Introduction
The purpose of this document is to inform employees of the health risks associated with laboratory animals and to describe means of disease prevention. Zoonotic diseases are infections of animals which, under certain circumstances, are communicable to humans. The infection in animals may produce a recognizable disease, such as rabies, or it may produce little, if any, signs of illness. In the latter case, the animal may be asymptomatic if it has developed resistance to the infectious agent, but if transmitted to a human with no specific immunity against the agent, illness could result.

Overall, the risk of ever contracting an illness from a laboratory animal is very low. Personnel in Occupational Health Facility, Environmental Health and Safety, Department of Laboratory Animal Medicine (DLAM), and others have implemented numerous programs to protect employee health. However, the primary responsibility for maintaining good health lies with each individual. Personnel should always follow company safety guidelines and exercise common sense. Examples include always maintaining a high level of cleanliness when working around animals and hand washing frequently. Wearing safety glasses and latex exam gloves protect employees in many ways. Using caution when working with needles and disposing of the needles attached to syringes, without recapping, directly into sharps containers are very important. Personnel must always wear the required protective clothing appropriate for the animal species. Reporting injuries such as bites and scratches to Occupational Health Services is mandatory. Consistently following just these precautions will protect employees from most health hazards.

Twenty­-one naturally occurring zoonotic diseases are described. It is beyond the scope of this document to be all inclusive. Not included in this document are zoonotic diseases which pose virtually no risk to employees in a controlled research environment. Many infectious agents are excluded due to practices such as purchasing only the highest quality animals, conducting quarantine programs when appropriate and maintaining the facilities at a high level of sanitation.

The intent of DLAM training programs on this subject is to increase employees' awareness on the importance of exercising necessary precautions when working with animals. Employees who have contact with primates or their tissues or body fluids are required to attend a separate orientation. It is also important to remember that if you become ill, tell your physician what type of exposures you may have had, in the event the illness is related to animal contact.

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Diseases which Affect Multiple Animal Species

Rabies 

  • Etiology: A rhabdovirus. 
  • Hosts: All warm ­blooded vertebrates are potentially susceptible; however, primates, opossums, rodents and rabbits are more resistant than dogs and cats. 
  • Disease in Animals: The incubation period is variable. Behavioral changes and/or unexplained paralysis are the most commonly reported signs. Behavioral changes may include shyness in normally friendly animals, anxiousness, excitability, sudden mood changes, pica, and/or aggressiveness. Paralysis progresses to eventual death. 
  • Mode of Transmission: Direct contact, usually from a bite. Ingestion or mucosal contact with the virus may result in infection. 
  • Disease in Humans: The incubation period can range from nine days to several years. Symptoms may include anxiety, irritation at the site of virus entry, hyperesthesia, hyperactivity, hydrophobia, acrophobia, increased salivation, laryngopharyngeal muscular spasms, convulsions, coma and death. 
  • Risk: Essentially no risk since all common laboratory animals are purpose-bred for research except primates. Primates may be purpose-bred or wild-caught, however, they are commonly considered resistant to rabies because reports of the disease in the common laboratory species are rare. Ferrets are raised in outdoor raised wire-mesh cages, and thus are very unlikely to come in contact with a rabid animal. 
  • Prevention: Avoid bites and other means of inoculation. If an animal-­related injury occurs, disinfect wound thoroughly and report to Occupational Health Services. LAR will be notified and the animal will be quarantined under observation. If the animal is euthanatized, the head may be sent to the County Health Laboratory for rabies testing. If other wild animals are used, additional special precautions may be implemented. Dogs are routinely vaccinated with approved rabies vaccines. 
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, p 621. Schwabe CW. Veterinary Medicine and Human Health, 3rd edition. Williams and Wilkins, Baltimore, 1984, pp 352-362. 

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Campylobacteriosis (Vibriosis)

  • Etiology: Campylobacter jejuni is the most common species. C. fetus ss fetus and C. fetus ss intestinalis are also implicated.
  • Hosts: Most animal species, i.e., primates, dogs, cats, swine, and other common domestic species.
  • Disease in Animals: Many animals are considered to be asymptomatic carriers or shedders. Stress from overcrowding or poor sanitation may increase signs of illness. Signs may include acute to chronic diarrhea which may be watery, bloody, or mucoid. Anorexia, fever, and vomiting may or may not occur. The disease is frequently self-limiting. 
  • Mode of Transmission: Fecal-oral transmission is possible though considered uncommon. People may also be infected by ingesting contaminated water or dairy or poultry products. 
  • Disease in Humans: The incubation period is 2 to 10 days. Susceptible individuals generally experience vague abdominal cramps followed by acute diarrhea for 3 to 5 days, usually with a fever. People often recover without treatment but antibiotics will decrease the amount of bacterial shedding.
  • Risk: Larger species (dogs, monkeys, swine, etc.) may carry Campy/obacterbutroutine rectal cultures seldom detect shedding. Risk is considered to be very low. 
  • Prevention: Higher risk animal species are routinely cultured for Campy/obacter. Wild caught primates may have a higher incidence than purpose­-bred animals since sanitary conditions at the breeder's fatalities are usually very good. Good personal hygiene should prevent transmission to employees. When entering a primate room, protective clothing must be worn which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots. Symptomatic animals are diagnosed by rectal culture and treated to decrease or eliminate shedding. 
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, p 621. Schwabe CW. Veterinary Medicine and Human Health, 3rd edition. Williams and Wilkins, Baltimore, 1984, pp 352-362. 

