Monday, 30 July 2007

What you must know about Zoonoses

Zoonoses Acquired From Pet Primates

David M. Renquist, D.V.M., M.A.
and Robert A. Whitney, Jr., D.V.M., M.S.

[Source: Veterinary Clinics of North America: Small Animal
Practice 17 (1) 219-240, 1987. With author's permission.]

Nonhuman primates are susceptible to many biological agents that
infect human beings but are not infectious to lower animals. The value of
this susceptibility in biomedical research is well known; however, the
infected nonhuman primate is a potential hazard to the research personnel
in contact with it. This hazard is even greater for the typical pet primate
owner, who is unfamiliar with the pathogenesis of disease. This article
reviews the most important infectious diseases that are found in the pet
nonhuman primate and present potential hazards to human beings.

Use of a monkey or ape as a pet should be strongly discouraged.
Although a current owner may be difficult to convince, a person considering
such a pet can generally be dissuaded. Most owners lack the knowledge,
devotion, and ambition necessary to prevent disease transmission and
maintain the health and welfare of the primate. Owners usually obtain the
primate as a curiosity or whim but lose interest rapidly as the problems of
puberty, nutrition, sanitation, and unpleasant habits appear. In addition,
the disease hazards to be discussed here far outweigh any advantages of
keeping the "cute little monkey." Therefore, veterinarians should
diplomatically discourage the practice of keeping a pet primate.

Fortunately, importation of primates for exclusive use as pets is now
prohibited by law; however, animals bred at wildlife parks, roadside zoos,
educational facilities, and (rarely) research facilities find their way
into the hands of pet owners.

There are more than 244 species of living primates, including the
great apes through the monkeys and prosimians such as lemurs, pottos,
galagos, tarsiers, and tupais. The groups principally seen in the United
States are described here.



The chimpanzee (Pan troglodytes) is a large, intelligent ape of West
African origin. In the past, small numbers were imported to perform in
circuses, for exhibition in zoologic collections, and, occasionally, for
private owners. Fortunately, the chimpanzee's cost ($10,000 and up) usually
prevents its being kept as a pet. Moreover, after puberty, the chimpanzee
is usually intractable and seen only in the protected environment of the
zoo or research facility.

The gibbon (Hylobates lar) is a smaller ape that was imported from
Indochina and Thailand in small numbers by military personnel and others.
It may be encountered as a pet even today, despite its status as an
endangered species.


The rhesus macaque (Macaca mulatta) is the principal species used in
biomedical research. These animals are not currently imported from the
wild. The domestically bred rhesus is expensive and, because of its size
and aggressive nature, it is rarely kept as a pet.

The cynomolgus monkey (Macaca fascicularis) is still being imported
from the Philippines for use in biomedical research. Its cost, considerably
less than that of a rhesus, may contribute to its occasional use
however, it too is an aggressive animal.

The vervet, or African green monkey (Cercopithecus aethiops), is a
lighter-bodied, more agile animal than the macaque. Its light yellow-green
haircoat and pleasant facial characteristics enhance its popularity as a

Baboons (Papio spp.) are very large (adult weight 25 kg plus) African
monkeys that are sometimes kept as pets when they are infants. Postpu-
bertal animals are rarely seen outside zoos or research facilities.


Until the 1974 prohibition, New World primates were used extensively
in the pet trade. Wooley monkeys (Lagothrix), capuchins (Cebus), squirrel
monkeys (Scuireus), marmosets of several species, and owl monkeys (Aotus),
in particular, are popular pets, with the squirrel monkey outranking all
the rest combined. In general, the South American monkey is less
aggressive but much harder to adapt to the pet environment.


Galagos (Galagidae), or "bushbabies," are occasionally seen as pets
because of their "teddy bear" appearance, but they are widely considered
unacceptable because of their fierce bite.


The infectious diseases of this large group of animals are as diverse
as the groups of animals they affect. The extensive bibliography at the end
of this article will provide further information about the diseases
presented as well as other related and distinct entities. In this article,
only the most important zoonotic hazards in the primates noted in the
preceding sections will be discussed. Discussion of the zoonotic diseases
will be limited to the Virchow definition: animal diseases transmissible to


Probably the most dangerous diseases, because they are so difficult to
diagnose and treat, are those of viral origin. Many viral diseases, such as
hepatitis or herpes B, can be transmitted from animal to man. A virus may
be latent in one species of primate, with little or no disease, yet be
fatal in another species of primate, including man.

Herpesvirus. Herpesviruses have been found in many different species
of primates. Some herpesviruses can produce a highly fatal systemic

Most primate herpes viruses are latent in one reservoir host species
and fatal in another species. Overt disease in the host species rarely
occurs other than as a mild skin lesion that is quickly self-limiting. The
most important of the zoonotic diseases is herpes B virus or Herpes simiae.

Herpes simiae (herpes B) produces a mild disease in some species of
monkeys that is analogous to the cold sores caused in humans by the virus
Herpes hominis (simplex), to which B virus is immunologically related. In
man, B virus can be fatal, causing an acute ascending myelitis. Of the 20
plus cases reported, only two patients have survived, and there is some
question on the confirmation of B virus in those two. Thus, the virus has a
possible mortality rate of 100 per cent in patients who develop clinical

Under natural conditions, the virus seems limited to the macaques,
with both the rhesus and cynomolgus considered primary natural hosts;
however, other macaque species are also incriminated from results of
serologic testing.

As high as 25 per cent of macaques, both imported and domestically
bred, have antibodies to herpes B virus. A short incubation period of 4 to
10 days is required from initial exposure. As with Herpes hominis,
recurrent infection can occur even in the presence of antibody; thus, all
macaques at any time should be considered potential carriers. As with other
herpes infections, viral shedding probably occurs only during periods of
active lesions.

The lesions in the primates can be difficult to detect because they
are usually on the mucosa of the buccal cavity. There may be vesicles or
ulcers around the lips and external nares, with an appearance very similar
to the cold sore of man; however, the most common site is the tongue. The
lesion resolves quickly and often goes unnoticed by the handler. A rate of
2 to 3 per cent has been reported for clinical evidence of lesions in the
macaque at any one time.

The primary transmissions are from monkey bites and aerosolization
of the virus. Most human infections have resulted from laboratory accidents
and monkey bites; however, one case was thought to have been caused by
droplet spread.

The hazard to the practitioner and the owner makes it imperative that
macaques not be kept as pets and that the risk be explained to the owner.
Any macaque being handled should be sedated with ketamine hydrochloride.
Face masks and rubber gloves should be used to prevent possible spread.
Serologic testing is available from primate reference services to determine
the presence of Herpes simiae and/or H. hominis antibody. An isolated
animal found negative for Herpes simae will remain negative unless brought
into contact with a primate shedding the virus. The virus can also
cause a fatal disease in the bonnet monkey (M. radiata).

Two other herpesviruses, Herpesvirus saimiri and Herpesvirus ateles,
which are found in the squirrel and spider monkey, respectively, are
oncogenic in other nonhuman primates, causing neoplasms of lymphoretic-
ular origin upon injection. The incidence of antibody to H. saimiri in
wild-trapped squirrel monkeys approaches 100 per cent; however, H. saimiri
and H. ateles are not considered zoonotic hazards to human beings. A
recent survey by NASA, using an indirect immunofluorescence test, showed
no positive serologic response to H. saimiri in human beings frequently
exposed to animals shedding the virus. Similar negative data exist for H.
ateles. These negative findings are mentioned here because of the
of New World monkeys, especially squirrel monkeys, as pets.

Poxviruses. Poxviruses cause foul diseases in nonhuman primates. All
four viruses are infective to man, although the incidence of human
for these viruses is low; monkeypox is the most frequent.

Monkeypox is serologically related to smallpox in man, so a smallpox
vaccination will prevent human development of monkeypox. Recent surveys
on purported "smallpox" outbreaks in Africa show that many of these cases
were monkeypox in unvaccinated individuals. The virus is found in both
New and Old World monkeys and apes with epithelial papular and vesicular
lesions. Protection is achieved through vaccination of animal and owner.

Benign epidermal monkeypox (BEMP) is known as "Tana pox" in the
human being. It was first recognized in 1965 in African children. The
reservoir hosts are macaques; New World primates are not infected. Clinical
signs are crusty elevations of the skin of the face, digits, and perineum.
Lesions usually regress in 3 to 6 weeks with no scarring. Immunity
following infection in the nonhuman primate lasts about 6 months.

Yaba virus infection is a rare disease of macaques, patas, baboon, and
man. The squirrel monkey and marmoset are resistant. Clinical lesions are
found as dermal tumors of the face, which regress spontaneously in 2 to 3
weeks for up to 4 months. The virus, which is arthropod-borne, is seen
only in newly imported macaques.

