Campylobacteriosis
Etiology:
Campylobacter jejuni, C. fetus, C. laridis.
Significance:
Moderate to high.
Hosts:
Man and non-human primates, cattle, sheep, poultry,
dogs, kittens, swine, rodents. Campylobacter jejuni
is common in all species of nonhuman primates.
Transmission:
Ingestion of meat contaminated with intestinal contents,
contaminated water, contact with animals. Asymptomatic
shedding by primates is common.
Clinical
disease: Clinical signs of campylobacter infection
are variable in both animals and humans. They range
from asymptomatic infection to acute typhoid-like illness.
Recurrent symptoms are reported. Immunological phenomena
such as reactive arthritis are possible sequelae to
infection. Diagnosis is by fecal culture.
Treatment/control:
Supportive care (oral electrolytes) and antibiotics
(erythromycin). Mild cases may resolve without antibiotics.
Carrier states are common. Colony primates should be
tested regularly and isolated and treated if positive.
Precautions against exposure include protective clothing,
shoe and head covers, face masks and gloves whenever
in contact with nonhuman primates.
Dermatophytosis
(Ringworm)
Agent:
Dermatophytic fungi: Microsporum canis, Trichophyton
mentagrophytes
Significance:
Low
Host:
Most mammals
Transmission:
Direct contact with infected skin or hair
Clinical
disease: Itchy red papule that spreads with central
clearing resulting in a ring-like appearance.
Treatment/control:
Topical or systemic antifungal drugs.
Herpes
B Virus
Etiology: Herpesvirus simiae-a herpesviruse host
adapted to non-human primates
Significance:
High-infection in humans is nearly uniformly fatal
Host:
Herpes B virus is present in about 25% of rhesus and
cynomolgus monkeys; only 2-3% of these monkeys have
clinical signs at a given time. Herpes B virus does
not infect baboons, squirrel monkeys or owl monkeys.
In general,
herpes viruses are species adapted and do not cause
disease in their natural hosts but infection can be
fatal to other primate species.
For instance, Herpesvirus saimiri and Herpesvirus tamarinus
cause no clinical disease in squirrel monkeys but are
lethal in owl monkeys and marmosets. Human herpes viruses
are highly pathogenic for owl monkeys and marmosets.
Herpes viruses are common in other primate species but
are not hazardous to humans.
Animal care
workers should take care to avoid cross contamination
between these species by shared equipment. Animal care
and research personnel should not work with New World
species when they have active cold sore lesions.
Transmission:
Infection of man may occur after bites, scratches, needle
sticks, splashes to the eye or injuries caused by macaque
caging. Virus is shed from active herpetic lesions and
in any body fluids.
Clinical
disease: While herpes B virus infection of humans
is very rare, when it occurs the disease is often fatal.
The incubation period of the disease in man is between
2 weeks and 6 months. Pain, numbness and weakness of
the affected arm may occur, accompanied by generalized
malaise and flu-like symptoms. Coma and death result
from central nervous system infection. Infected animals
may have very minor illness, with conjunctivitis or
ulcers or white plaques on the lips, nares, tongue,
palate or genitalia.
Treatment/control:
Diagnosis of Herpes B infection in monkeys is complicated
because infected animals may not have detectable antibody
and shed virus only intermittently. Thus, all macaque
monkeys must be assumed to be potential carriers of
this virus. Safe handling procedures to avoid bites
and scratches are essential. All injuries to humans
caused by macaques or mucosal exposures to macaque body
fluids and injuries sustained by personnel from cage
equipment have potential to transmit Herpes B. Use of
appropriate protective clothing, especially a facemask,
cannot be overemphasized. In the event of an injury,
washing the wound [Link] for 15 minutes is the most
important first step. The injured employee must report
the injury to the supervisor, the attending veterinarian
and occupational health services so that appropriate
evaluation of both human and primate is begun. Once
a wound has been acutely managed, any unusual symptoms
that develop later must be promptly reported.
Lymphocytic Chorio-meningitis Virus
(LCMV)
Agent:
Arenavirus
Significance:
High. Infection of wild rodent populations is not uncommon.
Host:
Mice, hamsters, guinea pigs, human
Transmission:
Aerosolization of urine, contaminated dust or bedding,
fecal contamination
Clinical
disease: In humans, often a flu-like illness with
fever progressive to meningitis or encephalitis. LCMV
infection is asymptomatic in animal hosts.
Treatment/control:
Treatment of clinical disease is difficult. Control
involves routine screening of rodents, guinea pigs and
hamsters for seroconversion and culling of any seropositive
animals. Introduction of virus into animal colonies
through contaminated cell lines has occurred. Prescreening
of cell lines intended for introduction into colony
animals is essential.
