confirmed by public-health or reference-laboratory serology and/or molecular testing. Clinicians should contact the appropriate health department promptly rather than delay critical care while awaiting confirmation.

Animal diagnosis

Routine testing of wild rodents around an individual home is generally not useful for clinical decision-making. Veterinary/public-health testing may be appropriate for epidemiologic investigations or pet-rat colonies when Seoul virus is a concern. Testing should be coordinated with public-health or veterinary authorities rather than attempted as an informal household screening program.

Differential diagnoses

Severe influenza, COVID-19 and other viral pneumonias, bacterial sepsis or pneumonia, leptospirosis, rickettsial disease, acute respiratory distress syndrome from other causes, cardiogenic pulmonary edema, pulmonary embolism, and HFRS or other hantavirus syndromes.

Treatment in humans

No antiviral therapy has proven effective for HPS. Early recognition, hospitalization, careful fluid management, oxygenation and ventilatory support, vasopressor/inotropic support when needed, and transfer to a center capable of advanced critical care are central. Extracorporeal membrane oxygenation may be considered for selected patients with refractory cardiopulmonary failure. Ribavirin has not shown benefit for HPS.

Treatment in animals—by species

No treatment is indicated for clinically normal wild reservoir rodents. Control focuses on excluding rodents from human environments rather than attempting to medicate wildlife. Pet rodents with suspected Seoul-virus infection require veterinary and public-health consultation regarding testing, isolation, disposition, and protection of exposed people.

Animal and environmental control

Prevent rodent entry into homes, cabins, barns, feed rooms, and animal facilities; remove food and nesting opportunities; use integrated rodent control; and store feed in rodent-resistant containers. Rodent-contaminated areas should be cleaned using current public-health wet-disinfection guidance rather than dry sweeping or vacuuming material that could aerosolize contaminated dust.

Prevention in humans

Avoid direct contact with wild rodents and their urine, droppings, saliva, and nesting material. Ventilate and assess long-closed rodent-infested structures before cleaning, follow CDC protective-equipment and wet-cleaning recommendations, wash hands after rodent or bedding contact, and obtain medical care promptly if fever or breathing difficulty develops after a credible exposure.

Human vaccination

No HPS vaccine is licensed for routine use in the United States. No vaccine is currently available for Andes virus in the United States.

Animal vaccination

No licensed veterinary vaccine is established for prevention of HPS-associated hantavirus infection in reservoir or companion animals.

Prognosis

Prognosis depends on rapid recognition and the severity of cardiopulmonary compromise. HPS has a substantial case-fatality rate, but survivors often improve rapidly after the critical capillary-leak phase and usually clear the human infection.

Reporting, legal, and regulatory considerations

Hantavirus disease is nationally notifiable in the United States. Suspected cases should be discussed promptly with state, tribal, local, or territorial public-health authorities. Occupational or institutional exposures may require coordinated public-health and workplace investigation.

Selected current sources

• CDC—Clinician Brief: Hantavirus Pulmonary Syndrome
• CDC—Hantavirus Prevention
• CDC—Hantavirus Case Definition and Reporting

HELICOBACTER

Synonyms and scope

Helicobacter infection; gastric helicobacteriosis. Human Helicobacter pylori infection is primarily a human-associated infection, not a conventional pet-borne zoonosis. This retained entry emphasizes the less common non-H. pylori gastric Helicobacter species of dogs, cats, and pigs that have possible zoonotic significance.

Etiologic agent

The genus Helicobacter contains numerous curved or spiral gram-negative bacteria. H. pylori is the dominant human gastric pathogen. Dogs and cats more commonly carry non-H. pylori species such as H. heilmannii-group organisms, H. felis, H. bizzozeronii, and H. salomonis; enterohepatic species also occur.

Animals involved and epidemiologic roles

• People: Principal reservoir for H. pylori; infection is associated with chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and gastric MALT lymphoma.
• Dogs and cats: Frequently harbor non-H. pylori gastric Helicobacter species; their role as sources of human infection is possible but incompletely defined.
• Pigs: Important host for H. suis, which is recognized in a minority of human gastric infections.
• Other mammals: Various Helicobacter species occur in wildlife and laboratory animals, but zoonotic importance is species-dependent.

Geographic distribution and occurrence

H. pylori occurs worldwide, with prevalence strongly influenced by age, household crowding, sanitation, geography, and socioeconomic conditions. Gastric non-H. pylori Helicobacter species are common in dogs and cats worldwide, but documented human infections are much less common.

Reservoir, life cycle, and transmission

H. pylori is maintained mainly among people, probably through oral-oral and fecal-oral routes within households. For animal-associated non-H. pylori species, direct or indirect animal-to-human transmission is biologically plausible and has been supported by selected household and molecular observations, but the magnitude of risk is uncertain. Routine pet contact should not be presented as a major established cause of human H. pylori infection.

Incubation period

A precise incubation period for chronic gastric colonization is not usually identifiable. Human acquisition often occurs in childhood and may persist for decades without treatment. Dogs and cats can remain colonized for prolonged periods, including while clinically normal.

Disease in humans

Most H. pylori infections are initially asymptomatic but cause chronic active gastritis. Some people develop dyspepsia, peptic ulcer disease, iron-deficiency anemia or other complications; long-term infection increases risk for gastric adenocarcinoma and MALT lymphoma. Non-H. pylori gastric species can also cause gastritis and have been associated with ulcers and gastric lymphoma, although they are much less common.

Disease in animals—by species

• Dogs: Gastric Helicobacter organisms are found in healthy and vomiting dogs. A direct causal relationship with chronic gastritis is inconsistent, although some infected animals have vomiting or histologic gastritis.
• Cats: Colonization is also common in healthy and symptomatic cats; clinical significance is uncertain.
• Pigs: H. suis colonizes the stomach and has been associated with gastritis and production effects in some settings.

Pathology

Human H. pylori produces chronic active gastritis and can progress to atrophy, intestinal metaplasia, ulceration, neoplasia, or MALT lymphoma. In dogs and cats, organisms are often present in gastric mucus and glands with variable lymphoplasmacytic inflammation; organism burden does not consistently predict clinical disease.

Human diagnosis

Common noninvasive tests for H. pylori include urea breath testing and stool antigen testing. Endoscopy with biopsy permits histology and additional testing when clinically indicated. Serology cannot reliably distinguish active from past infection. Confirmation of eradication after therapy is recommended using an appropriate test at the clinically recommended interval.

Animal diagnosis

Definitive evaluation of clinically significant gastric disease generally requires endoscopic gastric biopsies with histology and organism-directed testing. Cytology, urease-based methods, immunohistochemistry, and molecular assays may support identification. Positive detection alone does not prove that Helicobacter is the cause of vomiting or gastritis.

Differential diagnoses

In people: functional dyspepsia, gastroesophageal reflux, medication-associated gastritis, peptic ulcer from other causes, and gastric neoplasia. In dogs and cats: dietary disease, foreign body, parasitism, inflammatory enteropathy, pancreatitis, systemic disease, medication injury, gastric neoplasia, and other causes of acute or chronic gastritis.

Treatment in humans

Confirmed H. pylori infection is treated with guideline-based multidrug eradication therapy combining potent acid suppression with selected antimicrobials. Regimen choice should reflect current regional resistance patterns, previous antibiotic exposure, allergies, and local guidelines. Treatment success should be confirmed; persistent infection requires a different evidence-based salvage regimen.

Treatment in animals—by species

Because many healthy dogs and cats are colonized and causation is uncertain, treatment is generally reserved for animals with compatible chronic gastric disease in which organisms are considered clinically relevant. Veterinary protocols commonly combine acid suppression with multiple antimicrobials, but optimal regimens and durable eradication rates are not established. Clinical response and recurrence should be reassessed rather than repeatedly treating an incidental positive result.

Animal and environmental control

No evidence supports screening, isolation, or treatment of healthy household pets solely because a person has H. pylori. Provide routine veterinary care, manage chronic vomiting appropriately, remove feces promptly, maintain clean food and water bowls, and use good hand hygiene. Avoid unnecessary antimicrobials because of resistance and uncertain benefit.

Prevention in humans

Use safe water and food practices, hand hygiene after toileting and animal fecal contact, and appropriate sanitation. People with persistent dyspepsia, ulcer history, or other indications for testing should seek medical evaluation. Pet removal is not recommended as a routine strategy for preventing or treating human H. pylori.

Human vaccination

No licensed vaccine is currently available for H. pylori.

Animal vaccination

No licensed veterinary vaccine is available for gastric Helicobacter infection in dogs, cats, or pigs.

Prognosis

Human prognosis is excellent after successful eradication, although prior advanced gastric injury may confer continuing cancer risk. In dogs and cats, prognosis depends more on the underlying cause and severity of gastritis than on detection of Helicobacter alone.

Reporting, legal, and regulatory considerations

H. pylori and companion-animal gastric Helicobacter infections are generally not routinely reportable. Food-animal antimicrobial use must follow applicable prescription, residue, and withdrawal regulations. Unusual clusters or suspected foodborne or occupational transmission merit public-health or veterinary investigation.

Selected current sources

• Merck Veterinary Manual—Helicobacter Infection in Small Animals
• IARC/WHO—H. pylori Screen-and-Treat Strategies for Gastric Cancer Prevention

HEMORRHAGIC FEVER WITH RENAL SYNDROME [HFRS]

Synonyms and scope

HFRS; Korean hemorrhagic fever; epidemic hemorrhagic fever; nephropathia epidemica. HFRS is a group of rodent-borne hantavirus diseases characterized primarily by vascular leakage, thrombocytopenia, and acute kidney injury. It is distinct from, but related to, hantavirus pulmonary syndrome.

Etiologic agent

HFRS is caused by several orthohantaviruses, including Hantaan, Dobrava-Belgrade, Seoul, Puumala, and related viruses. Disease severity varies by virus. Seoul virus is globally distributed with Rattus rats and is the principal HFRS-associated hantavirus encountered in the United States.

Animals involved and epidemiologic roles

• Striped field mice (Apodemus agrarius): Major reservoir for Hantaan virus.
• Bank voles: Reservoir for Puumala virus.
• Yellow-necked and related mice: Reservoirs for Dobrava-Belgrade virus lineages.
• Norway and roof rats: Reservoirs for Seoul virus; infection can occur in wild, feeder, breeding, and pet rat populations.
• People: Accidental hosts after exposure to infected rodents or contaminated environments.

