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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. 
         
        PRIMATES SEEN AS PETS 
         
        APES
         
        
             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. 
         
        OLD WORLD MONKEYS
         
             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
        pet. 
        
             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. 
         
        NEW WORLD MONKEYS
         
        
             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. 
         
        LOWER PRIMATES (PROSIMIANS)
         
        
             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. 
         
        ZOONOTIC DISEASES 
         
        
             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
        man. 
         
        VIRAL DISEASES
         
        
             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
        disease. 
        
             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 
        disease. 
        
             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
        popularity 
        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
        infection 
        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
        infected. 
        
             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.
         
        BACTERIAL DISEASES
         
        
             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
        information. 
        
             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
        shigellosis. 
        
             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
        surface.
        
             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
        entity.
        
             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.
        
        FUNGAL DISEASE
        
        
             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
        technician.
        
        
             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.
        
        PARASITIC DISEASES
        
        
             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.
        
        NEMATODES
        
        
             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
        owner.
        
             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.
        
        CESTODES
        
        
             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.
        
        ARTHROPODS
        
        
             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.
        
        SUMMARY
        
        
             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.
        
        SUGGESTED READINGS
        
        Zoonoses of Primates: General
        
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        Viruses: General
        
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        Herpesvirus
        
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        Herpesvirus simiae (B virus)
        
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        Herpesvirus tamarinus (Herpes T)
        
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        Herpesvirus hominis (simplex)
        
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        laboratory colony. J Infect Dis 129:292-297, 1969.
        
        Oncogenic Herpesviruses
        
        1. Daniel M, et al: Herpesrirus saimiri. VII. Induction of malignant
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        8. Melendez LV, et al: Herpesvirus saimiri. II. Experimentally induced
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        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.
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        monkeys (Cercopithecus aethiops) caused by a new herpesvirus. Arch Gesamte
        Virusforsch 22:219-234, 1967.
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        Poxviruses
        
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        Benign Epidermal Monkey Pox (BEMP)
        
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        epidermal pox disease of rhesus monkeys. Am J Pathol 51:431-446, 1967.
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        of monkeys. J Infect Dis 119:80-88, 1969.
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        causing epidemic disease in monkeys. J Hyg 70:23-32, 1972.
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        6. McNulty WP Jr, et al: A pox disease in monkeys transmitted to man.
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        Caliciviruses
        
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        Yaba Virus Disease
        
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        monkeys. Nature 182:195-196, 1958.
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        NY Acad Sci 108:1123-1128, 1963.
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        Molluscum contagiosum
        
        1. Douglas JE, et al: Molluscum contagiosum in chimpanzees. J Am Vet Med
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        2. Schmidt RE, Butler TM: Molluscum contagiosum in a colony born
        chimpanzee. Lab Prim Newsletter 10:17, 1971
        
        Measles
        
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        in monkeys experimentally infected. J Exp Med 33:413-422, 1921.
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        Viral Hepatitis
        
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        related to hepatitis associated antigen. J Infect Dis 125:382-389, 1972.
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        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
        
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        Simian Hemorrhagic Feoer
        
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        SV 40 and Other Latent Viruses
        
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        reference to simian viruses. Bacteriol Rev 32:185-205, 1968.
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        5. Levy JA, et al: Presence of EBV antibodies in sera from wild
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        Poliomyelitis
        
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        2. Guilloud NB, et al: Paralytic poliomyelitis in laboratory primates. J Am
        Vet Med Assoc 155:1190-1193, 1969.
        
        Rabies
        
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        1969.
        3. Richardson JH: Rabies in nonhuman primates. CDC Prim Zoon Surv Rep
        5:18-20, 1970.
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        Marburg Virus
        
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        3. Marburg Virus Disease--South Africa. Morbid Mortal Weekly Rep 24:89-90,
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        Springer-Verlag, 1972, pp 97-153.
        
