Zoonotic Diseases — M–R

CHLAMYDIA ABORTUS

Synonyms and scope

Enzootic abortion of ewes (EAE); ovine enzootic abortion (OEA); chlamydial abortion. This is an important reproductive disease of sheep and goats and an uncommon but potentially severe zoonosis. Human risk is concentrated around infected placentas, aborted fetuses, uterine/vaginal discharges, contaminated bedding, and lambing or kidding environments; pregnancy greatly increases the consequences of infection.

Etiologic agent

Chlamydia abortus, an obligate intracellular bacterium. Older literature may use Chlamydophila abortus or classify the organism within Chlamydia psittaci. It is distinct from avian C. psittaci, which causes psittacosis.

Animals involved and epidemiologic roles

• Sheep: Principal reservoir and major host; infection commonly causes late-term abortion, stillbirth, or weak lambs.
• Goats: Important reservoir and clinical host; abortion outbreaks can be severe in naive herds.
• Cattle and other mammals: Sporadic infection and reproductive disease occur, but they are less important reservoirs than sheep and goats.
• People: Accidental hosts, with the greatest recognized risk in pregnant people exposed to infected birth products.

Geographic distribution and occurrence

Reported in many sheep- and goat-raising regions worldwide. Enzootic abortion is especially important in Europe and is also recognized in North America and other regions. Human infection is rare relative to the frequency of animal disease, but occupational and farm-family exposures occur.

Reservoir, life cycle, and transmission

Infected small ruminants can remain persistently infected and may shed large numbers of organisms around abortion or parturition. Exposure occurs mainly through contaminated placentas, fetal tissues, uterine or vaginal discharges, bedding, clothing, footwear, and dust or aerosols from lambing or kidding areas. Animal-to-animal spread is primarily associated with contaminated birth materials and environments. Human infection follows close contact or inhalation of contaminated material rather than ordinary casual contact with healthy animals.

Incubation period

The incubation period in people is not precisely defined because recognized cases are uncommon and exposure may be repeated. Illness after livestock exposure can develop over days to several weeks. In animals, infection acquired during one breeding season may not become apparent until placental infection and abortion late in a subsequent pregnancy.

Disease in humans

Human infection can cause fever, severe influenza-like illness, pneumonia, hepatitis, sepsis, and other systemic manifestations. Infection during pregnancy can cause placentitis, miscarriage, stillbirth, premature delivery, disseminated maternal illness, and rarely maternal death. Nonpregnant infections have been reported but are much less common.

Disease in animals—by species

• Sheep: Abortion typically occurs during the final 2–3 weeks of gestation; stillborn or weak lambs may be delivered. Dams may appear otherwise well.
• Goats: Late-term abortion, stillbirth, weak kids, retained placenta, and occasionally systemic or respiratory disease.
• Cattle: Sporadic placentitis and late-gestation abortion can occur.
• Neonates: Lambs or kids born alive after infected pregnancies may be weak and can occasionally develop pneumonia.

Pathology

Necrotizing placentitis is characteristic, with thickened, inflamed cotyledons and abnormal intercotyledonary tissue often covered by exudate. Fetal lesions may be mild or absent; when present they can include hepatitis, pneumonia, or lymphoid changes. In human pregnancy, placental inflammation and fetal compromise are central features of severe disease.

Human diagnosis

Diagnosis requires a compatible livestock exposure plus clinician- and public-health-directed laboratory testing. Molecular detection and serologic testing may be used depending on timing and specimen availability. Because illness can resemble influenza, pneumonia, Q fever, listeriosis, or other causes of pregnancy loss, the animal-exposure history should be communicated promptly.

Animal diagnosis

Submit placenta and appropriate fetal tissues through a veterinary diagnostic laboratory. PCR, immunohistochemistry or fluorescent-antibody methods, and serology may support diagnosis. Placenta is especially important because infection is concentrated there. Interpretation should distinguish C. abortus from other causes of small-ruminant abortion such as Coxiella burnetii, Campylobacter, Toxoplasma gondii, Listeria, and Salmonella.

Differential diagnoses

Q fever, campylobacteriosis, toxoplasmosis, listeriosis, salmonellosis, brucellosis, border disease, Cache Valley virus, nutritional or toxic causes of abortion, and other causes of febrile illness or pregnancy loss in exposed people.

Treatment in humans

Suspected human infection requires prompt physician and infectious-disease assessment, particularly during pregnancy. Treatment is antibiotic-based and must account for pregnancy status, disease severity, and current specialist guidance. Severe maternal disease may require hospitalization and obstetric monitoring.

Treatment in animals—by species

Veterinary management is flock- or herd-based. Tetracycline-class antimicrobials are used in some outbreak-control programs, but treatment does not reliably eliminate persistent infection. Management must also address isolation, reproductive losses, biosecurity, and region-specific drug-use rules.

Animal and environmental control

Immediately isolate aborting animals. Remove placentas, aborted fetuses, and heavily contaminated bedding using appropriate protective equipment; clean and disinfect contaminated lambing or kidding areas and equipment; and prevent dogs, cats, wildlife, or other livestock from scavenging birth materials. Manage affected groups with veterinary oversight and consider vaccination where available.

Prevention in humans

Pregnant people should not assist with lambing or kidding, handle aborted or newborn lambs or kids, placentas, uterine discharges, or contaminated clothing and footwear from affected flocks. Farm and veterinary personnel should use gloves, protective clothing, and appropriate respiratory/eye protection when exposure to contaminated birth material or dust is possible, followed by careful hand hygiene.

Human vaccination

No human vaccine is available.

Animal vaccination

Vaccines for sheep are available in some countries and can reduce abortion losses and shedding, but products, licensing, and schedules vary by region. Some products are live vaccines and require specific handling precautions; pregnant people should not handle live C. abortus vaccines.

Prognosis

Most nonpregnant human infections respond to appropriate treatment, but pregnancy-associated disease can be severe for both mother and fetus. In sheep and goats, affected dams commonly recover, but reproductive losses can be substantial and infection can persist in a flock or herd.

Reporting, legal, and regulatory considerations

Reporting requirements vary by jurisdiction. Abortion storms in livestock may trigger animal-health investigation, and severe or pregnancy-associated human infections should involve public health. Veterinary drug use, vaccine handling, carcass disposal, and occupational exposure management must follow local regulations.

Selected current sources

• UK Health Security Agency—Chlamydia abortus: Epidemiology, Transmission and Prevention
• Merck Veterinary Manual—Abortion in Sheep
• UK Government—Pregnancy: Advice on Contact with Animals Giving Birth

METHICILLIN-RESISTANT STAPHYLOCOCCUS AUREUS (MRSA)

Synonyms and scope

Methicillin-resistant Staphylococcus aureus infection or colonization. This entry covers animal-associated and bidirectional MRSA transmission. It does not imply that every MRSA infection in a person with animal contact was acquired from an animal.

Etiologic agent

Staphylococcus aureus strains carrying mecA or mecC, which confer resistance to methicillin and most other beta-lactam antimicrobials. Human-associated, livestock-associated, and less commonly animal-adapted lineages occur.

Animals involved and epidemiologic roles

• Pigs: Important reservoir for livestock-associated MRSA, particularly clonal complex 398 in many regions.
• Dogs and cats: Can be colonized or infected; household strains are often human-associated, so transmission can occur in either direction.
• Horses: Colonization and clinical infections occur, including veterinary-hospital outbreaks and occupational exposure.
• Cattle: Colonization and mastitis or other infections are reported; livestock-associated strains occur.
• Birds and other animals: MRSA has been reported in poultry, psittacines, turtles, and other species, but epidemiologic importance varies.
• People: May carry MRSA asymptomatically or develop skin, wound, postoperative, respiratory, bloodstream, bone/joint, or other invasive infection.

Geographic distribution and occurrence

Worldwide. The dominant MRSA lineages differ by country, animal industry, household, and healthcare setting. Livestock-associated MRSA is particularly important in some pig- and veal-producing regions.

Reservoir, life cycle, and transmission

Colonized people and animals are reservoirs. Transmission is primarily through direct contact with colonized or infected skin, wounds, nasal secretions, contaminated hands, equipment, bedding, or clinical environments. Companion animals commonly acquire human strains and may participate in household persistence; livestock-associated strains can move from animals to workers and their contacts.

Incubation period

Colonization may persist without symptoms. When infection follows wound contamination or other exposure, onset ranges from a few days to longer depending on the site and host. There is no single disease-specific incubation period for all MRSA syndromes.

Disease in humans

Most clinical disease involves skin and soft tissues, abscesses, wounds, or postoperative infection. Severe disease can include pneumonia, bacteremia, endocarditis, septic arthritis, osteomyelitis, sepsis, and toxic shock. Colonization without illness is common.

Disease in animals—by species

• Dogs and cats: Skin, wound, surgical-site, urinary, respiratory, ear, bone/joint, and invasive infections can occur; many colonized animals are asymptomatic.
• Horses: Wound, surgical-site, joint, respiratory, skin, and invasive infections are reported; colonization may occur without disease.
• Pigs: Usually colonized without signs; clinical infection is less common than carriage.
• Cattle: Mastitis and other opportunistic infections occur; asymptomatic carriage is also recognized.
• Birds/other animals: Clinical significance ranges from incidental carriage to opportunistic infection.

Pathology

MRSA causes the same pyogenic lesions as susceptible S. aureus: suppurative dermatitis, abscesses, wound infection, pneumonia, osteomyelitis, septic arthritis, endocarditis, or septicemia. Methicillin resistance affects treatment rather than the basic lesion type.

Human diagnosis

Diagnosis requires appropriate clinical specimens for culture and species identification with antimicrobial susceptibility testing. Resistance is confirmed by validated phenotypic or molecular methods when needed. Colonization screening is used selectively for infection-control or outbreak purposes rather than as routine testing of every exposed person.

Animal diagnosis

Culture clinically relevant deep or sterile-site specimens and request susceptibility testing. Interpret superficial or screening cultures cautiously because colonization is common. Repeated screening of healthy household animals is generally reserved for persistent transmission problems and should be coordinated with veterinary and human healthcare teams.

Differential diagnoses

Methicillin-susceptible S. aureus, Staphylococcus pseudintermedius including MRSP, streptococci, Pasteurella, gram-negative wound pathogens, dermatophytosis, sterile inflammatory skin disease, and other causes appropriate to the affected organ.

Treatment in humans

Drain and debride purulent foci when indicated and use antimicrobial therapy according to infection severity, site, local guidelines, and susceptibility results. Serious invasive infection requires prompt medical management. Colonization alone usually does not require systemic antimicrobial treatment.

Treatment in animals—by species

Treat clinical infection, not a laboratory result alone. Use drainage, wound care, source control, and culture-directed antimicrobials selected by a veterinarian. Avoid routine antimicrobial treatment or decolonization of healthy carrier pets or livestock unless an outbreak-control plan specifically calls for it.

Animal and environmental control

Use hand hygiene, gloves for wound care, clean and cover draining lesions, disinfect shared clinical equipment and high-touch surfaces, launder contaminated bedding, and apply veterinary infection-control precautions. During recurrent household transmission, coordinate medical and veterinary investigation rather than automatically removing or treating pets.

Prevention in humans

Wash hands after animal contact and before wound care, cover skin breaks, avoid sharing towels or personal items, and use appropriate PPE when handling infected wounds or heavily colonized livestock. People with invasive devices, major wounds, or substantial immune compromise should take extra precautions around draining animal lesions.

Human vaccination

No licensed human MRSA vaccine is available.

Animal vaccination

No broadly effective licensed MRSA vaccine is available for routine veterinary use.

Prognosis

Most localized infections resolve with adequate drainage and effective therapy. Prognosis worsens with bacteremia, pneumonia, endocarditis, bone/joint infection, delayed source control, or severe host comorbidity. Colonized animals and people often remain clinically healthy.

Reporting, legal, and regulatory considerations

Individual community MRSA infections are not uniformly nationally notifiable in the United States, but healthcare-associated surveillance, institutional outbreak reporting, occupational-health requirements, and local rules vary. Veterinary hospitals and animal facilities should follow infection-control and antimicrobial-stewardship policies.

Selected current sources

• CDC Healthy Pets, Healthy People—Zoonotic and Animal-Associated Diseases
• CDC—Dogs and Human Health
• Merck Veterinary Manual—Global Zoonotic Bacterial and Rickettsial Diseases

NEW WORLD SCREWWORM MYIASIS

Synonyms and scope

New World screwworm (NWS) myiasis; screwworm infestation. An obligate traumatic myiasis of living warm-blooded animals and people caused by larvae of Cochliomyia hominivorax.

Etiologic agent

Cochliomyia hominivorax, the New World screwworm fly. Larvae are obligate parasites of living tissue during their feeding stage.

Animals involved and epidemiologic roles

• Livestock: Cattle, horses, sheep, goats, pigs, and camelids are important susceptible hosts and can suffer severe production and welfare losses.
• Dogs and cats: Wounds, surgical sites, skin disease, and body openings can become infested.
• Wildlife: Many mammals and birds are susceptible; wildlife can sustain transmission where the fly is established.
• People: Accidental hosts when eggs are deposited at wounds or body openings.

Geographic distribution and occurrence

Historically endemic through tropical and subtropical areas of the Americas. Eradication programs eliminated established populations from the United States and much of Central America, but a major northward-moving outbreak re-emerged in Central America and Mexico. In June 2026 USDA confirmed the first U.S. animal case in the current outbreak; surveillance and eradication activities remain active.

Reservoir, life cycle, and transmission

Adult female flies are attracted to wounds and natural body openings and deposit egg masses. Larvae hatch, burrow into living tissue, feed for several days, then leave the host and pupate in soil. Transmission does not require direct contact between hosts; risk depends on exposure to adult flies where NWS is present. Even small wounds, tick bites, umbilical sites, mucosal lesions, or surgical wounds can attract flies.

Incubation period

Eggs can hatch within about a day after deposition, and painful wound deterioration may become apparent over the next several days as larvae feed. Timing varies with temperature, wound location, and burden.

Disease in humans

Infestation causes rapidly progressive painful wounds, bleeding or serosanguineous discharge, foul odor, swelling, visible or palpable larval movement, and tissue destruction. Eyes, ears, nose, mouth, genital, and anorectal sites can be affected. Secondary bacterial infection and extensive tissue damage may occur.

Disease in animals—by species

All warm-blooded species are susceptible. Livestock may develop enlarging wounds, restlessness, reduced feeding, weight loss, secondary infection, debilitation, and death when infestations are extensive. Companion animals and wildlife develop similar destructive myiasis, including infestation of wounds and body openings. Neonatal umbilici and reproductive or traumatic wounds are important risk sites.

Pathology

Larvae mechanically destroy viable tissue, producing deepening cavitary wounds with hemorrhage, necrosis, inflammation, exudation, and secondary bacterial contamination. Severe infestations can lead to systemic illness, toxemia, anemia, or death.

Human diagnosis

Diagnosis is based on compatible exposure and direct recognition of larvae in living tissue. Species confirmation should be obtained through public-health or reference entomology channels because other fly larvae can resemble NWS. Suspected cases require immediate reporting.

Animal diagnosis

Inspect all wounds and body openings carefully for egg masses and larvae, especially in animals from affected areas. Veterinarians should contact animal-health officials immediately for suspect cases so identification and regulatory response can be coordinated.

Differential diagnoses

Other wound myiases, bacterial or fungal wound infection, necrotizing soft-tissue disease, foreign-body wounds, neoplasia, chronic otitis or sinus disease, and nonparasitic causes of nonhealing wounds.

Treatment in humans

Prompt medical treatment requires complete physical removal of larvae, thorough wound assessment and cleansing, management of secondary infection when present, analgesia, and surgical care for extensive tissue damage. Deep or anatomically complex infestations may require specialist management.

Treatment in animals—by species

Veterinary treatment focuses on complete larval removal, wound cleaning and debridement as needed, pain control, treatment of secondary infection, and approved antiparasitic or wound products according to species and regulatory guidance. Food-animal drug restrictions and withdrawal requirements must be followed.

Animal and environmental control

Rapid detection and reporting are essential. Protect wounds, promptly treat injuries, inspect susceptible animals frequently in affected areas, control flies where appropriate, and follow official movement restrictions. Area-wide eradication relies heavily on coordinated surveillance and sterile-insect releases rather than individual animal treatment alone.

Prevention in humans

In affected areas, keep wounds clean and covered, use insect repellents and protective clothing, sleep in screened housing when possible, and seek care for wounds that worsen rapidly or contain larvae. Travelers with compatible lesions should disclose travel history immediately.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Excellent when infestation is recognized early and all larvae are removed with adequate wound care. Prognosis becomes guarded with deep anatomic involvement, severe tissue destruction, secondary sepsis, debilitation, or delayed treatment.

Reporting, legal, and regulatory considerations

In the United States, suspected human NWS should be reported immediately to the local or state health department. Veterinarians should immediately report suspected animal infestations to the State Animal Health Official and USDA APHIS. Animal movement, specimen submission, treatment, and eradication measures may be regulated during an outbreak.

Selected current sources

• CDC—Clinical Overview of New World Screwworm
• CDC—New World Screwworm Outbreak Situation Summary
• USDA APHIS—New World Screwworm

PSITTACOSIS / CHLAMYDIA PSITTACI

Synonyms and scope

Psittacosis; ornithosis; parrot fever; avian chlamydiosis. This is primarily a bird-associated zoonosis. The historic spelling “psitticosis” and older taxonomic name Chlamydophila psittaci may appear in legacy sources.

Etiologic agent

Chlamydia psittaci, an obligate intracellular bacterium. Multiple genotypes circulate in birds and can infect people.

Animals involved and epidemiologic roles

• Psittacine birds: Important companion-bird reservoirs, including parrots, parakeets, cockatiels, and macaws.
• Pigeons and doves: Commonly infected and may shed organisms with or without obvious illness.
• Poultry and other birds: Turkeys, ducks, chickens, shorebirds, and many other species can be infected and represent occupational exposure sources.
• People: Accidental hosts, especially bird owners, veterinarians, avian workers, poultry workers, and others exposed to contaminated bird secretions or excreta.

Geographic distribution and occurrence

Worldwide wherever susceptible birds and people interact. Human disease is uncommon but regularly recognized. Cases may be linked to pet birds, breeding facilities, pet shops, veterinary settings, poultry operations, rehabilitation centers, or wild-bird exposure.

Reservoir, life cycle, and transmission

Infected birds shed organisms in respiratory secretions and feces. People are infected mainly by inhaling dust or aerosols contaminated with dried droppings or respiratory material; bites and beak-to-mouth contact are less common routes. Birds may shed intermittently, and stress can increase shedding. Human-to-human transmission has been documented only rarely.

Incubation period

Usually 5–14 days after exposure, although later onset is reported.

Disease in humans

Illness ranges from mild respiratory disease to atypical pneumonia. Typical findings include abrupt fever, chills, severe headache, myalgia, malaise, and a dry cough. Severe cases can involve respiratory failure, hepatitis, myocarditis or endocarditis, encephalitis, sepsis, or other systemic complications. Properly treated disease is usually curable.

Disease in animals—by species

• Psittacine birds: Lethargy, anorexia, weight loss, conjunctivitis, nasal or ocular discharge, dyspnea, green or yellow-green droppings, hepatosplenomegaly, or sudden death; inapparent infection also occurs.
• Pigeons/doves: Often subclinical; conjunctivitis, respiratory disease, poor condition, or diarrhea may occur.
• Poultry: Clinical expression varies by species and strain and can include respiratory, systemic, or reproductive disease.

Pathology

Avian disease may include airsacculitis, pneumonia, hepatitis, splenitis, pericarditis, and serositis. Human disease primarily produces interstitial or atypical pneumonia, with possible hepatic, cardiac, neurologic, or systemic involvement in severe cases.

Human diagnosis

Diagnosis combines compatible bird exposure with laboratory testing. Nucleic-acid amplification testing, especially PCR from respiratory specimens, is preferred when available; serology may assist but has limitations and cross-reactivity. Notify the diagnostic laboratory and public-health authorities when psittacosis is suspected so testing can be appropriately coordinated.

Animal diagnosis

Veterinary diagnosis commonly uses PCR on appropriate respiratory, conjunctival, or cloacal/fecal specimens together with clinical findings and exposure history. Because shedding can be intermittent, test interpretation and sampling strategy should be directed by an avian veterinarian or diagnostic laboratory.

Differential diagnoses

Influenza, COVID-19, community-acquired bacterial pneumonia, Q fever, Legionella infection, Mycoplasma pneumonia, tularemia, and other causes of febrile respiratory illness in people; in birds, avian influenza, Newcastle disease, mycoplasmosis, aspergillosis, and other causes of respiratory or systemic disease.

Treatment in humans

Prompt clinician-directed antibiotic treatment is recommended. Doxycycline is generally preferred unless contraindicated; pregnancy, age, allergies, and disease severity affect drug selection. Severe pneumonia may require hospitalization and respiratory support.

Treatment in animals—by species

Bird treatment requires avian-veterinary supervision because species, formulation, route, duration, flock structure, and owner compliance affect success. Tetracycline-class therapy is commonly used. Treatment must be paired with environmental cleaning and management of exposed birds rather than unsupervised medication alone.

Animal and environmental control

Separate clinically ill or test-positive birds as directed, improve ventilation, reduce crowding and stress, wet-clean cages and surfaces before removing debris, and disinfect appropriately. Avoid dry sweeping or high-pressure cleaning that aerosolizes fecal material. Newly acquired birds should receive veterinary evaluation and risk-based quarantine.

Prevention in humans

Wash hands after bird contact, avoid beak-to-mouth contact, clean cages with wet methods, and use gloves and respiratory/eye protection for high-risk cleaning or veterinary procedures involving suspect birds. People at increased risk of severe infection should avoid direct contact with sick birds until veterinary evaluation is complete.

Human vaccination

No vaccine is available.

Animal vaccination

No routinely available commercial vaccine reliably prevents avian chlamydiosis in pet birds. Prevention relies on testing, quarantine, treatment, husbandry, and sanitation.

Prognosis

Human prognosis is excellent with prompt appropriate treatment; death is uncommon in properly treated disease. Avian prognosis varies with species, disease severity, chronicity, and treatment response; clinically recovered birds may require follow-up testing or management because shedding can recur.

Reporting, legal, and regulatory considerations

Psittacosis is reportable in many U.S. jurisdictions and may trigger public-health investigation of associated birds or facilities. Importation, quarantine, animal movement, and outbreak management may be regulated. Veterinary and public-health authorities should be involved in clusters involving pet shops, breeders, poultry facilities, or multiple human cases.

Selected current sources

• CDC—Clinical Overview of Psittacosis
• CDC—About Psittacosis
• NASPHV—Compendium of Measures to Control Chlamydia psittaci Infection

OTHER HEMORRHAGIC FEVERS

Synonyms and scope

Rodent-borne arenaviral hemorrhagic fevers; this retained umbrella entry includes Lassa fever and South American hemorrhagic fevers such as Argentine, Bolivian, Venezuelan, Brazilian, and Chapare hemorrhagic fevers. It does not replace the separate Marburg, Rift Valley fever, or other virus-specific entries on this site.

Etiologic agent

Pathogenic mammarenaviruses in family Arenaviridae, including Lassa virus, Junín virus, Machupo virus, Guanarito virus, Sabiá virus, Chapare virus, and Lujo virus. Lymphocytic choriomeningitis virus is addressed separately because its usual clinical syndrome differs from classic hemorrhagic fever.

Animals involved and epidemiologic roles

• Multimammate rats (Mastomys natalensis): Major reservoir for Lassa virus in West Africa.
• Drylands vesper mouse (Calomys musculinus): Reservoir for Junín virus in Argentina.
• Large vesper mouse (Calomys callosus): Reservoir for Machupo virus in Bolivia.
• Short-tailed cane mouse (Zygodontomys brevicauda): Reservoir for Guanarito virus in Venezuela.
• Other rodents: Reservoirs are known or suspected for several additional mammarenaviruses.
• People: Accidental hosts; person-to-person spread occurs with some viruses after zoonotic introduction.

Geographic distribution and occurrence

Lassa fever occurs principally in West Africa. Junín virus causes Argentine hemorrhagic fever in Argentina; Machupo and Chapare viruses occur in Bolivia; Guanarito virus occurs in Venezuela; Sabiá virus is associated with Brazil; and Lujo virus was recognized in southern Africa. Risk is highly focal and linked to the distribution and ecology of reservoir rodents.

Reservoir, life cycle, and transmission

Reservoir rodents generally carry persistent infection with little or no illness and contaminate environments with urine, feces, or saliva. People can be infected by inhalation of contaminated material, direct contact with excreta or nesting material, bites or scratches, or contaminated food. Certain arenaviruses, including Lassa, Machupo, Chapare, and Lujo viruses, can also spread person-to-person through direct exposure to infectious body fluids.

Incubation period

Varies by virus, generally within approximately 2–21 days. Examples include about 2–21 days for Lassa fever, 6–14 days for Junín virus, and 3–16 days for Machupo virus.

Disease in humans

Illness often begins with fever, weakness, headache, myalgia, and gastrointestinal symptoms. Severe disease can progress to shock, bleeding, neurologic abnormalities, organ dysfunction, respiratory compromise, and death. Not every patient develops obvious hemorrhage. Hearing loss is a recognized complication of Lassa fever, and neurologic manifestations may occur with South American hemorrhagic fevers.

Disease in animals—by species

Natural reservoir rodents usually remain clinically normal despite persistent infection and shedding. The absence of signs in a rodent does not indicate that it is free of an arenavirus. Domestic animals are not established maintenance reservoirs for the major hemorrhagic-fever mammarenaviruses.

Pathology

Severe human disease can involve endothelial and immune dysregulation, vascular leakage, thrombocytopenia, hepatic injury, shock, and multiorgan dysfunction. Lesion patterns vary by virus and are not specific enough to identify the agent without laboratory confirmation.

Human diagnosis

Any suspected viral hemorrhagic fever requires immediate public-health notification before specialized testing. Diagnosis may use RT-PCR, antigen or antibody assays, and other reference-laboratory methods selected according to the suspected virus and stage of illness. More common causes of fever after travel, including malaria, bacterial sepsis, and typhoid fever, must also be evaluated promptly.