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Salmonellosis

  • Etiology: Salmonella typhimurium and S. enteritidus over 1600 serotypes are recognized.
  • Hosts: Highest incidence in birds and reptiles (as high as 94%), also primates (20% innewly imported rhesus and cynomolqus), dogs (10% in the general canine population) and rodents.
  • Disease in Animals: Animals and humans may both act as asymptomatic carriers, shedding the bacteria periodically. Due to improved sanitation at vendors' facilities in more recent years, the incidence of the disease has decreased dramatically. When clinically, mild to marked gastroenteritis is observed which may become systemic with complications such as endocarditis or meningitis. Generally, the infection when limited to the gastrointestinal tract is localized in the ileum.
  • Risk: Larger species (dogs, monkeys, swine, etc.) may carry Campy/obacterbutroutine rectal cultures seldom detect shedding. Risk is considered to be very low. 
  • Prevention: Higher risk animal species are routinely cultured for Campy/obacter. Wild caught primates may have a higher incidence than purpose­bred animals since sanitary conditions at the breeder's fatalities are usually very good. Good personal hygiene should prevent transmission to employees. When entering a primate room, protective clothing must be worn which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots. Symptomatic animals are diagnosed by rectal culture and treated to decrease or eliminate shedding. 
  • Additional References: Willard MD, et al. Gastrointestinal zoonoses. Small Animal Practice, 1987, 17:152-155. Schwabe CW. Veterinary Medicine and Human Health, 3rd edition. Williams and Wilkins, Baltimore, 1984, p 615. Fox JG. Campylobacteriosis - a "new" disease in laboratory animals. Laboratory Animal Science, 1982, 32:615-637.

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Dermatophytoses (Ringworm, Dermatomycoses)

  • Etiology: Fungi (dermatophytes) principally in the genus Microsporum or Trichophyton. The most common species are M. cants, M. gypseum and T. mentagrophytes. M. gypseum inhabits the soil (geophilic), while the others are parasitic on animals (zoophilic) and humans.
  • Hosts: All common laboratory animal and domestic species.
  • Disease in Animals: Lesions on animals are variable depending on the specific pathogen, animal species and other factors affecting host resistance. Ringworm infection in rodents is often asymptomatic. In other species, clinical signs include dermal erythema, alopecia, and crusty circular lesions. 
  • Mode of Transmission: Transmission occurs both by direct or indirect contact with asymptomatic carriers, skin lesions of infected animals, contaminated bedding and equipment, or fungi present on dust which settles in animal rooms. 
  • Disease in Humans: Infection in humans is often mild and self-­limiting. Lesions may include dermalscaling, erythema, vesicles, and fissures. Other demmatophytes may produce eczema, folliculitis, circular lesions, tines capitis (infection of the scalp and hair), tines corporis (generalized body infection), tinea pedis (infection of the foot), and tinea unguim (infection of the nails). 
  • Risk: Ringworm is seldom reported and since these fungi are commonly found in the environment, the source of a human infection would be difficult to determine. Clinical manifestations of ringworm in animals are rarely observed. It is possible that some animals, such as dogs or primates, may be asymptomatic carriers. Rodents obtained from approved vendors should be free of pathogenic dermatophytes. 
  • Prevention: The use of Iatex examination gloves would prevent direct transmission when handling animals. The high level of sanitation maintained in the animal facilities further reduces the risk to employees 
  • Additional References: Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 631-633. Ripon JW. Medical Mycology, 2nd edition. W.B. Saunders, Philadelphia, 1982, pp 154-248.