Geographic distribution and occurrence

HFRS occurs predominantly in Europe and Asia. Seoul virus is an important exception because its rat reservoirs are worldwide, including North America. Human cases may follow occupational, household, travel, military, laboratory, or pet-rat exposure.

Reservoir, life cycle, and transmission

Reservoir rodents usually develop persistent asymptomatic infection and shed virus in urine, feces, and saliva. People are infected mainly by inhaling contaminated particles or through mucosal or broken-skin contact with rodent excreta; bites can also expose. Person-to-person transmission is not recognized for the usual HFRS viruses.

Incubation period

Symptoms commonly begin about 1–2 weeks after exposure but may be delayed for as long as approximately 8 weeks. The interval varies with virus and exposure.

Disease in humans

Illness may begin abruptly with fever, severe headache, back or abdominal pain, nausea, blurred vision, facial flushing, conjunctival injection, or rash. More severe disease can progress through hypotension and vascular leakage to thrombocytopenia, hemorrhage, acute kidney injury, oliguria, fluid overload, and later a polyuric recovery phase. Puumala and Seoul infections are often milder than Hantaan or Dobrava disease but can still require hospitalization.

Disease in animals—by species

• Reservoir mice, voles, and rats: Typically chronic asymptomatic infection with prolonged shedding.
• Pet rats: Seoul-virus infection is usually clinically inapparent, so appearance cannot establish infection status.
• Other domestic animals: No important HFRS reservoir role is established for dogs, cats, livestock, or horses.

Pathology

Endothelial dysfunction and increased vascular permeability produce edema, hypotension, and hemorrhagic manifestations. Renal involvement includes interstitial nephritis, medullary hemorrhage, tubular injury, and acute kidney dysfunction. Thrombocytopenia is common.

Human diagnosis

Consider HFRS in compatible febrile acute kidney injury with thrombocytopenia and rodent exposure or travel. Diagnosis is confirmed by hantavirus-specific serology and/or molecular testing through qualified clinical or public-health laboratories. Because early findings overlap with many infections, clinicians should involve public health when hantavirus is suspected.

Animal diagnosis

Testing of pet or breeding rats for Seoul virus may be recommended during investigations or before movement into certain colonies. Veterinary/public-health authorities can advise appropriate serologic or molecular testing. Routine testing of wild rodents around a home is generally not a substitute for exposure prevention.

Differential diagnoses

Leptospirosis, sepsis, acute pyelonephritis, thrombotic microangiopathy, other viral hemorrhagic fevers, rickettsial disease, acute glomerulonephritis, toxic nephropathy, severe influenza or COVID-19, and HPS.

Treatment in humans

Management is primarily supportive, with careful fluid and electrolyte balance, hemodynamic support, management of bleeding, and dialysis when indicated. Early critical-care and nephrology involvement is important in severe disease. Ribavirin has been used for severe HFRS in some settings, but evidence and recommendations vary by virus, timing, and country; specialist/public-health guidance is appropriate.

Treatment in animals—by species

No antiviral treatment is established for asymptomatic reservoir rodents. When Seoul virus is identified in pet, feeder, or breeding rats, management focuses on preventing human exposure and stopping spread among rats; testing, quarantine, movement restrictions, or humane depopulation may be directed by veterinary and public-health authorities.

Animal and environmental control

Exclude wild rodents from buildings and rat colonies, maintain secure feed storage, quarantine and appropriately source new rats, and use integrated pest management. Clean contaminated areas by wet-disinfection methods recommended by public health rather than dry sweeping or vacuuming rodent waste.

Prevention in humans

Avoid contact with rodent urine, feces, saliva, and contaminated bedding; wash hands after handling rats; keep wild rats away from pet-rat colonies; and use appropriate protective equipment for heavy infestations or occupational exposure. People at increased risk of severe infection should carefully consider the risks of keeping or handling pet rats.

Human vaccination

No HFRS vaccine is licensed in the United States. Hantavirus vaccines are used in some countries, particularly for selected HFRS viruses, under national programs.

Animal vaccination

No broadly used licensed veterinary vaccine is available for preventing Seoul or other HFRS-associated hantavirus infection in rats.

Prognosis

Most patients recover with appropriate supportive care. Severity varies by virus: Hantaan and Dobrava infections can have appreciable mortality, while Puumala and Seoul disease are often more moderate. Renal recovery can take weeks to months after severe illness.

Reporting, legal, and regulatory considerations

Hantavirus disease is nationally notifiable in the United States. Seoul-virus infections linked to pet or feeder rats may trigger coordinated human and animal contact tracing, testing, movement control, and breeder or distributor investigation.

Selected current sources

• CDC—Clinician Brief: Hemorrhagic Fever with Renal Syndrome
• CDC—Clinical Overview of Hantavirus
• CDC—Hantavirus Prevention

HEPATITIS E VIRUS INFECTION

Synonyms and scope

Hepatitis E; HEV infection. This entry distinguishes waterborne human HEV cycles from zoonotic foodborne infection. Zoonotic disease in industrialized regions is most strongly associated with HEV genotypes circulating in pigs, wild boar, and deer.

Etiologic agent

Hepatitis E virus (HEV), family Hepeviridae. Human disease is caused by several genotypes. Genotypes 1 and 2 are maintained mainly among people and are associated with waterborne outbreaks; genotypes 3 and 4 are zoonotic and circulate especially in domestic pigs and wild boar.

Animals involved and epidemiologic roles

• Domestic pigs: Major reservoirs of zoonotic HEV genotypes 3 and 4; infection is common and usually subclinical.
• Wild boar: Important wildlife reservoir and foodborne source.
• Deer: Can carry zoonotic HEV and have been linked to foodborne transmission.
• Rabbits and other mammals: Related HEV strains occur and some have zoonotic potential, but their population contribution is less important than swine in most settings.
• People: Reservoir for genotypes 1 and 2 and accidental hosts in zoonotic genotype 3/4 cycles.

Geographic distribution and occurrence

HEV occurs worldwide. Large waterborne outbreaks are concentrated in regions with inadequate sanitation, especially parts of Asia and Africa. Sporadic zoonotic genotype 3 and 4 infections occur in Europe, North America, and Asia, often without recognized travel.

Reservoir, life cycle, and transmission

HEV is shed in feces. Human-only genotypes spread mainly through fecally contaminated drinking water. Zoonotic infection is associated with eating raw or undercooked pork, pork liver, wild-boar meat, venison, and sometimes contaminated shellfish. Occupational pig exposure is associated with increased infection markers, although foodborne transmission is the dominant recognized zoonotic route.

Incubation period

Symptoms usually develop about 2–6 weeks after exposure, with an overall incubation range of roughly 2–10 weeks reported in major public-health references.

Disease in humans

Many infections are asymptomatic. Acute hepatitis can cause fatigue, fever, anorexia, nausea, abdominal discomfort, dark urine, pale stool, hepatomegaly, and jaundice. Severe acute liver failure is particularly important in pregnancy for some genotypes and settings. Chronic infection can occur in immunocompromised people, especially solid-organ transplant recipients, and may progress to cirrhosis.

Disease in animals—by species

• Pigs: Usually asymptomatic, transient infection and fecal shedding, commonly acquired while young.
• Wild boar/deer: Usually subclinical reservoir infection.
• Other susceptible mammals: Clinical significance varies by virus and host and is generally less well defined.

Pathology

Human disease is an acute viral hepatitis with hepatocellular injury and inflammatory infiltrates. Chronic infection can produce progressive fibrosis and cirrhosis. In pigs, infection generally causes little or no overt disease despite viral replication and mild microscopic hepatic changes.

Human diagnosis

Diagnosis uses HEV serology and/or detection of HEV RNA in blood or stool, interpreted in light of timing and immune status. Immunocompromised patients may have unreliable antibody responses, making molecular testing especially important. Other causes of acute hepatitis should be evaluated concurrently.

Animal diagnosis

HEV testing is not routinely indicated for individual healthy pigs. Herd, food-safety, or research surveillance may use serology or molecular detection under appropriate veterinary/public-health programs. A positive swine result does not by itself identify the source of an individual human case.

Differential diagnoses

Hepatitis A, B, C and other viral hepatitis; drug- or toxin-induced liver injury; leptospirosis; autoimmune hepatitis; biliary obstruction; ischemic hepatitis; and other causes of jaundice or elevated hepatic enzymes.

Treatment in humans

Most acute infections in immunocompetent people require supportive care only. Severe acute hepatitis requires hospital-based management. Chronic HEV in immunocompromised patients may respond to reduction of immunosuppression when feasible and specialist-directed ribavirin therapy; management should be individualized because treatment considerations differ with pregnancy, transplantation, anemia risk, and other comorbidities.

Treatment in animals—by species

No treatment is indicated for routine subclinical HEV infection in pigs, wild boar, or deer. Antimicrobial therapy has no role. Management is directed toward herd health, sanitation, food safety, and reduction of fecal contamination rather than attempting to eliminate infection from individual animals.

Animal and environmental control

Use good swine-facility hygiene, manage manure to reduce environmental contamination, provide clean water, and prevent cross-contamination during slaughter and food processing. Farm biosecurity may reduce transmission but cannot guarantee HEV-free pork. Wildlife carcasses should be handled hygienically.

Prevention in humans

Cook pork, pork liver, wild boar, and venison thoroughly; prevent raw-meat cross-contamination; wash hands after pig or carcass contact; and use safe drinking water in areas with inadequate sanitation. Pregnant, immunocompromised, and chronic-liver-disease patients should be particularly cautious about raw or undercooked animal products.

Human vaccination

A recombinant hepatitis E vaccine is licensed in China and has also been licensed in some other countries, but it is not licensed in the United States and is not globally available. WHO notes that it has been used as an outbreak-response measure.

Animal vaccination

No broadly used licensed veterinary HEV vaccine is established for pigs or wildlife.

Prognosis

Most immunocompetent patients recover completely. Prognosis is worse with acute liver failure, underlying liver disease, certain pregnancy-associated infections, or chronic infection in immunocompromised patients. Subclinical infection in pigs generally has an excellent animal-health prognosis.

Reporting, legal, and regulatory considerations

Reporting requirements for hepatitis E vary by country and U.S. jurisdiction. Foodborne clusters, transfusion-associated infection, or occupational clusters warrant public-health investigation. Food-animal management must comply with meat-inspection, food-safety, and medication-residue requirements.

