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Neutralization tests were done on sera from 141 horses from high elevation regions of California. Antibody prevalences to Jamestown Canyon, snowshoe hare, and California encephalitis viruses in the California serogroup and Northway virus in the Bunyamwera serogroup were 55%, 43%, 18%, and 46%, respectively. In 51 horses from rural low elevation regions, seroprevalences were 31%, 35%, 35%, and 37%, respectively. Twenty-four horses from a suburban lowland area were seronegative, except for a single horse with a low titer to snowshoe hare virus. Seroprevalence to Jamestown Canyon and snowshoe hare viruses was associated with increasing age. Only 2 of 177 rodents from the Sierra Nevada had antibodies to Northway virus; none had antibodies to Jamestown Canyon or snowshoe hare viruses.

From 1983 to 1985, 463 serum samples from 11 species of mammals in Redwood National Park (RNP) (California, USA) were evaluated for antibodies to Yersinia pestis by the passive hemagglutination method. Yersinia pestis antibodies occurred in serum samples from 25 (36%) of 69 black bears (Ursus americanus), one (50%) of two raccoons (Procyon lotor), five (3%) of 170 dusky-footed woodrats (Neotoma fuscipes), and one (less than 1%) of 118 deer mice (Peromyscus maniculatus). Two hundred seventy-three flea pools, consisting of 14 species of fleas, were collected from small mammals and woodrat nest cups. Viable Y. pestis were not isolated from any of the flea pools. Significant between-year variations in the frequencies of seropositive bear or small mammal sera were not observed. A significantly higher frequency of plague antibodies was observed in bear sera taken during September collections. Frequencies of seropositive bear sera did not vary significantly by sex or age group of bears. Significant differences were not observed in the frequencies of seropositive small mammals by forest habitat type in which they were captured. This is the first report of Y. pestis infection in Redwood National Park, and the first detailed report of Y. pestis activity in a temperate rainforest.

Approximately 20% of normal male and female feral mice (Mus musculus) from areas with populations having either high [Lake Casitas (LC) and La Puente] or low (Bouquet Canyon) spontaneous lymphoma incidence expressed murine mammary tumor virus (MuMTV) gp52 in specific tissues. Sera from a low percentage (6%) of mice from the same trapping areas contained precipitating antibody specific for MuMTV. Although moderate to high levels of MuMTV gp52 were expressed in mammary tumor tissues of 3 of 7 LC mice and 3 of 3 (C57BL/10ScSn X LC)F1 mice, the same animals showed no detectable MuMTV-precipitating antibody. Neither MuMTV antibody nor tumor-associated MuMTV gp52 was defected in 10 LC mice bearing lymphomas or in 5 LC mice bearing hepatomas. Low levels of MuMTV gp52 expression and MuMTV antibody were also detected in subspecies of M. musculus and in the more distantly related species M. cervicolar. Compared with normal and tumor-bearing inbred mice of high (C3H/HeN) and low (C3H/HeN foster-nursed on NIH Swiss) mammary tumor strains, normal and tumor-bearing feral mice express MuMTV gp52 and MuMTV-precipitating antibodies at low frequency.

Six species of rodents from Kern County, California, were inoculated subcutaneously with western equine encephalomyelitis (WEE) virus to determine their susceptibility to infection and their potential as natural hosts. Ammospermophilus nelsoni, Citellus beecheyi, Dipodomys heermanni, Dipodomys nitratoides, Peromyscus maniculatus, and Sciurus griseus were readily infected. Infection was usually fatal in Dipodomys species, C. beecheyi, and S. griseus, but was clinically inapparent in other species. Viremic responses varied greatly in magnitude and duration in different species and with different viral strains. Viremic animals that survived developed high titers of hemagglutination-inhibiting antibody. Hemagglutination-inhibiting and neutralizing antibodies persisted at high titers for at least 8 to 58 weeks after infection, except in P. maniculatus. If animals died during or shortly after the viremic phase of infection, the virus usually was recoverable from numerous organs. Long-term survival of virus could not be demonstrated in A. nelsoni and Dipodomys species. It is concluded that A. nelsoni and P. maniculatus are not important natural hosts of WEE virus; they are susceptible to infection and develop antibodies, but serological surveys of the same species rarely reveal evidence of infection. S. griseus, D. heermanni, D. nitratoides, and possibly C. beecheyi are aberrant hosts of WEE virus since most of them died when infected. Two species of ticks that are ectoparasitic on rodents in Kern County were evaluated as vectors of WEE virus. Dermacentor parumapertus failed to become infected after feeding on viremic hosts, and Ornithodorus parkeri became infected but failed to transmit virus.