Animal diagnosis

Routine clinical testing of wild rodents is not indicated for household exposure decisions. Reservoir surveillance is performed by specialized public-health or research programs. Suspect occupational or unusual animal-associated events should be referred to public-health and wildlife authorities.

Differential diagnoses

Malaria, typhoid fever, leptospirosis, meningococcemia, severe sepsis, dengue, yellow fever, Ebola or Marburg virus disease, Crimean-Congo hemorrhagic fever, Rift Valley fever, severe influenza, and other region-specific febrile illnesses.

Treatment in humans

Management is virus-specific and should occur with infectious-disease and public-health expertise. Early supportive care, careful fluid and electrolyte management, hemodynamic support, and treatment of complications are central. Some countries use virus-specific therapies or immune products for selected arenaviral diseases; these are not interchangeable and availability varies. Treatment should not be delayed while awaiting definitive confirmation when a high-consequence disease is strongly suspected.

Treatment in animals—by species

No treatment is recommended for wild reservoir rodents as a public-health control measure. Ill or exposed captive rodents should be managed through veterinary, occupational-health, and public-health risk assessment rather than empiric population treatment.

Animal and environmental control

Exclude commensal rodents from homes, food-storage areas, animal facilities, and workplaces; seal entry points; store food and feed securely; remove clutter and nesting material safely; and use integrated rodent control. Avoid creating dust from rodent-contaminated material; follow public-health guidance for cleaning heavily contaminated areas.

Prevention in humans

Avoid direct contact with wild rodents and their urine, feces, saliva, nesting materials, and contaminated food. Use appropriate protective equipment for occupational exposure. In affected regions, health-care facilities must use strict infection-control precautions for suspect cases because some arenaviruses can spread person-to-person.

Human vaccination

A licensed vaccine against Argentine hemorrhagic fever (Candid #1) is used in Argentina for people at risk from Junín virus but is not routinely available in the United States. No broadly licensed human vaccine is available for Lassa fever or the other major hemorrhagic-fever mammarenaviruses.

Animal vaccination

No animal vaccine is routinely available or used to control these reservoir infections.

Prognosis

Prognosis varies greatly by virus, timeliness of care, and disease severity. Mild infections occur, but recognized hemorrhagic-fever syndromes can have substantial mortality and prolonged recovery. Survivors may have persistent complications, including hearing impairment after Lassa fever.

Reporting, legal, and regulatory considerations

The major viral hemorrhagic fevers covered in this entry are nationally notifiable conditions in the United States under current surveillance definitions. Suspected cases require immediate health-department involvement; national notification urgency and jurisdiction-specific reporting requirements apply. Infection-control measures and coordinated reference testing are essential, and international notification or travel/contact management may apply during confirmed outbreaks.

Selected current sources

• CDC—About Viral Hemorrhagic Fevers
• CDC—Screening and Evaluating an Ill Person for Viral Hemorrhagic Fevers
• WHO—Lassa Fever

MARBURG VIRUS

Synonyms and scope

Marburg virus disease (MVD); formerly Marburg hemorrhagic fever. The historic term “green monkey disease” reflects the 1967 European outbreaks linked to imported African green monkeys, but those primates were not the natural reservoir.

Etiologic agent

Marburg virus and Ravn virus, orthomarburgviruses in family Filoviridae. Both can cause Marburg virus disease.

Animals involved and epidemiologic roles

• Egyptian fruit bats (Rousettus aegyptiacus): Natural reservoir and source of primary zoonotic infection.
• Nonhuman primates: Susceptible spillover hosts; infected primates were the source of the first recognized occupational outbreak in 1967.
• People: Spillover hosts who can sustain human-to-human transmission through direct contact with infectious body fluids.
• Other mammals: No established domestic-animal reservoir.

Geographic distribution and occurrence

Primary zoonotic risk is associated with sub-Saharan Africa, especially regions where Egyptian fruit bats inhabit caves or mines. Human outbreaks and sporadic cases have been reported in multiple African countries, with occasional exported cases. The disease remains rare but is a high-consequence infection.

Reservoir, life cycle, and transmission

Initial human infection can follow prolonged exposure to caves or mines inhabited by infected Egyptian fruit bats or contact with infected wildlife. Once introduced into people, transmission occurs through direct contact of broken skin or mucous membranes with blood or other infectious body fluids, or with contaminated materials. Transmission is associated with symptomatic illness; safe burial and health-care infection control are critical during outbreaks.

Incubation period

Usually 2–21 days; many patients develop symptoms around 8–10 days after exposure.

Disease in humans

Disease often begins abruptly with fever, severe headache, chills, myalgia, and profound malaise, followed by gastrointestinal symptoms, rash, and progressive systemic illness. Severe cases can develop bleeding, shock, neurologic abnormalities, multiorgan failure, and death. Case-fatality has varied widely among outbreaks.

Disease in animals—by species

• Egyptian fruit bats: Reservoir infection is generally inapparent.
• Nonhuman primates: Can develop severe systemic disease and die; outbreaks in primates should be treated as a serious occupational and public-health hazard.
• Domestic animals: No established role in maintenance or routine transmission.

Pathology

Severe human and primate disease can include hepatic injury, lymphoid depletion, hemorrhage, edema, necrosis, and widespread organ involvement. Pathology is not specific enough to distinguish Marburg disease from other viral hemorrhagic fevers without laboratory confirmation.

Human diagnosis

Immediately isolate and notify public health when MVD is suspected. Diagnosis is coordinated through specialized public-health laboratories and may include molecular detection, antigen testing, and serology. Concurrent evaluation for more common causes of severe febrile illness, especially malaria and bacterial sepsis, should not be delayed.

Animal diagnosis

Suspected infection in nonhuman primates or other mammals requires immediate veterinary and public-health/animal-health consultation. Diagnostic testing should be performed only through designated reference systems; routine clinical handling or necropsy of a suspect animal should be avoided until authorities provide direction.

Differential diagnoses

Malaria, Ebola virus disease, Lassa fever and other arenaviral hemorrhagic fevers, Crimean-Congo hemorrhagic fever, yellow fever, dengue, Rift Valley fever, typhoid fever, leptospirosis, meningococcemia, severe bacterial sepsis, and other causes of acute febrile illness with organ dysfunction.

Treatment in humans

No antiviral drug is currently approved as a proven cure. Early intensive supportive care—including careful rehydration, electrolyte correction, oxygenation, hemodynamic support, and treatment of complications—improves survival. Investigational vaccines and therapeutics may be available only through outbreak-response or clinical-trial protocols.

Treatment in animals—by species

No established curative treatment is recommended for suspect infected nonhuman primates or wildlife. Management is directed by veterinary and public-health authorities and emphasizes isolation, exposure prevention, humane care, and diagnostic confirmation.

Animal and environmental control

Avoid unnecessary entry into bat-inhabited caves or mines in outbreak areas. Facilities housing nonhuman primates should maintain quarantine, occupational-health programs, PPE, and rapid response to unexplained febrile or hemorrhagic illness. During outbreaks, contaminated materials and animal tissues must be managed under official high-consequence pathogen guidance.

Prevention in humans

Avoid direct contact with fruit bats, sick or dead nonhuman primates, and their tissues in affected regions. Health-care and veterinary workers should use appropriate PPE and infection-control measures. Do not handle bodies or contaminated materials from suspected human cases without trained outbreak-response procedures.

Human vaccination

No approved human vaccine is currently available for routine prevention of Marburg virus disease, although vaccine candidates are under clinical evaluation.

Animal vaccination

No licensed animal vaccine is available.

Prognosis

MVD can be rapidly fatal. Reported case-fatality rates have ranged from roughly one-quarter to nearly 90% in past outbreaks, with better outcomes where early intensive supportive care is available.

Reporting, legal, and regulatory considerations

Suspected MVD is an immediate public-health emergency and is reportable in the United States. Case isolation, testing, contact tracing, travel assessment, specimen management, and occupational exposures are coordinated by public-health authorities. Animal exposures involving nonhuman primates or bats may also require wildlife, animal-health, and workplace-safety involvement.

Selected current sources

• CDC—Clinical Overview of Marburg Virus Disease
• WHO—Marburg Virus Disease Fact Sheet
• CDC—Viral Hemorrhagic Fever Evaluation

MEASLES

Synonyms and scope

Rubeola; morbilli. Measles is retained on this animal-associated disease page because nonhuman primates are susceptible and outbreaks can occur in primate facilities. It is not an animal-maintained zoonosis: humans are the natural reservoir, and the principal direction of concern in managed primates is human-to-primate transmission.

Etiologic agent

Measles virus, an enveloped RNA virus in genus Morbillivirus, family Paramyxoviridae. It is distinct from canine distemper virus and other animal morbilliviruses.

Animals involved and epidemiologic roles

• People: Only established natural reservoir and source of sustained transmission.
• Old World monkeys and great apes: Highly susceptible to infection from people and can develop serious disease; outbreaks in captive groups can amplify exposure within the group.
• New World primates: Susceptibility varies, and some species can develop severe disease or adverse reactions to inappropriate modified-live vaccines.
• Domestic animals: Dogs, cats, livestock, and common pets are not reservoirs for human measles virus.

Geographic distribution and occurrence

Worldwide. Measles has been eliminated from sustained endemic transmission in some countries but is repeatedly reintroduced through travel and can cause outbreaks where vaccination coverage is insufficient. Captive nonhuman-primate facilities are at risk when susceptible animals are exposed to infected people.

Reservoir, life cycle, and transmission

Humans maintain measles virus. Transmission is airborne and respiratory, and the virus is extraordinarily contagious. Infected people can transmit virus to susceptible nonhuman primates. Animal reservoirs are not required for persistence, and routine animal contact is not a source of community measles in people.

Incubation period

In people, symptoms generally begin 7–14 days after infection, and rash typically appears about 14 days after exposure. Similar timing can occur in nonhuman primates, although facility outbreaks may make the exact exposure date uncertain.

Disease in humans

Measles causes high fever, malaise, cough, coryza, conjunctivitis, Koplik spots, and a descending maculopapular rash. Complications include otitis media, pneumonia, encephalitis, dehydration, pregnancy complications, and rarely subacute sclerosing panencephalitis years later. Severe disease is more likely in young children, adults, pregnant people, and immunocompromised patients.

Disease in animals—by species

• Macaques and other Old World monkeys: Fever, rash, conjunctivitis, nasal discharge, facial edema, pneumonia, immunosuppression, secondary infection, and death can occur.
• Great apes: Susceptible to human measles and may develop significant respiratory and systemic disease.
• New World monkeys: Susceptibility varies by species; some can develop severe infection, so vaccination choices require specialist guidance.

Pathology

Measles causes respiratory epithelial and lymphoid infection with marked immune suppression. Interstitial or giant-cell pneumonia, lymphoid depletion, and multinucleated syncytial cells may occur. Secondary bacterial pneumonia and other infections contribute substantially to morbidity.

Human diagnosis

Suspected measles should be reported immediately to the local health department. Laboratory confirmation generally uses RT-PCR from respiratory specimens and serology, interpreted with clinical and epidemiologic information. Sporadic cases and outbreaks require public-health confirmation.

Animal diagnosis

In a nonhuman primate with compatible disease, immediately restrict contact and involve an experienced zoo/laboratory-animal veterinarian and diagnostic laboratory. Diagnosis can use molecular testing and serology adapted to the species and outbreak context. Human cases among staff or visitors must be investigated concurrently.

Differential diagnoses

Rubella, roseola, parvovirus B19 infection, scarlet fever, drug eruptions, enteroviral exanthems, dengue or other febrile rash illnesses in people; in nonhuman primates, other morbillivirus-like disease, simian varicella, bacterial pneumonia, and other causes of febrile exanthem.

Treatment in humans

No specific antiviral treatment is routinely established. Management is supportive and complication-directed. Vitamin A is recommended in selected children with measles under clinical guidance, particularly when deficiency or severe disease is a concern; dosing must be age-appropriate rather than empirically extrapolated.

Treatment in animals—by species

There is no established virus-specific curative treatment in nonhuman primates. Isolate affected animals and provide specialist supportive care, hydration, nutritional support, oxygen or respiratory care when needed, and treatment of secondary bacterial infection when documented or strongly suspected.

Animal and environmental control

Prevent exposure of primates to people with fever, rash, or respiratory illness. Maintain employee vaccination and illness-exclusion policies, quarantine newly acquired primates, and use airborne/respiratory precautions during suspect outbreaks. Facility vaccination programs should be species-specific and directed by a veterinarian experienced with nonhuman primates.

Prevention in humans

Two appropriately timed doses of measles-containing vaccine provide the best routine protection. Susceptible staff working with nonhuman primates should meet current public-health vaccination recommendations. Suspected human cases require immediate isolation and airborne precautions to prevent transmission to both people and susceptible primates.

Human vaccination

Live attenuated measles-containing vaccines, usually MMR or MMRV as age-appropriate, provide highly effective prevention. Current national schedules and outbreak or travel recommendations should be followed.

Animal vaccination

Measles vaccination is used in selected nonhuman-primate populations, especially great apes and some Old World monkeys. Products and schedules are extralabel and species-dependent; modified-live measles vaccines can cause disease in some New World primates, so vaccination must be directed by an experienced veterinarian.

Prognosis

Most immunocompetent people recover, but serious complications and death still occur, particularly in unvaccinated or medically vulnerable patients. In nonhuman primates, prognosis varies by species, age, immune status, and severity of pneumonia or secondary infection.

Reporting, legal, and regulatory considerations

Measles is immediately reportable to public health in the United States and requires rapid case investigation and contact management. Outbreaks involving nonhuman primates also require facility occupational-health and veterinary response. Human vaccination records and employee exclusion may be governed by institutional and public-health policy.

Selected current sources

• CDC—Clinical Overview of Measles
• CDC—Measles
• Merck Veterinary Manual—Vaccine Recommendations for Nonhuman Primates

MELIOIDOSIS

Synonyms and scope

Pseudoglanders; Whitmore disease. Melioidosis is an environmental bacterial disease of people and many animal species. Most infections are acquired directly from contaminated soil or water rather than from animals, but infected animals can shed the organism and animal-associated exposure is a recognized zoonotic concern.

Etiologic agent

Burkholderia pseudomallei, a gram-negative environmental bacterium. The historical name Pseudomonas pseudomallei is obsolete. The organism is naturally associated with soil and surface water in endemic areas.

Animals involved and epidemiologic roles

• Sheep and goats: Among the more susceptible livestock species; outbreaks may include pneumonia, abscesses, mastitis, neurologic disease, and death.
• Pigs: Infection may be subclinical or produce splenic and other visceral lesions, septic arthritis, or systemic disease.
• Horses and other equids: Sporadic disease may resemble glanders and can include respiratory, cutaneous, lymphatic, gastrointestinal, or systemic signs.
• Dogs and cats: Sporadic acute, chronic, localized, or disseminated infections occur; underlying disease may increase susceptibility.
• Other animals: Cattle, camelids, deer, nonhuman primates, marine mammals, wildlife, birds, reptiles, and fish have been reported infected.
• People: Accidental hosts, usually infected from the environment rather than directly from animals.

Geographic distribution and occurrence

Melioidosis is widespread in tropical and subtropical regions, especially Southeast Asia and northern Australia, and is increasingly recognized in the Western Hemisphere. CDC recognizes environmental occurrence in Puerto Rico, the U.S. Virgin Islands, and the U.S. Gulf Coast, including Mississippi. Cases and environmental detections have also been reported in Central and South America, the Caribbean, Africa, the Middle East, and other regions. Heavy rainfall, flooding, and major soil or water disturbance can increase exposure risk.

Reservoir, life cycle, and transmission

Soil and surface water are the principal environmental reservoirs. Infection occurs through inoculation of contaminated material into damaged skin, inhalation of contaminated dust or water droplets, or ingestion of contaminated water or food. Most animal and human cases arise independently from environmental exposure. Direct animal-to-human transmission is uncommon but biologically possible because infected animals may shed organisms in wound exudate, respiratory secretions, milk, urine, feces, and other body fluids.

Incubation period

Human symptoms most often develop about 1–4 weeks after exposure, although onset may occur sooner and latent infection with illness months or years later is recognized. In animals, incubation is similarly variable and can range from days to prolonged latent or chronic infection.

Disease in humans

Clinical presentations range from localized skin infection to pneumonia, deep abscesses, osteomyelitis, neurologic disease, bacteremia, and rapidly progressive sepsis. Pulmonary disease is common and may resemble tuberculosis. Disseminated infection can involve the liver, spleen, prostate, joints, bones, lymph nodes, skin, or brain. Diabetes is a major risk factor for severe disease; chronic kidney or lung disease, hazardous alcohol use, and immune compromise also increase risk.

Disease in animals—by species

• Sheep: Fever, severe cough, respiratory distress, nasal or ocular discharge, pneumonia, abscesses, and occasionally neurologic disease.
• Goats: Pneumonia, mastitis, lymph-node or visceral abscesses, abortion, and systemic disease.
• Pigs: Often subclinical; splenic lesions may be found at slaughter. Arthritis, osteomyelitis, and disseminated disease also occur.
• Horses: Weakness, limb edema or lymphangitis, colic, diarrhea, cough, nasal discharge, skin lesions, or neurologic disease.
• Dogs: Acute septicemia, severe diarrhea, pneumonia, cutaneous/lymphatic disease, or chronic multisystem infection with abscesses.
• Cats: Localized ocular disease and systemic or suppurative infections have been reported.

Pathology

Melioidosis characteristically produces suppurative and granulomatous inflammation with single or multiple abscesses or caseous nodules. Common sites include lungs, spleen, liver, lymph nodes, and subcutaneous tissues, although essentially any organ can be involved. Pneumonia, meningoencephalitis, ocular inflammation, enteritis, polyarthritis, osteomyelitis, and disseminated lesions are possible.

Human diagnosis

Melioidosis should be considered with compatible illness plus residence in or travel to an endemic area, or exposure to potentially contaminated soil, freshwater, floodwater, or imported products. Diagnosis requires specialized laboratory confirmation. Because B. pseudomallei can be misidentified and poses an occupational hazard to laboratory personnel, clinicians should clearly communicate suspected melioidosis to the diagnostic laboratory and public-health authorities before routine processing.

Animal diagnosis

Clinical signs and gross lesions are not specific. Veterinary diagnosis relies on appropriate specimens submitted to a qualified diagnostic laboratory for validated organism-specific identification, including molecular methods where available. Serology can support investigation in some settings but has important sensitivity and specificity limitations, particularly in endemic regions. Suspected cases should be discussed with the diagnostic laboratory and animal-health authorities before specimen submission when required by jurisdiction.

Differential diagnoses

Glanders, tuberculosis and other mycobacterial disease, bacterial pneumonia or sepsis, nocardiosis, actinomycosis, fungal infections, pyogranulomatous disease, deep abscesses from other bacteria, septic arthritis or osteomyelitis, and malignancy. In people, differential diagnoses also include community-acquired pneumonia, tuberculosis, other causes of sepsis, and other endemic febrile illnesses.

Treatment in humans

Prompt treatment is essential and should involve infectious-disease and public-health consultation. Current CDC guidance uses a two-phase approach: an initial intensive phase with an active intravenous agent such as ceftazidime or meropenem, followed by a prolonged eradication phase, usually with trimethoprim-sulfamethoxazole. Duration depends on disease site, severity, and clinical response; deep-organ, neurologic, bone, and joint disease generally require longer therapy. Relapse can occur if therapy is inadequate or prematurely discontinued.

Treatment in animals—by species

Veterinary treatment is difficult, prolonged, and not consistently successful, with potential for recrudescence. Decisions should account for species, disease severity, zoonotic risk, local regulations, and antimicrobial susceptibility information. Severe cases have been managed using principles similar to human intensive and eradication therapy, but treatment of food animals or animals in regulated settings may be restricted or inappropriate. Abscesses or other focal lesions may require surgical management when clinically indicated.

Animal and environmental control

In endemic areas, reduce exposure to muddy soil, stagnant or flood water, and contaminated drinking water, particularly during heavy rainfall. Provide clean water and hygienic housing, promptly manage draining lesions and contaminated bedding, and prevent access to carcasses. Infected animals should be managed so that urine, feces, milk, respiratory secretions, and wound drainage do not contaminate people, other animals, feed, or water. Environmental eradication is generally impractical because the organism can persist naturally in suitable soil and water.

Prevention in humans

People in endemic areas should protect skin wounds from contact with soil or water, use waterproof footwear and gloves for high-risk wet-soil work, and avoid unprotected contact with drainage or body fluids from suspected infected animals. People with diabetes, chronic kidney or lung disease, hazardous alcohol use, or immune compromise should be especially cautious. Pasteurized milk should be used; raw milk from potentially infected livestock should not be consumed.

Human vaccination

No licensed human vaccine is available.

Animal vaccination

No effective licensed animal vaccine is available for routine prevention.

Prognosis

Prognosis depends strongly on disease severity, underlying health, prompt recognition, and completion of prolonged therapy. Human septicemic or disseminated disease can be fatal despite treatment. Localized disease generally has a better prognosis, but relapse is possible. In animals, acute disseminated disease and involvement of vital organs carry a guarded to poor prognosis; chronic infections may be difficult to eradicate.

Reporting, legal, and regulatory considerations

In the United States, melioidosis is a nationally notifiable condition. Suspected or confirmed human infection should be promptly coordinated with local or state public health authorities. Veterinary reporting requirements vary by jurisdiction; unusual animal cases, especially in nonendemic areas, should be discussed with state or federal animal-health officials. Diagnostic laboratories should be alerted when melioidosis is suspected so that appropriate occupational-safety and referral procedures can be followed.

Selected current sources

• CDC—Clinical Overview of Melioidosis
• CDC—About Melioidosis
• Merck Veterinary Manual—Melioidosis in Animals

MESOCESTODIASIS

Synonyms and scope

Mesocestoides infection; intestinal mesocestoidiasis; canine/feline peritoneal larval cestodiasis (tetrathyridiosis). Mesocestoides are tapeworms of carnivores. Human intestinal infection is very rare. Dogs and cats may have either adult intestinal infection or, less commonly but more seriously, invasive tetrathyridial infection of body cavities.

Etiologic agent

Cestodes of the genus Mesocestoides. Species implicated in human infections include M. lineatus and M. variabilis, although species relationships within the genus remain under study.

Animals involved and epidemiologic roles

• Definitive hosts: Wild and domestic carnivores, including canids, felids, mustelids, procyonids, and opossums.
• Vertebrate intermediate hosts: Numerous mammals, birds, reptiles, and amphibians may harbor tetrathyridia.
• Dogs and cats: Can be definitive hosts with adult intestinal tapeworms and can also develop aberrant/invasive tetrathyridial disease.
• Humans: Rare accidental definitive hosts with intestinal adult tapeworm infection.

Geographic distribution and occurrence

Mesocestoides occurs broadly in wild and domestic animals. CDC reports the genus from every inhabited continent except Australia. M. lineatus is reported from Europe, Asia, and Africa, while M. variabilis occurs in North America. Human cases are rare and have been reported from Japan, Korea, and the United States.

Reservoir, life cycle, and transmission

The complete life cycle remains incompletely resolved. Current evidence supports an indirect cycle involving a presumed arthropod first intermediate host, a vertebrate host containing tetrathyridia, and a carnivore definitive host. Dogs, cats, and other carnivores acquire adult intestinal infection by consuming tissues containing tetrathyridia. Reported human intestinal infections are believed to follow ingestion of inadequately cooked animal tissues or viscera containing tetrathyridia. Eggs passed by dogs or cats are not considered directly infective to people.

Incubation period

A precise incubation period for human disease is not established because cases are exceptionally uncommon. In natural carnivore definitive hosts, adult tapeworm development and passage of gravid segments can occur within several weeks after ingestion of infected tissues.

Disease in humans

Most recognized human infections have involved small numbers of adult intestinal worms. Infection may be asymptomatic or cause nonspecific recurrent gastrointestinal symptoms, including abdominal discomfort or diarrhea; motile proglottids may be noticed. CDC notes that human tetrathyridial larval-stage infection has not been documented.

Disease in animals—by species

• Dogs: Adult intestinal infection is commonly mild or subclinical. Tetrathyridia can invade the peritoneal cavity and cause peritonitis, ascites, abdominal distension, weight loss, lethargy, and recurrent disease; thoracic involvement is rare.
• Cats: Intestinal infection may be asymptomatic or mild. Peritoneal or thoracic tetrathyridiosis is reported but uncommon and can be serious.
• Wild carnivores: Important definitive hosts maintaining the parasite in wildlife cycles.
• Intermediate hosts: Larvae occur in body cavities or viscera of many mammals, birds, reptiles, and amphibians, often without obvious clinical disease.

Pathology

Adult worms attach to the small-intestinal mucosa and usually cause limited injury. In canine or feline tetrathyridiosis, numerous larvae may be present free or associated with serosal surfaces, producing granulomatous or proliferative peritonitis, serosal inflammation, ascites, adhesions, and occasionally pleural disease.

Human diagnosis

Diagnosis is based primarily on recognition of characteristic proglottids or other cestode material passed in stool, with specialist parasitologic identification when needed. Species-level identification can be difficult because of overlap within the genus. A history of ingestion of raw or undercooked animal tissues can support the diagnosis.

Animal diagnosis

Adult intestinal infection may be recognized by passage and morphologic identification of proglottids; routine fecal flotation can miss infection because eggs are retained within the parauterine organ of the segment. Suspected tetrathyridiosis is evaluated using abdominal or thoracic imaging, examination of effusions or aspirates, surgical findings, histopathology, and specialist parasitologic or molecular identification when indicated.

Differential diagnoses

For intestinal infection, differentials include other cestodes such as Dipylidium, Taenia, and diphyllobothriid tapeworms. In dogs and cats with peritoneal disease, consider neoplasia, bacterial or fungal peritonitis, pancreatitis, hepatic disease, protein-losing disorders, cardiac disease, and other causes of ascites or granulomatous inflammation.