Selected current sources

• WHO—Hepatitis E Fact Sheet
• CDC—Hepatitis E Basics

HEPATITIS A

Synonyms and scope

Hepatitis A virus infection; infectious hepatitis. Hepatitis A is primarily a human fecal-oral infection. This legacy zoonotic entry is retained because captive nonhuman primates can acquire HAV from people and have historically been associated with occupational transmission, but ordinary companion animals are not recognized reservoirs.

Etiologic agent

Hepatitis A virus (HAV), a nonenveloped RNA virus in genus Hepatovirus, family Picornaviridae. Human HAV is environmentally stable compared with many enveloped viruses and is shed in high concentrations in feces before symptoms appear.

Animals involved and epidemiologic roles

• People: Principal reservoir and source of most transmission.
• Nonhuman primates: Chimpanzees and several other primates can be infected, particularly in captive settings; infection is often acquired from humans and may create occupational exposure.
• Dogs, cats, livestock, rodents, and birds: Not established reservoirs of human HAV.

Geographic distribution and occurrence

HAV occurs worldwide. Endemicity is highest where sanitation and access to safe water are limited. In countries with lower endemicity, outbreaks occur among susceptible groups through person-to-person transmission or contaminated food and water. Animal-associated cases are uncommon compared with ordinary human transmission.

Reservoir, life cycle, and transmission

HAV is shed in feces and spreads primarily by the fecal-oral route through close contact, contaminated food or water, or contaminated hands and surfaces. Captive nonhuman primates may acquire human HAV and can potentially expose caretakers through fecal contamination. HAV does not establish chronic infection.

Incubation period

The incubation period averages about 28 days and generally ranges from approximately 15–50 days. People are most infectious before jaundice or other recognizable illness develops.

Disease in humans

Young children are often asymptomatic. Older children and adults more commonly develop abrupt fever, malaise, anorexia, nausea, abdominal discomfort, dark urine, pale stool, and jaundice. Illness usually resolves within weeks, although fatigue or relapsing symptoms can persist for months. Fulminant hepatitis is uncommon but risk increases with age and underlying liver disease.

Disease in animals—by species

• Nonhuman primates: Infection is often subclinical but can produce lethargy, anorexia, vomiting, jaundice, and increased hepatic enzymes. Captive outbreaks have historically occurred after introduction from infected people or primates.
• Other animals: No established clinical human-HAV reservoir syndrome.

Pathology

HAV causes acute hepatocellular inflammation and injury mediated largely by the host immune response. Histologic changes can include lobular inflammation, hepatocyte necrosis, and cholestasis. Chronic hepatitis and chronic carrier states do not occur.

Human diagnosis

Acute infection is diagnosed by serum IgM antibody to HAV in a compatible clinical setting. Total or IgG anti-HAV indicates immunity from prior infection or vaccination and does not by itself diagnose acute disease. Molecular testing is mainly used in specialized public-health investigations.

Animal diagnosis

Suspected HAV in a nonhuman primate should be managed with the institution's veterinarian, occupational-health program, and public-health authorities. Serology and molecular testing may be used through qualified laboratories. Routine testing of household pets is not indicated.

Differential diagnoses

Hepatitis B, C, E and other viral hepatitis; drug- or toxin-induced liver injury; leptospirosis; autoimmune hepatitis; biliary disease; Epstein-Barr virus or cytomegalovirus hepatitis; and other causes of jaundice and elevated hepatic enzymes.

Treatment in humans

There is no specific antiviral treatment. Most patients require rest, hydration, adequate nutrition, avoidance of alcohol and unnecessary hepatotoxic medications, and monitoring for complications. Severe disease or acute liver failure requires hospitalization and specialist care.

Treatment in animals—by species

There is no specific antiviral treatment for HAV in nonhuman primates. Provide veterinary supportive care, monitor hepatic function and hydration, and implement infection-control measures to prevent fecal-oral exposure. Management should be coordinated with occupational health because infected primates may expose personnel.

Animal and environmental control

In primate facilities, use rigorous hand hygiene, appropriate PPE for fecal or enclosure contact, prompt waste removal, safe food and water practices, and occupational-health oversight. Newly acquired or ill primates should be managed under facility-specific quarantine and health-screening programs based on current veterinary guidance rather than historical fixed quarantine periods.

Prevention in humans

Vaccination is the primary preventive measure. Wash hands after toileting, diapering, and animal fecal contact; use safe food and water practices; and maintain sanitation in primate facilities. After a recognized exposure, hepatitis A vaccine and/or immune globulin should be given as soon as possible, ideally within 2 weeks, according to age, immune status, liver disease, and public-health guidance.

Human vaccination

Highly effective inactivated hepatitis A vaccines are routinely recommended for children and for unvaccinated people at increased risk of infection or severe disease. Combined hepatitis A/hepatitis B vaccines are also available. Vaccination provides long-term protection.

Animal vaccination

No broadly applicable licensed veterinary HAV vaccine is established for nonhuman primates. Human vaccines have been studied or used in specialized primate settings, but institutional veterinary and regulatory guidance is required and such use should not be presented as routine companion-animal vaccination.

Prognosis

Most people and infected nonhuman primates recover completely. HAV does not become chronic. Human prognosis is more guarded in older adults and people with significant chronic liver disease who develop acute infection.

Reporting, legal, and regulatory considerations

Acute hepatitis A is nationally notifiable in the United States. Cases linked to food handling, childcare, congregate settings, travel, or nonhuman-primate facilities require rapid public-health assessment for contact prophylaxis. Primate facilities should follow occupational-health, animal-welfare, importation, and biosafety regulations.

Selected current sources

• CDC—Clinical Care of Hepatitis A
• CDC—Hepatitis A

HERPES B

Synonyms and scope

Also called B virus infection, macaque herpesvirus 1 infection, herpes B, monkey B virus, and historically herpesvirus simiae. This entry concerns zoonotic infection associated primarily with macaques.

Etiologic agent

Macacine alphaherpesvirus 1 (B virus), an alphaherpesvirus naturally carried by macaques.

Animals involved and epidemiologic roles

Macaques: the natural reservoir; infection is common in adult animals and usually inapparent or mild. Humans: accidental hosts, principally after occupational or other direct macaque exposure. Other nonhuman primates can become infected but are not established natural reservoirs.

Geographic distribution and occurrence

B virus occurs wherever macaques occur or are maintained. Human disease is extremely rare; documented cases have primarily involved people working with macaques or macaque tissues. Free-ranging macaques can also pose an exposure risk.

Reservoir, life cycle, and transmission

Infected macaques can intermittently shed virus in oral or genital secretions, including when they appear healthy. Human infection can follow bites, scratches, mucosal splash, or contamination of broken skin with macaque secretions or tissues. Fomite-associated exposures are possible when fresh contaminated material contacts susceptible tissue. Person-to-person transmission is extraordinarily rare.

Incubation period

Human illness usually begins within days to several weeks after exposure; timing is variable. Any compatible illness after macaque exposure warrants urgent evaluation rather than waiting for a defined incubation interval.

Disease in humans

Early illness can include fever, headache, myalgia, fatigue, local pain or vesicles near the exposure site, and neurologic symptoms. Infection can progress to ascending neurologic disease, encephalomyelitis, respiratory failure, coma, and death. Prompt recognition and antiviral therapy are critical.

Disease in animals—by species

Macaques: usually asymptomatic or mild oral/genital vesicular or ulcerative lesions; lifelong latency with intermittent reactivation/shedding can occur. Other nonhuman primates: infection acquired from macaques can be severe or fatal.

Pathology

Human disease is characterized primarily by viral spread along peripheral nerves and severe encephalomyelitis; disseminated disease may occur. Macaques typically have localized mucocutaneous infection followed by latency.

Human diagnosis

Diagnosis requires immediate consultation with public-health or specialized reference laboratories. Exposure history and clinical syndrome are essential. Validated molecular and serologic methods are used in appropriate settings. The receiving laboratory should be alerted before specimens from a suspected case are submitted.

Animal diagnosis

Routine testing of macaques may support colony management or exposure assessment, but a negative result does not prove that a macaque is incapable of shedding virus. Veterinary and institutional occupational-health protocols should guide evaluation.

Differential diagnoses

Human herpes simplex or varicella-zoster infection, bacterial wound infection, tetanus, rabies, other viral encephalitides, transverse myelitis, Guillain-Barré syndrome, and other causes of acute neurologic disease.

Treatment in humans

Potential exposures require immediate wound cleansing and urgent medical risk assessment. CDC guidance recommends post-exposure valacyclovir or acyclovir for specified higher-risk exposures and consideration for some lower-risk exposures. Established infection requires intravenous antiviral therapy; ganciclovir is preferred when central nervous system symptoms are present. Infectious-disease/public-health consultation is recommended.

Treatment in animals—by species

There is no treatment that reliably eliminates latent B virus from reservoir macaques. Clinical lesions in macaques require veterinary evaluation, and exposed animals should be managed under institutional primate-health and occupational-safety programs.

Animal and environmental control

Facilities housing macaques should use species-appropriate restraint, exposure-prevention programs, PPE, occupational-health plans, and prompt exposure-response procedures. Management should assume that an apparently healthy macaque may be infected.

Prevention in humans

Avoid touching or feeding free-ranging macaques. Occupationally exposed personnel should prevent bites, scratches and mucosal exposure and immediately cleanse any exposure. CDC advises thorough washing/scrubbing of an exposed wound or area for 15 minutes followed by running water for another 15–20 minutes, then prompt medical evaluation.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

No licensed vaccine is available for macaques or other animals.

Prognosis

Untreated neurologic human infection has historically had a very high fatality rate and survivors may have neurologic sequelae. Outcome is substantially better when exposure is recognized promptly and antiviral management begins before advanced neurologic disease.

Reporting, legal, and regulatory considerations

Suspected human B virus infection or significant macaque exposure should be handled urgently with occupational-health, infectious-disease, and public-health consultation. Animal-facility requirements vary by institution and jurisdiction.

Selected current sources

• CDC—B Virus
• CDC—Patient Care for B Virus
• CDC—B Virus Risk Factors and Prevention

HETEROPHYES HETEROPHYES

Synonyms and scope

Heterophyiasis (heterophyes infection), a foodborne intestinal trematode infection retained here because dogs, cats, other fish-eating mammals, birds, and people can share the parasite cycle.

Etiologic agent

Heterophyes heterophyes, a minute intestinal fluke (trematode).

Animals involved and epidemiologic roles

Humans, dogs, cats and other fish-eating mammals and birds: definitive hosts that can harbor adult flukes. Snails: first intermediate hosts. Fresh- or brackish-water fish: second intermediate hosts and the foodborne source for definitive hosts.