        Tuberculosis
        
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        Macaca mulatta monkey. Am J Pathol 34:337-347, 1958.
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        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,
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        4. Chaparas SD, et al: Comparison of the lymphocyte formation test with the
        tuberculin test in rhesus monkeys and chimpanzees. Am J Vet Res
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        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.
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        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,
        1971.
        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,
        1971.
        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,
        1970.
        7. Lott Stolz G: Yersinia pseudotuberculosis infection in pets. Publication
        no D-6300. German Federal Republic, Ciessen-Lahn, 1978, pp 205-208.
        8. McClure HM, Weaver RE, Kaufman AF: Pseudotuberculosis in nonhuman
        primates: Infection with organisms of the Yersinia enterocolis group. Lab
        Anim Sci 21:376-382, 1971.
        9. Respiratory diseases. CDC Prim Zoon Surv Rep 4:5-6, 1971.
        10. Selbitz HJ, Elze K, Seifert S: Detection and clinical importance of
        human- and animal-pathogenic serotypes of Escherichia coli in monkeys.
        Berlin, German Democratic Republic, Akademie-Verlag, 1983, pp 275-279.
        11. Shewen PE: Chlamydial infection in animals: A review. Can Vet J
        21:2-11, 1980. 
        12. Shive RJ, et al: Leptospirosis in Barbary apes (Macaca syltana). J Am
        Vet Med Assoc 155:1176-1178, 1969.
        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
        osteomyelitis in a macaque. J Am Vet Med Assoc 155:1190-1193 1969.
        15. Shane SM, Montrose MS: The occurrence and significance of Campylobacter
        jejuni in man and animals. Vet Res Comm 9:67-198 1985.
        16. Tribe GW, Mackenzie PS, Flemins MP: Incidence of thermophilic
        Campylobacter species in newly imported simian primates with enteritis
        (correspondence). Vet Rec 105:333, 1979.
        17. Tribe GW, Flemins MP: Biphasic enteritis in imported cynomolgus (Macaca
        fascicularis) monkeys infected with Shigella, Salmonella and Campylobacter
        species. Lab Anim 17:65-69, 1983.
        18. Wilson CD, Salt GF: Streptococci in animal disease. Soc Appl Bacteriol
        Symp Ser 7:143-156, 1978.
        
        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
        Am Vet Med Assoc 155:1163-1169 1969.
        3. Hironaga M, Fujigaki T, Watanabe S: Trichophyton mentagrophytes skin
        infections in laboratory animals as a cause of zoonosis. Mycopathologia
        73:101-104, 1981.
        4. Kaplan W: Dermatophilosis in primates. In Lloyd DH, Sellers KC (eds):
        Dermatophilus Infection in Animals and Man. New York, Academic Press, 1976,
        pp 128-138.
        5. King NW, et al: Cutaneous streptothricosis (dermatophiliasis) in owl
        monkeys. Lab Anim Sci 21:67-74, 1971.
        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
        mountain gorilla. J Am Vet Med Assoc 112:244, 1948.
        8. Schmidt RE: Dermatomycosis. In Garner FM, Stookey JL (eds): AFIP
        Syllabus: Diseases of Nonhuman Primates. Washington, DC, American Registry
        of Pathology, AFIP, 1968, pp 20-21.
        9. Takos MJ, Elton NW: Spontaneous cryptococcosis of marmoset monkeys in
        Panama. AMA Arch Pathol 55:403-407, 1953.
        10. Wikse SE, Fox JC, Kovatch RM: Candidiasis in simian primates. Lab Anim
        Care 20:957-963, 1970.
        
        Parasites: General
        
        1. Flynn RJ: Parasites of laboratory animals. Ames, lowa State University
        Press, 1973.
        2. Goldsmith JM: The intestinal helminthzoonoses of primates (abstract). In
        The 9th International Congress on Tropical Medicine and Malaria. Volume 1.
        Athens, Greece, 1973, pp 157-158.
        3. Goldsmith JM: Intestinal helminthzoonoses of primates in Rhodesia. Ann
        Soc Belse Med Trop 54:87-101, 1974.
        4. Hira PR: Some helminthozoonotic infections in Zambia. African J Med Sci
        7:1-7, 1978.
        5. Kunz RE (ed): Nonhuman primate parasites. Lah Anim Care 20(2):1970.
        