Treatment in humans

Because human infection is rare, treatment should be directed by a physician or infectious-disease/parasitology specialist. Praziquantel has been used for intestinal cestode infection; confirmation of parasite identity and clinical follow-up are appropriate.

Treatment in animals—by species

Dogs and cats with adult intestinal infection: praziquantel-containing anthelmintic therapy is used. Peritoneal or pleural tetrathyridiosis: treatment is substantially more difficult and recurrence is common. Veterinary management may combine surgical removal or lavage with prolonged antiparasitic therapy and supportive management of effusion and inflammation. Treatment should be individualized because no single regimen is uniformly curative.

Animal and environmental control

Treat infected dogs and cats and limit predation, scavenging, and access to raw carcasses or viscera. Because the complete natural cycle is unresolved, environmental eradication is not practical. Routine feces removal and general parasite-control hygiene remain appropriate.

Prevention in humans

Avoid eating raw or inadequately cooked wild-animal tissues or viscera, particularly reptiles and other potential intermediate hosts. Ordinary household contact with a dog or cat carrying adult Mesocestoides is not considered a direct route of human infection because shed eggs are not directly infective to people.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Human intestinal infections are generally mild and treatable. Prognosis for uncomplicated intestinal infection in dogs and cats is good. Prognosis for peritoneal or pleural tetrathyridiosis is more guarded because treatment can be difficult and recurrence is well recognized.

Reporting, legal, and regulatory considerations

Mesocestoidiasis is not generally a nationally notifiable human or animal disease in the United States. Unusual human infections should be identified with specialist assistance, and local reporting requirements should be checked. Veterinary cases involving unusual invasive disease may merit diagnostic-laboratory or parasitology consultation.

Selected current sources

• CDC DPDx—Mesocestoidiasis
• Merck Veterinary Manual—Tapeworms in Dogs and Cats
• Companion Animal Parasite Council—Mesocestoides

METAGONIMUS YOKOGAWAI (METAGONIMIASIS)

Synonyms and scope

Metagonimiasis is an intestinal food-borne trematode infection caused principally by Metagonimus yokogawai. It is included here because dogs, cats, other fish-eating mammals, and birds can participate as definitive hosts, although people acquire infection from infected fish rather than directly from companion animals.

Etiologic agent

Metagonimus yokogawai is a minute intestinal fluke (trematode) and one of the smallest flukes known to infect humans. Related Metagonimus species can also infect people in some regions.

Animals involved and epidemiologic roles

Freshwater snails, most often Semisulcospira species, serve as first intermediate hosts. Freshwater or brackish-water fish serve as second intermediate hosts and contain the infective metacercarial stage. Humans, dogs, cats, other fish-eating mammals, and fish-eating birds can serve as definitive hosts and pass eggs in feces.

Geographic distribution and occurrence

Human infection is concentrated in East Asia, particularly areas where raw or inadequately cooked freshwater fish are traditionally eaten. CDC also recognizes occurrence in Siberia, Manchuria, the Balkan states, Israel, and Spain. Distribution follows the presence of appropriate snail and fish hosts and dietary practices.

Reservoir, life cycle, and transmission

Eggs passed in feces enter aquatic environments and are taken up by suitable snails. Subsequent stages leave the snail and encyst as metacercariae in fish. Humans and other definitive hosts become infected by eating raw, undercooked, salted, or otherwise inadequately processed infected fish. Direct transmission from dogs, cats, or other animals to people does not occur.

Incubation period

A precise clinical incubation period is not well established because many infections are mild or asymptomatic. Intestinal adult flukes develop after ingestion of metacercariae, with clinical manifestations related largely to parasite burden and intestinal inflammation.

Disease in humans

Light infections may be asymptomatic. Symptomatic infection most often causes diarrhea, colicky abdominal pain, and other gastrointestinal discomfort. Heavy infections may cause more substantial intestinal inflammation. Rarely, eggs may reach extraintestinal tissues, including the heart or central nervous system, where they can provoke serious inflammatory lesions.

Disease in animals—by species

Dogs and cats: These species can harbor adult flukes in the small intestine after consuming infected fish. Light infections are often subclinical; heavier burdens may cause enteritis, diarrhea, abdominal discomfort, poor condition, or other gastrointestinal signs. Wild mammals and birds: Fish-eating species may serve as definitive hosts and contribute eggs to aquatic environments. Fish: Fish are second intermediate hosts and generally serve as the source of infection rather than developing the adult intestinal disease.

Pathology

Adult flukes attach to the mucosa of the small intestine and can produce mucosal irritation and inflammation. Disease severity generally increases with parasite burden. Rare ectopic deposition of eggs may result in granulomatous or other inflammatory lesions in extraintestinal tissues.

Human diagnosis

Diagnosis is usually based on microscopic recognition of characteristic small operculated trematode eggs in stool. The eggs are morphologically very similar or indistinguishable from those of Heterophyes heterophyes and can resemble Clonorchis and Opisthorchis eggs, so species-level attribution may require epidemiologic context and specialized parasitologic or molecular assessment.

Animal diagnosis

Veterinary diagnosis is based on compatible exposure to raw fish, gastrointestinal signs when present, and detection of small trematode eggs on fecal examination. Because egg morphology overlaps with other heterophyid and opisthorchiid flukes, definitive species identification may require specialist parasitology support.

Differential diagnoses

Human differentials include other food-borne intestinal trematodiases, especially heterophyiasis, as well as clonorchiasis, opisthorchiasis, other parasitic enteritides, and nonparasitic causes of diarrhea and abdominal pain. In dogs and cats, differentials include other intestinal parasites and common infectious, inflammatory, dietary, and infiltrative causes of enteritis.

Treatment in humans

Praziquantel is generally regarded as the treatment of choice for human metagonimiasis. Treatment should be directed by a physician familiar with parasitic disease, particularly when the diagnosis is uncertain, infection is heavy, or neurologic or cardiac involvement is suspected.

Treatment in animals—by species

When clinically significant infection is identified in dogs or cats, treatment should be selected by the attending veterinarian. Praziquantel has activity against many trematodes, but the regimen should be based on species, clinical condition, parasite identification, and locally available veterinary products. Preventing continued consumption of raw infected fish is essential to avoid reinfection.

Animal and environmental control

Do not feed dogs, cats, or other captive animals raw or inadequately cooked freshwater or brackish-water fish from endemic areas. Proper disposal of feces and protection of surface waters from fecal contamination reduce continuation of the parasite cycle. Control at the population level depends on sanitation and food-safety measures rather than treatment of a single animal reservoir.

Prevention in humans

Avoid raw, undercooked, inadequately salted, or otherwise insufficiently processed freshwater or brackish-water fish in endemic areas. Thorough cooking is the most reliable household preventive measure. Safe sanitation reduces contamination of aquatic environments with eggs from infected definitive hosts.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Most recognized intestinal infections have a good prognosis after appropriate treatment. Heavy intestinal burdens can cause greater morbidity. Rare extraintestinal egg embolization can produce substantially more serious disease depending on the organ involved.

Reporting, legal, and regulatory considerations

Metagonimiasis is not generally a nationally notifiable disease in the United States. Unusual cases, clusters associated with a shared food source, or imported food-associated infections may warrant consultation with public-health authorities. Requirements vary by jurisdiction.

Selected current sources

• CDC DPDx—Metagonimiasis
• CDC DPDx—Parasites A–Z

MIDDLE EAST RESPIRATORY SYNDROME CORONAVIRUS (MERS-COV)

Synonyms and scope

Middle East respiratory syndrome; MERS. MERS-CoV is a camel-associated zoonotic coronavirus that can also spread between people, especially during close or health-care-associated contact. Dromedary camels are the established animal reservoir linked to human infection.

Etiologic agent

Middle East respiratory syndrome coronavirus (MERS-CoV), an enveloped positive-sense RNA virus in genus Betacoronavirus, family Coronaviridae.

Animals involved and epidemiologic roles

• Dromedary camels: Principal animal reservoir and source of zoonotic exposure; many infections are mild or inapparent.
• People: Can acquire infection from camels and transmit infection to close contacts; substantial outbreaks have occurred in health-care settings.
• Bats: Related coronaviruses occur in bats, but bats are not the recognized direct source of most human MERS cases.
• Other livestock: No established major reservoir role.

Geographic distribution and occurrence

Human cases have occurred predominantly in or in travelers from the Arabian Peninsula. MERS-CoV or closely related camel viruses have been detected in dromedaries across much of the Middle East and Africa. Imported human cases and secondary outbreaks have occurred outside the region.

Reservoir, life cycle, and transmission

Dromedaries maintain MERS-CoV and can shed virus in respiratory secretions. Human infection is associated with direct or indirect camel contact, especially close contact with respiratory secretions, and may also be associated with raw camel milk or inadequately cooked camel products. Human-to-human spread occurs primarily through close contact and can be amplified in health-care settings.

Incubation period

Symptoms usually begin about 5 days after exposure, with a recognized range of approximately 2–14 days.

Disease in humans

Infection ranges from asymptomatic or mild illness to severe pneumonia, acute respiratory distress syndrome, shock, acute kidney injury, and death. Fever, cough, and dyspnea are common. Severe disease is more frequent in older adults and people with diabetes, chronic lung or kidney disease, or immune compromise. The case-fatality proportion among reported WHO cases has been about one third.

Disease in animals—by species

• Dromedary camels: Most infections are asymptomatic or cause mild upper-respiratory disease; young camels tend to shed more virus.
• Other domestic animals: Naturally important reservoir roles have not been established.

Pathology

Severe human disease is characterized by viral pneumonitis and diffuse alveolar injury that can progress to ARDS and multiorgan dysfunction. Characteristic clinically important lesions have not been defined in naturally infected camels because illness is usually mild.

Human diagnosis

Suspected cases require immediate public-health coordination. Diagnosis is based primarily on nucleic-acid amplification testing of respiratory specimens; lower-respiratory specimens may provide higher yield in severe disease. Serology is mainly useful for epidemiologic or retrospective assessment.

Animal diagnosis

Testing of suspect camels should be coordinated with veterinary and public-health authorities. Molecular testing of appropriate respiratory specimens is used in surveillance and outbreak investigations; serology is used to assess prior exposure at population level.

Differential diagnoses

Influenza, COVID-19, other viral pneumonias, community-acquired bacterial pneumonia, legionellosis, severe acute respiratory infections of other causes, and noninfectious causes of ARDS.

Treatment in humans

No specific antiviral therapy has been proven curative. Management is supportive and may include oxygen therapy, intensive respiratory support, hemodynamic support, renal support, and treatment of complications. Infection-control precautions are essential.

Treatment in animals—by species

No specific antiviral treatment is routinely recommended for naturally infected camels. Management is supportive when clinical signs occur. Decisions during outbreak investigation should follow veterinary and public-health direction.

Animal and environmental control

Use farm biosecurity, separate clinically ill camels when practical, minimize unnecessary close face-to-face contact, maintain hygiene around birthing and respiratory secretions, and avoid feeding raw camel products to susceptible animals or people. Veterinary surveillance is important in endemic regions.

Prevention in humans

Wash hands after camel contact; avoid touching the face with unwashed hands; avoid close contact with sick camels; and avoid raw camel milk, urine, or inadequately cooked camel meat. People at increased risk for severe disease should be especially cautious around camels in areas where MERS circulates.

Human vaccination

No licensed human MERS vaccine is currently available.

Animal vaccination

No routinely licensed camel vaccine is currently available for field prevention of MERS.

Prognosis

Mild infections recover fully, but severe human MERS has substantial mortality, particularly in older or medically vulnerable patients. Camel prognosis is generally excellent because disease is usually mild or inapparent.

Reporting, legal, and regulatory considerations

Suspected MERS requires prompt notification to the appropriate state or local health department and coordination with public-health authorities for testing, infection control, and case investigation. Reporting and international notification requirements depend on jurisdiction and outbreak context; animal testing, movement restrictions, and control measures should be coordinated with veterinary authorities.

Selected current sources

• CDC—Clinical Overview of MERS
• CDC—About MERS
• WHO—MERS-CoV

MICROSPORIDIOSIS

Synonyms and scope

Human and animal microsporidial infection. Microsporidia are spore-forming obligate intracellular fungal-related parasites. This umbrella entry emphasizes medically important species with plausible animal or environmental links rather than implying that all human microsporidiosis is zoonotic.

Etiologic agent

Human disease has been attributed to at least 15 microsporidian species, especially Enterocytozoon bieneusi, Encephalitozoon intestinalis, E. cuniculi, and E. hellem. Other genera cause less common ocular, muscular, disseminated, or other infections.

Animals involved and epidemiologic roles

• Rabbits: Major reservoir for E. cuniculi; many infections are subclinical.
• Dogs, cats, foxes, mink, and nonhuman primates: Occasional E. cuniculi hosts.
• Psittacine birds: Can carry E. hellem.
• Pigs, cattle, dogs, cats, primates, and wildlife: Some carry zoonotic genotypes of E. bieneusi.
• People: Especially susceptible to severe disease when immunocompromised.

Geographic distribution and occurrence

Worldwide. Infection is increasingly recognized with molecular diagnostics. Severe or disseminated disease occurs disproportionately in people with advanced immune suppression, transplant recipients, and other immunocompromised patients, although ocular and localized infections can occur in immunocompetent people.

Reservoir, life cycle, and transmission

Resistant spores are shed from infected hosts and occur in water and soil. Transmission for many species is incompletely defined but likely includes fecal-oral, urinary-oral, waterborne, environmental, and occasionally zoonotic exposure. Some E. cuniculi infections have also been donor-derived after organ transplantation. Direct proof of pet-to-person transmission is uncommon.

Incubation period

Not well defined and varies by organism, exposure route, and host immune status. Disease may become apparent long after acquisition in immunocompromised patients.

Disease in humans

Manifestations include chronic watery diarrhea and wasting, keratoconjunctivitis or keratitis, sinus or respiratory disease, nephritis, hepatitis, myositis, encephalitis, and disseminated infection. Clinical pattern depends strongly on species and immune status.

Disease in animals—by species

• Rabbits—E. cuniculi: Often subclinical; neurologic disease, vestibular signs, renal disease, uveitis, or cataract can occur.
• Dogs and cats: Rare neurologic, renal, ocular, or disseminated infection.
• Birds: E. hellem and related microsporidia may cause ocular, intestinal, renal, or systemic disease.
• Livestock and wildlife: Often asymptomatic carriage of E. bieneusi genotypes.

Pathology

Lesions reflect intracellular infection and host inflammation. Depending on species and tissue, findings may include villous injury, granulomatous nephritis or encephalitis, keratitis, myositis, hepatitis, or disseminated inflammatory lesions.

Human diagnosis

Diagnosis uses specialized microscopy or stains, histopathology, immunofluorescence, and increasingly PCR or sequencing on stool, urine, ocular samples, tissue, or other appropriate specimens. Species identification can affect treatment and epidemiologic interpretation.

Animal diagnosis

Diagnosis depends on species and syndrome. In rabbits, serology can document exposure but does not by itself prove active clinical disease; PCR of urine or tissue, histopathology, and clinicopathologic findings may support diagnosis. Similar molecular or histologic methods are used in other animals.

Differential diagnoses

Cryptosporidiosis, giardiasis, coccidiosis, other causes of chronic diarrhea, toxoplasmosis, viral or bacterial encephalitis, vestibular disease in rabbits, fungal keratitis, inflammatory bowel disease, and other opportunistic infections.

Treatment in humans

Treatment is species- and site-dependent. Albendazole is active against several Encephalitozoon species but is unreliable for E. bieneusi. Fumagillin has activity against some infections but availability and toxicity limit use. Immune restoration, when possible, is important in immunocompromised patients. Specialist infectious-disease or ophthalmology management is appropriate for severe, ocular, or disseminated disease.

Treatment in animals—by species

• Rabbits: Fenbendazole is commonly used under veterinary supervision for suspected clinical E. cuniculi, together with supportive treatment for vestibular, renal, nutritional, and ocular complications.
• Other animals: Treatment evidence is limited and should be individualized by species and syndrome.

Animal and environmental control

Maintain clean, dry housing; promptly remove urine and feces; prevent crowding; quarantine clinically ill or newly acquired animals when appropriate; and avoid sharing contaminated equipment. Routine eradication of latent E. cuniculi from rabbit populations is difficult.

Prevention in humans

Practice hand hygiene after animal contact, litter or cage cleaning, and gardening; avoid untreated water when immunocompromised; wear gloves when handling urine-soiled rabbit bedding or clinically ill animals; and use particular caution for severely immunocompromised household members.

Human vaccination

No human vaccine is available.

Animal vaccination

No licensed animal vaccine is available.

Prognosis

Prognosis ranges from excellent for localized disease to guarded for disseminated infection in severely immunocompromised people. Rabbits with mild neurologic disease may improve, but persistent vestibular deficits, renal injury, or ocular damage can remain.

Reporting, legal, and regulatory considerations

Microsporidiosis is generally not routinely reportable. Transplant-associated clusters, unusual zoonotic clusters, or waterborne outbreaks may warrant public-health investigation.

Selected current sources

• CDC DPDx—Microsporidiosis
• Merck Veterinary Manual—Encephalitozoonosis in Rabbits

MORGANELLA MORGANII

Synonyms and scope

Morganella morganii infection; opportunistic animal-associated wound infection. This organism is part of normal intestinal flora in people and many animals, so most human infections are not zoonotic. Its clearest animal association is secondary infection of traumatic wounds, especially snakebites.

Etiologic agent

Morganella morganii, a gram-negative facultatively anaerobic member of family Morganellaceae. It has intrinsic resistance to several commonly used antimicrobial classes and may acquire additional resistance.

Animals involved and epidemiologic roles

• Snakes: Oral and gastrointestinal carriage can contaminate bite wounds; M. morganii is among the most frequently recovered organisms from infected snakebite wounds in several regions.
• Other reptiles, mammals, and birds: Can carry the organism as intestinal flora.
• People: Often develop endogenous health-care-associated, urinary, wound, or bloodstream infection unrelated to animals.

Geographic distribution and occurrence

Worldwide. Human infection is uncommon relative to other Enterobacterales but occurs in health-care, urinary, intra-abdominal, and traumatic wound settings. Snakebite-associated infections are reported particularly from tropical regions with medically important snakes.

Reservoir, life cycle, and transmission

The organism colonizes intestinal tracts and environments. Animal-associated infection follows traumatic inoculation of contaminated oral or environmental flora into tissue, especially after snakebite. Person-to-person spread is not a characteristic zoonotic cycle.

Incubation period

No organism-specific incubation period is established. Secondary wound infection generally becomes evident over hours to days after tissue injury.

Disease in humans

Clinical syndromes include cellulitis, abscess, necrotic wound infection, urinary tract infection, bacteremia, sepsis, pneumonia, intra-abdominal infection, and occasional central nervous system infection. Risk rises with advanced age, hospitalization, immunocompromise, or major tissue injury.

Disease in animals—by species

• Reptiles: Often asymptomatic colonization; opportunistic wound or systemic infection can occur.
• Mammals and birds: Sporadic urinary, wound, respiratory, or septicemic disease has been reported, usually as an opportunistic infection.

Pathology

Pathology is syndrome-dependent and can include suppurative cellulitis, abscessation, necrosis, bacteremia, and sepsis. In snakebite patients, venom-mediated tissue injury can predispose to secondary bacterial invasion.

Human diagnosis

Obtain appropriate deep wound, tissue, blood, urine, or other clinical specimens when infection is suspected. Laboratory identification and antimicrobial susceptibility testing are important because resistance is variable. Clinical diagnosis of snakebite infection should distinguish infection from venom-related inflammation and necrosis.

Animal diagnosis

Culture or molecular identification from normally sterile sites or compatible lesions can confirm opportunistic infection. Isolation from oral or fecal samples alone may represent colonization and should not be interpreted as disease.

Differential diagnoses

Other polymicrobial bite-wound infections, Aeromonas, Enterococcus, Proteus, Pseudomonas, staphylococci, anaerobes, venom-induced sterile inflammation, compartment syndrome, and necrotizing soft-tissue infection.

Treatment in humans

Manage the primary injury, including wound irrigation, surgical assessment, drainage or debridement when indicated, and antivenom for envenomation when appropriate. Use antimicrobials for established or strongly suspected bacterial infection and tailor therapy to susceptibility results. Routine prophylactic antibiotics after snakebite are not consistently supported by evidence.

Treatment in animals—by species

Treat clinically significant infection based on the affected species, infection site, source control, and susceptibility testing. Colonization alone does not justify antimicrobial treatment.

Animal and environmental control

Prevent bites through safe animal handling and housing. Maintain good enclosure hygiene and promptly treat traumatic wounds in captive animals. There is no indication for attempting to eradicate normal intestinal carriage in healthy animals.

Prevention in humans

Avoid snake handling unless trained, use appropriate protective methods, seek urgent medical care after snakebite, and promptly clean animal-associated wounds. Do not use antibiotics routinely after every snakebite unless clinically indicated.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Usually good with timely source control and active antimicrobial therapy. Severe envenomation, deep necrosis, bacteremia, or multidrug-resistant infection can worsen outcome.

Reporting, legal, and regulatory considerations

M. morganii infection itself is generally not reportable. Snakebite reporting and occupational injury documentation vary by jurisdiction; unusual antimicrobial resistance may trigger laboratory or infection-control notification.

Selected current sources

• Systematic Review—Snakebite-Associated Infections
• Systematic Review—Antimicrobial Prophylaxis in Snakebite

MPOX (FORMERLY MONKEYPOX)

Synonyms and scope

Mpox; monkeypox. Current public-health terminology increasingly uses “monkeypox” for the disease in U.S. CDC materials, while WHO adopted “mpox” as a preferred synonym. This retained website anchor and title are preserved for continuity. The disease is a true zoonosis but recent large outbreaks have been driven predominantly by person-to-person transmission.

Etiologic agent

Monkeypox virus (MPXV), genus Orthopoxvirus, family Poxviridae. Two major clades, clade I and clade II, contain recognized subclades with differing epidemiology and severity.

Animals involved and epidemiologic roles

• African small mammals: Likely reservoirs or maintenance hosts include rope and sun squirrels, giant-pouched rats, African dormice, and other small mammals; the exact reservoir ecology is not fully resolved.
• Nonhuman primates: Susceptible spillover hosts and may develop clinical disease.
• Prairie dogs and other rodents: Can become infected and transmit virus, as demonstrated in the 2003 U.S. outbreak.
• Companion animals and other mammals: A broad mammalian host range is possible; human-to-animal transmission has been documented or is biologically plausible.
• People: Can acquire infection from animals or other people.

Geographic distribution and occurrence

Historically endemic in parts of Central and West Africa, with clade-specific regional patterns. Since 2022, clade IIb has caused sustained multinational person-to-person transmission. Clade I outbreaks have also produced international concern and travel-associated cases.

Reservoir, life cycle, and transmission

Transmission occurs through direct contact with skin or mucosal lesions, body fluids, contaminated materials, and close respiratory exposure. Animal-to-human transmission can follow bites, scratches, hunting, handling, or contact with infected tissues. Human-to-animal transmission is possible, so infected people should avoid close contact with susceptible mammals.

Incubation period

Usually approximately 3–17 days, though the recognized range varies somewhat among outbreaks and surveillance definitions.

Disease in humans

Typical illness includes rash or mucosal lesions, fever, lymphadenopathy, headache, myalgia, fatigue, or sore throat. Lesions may be localized or disseminated and can be painful. Severe complications include bacterial superinfection, proctitis, ocular disease, encephalitis, pneumonia, and disseminated disease, particularly in people with severe immune compromise.

Disease in animals—by species

• Rodents: Clinical disease ranges from subclinical infection to fever, lethargy, lymphadenopathy, conjunctivitis, rash, or death.
• Nonhuman primates: Fever, lymphadenopathy, and vesiculopustular lesions may occur.
• Companion mammals: Susceptibility varies; compatible skin lesions, fever, lethargy, respiratory signs, or lymphadenopathy after exposure warrant veterinary/public-health consultation.

Pathology

Lesions show ballooning degeneration, epidermal necrosis, vesiculation, pustule formation, and orthopoxviral cytoplasmic inclusions. Severe systemic disease can involve respiratory, neurologic, ocular, or other organs.

Human diagnosis

PCR testing of lesion material is the principal diagnostic method. Clinical appearance alone is insufficient because herpesvirus infections, varicella, syphilis, bacterial skin disease, and other poxviruses can mimic monkeypox.

Animal diagnosis

Animals meeting a suspect case definition should be evaluated in coordination with public-health and animal-health authorities. PCR testing of appropriate lesion or other specimens is used; routine testing of healthy exposed animals is generally not indicated unless directed.

Differential diagnoses

Varicella-zoster, herpes simplex, syphilis, molluscum contagiosum, bacterial folliculitis, hand-foot-and-mouth disease, other orthopoxvirus infections, and drug eruptions.

Treatment in humans

Most patients need supportive care and pain management. People with severe disease or high risk for complications may require specialist-directed antiviral or investigational therapy under current public-health guidance. Management recommendations can change as evidence evolves.

Treatment in animals—by species

There is no routinely established species-specific antiviral regimen for naturally infected animals. Isolate suspect animals, provide supportive veterinary care, avoid unnecessary procedures that increase exposure, and coordinate management with public-health and animal-health authorities.

Animal and environmental control

Separate infected people from susceptible mammals, prevent pets from contacting lesion material or contaminated linens, use PPE when handling suspect animals, and clean contaminated environments according to public-health guidance. Do not release exposed captive wildlife or exotic pets.

Prevention in humans

Avoid direct contact with lesions and contaminated materials, use recommended PPE for care, practice hand hygiene, and reduce high-risk animal exposure in endemic settings. Vaccination is recommended for people at increased risk and can be used after selected exposures.

Human vaccination

Vaccinia-based vaccines are available for prevention in people at increased risk and for postexposure prophylaxis according to current public-health recommendations.

Animal vaccination

No routinely licensed veterinary monkeypox vaccine is available for companion or production animals.

Prognosis

Most immunocompetent people recover, but severe or fatal disease can occur, especially with profound immune suppression or certain clade I infections. Prognosis in animals varies by species and disease severity.