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 Giardiasis

  • Etiology: Giardia spp., an enteric protozoa.
  • Hosts: Giardia is pan of the normal intestinal flora of most domestic and laboratory animal species. Many of these species of Giardia may not be pathogenic to humans.
  • Disease in Animals: Giardia are typically non­pathogenic to their hosts. Increased numbers of Giardia can be found in the feces of animals with diarrhea but it is uncertain whether they are a primary cause of disease or rather a secondary response of little clinical significance. Dogs may show signs of diarrhea, steatorrhea, and weight loss. 
  • Mode of Transmission: Infective cysts are passed in the feces of the affected host. Typically, people become infected after drinking contaminated water either during a camping trip or from a municipal water source that was contaminated with human Giardia. People may also become exposed if infected fecal material has contaminated skin or clothing and the infective material was subsequently ingested. 
  • Disease in Humans: Signs of giardiasis in humans include diarrhea, steatorrhea, malaise, anorexia and weight loss. 
  • Risk: Various species including dogs and primates may carry Giardia in their intestinal tracts but it is uncertain if they are pathogenic to humans. Reports of giardiasis are uncommon. 
  • Prevention: Good sanitary hygiene and wearing disposable latex examination gloves would prevent transmission. Maintaining a high level of sanitation in the animal facilities further reduces risk. Large animals are screened during the quarantine process by fecal examination and treated if positive. 
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 313, 6635-6636. Fraser CM, ed. The Merck Veterinary Manual, 6th edition. Merck and Co., Inc., Rahway, 1986, p 142. 

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Arthropod Infestations 

  • Etiology: Mites, ticks and fleas of numerous species.
  • Hosts: All animals have a potential for infestation of arthropods. Animals which arrive directly from their natural habitat would have a higher incidence.
  • Disease in Animals: Localized dermatitis of varying intensity is generally the most common clinical sign of arthropod infestations. The greater significance is the potential to serve as vectors for other systemic pathogens. Diseases which can be transferred include encephalitis (Western, Eastern and St. Louis), rickettsial pox, tularemia, psittacosis, Rocky Mountain Spotted Fever, plague, Q fever, Lyme Disease, etc. 
  • Mode of Transmission: Arthropods can be transmitted by direct or indirect methods. Viral bacterial and rickettsial pathogens are transmitted to humans typically by the bite of the arthropod.
  • Disease in Humans: Direct effects to humans are usually related to the irritation caused by the specific arthropod on the skin. The effects of the viral, bacterial, and rickettsial pathogens vary with the disease.
  • Risk: The incidence of arthropod infestations on laboratory animals is extremely low because of the high standards implemented by the breeders. Animals that are wild-caught, such as primates, undergo rigid conditioning programs which eliminate arthropods.
  • Prevention: Ensure that the arthropods do not infest the animal colonies by monitoring during quarantine and through the routine health surveillance programs. In addition, many arthropod species have a free-living phase in their life cycle which they are unable to complete due to the strict sanitary conditions in the animal facilities.
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 626-640.

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Tularemia 

  • Etiology: Francisella tularensis (small pleomorphic, gram negative coccobacillus)
  • Hosts: Francisella tularensis is capable of infecting domestic and wild mammals, birds, androdents such as squirrels, voles, and muskrats.
  • Disease in Animals: The clinical signs of this disease in animals are nonspecific. In advanced stages, animals exhibit lethargy, fever, anorexia, and listlessness. Terminally, clinical signs of septicemia (moribund, severe dehydration, petechia, or ecchymoses) are often present.
  • Mode of Transmission: Transmission to humans occurs most often through insect bites (ticks, flies, or other blood-feeding arthropods) or via contact with contaminated animal products. Additionally, aerosol droplets, contact with contaminated water or mud, and animal bites have been implicated in transmission of this disease. Although the organism has been reported to penetrate intact human skin, recent research has suggested that the organism penetrates only through cuts or abrasions.
  • Disease in Humans: Virulent forms of tularemia start abruptly after an average incubation period of 3 to 5 days. The onset may be accompanied by fever, chitis, headache, malaise, anorexia, and fatigue. More severe symptoms may include cough, muscle ache, abdominal pain, or diarrhea. Less virulent strains cause a milder, self-limiting form of the disease, and occur in up to 50% of infected patients. The most recognized form of this disease, called the ulceroglandular form, is characterized by ulcerative, punched-­out skin lesions at the point of a tick or other insect bite and swollen Iymph nodes. This condition is rarely fatal and responds well to antibiotic treatment.
  • Risk: The risk of contracting tularemia from purpose-­bred animals is considered low. Although some feral nonhuman primates are housed here, husbandry practices and vermin control procedures virtually eliminate exposure to tularemia vectors.
  • Prevention: Follow appropriate safety procedures for handling each animal species. Always wear gloves and wash hands after handling animals. Report sick or diseased animals to a staff veterinarian.
  • Additional References: Rohrbach BW. Tularemia. Journal of the American Veterinary Medical Association, Aug 15, 1988, 193:4. Steel JH, ed. CRC Handbook Series in Zoonoses, Section A, Volume II. CRC Press, Bola Raton, Florida, 1980, pp 161-193. Mandell GL, ed. Infectious Diseases, Volume 2. Churchill Livingstone, Inc., 1995, pp 2060-2068.