Molloscum contagiosum is seen only in chimpanzees and man as a
small, domelike waxy papule on the face and eyelids. The disease regresses
spontaneously and is mildly contagious from animal to man.

Measles (Rubeola). Measles is the most frequently reported viral
disease of nonhuman primates. In the wild, its incidence among them is
almost nonexistent; infection comes from exposure to infected children
during trapping. Upon infection, the primate sheds the virus and can
reinfect man. Measles is a highly infectious exanthematous viral disease of
children that causes a similar maculopapular rash in most nonhuman primate
species. Vaccination with 1/2 ml of an attenuated live virus is protective
for man and other primates. The disease in marmosets, tamarins, and owl
monkeys is usually fatal.

Rabies. Nonhuman primates are as susceptible to rabies as human
beings. Modified live vaccines for dogs and cats can cause rabies in the
nonhuman primate. Only killed vaccines or vaeeines suitable for man must
be used in nonhuman primates. Primates housed in rabies-endemic areas
are potentially at risk for indigenous wildlife and should be vaccinated.
Symptoms in the primate, as in man, are hydrophobia and paralysis. The
furious form is not usually seen in the nonhuman primate. Because of the
seriousness of this disease, the risk should be minimized by isolation,
environmental control, and a pre-exposure immunization program for
animals in an endemic area.

Marburg Virus. Although the vervet, or African green monkey, is rare
as a pet, the potential health hazard to human beings of this disease
requires its mention. Marburg virus was first reported in human beings in
Europe in 1967. Of the 31 cases in those outbreaks, 7 were fatal.

Twenty-five of these cases were found in laboratory personnel exposed
to African green tissue culture. No cases were reported in personell
handling the live African green monkey. The latest reports were of 300
fatalities in Sudan and Zaire (1976), caused by an unconfirmed but
morphologically indistinguishable virus, and 3 confirmed cases in Kenya
(1980). The reservoir host has never been determined; however, the virus is
virulent experimentally for vervet, rhesus, and squirrel monkeys. In man
there is a 4- to 9-day incubation period, accompanied by fever, weight
loss, vomiting, and diarrhea after 3 to 4 days. In nonhuman primates, death
occurs in 6 to 9 days with no signs until the day of death. Considering the
potential danger all African green monkeys should be handled as if

Viral Hepatitis. The virus of human infectious hepatitis (hepatitis A)
ean infect the chimpanzee, patas, wooley monkey (Lagothrix spp.), gorilla,
cebus, aotus, and some tamarins. Infection in the primate is usually
inapparent; however, the animal can carry the virus and be infective to
man. Several outbreaks have been reported in primate handlers in research
facilities. The disease in primate handlers appears to be related to
handling recently shipped animals; the virus is probably spread shortly
after exposure, antibodies develop, and the animals then become immune to
reinfection. Because chimpanzees have not been imported as pets for many
years, the few pet chimpanzees encountered probably present no danger of
hepatitis. However, the chimpanzee is susceptible to disease from infected
persons. Vaccines are being developed, but they are not reeommended for
routine primate vaccination.


Like man, the nonhuman primate is susceptible to the wide variety of
bacterial agents. There is little difference in susceptibility between most
primate species; however, the macaques are more susceptible to tubercu-
losis and enteric bacteria, whereas the New World primates are more
susceptible to the water-borne agents (Pseudomonas or Klebsiella). The
bacteria that deserve the most concern are Mycobacteriaciae, Shigella/
Salmonella, Campylobacter, and Klebsiella.

Mycobacteriaciae. Mycobacteria are responsible for tuberculosis, the
scourge of the primate owner and veterinarian. Tuberculosis has been
recognized as a common disease of captive primates for many years. Early
outbreaks were devastating, causing the loss of hundreds of primates of
many species. Species most susceptible are the macaques and apes; the
New World species seemingly are more resistant. Almost all species can
be experimentally infected. Historically, the three major species of myco-
bacteria--avium, bovis, and tuberculosis--have been incriminated as caus-
ing tuberculosis in the nonhuman primate. Recently, many atypical myco-
bacteria have also been reported in the nonhuman primate, including M.
kansasii and M. scrofulaceum, all of which are potential hazards to man.
The extreme susceptibility of monkeys to tuberculosis is often discussed;
the disease is usually miliary, and arrest and calcification are unusual.
The danger to owners and others who come in contact with infected monkeys
is obvious. Control requires an effective quarantine for newly arrived
primates, isolation from infected persons, and a rigorous testing program.
It is generally agreed that the route of initial infection is usually
respiratory (60 per cent) or intestinal (40 per cent). Because of their
fulminating nature, terminal infections often present difficulty in
establishing the portal of entry because so many organs are involved in the
generalized infection.

The clinical signs of tuberculosis are not striking until the disease
is in an advanced stage. The first sign may be a slight behavioral
alteration. The animal may be slower than normal or stay along the floor of
the enclosure rather than climb the enclosure or cage wall. Soon the
infected animal will exhibit a dull appearance, crouch in the corner, and
refuse to eat. The latter may be all the owner notices; coughing or other
respiratory signs are conspicuously absent. Less common signs that may or
may not be present with tuberculosis include diarrhea, skin ulceration,
suppuration of Iymph nodes, and visible enlargement of the spleen and
liver. Often there are no clinical signs, and the owner reports that the
animal died suddenly without explanation. Radiographs of the lungs, etc.,
are usually nondiagnostic because of the lack of calcification. The usual
presence of mite (Pneumonysis spp. ) lesions in normal rhesus monkeys
complicates the radiographic diagnosis.

The lesions seen at necropsy are fairly typical yellowish-white to
grey nodules that range from pinpoint size to several millimeters in
diameter and appear just under the surface of the affected organs. As the
disease progresses, the nodules fill with caseous material and may rupture
and produce cavitation. Caseous, enlarged mediastinal lymph nodes in the
rhesus monkeys are almost pathognomonic for tuberculosis. In baboons and
apes, the disease is much more like that seen in man, with caseation and
eventual calcification.

Cutaneous tuberculosis in primates usually migrates to the regional
Iymph nodes, and any draining lymph node should be suspected as a
tubercular lesion until proven otherwise. Tuberculosis of the spine, or
Pott's disease, also occurs in monkeys and should be considered whenever
there is unexplained paralysis of the hindlimbs.

Tuberculin skin testing must be part of any physical examination of a
nonhuman primate. Newly imported primates should be tested biweekly
and isolated until five negative tests have been certified. Approximately
15,000 tuberculin units (0.1 ml) of full-strength mammalian tuberculin is
given intradermally in alternating eyelids. The test is read at 24, 48, and
72 hours. A positive reaction is any erythema and/or edema that persists
for 48 hours or longer. Suspicious tests may be repeated at 7 days in the
opposite eyelid or abdomen. Stabilized Old World primates should be
tested quarterly, and New World monkeys semi-annually. Because of the
public health danger and the potential resistance to treatment, positive
animals should be euthanatized; treatment is not recommended. Atypical
tuberculosis, other serologic methods, and so on, are beyond the scope of
this article. The reader is referred to the bibliography for further

Shigella and Salmonella. Although shigellosis and salmonellosis are
caused by two separate organisms, the symptoms, signs, and treatment are
similar, so they will be discussed together. Shigella and salmonella are
frequently present in the alimentary tract of nonhuman primates. Isolation
of the organism from the carrier animal is difficult, requiring numerous
samples and enrichment techniques. A single negative culture means
nothing. Fortunately, the most serious human pathogens of these two
groups, Shigella dysenterriae type 1 and Salmonella typhi, have only rarely
been isolated from nonhuman primates; however, several others (Shigella
flexneri, S. sonnei, and Salmonella typhimirium, for example), which are
also infectious to man, have been recovered.

The literature contains many reports of infection in primates and few
reports of transmission to human beings. One of the earlier transmissions
reported was a case of shigellosis in a child who licked an ice cream cone
that had been touched by a monkey in a pet shop. This illustrates the
potential danger for infants and children in contact with the species.

Fortunately, the published reports of primate-to-man infections are
rare. The primate carrying the organism can have a fulminating fatal
infection at any time, with excretion of large numbers of organisms during
the course of the disease. This acute infection is usually precipitated by
some stress, such as environmental change of corticosteroids.