Reporting, legal, and regulatory considerations

Human monkeypox is reportable in many jurisdictions and suspected animal cases may require immediate public-health or animal-health notification. Animal movement, quarantine, testing, and disposition are jurisdiction-specific.

Selected current sources

• CDC—About Monkeypox
• CDC—Clinical Overview of Clade I and Clade II Monkeypox
• CDC—Veterinary Guidance for Monkeypox

MYCOBACTERIOSIS

Synonyms and scope

Nontuberculous mycobacterial infection; animal-associated mycobacteriosis; avian mycobacteriosis; aquarium- or fish-associated mycobacteriosis. This entry covers animal-associated nontuberculous mycobacteria (NTM) broadly and complements the separate Mycobacterium marinum monograph and the S–Z Tuberculosis monograph. Avian tuberculosis/mycobacteriosis caused by the M. avium complex is included here as NTM disease but is also discussed under Tuberculosis because of its traditional name.

Etiologic agent

NTM include numerous environmental mycobacteria. Important animal-associated examples include aquatic species such as Mycobacterium marinum, M. chelonae, M. fortuitum, and M. abscessus; and avian pathogens including M. avium subsp. avium, M. genavense, M. avium subsp. hominissuis, and M. intracellulare. These organisms occur widely in water, soil, sediments, biofilms, and contaminated animal environments.

Animals involved and epidemiologic roles

• Aquarium and cultured fish: important hosts for chronic granulomatous mycobacteriosis and a recognized source of traumatic aquatic exposure.
• Birds: domestic poultry, companion birds, zoo birds, and wild birds can develop avian mycobacteriosis; M. avium subsp. avium is especially important in poultry and M. genavense in pet/exotic birds.
• Reptiles and amphibians: can harbor several NTM species and may expose handlers through aquatic environments.
• Mammals: opportunistic NTM infection occurs in many species, including swine and companion animals.
• People: most NTM disease is acquired from environmental water, soil, aerosols, or traumatic inoculation rather than efficient animal-to-human transmission. Direct transmission from infected birds appears uncommon or unproven.

Geographic distribution and occurrence

Worldwide. NTM are ubiquitous environmental organisms. Fish mycobacteriosis occurs in freshwater and marine systems, especially intensive or recirculating environments. Avian mycobacteriosis occurs worldwide in poultry, aviaries, pet birds, zoo birds, and wildlife. Human MAC and other NTM disease occurs worldwide and is usually associated with environmental exposure rather than contact with infected animals.

Reservoir, life cycle, and transmission

NTM persist in environmental water, soil, biofilms, litter, and contaminated enclosures. Human aquatic infection typically follows inoculation through cuts, punctures, abrasions, fish-spine injuries, or contaminated water. Fish can shed organisms into system water. In avian mycobacteriosis, infected birds may shed organisms in feces, contaminating soil, litter, cages, food, and water; birds are commonly infected orally from contaminated environments. Human MAC disease is generally considered environmentally acquired rather than a direct consequence of bird contact.

Incubation period

Variable by species, route, and site. Cutaneous M. marinum disease often becomes apparent within several weeks but can be delayed. Avian mycobacteriosis is usually chronic and may remain subclinical for prolonged periods before progressive wasting or organ-specific signs develop.

Disease in humans

Aquatic NTM most often cause chronic skin and soft-tissue lesions, nodules, ulcers, or lymphocutaneous spread; tendon, joint, bursal, or bone infection can occur. MAC and other NTM can cause pulmonary disease, cervical lymphadenitis, skin/soft-tissue disease, and disseminated infection, particularly in immunocompromised people. Most human NTM disease is not attributable to direct animal transmission.

Disease in animals—by species

• Fish: chronic wasting, anorexia, skin ulcers, hemorrhage, exophthalmos, ascites, pallor, skeletal deformity, and internal granulomas; subclinical carriers occur.
• Birds: chronic progressive weight loss, anorexia or preserved appetite with wasting, depression, diarrhea, hepatosplenomegaly, abdominal masses, lameness or joint swelling, ocular lesions, and granulomatous disease of the intestine, liver, spleen, bone marrow, or other organs.
• Reptiles/amphibians: granulomatous skin, respiratory, visceral, or disseminated disease may occur.
• Other mammals: opportunistic localized or disseminated NTM infection is species-dependent.

Pathology

Typical lesions are chronic granulomatous inflammation containing acid-fast organisms. Fish commonly develop granulomas in kidney, spleen, liver, and other viscera. Birds often develop granulomas in the intestinal tract, liver, spleen, and bone marrow, with possible joint, ocular, skin, or disseminated lesions. Human disease may show granulomatous dermatitis, tenosynovitis, osteomyelitis, synovitis, pulmonary disease, or disseminated infection.

Human diagnosis

Diagnosis depends on the clinical syndrome and exposure history and may require imaging, tissue sampling, acid-fast staining, molecular identification, and mycobacterial culture. Species identification is important because NTM treatment differs substantially among organisms. Clinicians should not assume that human MAC disease was acquired from a household bird solely because the same broad organism group is present in birds.

Animal diagnosis

In fish, compatible granulomatous lesions and acid-fast organisms support the diagnosis, with definitive identification by specialized laboratory methods. In birds, diagnosis may involve imaging, hematology, cytology or biopsy, histopathology, acid-fast staining, and molecular testing. Fecal testing can identify some shedding birds but lacks sufficient sensitivity to exclude infection when negative.

Differential diagnoses

Deep fungal infection, nocardiosis, bacterial granulomas, neoplasia, foreign-body granuloma, sporotrichosis, leishmaniasis, chronic enteropathy, hepatic disease, parasitism, and other causes of chronic wasting or nodular/granulomatous disease. In birds, chlamydiosis and other systemic infections may mimic avian mycobacteriosis.

Treatment in humans

Therapy depends on NTM species, infection site and depth, susceptibility, and host factors and often requires prolonged multidrug treatment. Deep tendon, joint, bone, pulmonary, or disseminated disease may require specialist care and sometimes surgery.

Treatment in animals—by species

Fish: elimination is difficult; population-level control often relies on removal of affected fish, husbandry correction, and system management rather than antimicrobial therapy. Poultry: treatment of avian tuberculosis is generally not recommended. Companion/exotic birds: prolonged multidrug treatment may be considered in selected individual birds under an avian veterinarian, but therapy can extend for many months and relapse or treatment toxicity may occur. Other animals: treatment decisions are species- and case-specific and should consider zoonotic and collection-level implications.

Animal and environmental control

Reduce organic debris, maintain appropriate water quality and stocking density in aquatic systems, quarantine new animals, promptly remove dead or clinically affected animals, and prevent sharing contaminated wet equipment. For bird collections, minimize fecal contamination of food and water, improve enclosure hygiene, isolate affected birds when appropriate, and evaluate exposed collections. Environmental persistence can make eradication from soil-based aviaries difficult.

Prevention in humans

Wear waterproof gloves when cleaning aquariums or handling diseased fish, especially if skin is broken, and avoid immersing open wounds in aquarium or natural water. For known or suspected avian mycobacteriosis, use gloves and careful hand hygiene and minimize exposure to feces, dust, aerosols, and contaminated enclosure material. The zoonotic risk from infected birds appears low, but immunocompromised people should avoid high-exposure contact with infected birds or heavily contaminated environments.

Human vaccination

No vaccine is available to prevent human NTM disease. BCG vaccination is intended for M. tuberculosis-complex disease and does not provide reliable protection against environmental NTM.

Animal vaccination

No routinely available vaccine prevents fish, reptile, or companion-bird NTM infection, and vaccination is not a substitute for hygiene, quarantine, surveillance, and environmental control in affected collections.

Prognosis

Localized human NTM infection is often curable but may require prolonged therapy; delayed diagnosis increases the risk of deep structural involvement. Prognosis for system-level fish infection is guarded because eradication is difficult. In birds, advanced disseminated disease carries a guarded to poor prognosis; selected companion birds may respond to prolonged therapy, but relapse and persistent environmental exposure are concerns.

Reporting, legal, and regulatory considerations

Most NTM infections are not routinely reportable as ordinary human TB. Clusters related to commercial aquaculture, public exhibits, occupational exposure, poultry flocks, or managed bird collections may warrant public-health or veterinary investigation. Avian mycobacteriosis reporting requirements vary by jurisdiction. Food-fish antimicrobial use is regulated and must follow applicable residue requirements.

Selected current sources

• CDC—Tuberculosis Glossary: Nontuberculous Mycobacteria
• CDC—Environmental Control: Nontuberculous Mycobacteria and Water
• Merck Veterinary Manual—Bacterial Diseases of Fish
• Merck Veterinary Manual—Avian Mycobacteriosis in Pet Birds
• Merck Veterinary Manual—Tuberculosis in Poultry
• WOAH—Avian Tuberculosis
• CDC—Healthy Pets: Fish

MYCOBACTERIUM MARINUM

Synonyms and scope

Fish-tank granuloma; aquarium granuloma; swimming-pool granuloma. This is the best-established aquarium-associated nontuberculous mycobacterial zoonosis.

Etiologic agent

Mycobacterium marinum, a slow-growing photochromogenic nontuberculous mycobacterium associated with freshwater, brackish water, salt water, and aquatic animals.

Animals involved and epidemiologic roles

• Fish: Important hosts and sources of contaminated aquarium or aquaculture environments.
• Reptiles and amphibians: Can be associated with aquatic exposure and may harbor M. marinum.
• People: Accidental hosts following inoculation through damaged skin.

Geographic distribution and occurrence

Worldwide. Human cases occur after aquarium maintenance, fish handling, fishing, seafood handling, and natural-water injuries. Infection is uncommon but frequently delayed in diagnosis because lesions are indolent and routine antibacterial therapy is ineffective.

Reservoir, life cycle, and transmission

The organism persists in aquatic environments and infected fish. Human infection occurs when contaminated water, fish, or equipment contacts abrasions, puncture wounds, fish-spine injuries, or other breaks in the skin. Person-to-person transmission is exceptionally rare.

Incubation period

Often about 2–4 weeks, but onset can range from days to several months after exposure.

Disease in humans

Usually a slowly enlarging papule, nodule, plaque, or ulcer on an exposed extremity. Lesions may spread proximally along lymphatics in a sporotrichoid pattern. Deep infection can involve tendon sheaths, joints, bursae, or bone; disseminated disease is rare and mainly affects severely immunocompromised people.

Disease in animals—by species

• Fish: Chronic wasting, ulceration, exophthalmos, ascites, skeletal deformity, and granulomas in viscera; some fish remain subclinical.
• Reptiles/amphibians: Sporadic granulomatous skin or disseminated disease can occur.

Pathology

Human lesions are granulomatous and may extend into synovium, tendon sheaths, or bone. Fish typically develop multifocal granulomas in kidney, spleen, liver, and other organs.

Human diagnosis

Aquatic exposure history is crucial. Biopsy with histopathology, acid-fast staining, PCR or sequencing, and mycobacterial culture can establish the diagnosis. Alert the laboratory when M. marinum is suspected because standard routines may fail to detect it.

Animal diagnosis

Compatible granulomas plus acid-fast organisms are strongly suggestive. Definitive species identification uses specialized laboratory methods. Differentiate from other fish NTM because several species can produce similar lesions.

Differential diagnoses

Sporotrichosis, nocardiosis, cutaneous leishmaniasis, deep fungal infection, foreign-body granuloma, bacterial abscess, rheumatoid nodules, and neoplasia.

Treatment in humans

Prolonged antimycobacterial therapy is generally required, selected according to disease depth, susceptibility, drug interactions, and specialist guidance. Deep tendon, joint, or bone involvement may require surgical debridement in addition to medical therapy.

Treatment in animals—by species

There is no reliably curative population treatment for infected aquarium fish. Removal of affected fish and management of the contaminated system are generally favored. Individual treatment of valuable fish should be undertaken only with aquatic-veterinary guidance.

Animal and environmental control

Quarantine new fish, maintain good water quality, minimize crowding and organic loading, promptly remove dead or severely affected fish, and thoroughly manage contaminated systems before restocking. Shared wet equipment can spread infection between tanks.

Prevention in humans

Wear waterproof gloves during aquarium cleaning or when handling diseased fish, cover cuts, avoid immersion of open wounds, and wash fish-spine or aquarium injuries promptly. Immunocompromised people should consider having another person clean aquariums.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Localized skin disease usually resolves with appropriate prolonged therapy, but delayed diagnosis can lead to chronic tenosynovitis, arthritis, osteomyelitis, scarring, and functional impairment. Fish-population prognosis is guarded because infection can persist in the environment.

Reporting, legal, and regulatory considerations

Usually not reportable. Occupational clusters or infections linked to commercial aquaculture or public exhibits may merit workplace, public-health, or veterinary investigation.

Selected current sources

• CDC Yellow Book—Mycobacterium marinum Infection
• CDC—Nontuberculous Mycobacteria
• Merck Veterinary Manual—Fish Mycobacteriosis

MYCOBACTERIUM ULCERANS

Synonyms and scope

Buruli ulcer; Bairnsdale ulcer in parts of Australia. This is primarily an environmental nontuberculous mycobacterial disease. Animal infection is epidemiologically important in some regions, especially southeastern Australia, but routine direct animal-to-human transmission has not been established.

Etiologic agent

Mycobacterium ulcerans, an environmental mycobacterium that produces the lipid toxin mycolactone, responsible for local tissue necrosis and immunosuppression.

Animals involved and epidemiologic roles

• Possums in southeastern Australia: Can develop disease and shed M. ulcerans DNA or organisms; their distribution and fecal contamination correlate with human risk in some endemic areas.
• Dogs, cats, horses, koalas, and other mammals: Natural infections have been reported in endemic regions.
• Aquatic and terrestrial environments: Strongly associated with transmission ecology.
• People: Accidental hosts; exact acquisition route remains unresolved.

Geographic distribution and occurrence

Reported in more than 30 countries in Africa, the Americas, Asia, and the Western Pacific. Most cases occur in tropical or subtropical regions, but important temperate foci occur in southeastern Australia and Japan. Geographic risk is highly focal.

Reservoir, life cycle, and transmission

The precise transmission route remains unknown. Environmental exposure is central, and insect vectors have been investigated in some regions. In Australia, possums appear to participate in local ecology, but direct transmission from possums, pets, fish, or other animals to people has not been proven as the routine route.

Incubation period

Usually prolonged and difficult to determine; epidemiologic studies suggest a typical interval of several months, with reported ranges from weeks to many months.

Disease in humans

Disease commonly begins as a painless nodule, papule, plaque, or area of edema and progresses to a painless ulcer with undermined edges. Delayed treatment can cause extensive tissue loss, scarring, contracture, osteomyelitis, deformity, and disability.

Disease in animals—by species

• Possums: Ulcerative skin lesions may occur; some infected animals may shed organisms in feces.
• Dogs and cats: Chronic nonhealing skin ulcers or nodules can occur in endemic areas.
• Horses and other mammals: Sporadic ulcerative disease has been reported.

Pathology

Mycolactone causes extensive coagulative necrosis of skin and subcutaneous tissue with relatively limited early inflammation. Acid-fast organisms may cluster in necrotic tissue. Bone can be involved in advanced disease.

Human diagnosis

In an endemic setting, diagnosis is based on compatible lesions and laboratory confirmation, most commonly PCR. Histopathology, microscopy, or other reference methods may support diagnosis. Early confirmation is important because treatment can prevent extensive tissue loss.

Animal diagnosis

In endemic regions, chronic compatible ulcers should prompt veterinary investigation. PCR, histopathology, and other mycobacterial testing may be used. Results should be interpreted with regional epidemiology because environmental contamination is possible.

Differential diagnoses

Cutaneous tuberculosis, leprosy, deep fungal infection, tropical ulcer, pyoderma gangrenosum, squamous-cell carcinoma, vascular ulceration, traumatic wounds, and other chronic bacterial infections.

Treatment in humans

WHO recommends combination antimicrobial therapy, currently commonly rifampicin plus clarithromycin, together with wound care. Surgery, skin grafting, and physiotherapy may be needed for extensive lesions or functional impairment. Regimens should follow current regional and specialist guidance.

Treatment in animals—by species

Veterinary treatment is case-specific and may involve prolonged antimycobacterial therapy, wound management, and surgery. Evidence is limited, and public-health consultation may be appropriate in endemic areas.

Animal and environmental control

No proven animal-control program eliminates human risk because transmission is unresolved. In endemic Australian regions, surveillance of possums and animal cases can support public-health risk mapping. Manage wounds, reduce mosquito exposure where locally recommended, and avoid unnecessary contact with contaminated environmental material.

Prevention in humans

No single proven preventive measure exists. In endemic areas, promptly clean and cover skin injuries, use protective clothing during outdoor activities, and follow local mosquito-bite prevention recommendations. Seek early evaluation of persistent painless nodules, swelling, or ulcers.

Human vaccination

No specific vaccine is available. BCG may provide limited or transient protection but is not relied upon as a Buruli-ulcer prevention strategy.

Animal vaccination

No vaccine is available.

Prognosis

Excellent when diagnosed and treated early. Delayed diagnosis increases the risk of extensive ulceration, osteomyelitis, scarring, contractures, and long-term disability. Animal prognosis depends on lesion extent and response to therapy.

Reporting, legal, and regulatory considerations

Buruli ulcer is subject to surveillance in endemic countries and may be reportable regionally. Animal cases in endemic Australian jurisdictions may be epidemiologically important and should follow local veterinary/public-health notification guidance.

Selected current sources

• WHO—Buruli Ulcer
• WHO—Buruli Ulcer Fact Sheet

MURINE TYPHUS

Synonyms and scope

Flea-borne typhus; endemic typhus. A zoonotic rickettsial disease transmitted to people by infected fleas. The classic rat–rat flea cycle remains important, while cat fleas and periurban hosts such as opossums, cats, and dogs are epidemiologically relevant in some regions.

Etiologic agent

Rickettsia typhi, an obligate intracellular bacterium in the typhus group rickettsiae.

Animals involved and epidemiologic roles

• Rats and other rodents: Principal reservoir hosts in the classic urban cycle.
• Opossums, cats, and dogs: Can host infected fleas and contribute to periurban transmission cycles in some areas; they are not ordinarily direct sources to people.
• Fleas: Particularly Xenopsylla cheopis and, in some settings, Ctenocephalides felis; infected flea feces are the usual source of human inoculation.
• People: Incidental hosts.

Geographic distribution and occurrence

Occurs worldwide, especially in tropical and subtropical regions. In the United States, most reported cases occur in southern California, Texas, and Hawaii, with increasing recognition in some endemic areas.

Reservoir, life cycle, and transmission

Fleas acquire infection while feeding on rickettsemic reservoir hosts. People are infected when contaminated flea feces are rubbed into bites, abrasions, or mucous membranes; inhalation of contaminated flea dirt is also possible. Person-to-person transmission is not expected.

Incubation period

Usually about 7–14 days; illness may begin roughly 3–14 days after exposure.

Disease in humans

Fever, severe headache, myalgia, malaise, nausea, abdominal pain, cough, and sometimes rash. Rash often begins on the trunk and may be absent. Severe disease can include hepatitis, pneumonia, meningoencephalitis, renal dysfunction, or shock; death is uncommon but possible.

Disease in animals—by species

• Rodents: Reservoir infection is usually subclinical.
• Cats, dogs, and opossums: Generally do not develop a characteristic clinical syndrome from R. typhi; their importance is primarily as hosts for infected fleas.

Pathology

Rickettsial infection of vascular endothelial cells produces systemic vasculitis and increased vascular permeability. Severe cases may involve lungs, central nervous system, liver, kidneys, and other organs.

Human diagnosis

Diagnosis is based on compatible illness and exposure plus laboratory support. Paired IgG serology demonstrating a fourfold rise is the usual confirmatory method; PCR may support early diagnosis but a negative result does not exclude disease. Treatment should not be delayed while awaiting confirmation.

Animal diagnosis

Routine testing of healthy pets or wildlife is not generally indicated. Public-health or research investigations may use serologic or molecular methods to assess reservoir or flea exposure.

Differential diagnoses

Rocky Mountain spotted fever and other rickettsioses, leptospirosis, dengue, viral syndromes, meningococcemia, typhoid fever, ehrlichiosis, anaplasmosis, and other febrile illnesses.

Treatment in humans

Doxycycline is the treatment of choice for suspected flea-borne typhus in adults and children of all ages. Clinicians should treat empirically when clinical suspicion is significant rather than waiting for laboratory confirmation.

Treatment in animals—by species

No routine antimicrobial treatment is indicated for clinically normal animals solely because they may have been exposed to infected fleas. Treat any identified animal illness on its own merits and institute effective flea control.

Animal and environmental control

Maintain effective flea control on pets, reduce rodent and opossum harborage, secure food and refuse, and coordinate rodent control with flea control so displaced infected fleas do not seek new hosts.

Prevention in humans

Avoid flea exposure, use EPA-registered repellents as directed, keep pets on effective flea preventives, and reduce contact with rodents and flea-infested wildlife environments.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Excellent with prompt doxycycline treatment. Delayed therapy increases the risk of hospitalization and severe organ involvement.

Reporting, legal, and regulatory considerations

Reporting requirements vary by jurisdiction. CDC advises that suspected clusters and cases in endemic settings be reported to state or local public-health authorities as required.

Selected current sources

• CDC—Clinical Overview of Flea-borne Typhus
• CDC—About Flea-borne Typhus

NANOPHYETIASIS

Synonyms and scope

Nanophyetus infection; salmon-fluke infection. A foodborne intestinal trematode infection acquired from raw or inadequately cooked fish. In dogs, the far more serious associated problem is salmon poisoning disease caused by Neorickettsia helminthoeca carried by the fluke; that bacterial disease is not known to infect people.

Etiologic agent

Nanophyetus salmincola and related Nanophyetus species, minute intestinal trematodes.

Animals involved and epidemiologic roles

• Dogs, cats, wild canids, mustelids, bears, and other fish-eating mammals: Definitive hosts.
• Fish-eating birds: Can serve as definitive hosts.
• Freshwater snails: First intermediate hosts.
• Salmonids and some other fish: Second intermediate hosts carrying metacercariae.
• People: Accidental definitive hosts after eating infected fish or roe.

Geographic distribution and occurrence

Occurs along portions of the Pacific coast of North America and in parts of Eurasia. In North America the parasite is associated particularly with the Pacific Northwest and adjacent coastal regions.

Reservoir, life cycle, and transmission

Eggs from infected definitive hosts enter water and continue development through snail and fish hosts. People and other definitive hosts become infected by eating raw, undercooked, or otherwise inadequately processed infected fish or fish roe. Ordinary contact with infected dogs, cats, wildlife, or fish does not transmit infection.

Incubation period

Not precisely defined for human disease. Gastrointestinal symptoms, when they occur, generally follow acquisition of mature intestinal flukes after ingestion of infected fish.

Disease in humans

Human infection is uncommon and usually mild. Abdominal discomfort, nausea, diarrhea, increased bowel activity, fatigue, or eosinophilia may occur; some infections are asymptomatic.

Disease in animals—by species

• Dogs: The fluke itself may cause enteritis when burdens are heavy. More importantly, infected flukes can transmit Neorickettsia helminthoeca, causing salmon poisoning disease with fever, vomiting, diarrhea, lymphadenopathy, weakness, weight loss, and potentially death if untreated.
• Cats and wild fish-eating mammals: Intestinal fluke infection is often mild or subclinical.
• Fish: Metacercariae may be present in tissues without obvious external signs.

Pathology

Adult flukes attach between small-intestinal villi and can cause focal mucosal inflammation and enteritis. In canine salmon poisoning disease, systemic inflammation results from the associated Neorickettsia infection rather than from the fluke alone.

Human diagnosis

Diagnosis is by identification of characteristic operculated eggs in stool, supported by compatible dietary exposure. Specialist parasitology review may be needed because trematode eggs can resemble those of other species.

Animal diagnosis

Fecal examination can identify Nanophyetus eggs in definitive hosts. Dogs with compatible systemic illness after raw salmonid exposure should be evaluated promptly for salmon poisoning disease using appropriate veterinary diagnostic testing.

Differential diagnoses

Other intestinal trematodes, giardiasis, bacterial or viral gastroenteritis, food intolerance, inflammatory enteropathy, and in dogs parvoviral enteritis, distemper, pancreatitis, and other causes of febrile gastrointestinal disease.

Treatment in humans

Praziquantel is generally effective for reported human intestinal infection; treatment should be clinician-directed.

Treatment in animals—by species

• Dogs/cats with intestinal flukes: Veterinary antiparasitic therapy is effective; product selection and dosing are species-specific.
• Dogs with salmon poisoning disease: Require prompt doxycycline-based treatment, flukicidal therapy, and supportive care as indicated.

Animal and environmental control

Do not feed raw salmon, trout, steelhead, or related fish from endemic areas to dogs or other susceptible carnivores. Prevent scavenging of raw fish carcasses and offal.

Prevention in humans

Thoroughly cook fish and roe from endemic areas. Raw, lightly cured, inadequately frozen, or undercooked fish may retain infective metacercariae.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available against Nanophyetus or salmon poisoning disease.

Prognosis

Human intestinal infection generally has an excellent prognosis. Canine salmon poisoning disease can be fatal without treatment but responds well when recognized and treated promptly.

Reporting, legal, and regulatory considerations

Nanophyetiasis is generally not reportable. Foodborne clusters or unusual regional cases may warrant public-health investigation.

Selected current sources

• Merck Veterinary Manual—Zoonotic Diseases
• Merck Veterinary Manual—Salmon Poisoning Disease in Dogs

NEISSERIA CANIS

Synonyms and scope

Animal-associated Neisseria canis wound infection. This is a rare opportunistic zoonotic infection rather than a common transmissible disease.

Etiologic agent

Neisseria canis, a gram-negative member of the genus Neisseria that can occur in the oral flora of dogs and cats.

Animals involved and epidemiologic roles

• Dogs: Oral carriage provides a source for bite-associated inoculation.
• Cats: Oral carriage has also been reported and rare cat-associated infections have occurred.
• People: Accidental hosts, usually after bites or contamination of traumatic wounds.