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Diseases which Primarily Affect Non-Human Primates

Herpes B Infection (B­Virus or Cercopithecine herpesvirus 1 Infection)

  • Etiology: Herpesvirus simiae.
  • Hosts: Macaca mulatta (rhesus) and Macaca fascicularis (cynomolqus).
  • Disease in Animals: The only signs which may be seen are formation of vesicles or ulcers on the lips, gingiva, hard palate and/or tongue. These lesions persist for 10 to 14 days. It is thought that the virus becomes latent thus infecting the animal for life. At various times, particularly in stressful situations, the virus may become reactivated and shedding may occur in saliva and other secretions. Shedding may occur in the absence of clinical signs.
  • Mode of Transmission: Exposure to contaminated monkey saliva through bites and scratches is the most common means of transmission. Monkey tissues, body fluids and contaminated primate kidney cell cultures are all possible sources of infection.
  • Disease in Humans: Herpes B causes an ascending encephalomyelitis which is usually fatal. Fewer than 30 documented cases have been described. Initial symptoms include minor vesicular lesions and numbness at the site of inoculation, flu-like symptoms, ataxia, nausea, convulsions, coma and death.
  • Risk: The majority of wild-caught macaques are probably latent carriers. Risk of infection is very low if proper precautions are followed.
  • Prevention: Most importantly, avoid primate bites, scratches, needle sticks and other injuries that may constitute an exposure. Protective clothing must be worn which includes a disposable respirator, eye protection, disposable coveralls, latex exam gloves and boots. Leather gloves and other restraint devices are required if handling conscious animals is necessary. If an injury occurs, specific first­ aid procedures must be implemented immediately after the injury occurs. Directions and supplies can be obtained from Monkey Bite/Scratch First Aid Kits. Immediately after completing the first ­aid procedures, employees must report to Occupational Health Services or, if after hours, to UCLA Ronald Reagan Medical Center Emergency Medicine Center for further medical treatment. Additional training is required for all personnel working with primates, or with their tissues and body fluids.
  • Additional References: Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 317, 619-620.

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Measles (Giant Cell Pneumonia, Rubeola)

  • Etiology: Etiology: Measles virus, a paramyxovirus.
  • Hosts: Humans are the primary reservoir; New World and Old World monkeys become secondarily infected.
  • Disease in Animals: Large outbreaks can occur in susceptible colonies of New World and Old World monkeys. Higher mortality rates are observed in New World monkeys. Animals exhibit an exanthematous rash, a mild conjunctivitis and occasionally gingival ulceration and diarrhea. The illness can progress to giant cell pneumonia and death. Immune system dysfunction is thought to occur during the course of the disease.
  • Mode of Transmission: Measles is one of the most readily transmitted of all infectious diseases. The measles virus can be potentially transmitted from monkeys to man and from man to monkeys. It is shed beginning in the prodromal stage and extends through the exanthematous phase. Viral excretion occurs from the mucous membranes of the eye and pharynx and later from the respiratory and urinary tracts.
  • Disease in Humans: After a 1- to 2-week incubation period in a susceptible person, the illness begins with prodromal fever, coryza, cough and conjunctivitis. Bluish­-white Koplik's spots appear 2 to 4 days later, usually on the buccal mucosa. The skin rash appears 1 to 2 days after the Koplik's spots appear. Pneumonia (especially in the young), otitis media and other secondary bacterial infections are relatively common complications. Mortality rate is low.
  • Risk: In recent years there have been no confirmed cases of measles in monkeys at our institution. Since the majority, if not all employees, have antibody titers through natural exposure or from childhood vaccination, the risk is very low.
  • Prevention: People who have had measles are immune for life. Other employees who may be at risk should consult with a physician. In general, if the employee's immune status is unknown, an antibody titer should be determined if a potential for risk exists. If a protective titer is not demonstrated, vaccination can be provided. Pregnant women should not be vaccinated. Protective clothing must be worn when entering primate rooms which includes a disposable respirator, eye protection, disposable coveralls, latex gloves and boots.
  • Additional References: Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 317, 350, 618-619.
    Berkow R, ed. The Merck Manual, 15th edition. Merck and Co., Inc., Rahway, 1987, pp 2022-2028.