Geographic distribution and occurrence

Human infection is reported particularly in Egypt and other parts of the Middle East and in parts of Asia where suitable snail and fish hosts occur and raw or inadequately cooked fish is eaten.

Reservoir, life cycle, and transmission

Eggs from definitive hosts enter aquatic environments; the parasite develops through snail and fish hosts. People and other definitive hosts acquire infection by eating infected raw, salted, pickled, or inadequately cooked fish. Direct transmission from a dog, cat, bird, or fish to a person does not occur.

Incubation period

Following ingestion of infected fish, maturation to intestinal adults occurs over a short period measured in days to weeks. Clinical timing varies with parasite burden and host response.

Disease in humans

Many infections are mild. Symptomatic disease can include diarrhea, abdominal discomfort or colicky pain and intestinal inflammation. Rarely, eggs have been reported in extraintestinal sites such as the heart or central nervous system, with potentially severe consequences.

Disease in animals—by species

Dogs/cats and other fish-eating mammals: often subclinical; heavier burdens may cause enteritis, diarrhea or poor condition. Fish: larval stages occur in tissues without representing direct zoonotic transmission by handling alone. Birds: may serve as definitive hosts.

Pathology

Adults inhabit the small intestine and can produce mucosal irritation and inflammation. Rare ectopic deposition of eggs has been associated with granulomatous or vascular injury in extraintestinal tissues.

Human diagnosis

Diagnosis is usually by detection of small operculated trematode eggs in stool. Eggs overlap morphologically with Metagonimus and resemble those of Clonorchis and Opisthorchis, so species-level identification may be difficult.

Animal diagnosis

Veterinary diagnosis is based on compatible exposure and fecal parasite evaluation. Because small trematode eggs can be difficult to distinguish, interpretation may require veterinary parasitology expertise.

Differential diagnoses

Other intestinal flukes including Metagonimus, Clonorchis and Opisthorchis; giardiasis; bacterial or viral enteritis; inflammatory bowel disease; and other causes of diarrhea and abdominal pain.

Treatment in humans

Praziquantel is generally regarded as the treatment of choice for intestinal heterophyid infections; treatment should be directed by a clinician familiar with foodborne trematodes, particularly when extraintestinal disease is suspected.

Treatment in animals—by species

Infected dogs or cats with clinically significant disease should be treated under veterinary direction with an appropriate anthelmintic and reassessed for continuing access to raw fish. Drug choice and dosing depend on species, patient factors, and local availability.

Animal and environmental control

Prevent dogs and cats from eating raw or inadequately cooked fish and dispose of feces hygienically. Community control depends on sanitation that prevents fecal contamination of aquatic habitats and on safe preparation of fish.

Prevention in humans

Do not eat raw or inadequately cooked fresh- or brackish-water fish from endemic areas. Salting or pickling should not be assumed to make infected fish safe. Hand hygiene and sanitary fecal disposal reduce environmental contamination.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Most intestinal infections respond well to treatment. Heavy infections and rare ectopic egg-associated disease can be more serious.

Reporting, legal, and regulatory considerations

Heterophyiasis is not generally a nationally notifiable disease in the United States. Local reporting requirements may differ, and unusual clusters or foodborne outbreaks should be discussed with public-health authorities.

Selected current sources

• CDC DPDx—Heterophyiasis

HYMENOLEPIS DIMINUTA

Synonyms and scope

Rat tapeworm infection; Hymenolepis diminuta infection. Human infection is uncommon and occurs through accidental ingestion of infected arthropods rather than direct contact with rodents.

Etiologic agent

Hymenolepis diminuta, a cestode commonly found in rodents; adult worms are much larger than the dwarf tapeworm H. nana.

Animals involved and epidemiologic roles

Rodents: principal definitive hosts and reservoir. Humans: accidental definitive hosts. Arthropods, especially grain beetles and other insects, serve as required intermediate hosts.

Geographic distribution and occurrence

The parasite occurs worldwide in rodents. Human infections are rare but have been reported in multiple regions, particularly where food or environments permit accidental ingestion of infected insects.

Reservoir, life cycle, and transmission

Rodent feces release eggs that are ingested by susceptible arthropods, in which infective cysticercoids develop. Rodents or people become infected by swallowing infected arthropods, including insects contaminating stored foods. Direct fecal-oral transmission of H. diminuta eggs to humans does not complete the cycle.

Incubation period

Adult maturation in the mammalian intestine occurs in roughly several weeks after ingestion of an infected arthropod. Many infections remain asymptomatic.

Disease in humans

Most reported human infections are asymptomatic or mild. Heavier infections can be associated with abdominal discomfort, diarrhea, nausea, reduced appetite or other nonspecific gastrointestinal complaints.

Disease in animals—by species

Rodents: commonly subclinical; heavy intestinal burdens may be associated with enteritis or poor condition. Other mammalian hosts are uncommon.

Pathology

Adult tapeworms inhabit the small intestine. Heavy burdens can cause local mucosal irritation or catarrhal enteritis.

Human diagnosis

Diagnosis is by demonstration of characteristic eggs in stool. H. diminuta eggs are larger than H. nana eggs and lack the polar filaments characteristic of H. nana.

Animal diagnosis

Rodent infection can be diagnosed by fecal parasite examination. In colonies or facilities, identification should be interpreted with attention to rodent and arthropod control.

Differential diagnoses

Hymenolepis nana and other cestode infections; protozoal, bacterial or viral enteritis; dietary and inflammatory causes of gastrointestinal signs.

Treatment in humans

Praziquantel is the CDC treatment of choice for hymenolepiasis; alternative agents may be considered by the treating clinician. Because human H. diminuta infection is uncommon, species identification and clinical context are useful.

Treatment in animals—by species

Veterinary treatment of infected rodents or other animals should be directed by a veterinarian and accompanied by correction of insect and food-storage problems to prevent reinfection.

Animal and environmental control

Integrated rodent and insect control is central. Protect cereals, pet foods and other stored products from rodents and beetles; clean contaminated storage areas and prevent access to rodent feces.

Prevention in humans

Store food in insect- and rodent-resistant containers, discard infested food, control rodents and pantry insects, and supervise young children in environments where contaminated insects could be ingested.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Prognosis is excellent in most human cases after appropriate therapy. Animal infections are usually mild unless parasite burdens are high.

Reporting, legal, and regulatory considerations

Human H. diminuta infection is not generally nationally notifiable in the United States. Clusters suggesting contaminated food or unusual exposure should be discussed with public-health authorities.

Selected current sources

• CDC DPDx—Hymenolepiasis
• CDC—Clinical Care of Hymenolepiasis

HYMENOLEPIS NANA

Synonyms and scope

Dwarf tapeworm infection; hymenolepiasis. Unlike H. diminuta, H. nana can complete its cycle in a single human or rodent host and can spread directly by ingestion of eggs.

Etiologic agent

Hymenolepis nana (dwarf tapeworm; also classified as Rodentolepis nana in some taxonomies), a small intestinal cestode.

Animals involved and epidemiologic roles

Humans: important definitive hosts and sources of directly infective eggs. Rodents: animal hosts/reservoirs. Beetles and fleas: can serve as optional intermediate hosts, but an arthropod is not required for direct egg transmission.

Geographic distribution and occurrence

Worldwide. Infection is more common in children, institutional settings, and communities with inadequate sanitation.

Reservoir, life cycle, and transmission

Eggs passed in feces are immediately infective and can be swallowed through fecally contaminated hands, food or water. Internal autoinfection can maintain or increase parasite burden. Infection can also follow ingestion of an infected arthropod intermediate host.

Incubation period

After ingestion, development to egg-producing adults occurs over approximately a few weeks. Autoinfection can prolong infection without a new external exposure.

Disease in humans

Many infections are asymptomatic. Heavier burdens, particularly in children, can cause abdominal pain, diarrhea, nausea, weakness, loss of appetite, headache, sleep disturbance or perianal itching.

Disease in animals—by species

Rodents: often subclinical; heavy burdens may cause enteritis, diarrhea or reduced condition. Dogs and cats are not considered major reservoirs for ordinary human H. nana transmission.

Pathology

Larval stages develop transiently in intestinal villi and adults occupy the small-intestinal lumen. Heavy infection can produce mucosal inflammation.

Human diagnosis

Diagnosis is by detection of characteristic eggs in stool. Repeated examinations or concentration methods can improve detection of light infections. Eggs have polar filaments that help distinguish them from H. diminuta.

Animal diagnosis

Veterinary diagnosis is by fecal parasite examination in susceptible rodents or other hosts, interpreted with colony, sanitation and exposure history.

Differential diagnoses

H. diminuta and other cestodes; giardiasis and other intestinal parasites; bacterial or viral gastroenteritis; inflammatory or dietary gastrointestinal disease.

Treatment in humans

CDC identifies praziquantel as the treatment of choice; niclosamide and nitazoxanide are alternatives in appropriate circumstances. Reinfection or autoinfection may require follow-up and occasionally repeat treatment.

Treatment in animals—by species

Clinically significant animal infection should be treated under veterinary direction. Environmental sanitation and rodent/insect management are important to reduce reinfection.

Animal and environmental control

Improve sanitation, promptly remove fecal contamination, control rodents and insects, and protect stored foods and animal feeds from contamination.

Prevention in humans

Handwashing after toileting or diaper changes and before food preparation is central. Use safe food and water practices, especially where sanitation is limited, and control rodents and food-infesting insects.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Prognosis is generally excellent with treatment. Heavy or persistent infection may cause more significant symptoms, especially in children or immunocompromised patients.

Reporting, legal, and regulatory considerations

Hymenolepiasis is not generally nationally notifiable in the United States. Institutional clusters or suspected food/water-associated outbreaks should be evaluated with local public-health authorities.

Selected current sources

• CDC DPDx—Hymenolepiasis
• CDC—About Hymenolepiasis
• CDC—Clinical Care of Hymenolepiasis

INFLUENZA

Synonyms and scope

This zoonotic entry focuses on influenza A viruses at the human–animal interface, including avian and swine influenza and infections in other mammals. Seasonal human influenza is included where necessary for comparison and prevention.

Etiologic agent

Influenza A viruses, family Orthomyxoviridae. Subtypes are defined by hemagglutinin (H) and neuraminidase (N) surface proteins. Influenza B primarily circulates in people and is not a major zoonotic virus.

