A number of herpesviruses affect nonhuman primates; many exist as latent or subclinical infections in reservoir hosts but cause severe disease or death when transmitted naturally to other hosts. All macaques are considered to be potential shedders of Cercopithecine herpesvirus type 1 (Herpesvirus simiae, B virus). The infection is generally subclinical or mild (conjunctivitis or oral vesicles) in Macaca spp but usually causes a fatal encephalitis and encephalomyelitis in people. Transmission may occur via a bite, scratch, or contamination of a superficial wound or mucous membranes (eg, conjunctiva) with infectious saliva, conjunctival secretion, or genitourinary secretions. Human fatalities due to B virus encephalitis illustrate the importance of using appropriate precautions and personal protective equipment to prevent direct or indirect contact with macaque secretions and body fluids. Captive-born and raised animals should still be screened when first presented in a clinical setting and subsequently every year afterward in a private facility.
Saimiriine herpesvirus type 1 (herpesvirus T) causes mild herpetic lingual ulcers and stomatitis in squirrel monkeys, but fatal epizootics have followed natural transmission to owl monkeys and marmosets. The human herpesvirus, herpes simplex virus type 1, causes a mild infection in people and certain other primates, but owl monkeys, gibbons, capuchins, and tree shrews (Tupaia glis) are highly susceptible and may die; signs may include ulcerations of the mucous membrane or skin, conjunctivitis, meningitis, or encephalitis. Human caretakers with oral lesions should be replaced until the infection regresses, and any interaction with the public should be discouraged.
Naturally occurring, clinically silent infections of hepatitis A virus (enterically transmitted hepatitis virus) have been seen in chimpanzees (Pan troglodytes) and monkeys. Increased AST and ALT values are of diagnostic significance in nonhuman primates. Human infections have been contracted from chimpanzees.
Because some vaccines are not available to protect nonhuman primate colony personnel or the primates against herpes and some viral hepatitis infections, exposure should be prevented. This is best accomplished by carefully training personnel in the handling of nonhuman primates, using personal protective equipment (clothing, face masks, goggles or shields, and gloves), separating primates in species-specific rooms, and paying strict attention to hygienic standards. In private facilities, prescreening the primates by serologic and PCR testing is recommended.
Several other viruses commonly produce clinical disease in newly imported primates. Rubeola infection (measles) acquired via human contact can assume epizootic proportions. The virus causes a nonpruritic, exanthematous rash on the face, chest, and lower portions of the body; it may also cause interstitial giant-cell pneumonia, rhinitis, conjunctivitis, and, particularly in New World monkeys, gastroenteritis. Marmosets are extremely susceptible, and children, especially, should not be encouraged to interact with this species. There is no specific treatment. Vaccination of infant rhesus monkeys and other macaques with human measles vaccine is recommended. Modified-live measles vaccine can cause disease in marmosets and is not recommended. Monkeypox and other poxvirus infections may be seen in primate colonies. Monkeypox is a reportable, zoonotic disease characterized by a maculopapular rash and variolous pustules (see Zoonotic Diseases). Affected monkeys usually survive; after recovery, they are immune to challenge.
Immunosuppressive disease in nonhuman primates may be caused by a number of retroviruses, including several orthoretroviruses formerly called type C and type D oncornaviruses, and several simian immunodeficiency viruses (SIV). The SIV are lentiviruses closely related to human immunodeficiency virus 1 (HIV-1) and HIV-2. Unique isolates have been found in different species of nonhuman primates. SIV are of low pathogenicity in the natural hosts, African species, and infections are often clinically silent but may cause devastating disease similar to AIDS in macaques after cross-species transmission. SIV has been demonstrated to infect people, although the longterm consequences of infection are unknown. Infection with orthoretroviruses in the genus Betaretrovirus (formerly the type D retroviruses SRV, 5 serotypes) may cause an immunodeficiency predisposing to a complex of diseases such as fibromatosis, atypical mycobacteriosis, intestinal cryptosporidiosis, pneumocystic pneumonia, disseminated cytomegalovirus infection, and candidiasis in colonies of macaques. Infection with oncornaviruses in the genus Deltaretrovirus (formerly Type C retrovirus) results primarily in lymphoproliferative disease, and rarely T-cell lymphoma, in Old World monkeys and apes. There is great host-interspecies variation in clinical signs and susceptibility from virus to virus. Transmission between nonhuman primates is via direct or indirect contact with infected blood and other body fluids or from dam to offspring.
Hemorrhagic viral zoonoses, such as Ebola, Marburg, and mosquito-borne yellow fever, are risks with wild-caught animals. An important differential diagnosis for these zoonoses is simian hemorrhagic fever. This Arterivirus infection is subclinical in African monkeys but is highly contagious and fatal for Asian species. Hemorrhagic necrosis of the proximal duodenum is a pathognomonic lesion. Captive populations that ultimately are housed in private facilities are a low risk.
Last full review/revision August 2014 by Terri Parrott, DVM