Clinical signs of shigellosis and salmonellosis are weakness,
prostration edema of the face and neck, emaciation, and diarrhea with mucus
and/or blood. As a rule, a bloody dysentery eventually occurs in

Prolapse of the rectum is commonly seen, with death in a few days to 2
weeks after the onset of signs. At necropsy, the large intestine is
distended and the serosol surface has a red tinge. A catarrhal and
diphtheritic colitis occurs with a varying degree of exudation and necrosis
of the mucous membrane and ulceration that may penetrate the serosal

Diagnosis is based on signs, necropsy, and culture results. Culture
must be fresh, but, even so, the isolation rate is low. Treatment for both
entities is as follows: (1) take offor reduce feed; (2) provide
fluids--lactated Ringers, 1/2 strength with 2.5 per cent dextrose given at
a rate of 20 ml per kg or higher, depending on the state of dehydration;
(3) administer antibiotics--trimethoprim and sulfadiazine (Tribrissen) will
eliminate the carrier state if given conscientiously; and (4) administer
kaolin plus pectin (Pectolin).

The family medical practitioner should be made aware of any pet
monkey with symptoms of these diseases, particularly if children are or
will be in contact with the primate.

Campylobacteriosis. Campylobacters were originally classified as a
member of the family Vibriacae but recently have been reclassified as a
separate group. Campylobacter jejuni, the etiologic agent seen most fre-
quently in the nonhuman primate, is a small, gram-negative, non-spore-
forming, curved rod causing a moderate to severe enterocolitis in a variety
of mammals and birds, including man. The review article by Shane and
Montrose (1985) is highly recommended for a full description of the disease
and its pathogenesis. Because Campylobacter has been one of the leading
causes of diarrhea in human beings, it is keenly important as a zoonotic
biohazard. The original report by King (1957) on the isolation of C. jejuni
from the blood of children with diarrhea was the first account of the
organism's pathogenicity. Since that time, the organism has been recognized
as a significant problem in a variety of domestic and exotic animals.

The signs and lesions of campylobacteriosis have been extensively
reviewed by Butzler and Skerrow. A usual incubation period of 3 to 5 days
is followed by a febrile period accompanied by malaise, dizziness, myalgia,
and abdominal pain. The stool is watery, bile-stained, and malodorous, and
may contain blood. The diarrhea phase usually lasts for 3 days but may
recur up to 2 weeks. It is most severe in infants, children, and
prepubertal primates (Morton et al., 1981) and in immunocompromised adults,
in whom the infection can be fatal. Poor self-hygiene in the pet owner can
be directly related to infection. In the adult primate, the disease is
usually a mild, self-limiting enteritis, but it is a significant hazard to
the handler or owner from fecal spray and droplet contamination. The
carrier reservoir condition, as with shigella and salmonella, is frequently
a sequel to an active clinical infection. Surveys in companion domestic
animals have shown direct correlation between positive animals and positive
household members. The organism is quite resistant, being found to remain
viable in streamwater at 4x C far up to 4 weeks. Contamination of the
environment by the pet primate poses a significant threat to human beings.

Diagnosis is through culture, which must be specific for the
organism's growth requirement of 43x C and reduced oxygen tension. Normal
anaerobic/aerobic culture techniques at 37x C will not pick up the
organism, andthe diagnosis will be missed or attributed to a nonspecific

Treatment is similar for shigella and salmonella: erythromycin is the
antibiotic of choice. Vaccines provide partial protection for 3 to 6 months
to nonimmune individuals in highly endemic areas. However, the routine use
of vaccines is not recommended.

Klebsiella. Klebsiella and other water-borne, gram-negative bacteria
(Pseudomonas) are primarily opportunists affecting primates that have a
lowered resistance. Primates with inadequate nutrition (the fruit-fed
squirrel or owl monkey, for example) are prime candidates for this disease.
The infected primate is a real threat to the infant or child with a mild
respiratory infection whose reduced level of health increases the potential
for infection. Klebsiella is present in stagnant water, dirty drinking
receptacles, and soil, and as flora of the alimentary tract.

The clinical signs are coughing, sneezing, facial edema (air
sacculitis in owl monkeys), nasal discharge, dyspnea, and anorexia. The
lesions consist of pleural congestion and red to gray hepatization of the
lungs. The airsacs of the owl monkey may be filled with a clear fluid,
eventually leading to a severe bronchopneumonia.

Diagnosis is by isolation of the organism, a nonmotile, gram-negative
short bacillus with rounded ends and a thick capsule.

Treatment is with an organism-sensitive antibiotic such as streptomy-
cin, kanamycin, colimycin, or gentacin. The organism may develop multiple
resistance to antibiotics, however. Aerosol installation of kanamycin in an
incubator has been reported to be effective.


Several reports have been made on systemic and superficial mycoses
in primates. Fortunately, these are isolated cases; however, there is a
potential danger to human beings. The primary pathogens are Dermato-
philus congolensis, Candida albicans, and Trichophyton mentagrophytes.
The systemic fungi, nocardia, coccidiomyces, and crYptococcus have been
reported and are included in the bibliography.

Dermatophilus congolensis. Streptothricosis (D. congolensis) is caused
by an actinomycete with gram-positive but non-acid-fast mycelium and
spores. Natural disease has been reported in Aotus and Lagothrix, and
experimental infection was successful in rhesus, cynomolgus, and squirrel
monkeys. The disease was reviewed by Kaplan in 1976.

Clinically, the disease is characterized by erythema that becomes
scaly and progresses to an exudative papillomatous crusty lesion. When the
crust is removed, a raw bleeding area is left, resembling a strawberry
surface. Diagnosis is through gram smears of the exudate; branched
filaments forming packets up to eight coccoid cells wide are seen. The
disease is treated with penicillin, ampicillin, or streptomycin applied
with a topical iodine tincture on the lesions. Strict sanitation and
isolation are necessary to avoid contamination of the pet owner or

Candida albicans. Candidiasis is a fungal infection of the mucous
membranes. It has been reported in a variety of primates, but it is usually
secondary to nutritional deficiency, other disease, or extensive antibiotic
treatment. Syrnptoms vary with the site of infection. Intertriginous infec-
tions appear as pruritic, exuclative patches between the skin folds (the
toes, for example). Oral candidiasis appears as creamy white patches of
exudate that can be scraped offthe inflammed tongue or buccal mucosa. The
disease in individuals with an immune deficiency may be quite severe. Man
is susceptible to the infection; however, it usually requires a favorable
moist environment or reduced defenses caused by another disease. The infant
with a mild diaper rash would be a prime candidate for candida transmission
from the pet primate.

Diagnosis is by finding yeast cells and hyphae in gram-stained prepa-
ration. Because candida is often found as a commensal organism, the culture
of a species from skin, vagina, urine, sputum, or stool should be
interpreted cautiously. Confirmation is based on the presence of the
characteristic lesion and, if necessary, a histologic biopsy of the area.
Treatment is contact application of nystatin, clotrimazole, or micono-
zole. A vehicle appropriate to the site of infection should be used in
light of the primate's habit of licking or rubbing off applied ointments.
Recalcitrant or recurrent cases, especially of oral or mucogenital candida,
have been treated with nystatin oral suspension or tablets.

Ringworm. Trichophyton mentagrophytes is the usual cause of ring-
worm in primates. Signs, diagnosis, and treatment are similar to that for
the dog and cat. Treatment is oral griseofulvin (microsize 125 to 150 mg
orally with mashed feed). The owner should be warned of the hazard, and
the animal should be isolated during treatment. All primates are
susceptible to the infection.


Most primates inhabit tropical and subtropical regions. In the wild,
many scavenge about villages and share not only food but also the parasites
of the human inhabitants. Danger to the pet owner from imported animals,
therefore, is usually during the first few months after the animal's
arrival in the country. If the parasites are effectively eliminated during
the initial quarantine adaptation period, the danger of transmission to the
pet owner can be eliminated. Parasites that need an intermediate host are
self-limiting but those having a direct cycle become a continual problem.
Possible human infection from primate carriers is a constant threat.
Numerous articles and monographs have been written on the primate
parasites. In this article, discussion is limited to examples of protozoa,
nematodes, tapeworms, and arthropods that have a direct life cycle and are
infectious to man.

Protozoa. Many protozoa require arthropod vectors; with vector con-
trol, they do not cause a significant problem to man outside the environ-
mental range of the arthropod. Giardia and Entamoeba histolytica are the
two primary pathogens not requiring an arthropod vector. Although plas-
modia cause malaria, a disease of major importance, they are usually
specific for each primate except in experimental situations and are rarely
transmitted between primates and man in North America. References for
malaria can be found in the bibliography.

Giardiosis. Giardia is becoming a frequent cause of recurrent diarrhea
in man and primate. Trophozoites of Giardia are found in the upper part
the small intestine, where they live adhering closely to the mucosa. The
gellate is capable of almost limitless proliferation; diarrheic stools may
contain countless cysts or trophozoites. Diarrhea is the most common
symptom associated with Giardia infection, although some reports show
that the infection mimics biliary disease or even chronic cholecystitis.
The stools frequently contain mucus, but not blood. Giardia, like other
agents potentially transmissible from the primate, is also considerably
more common in children than adults.