Animals involved and epidemiologic roles

Wild aquatic birds: major natural reservoir for diverse influenza A viruses. Domestic poultry: can develop low- or highly pathogenic avian influenza. Swine: maintain swine influenza A lineages and can occasionally transmit variant viruses to people. Other mammals: horses, dogs, cats, ferrets, seals and cattle can be infected by particular influenza A viruses. Humans: usually maintain seasonal human strains but can acquire novel animal-origin influenza A viruses.

Geographic distribution and occurrence

Influenza A viruses circulate globally. Zoonotic risk varies by subtype, geography and current animal outbreaks. Avian and swine influenza events are continuously monitored because sporadic human infections can occur and novel viruses may have pandemic potential.

Reservoir, life cycle, and transmission

Transmission within susceptible species is mainly respiratory. Zoonotic infections most often follow close, unprotected exposure to infected animals or contaminated environments, particularly poultry, wild birds, swine or affected mammals. Most animal-origin influenza viruses do not spread efficiently from person to person.

Incubation period

Human influenza generally develops about 1–4 days after infection, although incubation with some zoonotic influenza viruses may vary. Animal incubation depends on host species and virus.

Disease in humans

Illness ranges from conjunctivitis or mild upper-respiratory disease to typical influenza-like illness, pneumonia, acute respiratory distress syndrome, encephalopathy, multiorgan disease and death, depending on the zoonotic virus and patient factors.

Disease in animals—by species

Birds: signs range from inapparent infection to severe systemic highly pathogenic avian influenza with high mortality. Swine: acute fever, cough, nasal discharge, anorexia and reduced activity are typical. Horses: fever, cough and nasal discharge. Dogs/cats/ferrets: respiratory disease of variable severity; cats and some other mammals can develop severe disease with certain avian influenza viruses. Cattle: particular influenza A viruses can produce species-specific syndromes and require current outbreak guidance.

Pathology

Respiratory epithelial injury and inflammation predominate in uncomplicated disease. Severe infections can cause viral pneumonia, diffuse alveolar damage and secondary bacterial pneumonia; some zoonotic strains can produce systemic lesions in susceptible animal species.

Human diagnosis

Human testing should use current public-health guidance. Suspected novel or zoonotic influenza requires prompt notification of public-health authorities so appropriate respiratory testing and subtype characterization can be arranged. Exposure history to animals is essential.

Animal diagnosis

Veterinary diagnosis depends on species, syndrome and current outbreak context. Suspected reportable avian influenza or other regulated animal influenza should be referred promptly to animal-health authorities; validated molecular testing is generally central to confirmation.

Differential diagnoses

COVID-19 and other viral respiratory infections; bacterial pneumonia; infectious tracheobronchitis and other species-specific respiratory diseases; Newcastle disease and other important poultry diseases; and noninfectious causes of respiratory distress.

Treatment in humans

CDC recommends prompt influenza antiviral treatment for hospitalized patients, severe/progressive illness, and people at increased risk for complications. Oseltamivir is commonly used and is also used for many suspected novel influenza A infections while public-health guidance is obtained. Management of severe zoonotic influenza should involve infectious-disease and public-health specialists.

Treatment in animals—by species

Treatment is species- and virus-specific and is primarily supportive for many animal influenza infections. Antiviral use in animals is generally not routine and may be restricted or discouraged because of public-health and resistance concerns. Secondary bacterial infection should be treated when clinically indicated. Regulated poultry outbreaks follow official control policy rather than individual-animal treatment.

Animal and environmental control

Separate sick animals, reduce movement and mixing, use appropriate PPE and biosecurity, and follow current animal-health authority instructions. Control of reportable avian influenza can include quarantine, movement controls, surveillance, depopulation of affected flocks, cleaning/disinfection and other official measures.

Prevention in humans

Avoid unprotected contact with sick or dead birds and other animals involved in influenza outbreaks. People with occupational exposure should follow current PPE and monitoring guidance. Seasonal influenza vaccination does not prevent zoonotic avian or swine influenza infection, but is recommended for eligible people and helps reduce concurrent human influenza.

Human vaccination

Annual seasonal influenza vaccination is recommended in the United States for everyone 6 months and older who does not have a contraindication. Seasonal vaccines are not designed to protect against most novel animal-origin influenza A viruses; candidate vaccines may be developed for specific pandemic threats.

Animal vaccination

Vaccines are available for selected animal populations, including horses and swine, and poultry vaccines may be used under national or regional policy. Availability, strain matching, indications and regulatory policy vary by species and jurisdiction.

Prognosis

Most uncomplicated seasonal influenza resolves, but zoonotic influenza severity varies widely by virus. Some avian influenza viruses have caused severe or fatal human disease. Animal prognosis likewise ranges from rapid recovery to high mortality depending on host and strain.

Reporting, legal, and regulatory considerations

Human infection with a novel influenza A virus is nationally notifiable in the United States and requires public-health investigation. Suspected highly pathogenic avian influenza and other regulated animal influenza events should be reported immediately to state/federal animal-health authorities. Requirements change with outbreak conditions.

Selected current sources

• CDC—Influenza A in Animals
• CDC—Influenza Antiviral Treatment
• CDC—Preventing Seasonal Influenza
• CDC—Novel Influenza Outbreak Investigations
• CDC—A(H5) Bird Flu: Current Situation
• USDA APHIS—H5N1 HPAI Resources and Guidance

KASOKERO VIRUS

Synonyms and scope

Kasokero virus infection; a very rare emerging zoonotic orthonairovirus infection. Human disease is documented principally from four laboratory-associated infections reported in Uganda in the 1970s; the natural human disease burden remains unknown.

Etiologic agent

Kasokero virus (KASV), an enveloped negative-sense RNA virus in the genus Orthonairovirus, family Nairoviridae.

Animals involved and epidemiologic roles

Egyptian rousette fruit bats (Rousettus aegyptiacus): important vertebrate hosts. Soft ticks: Ornithodoros (Reticulinasus) faini associated with rousette bat roosts appear to participate in enzootic maintenance. Humans: incidental hosts; naturally acquired clinical cases have not been well characterized.

Geographic distribution and occurrence

KASV was first recognized from bats in Uganda. Virus has subsequently been detected in bat-associated soft ticks in Uganda and South Africa. The geographic range and frequency of human infection are poorly defined.

Reservoir, life cycle, and transmission

Current evidence supports an enzootic bat–soft-tick cycle. Human spillover could plausibly occur in bat-roost environments through infected ticks or other exposure, but the routes responsible for naturally acquired human infection have not been established. The historical human cases were associated with laboratory exposure.

Incubation period

Not established for naturally acquired infection. The small number of historical occupational cases does not permit a reliable general incubation estimate.

Disease in humans

The four reported occupational infections ranged from a mild febrile illness to prolonged systemic disease with fever, headache, myalgia, arthralgia, abdominal symptoms, nausea, diarrhea, chest pain and cough; neurologic hyperreflexia was reported in some patients. No population-based clinical spectrum is available.

Disease in animals—by species

Egyptian rousette bats: naturally infected bats have yielded KASV; available evidence indicates infection may occur without obvious clinical disease. Disease in other naturally infected animal species has not been adequately defined.

Pathology

Human and naturally occurring animal pathology is insufficiently characterized to provide a reliable lesion profile. Findings from experimental research should not be assumed to represent naturally occurring clinical disease.

Human diagnosis

No routine clinical diagnostic pathway is established. A suspected case should prompt infectious-disease and public-health consultation, detailed exposure history, and referral to an appropriate specialized public-health/reference laboratory using validated methods.

Animal diagnosis

No routine veterinary clinical test is established. Suspected infection associated with bat or tick investigations should be coordinated with wildlife/public-health authorities and specialized reference laboratories rather than routine practice testing.

Differential diagnoses

Other acute febrile illnesses relevant to geography and exposure, including malaria, arboviral and tickborne infections, leptospirosis, rickettsioses and other bat-associated zoonoses. Differential diagnosis should be driven by travel, cave/bat/tick exposure and clinical syndrome.

Treatment in humans

No virus-specific therapy has been established. Management is supportive and should involve infectious-disease specialists for significant illness. Treatment recommendations cannot be extrapolated reliably from other orthonairoviruses without expert guidance.

Treatment in animals—by species

No specific veterinary treatment is established or indicated for apparently healthy wild reservoir hosts. Wildlife should not be treated empirically for KASV.

Animal and environmental control

Avoid unnecessary disturbance of bat colonies and control human exposure to bat-roost-associated ticks. Wildlife, occupational and public-health authorities should coordinate investigations. Routine destruction of bat colonies is not recommended as a public-health response.

Prevention in humans

People entering bat caves, mines or dense rousette roosts should minimize direct contact with bats and bat-associated arthropods and use risk-appropriate protective measures. Bites, scratches or significant exposures should receive prompt medical evaluation based on the full zoonotic differential.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

No licensed animal vaccine is available.

Prognosis

Too few human cases have been described to define prognosis. Historical cases ranged from mild to prolonged severe illness. The clinical significance of infection in reservoir bats appears limited based on available observations.

Reporting, legal, and regulatory considerations

KASV is an emerging zoonotic virus without a routine U.S. case-reporting framework specific to KASV. Suspected human infection should nevertheless be discussed promptly with local/state public health authorities because specialized testing and investigation would be required.

Selected current sources

• CDC Emerging Infectious Diseases—Human-Pathogenic Kasokero Virus in Field-Collected Ticks
• Scientific Reports/PubMed—Egyptian rousette bat host model and zoonotic spillover mechanisms
• American Journal of Tropical Medicine and Hygiene/PubMed—Original human infections

LEISHMANIASIS

Synonyms and scope

Leishmaniasis includes cutaneous, mucosal/mucocutaneous and visceral disease (kala-azar). Historical regional names include oriental sore, Aleppo boil, chiclero ulcer, espundia and uta.

Etiologic agent

Protozoan parasites of the genus Leishmania. Species and geographic origin strongly influence clinical form, reservoir ecology and treatment.

Animals involved and epidemiologic roles

Dogs: major domestic reservoir for zoonotic visceral leishmaniasis caused by L. infantum in many endemic regions. Wild mammals and rodents: reservoirs for various species. Humans: reservoir hosts in some anthroponotic transmission cycles. Sand flies: biological vectors.

Geographic distribution and occurrence

Endemic in parts of the tropics, subtropics and southern Europe, with transmission patterns varying by species. U.S. cases are commonly travel-associated, although competent vectors and enzootic transmission occur in parts of the Americas.