Geographic distribution and occurrence

Human cases are rare and have been reported sporadically in several countries. The organism is likely underrecognized because bite wounds are commonly polymicrobial and older laboratory methods may not identify unusual animal-associated Neisseria reliably.

Reservoir, life cycle, and transmission

The reservoir is the oral and upper respiratory flora of dogs and cats. Human infection follows traumatic inoculation, especially bites, scratches contaminated with saliva, or contamination of an existing wound. Person-to-person transmission is not a recognized epidemiologic concern.

Incubation period

No organism-specific incubation period is established. Bite-wound infection generally becomes apparent within hours to several days.

Disease in humans

Reported disease includes localized wound infection, cellulitis, purulent drainage, and occasionally deeper soft-tissue infection. Clinical findings are similar to other infected dog- or cat-bite wounds.

Disease in animals—by species

N. canis is primarily recognized as commensal oral flora in dogs and cats. A characteristic clinical disease syndrome in animals is not established.

Pathology

Human disease consists of bite- or wound-associated suppurative inflammation and cellulitis. Deeper extension can occur when inoculation involves tendon, joint, bone, or poorly perfused tissue.

Human diagnosis

Obtain appropriate deep wound specimens when infection is clinically significant. Culture and modern species identification, such as MALDI-TOF or molecular methods, may be needed for unusual isolates. Bite wounds often contain multiple organisms.

Animal diagnosis

No screening is recommended for healthy dogs or cats after a human bite injury. Animals with clinical oral, respiratory, or wound disease should be evaluated according to the presenting problem.

Differential diagnoses

Pasteurella multocida, Capnocytophaga species, streptococci, staphylococci, anaerobes, other gram-negative oral flora, retained foreign body, tendon injury, septic arthritis, and osteomyelitis.

Treatment in humans

Management follows established dog- and cat-bite principles: prompt cleansing and irrigation, assessment of tendon/joint/bone injury, drainage or debridement when required, and antimicrobial treatment when clinically indicated. Empiric bite-wound therapy generally covers polymicrobial oral flora and should be adjusted to culture and susceptibility results.

Treatment in animals—by species

No treatment is indicated for a clinically normal dog or cat solely because N. canis was recovered from a human bite wound. Treat animal disease only when a clinical diagnosis is established.

Animal and environmental control

Prevent bites through appropriate handling, training, restraint, and behavior management. No environmental disinfection or animal isolation program is specifically indicated for this commensal organism.

Prevention in humans

Promptly wash and irrigate animal bites and saliva-contaminated wounds and obtain medical assessment for deep punctures, hand wounds, facial wounds, immunocompromised patients, or progressive pain, swelling, drainage, or fever.

Human vaccination

No vaccine exists. Tetanus and rabies prevention should be assessed separately after animal bites.

Animal vaccination

No vaccine exists or is indicated.

Prognosis

Generally good with appropriate wound care and treatment. Prognosis worsens with delayed care or deep-structure involvement.

Reporting, legal, and regulatory considerations

N. canis infection itself is not routinely reportable. Animal-bite reporting, rabies assessment, and occupational documentation requirements vary by jurisdiction.

Selected current sources

• PubMed—Infected Dog Bite With Neisseria canis: Case Report and Review

NIPAH VIRUS INFECTION

Synonyms and scope

Nipah virus disease; NiV infection. A severe emerging bat-associated zoonosis that can involve animal-to-human, foodborne, and person-to-person transmission.

Etiologic agent

Nipah virus, genus Henipavirus, family Paramyxoviridae.

Animals involved and epidemiologic roles

• Pteropodid fruit bats: Natural reservoir hosts.
• Pigs: Important amplifying hosts in the Malaysian/Singapore emergence; can transmit infection to people and other pigs.
• Horses: Have been implicated in the Philippine outbreak and can develop fatal neurologic disease.
• Dogs and cats: Susceptible to infection but not established maintenance reservoirs.
• People: Accidental hosts; person-to-person spread can sustain outbreaks.

Geographic distribution and occurrence

Human disease has been reported in Malaysia, Singapore, Bangladesh, India, and the Philippines. Bangladesh has experienced recurrent outbreaks, and India has had periodic outbreaks, including cases reported in 2026.

Reservoir, life cycle, and transmission

Fruit bats shed virus in secretions and excretions. Spillover can occur directly from bats, through food contaminated by bats such as raw date-palm sap, or through infected domestic animals. Pigs can efficiently amplify and spread virus within farms. Close person-to-person transmission occurs, particularly through contact with respiratory secretions or body fluids of infected patients.

Incubation period

Human incubation is usually several days to about two weeks but longer intervals have been reported. In pigs, incubation is commonly approximately 1–2 weeks.

Disease in humans

Illness ranges from asymptomatic infection to acute febrile respiratory disease and severe encephalitis. Headache, confusion, seizures, reduced consciousness, cough, dyspnea, coma, and death may occur. WHO estimates an overall case-fatality rate of approximately 40–75%, varying by outbreak.

Disease in animals—by species

• Fruit bats: Usually clinically normal reservoir hosts.
• Pigs: Fever, severe cough, respiratory distress, nasal discharge, tremors, fasciculations, paresis, seizures, or sudden death; morbidity can be high while mortality is often lower except in young pigs.
• Horses: Acute neurologic disease and sudden death have been reported.
• Dogs/cats: Susceptible; clinical disease has been documented but is less well characterized.

Pathology

Systemic vasculitis, endothelial infection, thrombosis, and necrosis can involve brain, lungs, and other organs. Human encephalitis and severe pulmonary disease are the principal life-threatening manifestations.

Human diagnosis

Suspected cases require immediate public-health coordination. Molecular testing during acute illness and serology during later phases are used for confirmation in designated reference systems.

Animal diagnosis

Because clinical signs are nonspecific and NiV is a regulated high-consequence disease, suspected animal infections require immediate veterinary-authority involvement and testing through official reference pathways.

Differential diagnoses

Japanese encephalitis and other viral encephalitides, rabies, bacterial meningoencephalitis, influenza and other severe respiratory infections, African swine fever or classical swine fever in pigs, and toxic or metabolic neurologic disease.

Treatment in humans

No licensed curative antiviral treatment is established. Early intensive supportive care, including respiratory and neurologic support, is central. Candidate therapeutics are under investigation.

Treatment in animals—by species

No specific curative therapy is established. In affected livestock populations, official disease-control measures—not routine treatment—govern management.

Animal and environmental control

Prevent bat access to livestock feed, water, fruit trees over animal areas, and collection vessels for food products. Use strict farm biosecurity, restrict movement during outbreaks, and follow official quarantine, testing, culling, and disposal directions when infection is suspected or confirmed.

Prevention in humans

Avoid contact with sick pigs, horses, or bats in affected areas; avoid raw date-palm sap or fruit contaminated by bats; use appropriate PPE for animal care; and use strict infection-control measures around human cases.

Human vaccination

No licensed human vaccine is currently available, although candidate vaccines are in development.

Animal vaccination

No licensed animal vaccine is currently available.

Prognosis

Guarded to poor in severe human encephalitis or respiratory disease. Survivors may have persistent neurologic sequelae. Animal prognosis depends on species and disease severity.

Reporting, legal, and regulatory considerations

Nipah virus infection in susceptible domestic animals is internationally notifiable to WOAH. Suspected human disease requires urgent public-health notification. Animal movement and outbreak-control measures are legally regulated.

Selected current sources

• WHO—Nipah Virus Fact Sheet
• WOAH—Nipah Virus

NEWCASTLE DISEASE

Synonyms and scope

Newcastle disease; virulent Newcastle disease (vND); historically exotic Newcastle disease. A highly contagious avian disease with only rare, mild occupational infection in people.

Etiologic agent

Virulent strains of avian orthoavulavirus 1 (Newcastle disease virus), family Paramyxoviridae.

Animals involved and epidemiologic roles

• Domestic poultry: Major susceptible hosts; chickens are especially vulnerable to virulent strains.
• Wild and captive birds: Numerous species can be infected and may contribute to spread.
• People: Rare accidental hosts, usually after intense occupational exposure to infected birds or live vaccine virus.

Geographic distribution and occurrence

Occurs worldwide. Virulent Newcastle disease remains endemic in some regions and causes major poultry outbreaks and trade restrictions when introduced into disease-free areas.

Reservoir, life cycle, and transmission

Infected birds shed virus in respiratory secretions and feces. Transmission occurs by direct contact, contaminated equipment, clothing, vehicles, litter, feed, and aerosols over short distances. Human infection is usually associated with direct ocular or respiratory exposure in poultry or laboratory settings.

Incubation period

In birds, usually several days and commonly within 2–15 days depending on strain, dose, and species. Human conjunctivitis generally appears within a few days of exposure.

Disease in humans

Human disease is rare and usually limited to transient conjunctivitis, eye irritation, and occasionally mild influenza-like symptoms. Severe systemic disease is not typical.

Disease in animals—by species

• Chickens/turkeys: Sudden death, respiratory distress, green diarrhea, depression, decreased egg production, tremors, torticollis, paralysis, and high mortality with virulent strains.
• Other birds: Disease ranges from inapparent infection to severe respiratory, gastrointestinal, or neurologic illness.

Pathology

Virulent infection can cause hemorrhagic and necrotic lesions in the gastrointestinal tract and lymphoid tissues, respiratory inflammation, and encephalitis. Lesions vary by viral pathotype and host species.

Human diagnosis

Most occupational conjunctivitis is diagnosed clinically from exposure history. Unusual or severe cases should be evaluated medically and, when needed, coordinated with public-health authorities.

Animal diagnosis

Clinical signs alone are not specific. Suspected virulent Newcastle disease requires immediate animal-health notification and confirmation through authorized molecular and virologic testing.

Differential diagnoses

Highly pathogenic avian influenza, infectious bronchitis, infectious laryngotracheitis, avian cholera, avian encephalomyelitis, toxins, and other causes of neurologic or respiratory flock disease.

Treatment in humans

Human infection is usually self-limited and treated symptomatically. Persistent eye pain, visual change, or severe systemic illness warrants medical evaluation.

Treatment in animals—by species

No antiviral treatment eliminates virulent Newcastle disease in poultry. In regulated outbreaks, official quarantine, movement controls, depopulation, vaccination strategy, and disposal policies determine management.

Animal and environmental control

Use flock biosecurity, quarantine new birds, control movement of people and equipment, clean and disinfect appropriately, prevent contact with wild birds, and follow vaccination programs where recommended. Suspected virulent disease must be reported before moving birds or samples.

Prevention in humans

Wear eye protection, gloves, and appropriate respiratory protection when handling suspect infected birds or administering live aerosolized vaccine. Wash hands and avoid touching the eyes during bird work.

Human vaccination

No human vaccine is licensed or indicated.

Animal vaccination

Multiple live and inactivated poultry vaccines are available and widely used. Vaccination reduces disease but does not necessarily prevent infection or shedding, so biosecurity remains essential.

Prognosis

Human prognosis is excellent. In susceptible poultry, virulent Newcastle disease can cause very high mortality and major flock losses.

Reporting, legal, and regulatory considerations

Virulent Newcastle disease is a regulated, internationally reportable animal disease. In the United States, suspicion requires immediate contact with state animal-health officials or USDA APHIS.

Selected current sources

• USDA APHIS—Virulent Newcastle Disease

OPHIONYSSUS NATRICIS INFESTATION

Synonyms and scope

Snake-mite infestation; snake-mite dermatitis. An animal-associated ectoparasitic hazard rather than a persistent human infestation.

Etiologic agent

Ophionyssus natricis, a hematophagous macronyssid mite of reptiles.

Animals involved and epidemiologic roles

Snakes are the principal hosts; lizards are less commonly affected. Humans and other mammals are incidental feeding hosts.

Geographic distribution and occurrence

Worldwide, especially in captive reptile collections; spread is facilitated by movement of infested reptiles and equipment.

Reservoir, life cycle, and transmission

Mites feed on reptiles and spend important portions of their life cycle in cage cracks, furnishings, and other environmental sites. They may leave heavily infested enclosures and temporarily bite people; they do not normally establish a reproducing infestation on humans.

Incubation period

In reptiles, signs may become apparent after mite populations increase; there is no single fixed clinical incubation period. Human pruritic lesions may develop soon after bites.

Disease in humans

Transient bites cause intensely pruritic erythematous papules and occasionally vesicular or vesiculobullous dermatitis. Persistent disease usually reflects continuing environmental exposure.

Disease in animals—by species

Snakes: restlessness, excessive soaking, rubbing, dysecdysis, dermatitis, anemia, debility, and secondary infection with heavy burdens. Lizards: similar signs are possible but infestation is less common.

Pathology

Repeated blood feeding causes cutaneous irritation and blood loss; severe burdens may contribute to anemia and compromised condition.

Human diagnosis

Exposure history plus recovery and identification of mites from the reptile, enclosure, clothing, or skin. Other arthropod bites and dermatitis should be considered.

Animal diagnosis

Direct inspection of the reptile and enclosure, including folds and crevices, with microscopic identification of collected mites when needed.

Differential diagnoses

Other reptile mites or ticks, dysecdysis from husbandry problems, bacterial or fungal dermatitis, and in people bedbugs, fleas, scabies, bird/rodent mites, and contact dermatitis.

Treatment in humans

Usually symptomatic treatment and prevention of further bites; persistent or severe dermatitis warrants medical evaluation.

Treatment in animals—by species

Treat the affected reptile and all epidemiologically linked animals under veterinary guidance, selecting products appropriate for the species because some acaricides are hazardous to reptiles.

Animal and environmental control

Quarantine new reptiles; treat animals and their environment concurrently; clean enclosures and furnishings; prevent transfer on equipment, substrate, or hands.

Prevention in humans

Avoid handling infested reptiles or contaminated furnishings without appropriate protection; wash hands and clothing after contact and correct the animal/environmental infestation.

Human vaccination

None.

Animal vaccination

No vaccine.

Prognosis

Excellent for human dermatitis after exposure ends. Reptile prognosis is generally good with effective eradication, but severe anemia or secondary disease worsens prognosis.

Reporting, legal, and regulatory considerations

Not generally reportable as a human or animal disease. Commercial, institutional, or zoological collections should follow applicable animal-care and pest-control requirements.

Selected current sources

Amanatfard et al.—Human dermatitis caused by O. natricis; Orlova et al. 2024—distribution and biology review.

OESOPHAGOSTOMIASIS

Synonyms and scope

Nodular worm disease; oesophagostomosis. A soil-transmitted strongylid nematode infection of livestock and nonhuman primates with focal human disease, especially in parts of West Africa.

Etiologic agent

Oesophagostomum species; O. bifurcum is the principal species recognized in human infections in West Africa.

Animals involved and epidemiologic roles

• Sheep, goats, pigs, cattle, and other livestock: Common hosts for various Oesophagostomum species.
• Nonhuman primates: Hosts for species including O. bifurcum.
• People: Can serve as definitive hosts; in northern Ghana and Togo, human transmission of O. bifurcum appears to be maintained largely within human populations rather than by direct primate transmission.

Geographic distribution and occurrence

Animal infections are widespread, particularly in tropical and subtropical regions. Human disease is concentrated in northern Ghana and Togo, with sporadic cases reported elsewhere in Africa, South America, and Asia.

Reservoir, life cycle, and transmission

Eggs pass in feces and develop in the environment to infective larvae. Hosts are infected by ingesting larvae from contaminated soil, food, or water. Larvae enter the intestinal wall and form nodules before returning to the lumen and maturing. Direct animal contact is not required for transmission.

Incubation period

Egg production can begin about one month after infection. The interval to clinical disease is variable and depends on larval burden, intestinal inflammation, and nodule formation.

Disease in humans

Many infections are mild or asymptomatic. Symptomatic disease may cause abdominal pain, fever, diarrhea, gastrointestinal bleeding, inflammatory masses, or acute abdomen mimicking appendicitis. Nodules or abscesses can occasionally perforate or obstruct the intestine.

Disease in animals—by species

• Ruminants and pigs: Diarrhea, weight loss, poor growth, anemia, protein loss, and nodular enteritis with heavy burdens.
• Nonhuman primates: Abdominal pain, diarrhea or dysentery, intestinal nodules, peritonitis, and rarely death from perforation.

Pathology

Larvae produce granulomatous nodules in the intestinal wall. Secondary bacterial infection, abscessation, edema, ulceration, obstruction, and peritonitis can occur in severe disease.

Human diagnosis

Stool eggs resemble hookworm eggs and are not reliably species-specific. Definitive diagnosis may require recovery of a worm or tissue-stage parasite, supported by imaging or specialist parasitology methods.

Animal diagnosis

Fecal egg detection can demonstrate strongylid infection but may not distinguish Oesophagostomum from related nematodes. Herd or colony diagnosis may require species-specific parasitologic or molecular testing where available.

Differential diagnoses

Hookworm infection, appendicitis, amebiasis, schistosomiasis, inflammatory bowel disease, intestinal tuberculosis, neoplasia, and other causes of abdominal masses or enteritis.

Treatment in humans

Anthelmintic treatment is effective for uncomplicated infection; albendazole is commonly used in endemic control programs. Surgical management may be required for obstruction, abscess, perforation, or diagnostic uncertainty.

Treatment in animals—by species

Use species-appropriate anthelmintics under veterinary guidance and incorporate fecal monitoring, pasture management, and resistance-aware parasite control.

Animal and environmental control

Reduce fecal contamination of feed and water, manage manure, avoid overcrowding, rotate or manage pasture where appropriate, and use evidence-based parasite-control programs rather than indiscriminate treatment.

Prevention in humans

Improve sanitation, use latrines, wash produce, avoid ingestion of soil-contaminated food or water, and practice hand hygiene after animal or soil contact.

Human vaccination

No vaccine is available.

Animal vaccination

No broadly used vaccine is available.

Prognosis

Generally good with treatment. Complicated nodular disease with perforation, obstruction, or peritonitis can be serious.

Reporting, legal, and regulatory considerations

Usually not routinely reportable. Local public-health investigation may be appropriate in endemic clusters. Food-animal treatment must follow drug-approval and withdrawal requirements.

Selected current sources

• CDC DPDx—Oesophagostomiasis

OPISTHORCHIASIS

Synonyms and scope

Cat liver fluke disease; Southeast Asian liver fluke disease. A foodborne trematode infection of the biliary tract acquired from raw or inadequately cooked freshwater fish.

Etiologic agent

Opisthorchis viverrini and Opisthorchis felineus.

Animals involved and epidemiologic roles

• Humans, cats, dogs, pigs, and other fish-eating mammals: Definitive hosts.
• Freshwater snails: First intermediate hosts.
• Freshwater fish: Second intermediate hosts carrying infective metacercariae.

Geographic distribution and occurrence

O. viverrini is endemic in parts of Southeast Asia, especially the Mekong region. O. felineus occurs in parts of eastern Europe, Russia, Kazakhstan, and neighboring areas.

Reservoir, life cycle, and transmission

Eggs from infected definitive hosts reach freshwater, develop through snail and fish hosts, and become infective metacercariae in fish. Humans and animals acquire infection by eating raw, undercooked, fermented, salted, or otherwise inadequately processed freshwater fish. Direct transmission from cats, dogs, or pigs does not occur.

Incubation period

Symptoms may begin within weeks after infection, but many infections remain asymptomatic for years. Chronic hepatobiliary complications reflect long-standing infection and repeated exposure.

Disease in humans

Light infection is often asymptomatic. Acute or chronic disease may cause abdominal pain, dyspepsia, fever, hepatomegaly, cholangitis, cholecystitis, pancreatitis, or biliary obstruction. Chronic O. viverrini infection is a proven cause of cholangiocarcinoma. Evidence is insufficient to classify O. felineus as carcinogenic to humans.

Disease in animals—by species

• Cats and dogs: Often subclinical; heavy or chronic infection may cause cholangitis, biliary hyperplasia and fibrosis, hepatomegaly, jaundice, or poor condition.
• Pigs and wildlife: Can maintain adult biliary infection and contribute eggs to the environment.

Pathology

Adult flukes in bile ducts cause epithelial hyperplasia, chronic inflammation, periductal fibrosis, and biliary obstruction. Recurrent pyogenic cholangitis and liver abscesses can occur. Chronic O. viverrini infection promotes carcinogenic biliary changes.

Human diagnosis

Diagnosis is usually based on detection of characteristic eggs in stool. Eggs are difficult to distinguish from Clonorchis and some small intestinal flukes; imaging can identify biliary disease, and molecular methods can assist species identification where available.

Animal diagnosis

Fecal examination can detect eggs in definitive hosts, but species-level differentiation may be difficult. Ultrasound, hepatobiliary imaging, or necropsy findings may support diagnosis in clinically affected animals.

Differential diagnoses

Clonorchiasis, fascioliasis, gallstones, bacterial cholangitis, pancreatitis, viral hepatitis, hepatobiliary neoplasia, and other causes of eosinophilic or obstructive hepatobiliary disease.

Treatment in humans

Praziquantel is the treatment of choice. Albendazole is an alternative in some circumstances. Advanced cholangitis, obstruction, or suspected cholangiocarcinoma requires specialist management.

Treatment in animals—by species

Veterinary antiparasitic treatment may be used for infected dogs or cats, but prevention of raw-fish feeding and reinfection is essential. Food-animal therapy must comply with local drug and withdrawal regulations.

Animal and environmental control

Do not feed raw endemic freshwater fish to dogs, cats, or pigs. Improve sanitation to prevent fecal contamination of freshwater and reduce access of reservoir animals to aquaculture or fish-processing waste.

Prevention in humans

Avoid raw, undercooked, fermented, or inadequately processed freshwater fish in endemic areas. Safe cooking is the most reliable preventive measure.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Excellent for uncomplicated infection after effective therapy, but chronic biliary injury may persist. Long-standing O. viverrini infection carries a substantial risk of cholangiocarcinoma.

Reporting, legal, and regulatory considerations

Usually not routinely reportable. Foodborne clusters and endemic control programs may involve public-health, food-safety, fisheries, and veterinary authorities.

Selected current sources

• CDC—Clinical Overview of Opisthorchis
• CDC DPDx—Opisthorchiasis
• WHO—Opisthorchiasis

ORNITHONYSSUS BACOTI INDUCED DERMATITIS (TROPICAL RAT MITE)

Synonyms and scope

Tropical rat-mite dermatitis; rodent-mite dermatitis.

Etiologic agent

Ornithonyssus bacoti, a blood-feeding macronyssid mite.

Animals involved and epidemiologic roles

Rats are principal hosts; mice and other small mammals may be infested. Humans and pets are incidental hosts when mites leave rodent nests or harborages.

Geographic distribution and occurrence

Cosmopolitan, especially where commensal rodents occur in buildings, animal facilities, warehouses, or residences.

Reservoir, life cycle, and transmission

Mites feed on rodents but can survive off host in the environment and disperse after rodent control or nest abandonment. Humans are bitten when mites migrate from nests, wall voids, ceilings, cages, or furnishings.

Incubation period

No fixed incubation period; pruritic lesions can appear shortly after bites, and new lesions continue while environmental mites remain.

Disease in humans

Intensely pruritic erythematous papules or wheals, often clustered. Systemic illness is not typical; the principal established human problem is dermatitis.

Disease in animals—by species

Rodents may be asymptomatic; heavy infestations can cause pruritus, alopecia, anemia, and debility. Incidental pets may develop pruritus and dermatitis.

Pathology

Bite-associated hypersensitivity and local inflammation; heavy burdens in small hosts can cause clinically important blood loss.

Human diagnosis

Clinical pattern plus evidence of rodent activity and identification of mites collected from the environment or patient.

Animal diagnosis

Inspect rodents, nests, cages, and environmental sites; identify collected mites morphologically when confirmation is needed.

Differential diagnoses

Bedbugs, fleas, scabies, bird mites, O. natricis, contact dermatitis, papular urticaria, and other arthropod bites.

Treatment in humans

Symptomatic antipruritic/anti-inflammatory care as medically appropriate; treatment fails if the environmental source persists.

Treatment in animals—by species

Treat infested pets or captive rodents under veterinary direction while simultaneously addressing the environment.

Animal and environmental control

Integrated rodent control plus removal of nests and mite control. Seal rodent entry points and clean affected areas using appropriate pest-management methods.

Prevention in humans

Avoid direct contact with rodent nests and contaminated materials; use gloves/protective clothing during cleanup and obtain professional pest control for persistent infestations.

Human vaccination

None.

Animal vaccination

No vaccine.

Prognosis

Excellent once mites are eliminated; recurrent lesions indicate continuing exposure.

Reporting, legal, and regulatory considerations

Not generally reportable. Rodent-control and pesticide use must comply with local regulations and product labeling.

Selected current sources

Current clinical literature on tropical rat-mite dermatitis and integrated rodent/ectoparasite control; veterinary parasitology references.

PASTEURELLA AEROGENES

Synonyms and scope

Pig-associated Pasteurella aerogenes wound infection.

Etiologic agent

Pasteurella aerogenes, a gram-negative bacterium associated particularly with the porcine gastrointestinal tract.

Animals involved and epidemiologic roles

Pigs are the principal animal association. Human cases are rare and usually follow pig bites, goring injuries, or contamination of wounds.

Geographic distribution and occurrence

Reported internationally wherever close occupational or agricultural contact with pigs occurs; human disease is uncommon.

Reservoir, life cycle, and transmission

Traumatic inoculation of porcine oral or gastrointestinal flora into damaged human tissue is the important route. Casual contact is not a recognized common cause of infection.

Incubation period

Variable; wound inflammation generally develops over hours to days depending on injury and microbial burden.

Disease in humans

Cellulitis, painful wound infection, abscess, purulent drainage, and occasionally deeper infection; pig-bite wounds are frequently polymicrobial.

Disease in animals—by species

Usually part of porcine flora rather than a major primary pathogen; its zoonotic significance is chiefly contamination of traumatic wounds.

Pathology

Acute suppurative inflammation, cellulitis, abscessation, and potentially deeper soft-tissue involvement.

Human diagnosis

Clinical assessment of the wound with bacterial identification and susceptibility testing when infection is significant, progressive, deep, or unusual.