        Malaria
        
        1. Chin W, et al: A naturally acquired quotidian-type malaria in man
        transferable to monkeys. Science 149:865, 1965.
        2. Coatney RG, et al: The primate malarias. Washington, DC, Department of
        Health, Education and Welfare, US Government Printing Office, 1971.
        3. Contacos P, et al: Quartan-type malaria parasite of New World monkeys
        transmissible to man. Science, 142:676, 1963.
        4. Collins WE: Simian malaria. In Jacobs L, Arambulo P (eds): CRC Handbook
        Series in Zoonoses. Section C: Parasitic Zoonoses. Volume I. Boca Raton,
        Florida, CRC Press, Inc, 1982, pp 141-150.
        4. Druilhe P, Trape JF, Gentilini M: Accidental human infections by
        Plasmodium-Cynomolgi-Bastianellii: A serological and clinical study of 2
        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
        subperiodic Brusia malayi in Malaysia: Problems in its control. Acta
        Tropica 39:237-245, 1982.
        6. Kalra NL: Emergence of malaria zoonosis of simian origin as natural
        phenomenon in Greater Nicobars, Andaman & Nicobar Islands: A preliminary
        note. J Comm Dis 12:49-54, 1980.
        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.
        2. Hiepe F, Hiepe T: Experimental infection of man and monkeys
        (Cercopithecus callithrichus) with sarcosporidian cysts from cattle and
        pigs. Arch Exp Veterinarmed 33:819-830, 1979.
        3. Jueco NL: Bertiella infection. In Jacobs L, Arambulo P (eds): CRC
        Handbook Series in Zoonoses. Section C: Parasitic Zoonoses. Volume I. Boca
        Raton, Florida, CRC Press, Inc, 1982, pp 215-216.
        4. Levine ND: Protozoan parasites of nonhuman primates as zoonotic agents.
        Lab Anim Care 20:377-382, 1970.
        5. Lushbaush WB, Pittman FE: Amebiasis. In Jacobs L, Arambulo P (eds): CRC
        Handbook Series in Zoonoses. Section C: Parasitic Zoonoses. Volume I. Boca
        Raton, Florida, CRC Press, Inc, 1982, pp 5-13.
        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.
        5. Clark JD: Coenuris in a gelada baboon. J Am Vet Med Assoc 155:1258-1263,
        1969.
        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,
        1970.
        11. Graham GL: Parasitism in monkeys from care and diseases of the research
        monkey. Ann NY Acad Sci 85:842-860, 1960.
        12. Hira PR: Some helminth zoonotic infections in Zambia. Afr J Med Sci
        7:1-8, 1978.
        13. Kazacos KR, Vestre WA, Kazacos EA: Experimental ocular larva migrans
        and cerebrospinal nematodiasis due to Baylisascaris-Procyonis in subhuman
        primates. In Parasites: Their World and Ours. Amsterdam, Elsevier, 1982, pp
        261-262.
        14. Kazacos KR, Wirtz WL, Burger PP, et al: Raccoon ascarid larvae as a
        cause of fatal central nervous system disease in subhuman primates. J Am
        Vet Med Assoc 179:1089-1094, 1981.
        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.
        17. Nelson B, Cosgrove C, Gengozian N: Diseases of an imported primate,
        Tarnarinus nigricollis. Lab Anim Care 16:255-275, 1966.
        18. Nelson GS: Wild animals as reservoir hosts of parasitic diseases of man
        in Kenya. In Dunsmore JDJ (ed): Tropical Parasitoses and Parasitic
        Zoonoses. Perth, Australia, World Association for the Advancement of
        Veterinary Parasitology, 1983, pp 59-72.
        19. Orihel TC: The helminth parasites of nonhuman primates and man. Lab
        Anim Care 20:395-401, 1970.
        20. Simmons CF Jr, Winter HS, Berde C, et al: Zoonotic filariasis with
        Iymphedema in an immunodeficient infant. N Engl J Med 310:1243-1245, 1984.
        21. Van Riper D, et al: Intestinal parasites of recently imported
        chimpanzees. Lab Anim Care 16:360-363, 1966.
        22. Varela-Diaz VM, Coltorti EA, Zavaleta O de, et al: Immunodiagnosis of
        human hydatid disease: Applications and contributions to a control program
        in Argentina. Am J Trop Med Hyg 32: 1079-1087, 1983.
        23. Vickers JH, Penner LR: Cysticercosis in four rhesus brains. J Am Vet
        Med Assoc 153:868-871, 1968.
        
        Arthropod Parasites
        
        1. Flatt RE, Patton NM: A mite infestation in squirrel monkeys. J Am Vet
        Med Assoc 155:1233-1235, 1969.
        2. Hull WB: Respiratory mite parasites in nonhuman primates. Lab Anim Care
        20:354-360, 1970.
        3. Peddle JG, Larson EJ: Demodectic acariasis in a woolly monkey. Vet Med
        Small Anim Clin 66:485-488, 1971.
        4. Schwartz LW: Pulmonary acariasis. In Garner FM, Stookey JL (eds): AFIP
        Syllabus: Diseases of Nonhuman Primates. Washington, DC, American Registry
        of Pathology, AFIP, 1968, pp 51-52.
        
        Human Disease and Its Treatment
        
        1. Berkow R (ed): The Merck Manual of Diagnosis and Therapy. Edition 14.
        Rahway, New Jersey, Merck Sharp & Dohme Research Laboratories, 1982.