Diagnosis of Giardia is easy, the organism being one of the most
recognizable intestinal protozoa. The trophozoite is bilaterally symmetric
and pear-shaped with an attenuated posterior end. The two nuclei and the
rodlike median bodies resemble a face with eyes and mouth.

Nonhuman primates can be asymptomatic carriers to man, with infec-
tin via direct contact.

Treatment using metronidazole is usually successful at a dose of 10 to
35 mg per kg per day, three times a day, for 7 days. This drug, however,
is currently not licensed for use with Giardia, and there is concern over
its potential carcinogenicity. Quinacrine at 10 mg per kg per day, three
times a day, for 5 days is 70 to 95 per cent effective but is not tolerated
well by squirrel monkeys, often causing some gastrointestinal disturbances.

Proper hygienic practices with routine fecal smears will minimize the
pet's disease potential to the owner.

Entamoeba histolytica. Amebiasis is a severe disease of man and
primate; it causes a protracted diarrhea from chronic colitis and
occasionally abscesses in the brain, liver, or lungs. The cyst must be
ingested to cause disease; the trophozoite in fresh stools is rarely
infective. The organisms involve the intestinal mucosa and form small
colonies that extend into the submucosa and, occasionally, the muscularis,
producing the typical bottle- or flask-shaped ulcers. The frequency of this
tissue invasion varies within an individual; most patients are
asymptomatic. When symptoms do occur, they vary according to geography. In
temperate climates, the disease is usually characterized by a mild,
intermittent diarrhea and constipation, flatulence, and cramping abdominal
pain in both primate and man. In tropical environments, the disease may be
characterized by a frank dysentery with episodes of frequent semifluid
stools, often containing blood and mucus. Complications may involve hepatic
abscess and/or brain abscesses.

Diagnosis is confirmed by the presence of the trophozoite in fresh
stools. Diagnosis may require examination of three to six stool specimens.
controlling the spread of E. histolytica requires proper hygiene to prevent
direct oral contact with human or primate feces. The high incidence of
symptomatic carriers complicates the problem.

Metronidazole is the treatment of choice for both intestinal and
extra-intestinal amebiasis. A dose of 30 to 50 mg per kg per day given
orally in three divided doses for 10 days is recommended. Severe cases may
require combination with diiodohydroxyquin at a dose of 30 to 40 mg per kg
per day in three individual doses.

Three negative stools, obtained on three successive days, are usually
indicative of cure. Reexamination of the stools at 1, 3, and 6 months after
treatment is recommended.


This is a group of elongated cylindrical worms that infect all species
of primates; the agent depends on species and location. The principal
infective nematode from primate to man is Strongyloides spp.

Strongyloides is common in many species of primates and, because of
its direct life cycle, can be infectious for man. Three species are
involved: S. fillleborni, S. cebus, and S. stercoralis. The infective
third-stage filariform larvae (rhabditiform), found as a free-living stage
or in fresh feces, penetrates the skin or mucosa and migrates via the blood
to the lungs, alveoli, and trachea. They are swallowed and cause a severe
acute enteritis. The invasion through the skin can cause pruritus and
erythema. The passage through the lungs can cause pneumonia and possibly
death due to pericarditis. The affected primate, unless treated and tested
frequently, can reinfect itself and may be a continual hazard to the pet

Diagnosis is confirmed by finding ova or larvae in the feces, coupled
with the clinical signs. Treatment is effective, with thiabendazole at 100
mg per kg repeated in 2 weeks. Sanitation is essential in preventing
reinfection. Veterinarians and technicians handling fecal specimens are
advised to wear gloves during all diagnostic procedures to avoid potential
skin penetration of the infective larvae.


The nonhuman primate is susceptible to a variety of cestodes; however,
the only cestode considered a potential zoonosis from nonhuman primates
is Hymenolepsis nana.

Hymenolepsis has a direct life cycle but can also pass through an
intermediate host such as a beetle or flea. The life span of the adult in
the intestine is only a few weeks. The tapeworm causes a catarrhal
enteritis with abscesses of the mesenteric lymph nodes.

The principal signs are diarrhea and abdominal pain, exhibited in the
nonhuman primate by crouching and tucking of the abdomen. The diagnosis
is through fecal examination with demonstration of the typical proglottid.
Treatment is the use of niclosamide at 20 mg per kg per day.


A variety of lice, mites, and fleas infest nonhuman primates. Most of
these can be transmitted to humans through contact. Of these, the most
likely problems are with Sarcoptes scabiei (the itch mite), Pediculus
humanas (the human head or body louse), Tunga penetrans (the chigoe
flea), and Ornithodorus (tick). Disease caused by these arthropods involve
the skin and are characterized by pruritus and scaling, which, in the case
of the chigoe flea, can lead to severe inflammation and ulceration. Fortu-
nately, the grooming habits of healthy primates prevent severe infestation
of most ectoparasites. Sarcoptic mange is the only significant threat among
most animals.

The most serious danger to man and primate is the role of the
arthropods as an intermediate biological host for parasitic diseases and as
a mechanical vector for infectious organisms. The tick (Ornithodorus) is an
intermediate host for relapsing fever. Yellow fever, an important disease
of Central and South America, has its reservoir host in the primate and
utilizes the mosquito (Aedes) as an important vector. Control is through
environmental sanitation and direct treatment of the primate. Treatment is
difficult because of the grooming, licking nature of the primate; however,
dusts and ointments suitable for cats and humans can be used with
discretion on the primate.


Laws regulating the importation of primates have drastically reduced
the number of primates seen as pets and, thus, the hazard both to the
potential owner and veterinarian. Active disease and latent carrier states
in primates potentially have severe consequences for the contact person.
This potential for human transmission makes it imperative that medical and
veterinary professionals collaborate to educate the public on the danger of
the primate as a pet.


Zoonoses of Primates: General

1. Fernandes MV, Arambulo PV, Moro M: Planning of national zoonosis control
programs in developing countries. In Third International Symposium in
Veterinary Epidemiology and Economics, Arlington, Virginia, 1982.
Edwardsville, Kansas, Veterinary Medicine Publishing Co, 1983, pp 631-639.
2. Fiennes R (ed): Pathology of simian primates. Part I. General Pathology.
Part II. Infectious and Parasitic Diseases. Basel, Switzerland, Karger,
3. Fiennes R: Zoonoses of Primates. Ithaca, New York, Cornell University
Press, 1975.
4. McLean RG, Trevino HA, Sather GE: Prevalence of selected zoonotic
diseases in vertebrates from Haiti, 1972. J Wildlife Dis 15:327-30 1979.
5. Melby EC, Altman NH (eds): Handbook of Laboratory Animal Science. Volume
2. Cleveland, CRC Press, 1974.
6. Milhaud CL, Klein MJ: Diseases of primates transmissible to man.
Sciences et Techniques de l'Animal de Laboratoire 4:27-41, 1979.
7. Mortelmans J, Kumar V, Brandt J, et al: Import of exotic diseases in
pets and other animals. Symposium on Tropical Medicine Outside of the
Tropics, Antwerp, Belgium, 1983. Ann Soc Belse Med Trop 65:109, 1984.
8. Ruch TC: Diseases of Laboratory Primates. Philadelphia, WB Saunders Co,
9. Sedswick CJ, Robinson PT, Lochner FK: Zoonoses: A zoo s concern. J Am
Vet Med Assoc 167:828-829, 1975.
10. St Whitelock OV (ed): Care and Diseases of the Research Monkey. New
York, New York Academy of Science, 1960.
11. Tauraso NM: Review of recent epizootics in nonhuman primate colonies:
Their relation to man. Lab Anim Sci 23:201-210, 1973.
12. Tribe GW, Noren E: Incidence of bites from cynomolgus monkeys in
attending animal staff--1975-80. Lab Anim 17:110, 1983.
13. Valerio DA: Nonhuman Primates: Standards and Guidelines for the
Breeding, Care, and Management of Laboratory Animals. Edition 2. Revised.
Washington, DC, National Academy of Sciences, 1973.
14. Vitali E: Viral, Bacterial, and Parasitic Diseases of Primates in
Captivity. Berlin, German Democratic Republic, Akademie-Verlag, 1980.
15. Whitney R, Johnson D, Cole W: Laboratory Primate Handbook. New York,
Academic Press.