Reservoir, life cycle, and transmission

Infected female phlebotomine sand flies transmit parasites while blood feeding. Reservoirs vary among parasite species and regions. Less common human transmission routes include congenital transmission, contaminated needles and transfusion.

Incubation period

Variable. Cutaneous lesions may appear weeks to months after infection; visceral disease commonly develops over months and may occasionally present much later.

Disease in humans

Cutaneous disease produces one or more papules, nodules or ulcers, often with raised borders, and can scar. Mucosal disease may involve the nose, mouth or pharynx and can be destructive. Visceral disease causes prolonged fever, weight loss, hepatosplenomegaly, cytopenias and can be fatal without treatment.

Disease in animals—by species

Dogs: L. infantum infection ranges from subclinical to chronic systemic disease with lymphadenopathy, weight loss, dermatologic lesions, ocular disease, epistaxis, renal disease and other manifestations. Wild mammals/rodents: infection is often subclinical but varies by host and species.

Pathology

Cutaneous disease produces chronic granulomatous inflammation. Visceral disease involves the mononuclear-phagocyte system, especially spleen, liver, bone marrow and lymph nodes. Canine disease commonly involves skin, lymphoid tissues and kidneys.

Human diagnosis

Diagnosis integrates exposure/geography and clinical form with demonstration of the parasite or parasite DNA in appropriate clinical specimens; serology can support visceral disease but is less useful for some cutaneous infections. Species identification can guide prognosis and therapy.

Animal diagnosis

Canine diagnosis requires compatible clinical findings plus appropriate serology, cytology/histopathology and/or molecular testing interpreted in the context of endemicity and vaccination history where relevant. Subclinical infection is common in endemic areas.

Differential diagnoses

Cutaneous ulcers from bacterial, fungal, mycobacterial, neoplastic and inflammatory causes; mucosal infections and malignancy; visceral disease differentials include malaria, typhoid, brucellosis, tuberculosis, lymphoma and other causes of fever with splenomegaly.

Treatment in humans

Treatment is individualized by clinical form, Leishmania species, acquisition region and host factors. In the United States, liposomal amphotericin B is generally preferred for visceral leishmaniasis. Miltefosine is FDA-approved for selected species/forms in eligible patients. Expert consultation is recommended.

Treatment in animals—by species

Dogs: treatment may improve clinical disease but usually does not reliably eliminate infection; protocols vary by country and drug availability and may include antileishmanial therapy plus management of renal/other complications. Treatment decisions should consider local regulations and public-health implications.

Animal and environmental control

Integrated control emphasizes sand-fly control, reducing vector exposure, surveillance and locally appropriate reservoir management. Infected dogs should receive veterinary management and vector protection; indiscriminate dog removal is not an adequate stand-alone control strategy.

Prevention in humans

Prevent sand-fly bites with protective clothing, EPA-registered repellents, screened/air-conditioned lodging and appropriately selected fine-mesh bed nets in endemic areas. There is no routinely recommended preventive drug for travelers.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

Canine vaccines are licensed in some countries but are not universally available and do not replace vector prevention or testing/control programs. Product availability and recommendations are jurisdiction-specific.

Prognosis

Localized cutaneous disease may heal but can scar or relapse. Mucosal disease can cause major morbidity. Untreated visceral leishmaniasis can be fatal; prognosis improves substantially with appropriate therapy. Canine infection is generally chronic and relapses can occur.

Reporting, legal, and regulatory considerations

Human reporting requirements vary by jurisdiction. Imported or unusual cases should be discussed with public-health authorities when indicated. Animal importation, testing and control requirements vary, particularly for dogs from endemic regions.

Selected current sources

• CDC—Clinical Overview of Leishmaniasis
• CDC—Clinical Care of Leishmaniasis
• CDC—Preventing Leishmaniasis

LEPROSY

Synonyms and scope

Hansen disease (Hansen’s disease). A chronic infection affecting skin, peripheral nerves, eyes and upper respiratory mucosa.

Etiologic agent

Primarily Mycobacterium leprae; Mycobacterium lepromatosis also causes Hansen disease. These are slow-growing obligate intracellular bacteria.

Animals involved and epidemiologic roles

Humans: principal recognized source in most transmission settings. Nine-banded armadillos: naturally infected in parts of the southern United States and can rarely transmit infection to people. Natural infection has also been reported in some nonhuman primates and red squirrels, but their public-health role is geographically limited.

Geographic distribution and occurrence

Occurs in more than 120 countries, with most new cases in endemic tropical/subtropical regions. U.S. cases are uncommon; many are associated with prior residence in endemic areas, while some southern U.S. cases have epidemiologic or molecular links to armadillos.

Reservoir, life cycle, and transmission

Human-to-human transmission is believed to require prolonged, close, repeated exposure to respiratory droplets from an untreated person. Casual contact does not spread leprosy. Zoonotic transmission from naturally infected armadillos is possible but uncommon.

Incubation period

Usually prolonged: symptoms may appear within a year but can take 5 years or substantially longer; WHO notes that incubation can extend to 20 years or more.

Disease in humans

Clinical disease spans paucibacillary to multibacillary forms. Key findings include hypopigmented or erythematous skin lesions with sensory loss, peripheral nerve enlargement/dysfunction, weakness, neuropathic injury, ocular involvement and, in multibacillary disease, diffuse/nodular skin and mucosal disease. Immune reactions can cause acute nerve injury.

Disease in animals—by species

Armadillos: natural infection may be systemic and resemble multibacillary disease, although many infected animals are not recognized clinically. Other naturally infected wildlife species have variable manifestations. Leprosy is not a common clinical disease of household pets.

Pathology

Granulomatous inflammation of skin and peripheral nerves is characteristic. Bacillary burden varies with host cellular immunity; multibacillary disease can involve skin, nerves, upper-airway mucosa, eyes and other tissues.

Human diagnosis

Diagnosis is primarily clinical, supported when needed by skin or nerve biopsy and organism-specific testing. Cardinal findings include sensory loss in a characteristic skin lesion, thickened peripheral nerve with sensory/motor deficit, or demonstration of acid-fast bacilli in appropriate specimens.

Animal diagnosis

Routine veterinary testing of healthy pets is not indicated. Suspected naturally occurring disease in wildlife or unusual species should be evaluated with wildlife/public-health specialists and appropriate reference pathology/testing.

Differential diagnoses

Peripheral neuropathies, vitiligo and other pigment disorders, dermatophytosis, sarcoidosis, cutaneous tuberculosis/atypical mycobacterial disease, syphilis and other causes of chronic skin lesions with sensory or nerve abnormalities.

Treatment in humans

Leprosy is curable with multidrug therapy. WHO recommends rifampicin, dapsone and clofazimine, with duration based on paucibacillary versus multibacillary classification. U.S. patients should be managed with the National Hansen’s Disease Program or experienced specialists; reactions and neuropathy may require additional treatment.

Treatment in animals—by species

No routine treatment program is indicated for wildlife reservoirs. Management of a suspected animal case should be coordinated with wildlife/public-health experts rather than extrapolated from human multidrug therapy.

Animal and environmental control

Public-health control centers on early human diagnosis and effective treatment, contact evaluation and locally recommended prophylaxis. There is no rationale for broad wildlife eradication. Avoid handling wild armadillos unnecessarily.

Prevention in humans

Avoid prolonged close exposure to untreated human cases and direct contact with wild armadillos, particularly handling or consuming armadillo meat. People with concerning skin lesions or sensory changes should seek medical evaluation. Treated patients are not considered infectious once effective therapy begins.

Human vaccination

No leprosy-specific vaccine is licensed. BCG vaccination provides partial protection in some populations and is incorporated into control strategies in certain countries, but it is not a dedicated leprosy vaccine.

Animal vaccination

No licensed animal vaccine is used for leprosy prevention.

Prognosis

Curable with appropriate multidrug therapy. Early treatment limits nerve damage and disability; established neuropathy and deformity may be permanent. Social stigma remains an important avoidable source of harm.

Reporting, legal, and regulatory considerations

Human reporting requirements vary by country and U.S. jurisdiction. U.S. clinicians can consult the National Hansen’s Disease Program. Animal/wildlife findings of suspected zoonotic significance should be coordinated with appropriate public-health and wildlife agencies.

Selected current sources

• WHO—Leprosy Fact Sheet
• CDC—About Leprosy
• CDC—Clinical Overview of Leprosy

LEPTOSPIROSIS

Synonyms and scope

Leptospirosis; severe icteric disease is historically termed Weil disease. A globally important bacterial zoonosis affecting people and many domestic and wild animals.

Etiologic agent

Pathogenic spirochetes in the genus Leptospira, comprising numerous species and more than 300 pathogenic serovars.

Animals involved and epidemiologic roles

Rodents and wildlife: important maintenance hosts. Dogs, cattle, pigs, horses, sheep and goats: susceptible hosts and, depending on serovar, potential maintenance/shedding hosts. Marine mammals: important in some ecosystems. Cats: infection occurs but clinical disease is less common.

Geographic distribution and occurrence

Worldwide, particularly common in tropical/subtropical climates and after heavy rainfall or flooding. Infection occurs throughout the United States.

Reservoir, life cycle, and transmission

Infected animals shed leptospires in urine, contaminating water and moist soil. Infection follows contact of mucous membranes or damaged skin with infected urine, tissues or contaminated water/soil. Maintenance hosts may shed organisms for prolonged periods.

Incubation period

Human incubation is usually 5–14 days, with a reported range of approximately 2–30 days.

Disease in humans

Illness ranges from asymptomatic infection to acute fever, headache, severe myalgia, conjunctival suffusion, nausea/vomiting, diarrhea and rash. Severe disease may cause jaundice, acute kidney injury, hemorrhage, meningitis, pulmonary hemorrhage/respiratory failure, shock and multiorgan failure.

Disease in animals—by species

Dogs: acute kidney injury, hepatic injury, fever, lethargy, vomiting, dehydration and altered urination; pulmonary hemorrhagic disease can occur. Cattle/pigs/small ruminants: reproductive loss, infertility, weak offspring and occasionally systemic disease. Horses: recurrent uveitis, reproductive loss and renal disease. Cats: often subclinical. Marine mammals: renal disease is important.

Pathology

Lesions reflect vasculitis/endothelial injury and organ involvement, especially kidneys and liver; interstitial nephritis, hepatic dysfunction and pulmonary hemorrhage may occur. Reproductive tissues may be affected in livestock.

