Serum samples obtained from 38 free-ranging Florida panthers (Felis concolor coryi) in southern Florida, March 1978 through February 1991, were tested for antibodies against eight bacterial, parasitic, and viral disease agents. Sera were positive for antibodies against feline panleukopenia virus (FPV) (78%), feline calicivirus (56%), feline immunodeficiency virus/puma lentivirus (37%), feline enteric coronavirus/feline infectious peritonitis virus (19%), and Toxoplasma gondii (9%). All samples were seronegative for Brucella spp., feline rhinotracheitis virus, and pseudorabies virus. In addition, all the animals tested were negative for feline leukemia virus p27 antigen as determined by enzyme-linked immunosorbent assay. Feline panleukopenia virus was considered to be a potentially significant disease agent; FPV antibodies occurred in the highest prevalences in older age classes (P = 0.027) and in panthers living in the dense mixed hardwood swamps in the western portion of their range compared to the open cypress and sawgrass prairies to the east (P = 0.096). Because < 50 animals remain in this relict population and the probable resultant depression of genetic diversity and lowered disease resistance, FPV or other disease agents could contribute to the extinction of this endangered subspecies.

We have previously demonstrated antibody-dependent enhancement of feline infectious peritonitis virus (FIPV) infection of macrophages using both virus-specific antisera and monoclonal antibodies (MAbs) to the spike (S) protein of FIPV. To increase our understanding of this phenomenon, six representative MAbs from a previously documented group of 12 enhancing MAbs were used to identify epitopes that mediate antibodydependent enhancement of FIPV infectivity. Analysis of the results of kinetics-based competitive ELISA (KcELISA) among these six enhancing MAbs grouped the epitopes into two clusters. Because transmissible gastroenteritis virus (TGEV) and FIPV are so closely related antigenically, we also conducted K-cELISA experiments between the FIPV MAbs and TGEV S protein-specific MAbs for which the epitopes had previously been mapped to specific sites on the TGEV S protein. Results of these assays indicated that the two FIPV epitope clusters are homologues of the previously defined TGEV S protein sites A and E/F. In addition, two TGEV S protein-specific MAbs also induced antibody-dependent enhancement of FIPV infection of macrophages. This functional cross-reactivity provides further support for the close antigenic relationship between FIPV and TGEV. Our results provide a preliminary localization of several enhancing epitopes within the amino acid sequence of the FIPV S protein.

Multiple congenital malformations occurred in kittens of three cats treated orally at weekly intervals with 500-1000 mg of the antifungal drug griseofulin. Malformations of the brain included exencephaly, malformed prosencephalon, caudal displacement, and hydrocephalus. Skeletal malformations included cranium bifidium, spina bifida (C1 through C4, and sacral), abnormal atlantooccipital articulation, cleft palate, absence of maxillae, and lack of tail vertebrae. Cyclopia and anophthalmia with absence of optic nerves and rudimentary optic tracts were also observed. Atresia ani, atresia coli, lack of atrioventricular valves in the heart, and absence of external nares and soft palate were other abnormalities present.