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Hepatitis A (Infectious Hepatitis, Simian Hepatitis)

  • Etiology: Etiology: Hepatitis A virus, a picorna virus.
  • Hosts: Man is the principle reservoir; primates, especially chimpanzees, are secondary reservoirs.
  • Disease in Animals: Usually unapparent. The incubation period is 2 to 6 weeks. In the acute phase of infection, serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) will rise significantly for 2 to 3 weeks and then return to normal. Serum IgM will remain detectable for approximately the same period.
  • Mode of Transmission: Food or water vehicles or fecal­oral contact only during the acute phase of infection. 
  • Disease in Humans: Unapparent as in primates, or people may experience an acute onset of fever, nausea and anorexia. This is in contrast to Hepatitis B (serum hepatitis) which has an insidious onset but is more severe.
  • Risk: Feral primates probably contract the virus when exposed to man. The majority of wild-caught primates have titers to Hepatitis A when first brought into quarantine and are no longer infectious. A few previously seronegative animals may seroconvert and are infectious for several weeks. Standard sanitary precautions will prevent transmission so risk to employees is very low.
  • Prevention: General, sanitary precautions will prevent infection. When entering a primate room, protective clothing must be worn which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots.
  • Additional References: Burke DS, Heisey GB. Wild malaysian cynomolgus monkeys are exposed to Hepatitis A. American Journal of Tropical Medicine and Hygiene, 1984,33(5) :940-944. Eichberg JW, Kalter SS. Hepatitis A and B: serologic survey of human and nonhuman primate sera. Laboratory Animal Sciences, 1980, 30(3):541-543.

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Tuberculosis (TB)

  • Etiology: Mycobacterium bovis, M. avian, M. tuberculosis, acid-fast bacilli.
  • Hosts: The major reservoir hosts are cattle, birds and humans, respectively. Other domestic species and monkeys are also susceptible.
  • Disease in Animals: Old World monkeys are the most common species likely to be infected in a research animal facility. Wild-caught monkeys contract the disease typically from humans in the country of origin. Three to 4 weeks after exposure, monkeys will start to shed the organisms, primarily by aerosolized droplets from coughing. Ingestion and fomite transmission may also occur. The course of the disease from exposure to death may last 1 year, but could be shorter depending on various factors such as host resistance. Initially, animals are asymptomatic. Clinical signs include coughing, dyspnea, anorexia, depression, weight loss and chronic diarrhea. Death results from pleuropneumonia or the disseminated miliary form.
  • Mode of Transmission: In a research setting, inhalation is the major portal of entry for humans.
  • Disease in Humans: Similar to clinical signs seen in monkeys. People may remain asymptomatic for months to years. Clinically, the disease may manifest itself by cough, sputum production, hemoptysis, anorexia, weight loss, malaise, fatigue, fever, chills and cachexia. The disseminated miliary form may affect any organ, including bones.
  • Risk: Only purpose-­bred or preconditioned monkeys are purchased. Multiple TB tests and other health assessment procedures are included in the conditioning programs. Risk for employees working with the general monkey population is low. Risk for those working in the monkey quarantine area may be slightly higher until tuberculin testing is complete. Quarantine monkeys are tuberculin tested at least three times at 2­week intervals before release. Monkeys in the colonies are tested quarterly and employees are tested annually to ensure that the animal colonies remain TB­free.
  • Prevention: Employees with a potential for occupational exposure are TB­ tested annually. When entering a primate room, protective clothing must be worn, which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots. 
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 310-313, 627-628. Hubbert WT, McCulloch WF, et al., eds. Diseases Transmitted from Animals to Man. Charles Thomas, Springfield, 1 97S, pp 303-360.

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 Shigellosis

  • Etiology: Shigella flexneri, S. sonnet and S. dysenteriae, a gram negative, non-spore forming bacilli.
  • Hosts: Humans are the primary reservoir; primates acquire the disease after capture in the wild.
  • Disease in Animals: Shigellosis is one of the most common enteric pathogens of primates. Animals may be asymptomatic carriers or they may exhibit a wide range of clinical signs. Intermittent diarrhea with mucous and/or blood may be observed. The more severe form may be present as acute dysentery which may be life-­threatening if fluid and electrolyte imbalances are not corrected. When localized, the bacteria are commonly found in the colon.
  • Mode of Transmission: Contact with infected animals or contaminated feces. People may become exposed if infected fecal material has contaminated skin or clothing and the infective material was subsequently ingested.
  • Disease in Humans: As in primates, the disease can vary from asymptomatic to acute dysentery. In the most severe form, the signs include diarrhea with blood and mucous, abdominal cramping, tenesmus, weight loss and anorexia. Mortalities have been reported, especially in children, if prompt medical attention is not provided.
  • Risk: Risk is considered low since all primates are screened for Shigella and other enteric pathogens during quarantine. Typically, the organisms are not found.
  • Prevention: Good sanitary hygiene will prevent transmission. Continual health surveillance will ensure that the primate colonies will not be contaminated. When entering a primate room, protective clothing must be worn which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots.
  • Additional References: Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 30-310, 629-630.