Animal diagnosis

Not usually indicated in healthy pigs solely because a human wound isolate is identified; investigate clinically affected animals as appropriate.

Differential diagnoses

Other organisms in pig wounds including Pasteurella multocida, Actinobacillus suis, streptococci, staphylococci, anaerobes, and Enterobacterales.

Treatment in humans

Prompt wound cleansing, assessment of tetanus status, drainage/debridement when indicated, and clinician-selected antimicrobials for infected or high-risk wounds.

Treatment in animals—by species

Treat clinically affected animals based on veterinary examination and culture/susceptibility where indicated; routine treatment of healthy source pigs is not warranted.

Animal and environmental control

Safe pig handling and restraint, wound prevention, sanitation, and prompt management of bite/goring injuries.

Prevention in humans

Wash wounds promptly and seek medical assessment for deep bites, hand injuries, progressive inflammation, systemic signs, or immunocompromised patients.

Human vaccination

None.

Animal vaccination

No vaccine specifically for P. aerogenes.

Prognosis

Usually good with prompt wound care; delayed treatment of deep or polymicrobial injuries can lead to serious complications.

Reporting, legal, and regulatory considerations

Human cases are not generally specifically reportable; occupational injuries may be subject to workplace requirements.

Selected current sources

Microbiology of animal bite wound infections—pig-associated organisms.

PASTEURELLOSIS

Synonyms and scope

Pasteurella infection; animal-bite pasteurellosis. This section focuses on zoonotic Pasteurella multocida and related species.

Etiologic agent

Most commonly Pasteurella multocida; other Pasteurella species can cause animal and human disease.

Animals involved and epidemiologic roles

Cats and dogs commonly carry P. multocida in the oral/upper respiratory tract and are the most important companion-animal sources. Rabbits and many other mammals and birds may also carry or develop disease.

Geographic distribution and occurrence

Worldwide. Human disease is most often associated with cat bites/scratches, dog bites, licking of wounds, or close exposure in susceptible people.

Reservoir, life cycle, and transmission

Usually inoculation through bites, scratches, or saliva contacting broken skin; less commonly respiratory exposure or infection without recognized trauma.

Incubation period

Soft-tissue infection can develop rapidly, often within 24 hours after a bite or scratch.

Disease in humans

Rapidly progressive cellulitis with pain, erythema and swelling; abscess, tenosynovitis, septic arthritis, osteomyelitis, bacteremia, pneumonia, meningitis, endocarditis, and other invasive disease can occur.

Disease in animals—by species

Cats/dogs: often asymptomatic carriers but may develop respiratory, wound, or systemic infections. Rabbits: rhinitis, pneumonia, otitis, abscesses, reproductive disease, and septicemia are important manifestations. Other species have host-specific syndromes.

Pathology

Suppurative cellulitis and abscessation predominate after inoculation; invasive cases may involve joints, bone, respiratory tract, bloodstream, or other organs.

Human diagnosis

Clinical exposure history plus culture or molecular identification from infected tissue, blood, joint fluid, or other appropriate specimens; susceptibility testing is useful in serious disease.

Animal diagnosis

Diagnosis depends on species and syndrome; culture/PCR and cytology/histopathology may support veterinary cases.

Differential diagnoses

Other bite-wound bacteria, Capnocytophaga, staphylococci, streptococci, anaerobes, cat-scratch disease, and noninfectious traumatic inflammation.

Treatment in humans

Immediate wound irrigation and medical assessment; infected or high-risk bite wounds receive clinician-directed antimicrobial therapy, with drainage/debridement and treatment of deep infection as needed.

Treatment in animals—by species

Species- and syndrome-specific veterinary treatment guided by culture/susceptibility when practical; chronic rabbit disease can be difficult to eradicate.

Animal and environmental control

Prevent bites and scratches; manage clinically infected animals; use good veterinary infection-control and wound-care practices.

Prevention in humans

Wash bites/scratches immediately, avoid allowing animals to lick open wounds, and obtain prompt care for cat bites, deep hand wounds, rapidly progressive inflammation, or high-risk patients.

Human vaccination

None.

Animal vaccination

No general zoonosis-prevention vaccine; some animal vaccines exist for specific production-animal pasteurellosis syndromes but are not substitutes for bite prevention.

Prognosis

Excellent for uncomplicated superficial infection treated promptly; guarded with delayed treatment, immunocompromise, bacteremia, or deep-tissue involvement.

Reporting, legal, and regulatory considerations

Reporting varies by jurisdiction and syndrome; animal bites may trigger local rabies/public-health requirements independent of Pasteurella infection.

Selected current sources

CDC/clinical guidance on animal-bite wound management; veterinary references on Pasteurella infections.

PENTASTOMIASIS

Synonyms and scope

Pentastomid infection; visceral pentastomiasis; linguatuliasis is a related pentastomid disease with a distinct cycle.

Etiologic agent

Pentastomid parasites, especially Armillifer and Porocephalus species for visceral disease; Linguatula serrata causes linguatuliasis.

Animals involved and epidemiologic roles

Snakes are definitive hosts for important zoonotic Armillifer/Porocephalus species; mammals serve as intermediate hosts. Canids are definitive hosts for L. serrata. Humans are accidental intermediate or aberrant hosts.

Geographic distribution and occurrence

Human cases occur particularly in parts of Africa and Asia and are associated with snake exposure or consumption; sporadic cases occur elsewhere.

Reservoir, life cycle, and transmission

Humans acquire visceral infection by ingesting eggs contaminating hands, food, or water after contact with infected reptiles/environments; consumption of raw or undercooked infected tissues can also be involved.

Incubation period

Often months to years before incidental detection; a precise incubation period is not established.

Disease in humans

Many infections are asymptomatic. Symptomatic visceral disease can cause abdominal pain, peritonitis, obstruction, hepatic or pulmonary signs, ocular disease, or disseminated involvement depending on location and burden.

Disease in animals—by species

Snakes: adults inhabit the respiratory tract and may cause respiratory irritation or disease with heavy burdens. Intermediate mammalian hosts: encysted larvae are often incidental findings. Canids with linguatuliasis may have nasal disease.

Pathology

Encysted larvae provoke granulomatous inflammation and may later calcify; location determines clinical significance.

Human diagnosis

Imaging may reveal characteristic calcified larvae; definitive diagnosis can follow surgical/pathologic recovery with morphologic or molecular identification.

Animal diagnosis

In reptiles, endoscopy/imaging and parasite recovery may support diagnosis; intermediate-host lesions are often found incidentally.

Differential diagnoses

Other calcified granulomas, parasitic cysts, neoplasia, tuberculosis, echinococcosis, and causes of eosinophilic or granulomatous disease.

Treatment in humans

Observation may be appropriate for asymptomatic visceral infection; surgical removal is considered for symptomatic, obstructive, ocular, or localized disease. No consistently proven drug regimen exists.

Treatment in animals—by species

Veterinary removal/treatment is case-dependent and should be directed by a reptile or species-experienced veterinarian; environmental control is important.

Animal and environmental control

Hygiene when handling reptiles and cleaning enclosures; prevent contamination of food/water and do not feed or consume raw potentially infected tissues.

Prevention in humans

Wash hands after reptile contact, use gloves for enclosure cleaning, avoid raw/undercooked snake meat or viscera, and prevent hand-to-mouth contamination.

Human vaccination

None.

Animal vaccination

No vaccine.

Prognosis

Most incidental infections remain asymptomatic; prognosis depends on parasite location, burden, and complications.

Reporting, legal, and regulatory considerations

Generally not specifically reportable, though imported wildlife, food safety, and animal-health regulations may apply.

Selected current sources

Current parasitology and tropical-medicine reviews of pentastomiasis; CDC/DPDx resources where available.

PIGBEL

Synonyms and scope

Enteritis necroticans; clostridial necrotizing enteritis; Darmbrand. Historically called pigbel in Papua New Guinea.

Etiologic agent

Beta-toxin-producing Clostridium perfringens type C.

Animals involved and epidemiologic roles

Humans can develop enteritis necroticans. Type C disease also occurs in animals, especially neonatal piglets and sometimes calves, lambs, and other species. Pigs are not a required direct reservoir for human disease.

Geographic distribution and occurrence

Historically important in the Papua New Guinea highlands; now uncommon there but sporadic cases and outbreaks continue to be reported worldwide.

Reservoir, life cycle, and transmission

Human disease follows ingestion of food containing type C organisms under conditions that allow beta toxin to remain active. Historical pig-feast associations gave the disease its name, but this is not a conventional direct pig-to-human zoonosis.

Incubation period

Usually acute after the implicated meal/exposure; exact timing varies and is not reliably defined for all cases.

Disease in humans

Severe abdominal pain, distention, vomiting, bloody diarrhea, intestinal necrosis, toxemia, perforation, peritonitis, shock, and death. Diabetes and conditions reducing intestinal protease activity can increase risk.

Disease in animals—by species

Piglets: peracute or acute hemorrhagic necrotizing enteritis, bloody diarrhea, collapse, and very high mortality, especially in the first days of life. Calves/lambs: analogous type C enteric disease can occur.

Pathology

Segmental to extensive hemorrhagic necrosis of the small intestine, often jejunum/ileum; beta toxin damages mucosa and vascular endothelium.

Human diagnosis

Clinical/surgical recognition of necrotizing enteritis supported by demonstration of type C/beta toxin or toxin genes in appropriate clinical material.

Animal diagnosis

Compatible lesions plus identification/toxin typing of C. perfringens in appropriate specimens; interpretation requires correlation with pathology.

Differential diagnoses

Other causes of acute abdomen, ischemic/necrotizing enteritis, severe bacterial enteritis, intussusception/obstruction, and in neonates other causes of hemorrhagic diarrhea.

Treatment in humans

Medical emergency: aggressive supportive care, clinician-directed antimicrobials, and surgical management when necrotic or perforated bowel is present.

Treatment in animals—by species

Rapid progression may limit treatment success in neonatal livestock; veterinary therapy and intensive supportive care are combined with immediate herd/flock control.

Animal and environmental control

Food hygiene and sanitation; in livestock, farrowing/lambing hygiene, adequate colostrum, and immunization of pregnant dams where appropriate.

Prevention in humans

Safe food preparation and cooking, particularly in settings with poor sanitation or high-risk traditional food practices.

Human vaccination

No routinely available human vaccine. Historical toxoid vaccination contributed to control in endemic Papua New Guinea but is not a routine global vaccine program.

Animal vaccination

Commercial type C toxoid-containing vaccines are used in susceptible livestock, commonly through maternal immunization programs.

Prognosis

Potentially fatal in severe human disease; prompt recognition and surgery/supportive care improve outcome. Peracute neonatal animal disease has a poor prognosis once severe signs develop.

Reporting, legal, and regulatory considerations

Not generally a routine nationally notifiable human disease; outbreaks warrant public-health investigation. Animal requirements vary by jurisdiction.

Selected current sources

PLOS NTD 2025 review—enteritis necroticans; Merck Veterinary Manual—type C enteritis in pigs.

PLAGUE

Synonyms and scope

Bubonic plague; septicemic plague; pneumonic plague. The baseline cross-reference is expanded here because animal exposure is central to zoonotic risk.

Etiologic agent

Yersinia pestis.

Animals involved and epidemiologic roles

Wild rodents and their fleas maintain enzootic cycles. Cats are highly susceptible and are an important direct source for some human cases; dogs are less likely to become severely ill but can carry infected fleas or occasionally develop disease. Other mammals can be infected.

Geographic distribution and occurrence

Persistent natural foci occur in parts of Africa, Asia, and the Americas. In the United States, plague occurs mainly in rural/semi-rural areas of western states.

Reservoir, life cycle, and transmission

Most human infections follow bites from infected fleas or handling infected animals. Cats can transmit through bites, scratches, infectious exudates, and respiratory droplets when pneumonic. Person-to-person transmission is primarily a concern with pneumonic plague.

Incubation period

Usually 1–7 days depending on form and route; pneumonic disease can develop after a shorter incubation.

Disease in humans

Bubonic disease causes fever and painful lymphadenopathy; septicemic disease causes systemic toxicity and may cause DIC/necrosis; pneumonic plague causes rapidly progressive pneumonia and is transmissible by respiratory droplets.

Disease in animals—by species

Cats: fever, lethargy, anorexia and commonly submandibular lymphadenitis/abscess-like buboes; septicemic or pneumonic disease may occur. Dogs: often milder or subclinical but can develop febrile systemic illness. Wild rodents: susceptibility varies and epizootic mortality may be conspicuous.

Pathology

Necrotizing suppurative lymphadenitis, bacteremia/sepsis, hemorrhage, tissue necrosis, and severe pneumonia depending on form.

Human diagnosis

Suspect from compatible illness plus exposure in an endemic area. Obtain appropriate diagnostic specimens when feasible, notify public health immediately, and do not delay treatment while awaiting results.

Animal diagnosis

Suspect in febrile cats or other mammals with lymphadenitis, pneumonia, sepsis, or relevant wildlife/flea exposure in endemic areas; coordinate diagnostic testing with public-health/animal-health authorities.

Differential diagnoses

Tularemia, bacterial lymphadenitis/abscess, cat-bite abscess, sepsis from other bacteria, severe pneumonia, and other causes of acute febrile lymphadenopathy.

Treatment in humans

Prompt effective antimicrobial therapy is lifesaving and should begin on clinical suspicion; supportive care and isolation precautions are added according to disease form.

Treatment in animals—by species

Prompt veterinary antimicrobial treatment and supportive care; suspected cats require infection-control precautions and public-health coordination because of zoonotic risk.

Animal and environmental control

Integrated flea and rodent management; avoid handling sick/dead wildlife; control fleas on pets; prevent pets from hunting rodents in endemic areas; isolate suspected animal cases appropriately.

Prevention in humans

Use EPA-registered repellents when indicated, avoid rodent carcasses and flea-infested habitats, maintain pet flea control, and seek urgent medical care after compatible exposure/illness.

Human vaccination

No routinely available plague vaccine for the general U.S. public.

Animal vaccination

No routinely used animal vaccine for prevention of zoonotic plague.

Prognosis

Excellent with early appropriate treatment in many cases; untreated pneumonic or septicemic plague can progress rapidly and be fatal.

Reporting, legal, and regulatory considerations

Suspected human plague requires immediate notification to public-health authorities in the U.S. and is nationally notifiable. Suspected animal cases in endemic areas warrant prompt coordination with public-health/animal-health authorities.

Selected current sources

CDC—Clinical Testing and Diagnosis for Plague, 2026; CDC—Veterinary Guidance for Plague.

PLASMODIUM SPP.

Synonyms and scope

Malaria parasites; simian or zoonotic malaria. This retained umbrella entry focuses on animal-associated Plasmodium infections, especially malaria parasites maintained in nonhuman primates that can infect people. It does not imply that the major human malaria parasites are ordinarily maintained by animals.

Etiologic agent

Protozoa of genus Plasmodium. The best-established zoonotic species is P. knowlesi; human infections have also been documented with simian parasites including P. cynomolgi, P. inui, and P. coatneyi. In South America, lineages closely related to P. vivax/P. simium and P. malariae/P. brasilianum can circulate across human–nonhuman-primate interfaces.

Animals involved and epidemiologic roles

• Macaques: Long-tailed and pig-tailed macaques are important reservoirs for P. knowlesi in Southeast Asia; macaques also maintain other simian malaria parasites.
• New World primates: Several species can harbor P. simium- or P. brasilianum-like parasites in parts of South America.
• Anopheles mosquitoes: Biological vectors required for ordinary zoonotic transmission.
• People: Accidental or spillover hosts for simian malaria; human-to-mosquito-to-human transmission is not considered the principal maintenance cycle for P. knowlesi.

Geographic distribution and occurrence

P. knowlesi is an important cause of human malaria in parts of Southeast Asia, especially Malaysia and neighboring areas where competent vectors and macaque reservoirs overlap. Other simian-malaria spillovers are reported more sporadically in Southeast Asia and the Amazon region.

Reservoir, life cycle, and transmission

Infected primates develop blood-stage parasitemia that can infect competent female Anopheles mosquitoes. Mosquitoes then transmit infective stages during later blood meals. Human infection is therefore vector-borne rather than acquired by touching, feeding, or caring for an infected primate. Blood-borne transmission is possible in principle but is not the ordinary zoonotic route.

Incubation period

Usually about 1–3 weeks for mosquito-acquired malaria, with variation by species. Relapsing species such as P. cynomolgi can form dormant liver stages and may cause later relapses.

Disease in humans

Zoonotic malaria typically causes fever, chills, headache, malaise, myalgia, anemia, and thrombocytopenia. P. knowlesi can multiply rapidly and may progress to severe malaria with jaundice, acute kidney injury, respiratory distress, shock, or death. Clinical appearance alone cannot reliably distinguish species.

Disease in animals—by species

• Natural nonhuman-primate reservoirs: Often have low-grade or subclinical parasitemia, although illness can occur depending on host and parasite combination.
• Captive nonhuman primates: Clinical malaria may include fever, anemia, splenomegaly, lethargy, and reduced condition; imported animals can carry infections without obvious signs.

Pathology

Blood-stage parasites infect erythrocytes, producing hemolysis, anemia, splenic enlargement, and systemic inflammation. Severe human P. knowlesi disease may involve microvascular dysfunction, renal injury, hepatic dysfunction, and pulmonary complications.

Human diagnosis

Urgent malaria testing is required for compatible febrile illness after exposure in an endemic region. Microscopy and rapid diagnostic tests identify malaria, but species identification can be difficult; molecular confirmation is useful when P. knowlesi or another simian species is possible.

Animal diagnosis

In nonhuman primates, diagnosis may use blood-film examination and molecular testing through veterinary or reference laboratories. Species-level identification is important because morphology can overlap among simian and human malaria parasites.

Differential diagnoses

Dengue, chikungunya, leptospirosis, rickettsial infections, typhoid fever, viral hepatitis, sepsis, babesiosis, and malaria caused by the major human Plasmodium species.

Treatment in humans

Treat malaria promptly according to species, disease severity, acquisition geography, and current resistance guidance. Under current CDC guidance, patients with P. knowlesi should initially be hospitalized because infection can progress rapidly to severe disease; species confirmation by PCR is preferred because P. knowlesi may be confused microscopically with P. malariae or P. falciparum. Confirmed uncomplicated P. knowlesi monoinfection can be treated with chloroquine/hydroxychloroquine or an effective regimen used for chloroquine-resistant P. falciparum; severe malaria requires emergency parenteral therapy, typically intravenous artesunate in the United States. Simian species with hypnozoites, including P. cynomolgi, require consideration of liver-stage eradication under specialist guidance.

Treatment in animals—by species

Treatment of malaria in captive nonhuman primates should be directed by a veterinarian experienced with primates and selected for the identified parasite, host species, clinical severity, and regional drug susceptibility. Relapsing species require consideration of liver-stage infection. Treatment of free-ranging reservoir primates is not a practical population-control strategy.

Animal and environmental control

Use mosquito exclusion and control in primate facilities, screen imported or clinically suspect nonhuman primates as required by institutional or regulatory programs, and prevent mosquito access to infected animals. Wildlife-reservoir control is neither feasible nor appropriate for routine zoonotic-malaria prevention.

Prevention in humans

Prevent mosquito bites with repellents, protective clothing, screened or air-conditioned housing, and appropriate travel chemoprophylaxis for human malaria risk. People working with nonhuman primates in endemic areas should use vector protection; ordinary animal contact itself is not the transmission route.

Human vaccination

WHO-recommended malaria vaccines such as RTS,S and R21 are directed against P. falciparum in children in endemic settings. They are not established vaccines against P. knowlesi or other simian malaria parasites.

Animal vaccination

No routinely licensed vaccine is available to prevent simian malaria in nonhuman primates.

Prognosis

Usually good with prompt diagnosis and effective therapy, but P. knowlesi can become severe rapidly and fatalities occur. Delay in recognizing malaria is a major preventable risk.

Reporting, legal, and regulatory considerations

Human malaria is reportable in many jurisdictions, including the United States. Imported nonhuman primates are subject to public-health and animal-import requirements. Zoonotic-malaria surveillance may require coordination among human health, wildlife, veterinary, and vector-control authorities.

Selected current sources

• CDC Yellow Book—Malaria
• CDC—Nonhuman Primate Policy Statements: Malaria
• WHO—Technical Consultation on Control of Zoonotic Malaria

POXVIRUS

Synonyms and scope

Animal-associated poxvirus infections. This is an umbrella entry for zoonotic poxviruses other than conditions given their own monographs on this site, such as mpox, tanapox, and yabapox. Important examples include orf (contagious ecthyma), pseudocowpox/milker's nodules, bovine papular stomatitis, cowpox, and zoonotic vaccinia infections.

Etiologic agent

Viruses in family Poxviridae, principally zoonotic members of genera Parapoxvirus and Orthopoxvirus. Agent identity matters because host range, severity, vaccination, and public-health response differ substantially.

Animals involved and epidemiologic roles

• Sheep and goats: Major hosts for orf virus.
• Cattle: Hosts for pseudocowpox and bovine papular stomatitis viruses; vaccinia-like infections occur in some regions.
• Wild rodents: Important reservoirs for cowpox virus in Europe; pet rats and other mammals can serve as bridge hosts.
• Cats and zoo/exotic mammals: Can acquire cowpox and transmit it to people through lesions.
• People: Usually accidental hosts after direct inoculation through damaged skin.

Geographic distribution and occurrence

Parapoxvirus infections occur worldwide wherever susceptible livestock are raised. Cowpox is primarily Eurasian. Zoonotic vaccinia occurs focally, especially where vaccinia-like viruses circulate among livestock. Distribution of individual poxviruses should be assessed separately.

Reservoir, life cycle, and transmission

Transmission generally follows direct contact with animal skin or oral lesions, scabs, secretions, or contaminated equipment, with virus entering through cuts or abrasions. Some poxviruses persist for prolonged periods in dried scabs and contaminated environments. Person-to-person transmission is uncommon for orf and several other animal parapoxviruses.

Incubation period

Varies by virus. Human orf lesions commonly appear within several days after exposure; other zoonotic poxvirus infections may have incubation periods of roughly one to several weeks.

Disease in humans

Most animal-associated poxvirus infections cause one or a few papules, nodules, pustules, or ulcerative lesions on the hands, forearms, face, or other inoculation sites, sometimes with regional lymphadenopathy or fever. Immunocompromised people, people with extensive skin disease, and pregnant patients may be at risk for more severe complications with selected poxviruses.

Disease in animals—by species

• Sheep/goats—orf: Proliferative crusting lesions around the lips, muzzle, oral cavity, teats, and feet; young animals may have difficulty nursing.
• Cattle—parapoxviruses: Papules or nodules on teats, muzzle, oral mucosa, or other skin sites.
• Cats/rodents/exotic mammals—cowpox: Localized or disseminated skin lesions and, occasionally, systemic disease.

Pathology

Poxviruses produce epidermal hyperplasia, ballooning degeneration, vesiculation or pustulation, necrosis, crust formation, and characteristic cytoplasmic inclusions. Lesion pattern varies with virus and host.

Human diagnosis

Diagnosis is often clinical when the lesion and animal exposure are characteristic. PCR or other reference-laboratory testing can distinguish poxviruses when confirmation is needed, particularly for severe, atypical, or epidemiologically important cases.

Animal diagnosis

Veterinary diagnosis uses lesion appearance, herd or flock history, and confirmatory molecular or histopathologic testing when needed. Vesicular or erosive livestock diseases must be differentiated from regulated diseases such as foot-and-mouth disease or vesicular stomatitis.

Differential diagnoses

Mpox, cutaneous anthrax, tularemia, bacterial pyoderma, dermatophytosis, herpesvirus lesions, sporotrichosis, milker's nodules, contagious ecthyma, neoplasia, and regulated vesicular livestock diseases.

Treatment in humans

Most localized parapoxvirus infections are self-limited and require wound protection, pain control, and treatment of secondary bacterial infection only when present. Severe or progressive orthopoxvirus disease requires infectious-disease and public-health consultation; antiviral therapy may be considered depending on the specific virus and patient risk.

Treatment in animals—by species

Most uncomplicated livestock parapoxvirus infections are managed supportively with attention to nutrition, nursing ability, mastitis, and secondary infection. Severe cowpox or other orthopoxvirus disease in companion or exotic animals requires species-specific veterinary care and infection-control measures.

Animal and environmental control

Isolate clinically affected animals when practical, use dedicated equipment, remove heavily contaminated bedding and scabs safely, and clean/disinfect according to veterinary guidance. Prevent movement of animals with undiagnosed vesicular or proliferative lesions until regulated diseases are excluded.

Prevention in humans

Wear nonpermeable gloves when handling animals with suspicious skin or oral lesions, especially if cuts are present; wash hands and wounds promptly; avoid direct contact with scabs; and clean contaminated equipment. Immunocompromised people should avoid handling animals with active poxvirus lesions.

Human vaccination

No universal human vaccine prevents all animal poxvirus infections. Orthopoxvirus vaccines are used for selected occupational or outbreak indications and for mpox prevention under current guidance; they do not provide routine prevention of orf and other parapoxvirus infections.

Animal vaccination

No universal poxvirus vaccine exists. Live orf vaccines are available in some regions for sheep and goats and should be used under veterinary guidance because vaccine virus can establish infection in previously clean premises and can infect people.

Prognosis

Excellent for most localized human and animal parapoxvirus infections. Prognosis is more guarded with disseminated orthopoxvirus disease or infection in severely immunocompromised hosts.

Reporting, legal, and regulatory considerations

Reporting depends on the specific poxvirus and jurisdiction. Suspected mpox, unusual orthopoxvirus disease, or vesicular disease of livestock may require immediate public-health or animal-health notification. Animal movement and vaccination may be regulated during outbreaks.

Selected current sources

• CDC—About Orf Virus
• CDC—Orf Virus in Animals
• CDC—Smallpox/Orthopoxvirus Vaccines

PROTEUS VULGARIS

Synonyms and scope

Animal-associated Proteus vulgaris wound infection. This is an uncommon opportunistic infection rather than a major independent zoonosis; the retained entry is most relevant to contaminated animal-bite wounds, particularly snakebite.