Human diagnosis

Diagnosis combines compatible exposure and illness with validated molecular testing and/or serology, interpreted according to illness timing. Treatment should not be delayed when clinical suspicion is high.

Animal diagnosis

Animal diagnosis integrates clinical syndrome, vaccination history and exposure with PCR and serology interpreted by species and timing. Paired serology can help distinguish acute infection; vaccination and endemic exposure complicate interpretation.

Differential diagnoses

Influenza and other febrile illnesses, hantavirus disease, dengue and other arboviruses, rickettsial disease, hepatitis, pyelonephritis, immune-mediated disease, toxin exposure and other causes of acute kidney/liver injury. In dogs, consider other infectious and toxic causes of AKI.

Treatment in humans

Early antibiotics are recommended. CDC lists doxycycline for mild disease when appropriate, with alternatives including azithromycin, ampicillin or amoxicillin; severe disease is treated with IV penicillin or ceftriaxone plus organ-supportive care. Do not wait for laboratory confirmation when suspicion is high.

Treatment in animals—by species

Dogs: prompt antimicrobial therapy and aggressive supportive care for renal/hepatic disease; dialysis may be lifesaving when available. Livestock/horses: antimicrobial treatment and herd-level management depend on species, serovar and production context. Veterinary therapy should also address urinary shedding and zoonotic precautions.

Animal and environmental control

Vaccinate susceptible domestic species where indicated, control rodents, restrict access to stagnant/contaminated water, manage livestock reproductive disease, separate clinically affected animals and use urine precautions during treatment. Environmental risk rises after flooding.

Prevention in humans

Avoid contact with potentially contaminated floodwater, freshwater, soil and animal urine; cover skin wounds and use protective footwear/gloves for occupational or cleanup exposure. Use appropriate PPE when caring for suspect animals and perform careful hand hygiene.

Human vaccination

No routinely available human leptospirosis vaccine is licensed in the United States; vaccines are used in selected countries or occupational programs.

Animal vaccination

Vaccines are available in the United States for dogs, horses, cattle, sheep, goats and pigs. Vaccines are serovar-specific and do not provide complete protection; recommended products and schedules depend on species and risk.

Prognosis

Most treated human cases recover, but severe pulmonary, renal or multiorgan disease can be fatal. Early veterinary treatment improves outcome, although permanent organ damage may occur. Reproductive losses can be substantial in livestock.

Reporting, legal, and regulatory considerations

Human leptospirosis is nationally notifiable in the United States. Animal reporting requirements vary by jurisdiction and species. Suspected outbreaks associated with flooding, occupational exposure, livestock or clusters of human/animal illness warrant public-health and animal-health coordination.

Selected current sources

• CDC—Clinical Overview of Leptospirosis
• CDC—Leptospirosis in Animals
• CDC—About Leptospirosis

LISTERIOSIS

Synonyms and scope

Listeriosis; infection with Listeria monocytogenes. Human disease is primarily foodborne, while animal listeriosis is also associated with contaminated feed and environmental exposure.

Etiologic agent

Listeria monocytogenes, a gram-positive facultatively intracellular bacterium widely present in soil, water, decaying vegetation and food-production environments.

Animals involved and epidemiologic roles

Ruminants: cattle, sheep and goats are important veterinary hosts and may develop encephalitis, abortion or septicemia. Other mammals and birds: infection occurs sporadically. Humans: most disease results from contaminated food rather than direct animal contact.

Geographic distribution and occurrence

Worldwide. Sporadic disease and foodborne outbreaks occur in many countries. The organism is environmentally widespread and can persist in food-processing environments.

Reservoir, life cycle, and transmission

People are infected predominantly by eating contaminated ready-to-eat or refrigerated foods. Pregnant people can transmit infection to the fetus/newborn. Direct zoonotic transmission is uncommon but exposure to infected fetal tissues, placenta and uterine discharges from livestock can pose occupational risk. Ruminant disease is often associated with poor-quality silage.

Incubation period

Invasive human listeriosis commonly develops within days to several weeks after exposure; pregnancy-associated disease can have a longer recognized exposure window. Acute febrile gastroenteritis generally has a shorter incubation.

Disease in humans

Healthy people may develop self-limited febrile gastroenteritis. Invasive listeriosis primarily affects pregnant people/newborns, adults 65 years and older and immunocompromised persons, causing sepsis, meningitis or meningoencephalitis. Pregnancy may cause mild maternal illness but fetal loss, preterm delivery or neonatal infection.

Disease in animals—by species

Ruminants: encephalitis/meningoencephalitis (“circling disease”), abortion, stillbirth, neonatal septicemia, mastitis and occasionally septicemia. Other species: sporadic septicemic, neurologic or reproductive disease can occur.

Pathology

Neurologic ruminant disease characteristically produces microabscesses and inflammation in the brainstem. Septicemia causes multifocal organ lesions. Placental/fetal infection can produce necrotizing placentitis and fetal lesions.

Human diagnosis

Invasive disease is diagnosed from appropriate normally sterile clinical specimens using routine validated clinical microbiology methods. Exposure history and pregnancy/immunocompromise are important. Routine stool testing is not useful for diagnosing invasive listeriosis.

Animal diagnosis

Animal diagnosis is based on compatible neurologic, reproductive or septicemic disease with appropriate pathology and laboratory confirmation from clinical tissues/specimens. Feed history, especially silage quality in ruminants, is important.

Differential diagnoses

Human meningitis/sepsis from other bacteria; pregnancy-associated infections; gastroenteritis from other foodborne pathogens. In ruminants: rabies, polioencephalomalacia, thromboembolic meningoencephalitis, otitis-associated neurologic disease, pregnancy toxemia and other infectious causes of abortion.

Treatment in humans

Invasive human listeriosis requires antimicrobial therapy; ampicillin is commonly first-line, often with specialist-directed consideration of gentamicin in selected severe cases. Trimethoprim-sulfamethoxazole is an important alternative when beta-lactams cannot be used. Supportive care is guided by sepsis/CNS disease.

Treatment in animals—by species

Ruminants: early antimicrobial treatment can be effective, particularly before severe neurologic dysfunction; supportive care is important. Abortion outbreaks require herd/flock evaluation, feed correction and biosecurity. Treatment protocols should be selected by the attending veterinarian.

Animal and environmental control

Discard spoiled or poorly fermented silage, improve feed storage, separate clinically affected/aborting animals, safely manage placentas/fetuses and contaminated bedding, and clean contaminated areas. Food-industry control depends on sanitation, temperature control and regulatory food-safety programs.

Prevention in humans

People at increased risk should follow CDC food-safety recommendations, including avoiding high-risk refrigerated ready-to-eat foods unless appropriately heated and choosing pasteurized dairy products. Wear gloves and use careful hygiene when handling aborted livestock fetuses, placentas and uterine discharges.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

No broadly used licensed animal vaccine is relied upon for listeriosis control in the United States; prevention centers on feed quality and management.

Prognosis

Invasive human listeriosis is serious: nearly all recognized invasive cases require hospitalization and CDC estimates case fatality around 20%; pregnancy-associated infection can cause fetal/neonatal loss. Early-treated animal cases may recover, but advanced neurologic disease has a guarded prognosis.

Reporting, legal, and regulatory considerations

Human listeriosis is nationally notifiable in the United States and foodborne clusters require rapid public-health investigation. Animal reporting requirements vary. Suspected food/feed-associated clusters or occupationally linked human and livestock cases warrant coordinated public-health, veterinary and food-safety investigation.

Selected current sources

• CDC—Clinical Overview of Listeriosis
• CDC—About Listeria Infection
• CDC—Preventing Listeria Infection

LYME DISEASE

Synonyms and scope

Lyme borreliosis; Lyme disease. A tick-borne bacterial zoonosis of people and several animal species. Animals do not ordinarily transmit Lyme disease directly to people; infected Ixodes ticks link wildlife reservoirs, domestic animals, and humans.

Etiologic agent

Lyme borreliosis is caused by pathogenic members of the Borrelia burgdorferi sensu lato complex. B. burgdorferi sensu stricto causes essentially all locally acquired human Lyme disease in the United States; additional genospecies are important in Europe and Asia.

Animals involved and epidemiologic roles

Small mammals and some birds maintain enzootic transmission by infecting feeding ticks. White-footed mice are important reservoir hosts in much of eastern North America. Deer are important hosts for adult Ixodes ticks but are not considered important reservoirs for B. burgdorferi. Dogs and horses are frequently exposed and may develop clinical disease; cats can be infected but recognized clinical disease is uncommon. Pets may carry unattached ticks into human environments but are not the usual direct source of human infection.

Geographic distribution and occurrence

Lyme borreliosis occurs in temperate regions of North America, Europe, and Asia where competent Ixodes vectors and reservoir hosts coexist. In the United States, human disease is concentrated in the Northeast, mid-Atlantic, and upper Midwest, with additional transmission along the Pacific Coast. Geographic risk changes as tick ranges expand.

Reservoir, life cycle, and transmission

Immature ticks acquire Borrelia while feeding on infected reservoir hosts and may transmit infection during later blood meals. In the United States the principal vectors are Ixodes scapularis in the East and upper Midwest and I. pacificus in the West. Risk increases with duration of tick attachment. Lyme disease is not spread to people by ordinary contact with infected dogs, cats, or horses.

Incubation period

In people, erythema migrans and early systemic manifestations generally begin days to weeks after an infectious tick bite. In dogs, clinical illness attributed to Lyme borreliosis commonly appears weeks after infection. Timing varies with manifestation and host.

Disease in humans

Early disease may cause erythema migrans, fever, chills, headache, fatigue, myalgia, arthralgia, and lymphadenopathy. Untreated infection can disseminate and cause facial palsy or other neurologic disease, Lyme carditis, and arthritis. Most appropriately treated patients recover; some have prolonged fatigue, pain, or cognitive symptoms after recommended therapy, for which additional prolonged antibiotics have not been shown to provide benefit.

Disease in animals—by species

Dogs: Most exposed dogs remain clinically normal. Recognized disease most often causes fever, lethargy, anorexia, lymphadenopathy, painful joints, and intermittent or shifting-leg lameness. A severe protein-losing nephropathy has been associated with Lyme disease but is uncommon. Horses: Most seropositive horses are asymptomatic; well-supported manifestations include neuroborreliosis, uveitis, nuchal bursitis, and cutaneous pseudolymphoma. Cats: Infection occurs, but naturally occurring clinical disease is rarely documented. Wildlife primarily supports the tick–reservoir cycle.