Measles
Virus
Etiology:
Paramyxovirus
Significance: Moderate, since vaccination protection
is not complete in all people
Hosts:
Nonhuman primates (New World monkeys are more susceptible
to measles than are Old World monkeys), puppies, humans
Transmission:
Contact, aerosol of respiratory particles
Clinical
disease: The incubation period in monkeys is usually
5-15 days. Affected animals develop conjunctivitis,
lethargy, and a diffuse rash. Pneumonia, abortion, secondary
bacterial infection and death can occur.
Treatment/control:
Measles is rare in wild monkeys but unvaccinated monkeys
acquire the disease readily from other monkeys or from
infected people. Unvaccinated or improperly vaccinated
people may contract the disease from monkeys during
an outbreak. Improperly vaccinated people may introduce
the infection into a primate colony.
Orf
(Contagious Ecythma)
Agent:
Parapoxvirus
Significance:
Moderate
Host:
Sheep and goats, human
Transmission:
Direct skin contact with infected tissue, scabs, or
contaminated bedding or equipment
Clinical
disease: In sheep and goats, infection with parapoxvirus
causes proliferative papules or crusted vesicles on
the skin of the lips, nostrils, around the eyes or on
teats of nursing females. The infection is very contagious,
but causes little mortality, unless nursing is inhibited
in lambs or goat kids. In humans large nodules with
surrounding inflamed skin can occur. The lesions may
itch and disappear slowly after 4-6 weeks.
Treatment/control:
There is little treatment for lesions, but control
is through use of good hygiene practices when handling
ruminants. Whenever suspicious oral lesions are seen,
the use of protective clothing (esp. gloves) is essential
to prevent exposure. Procurement of small ruminants
from reputable dealers, rather than use of random source
or auctioned animals decreases chance of infection in
experimental animals.
Q
Fever
Etiology:
Coxiella burnetti, a rickettsia.
Significance:
Moderate to high-- the agent is widespread, and the
potential for chronic, debilitating disease exists.
Hosts:
Livestock, especially sheep and goats, birds, and humans.
Transmission:
The organism is shed in urine, feces and milk during
active infection. The organism is concentrated in amnionic
fluid, placenta, and fetal membranes. Thus experiments
involving ovine fetal surgery or allowing birth of lambs
have the greatest potential for exposure of investigators
and animal care personnel. The organism is spread by
aerosol from fetal membranes and fluids, or contaminated
bedding.
Clinical
Disease: Infection in animals is generally asymptomatic.
In humans, symptoms of fever, headache and chills develop
after a 14-28 day incubation period. Most patients develop
a self-limiting illness of only 2 weeks duration, but
some individuals develop liver disease or cardiac valve
endocarditis. Exposure of immunosuppressed individuals
or those having had a cardiac valve replacement is of
greatest concern. Diagnosis is by serology.
Treatment/control:
Control is best accomplished by the use of sheep from
Q-fever negative flocks. If this is not possible, testing
of individual females before use in peri-parturient
studies and rejection of any animals with positive serology
is advisable. Use of male sheep or goats decreases risk.
When peri-parturient animals, fetal membranes or newborn
lambs are handled, BL-2 precautions must be in place,
including protective clothing, shoe and head covers,
facemask and gloves. Peri-parturient animal must be
transported in filtered cages, and bedding collected
withing for 48 hours after birth should be decontaminated.
Immunocompromised
individuals, including those with a positive test for
the AIDS virus, or those with congenital cardiac disease
or valvular disease should not work with sheep or goats
at the time of parturition.
Rabies
Virus
Etiology:
Rhabdovirus
Significance:
Low in terms of incidence and potential exposure from
laboratory animals; high risk in dealing with wild populations
especially of bats. The consequences of infection are
very severe.
Hosts:
Most mammals. Common wild animal reservoirs include
skunks, raccoons, foxes, coyotes, and bats. Rodents
and rabbits are not known to be naturally infected.
Transmission:
Saliva (bite or scratch) from an infected animal, contact
with tissue from an infected animal, inhalation of aerosolized
virus
Clinical
disease: A latent period of weeks, months or years
can occur. Symptoms begin with fatigue, malaise or headache
and progress to severe central nervous system disease
with paralysis, coma and death. Numbness or tingling
at the bite or scratch site may be the initial sign.
Rabies is almost uniformly fatal once clinical disease
develops. It is important to note that the initial clinical
signs in animals are highly variable and nonspecific.
Any abnormal behavior in wild-caught unvaccinated animals
should arouse suspicion and extreme precautions.
Treatment/control:
Consider any wild-caught or random source mammals as
potentially infected and exercise extreme care in handling
these animals. Appropriate protective clothing and restraint
procedures must be used when handling them. All personnel
whose work places them in contact with such animals
should be vaccinated with human diploid cell vaccine.
All bites or scratches from potentially rabid animals
must be reported immediately to an animal care supervisor
and attending veterinarian so that appropriate diagnostic
evaluation can be arranged.
