An overview of successful TGEV vaccination strategies and discussion on the interrelationship between TGEV and PRCV.

Porcine respiratory coronavirus (PRCV) is a new variant of TGE with an altered pathogenesis. PRCV multiplies mainly in tonsilar tissues and the respiratory tract. There are no enteric symptoms and in experimentally infected pigs, even the respiratory tract infection is usually asymptomatic. PRCV is spread aerogenically through herds and the significance of PRCV as a pathogen in swine has yet to be determined. Despite the differences in pathogenesis and tissue tropism, the behavior of TGEV and PRCV are closely related antigenically. PRCV induces an antibody response in pigs that cannot be distinguished from TGEV-infected pigs by conventional serological assays. PRCV sensitized animals are not protected from TGEV challenge nor is the milk antibody provided to nursing piglets completely effective in prevention of TGEV infections; thus PRCV is not a good vaccine candidate for TGEV infections. PRCV subclinical infections have led to several reported cases of enzootic TGEV in herds that had been diagnosed as TGEV immune strictly on the basis of serum neutralizing titers which were later found to be due to exposure to PRCV. Vaccination studies conducted with the Ambico, oral modified live TGEV vaccine have led to some startling new results: (1) Use of Ambico TGEV modified live vaccine has been shown to provide complete protection against subsequent PRCV challenge and (2) the effectiveness of TGEV vaccination is actually enhanced by previous exposure to PRCV (3) Weanling pigs which have passively acquired circulating TGEV neutralizing antibodies are protected from subsequent PRCV infections.

Adaptation and serial passage of porcine group C rotavirus in ST-cells, an established diploid swine testicular cell line.

A porcine group C rotavirus (strain Cowden-AmC-1) was adapted and serially passaged in an established diploid swine testicular cell line (ST cells). Growth of group C rotavirus in ST cells, which in maintenance medium required trypsin, but not pancreatin resulted in cytopathic effect characterized by cellular stranding and subsequent cell lysis. Active replication and assembly were confirmed by RNA profile analysis, immune electron microscopy and immunofluorescence. Adaptation of non-group A rotavirus to a continuous cell line has not previously been reported and should facilitate progress in diagnostic procedures and vaccine development.

Evaluation of killed and modified live porcine rotavirus vaccines in cesarean derived colostrum deprived pigs.

Twenty-eight cesarean derived, colostrum deprived (CDCD) piglets were used to evaluate the efficacy of killed and modified live rotavirus (MLV) vaccines against challenge with virulent A-1 and A-2 rotaviruses. Two killed rotavirus vaccines were evaluated: an experimental vaccine and a commercially available vaccine. Efficacy parameters included: average daily weight gains, rotavirus shedding in feces, morbidity incidence and duration, and rotavirus serum antibody conversion post-vaccination and post-challenge. Piglets vaccinated orally/intramuscularly with the modified live vaccine were completely protected from A-1 and A-2 virulent rotavirus challenge. Nonvaccinated control piglets and piglets receiving killed rotavirus vaccines developed diarrhea, shed virus and exhibited reduced weight gains post-challenge. Only the MLV rotavirus vaccine was able to prevent virus shedding in feces after virulent challenge. Both controls and pigs which received killed vaccines intraperitoneally, orally or intramuscularly shed virus in the feces for 7 days post-challenge and virus peak titers approached 10(7) fluorescent antibody infectious dose (FAID)50/g feces. These studies clearly reflected the inability of killed rotavirus vaccines to induce active local immunity to rotaviral diarrhea in piglets.

Cephamycin C treatment of induced swine salmonellosis.

Weanling pigs in groups of 12 were infected orally with Salmonella choleraesuis and were treated intramuscularly with doses of cephamycin C ranging from 12.5 to 337.5 mg twice daily for 10 days beginning 1 day postinoculation. Pigs in two other infected groups either received 300 mg of tetracycline orally on a similar schedule or served as nonmedicated controls. Optimal responses to cephamycin C were achieved at a twice daily dose of 112.5 mg. With this regimen, the febrile response was significantly reduced on day 2 and eliminated by day 5 postinfection, and the shedding of Salmonella spp. in feces was eliminated by day 5 postinfection; essentially, no lesions were found in the gastrointestinal tract at necropsy (day 26 postinfection). There was no mortality among recipients of the 112.5-mg dose; diarrhea was present on only 2% of the observation days. In contrast, 83% of the infected, nonmedicated pigs and 25% of the tetracycline-medicated pigs died, and diarrhea was present in these groups on 63 and 54% of the observation days, respectively. The striking benefits of cephamycin C treatment was achieved without adverse reactions. The weight gain and feed efficiency of the infected pigs treated with the 112.5-mg dose of cephamycin C and the noninfected, nonmedicated control pigs were equivalent.