Viruses: General

1. Bauer K: Newly appearing virus diseases in animals and humans. Tierarztl
Prax 8:307-312, 1980.
2. Hull RN: The simian viruses. In Virology Monographs 2. New York,
Springer-Verlag, 1968, pp 1-66.
3. Jerath R: Recent advances in viral zoonoses. Int J Zoonoses 6:49-60,
4. Kalter SS: Virus research. In Bourne GH (ed): Nonhuman Primates and
Medical Research. New York, Academic Press, 1973, pp 61-65.
5. Mayr A: New emerging viral zoonoses. Vet Rec 106:503-506, 1980.
6. Zuckerman A: Exotic viruses (Marburg disease, Lassa fever, rabies).
Nature 263 (5579):625-626. 1976.


1. Daniel MD: The herpesvirus group. In Fiennes RN (ed): Pathology of
Simian Primates. Part 2. New York, S Karger, 1972, pp 592-611.
2. Hunt RD, Melendez LV: Herpesvirus infections of nonhuman primates:
Review. Lab Anim Care 19:221-234. 1969.

Herpesvirus simiae (B virus)

1. Cole WC, Bostrom RE, Whitney RA: Diagnosis and handling of B virus in
rhesus monkey (Macaca mulatta). J Am Vet Med Assoc 153:894-898, 1968.
2. Espana C: Herpesvirus simiae infection in Macaca radiata. Am J Phys
Anthropol 38:447-454, 1973.
3. Hartley EG: Naturally occuring "B" virus infection in cynomolgus. Vet
Rec 76:555-557, 1964.
4. Hartley EG: B virus: Herpesvirus simiae. Lancet 1:87, 1966.
5. Keeble SA, Christofinis GJ, Wood W: Natural virus-B infection in rhesus
monkeys. Pathol Bacteriol 76:189-199, 1958.
6. Sabin AB, Wright AM: Acute ascending myelitis following a monkey bite
with the isolation of a virus capable of reproducing the disease. J Exp Med
59:115-136, 1934.

Herpesvirus tamarinus (Herpes T)

1. Holmes AW, Calwell RG, Dodmon RE, et al: Isolation and characterization
of a new herpes virus. J Immunol 92:602-610, 1964.
2. Hunt RD, Melendez LV: Spontaneous herpes-T infection in the owl monkey
(Aotus trivirgatus). Pathol Vet 3:1-26, 1966.
3. King NW, Hunt RD, Daniel MD, et al: Overt herpes-T infection in squirrel
monkeys (Saimiri sciureus). Lab Anim Care 17:412-423, 1967.
4. Melnick JL, Midulla M, Wimberly I, et al: A new member of the
herpesvirus group isolated from South Americall marmosets. J Immunol
92:596-601, 1964.
5. Tate CL, Lewis JC, Huxsoll DL, et al: Herpesvirus T as cause of
encephalitis in an owl monkey (Aotus trivirgatus). Lab Anim Sci 21:743-745,

Herpesvirus hominis (simplex)

1. Emmons RW, Lennette EH: Natural Herpesvirus hominis infection of a
gibbon (Hylobates lar). Arch Gesamte Virusforsh 31:215-218, 1970.
2. Heldstab AH, Ruedi D, Sonnabend W, et al: Spontaneous generalized
Herpevirus hominis infection of a lowland gorilla (Gorilla gorilla
gorilla). J Med Primatol 10:129-135, 1981.
3. Kalter SS, et al: Experimental herpesvirus hominis type 2 infection in
non-human primates. Proc Soc Exp Biol Med 139:964-968, 1972.
4. Katzen DS, Connor JD, Wilson LA, et al: Experimental Herpes simplex
infection in the owl monkey. Proc Soc Exp Biol Med 125:391-398, 1967.
5. London WT, et al: Genital Herpesvirus hominis type 2 infection of
monkeys. Obstet Gynecol 35:501-509, 1971.
6. McClure HM: Natural Herpes-irus horninis infection of tree shrews
(Tupaia glis). Lab Anim Sci 22:517-521, 1972.
7. Melendez LV, Espana C, Hunt RD, et al: Natural Hetpes simplex infection
in the owl monkey (Aotus trivirgatus). Lab Anim Care 19:38-45, 1969.
8. Smith PC, Yuill TM, Buchanan RD, et al: The gibbon (Hylobates lar): A
new primate host for Herpesvirus hominis. 1. A natural epizootic in a
laboratory colony. J Infect Dis 129:292-297, 1969.

Oncogenic Herpesviruses

1. Daniel M, et al: Herpesrirus saimiri. VII. Induction of malignant
lymphoma in New Zealand white rabbits. J Natl Cancer Inst 53:1803-1807,
2. Hull D, et al: Recovery and characterization of a new simian herpesvirus
from a fatally infected spider monkey. J Natl Cancer Inst 49:225-230, 1972.
3. Hunt RD, et al: Morphology of a disease with features of malignant
Iymphoma in marmosets and owl monkeys inoculated with Herpesvirus saimiri.
J Natl Cancer Inst 44:447-465, 1970.
4. Hunt RD, et al: Pathologic features of Herpesvirus ateles Iymphoma in
cotton-topped marmosets (Saguinus oedipus). J Natl Cancer Inst
49:1631-1639, 1972.
5. Hunt RD, et al: Spontaneous Herpesvirus saimiri Iymphoma in an owl
monkey. J Infect Dis 127:723-725, 1973.
6. Melendez LV, Daniel MD, Hunt RD, et al: An apparently new herpesvirus
from primary kidney cultures of the squirrel monkey (Saimiri sciureus). Lab
Anim Care 18:374-381, 1968.
7. Melendez LV, et al: Herpesvirus saimiri. 1. Further characterization
studies of a new virus from the squirrel monkey. Lab Anim Care 19:372-377,
8. Melendez LV, et al: Herpesvirus saimiri. II. Experimentally induced
malignant lymphoma in primates. Lab Anim Care 19:378-386 1969.
9. Melendez LV, et al: Herpesrirus ateles, a new Iymphoma virus of monkeys.
Nature (New Biol) 235: 182- 184, 1972.
10. Melendez LV, et al: Two new herpesviruses from spider monkeys (Ateles
geoffroyi). J Natl Cancer Inst 49:233-238, 1972.
11. Wolfe LG, Falk LA, Reinhardt F: Oncogenicity of Herpesvirus saimiri in
marmoset monkeys. J Natl Cancer Inst 47:1145-1162, 1971.

Other Herpesviruses

1. Allen WP, Felsenfeld AD, Wolf RH, et al: Recent studies on the isolation
and characterization of delta herpesvirus. Lab Anim Sci 24:222-228, 1974.
2. Ayers JP: Studies of the delta herpesvirus isolated from the patas
monkey (Erythrocebus patas). Lab Anim Sci 21:685-695, 1971.
3. Clarkson MJ, Thorpe E, McCarty K: A virus disease of captive vervet
monkeys (Cercopithecus aethiops) caused by a new herpesvirus. Arch Gesamte
Virusforsch 22:219-234, 1967.
4. Heuschele WP: Varicella (chicken pox) in three young anthropoid apes. J
Am Vet Med Assoc 136:256-257, 1960.
5. Mialherbe H, Strickland-Cholmley M: Simian herpesvirus SA8 from a
baboon. Lancet 2(7635):1427, 1969.
6. McCarthy K, et al: Exanthematous disease in patas monkeys caused by a
he*rpes virus. Lancet 2(7573):856-857, 1968.
7. White RJ, Simmon L, Wilson RB: Chickenpox in young anthropoid apes:
Clinical and laboratory findings. J Am Vet Med Assoc 161:690-692, 1972.


1. Arita I, Jezek Z., Khodakevich L., et al.: Human monkey pox: A newly
emerged orthopoxvirus zoonosis in the tropical rain forests of Africa. Am J
Trop Med Hyg 34:781-789. 1985.
2. Cho CT, Wenner HA: Monkeypox virus. Bacteriol Rev 37:1-18, 1973.
3. Foster SO, et al: Human monkeypox. Bull WHO 46:569-576, 1972.
4. Jezek Z, Gromyko AI, Szczeniowski MV: Human monkeypox. J Hyg Epidemiol
Microbiol Immunol 27:13--28, 1983.
5. Leone L, Leona S: Human infection with monkeypox. Centers for Disease
Control Veterinary Public Health Notes. US Department of Health, Education
and Welfare, Public Health Service. Atlanta, Georgia, Centers for Disease
Control, 1971.
6. Mayr A, Danner K: Vaccination against pox diseases under
immunosuppressive conditions. Dev Biol Stand 41:225-234, 1978.
7. McConnell SJ, et al: Protection of rhesus monkeys against monkeypox by
vaccinia virus immunization. Am J Vet Res 25:192-195, 1964.
8. Mutombo M, Arita I, Jezek Z: Human monkeypox transmitted by a chimpanzee
in a tropical rain-forest area of Zaire. Lancet 1(8327):735-737, 1983.
9. Prier JE, Sauer RM, Malsberger RG, et al: Studies on a pox disease of
monkeys. II. Isolation of the etiologic agent. Am J Vet Res 21:381-384,
10. Sauer RM, et al: Studies on a pox disease of monkeys. I. Pathology. Am
J Vet Res 21:377-380, 1960.
11. Von Magnus P, Anderson EK, Peterson KB, et al: A pox-like disease in
cynomolgus monkeys. Acta Path Micr Scand 46:156-176, 1959.