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Amebiasis 

  • Etiology: Entamaeba histolytica, a protozoan parasite. 
  • Hosts: Primates.
  • Disease in Animals: E histolytica is a common intestinal inhabitant of primates which seldom causes any illness. If the animal is stressed, or if the normal intestinal flora is disrupted, the organism may produce an enteritis.
  • Mode of Transmission: People may become exposed if infected fecal material contaminated skin or clothing and the infective cyst forms were subsequently ingested.
  • Disease in Humans: Humans will not typically become ill when infected. Under certain circumstances, the parasites may infect the large bowel wall causing an amebic colitis. Signs may include mild watery diarrhea to acute fulminating bloody or mucoid dysentery with fever and chills. If not cured, the disease could persist with periods of exacerbation for months. Rare complications may include amebic abscesses in various organs.
  • Risk: Primates should generally be considered as asymptomatic carriers and a potential source of infection. Animals with clinical signs are treated to decrease shedding.
  • Prevention: Good sanitary hygiene will prevent transmission from animals to humans. When entering a primate room, protective clothing must be worn which includes latex gloves, a disposable respirator, eye protection, disposable coveralls and boots.
  • Additional References: Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 313, 634. Berkow R. ed. The Merck Manual, 15th edition. Merck and Co., Inc., Radway, 1987, pp 197-204. 

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Diseases which Primarily Affect Sheep, Goats & Pigs  

Contagious Ecthyma (ORF, Contagious Pustular Dermatitis)

  • Etiology: Contagious Ecthyma virus, a parapox virus.
  • Hosts: Sheep, goats
  • Disease in Animals: Papular, becoming pustular lesions on lips, mouth, nostrils, ears, teats and udder.
  • Mode of Transmission: Direct contact with lesions.
  • Disease in Humans: Dermal papules progressing to pustules, generally on hand or fingers. Slow recovery in 1 to 2 months.
  • Risk: Minimal if precautions are followed.
  • Prevention: Lambs and kids are vaccinated, if a vaccine is available. Wear latex gloves when handling affected animals. 
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 622-623. Schwabe CW. Veterinary Medicine and Human Health, 3rd edition. Williams and Wilkins, Baltimore, 1984, p 615. 

 Q Fever

  • Etiology: Coxiella burnetti, a rickettsia.
  • Hosts: Cattle, sheep, goats and certain wild mammals.
  • Disease in Animals: Abortion in the absence of other clinical signs.
  • Mode of Transmission: The organism is spread in urine, feces, milk and especially birth products such as the placenta. The organism can survive for months in the environment. Transmission generally occurs via inhalation of infective aerosols. Ticks may also act as vectors.
  • Disease in Humans: The incubation period is 2 to 4 weeks. Symptoms include fever, chills, profuse sweating, malaise, anorexia, myalgia, nausea and vomiting. Subacute endocarditis is particularly a concern in patients with pre-existing valvular disease. Other infections may also occur such as encephalitis, hepatitis and pneumonia. Most cases resolve in two weeks but protracted recoveries may occur, especially in the elderly.
  • Prevention: If pregnant or post­-parturient sheep are housed indoors, no room air should be recirculated. To enter a post­parturient sheep room, disposable masks, coveralls, gloves and shoe covers must be worn. Employees with valvular or congenital heart defects are evaluated for risk prior to potential exposure to tissues or body fluids produced during parturition of sheep, cattle or goats. Antibody titers against C. burnetti are determined before working with susceptible species. If titers are not considered protective, immunization is provided. Routine titers should be taken periodically.
  • Additional References: Bernard KW, et al. Q Fever control measures: recommendations for research facilities using sheep. Infection Control, 1982, 3(6):461-465. Fox JO, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 622-623. Grant CG, et al. Q Fever and experimental sheep. Infection Control, 1985, 6(3):122-123.

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Erysipelas (Diamond Skin Disease in Swine, Erysipeloid in Humans)

  • Etiology: Erysipelothrix rhusiopathiae (E. insidiosa) a gram positive, non-acid fast, facultative aerobe.
  • Hosts: Primarily swine, but also sheep, fish and man, rarely in cattle, fowl and rodents.
  • Disease in Animals: In swine, three basic forms of the disease exist: acute septicemia form, the skin form and the chronic arthritic form. The different forms represent progressive stages of the disease. Swine may die during the acute septicemic stage. Skin lesions typically form a diamond shaped configuration. Recovered animals may shed the bacteria in their feces for a prolonged time.
  • Mode of Transmission: Man is infected through contamination of wounds and abrasions. Rodents may serve as reservoirs. Insect vectors and ticks may transmit the bacteria mechanically.
  • Disease in Humans: Erysipeloid usually begins as a localized wound infection but may progress to a generalized septicemia. First signs appear after a 2- to 7-day incubation period. Skin lesions, arthritis and endocarditis may also develop. 
  • Risk: Very low to none. Swine are only purchased from Erysipelas-free vendors.
  • Prevention: In addition to using only Erysipelas-free swine, good hygiene will prevent infections. These practices include: wearing latex gloves, frequent hand washing with a disinfectant soap and prompt medical treatment of cuts and abrasions.
  • Additional References: Steele JA, ed. CRC Handbook in Zoonoses. CRC Press, Boca Raton, 1979, Sec. A, Vol. I. Fraser CM, ed. The Merck Veterinary Manual, 6th edition. Merck and Co., Inc., Rahway, 1986, pp 372­374.