Pathology

Pathologic changes vary with organ involvement. Synovitis may accompany arthritis; carditis and inflammatory neurologic lesions occur in disseminated human disease. In dogs with suspected Lyme-associated nephropathy, severe protein-losing glomerular disease may occur.

Human diagnosis

Erythema migrans in a person with compatible epidemiologic exposure is primarily a clinical diagnosis and treatment should not be delayed for early serology. When laboratory testing is indicated, CDC recommends FDA-cleared two-step serologic testing. Antibody tests can be negative early and may remain positive for years after infection, so seropositivity alone does not prove active disease or treatment failure.

Animal diagnosis

Diagnosis requires compatible clinical signs, plausible tick exposure, supportive testing, and exclusion of other causes. Because many healthy dogs and horses in endemic areas are seropositive, a positive antibody test demonstrates exposure but does not by itself establish that current illness is caused by Lyme borreliosis. Evaluate clinically ill animals for coinfections and organ-specific abnormalities, including proteinuria when appropriate.

Differential diagnoses

Consider other tick-borne infections such as anaplasmosis, ehrlichiosis, babesiosis, and rickettsial disease; immune-mediated polyarthritis; septic arthritis; orthopedic disease; other causes of facial paralysis, meningitis/radiculitis, carditis, and arthritis in people; and other renal, neurologic, ocular, or musculoskeletal disorders in animals.

Treatment in humans

Early diagnosis and guideline-directed antibiotic therapy are highly effective. Common agents include doxycycline, amoxicillin, and cefuroxime axetil, with drug, route, and duration selected according to manifestation, age, pregnancy status, allergies, and other patient factors. Neurologic disease, carditis, and arthritis require manifestation-specific regimens. Persistent nonspecific symptoms after recommended treatment should prompt clinical reassessment rather than automatic prolonged antibiotic therapy.

Treatment in animals—by species

Clinically affected dogs are commonly treated with an approximately 4-week antimicrobial course; doxycycline is frequently first-line, with alternatives selected according to patient factors. Supportive treatment is directed to pain, renal disease, or other organ involvement. Equine treatment likewise uses prolonged appropriate antimicrobial therapy selected by the veterinarian; neuroborreliosis may require different drug selection and intensive supportive care. Routine antimicrobial treatment of healthy seropositive animals is controversial because exposure does not equal clinical disease.

Animal and environmental control

Use veterinarian-recommended tick preventives consistently, check animals for ticks after exposure, remove attached ticks promptly, and reduce tick habitat around homes and animal areas. Keep grass and brush controlled and reduce leaf litter where practical. Pets should be checked before entering living areas because unattached ticks can be carried indoors.

Prevention in humans

Avoid tick-infested brush and tall vegetation when possible; use EPA-registered repellents and appropriately treated clothing; perform body, clothing, gear, and pet tick checks; shower after outdoor exposure; and remove attached ticks promptly. In selected high-risk tick bites, a clinician may recommend single-dose doxycycline prophylaxis when established criteria are met.

Human vaccination

No Lyme disease vaccine is currently licensed for people in the United States as of 2026. New human vaccine candidates are in clinical development.

Animal vaccination

Several Lyme vaccines are licensed for dogs. Vaccination is noncore and should be based on geographic and lifestyle risk. Vaccination does not replace effective tick prevention and does not protect people from ticks. No routinely recommended Lyme vaccine is established for cats or horses in the United States.

Prognosis

Most people treated appropriately, particularly early, recover completely. Delayed treatment can permit neurologic, cardiac, or arthritic complications. Dogs with uncomplicated febrile/arthritic disease often respond rapidly, whereas severe protein-losing nephropathy carries a guarded to poor prognosis. Prognosis for equine neurologic disease varies with severity and timing of treatment.

Reporting, legal, and regulatory considerations

Human Lyme disease is nationally notifiable in the United States, with case reporting handled through state and local public-health systems. Animal Lyme disease reporting requirements vary by jurisdiction. Surveillance data should be interpreted separately from individual clinical diagnosis.

Selected current sources

• CDC—Clinical Care of Lyme Disease
• CDC—Preventing Lyme Disease
• CDC—Lyme Disease Vaccine
• Merck Veterinary Manual—Lyme Borreliosis in Animals

LYMPHOCYTIC CHORIOMENINGITIS - LCM

Synonyms and scope

Lymphocytic choriomeningitis (LCM); LCMV infection. A rodent-associated viral zoonosis of particular importance during pregnancy and in immunocompromised people.

Etiologic agent

Lymphocytic choriomeningitis virus (LCMV), an enveloped RNA virus in the family Arenaviridae, genus Mammarenavirus.

Animals involved and epidemiologic roles

The common house mouse (Mus musculus) is the principal natural reservoir and can remain persistently infected without obvious illness. Hamsters and other pet, feeder, or captive rodents—including guinea pigs, rats, and mice—can become infected after exposure to infected mice or contaminated rodent populations. Humans are accidental hosts.

Geographic distribution and occurrence

LCMV has a worldwide distribution associated with house mice and has been reported in Europe, the Americas, Australia, and Japan. Human disease is probably underrecognized. Risk is determined more by exposure to infected rodents than by a narrow geographic boundary.

Reservoir, life cycle, and transmission

Persistently infected house mice shed virus in urine, feces, saliva, and other secretions. People are infected through direct or indirect exposure of mucous membranes or broken skin to contaminated rodent material, inhalation of contaminated particles, or occasionally bites. Pet rodents can serve as a bridge when infected by wild mice or within an affected breeding/supply population. Person-to-person spread has not been documented except transplacental transmission and rare transmission through organ transplantation.

Incubation period

Human symptoms usually begin approximately 8–13 days after infection, although clinical timing can vary.

Disease in humans

Most infections are asymptomatic or mild. Symptomatic disease may begin with fever, malaise, anorexia, myalgia, headache, nausea, and vomiting. Some patients improve and then develop a second neurologic phase with aseptic meningitis, encephalitis, or meningoencephalitis. Congenital infection can cause miscarriage, hydrocephalus, intracranial calcifications, chorioretinitis, visual impairment, and long-term neurologic disability. Immunocompromised patients, particularly transplant recipients, can develop severe multisystem disease.

Disease in animals—by species

House mice: Commonly persistently infected and clinically normal; disease expression depends on age, immune status, and timing of infection. Hamsters: May remain infected or develop wasting, decreased activity and appetite, unkempt coat, weight loss, hunched posture, blepharitis, neurologic signs, and death. Other rodents: Rats, guinea pigs, and other rodents can be infected, particularly after contact with wild mice or infected rodent populations; clinical expression varies.

Pathology

Human neurologic disease is characterized by inflammatory involvement of the meninges and sometimes brain or spinal cord. Congenital infection may produce hydrocephalus, periventricular calcification, and chorioretinal lesions. Persistently infected rodents can develop immune-mediated lesions, including glomerular disease, depending on host and infection pattern.

Human diagnosis

Diagnosis should be considered when compatible febrile or neurologic illness follows rodent exposure, and in unexplained congenital hydrocephalus/chorioretinitis or severe illness in transplant recipients. Clinical laboratories and public-health authorities can guide appropriate validated serologic or molecular testing. Routine testing of asymptomatic people is not generally used as population screening.

Animal diagnosis

Suspected infection in pet, breeding, feeder, or research-associated rodents should be evaluated with a veterinarian and, when human exposure is possible, public-health professionals. Validated testing can identify infection or exposure; interpretation depends on species, population history, and purpose of testing. Avoid unnecessary handling of suspect rodents and their excreta.

Differential diagnoses

In people consider other viral meningitides/encephalitides, bacterial meningitis, influenza-like infections, arboviral disease, and other congenital infections that cause hydrocephalus or chorioretinitis. In rodents consider other infectious, nutritional, neoplastic, and husbandry-related causes of wasting, neurologic signs, or reproductive loss.

Treatment in humans

No specific antiviral therapy has established efficacy for routine LCM. Management is supportive; patients with meningitis, encephalitis, severe systemic disease, pregnancy-associated infection, or immunosuppression require specialist assessment and may need hospitalization. Ribavirin has been considered in severe cases, but evidence is insufficient to support routine use and decisions should involve infectious-disease experts.

Treatment in animals—by species

There is no established curative treatment that reliably eliminates LCMV carriage from infected reservoir rodents. For an individual pet rodent, management decisions should be made with a veterinarian and public-health guidance, especially when pregnant or immunocompromised people may have been exposed. Population-control decisions should prioritize prevention of human exposure rather than attempts to medically clear infected colonies.

Animal and environmental control

Prevent wild-mouse access to homes, animal rooms, food, bedding, and pet-rodent housing. Store feed securely, exclude rodents, and clean contaminated areas using public-health rodent-cleanup guidance rather than dry sweeping or vacuuming fresh droppings. Suspected infected rodent populations should be managed with veterinary/public-health guidance to prevent spread to other animals and people.

Prevention in humans

Avoid contact with wild mice and their urine, feces, saliva, nesting material, and contaminated dust. Wash hands after handling pet rodents or their supplies and keep pet-rodent environments protected from wild mice. Pregnant people should avoid handling wild rodents and should have another person manage pet-rodent cage cleaning and rodent infestations. Immunocompromised people should discuss rodent exposure risk with their healthcare team.

Human vaccination

No licensed human vaccine is available for LCMV.

Animal vaccination

No licensed LCMV vaccine is routinely available for pet rodents. Prevention depends on biosecurity, wild-rodent exclusion, and sourcing/management practices.

Prognosis

Most immunocompetent people recover and overall mortality is low, although neurologic sequelae can occur. Prognosis is substantially worse in severely immunocompromised patients. Fetal infection can cause pregnancy loss, severe congenital neurologic/ocular disease, or lifelong disability. Prognosis in infected rodents depends on species, age at infection, and immune response.

Reporting, legal, and regulatory considerations

LCM is not uniformly reportable in all jurisdictions. Severe human cases, congenital infections, transplant-associated infections, clusters, or infections linked to commercial pet/feeder-rodent distribution warrant prompt consultation with local or state public-health authorities. Animal reporting requirements vary by jurisdiction and setting.

Selected current sources

• CDC—About Lymphocytic Choriomeningitis
• CDC—LCM Training for Healthcare Providers
• Merck Veterinary Manual—Zoonotic Diseases
• Merck Veterinary Manual—Hamsters: Zoonotic Risk