BULLETIN FLORIDA STATE MUSEUM VOL. 33(4)


range. Lembeck (1978, 1986) and Gould (1980) recorded confirmed deaths of
bobcats from FPLV in California. In an unharvested population studied by
Lembeck (1986) from 1976 to 1982, 11 of 22 deaths from known, non
study-related causes resulted from natural causes, and five of these were
attributable to panleucopenia. FPLV was the probable cause of death of two
of five radio-collared bobcats in a study on the Savannah River Plant, South
Carolina (Griffith and Fendley 1986). Fox (1983) concluded that feline
panleukopenia was probably an important cause of bobcat mortality in New
York based upon diagnosed cases of the disease in the Adirondack and Catskill
mountains and a relatively high (21%) prevalence of FPLV antibodies in a
statewide sample of bobcats.
 Our data suggest that FPLV could have been transmitted indirectly through
 contaminated feces or urine (Csiza et al. 1971), as well as by actual contact
 between animals. Bobcat marking with exposed scats was most frequent
 during winter, and bobcats were known to visit each other's marking sites.
 Bouillant and Hanson (1965) found that healthy mink (Mustela vison) who
 received stomach inoculations of 20% suspended feces passed by animals
 experimentally infected with mink enteritis virus (MEV) developed clinical
 symptoms of MEV, even when carrier feces were half-buried for several
 months during cold, damp weather, which favored survival of the virus. The
 winter of 1979-1980 in south-central Florida was relatively cool and wet. These
 facts suggest that bobcats might become infected through investigating
 contaminated feces and that weather conditions could influence the probability
 of an outbreak by affecting survival of the virus. The higher incidence of FPLV
 mortality in males than females suggested by our data may reflect the larger
 home range size of males (see below), which might increase their probability of
 contacting infected animals and/or feces. Further, FPLV infections occurred
 during the peak period of marking, which might also have increased chances of
 virus transmission.
 In addition to being a cause of death of young or adult bobcats, FPLV may
 also kill embryos or fetuses of pregnant females with a sublethal infection
 (Povey and Davis 1977). It may be significant in this connection that female
 Fl, believed to have had a sublethal infection during winter 1979-80, produced
 only two young in her first litter following this period, whereas her two
 previous litters and subsequent two litters numbered three, four, and five, four,
 respectively. In addition, F4, also suspected of having a sublethal infection, was
 the only collared female in the population who did not rear a litter in the year
 following the epizootic.
 Although FPLV was probably spread through the bobcat population by
contact with infected individuals or contaminated feces, other potential vectors,
including free-ranging domestic cats (Felis catus) and raccoons (Procyon lotor),
were present in the study area. Feline panleukopenia is common in domestic
cats throughout the United States, and Goss (1948) reported that raccoons are