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Diseases which Primarily Affect Dogs & Cats 

Cat & Dog Bites

  • Etiology: Pasteurella multocida is reported to be the most common cause of infection following a cat or dog bite. It is a non-spore forming, gram-negative coccobacillus.
  • Hosts: P. multocida is part of the normal mouth flora of dogs (66% incidence), cats (70% incidence) and other domestic species.
  • Disease in Animals: None in dogs or cats. In rabbits, clinical signs include rhinitis (snuffles), pneumonia, otitis media and interna, conjunctivitis, abscesses. Vulvovacinitis pyometra, balanoposthitis, orchitis and septicemia.
  • Mode of Transmission: Bites or scratches from carrier animals.
  • Disease in Humans: Signs develop at the wound site, usually a hand or finger. Incubation is 12 to 72 hours. Signs include local cellulitis, pain, swelling, serosanguineous or purulent drainage and Iymphangitis in the affected limb. Complications may include septicemia, meningoencephalitis, osteomyelitis and purulent tenosynovitis.
  • Risk: Since P. multocida may be part of the normal mouth flora of dogs and cats, infection may occur following a bite or scratch. Rabbits used at our institution are pasteurella-free.
  • Prevention: Avoid bites and scratches. If a bite or scratch occurs, prompt first aid treatment is necessary followed by medical treatment at Occupational Health Services or at an emergency room. First aid treatment should include cleansing with an antibacterial detergent and irrigation with large amounts of water.
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 217-218, 640. Arons MS, et al. Pasteurella multocida - The major cause of hand bites following domestic animal bites. The Journal of Hand Surgery, 1982, 7(1):47-51. 

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Toxoplasmosis

  • Etiology: Toxoplasma gondii an obligate intestinal coccidium.
  • Hosts: Cats are the primary reservoir; a wide range of other species, including humans, are intermediate hosts. The infective oocyst is only produced and shed by cats.
  • Disease in Animals: Most infected cats are asymptomatic. Severely infected cats may exhibit signs which include fever, dyspnea, coughing, Iymphadenopathy, myalgia, vomiting, diarrhea, splenomegaly, neurologic signs and retinochoroiditis.
  • Mode of Transmission: People are infected by ingestion of sporulated oocysts from cats. Sporulation of oocysts occurs one to five days after shedding in the feces. Outside of the research setting, transmission may occur by ingestion of infected, partially cooked meat (particularly lamb and pork), ingestion of sporulated oocysts from a pet's litter pan, or from soil, or by the congenital transplacental route.  
  • Disease in Humans: In adult, immunocompetent people, most infections are subclinical. Occasionally, a transient fever and Iymphadenopathy may be observed. Immunocompromised persons suffer from a more severe form of the disease, which includes encephalitis. Women who contract the disease during pregnancy may transmit the parasite to the fetus. Congenital infections may manifest in one of several different ways. A small percentage of babies may develop brain and ocular lesions, and some may die.
  • Risk: The risk is extremely low, even for those who work with cats. Generally, only Toxoplasma-free cats are purchased. Oocyst shedding in exposed cats usually only occurs once in a lifetime, and the period of shedding only lasts 10 to 15 days. Since cages are cleaned once or twice a day, the feces are disposed of before sporulation of the oocysts can occur.
  • Prevention: Good sanitary hygiene will prevent transmission. Personnel should wear gloves when handling feces. Pregnant women should completely avoid contact with cat feces.
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 633-634.
    August JR, Chase TM. Toxoplasmosis. Small Animal Practice, 1987, 17:55-71.

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Diseases which Primarily Affect Rodents 

Lymphocytic Choriomeningitis (LCM)