Benign Epidermal Monkey Pox (BEMP)

1. Casey HW, Woodruff JM, Butcher WI: Electron microscopy of a benign
epidermal pox disease of rhesus monkeys. Am J Pathol 51:431-446, 1967.
2. Crandell RA, Casey HW, Brumlow WB: Shldies of newly recognized poxvirus
of monkeys. J Infect Dis 119:80-88, 1969.
3. Downie AW, et al: Tanapox: A new disease caused by a poxvirus. Br Med J
1(5745):363-368 1971.
4. Downie AW, Espana C: Comparisons of tanapox and Yaba-like viruses
causing epidemic disease in monkeys. J Hyg 70:23-32, 1972.
5. Hall AS, McNulty WP Jr: A contagious pox disease in monkeys. J Am Vet
Med Assoc 151:833-838, 1967.
6. McNulty WP Jr, et al: A pox disease in monkeys transmitted to man.
Clinical and histological feahlres Arch Dermatol 97:286-293, 1968.


1. Smith AW, Prato C, Skillins DE: Caliciviruses infecting monkeys and
possibly man. Am J Vet Res 39:287-289, 1978.

Yaba Virus Disease

1. Bearcroft WGC, Jamiesen MF: An outbreak of subcutaneous tumors in rhesus
monkeys. Nature 182:195-196, 1958.
2. Grace T Jr, Mirand EA: Human susceptibility to a simian tumor virus. Ann
NY Acad Sci 108:1123-1128, 1963.
3. Kupper JL, Casey HW, Johnson DK: Experimental Yaba and benign epidermal
monkey pox in rhesus monkeys. Lab Anim Care 20:979-988, 1970.
4. Neven JSF, et al: Subcutaneous "growths" in monkeys produced by a
poxvirus. J Pathol Bacteriol 81:1-14, 1961.
5. Wolfe LG, Griesemer RA, Farrell RL: Experimental aerosol transmission of
Yaba virus in monkeys. J Natl Cancer Inst 41:1175-1195, 1968.

Molluscum contagiosum

1. Douglas JE, et al: Molluscum contagiosum in chimpanzees. J Am Vet Med
Assoc 151:901-904, 1967.
2. Schmidt RE, Butler TM: Molluscum contagiosum in a colony born
chimpanzee. Lab Prim Newsletter 10:17, 1971


1. Blake FG, Trask JD: Studies on measles. lI. Symptomatology and pathology
in monkeys experimentally infected. J Exp Med 33:413-422, 1921.
2. Hall WC, et al: Pathology of measles in rhesus monkeys. Vet Pathol
8:397-419, 1971.
3. Levy BM: An acute epizootic of measles in marmosets. Lab Anim Sci
21:33-39, 1971.
4. Meyer HM, et al: Ecology of measles in monkeys. Am J Dis Child
102:307-313, 1966.
5. Potkav S, Ganaway JR, Rogers NG, et al: An epizootic of measles in
colony of rhesus monkeys (Macaca mulatta). Am J Vet Res 27:33-39, 1971.

Viral Hepatitis

1. Davenport RM, Hennessy AV, Christopher N, et al: A common source
multi-household outbreak of chimpanzee-associated hepatitis in humans. Am J
Epidemiol 83:146-151, 1966.
2. Deinhardt F: Hepatitis in subhuman primates and the hazards to man. In
Balner H, Beveridge WIB (eds): Infections and Immunosuppression in Subhuman
Primates. Copenhagen, Munksgaard, 1970, pp 55-63.
3. Friedman CTH, et al: Chimpanzee-associated infectious hepatitis among
personnel at an animal hospital. J Am Vet Med Assoc 159:541-545, 1971.
4. Hillis WD: Viral hepatitis associated with subhuman primates.
Transfusion 3:445-454, 1963.
5. Kessler H, Tsiquaye KN, Smith H, et al: Hepatitis A and B at the London
Zoo. J Infect Dis 33:63-67, 1982.
6. London WT et al: Serial transmission in rhesus monkeys of an agent
related to hepatitis associated antigen. J Infect Dis 125:382-389, 1972.
7. Mosley JW, Reinhart HP, Hassler FR: Chimpanzee-associated hepatitis. J
Am Vet Med Assoc 199:695-697, 1967.
8. Sly DL, London WT, Purcell RH: Illness in a chimpanzee inoculated with
hepatitis B virus. J Am Vet Med Assoc 175:987-988, 1979.

Yellow Fever

1. Birch CL: Jungle yellow fever. In Hull TG (ed): Diseases Transmitted
from Animal to Man. Edition 5. Springfield, Illinois Charles C Thomas,
1963, pp 792-811.
2. Kalter SS, Jeffried-Klitch H: Yellow fever vaccination of primates. Am J
Trop Med Hyg 18:466-469, 1969.

Simian Hemorrhagic Feoer

1. Allen AM, et al: Simian hemorrhagic fever. II. Studies on pathology. Am
J Trop Med Hyg 17:413-421 1968.
2. Espana C: Review of some outbreaks of viral disease in captive nonhuman
primates. Lab Anim Sci 21:1023-1031, 1971.
3. London WT: Simian hemorrhagic fever. In Goodwin WJ, Palmer A (eds):
Proceedings of the Workshop in the Clinical Care of Nonhuman Primates,
National Institutes of Health Bethesda, Maryland, 1973, pp 21-24.
4. Palmer AE, et al: Simian hemorrhagic fever. I. Clinical and epizootic
aspects of an outbreak among quarantined monkeys. Am J Trop Med Hyg
17:404-412, 1968.
5. Tauraso NM, et al: Simian hemorrhagic fever. II. Isolation and
characterization of a viral agent. Am J Trop Med Hyg 17:422-431, 1968.

SV 40 and Other Latent Viruses

1. Hsiung GD: Latent virus infections in primate tissues with special
reference to simian viruses. Bacteriol Rev 32:185-205, 1968.
2. Kalter SS, Heberling RL: Viral flora of tissue sources simian and human.
In NCI Monographs 29, Bethesda, Maryland, National Cancer Institute, 1968,
pp 149-160.
3. Kalter SS, Heberling RL: Comparative virology of primates. Bacteriol Rev
35:310-365, 1971.
4. Kissling RE, Murphy FA, Henderson BE: Marburg virus. Ann NY Acad Sci
174:932-915, 1970.
5. Levy JA, et al: Presence of EBV antibodies in sera from wild
chimpanzees. Nature 233 (5231):559-560, 1971.


1. Allmond BW Jr, Froeschle JE, Guilloud NB: Paralytic poliomyelitis in
larger laboratory primates: Virologic investigations and report on the use
of oral poliomyelitis virus (OPV) vaccine. Am J Epidemiol 85:229-239, 1967.
2. Guilloud NB, et al: Paralytic poliomyelitis in laboratory primates. J Am
Vet Med Assoc 155:1190-1193, 1969.


1. Diaz AMO: Pre-exposure rabies immunization of man with suckling mouse
brain vaccine. Am J Epidemiol 115:274-277, 1982.
2. Kaplan C: Rabies in nonhuman primates. Lab Anim Handbook, 4:117-118,
3. Richardson JH: Rabies in nonhuman primates. CDC Prim Zoon Surv Rep
5:18-20, 1970.
4. Richardson JH: Rabies in nonhllman primates. CDC Prim Zoon Surv Rep
5:14, 1971.

Marburg Virus

1. Gordon-Smith CE, et al: Fatal human disease from vervet monkeys. Lancet
2(7526):1119-1121, 1967.
2. Hennessen W: Epidemiology of Marburg virus disease. Lab Anim Handbook
4:137-142, 1970.
3. Marburg Virus Disease--South Africa. Morbid Mortal Weekly Rep 24:89-90,
4. Siegert R: Marburg virus. In Virology Monographs 11. New York,
Springer-Verlag, 1972, pp 97-153.


