SEROLOGIC EVIDENCE OF INFECTION WITH LYMPHOCYTIC CHORIOMENINGITIS VIRUS, THE AGENT OF CALLITRICHID HEPATITIS, IN PRIMATES IN ZOOS, PRIMATE RESEARCH CENTERS, AND A NATURAL RESERVE

Callitrichid hepatitis (CH) occurs in sporadic epizootics in marmosets and tamarins in zoos and animal parks. This disease is caused by acci dental infection of callitrichids with an arenavirus, lymphocytic chor iomeningitis virus (LCMV), derived from persistently infected murine r eservoirs. In callitrichids, LCMV infection is associated with a high case/fatality ratio, The rate of LCMV exposure of callitrichids and ot her nonhuman primates in 31 zoos and animal parks, 6 primate research centers, and a wild golden lion tamarin (Leontopithecus rosalia) reser ve in Brazil was determined by detection of LCMV-specific antibody usi ng a solid-phase immunoassay. Sera from 15 New World and 12 Old World primate species were tested, and 33 of 730 animals (4.5%) were LCMV se ropositive. These seropositive animals were all located at 10 domestic zoos and animal parks; 32/33 (97.0%) of the animals were housed at, o r transferred from, locations that had experienced CH outbreaks. Three of the seropositive animals (9.1%) had a clinical history of CH. Amon g the golden lion tamarins in zoos, 11 of 88 (12.5%) were seropositive for LCMV. None of the sera from 211 primates in the primate research centers and the golden lion tamarin reserve had detectable LCMV antibo dies. Our data demonstrate that rates of LCMV infection differ among p rimate species and among primates maintained under different condition s. The data indicate that Callitrichidae are highly susceptible to LCM V infection, often resulting in fatal hepatitis. Consequently, the com mon practice of feeding neonatal mice to nonhuman primates should be d iscontinued, and wild mice should be eradicated from cages housing cal litrichids because of the risk that the mice may have inapparent LCMV infections.