  • Etiology: LCM virus, an arena virus.
  • Hosts: Rodents, primarily mice and hamsters.
  • Disease in Animals: Clinical signs of LCMV infection vary depending on the strain of the mouse and virus, age at inoculation and route of inoculation. The cerebral form — induced in adult mice by intracerebral inoculation, may lead to neurological signs and death.
    • The visceral form — induced in adult mice by peripheral routes of inoculation, variable signs may be produced.
    • Late onset disease — found in persistently infected mice when they reach 9 to 12 months of age. 
    • Runting and death — found in neonatally infected mice.
  • Mode of Transmission: LCMV can contaminate cells lines derived from infected animals. Human infection can occur by direct inoculation from infected cell lines, animals, feces, or urine. Indirect transmission may occur from inhalation of dried excrete carried on aerosolized dust from an animal room.
  • Disease in Humans: Most frequently it occurs as a mild flu-like syndrome, with or without central nervous system involvement. Under certain circumstances, LCMV infection can be fatal.
  • Risk: Almost none. Persons at greatest risk are those who may handle untested murine cell cultures.
  • Prevention: The LAR QC/Diagnostic Laboratory routinely monitors all susceptible animal rooms serologically for LCMV. The Laboratory also tests for the virus in the Vendor Monitoring Program. Since these programs started, LCMV has never been detected in any vendor area. All murine derived cell lines must be screened by the Mouse or Rat Antibody Production test prior to use.
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. Academic Press, Orlando, 1984, pp 59-62, 135-136, 598, 617-618, 659, 672. Bhatt N. Jacoby RD, Barthold SW. Contamination of transplantable murine tumors with Iymphocytic choriomeningitis virus. Laboratory Animal Science, 1986, 36:136-139. 

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Rat Bite Fever (Sodoku, Haverhill Fever)

  • Etiology: Etiology: Streplobacillus moniliformis or Spirillium minus.
  • Hosts: Rats and mice primarily, rarely other domestic species.
  • Disease in Animals: These organisms grow in the oral cavity and upper respiratory tracts of asymptomatic rodents. Rodent colonies at do not harbor these microorganisms.
  • Mode of Transmission: The usual source of infection is the bite of a carrier rodent.
  • Disease in Humans: Incubation period of S. moniliformis is a few hours to 3 days, and 1 to 6 weeks with S. minus. Inflammation at the injury site followed by regional Iymphadenopathy, fever, headaches, malaise, myalgia and chills are frequent signs. If not treated properly, complications may include arthritis, pneumonia, hepatitis, pyelonephritis, enteritis and endocarditis.
  • Prevention: Avoid bites. If a bite occurs, cleanse the wound immediately with an antibacterial detergent and seek medical attention. The Vendor Screening Program monitors animals for these microorganisms but has never detected them.
  • Additional References: Fox JG, Cohen BJ, Loew FM, eds. Laboratory Animal Medicine. AcademicPress, Orlando, 1984, pp 640-641. Berkow R. ed. The Merck Manual, 1Sth edition. Merck and Co., Inc., Rahway, 1987, p 136.

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Hantavirus

  • Etiology: Strains from the genus Hantavirus (Seoul, Hantasn, Puumala, Sin Nombre (SNV) Prospect Hill), family Bunyaviridae.
  • Hosts: Each member of the genus is associated with a specific rodent host. Seoul virus- Rattus norvegicus, the urban sewer rat, found worldwide. 
    • Hantaan virus — Apodemus agrarius, the striped field mouse, found in Asia.
    • Sin Nombre virus — Peromyscus maniculatus, the deer mouse, found throughout the United States. 
    • Prospect Hill virus — M'crotus pennsylvanicus, the meadow vole, found in the United States.
  • Disease in Animals: Hantaviruses do not cause apparent illness in their rodent hosts. The host does, however, remain persistently infected for life, and may shed virus for weeks in saliva, urine and feces.
  • Mode of Transmission: Inhalation of aerosols or dust containing saliva or excrete from infected rodents is the principal mode of disease transmission to humans. The bites of infected rodents may also transmit the disease, as virus is shed in saliva.
  • Disease in Humans: Different strains of Hantaviruses cause different clinical syndromes. The Hantaan, Puumala and Seoul strains cause hemorrhagic fevers of varying severity accompanied by renal insufficiency. The Sin Nombre virus, recently identified as a human pathogen in the Western United States, causes Hantavirus Pulmonary Syndrome (HPS), which is characterized by a febrile prodrome, followed by development of noncardiogenic pulmonary edema, hypotension or shock and respiratory failure.
  • Risk: Exposure to infected rodent excrete, necropsy materials and rodent bedding are presumed to be associated with risk of infection. procures animals which are vendor-tested negative for Hantaviruses, and performs in-house testing for colonies maintained on site. If researchers need to procure rodents from non-approved sources, the LAR QC/Diagnostic Laboratory will first screen the animals for human and murine pathogens. Only animals that meet LAR's health specifications can enter our facilities.
  • Prevention: LAR will continue procuring and maintaining Hantavirus-free rodent colonies. Changes in the disease status of our colony will be managed appropriately. Follow all applicable dress and rodent handling guidelines.
  • Additional References: Mandell GL, ed. Principles and Practice of Infectious Diseases, fourth edition. Churchill Livingstone, Inc., 1995, pp 1567-1572. Morbidity and Mortality Weekly Report, CDC 43:RR-7, May 13,1994. 

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