1. Allen AM, Kinard RF: Primary cutaneous inoculation tuberculosis in the
Macaca mulatta monkey. Am J Pathol 34:337-347, 1958.
2. Bellson RE, Femming BD, Young RJ: A tuberculosis outbreak in a Macaca
mulatta colony. Am Rev Tuberc Pulmon Dis 72:204-209, 1955.
3. Cappucci DT Jr, O Shea JL, Smith GD: An epidemiologic account of
tuberculosis transmitted from man to monkey. Am Rev Respir Dis 106:819-823,
4. Chaparas SD, et al: Comparison of the lymphocyte formation test with the
tuberculin test in rhesus monkeys and chimpanzees. Am J Vet Res
31:1437-1411, 1970.
5. Chrisp CE, et al: Tuberculosis in a squirrel monkey (Saimiri sciureus).
J Am Vet Med Assoc 153:918-922, 1968.
6. Christensen LR, et al: Suggested standard procedures for detection of
tuberculosis. ILAR News 10:3-5, 1967.
7. Clarke GL, Schmidt JP: Effect of prophylactic isoniazid on early
developing experimental tuberculosis in Macaca mulatta. Am Rev Respir Dis
100:224-227, 1967.
8. Fife EH, et al: Serodiagnosis of simian tuberculosis by soluble antigen
fluorescent antibody (SAFA) tests. Lab Anim Care 20:969-978, 1970.
9. Gibson JP, Rohovsky MW, Newberne JW: Modification of the tuberculin
response of rhesus monkeys by isoniazid therapy. Lah Anim Sci 21:62-66,
10. Hessler JR, Moreland AF: Pulmonary tuberculosis in a squirrel monkey
(Saimiri sciureus). J Am Vet Med Assoc 153:923-927, 1968.
11. Keeling ME, Froehlick RE, Ediger RD: An epizootic of tuberculosis in a
rhesus monkey conditioning colony. Lab Anim Care 19:629-634, 1969.
12. Kehoe M, Phin CS, Chu CL: Tuberculosis in an orangutan. Aust Vet J
61:128, 1984.
13. Martin JE, Cole WC, Whitney RA: Tuberculosis of the spine (Pott's
disease) in a rhesus monkey (Macaca mulatta). J Am Vet Med Assoc
153:914-917, 1968.
14. Middlebrook G: The mycobacteria. In Dubos RJ, Hirsch JG (eds):
Bacterial and Mycotic Infections of Man. Edition 4. Philadelphia, JB
Lippincott Co, 1965, pp 510-511.
15. Moreland AF: Tuberculosis in New World primates. Lab Anim Care
20:262-264, 1970.
16. Peters JH, Gordon GR: Susceptibility of squirrel monkeys to the
convulsant action of isoniazid. Lab Prim Newsletter 10:1-3, 1971.
17. Rao AT, Acharjyo LN, Nayak BC: Tuberculosis in some ungulates and
primates at Nandankanan Biological Park. Indian J Pathol Microbiol
25:199-202, 1982.
18. Renquist DM, Potkay S: Mycobacterium scrofulaceum infection in E. patas
monkeys. Lab Anim Sci 29:97-101, 1979.
19. Riordan JT: Rectal tuberculosis in monkeys from the use of contaminated
thermometers. J Infect Dis 73:93-94, 1943.
20. Sedgewick CS, Parher J, Durham R: Atypical mycobacterial infection in
the pig-tailed macaque. J Am Vet Med Assoc 157:724-725, 1970.
21. Sibinovic S: Tuberculin testing in monkeys (Macaca mulatta) with
naturally occurring tuberculosis. Lab Anim Care 19:621-632, 1969.
22. Smith AW, Wolochow H: Comparison of old tuberculin and purified protein
derivative in Macaca mulatta. Lab Anim Sci 23:3, 1973.
23. Smith EK, et al: Avian tuberculosis in monkeys. Am Rev Respir Dis
107:469-471, 1973.
24. Snyder S, Peace R, Soave O: Tuberculosis in an owl monkey (Aotus
triuirgatus). J Am Vet Med Assoc 1 i7:712-713, 1970.
25. Thorel MF: Isolation of Mycobacterium africanum from monkeys. Tubercle
61:101-104, 1980.

Mycobacterium leprae

1. Hasstad HV: Leprosy in sub-human primates: Potential risk for transfer
of M. leprae to humans. Int J Zoonoses 10:127-131, 1983.
2. Walsh GP, Meyers WM, Binford CH, et al: Leprosy: A zoonosis. Lepr Rev
52(suppl 1):77-83, 1981.
3. Walsh GP, Meyers WM, Brown HL, Binford CH, Gerone PJ, Wolfe RH:
Naturally acquired leprosy in a mangabey monkey Cercocebus-Sp. (abstract).
Annual Meeting of the American Society of Microbiologists, 1981, p 34.

Mycobacterium simiae

1. Boisvert H, Truffot C: Mycobacterium simiae in Africa (summary). Ann
Microbiol 131A:98, 1980.

Shigellosis and Salmonellosis

1. Surveillance of Enteric Disease. CDC Prim Zoon Surv Rep 4:1-5, 1971.
2. Good RC, May BD, Kawatomari T: Enteric pathogens in monkeys. J Bacteriol
97:1048-1055, 1969.
3. Mulder JB: Shigellosis in nonhuman primates: A review. Lab Anim Sci
21:734-738, 1971.
4. Schneider NJ: Enteric bacteriological studies in a large colony of
primates. Ann NY Acad Sci 85:935-941, 1980.
5. Weil JD, Ward MK, Spertzel RO: Incidence of Shigella in conditioned
rhesus monkeys (Macaca mulatta). Lab Anim Sci 21:4, 1971.
6. Yeary RA: Furazolidone: The therapeutic use of furazolidone to control
an epidemic of shigellosis in monkeys (Macaca mulatta). Proc Care Panel
10:83-84, 1960.

Other Bacterial Infections

1. Benjamin SA, Lang CM: Acute pasteurellosis in owl monkeys (Aotus
trivirgatus). Lab Anim Sci 21:258-262, 1971.
2. Anusz Z: Brucellosis and other zoonoses. Przegl Epidemiol (Warsaw)
34:111-117, 1980.
3. Good RC, May BD: Respiratory pathogens in monkeys. Infect Immun 3:87-93,
4. Greenstein ET, Doty RW, Lowy K: An outbreak of fulminate infectious
disease in the squirrel monkey (Saimiri sciureus). Lab Anim 15:74-79, 1965.
5. Fear FA, et al: Leptospirosis in a baboon (Papio sp.) colony. Lab Anim
Care 18:22-28, 1968.
6. Krushak DH, Zimmerman RA, Murphy BL: Induced group A hemolytic
streptococci infection in chimpanzees. J Am Vet Med Assoc 157:742-744,
7. Lott Stolz G: Yersinia pseudotuberculosis infection in pets. Publication
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11. Shewen PE: Chlamydial infection in animals: A review. Can Vet J
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13. Siebold HR, Perrin EA, Garner AC: Pneumonia associated with Bordatella
bronchiseptica in Callicebus spp. primates. Lab Anim 20:456-461, 1970.
14. Strauss JM, et al: Melioidosis with spontaneous remission of
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15. Shane SM, Montrose MS: The occurrence and significance of Campylobacter
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17. Tribe GW, Flemins MP: Biphasic enteritis in imported cynomolgus (Macaca
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18. Wilson CD, Salt GF: Streptococci in animal disease. Soc Appl Bacteriol
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Fungal Diseases

1. Al-Doory T, et al: Pulmonary nocardiosis in a vervet monkey. J Am Vet
Assoc 155:1179-1180, 1969.
2. Gerner FM, Ford DF, Ross MA: Systemic cryptococcosis in two monkeys. J
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3. Hironaga M, Fujigaki T, Watanabe S: Trichophyton mentagrophytes skin
infections in laboratory animals as a cause of zoonosis. Mycopathologia
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4. Kaplan W: Dermatophilosis in primates. In Lloyd DH, Sellers KC (eds):
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5. King NW, et al: Cutaneous streptothricosis (dermatophiliasis) in owl
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6. Martin JE, et al: Rhino-orbital phycomycosis in a rhesus monkey (Macaca
mulatta). J Am Vet Med Assoc 155:1253-1257, 1969.
7. McKenney FD, Traum J, Bonestall AE: Acute coccidioidomycoses in a
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Parasites: General

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4. Hira PR: Some helminthozoonotic infections in Zambia. African J Med Sci
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5. Kunz RE (ed): Nonhuman primate parasites. Lah Anim Care 20(2):1970.