Etiologic agent

Proteus vulgaris, a gram-negative facultatively anaerobic bacterium in family Morganellaceae. Other Proteus species can cause similar opportunistic infections.

Animals involved and epidemiologic roles

• Snakes: Proteus species occur in oral and gastrointestinal flora of some snakes and have been recovered from infected snakebite wounds.
• Other animals: May carry Proteus in the gastrointestinal tract or environment without disease.
• People: Most Proteus infections arise from endogenous or healthcare-associated sources; animal inoculation is an uncommon pathway.

Geographic distribution and occurrence

Worldwide. Animal-associated human cases are sporadic. The clinical importance of Proteus after snakebite varies with geography, snake species, wound severity, local flora, and prior care.

Reservoir, life cycle, and transmission

The organism is widely present in intestines, soil, sewage, and decomposing organic material. Zoonotic exposure occurs through traumatic inoculation of contaminated animal oral flora into tissue, not through a specialized life cycle or routine casual animal contact.

Incubation period

No organism-specific incubation period is established for bite-associated infection; clinically apparent secondary wound infection usually develops over hours to several days.

Disease in humans

Possible manifestations include cellulitis, abscess, wound necrosis, deeper soft-tissue infection, bacteremia, and sepsis. Outside animal exposures, P. vulgaris can also cause urinary, intra-abdominal, and healthcare-associated infections.

Disease in animals—by species

Most colonized animals are asymptomatic. Opportunistic urinary, wound, ear, respiratory, or systemic infections can occur in various species but are not a defining zoonotic syndrome.

Pathology

Suppurative inflammation, tissue necrosis, abscessation, and occasionally invasive infection occur when bacterial proliferation follows tissue injury. Snake venom itself can cause edema, necrosis, and inflammation that mimic infection.

Human diagnosis

Diagnosis requires clinical evidence of infection plus identification of the organism from an appropriate wound, tissue, blood, or other specimen. Antimicrobial susceptibility testing is important because resistance patterns vary.

Animal diagnosis

Testing healthy source animals is not generally useful after a human bite. Clinically affected animals should be evaluated according to the affected organ system with routine veterinary diagnostic methods.

Differential diagnoses

Venom-mediated sterile inflammation, necrotizing soft-tissue injury, compartment syndrome, and polymicrobial bite infection involving Morganella, Providencia, Enterococcus, Pseudomonas, staphylococci, anaerobes, or other Enterobacterales.

Treatment in humans

Snakebite requires urgent envenomation assessment and appropriate antivenom when indicated. Antibiotics are not recommended routinely for every snakebite; established or strongly suspected secondary bacterial infection should be treated with wound care, drainage or debridement when necessary, and antimicrobials guided by local patterns and susceptibility results.

Treatment in animals—by species

No treatment is indicated for a clinically normal source animal solely because P. vulgaris is recovered from a human wound. Treat veterinary infections according to site, severity, and susceptibility results.

Animal and environmental control

Prevent bites through safe handling and appropriate barriers. Maintain clean animal housing and equipment. There is no evidence-based role for screening or treating healthy reptiles to eradicate Proteus carriage.

Prevention in humans

Avoid handling venomous snakes without appropriate training and equipment. After any bite, seek urgent medical care; do not incise, suction, or otherwise manipulate the wound. Monitor for progressive erythema, purulence, fever, worsening pain, or tissue breakdown.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Generally good for localized bacterial infection recognized and treated promptly; prognosis after snakebite is driven primarily by envenomation severity, tissue injury, delay to care, and invasive infection.

Reporting, legal, and regulatory considerations

Proteus infection itself is not generally reportable. Venomous-animal ownership, occupational injury, and antivenom access may be regulated locally.

Selected current sources

• Snakebite-Associated Infections—Systematic Review and Meta-analysis
• CDC—Wildlife Safety and Animal Bites

PROVIDENCIA SPP.

Synonyms and scope

Animal-associated Providencia infection. This retained entry concerns uncommon opportunistic wound infection associated with animal trauma, especially snakebite, rather than a common stand-alone zoonosis.

Etiologic agent

Species of genus Providencia, particularly P. rettgeri and P. stuartii, gram-negative members of family Morganellaceae.

Animals involved and epidemiologic roles

• Snakes: Providencia, especially P. rettgeri, has been recovered from snake oral flora and from some infected snakebite wounds.
• Other animals: May carry the organism in intestinal or environmental flora.
• People: Most infections are opportunistic and healthcare-associated rather than zoonotic.

Geographic distribution and occurrence

Worldwide as an environmental and intestinal organism. Animal-associated human disease is sporadic and most often described in the context of contaminated traumatic wounds.

Reservoir, life cycle, and transmission

No specialized animal-to-human life cycle exists. Infection follows opportunistic inoculation into damaged tissue or, more commonly outside animal settings, arises from endogenous flora or healthcare exposures.

Incubation period

No specific incubation period is defined; bite-wound infection generally becomes apparent within hours to several days.

Disease in humans

Wound and soft-tissue infection, urinary tract infection, bacteremia, and other opportunistic infections occur. After snakebite, Providencia may be one component of a polymicrobial secondary infection.

Disease in animals—by species

Usually colonization without disease. Opportunistic infections have been reported in multiple animal species, but no characteristic zoonotic animal syndrome is established.

Pathology

Suppurative cellulitis, abscessation, and tissue necrosis can occur. In snakebite patients, venom-associated necrosis can resemble or predispose to secondary bacterial infection.

Human diagnosis

Confirm clinically significant infection with bacterial identification from an appropriate specimen and antimicrobial susceptibility testing. Resistant strains occur and may limit empiric options.

Animal diagnosis

Healthy source animals do not require routine testing after human exposure. Clinically ill animals should be investigated according to the affected organ system.

Differential diagnoses

Venom-induced tissue injury and polymicrobial infection involving Proteus, Morganella, Pseudomonas, enterococci, staphylococci, anaerobes, and other gram-negative organisms.

Treatment in humans

Prioritize emergency snakebite management when relevant. Do not give antibiotics routinely solely because a snakebite occurred; treat demonstrated or strongly suspected infection with wound care, drainage or debridement when indicated, and susceptibility-guided antimicrobials.

Treatment in animals—by species

No treatment is indicated for asymptomatic animal carriage. Treat confirmed veterinary infections based on clinical site, severity, and susceptibility testing.

Animal and environmental control

Prevent bites, use appropriate handling equipment, and maintain enclosure hygiene. Attempted eradication of normal intestinal/oral carriage in healthy reptiles is not recommended.

Prevention in humans

Use trained handling and bite-prevention practices. Seek urgent medical evaluation after snakebite and return promptly for fever, purulent drainage, progressive erythema, worsening pain, or tissue necrosis.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Usually favorable when localized infection is recognized early and active therapy is selected. Multidrug resistance, deep infection, and severe envenomation worsen outcome.

Reporting, legal, and regulatory considerations

Providencia infection is not generally reportable. Occupational injuries and regulated venomous-animal keeping may have local requirements.

Selected current sources

• Snakebite-Associated Infections—Systematic Review and Meta-analysis
• CDC—Wildlife Safety and Animal Bites

Q-FEVER

Synonyms and scope

Q fever; coxiellosis. A highly infectious zoonosis associated especially with ruminant birth products and contaminated farm environments.

Etiologic agent

Coxiella burnetii, an obligate intracellular bacterium with environmentally resistant forms that can persist in dust and contaminated materials.

Animals involved and epidemiologic roles

• Goats and sheep: Major zoonotic sources, especially during abortion and parturition.
• Cattle: Important reservoir and shedding host; reproductive disease may occur.
• Cats and dogs: Can become infected and have occasionally been linked to human exposure, particularly around parturition.
• Other mammals, birds, and wildlife: Many species can be infected; their human-health importance varies by region.
• Ticks: Can participate in animal cycles but are not the principal route of human infection in most settings.

Geographic distribution and occurrence

Worldwide with notable regional variation; large livestock-associated outbreaks have occurred in several countries. People with occupational exposure to sheep, goats, cattle, and birth materials are at increased risk.

Reservoir, life cycle, and transmission

Infected animals may shed C. burnetii in placenta, amniotic fluid, vaginal secretions, milk, urine, and feces, with especially heavy contamination during birth or abortion. People are infected mainly by inhaling contaminated aerosols or dust. Raw milk is a potential exposure; person-to-person transmission is rare.

Incubation period

Typically about 2–3 weeks after exposure, with variation related to exposure intensity and host factors.

Disease in humans

Many infections are asymptomatic. Acute Q fever can cause abrupt fever, severe headache, myalgia, fatigue, pneumonia, or hepatitis. Persistent focalized infection can develop months to years later, most importantly endocarditis or vascular infection. Pregnancy infection can increase risk of miscarriage, stillbirth, preterm delivery, or low birth weight.

Disease in animals—by species

• Sheep/goats: Usually asymptomatic, but abortion, stillbirth, premature delivery, and weak offspring may occur.
• Cattle: Infertility, metritis, abortion, stillbirth, and weak calves are reported; many infections remain subclinical.
• Cats/dogs: Often asymptomatic; reproductive disease has been reported and birth materials can pose exposure risk.

Pathology

In people, acute disease may cause hepatitis and interstitial pneumonia; persistent infection commonly targets abnormal heart valves or vascular tissue. In ruminants, placentitis is a major lesion associated with abortion and intense shedding.

Human diagnosis

Diagnosis combines exposure history with serology and, early in illness, PCR. Because serology can be negative early, treatment should not be delayed when clinical suspicion is strong. Persistent infection requires specialist interpretation of phase-specific antibody responses and imaging as indicated.

Animal diagnosis

Veterinary diagnosis is most informative at the herd or flock level and may use PCR on placenta or reproductive material together with serology and investigation of abortion patterns. A positive antibody result alone does not establish that an individual animal is actively shedding.

Differential diagnoses

Influenza-like viral illness, leptospirosis, brucellosis, psittacosis, tularemia, rickettsial disease, bacterial pneumonia, viral hepatitis, culture-negative endocarditis, and other causes of livestock abortion.

Treatment in humans

Doxycycline is first-line treatment for symptomatic acute Q fever and should be started promptly on clinical suspicion. Persistent focalized infection requires prolonged specialist-directed combination therapy and follow-up, especially for endocarditis or vascular infection.

Treatment in animals—by species

Treatment does not reliably eliminate infection or environmental shedding from a herd or flock. Manage affected livestock under veterinary direction, addressing reproductive losses, concurrent disease, and herd-level control; antimicrobial use in food animals must comply with residue and withdrawal regulations.

Animal and environmental control

Immediately contain and safely dispose of placentas, aborted fetuses, and heavily contaminated bedding; segregate aborting animals when practical; improve birthing-area hygiene and ventilation; manage manure to reduce dust; and avoid aerosol-generating cleanup. Vaccination of livestock is used in some countries where licensed products are available.

Prevention in humans

Use gloves and protective clothing for births and abortions, minimize exposure to contaminated dust, wash hands, and avoid raw milk. Pregnant people and those with valvular heart disease, vascular abnormalities, or significant immunocompromise should avoid high-risk exposure to birthing ruminants and contaminated birth materials.

Human vaccination

No Q fever vaccine is licensed for routine use in the United States. A human vaccine is used in Australia for selected high-risk people under a pre-vaccination screening program.

Animal vaccination

Vaccines are available for livestock in some countries and may reduce abortion and shedding, but availability and indications vary. Vaccination does not replace birth-product management and environmental control.

Prognosis

Most acute infections recover completely, but persistent focalized infection can be life-threatening and requires prolonged treatment. Animal prognosis is generally good for the dam, although reproductive losses can be substantial.

Reporting, legal, and regulatory considerations

Human Q fever is nationally notifiable in the United States. Animal reporting requirements vary by jurisdiction; Q fever is a WOAH-listed disease. Occupational exposures, abortion storms, and community clusters warrant public-health and veterinary investigation.

Selected current sources

• CDC—Q Fever
• CDC—Clinical Guidance for Q Fever
• WOAH—Q Fever

RABIES

Synonyms and scope

Rabies; hydrophobia. This entry addresses classical rabies caused by rabies lyssavirus. Other lyssaviruses are covered in the F–L Lyssavirus monograph.

Etiologic agent

Rabies lyssavirus (RABV), genus Lyssavirus, family Rhabdoviridae. Distinct reservoir-associated variants circulate in different mammalian populations.

Animals involved and epidemiologic roles

• Dogs: Principal source of human rabies deaths globally.
• Bats: Major wildlife reservoirs in the Americas and important sources of human exposure.
• Raccoons, skunks, foxes, mongooses, and other carnivores: Region-specific wildlife reservoirs.
• Cats, livestock, horses, and other mammals: Susceptible spillover hosts that can expose people.
• Small rodents and lagomorphs: Rarely infected and very rarely sources of human rabies; risk assessment remains exposure- and jurisdiction-specific.

Geographic distribution and occurrence

Rabies occurs in more than 150 countries and territories. Dog-mediated rabies causes the great majority of human deaths worldwide, especially in Africa and Asia. In the United States, most rabid animals are wildlife, particularly bats, raccoons, skunks, and foxes.

Reservoir, life cycle, and transmission

Virus is shed mainly in saliva and is transmitted through bites, scratches contaminated with saliva, or saliva contact with mucosa or broken skin. After local replication, virus travels through peripheral nerves to the central nervous system and later to salivary glands. Casual contact, intact skin, urine, and feces are not ordinary transmission routes.

Incubation period

Usually weeks to months in people and animals but highly variable. Wound location, severity, viral dose, host species, and other factors influence the interval.

Disease in humans

Early fever, malaise, headache, and pain or paresthesia at the exposure site progress to encephalitis. Furious rabies causes agitation, hydrophobia, aerophobia, dysphagia, and autonomic instability; paralytic rabies causes progressive weakness and paralysis. Once clinical signs appear, rabies is virtually always fatal.

Disease in animals—by species

• Dogs/cats/ferrets: Behavior change, aggression or unusual friendliness, dysphagia, hypersalivation, ataxia, paralysis, seizures, and rapid death.
• Livestock/horses: Behavioral change, lameness, colic-like signs, dysphagia, ataxia, recumbency, or paralysis; furious behavior is not required.
• Wildlife/bats: Loss of fear, abnormal daytime activity, aggression, inability to fly, weakness, ataxia, or paralysis.

Pathology

Acute nonsuppurative encephalomyelitis with neuronal degeneration and gliosis is typical; Negri bodies may be present but are not required. Gross lesions are often absent.

Human diagnosis

Immediately involve public health. Antemortem diagnosis uses multiple specimen types and specialized molecular, antigen, and antibody testing because no single test is sufficient in all cases. Postmortem testing of brain tissue confirms infection.

Animal diagnosis

There is no approved routine antemortem test that rules out rabies in animals. Diagnostic confirmation requires postmortem examination of brain tissue by an authorized rabies laboratory. Do not perform unnecessary necropsy or brain sampling outside official protocols.

Differential diagnoses

Canine distemper, tetanus, botulism, toxicities, trauma, metabolic encephalopathy, listeriosis, viral or bacterial encephalitis, pseudorabies where present, and other causes of acute behavior change, dysphagia, or paralysis.

Treatment in humans

No treatment reliably cures established clinical rabies. Intensive supportive and palliative care and infection-control measures are required. The life-saving intervention is post-exposure prophylaxis before symptoms: immediate wound cleansing plus rabies vaccine and, when indicated, human rabies immune globulin according to current guidance.

Treatment in animals—by species

There is no curative treatment for clinically suspect rabies. Immediately isolate the animal, prevent saliva exposure, and contact public-health or animal-health authorities. Observation, quarantine, booster vaccination, euthanasia, and testing depend on species, vaccination status, exposure circumstances, and local law.

Animal and environmental control

Maintain legally required vaccination of dogs, cats, and ferrets; vaccinate at-risk livestock and other species when indicated; control canine rabies through mass dog vaccination; reduce wildlife exposure; and use authorized wildlife-vaccination programs where appropriate. Routine indiscriminate dog culling is not an effective rabies-control strategy.

Prevention in humans

Avoid contact with bats and unfamiliar wildlife, vaccinate pets, teach bite prevention, and use appropriate PPE when handling suspect animals. Wash potential exposure wounds immediately and seek urgent public-health or medical risk assessment; do not wait for symptoms.

Human vaccination

Modern rabies vaccines are used for risk-based pre-exposure vaccination and for post-exposure prophylaxis. PEP schedules depend on prior vaccination and immune status; previously unvaccinated people who require PEP also receive rabies immune globulin when indicated.

Animal vaccination

Licensed rabies vaccines are available for dogs, cats, ferrets, horses, cattle, sheep, and selected wildlife applications depending on country. Vaccination schedules and who may administer vaccine are legally regulated.

Prognosis

Clinical rabies is almost invariably fatal in people and animals. Correctly administered post-exposure prophylaxis before symptom onset is highly effective at preventing disease.

Reporting, legal, and regulatory considerations

Rabies is urgently reportable in people and animals. Animal quarantine, observation, euthanasia, testing, vaccination, movement, and exposure management are governed by jurisdiction-specific law. Coordinate suspected cases with public-health and animal-health authorities.

Selected current sources

• CDC—About Rabies
• CDC—Information for Veterinarians
• CDC—Rabies Post-exposure Prophylaxis
• WHO—Rabies

RAT BITE FEVER

Synonyms and scope

Rat-bite fever (RBF); streptobacillary fever; Haverhill fever; sodoku. A rodent-associated bacterial zoonosis acquired through bites, scratches, secretions, urine, contaminated materials, or contaminated food and drink.

Etiologic agent

Streptobacillus moniliformis causes most RBF in North America and is responsible for Haverhill fever. Spirillum minus causes sodoku and is reported more often in Asia.

Animals involved and epidemiologic roles

• Rats: Principal reservoir; often carry the organisms in the upper respiratory/oral tract without illness.
• Mice, gerbils, guinea pigs, squirrels, and other rodents: Can carry RBF organisms and expose people.
• Dogs, cats, ferrets, and rabbits: Rarely can acquire infection through rodent contact and have occasionally been implicated in human exposure.
• People: Accidental hosts; person-to-person transmission is not recognized as an important route.

Geographic distribution and occurrence

RBF occurs worldwide but is uncommon and probably underdiagnosed. Pet-rodent ownership, rodent infestation, animal-care work, and laboratory or pet-store exposure increase risk. S. minus disease is reported mainly in Asia.

Reservoir, life cycle, and transmission

Reservoir rodents can carry organisms in oral, nasal, conjunctival, and urinary secretions without appearing ill. People become infected after bites or scratches, saliva or urine contacting broken skin or mucosa, close contact with contaminated bedding or cages, or ingestion of contaminated food or water.

Incubation period

S. moniliformis disease usually begins 3–10 days after exposure and can occur up to about 21 days later. S. minus typically has a longer interval, often 7–21 days.

Disease in humans

S. moniliformis commonly causes fever, chills, headache, myalgia, vomiting, rash—often involving hands and feet—and migratory polyarthralgia or polyarthritis. S. minus more often causes recurrent fever, ulceration at the healed bite site, lymphangitis, lymphadenopathy, and a violaceous rash. Untreated disease can lead to abscesses, septic arthritis, pneumonia, hepatitis, meningitis, or endocarditis.

Disease in animals—by species

• Rats and many reservoir rodents: Usually asymptomatic carriers.
• Mice: Some strains or hosts can develop systemic illness, arthritis, or septic disease.
• Other mammals: Sporadic clinical infection can occur after rodent exposure but is uncommon.

Pathology

Human disease is a bacteremic systemic infection that can seed joints, heart valves, lungs, central nervous system, and other organs. Septic arthritis and endocarditis are important severe complications.

Human diagnosis

Diagnosis depends on recognizing the rodent exposure and identifying the causative organism from blood, joint fluid, tissue, or other appropriate specimens with specialized laboratory support when necessary. The laboratory should be informed that RBF is suspected because routine systems may not reliably detect all cases.

Animal diagnosis

Routine screening of healthy pet rodents is not recommended as a reliable way to establish human safety because colonized rodents can appear normal and tests may not predict shedding. Clinically ill animals should receive veterinary evaluation.

Differential diagnoses

Rocky Mountain spotted fever and other rickettsioses, meningococcemia, disseminated gonococcal infection, viral exanthems, leptospirosis, Lyme disease, septic arthritis, infective endocarditis, and other causes of fever with rash and arthralgia.

Treatment in humans

Prompt antibiotic treatment is important. Penicillin-class therapy is traditional first-line treatment; doxycycline is an alternative and is especially useful when RBF and a tick-borne rickettsial disease are both being considered. Endocarditis or other focal complications require prolonged, specialist-directed therapy.

Treatment in animals—by species

Treatment of clinically ill animals should be directed by a veterinarian. Attempting to eliminate asymptomatic carriage from healthy pet rodents with routine antibiotics is not an established public-health strategy and may not reliably prevent recurrence or transmission.

Animal and environmental control

Use good rodent husbandry, keep cages clean, control wild-rodent infestations, prevent pet rodents from contact with wild rodents, and obtain animals from responsible sources. Avoid kissing rodents or allowing them close to the face.

Prevention in humans

Wash hands after handling rodents, bedding, cages, or feeder rodents; wear gloves for contaminated bedding if skin is broken; promptly wash bites and scratches; and seek medical care for fever, rash, or joint pain after rodent exposure. Young children, older adults, pregnant people, and immunocompromised people should use additional caution with pet rodents.

Human vaccination

No vaccine is available.

Animal vaccination

No vaccine is available.

Prognosis

Generally excellent with prompt appropriate antibiotics. Delayed diagnosis can result in life-threatening endocarditis, meningitis, pneumonia, or other invasive complications.

Reporting, legal, and regulatory considerations

RBF is not nationally notifiable in the United States and is not routinely reportable in most jurisdictions, but clusters associated with pet stores, breeding facilities, food contamination, or occupational settings warrant public-health consultation.

Selected current sources

• CDC—About Rat-bite Fever
• CDC—Clinical Overview of Rat-bite Fever
• CDC—Small Mammals and Healthy Pets

RETROVIRUSES

Synonyms and scope

Retroviruses are a large viral family; this monograph is limited to animal-associated retroviruses with demonstrated or plausible zoonotic relevance, especially simian foamy viruses and other nonhuman-primate retroviruses. HIV-1 and HIV-2 have ancient primate origins but are now maintained by human-to-human transmission and are not ordinarily acquired from contemporary pet or domestic-animal contact.

Etiologic agent

Retroviridae are enveloped RNA viruses that reverse-transcribe their genome into DNA and integrate a provirus into host cells. Zoonotic concern is virus-specific; the family name alone does not imply a zoonotic hazard.

Animals involved and epidemiologic roles

Nonhuman primates are the principal animals of concern for recognized cross-species simian retrovirus exposure. Simian foamy viruses are widespread in many primates. Simian T-lymphotropic viruses and simian immunodeficiency viruses have also crossed species historically. Ordinary dogs, cats, livestock, birds, reptiles, and small mammals are not recognized reservoirs for human retroviral infection merely because they harbor species-specific retroviruses.

Geographic distribution and occurrence

Animal retroviruses occur worldwide. Human infection with simian foamy virus has been documented particularly in people with occupational, hunting, butchering, bite, or other close exposure to nonhuman primates in Africa and Asia.

Reservoir, life cycle, and transmission

Transmission risk depends on the virus. For simian foamy virus, bites and contact with primate saliva or tissues are important recognized exposures. Persistent infection can follow spillover. Sustained human-to-human transmission of simian foamy virus has not been established.

Incubation period

No single incubation period applies to retroviruses. Spillover infection may remain asymptomatic for years; incubation and latency are virus-specific and often cannot be defined from the exposure event.

Disease in humans

Most documented simian foamy virus infections in people have not been associated with a clearly established clinical syndrome. Historical cross-species transmission of primate lentiviruses and T-lymphotropic viruses demonstrates that some retroviral spillovers can have major long-term consequences, but those viruses must be evaluated individually.

Disease in animals—by species

Nonhuman primates commonly carry species-adapted retroviruses without obvious illness, although some simian retroviruses can cause immunologic, hematologic, or neoplastic disease. Species-specific retroviruses of domestic animals cause important veterinary diseases but generally are not human zoonoses.

Pathology

Pathology is virus-specific. Retroviral integration can produce persistent infection; disease mechanisms may include immune dysfunction, lymphoproliferation, oncogenesis, or no recognized tissue injury.

Human diagnosis

Diagnosis after a significant nonhuman-primate exposure should be coordinated with occupational medicine or public health when a simian retrovirus is suspected. Serologic and molecular methods are virus-specific; routine human clinical panels do not screen for all simian retroviruses.

Animal diagnosis

Animal diagnosis is specialized and depends on species, colony health programs, and the retrovirus of concern. Testing of nonhuman primates is generally performed within institutional veterinary and biosafety programs.

Differential diagnoses

Differentials depend on the clinical syndrome and include other causes of lymphadenopathy, cytopenias, immune dysfunction, neurologic disease, and neoplasia. A history of nonhuman-primate exposure is essential when considering a simian retrovirus.

Treatment in humans

There is no established antiviral treatment for asymptomatic simian foamy virus infection. Management of other retroviral infections is virus-specific and should follow specialist guidance.

Treatment in animals—by species

Treatment of retroviral disease in animals is species- and virus-specific. Colony management may be more important than individual therapy for regulated or research nonhuman-primate populations.

Animal and environmental control

Prevent bites, scratches, mucosal exposure, and contact with nonhuman-primate blood, saliva, and tissues. Occupational programs should include exposure-response procedures and appropriate personal protective equipment. Pet ownership of nonhuman primates may carry additional infectious-disease risks beyond retroviruses.

Prevention in humans

People working with or handling nonhuman primates should use established occupational safeguards and promptly wash and report bites, scratches, and mucosal exposures. Post-exposure evaluation should address the full range of primate-associated pathogens, not retroviruses alone.

Human vaccination

No licensed human vaccine is available specifically to prevent simian foamy virus or the other occupational simian retroviral infections discussed here.