Shigellosis
Etiology:
Shigella flexneri, S. boydii, S. sonnei, S. dysenteriae
Significance:
Very high.
Hosts:
Humans and primates. Shigella flexneri is a common cause
of diarrhea in macaque monkeys. Humans may also be the
reservoir for monkey infections, but asymptomatic carriers
may maintain the infection in the colony between outbreaks.
Transmission: Fecal-oral. Shigella is very infectious
and as few as 500 bacteria will causes infection. Children
are more susceptible than adults.
Clinical
disease: Diarrhea with blood and mucous is the most
common clinical sign. Shigellosis may be fatal in monkeys
if untreated, but most animals respond rapidly to antibiotics
and parenteral fluids. The human disease is often mild
in adults, but may be very debilitating or fatal in
children. Monkeys also may harbor other bacteria that
cause debilitating diarrhea in people, and may shed
large numbers of bacteria in their feces without serious
illness. People may also shed these bacteria asymptomatically.
Diagnosis of all of these infections is by culture of
the feces.
Treatment/control:Multi-antibiotic
resistant strains are present throughout the world.
All nonhuman primates should have regular fecal cultures,
and any infected animals should be isolated and treated.
Appropriate protective clothing, shoe and head covers
and gloves when in contact with nonhuman primates are
of greatest importance in preventing exposure. Prevention
of fecal contact with any equipment that may subsequently
contact hands or mouth must be prevented.
Tuberculosis
Etiology:
Mycobacterium tuberculosis
Significance:
High
Hosts:
All non-human primates. Tuberculosis is rare in wild
monkeys but can readily be acquired from infected humans.
Transmission:
Aerosol of infectious particles from respiratory secretions
Clinical
disease: People may have asymptomatic infections
or may suffer severe respiratory disease and weight
loss. Routine tuberculin testing detects most human
cases in non-vaccinated populations. Chest radiographs
are required to make a positive diagnosis of disease
in BCG-vaccinated people.
Treatment/control:
Tuberculosis causes severe weight loss, lethargy and
coughing and is almost always fatal in monkeys, but
the disease can go unrecognized for months during which
time other animals may be infected. Strict quarantine
of new animals and regular testing of the entire colony
identifies asymptomatic monkeys. Old world primates
are tested quarterly and New world primates are tested
annually. All personnel who work with primates should
be tuberculin tested annually. Infected animals are
not treated, but are culled from the colony. Treament
of humans requires a prolonged course of systemic antibiotics.
All individuals
who work with monkeys, including visiting faculty and
students, must have annual skin tests showing that they
do not have tuberculosis. Individuals with positive
skin tests must have an alternate evaluation such as
a chest radiograph by a health professional within the
calendar year prior to working with primates.
Harvard Medical
School staff and students may obtain tuberculin skin
tests or radiographs at no charge from the University
Health Services. Individuals with other primary affiliations
should be tested at their home institution. Written
documentation of tuberculin skin test results must be
presented to the ARCM Associate Director for Operations
before requesting access to nonhuman primate facilities.
Immunodeficiency Viruses
Etiology:
Various retroviruses
Significance: Unknown
Hosts: Non-Human Primates, primarily old world
monkeys and apes; Humans
Transmission: Cell associated transmission; blood
borne.
Treatment: Anti-retroviral therapy
Infection
of monkeys with simian Immunodeficiency Virus (SIV)
causes an AIDS-like syndrome in macaques but only occurs
in experimental infectious disease laboratories. There
are no macaques infected with SIV at the Longwood campus.
SIV is not known to be pathogenic to people, but it
is closely related to human immunodeficiency virus (HIV)
and the virus can infect human cells in tissue culture.
Type D retrovirus is another immunosuppressive macaque
retrovirus that can cause diarrhea, weight loss and
recurrent infections. Macaques at the Longwood Medical
Area are regularly screened for this virus to prevent
inadvertent introduction of infected animals. D retrovirus
is not infectious to people.
Other Enteric Bacteria and Parasites
- Yersinia
enterocolitica is more rare than the previously
mentioned pathogens, but can also cause severe diarrhea
and dehydration in people and monkeys.
- Salmonella
is not common in nonhuman primates. Infection can
occur from contact with an infected person or from
consumption of contaminated food, especially poultry.
Mild or severe diarrhea can occur.
- Escherichia
coli occasionally causes diarrhea which may either
watery or contain blood and mucous. Giardia lamblia,
Cryptosporidium parvum, Enterocytozoan bieneusi,
Balantridium coli, and Entameba histolytica
are all intestinal protozoa that can infect monkeys
and man. Diarrhea can range from mild to severe. These
parasites are rare in most laboratory primates.
- Wild-caught
monkeys occasionally harbor other parasites that can
infect people.
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