1. Chin W, et al: A naturally acquired quotidian-type malaria in man
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transmissible to man. Science, 142:676, 1963.
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recent cases. Southeast Asian J Trop Med Public Health 12:444, 1981.
5. Mak JW, Cheons WH, Yen PKF, et al: Studies on the epidemiology of
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6. Kalra NL: Emergence of malaria zoonosis of simian origin as natural
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7. Tsukamoto M: Simian malarias as zoonoses: A review of cases of human
infection. J Uoeh (Japan) 1:515-534, 1979.
8. Warren M: Simian and anthropoid malarias: Their role in human disease.
Lab Anim Care 20:368-376, 1970.
9. Young MD: Natural and induced malarias in Western Hemisphere monkeys.
Lab Anim Care 20:361-367. 1970.

Other Protozoa

1. Bullock BC, Wolf RH, Clarkson TB: Myocarditis associated with
trypanosomiasis in a cebus monkey (Cebus albifrons). J Am Vet Med Assoc
151:920-922, 1967.
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Lab Anim Care 20:377-382, 1970.
5. Lushbaush WB, Pittman FE: Amebiasis. In Jacobs L, Arambulo P (eds): CRC
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6. Siebold HR, Wolf RH: Toxoplasmosis in Aotus trivirgatus and Callicebus
moloch. Lab Anim Sci 21:118-120. 1971.

Helminth Parasites

1. Asrawal MC, Shah HL: Stephanofilarial dermatitis in India. Vet Res
Commun 8:93-102, 1984.
2. Bingham GA, Rabstein MM: A study of thiabendazole in the rhesus monkey.
Lab Anim Care 14:357, 1964.
3. Brown RJ: Acanthocephalin myositis in a bushbaby. J Am Vet Med Assoc
155:1141-1143, 1969.
4. Eberhard ML: Intestinal parasitism in an outdoor breeding colony of
Macaca mulatta. Lab Anim Sci 31:282-285, 1981.
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6. Cosgrove GE: The trematodes of laboratory primates. Lab Anim Care
16:23-29, 1966.
7. Deinhardt F, et al: Marmosets as laboratory animals. IV. The
microbiology of laboratory kept marmosets. Lab Anim Care 17:48-70, 1967.
8. Else JG, Satzger M, Sturrock RF: Natural infections of Schistosoma
Mansoni and S. Haematobium in Cercopithecus monkeys in Kenya. Ann Trop Med
Parasitol 76:111-112, 1982.
9. Fauran P, Lacoste J, Combes D, et al: Wuchereria bancrofti human
aperiodic filariasis in French territory of Wallis and Futuna. Med Trop
(Marseille) 41:665-669, 1981.
10. Fox JG, Hall WC: Fluke (Gastrodiscoides hominis) in a rhesus monkey
with related intussusception of the colon. J Am Vet Med Assoc 157:714-716,
11. Graham GL: Parasitism in monkeys from care and diseases of the research
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12. Hira PR: Some helminth zoonotic infections in Zambia. Afr J Med Sci
7:1-8, 1978.
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primates. In Parasites: Their World and Ours. Amsterdam, Elsevier, 1982, pp
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cause of fatal central nervous system disease in subhuman primates. J Am
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15. Middleton CC: Acanthocephala (Prosthenorchus elegans) infection in
squirrel monkeys (Saimiri sciureus). Lab Anim Dis 2:16-17, 1966.
16. Moore JC: Epizootic of acanthocephaliasis among primates. J Am Vet Med
Assoc 157:699-705, 1970.
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Tarnarinus nigricollis. Lab Anim Care 16:255-275, 1966.
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Arthropod Parasites

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Med Assoc 155:1233-1235, 1969.
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Human Disease and Its Treatment

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Saturday, 28 July 2007

Three million procedures were carried out.

United Kingdom Review ordered on lab test labels

The British Union for the Abolition of Vivisection (Buav) claimed that the licences underplayed the severity of suffering that the animals experienced.

Buav complained about experiments on marmosets
The licences given to scientists that allow them to carry out experiments on animals are being mislabelled, according to a High Court ruling.

The High Court found for Buav on this ground, but rejected three other claims brought by the campaign group.

The Home Office has been granted leave to appeal against the decision.

If it is unsuccessful, the government will have to re-examine the way it classifies the severity of lab animal tests.

We have proven that the government misleads the public and parliament about the severity of animal experiments licensed in the UK

Michelle Thew, Buav

The ruling followed a judicial review that took place earlier this week.

It was prompted by a 10-month investigation carried out by Buav at Cambridge University in 2000-2001.

Lost grounds

The campaigning group said that experiments that had been taking place on marmosets were causing far more suffering than their licence implied.

The Home Office grants licences for all experiments carried out in the UK that involve animals.

The Home Office issues licences for animal research
Each licence is categorised as "mild", "moderate", "substantial" or "unclassified" (meaning the animal is under anaesthetic). This is based on the likely experience of the "average" animal in the experiment.

The licence for the marmoset research was classified as moderate, but Buav argued that the experiments should have been classed as severe, leading the group to call for a judicial review, stating that the Home Office was failing to ensure animal suffering was kept to a minimum.

The High Court ruled that Buav was correct in stating that the government was failing to correctly determine the severity limits for animal experiments.

However, it rejected three other grounds the campaigning group put forward: on the fact that animal death should be labelled as an "adverse effect", a technical notice that failed to follow correct legislative procedure, and failings on post-operative care.

'Misleading the public'

Buav chief executive Michelle Thew said: "We have proven that the government misleads the public and Parliament about the severity of animal experiments licensed in the UK.

The Home Office is obviously disappointed not to have successfully defended all of the grounds of claim

A Home Office spokesperson
"The government can no longer pretend it has the strictest regulation of animal experiments in the world. This case demonstrates it has ridden roughshod over the public's trust in this matter."

A Home Office spokesperson said: "The Home Office is obviously disappointed not to have successfully defended all of the grounds of claim, and has been granted leave to appeal against the decisions in the instances where the judge had found in favour of Buav.

"The Home Office believes it has been rigorous in applying the strict criteria of the Animals (Scientific Procedures) Act 1986 with a view to making proper provision for the protection of animals used for experimental and other scientific purposes."

Rising statistics

This week, the Home Office announced its official figures on animal tests.

A total of three million procedures were carried out on animals in 2006, a rise of 4% on the previous year.

Scientists said tests were necessary to help cure life-threatening diseases; however antivivisectionists said the rise was too high.

In 2003, the Chief Inspector of the Animals (Scientific Procedures) Inspectorate rejected the notion that Cambridge University had breached its licence when it considered Buav's complaints.

The inspector's inquiry found that the severity levels of the procedures had been correctly assigned; and concluded that "nothing seriously untoward has been discovered about the licensing and running of these projects".

Thursday, 5 July 2007

Orang-utans are clever

Orang-utans are clever enough to use water as a problem-solving tool, an experiment inspired by Aesop's fables has demonstrated.

When presented with a peanut floating deep down inside a transparent tube, the animals spat their drinking water into the tube to raise the treat to the top, where they could grab it. Researchers say that the study is novel because it shows the insightful use of a liquid tool by a non-human primate.

Natacha Mendes at the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, recalls that the idea for the study came out of a discussion with her colleagues about Aesop's fables.

The team focused on one particular story, in which a clever crow throws stones into a pitcher to elevate the water to a level where the bird can access it for drinking. Mendes and her fellow researchers wondered whether the orang-utans they worked with could have a similarly smart insight.

Speedy learning
To test this out, the scientists presented five orang-utans (Pongo abelii) with clear plastic tubes, each containing a small amount of water along with a peanut. But, to the orang-utans' great dismay, the peanuts floated too far down the tube for them to reach.

The frustrated apes tried everything they could to get to the peanuts – including biting, hitting, and kicking the tube.

It only took them about nine minutes on average, though, to figure out that a little bit of extra water could do the trick. At this point the orang-utans began taking mouthfuls of water from their drink dispenser and spitting the liquid into the tube, a trick that elevated the peanuts to an accessible point.

"This seems to be insightful behaviour because they haven't seen this test before," Mendes explains. "And as soon as they got the idea they continued to do it."

And do it faster, Mendes adds. She presented each orang-utan with the peanut-containing tube 10 times. By the tenth attempt, it took the animals only 30 seconds before they started spitting water into the tube.

Intelligent spitting
Researchers also conducted control experiments, including one in which they taped the peanut to the top of the tube. The orang-utans did not spit into the tube, but instead simply grabbed the treat with their hands.

Mendes notes that archer fish (Toxotes jaculatrix) can spit water at flies to knock them into the water for eating (see Fast food for fish with perfect aim). But she says the orang-utans' use of water represents a more sophisticated behaviour.

"There's no comparison," she says, pointing out that the apes have a conscious idea of what they are doing and consider other options, such as kicking the tube. "With orang-utans we are talking about a flexible strategy – that's the big difference."

Journal reference: Biology Letters (DOI: 10.1098/rsbl.2007.0198)