Animal vaccination

No routine animal vaccine is available to eliminate the simian retroviruses of primary zoonotic concern. Management relies on husbandry, colony surveillance where appropriate, and exposure prevention.

Prognosis

For documented simian foamy virus infection, available observations have generally been reassuring, but long-term clinical significance is still being studied. Prognosis for other retroviral infections varies widely by virus.

Reporting, legal, and regulatory considerations

Reporting requirements vary by virus and jurisdiction. Occupational nonhuman-primate exposures should be documented under institutional protocols. Human HIV and HTLV reporting rules are separate from the animal-associated spillover focus of this monograph.

Selected current sources

CDC Emerging Infectious Diseases: Primate-to-Human Retroviral Transmission in Asia; CDC/NIOSH and institutional nonhuman-primate occupational-health guidance; current peer-reviewed reviews of simian foamy virus epidemiology.

RHODOCOCCUS EQUI INFECTION

Synonyms and scope

Rhodococcosis; Rhodococcus equi infection; historically Corynebacterium equi. An environmentally associated opportunistic infection important in foals and increasingly recognized as an occupational, food-associated, or animal-associated zoonotic pathogen in susceptible people.

Etiologic agent

Rhodococcus equi, a facultative intracellular, gram-positive actinomycete. Virulence-associated plasmid types show host associations, including equine, porcine, and bovine/caprine lineages, while human infections involve multiple plasmid types.

Animals involved and epidemiologic roles

• Horses: Foals are the classic clinical host, developing pyogranulomatous pneumonia and lymphadenitis; contaminated soil and manure are major environmental sources.
• Pigs: Often have lymph-node lesions or subclinical infection and can carry porcine-associated virulence types.
• Cattle and goats: Infections occur and bovine/caprine-associated virulence types have been recovered from human cases.
• Dogs and cats: Opportunistic pulmonary, cutaneous, wound, or systemic disease occurs; draining lesions may pose risk to highly susceptible owners.
• People: Opportunistic infection, especially in transplant recipients, people with advanced HIV infection, malignancy, corticosteroid therapy, or other immune compromise.

Geographic distribution and occurrence

Worldwide wherever horses and livestock are raised. The organism persists in soil and manure, and disease in foals is especially associated with endemic breeding farms and dusty, heavily contaminated environments.

Reservoir, life cycle, and transmission

Soil and animal manure are major reservoirs. Human exposure can occur through inhalation of contaminated dust or aerosols, traumatic inoculation, contact with diseased animals or draining lesions, and possibly ingestion of undercooked pork or bovine products contaminated during slaughter. Most human cases cannot be attributed to a single animal, so routine direct horse-to-human transmission should not be assumed.

Incubation period

No single incubation period is established. Disease may emerge weeks to months after exposure, particularly in immunocompromised people. Foal disease usually becomes clinically apparent during the first months of life after early environmental exposure.

Disease in humans

Chronic or subacute pneumonia is most common, often with nodular or cavitary pulmonary lesions, fever, cough, dyspnea, and systemic illness. Bacteremia, brain abscess, endocarditis, bone/joint infection, skin and soft-tissue disease, and other disseminated forms occur, especially with impaired immunity.

Disease in animals—by species

• Foals: Suppurative/pyogranulomatous bronchopneumonia, pulmonary abscesses, tracheobronchial lymphadenopathy, fever, cough, tachypnea, and poor growth; extrapulmonary disorders include colitis, abdominal lymphadenitis, polysynovitis, osteomyelitis, and abscesses.
• Adult horses: Disease is uncommon and usually associated with immune compromise or another predisposing condition.
• Pigs/cattle/goats: Lymphadenitis, abscesses, pulmonary or other pyogranulomatous lesions, sometimes detected at slaughter.
• Dogs/cats: Pulmonary, cutaneous/subcutaneous, wound, lymph-node, or disseminated infections.

Pathology

Characteristic lesions are suppurative to pyogranulomatous inflammation with macrophages, neutrophils, necrosis, and abscess formation. Pulmonary lesions can coalesce into nodules or cavities; lymph nodes and many extrapulmonary organs may be involved.

Human diagnosis

Obtain cultures and histopathology from involved tissue, respiratory specimens, blood, or other sterile sites and request accurate species identification plus susceptibility testing. The organism can be mistaken for diphtheroids, Nocardia, or mycobacteria, so clinical context and modern identification methods are important.

Animal diagnosis

In foals, combine clinical examination, thoracic imaging, hematology, and sampling of lower-airway or lesion material for cytology and culture/PCR as indicated. Farm screening findings alone do not prove clinical disease. Other species require lesion-directed culture and histopathology.

Differential diagnoses

In people: tuberculosis, nontuberculous mycobacteria, nocardiosis, fungal pneumonia, bacterial lung abscess, malignancy, and other causes of cavitary lung disease. In foals: other bacterial pneumonia, viral respiratory disease, aspiration, parasitic lung disease, and noninfectious pulmonary disorders.

Treatment in humans

Invasive human rhodococcosis usually requires prolonged specialist-directed combination antimicrobial therapy guided by susceptibility and infection site, with drainage or surgical source control when indicated. Management of underlying immunosuppression is important when feasible.

Treatment in animals—by species

Foal treatment typically requires prolonged combination antimicrobial therapy selected by the attending veterinarian, with monitoring for adverse effects and response. Abscess drainage or other surgery may be needed in selected extrapulmonary disease. Treatment of food animals must comply with drug-use and withdrawal regulations.

Animal and environmental control

Reduce excessive dust and manure accumulation on endemic farms, avoid overcrowding, and identify clinically affected foals promptly. No farm intervention reliably eliminates the organism from soil. Use gloves and hygiene around draining lesions and contaminated dressings.

Prevention in humans

Immunocompromised people should avoid heavy exposure to dusty livestock environments and direct contact with draining lesions from affected animals, and should avoid undercooked pork and bovine products. Cover wounds and use appropriate PPE for veterinary, farm, necropsy, and wound-care tasks.

Human vaccination

No human vaccine is available.

Animal vaccination

No broadly effective licensed vaccine is available for routine prevention of equine rhodococcosis.

Prognosis

Foal prognosis is often good with early recognition and effective treatment but worsens with extensive pulmonary disease or severe extrapulmonary complications. Human prognosis depends strongly on immune status, dissemination, site, and timeliness of effective therapy.

Reporting, legal, and regulatory considerations

Rhodococcosis is not generally nationally notifiable in the United States. Clusters in animal facilities, occupational cases, unusual food-associated infections, or antimicrobial-resistance concerns may warrant local public-health, veterinary, or infection-control consultation.

Selected current sources

• Merck Veterinary Manual—Rhodococcus Infection in Animals
• Merck Veterinary Manual—Global Zoonotic Bacterial and Rickettsial Diseases

RICKETTSIA FELIS

Synonyms and scope

Rickettsia felis infection is a flea-associated spotted-fever-group rickettsiosis. It should be distinguished from flea-borne (murine) typhus caused by R. typhi.

Etiologic agent

Rickettsia felis is an obligately intracellular spotted-fever-group Rickettsia.

Animals involved and epidemiologic roles

Cat fleas (Ctenocephalides felis) are the best-established vector and maintenance host. Dogs, cats, opossums, rodents, and other vertebrates may participate in local flea ecology, but their reservoir competence and importance vary by setting.

Geographic distribution and occurrence

R. felis and infected fleas have been detected worldwide, with human cases reported in multiple tropical, subtropical, and temperate regions. True incidence is uncertain because diagnostic cross-reactivity and limited testing complicate surveillance.

Reservoir, life cycle, and transmission

People are thought to become infected primarily through exposure to infected fleas. Fleas can maintain R. felis across generations. Direct transmission from a dog or cat to a person has not been established as the usual route; pets primarily increase exposure by carrying infected fleas.

Incubation period

The incubation period is not as well defined as for several other rickettsioses; illness is generally reported within days to roughly two weeks after arthropod exposure.

Disease in humans

Reported human illness commonly includes fever, headache, myalgia, and sometimes rash or an inoculation eschar. Clinical severity varies, and attribution can be difficult in areas where several rickettsiae circulate.

Disease in animals—by species

Dogs and cats with infected fleas are usually not clinically ill from R. felis itself. Their principal epidemiologic role is association with flea populations. Disease attribution in animals requires caution because molecular detection does not necessarily establish causation.

Pathology

Human disease is consistent with a rickettsial vasculitic process, although pathology is less completely characterized than RMSF. Animal pathology specifically attributable to R. felis is not well established.

Human diagnosis

Diagnosis combines compatible illness and exposure with rickettsial serology and, where appropriate, molecular testing. Cross-reactivity among spotted-fever-group rickettsiae can prevent species-level assignment from a single serologic result.

Animal diagnosis

Routine testing of healthy pets for R. felis is generally not useful for individual human risk assessment. Flea identification/control is more actionable. Specialized molecular testing may be used in epidemiologic investigations.

Differential diagnoses

Differentials include flea-borne typhus, RMSF and other spotted fever rickettsioses, ehrlichiosis, anaplasmosis, viral febrile illnesses, and other causes of fever with rash.

Treatment in humans

Doxycycline is the preferred treatment for suspected clinically significant rickettsial infection; treatment should be based on clinical judgment and should not be delayed when a serious rickettsiosis is possible.

Treatment in animals—by species

No specific treatment is indicated for an otherwise healthy animal solely because fleas or a screening sample contain R. felis. Treat clinically ill animals according to the actual diagnosis and institute effective flea control.

Animal and environmental control

Year-round integrated flea control for pets and the home environment is the central preventive measure. Treat all susceptible household animals with veterinarian-recommended flea preventives and address environmental infestation.

Prevention in humans

Avoid flea bites, use effective pet flea control, wash hands after handling flea debris, and reduce rodent/opossum access around homes where feasible.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Most recognized human cases respond well to appropriate treatment. Prognosis in animals is generally favorable because most infected animals do not develop a clearly attributable illness.

Reporting, legal, and regulatory considerations

R. felis infection is not generally a nationally notifiable disease in the United States; requirements may differ locally. Clusters or unusual severe cases should prompt consultation with public health authorities.

Selected current sources

CDC Vector-Borne Diseases Rickettsial Isolate Reference Collection (2025); CDC guidance for spotted-fever rickettsioses; current peer-reviewed reviews of R. felis and flea-associated rickettsiae.

RICKETTSIALPOX

Synonyms and scope

Rickettsialpox is a mite-borne spotted-fever-group rickettsiosis associated classically with house mice and their mites.

Etiologic agent

Rickettsia akari is an obligately intracellular spotted-fever-group bacterium.

Animals involved and epidemiologic roles

The house mouse (Mus musculus) is the principal vertebrate host in the classic urban cycle. The house-mouse mite Liponyssoides sanguineus is the vector and an important maintenance host. Dogs and cats are not recognized as principal reservoirs.

Geographic distribution and occurrence

First recognized in New York City, rickettsialpox has been reported in the United States and other regions. Cases are uncommon and probably underrecognized.

Reservoir, life cycle, and transmission

Infected mouse mites bite people when rodent hosts are unavailable or when infestations bring mites into human living spaces. Person-to-person transmission is not expected.

Incubation period

An eschar usually develops about a week after the mite bite, followed several days later by systemic illness and rash; exact timing varies.

Disease in humans

Typical disease includes a papule that becomes a dark eschar, followed by fever, headache, myalgia, and a generalized papulovesicular rash. Illness is usually milder than RMSF.

Disease in animals—by species

House mice generally serve as hosts without a recognized clinical syndrome. The disease is principally a human illness arising from a rodent-mite cycle.

Pathology

Human lesions reflect local inoculation injury and systemic rickettsial infection with small-vessel involvement. Characteristic skin lesions include the inoculation eschar and papulovesicular eruption.

Human diagnosis

Diagnosis is based on compatible clinical findings and rodent/mite exposure, supported by spotted-fever-group serology or molecular testing when available. Species-level confirmation may require specialized testing.

Animal diagnosis

Animal testing is rarely clinically indicated. Identification of a mouse and mite infestation is more useful for control than testing individual rodents.

Differential diagnoses

Differentials include varicella, mpox, insect bites, bacterial ecthyma, other eschar-associated spotted fevers, and RMSF.

Treatment in humans

Doxycycline is the treatment of choice for rickettsialpox and other suspected spotted-fever rickettsioses.

Treatment in animals—by species

No treatment is required for reservoir mice as a clinical intervention. Control focuses on coordinated rodent and mite management rather than treating individual wildlife or commensal rodents.

Animal and environmental control

Control mice and their mites together. Rodent removal without mite control can temporarily increase human biting as mites seek alternative hosts. Seal entry points and use professional pest management when infestation is substantial.

Prevention in humans

Avoid contact with rodent nests and contaminated areas, use gloves during cleanup, and address mite exposure promptly when rodent infestations are discovered.

Human vaccination

No human vaccine is available.

Animal vaccination

No animal vaccine is available.

Prognosis

Prognosis is excellent with appropriate treatment; severe or fatal disease is rare.

Reporting, legal, and regulatory considerations

Rickettsialpox is not generally nationally notifiable in the United States. Local reporting rules may vary, and unusual clusters should be discussed with public health authorities.

Selected current sources

CDC: Other Spotted Fever Rickettsioses; CDC Clinical Care of Other Spotted Fever Rickettsioses (2025); CDC Rickettsial Isolate Reference Collection (2025).

RIFT VALLEY FEVER

Synonyms and scope

Rift Valley fever (RVF) is a mosquito-borne and animal-contact zoonosis that causes major abortion storms and neonatal mortality in susceptible livestock and can cause febrile, ocular, neurologic, or hemorrhagic disease in people.

Etiologic agent

Rift Valley fever virus is a phlebovirus in the family Phenuiviridae, order Bunyavirales.

Animals involved and epidemiologic roles

Sheep, goats, cattle, buffalo, camels, and other ruminants are important amplifying hosts. Young lambs and kids are particularly susceptible. Mosquitoes are vectors and can contribute to long-term maintenance through vertical transmission. Humans are incidental hosts.

Geographic distribution and occurrence

RVF is endemic in much of sub-Saharan Africa and has caused outbreaks in Egypt, the Arabian Peninsula, and Indian Ocean islands. Recent outbreaks continue to occur in Africa, including West and East Africa.

Reservoir, life cycle, and transmission

Mosquitoes transmit virus among animals and to people. Humans are also commonly infected through contact with blood, body fluids, organs, fetuses, placentas, or tissues of infected livestock. Person-to-person transmission has not been documented.

Incubation period

Human symptoms usually begin about 2–6 days after exposure. Incubation in animals is short and varies with species, age, and exposure.

Disease in humans

Most human infections are asymptomatic or cause an acute influenza-like febrile illness. A minority develop ocular disease, meningoencephalitis, or hemorrhagic manifestations; severe disease can be fatal.

Disease in animals—by species

Sheep/goats: abortion storms and very high mortality in neonates; adults may have fever and hepatic disease. Cattle: abortions, neonatal disease, and variable adult illness. Camels and other ruminants: reproductive loss and variable systemic disease. Wildlife may be infected and contribute to ecology.

Pathology

Hepatic necrosis is a major lesion in susceptible animals, especially neonates. Human severe disease can involve hepatitis, hemorrhage, encephalitis, and retinal injury.

Human diagnosis

Clinical suspicion depends on travel/residence, mosquito exposure, and contact with livestock during an outbreak. Confirmation requires specialized public-health laboratory testing; U.S. clinicians should immediately involve health departments when RVF is suspected.

Animal diagnosis

Animal diagnosis combines outbreak pattern—especially abortions and neonatal deaths—with official laboratory confirmation. Suspected cases in non-endemic countries require immediate veterinary-authority involvement.

Differential diagnoses

Human differentials include malaria, dengue and other arboviruses, leptospirosis, severe bacterial sepsis, hepatitis, and other viral hemorrhagic fevers. Animal differentials for abortion storms include brucellosis, Q fever, chlamydiosis, leptospirosis, bluetongue and other reproductive diseases.

Treatment in humans

No licensed specific antiviral therapy is established for routine human RVF. Most cases receive supportive care; severe cases require hospital-based management of neurologic, ocular, hemorrhagic, or organ complications.

Treatment in animals—by species

There is no specific curative antiviral treatment for livestock. Care is supportive where practical, while outbreak management emphasizes movement controls, vector reduction, biosecurity, and vaccination programs authorized by veterinary authorities.

Animal and environmental control

In endemic regions, vaccination of livestock before outbreaks, surveillance, mosquito control, movement management, and safe handling of abortions and carcasses are central. During outbreaks, veterinary authorities direct vaccination and movement/slaughter measures.

Prevention in humans

People should avoid unprotected contact with blood, birth products, carcasses, and raw animal products in affected areas and prevent mosquito bites. Veterinarians, farmers, abattoir workers, and animal-health responders require appropriate PPE.

Human vaccination

No licensed human RVF vaccine is currently available for routine use.

Animal vaccination

Live-attenuated and inactivated RVF vaccines are used in animals in some endemic countries. Product choice and use depend on national programs; some live vaccines can cause fetal adverse effects and are unsuitable in certain pregnant animals.

Prognosis

Most human cases recover, but ocular, neurologic, and hemorrhagic forms can cause permanent disability or death. Prognosis in young susceptible livestock can be poor, and reproductive losses may be extensive.

Reporting, legal, and regulatory considerations

RVF is a WOAH-listed disease and relevant animal infections/outbreaks are subject to international notification requirements. In the United States, suspected human or animal RVF requires immediate coordination with public-health and animal-health authorities.

Selected current sources

CDC: About Rift Valley Fever (reviewed 2024); WOAH: Rift Valley fever disease page and 2026 State of the World’s Animal Health report; WOAH statements on 2025 West African outbreaks.

ROCKY MOUNTAIN SPOTTED FEVER

Synonyms and scope

Rocky Mountain spotted fever (RMSF) is a potentially fatal tick-borne spotted-fever-group rickettsiosis. Dogs are important sentinels for shared tick exposure but do not directly transmit RMSF to people.

Etiologic agent

Rickettsia rickettsii is an obligately intracellular spotted-fever-group bacterium.

Animals involved and epidemiologic roles

Ticks are vectors and maintenance hosts. Important U.S. vectors include Dermacentor variabilis, D. andersoni, and, in parts of the Southwest and Mexico, Rhipicephalus sanguineus sensu lato. Dogs can develop clinical RMSF and can transport infected ticks into human environments.

Geographic distribution and occurrence

RMSF occurs in the Americas. In the United States, cases are reported most often from several south-central and southeastern states, although exposure can occur elsewhere where competent vectors are present.

Reservoir, life cycle, and transmission

People and dogs become infected through bites of infected ticks. Direct dog-to-human transmission does not occur. Removing or crushing attached ticks with bare fingers can create avoidable exposure to tick contents.

Incubation period

Human symptoms usually begin 3–12 days after an infected tick bite. Canine incubation is commonly several days to about two weeks.

Disease in humans

Early human illness commonly includes fever, severe headache, myalgia, gastrointestinal signs, and sometimes periorbital or hand edema. Rash often appears later and may be absent early. Untreated disease can rapidly progress to neurologic injury, respiratory failure, shock, organ failure, and death.

Disease in animals—by species

Dogs may develop fever, lethargy, anorexia, lymphadenopathy, thrombocytopenia, petechiae/ecchymoses, edema, joint pain, neurologic abnormalities, and ocular lesions. Many exposed animals remain subclinical.

Pathology

R. rickettsii targets vascular endothelial cells, producing systemic vasculitis, increased vascular permeability, edema, hemorrhage, and ischemic organ injury.

Human diagnosis

RMSF is a clinical diagnosis supported by epidemiology and testing. Serology is often negative early; paired serology is useful retrospectively. Treatment must not wait for laboratory confirmation when RMSF is suspected.

Animal diagnosis

Canine diagnosis uses clinical findings, tick exposure, CBC/chemistry abnormalities, paired serology and, selectively, molecular testing. A single positive antibody titer can reflect prior exposure rather than current disease.

Differential diagnoses

Differentials in people include meningococcemia, ehrlichiosis, anaplasmosis, other spotted fevers, viral exanthems, leptospirosis and sepsis. In dogs, consider ehrlichiosis, anaplasmosis, immune-mediated thrombocytopenia, leptospirosis, sepsis and other tick-borne infections.

Treatment in humans

Doxycycline is the treatment of choice for adults and children of all ages with suspected RMSF. Early treatment is critical; delay beyond the first several days of illness markedly increases the risk of severe disease and death.

Treatment in animals—by species

Doxycycline is also commonly the treatment of choice for clinically affected dogs. Supportive therapy is tailored to dehydration, hemorrhage, neurologic disease, renal injury, or other complications.

Animal and environmental control

Use effective tick prevention on dogs, inspect pets and people after tick exposure, manage yard habitat, and remove attached ticks promptly with appropriate technique. Treat the environment when brown dog tick infestation is present.

Prevention in humans

Avoid tick bites with repellents, protective clothing, prompt tick checks, and careful tick removal. Pet tick prevention reduces ticks entering the home but does not replace personal precautions.

Human vaccination

No human vaccine is available.

Animal vaccination

No licensed animal vaccine is available.

Prognosis

With early doxycycline, prognosis is usually good. Delayed human treatment can result in severe complications or death. Dogs generally respond well when treated before advanced vasculitic injury.

Reporting, legal, and regulatory considerations

Spotted fever rickettsioses are nationally notifiable in the United States under the surveillance category used by CDC; state requirements vary. Veterinarians should follow local requirements for animal disease and tick-borne surveillance.

Selected current sources

CDC: Clinical Overview of RMSF; CDC: Clinical Signs and Symptoms of RMSF; CDC: About RMSF; current veterinary infectious-disease references for canine RMSF.

ROTAVIRUS

Synonyms and scope

Rotaviruses are major causes of acute gastroenteritis in young humans and many animal species. Most infections are host-adapted; animal-to-human transmission and human-animal reassortment occur but account for a minority of routine human rotavirus disease.

Etiologic agent

Rotaviruses are non-enveloped segmented double-stranded RNA viruses in the family Sedoreoviridae. Group A rotaviruses cause most human disease and many veterinary infections.

Animals involved and epidemiologic roles

Humans, cattle, pigs, horses, dogs, cats, birds, and numerous wildlife species carry distinct and sometimes overlapping rotavirus lineages. Young animals are most likely to develop clinical diarrhea. Animals can contribute genes to reassortant human strains, but ordinary human transmission is predominantly person-to-person.

Geographic distribution and occurrence

Rotaviruses occur worldwide. Human vaccination has greatly reduced severe pediatric disease in countries with high vaccine coverage, while animal rotavirus remains an important cause of neonatal enteric disease in livestock.

Reservoir, life cycle, and transmission

Transmission is primarily fecal-oral through contaminated hands, surfaces, food, water, and close contact. Rotaviruses are environmentally stable. Cross-species infection can occur, and mixed infection can generate reassortant viruses containing both human- and animal-associated gene segments.

Incubation period

Human incubation is usually about 2 days. Incubation in young animals is generally short, often 1–3 days depending on host and strain.

Disease in humans

Human disease typically causes acute vomiting, watery diarrhea, fever, and abdominal pain, with dehydration the major complication, especially in infants and young children.

Disease in animals—by species

Calves: neonatal watery diarrhea and dehydration, often as part of multifactorial calf diarrhea. Piglets: diarrhea, poor growth and dehydration, with severity influenced by age and maternal immunity. Foals, puppies, kittens and other young animals may develop enteritis, although clinical importance varies by species and strain.

Pathology

Rotavirus infects mature villous enterocytes of the small intestine, causing villous atrophy, malabsorption, enzyme loss, and secretory diarrhea. Lesions are usually most important in young animals.

Human diagnosis

Human diagnosis is usually clinical in uncomplicated cases. Stool antigen or molecular assays may be used in hospitalized patients, outbreaks, or surveillance. Genotyping is mainly epidemiologic and can identify unusual human-animal reassortants.

Animal diagnosis

Animal diagnosis is based on age, herd/flock history, clinical pattern, and fecal testing interpreted with other enteric pathogens. Detection alone may not prove causation in mixed infections.

Differential diagnoses

Human differentials include norovirus, adenovirus, astrovirus, bacterial enteritis and other causes of acute gastroenteritis. Veterinary differentials depend on species and include coronavirus, enterotoxigenic bacteria, Cryptosporidium, coccidia and nutritional diarrhea.

Treatment in humans

Treatment is primarily oral or intravenous rehydration and electrolyte replacement according to severity. Antibiotics do not treat rotavirus. Severe dehydration requires prompt medical care.

Treatment in animals—by species

Animal treatment is supportive, emphasizing fluids, electrolytes, warmth, nutrition and correction of acid-base abnormalities. Concurrent bacterial or protozoal disease is treated only when specifically diagnosed or strongly suspected.

Animal and environmental control

Control in animal facilities relies on maternity hygiene, colostrum management, age-group separation, cleaning/disinfection appropriate for a non-enveloped virus, reduction of fecal contamination, and species-specific vaccination programs where available.

Prevention in humans

Hand hygiene, safe diapering and sanitation reduce spread, but vaccination is the most effective prevention of severe childhood rotavirus disease. People handling diarrheic young animals should use routine fecal-oral precautions.

Human vaccination

Live oral rotavirus vaccines are recommended routinely for infants in the United States according to the childhood immunization schedule. They substantially reduce severe rotavirus gastroenteritis and hospitalization.

Animal vaccination

Vaccines are available for some livestock species, commonly administered to pregnant dams to increase colostral antibody for neonates. Products and schedules vary by species and country. No universal companion-animal rotavirus vaccine is recommended.

Prognosis

Most human and animal infections are self-limited when dehydration is prevented or corrected. Severe dehydration can be life-threatening in infants and neonatal animals.

Reporting, legal, and regulatory considerations

Individual human rotavirus cases are not nationally notifiable in the United States, although outbreaks may be reportable under state/local rules. Animal reporting is generally not required for routine rotavirus enteritis.

Selected current sources

CDC Manual for the Surveillance of Vaccine-Preventable Diseases, Chapter 13: Rotavirus; CDC childhood rotavirus vaccination guidance; current veterinary references on neonatal rotaviral enteritis.