Pathogenicity of experimental infection with 'pneumotropic' porcine coronavirus.

Virus localisation and lesions were studied in 14-one-week-old piglets following combined intranasal-oral inoculation with a British isolate of 'pneumotropic' porcine coronavirus (PCV) and were compared with the effects of transmissible gastroenteritis virus (TGEV) infection in five piglets. Unlike TGEV-infected piglets, all PCV-inoculated piglets remained clinically healthy. Seroconversion was detected at seven days after inoculation. Mild bronchointerstitial pneumonia involving terminal airways was consistently present at two days after infection and thereafter. Both PCV and TGEV infected bronchiolar epithelium and alveolar macrophages but, unlike TGEV, replication by PCV in villous enterocytes was limited and did not cause villous atrophy.

Outbreaks of classical swine influenza in pigs in England in 1986.

Serum samples from pig herds in Great Britain have been examined for antibodies to influenza virus since 1968. Antibodies to H3N2 virus strains have been found since 1968 and the serological data presented here suggests that H3N2 virus strains continue to persist in the pig population. An outbreak of acute respiratory disease occurred in a 400-sow unit. The outbreak was characterised by coughing, anorexia, fever, inappetence and loss of condition. The gilts and weaners were affected and the morbidity approached 100 per cent. An influenza A virus designated A/Swine/Weybridge/117316/86 (H1N1) was isolated from the herd and 28 paired serum samples from the affected animals showed increases in the haemagglutination inhibition titres to this isolate. Haemagglutinin and neuraminidase characterisation indicated that the virus is similar to H1N1 viruses isolated recently from pigs in Europe. A total of 91 herds experiencing respiratory disease were investigated, of which 42 gave positive reactions in the haemagglutination inhibition test. Antibodies to A/Port Chalmers/1/73 (H3N2) were also detected in some of the herds but it is not known whether this strain plays any role in the current respiratory disease problems in pigs.

Maternally-derived antibodies to porcine parvovirus and their effect on active antibody production after vaccination with an inactivated oil-emulsion vaccine.

Two sows which had been vaccinated with an oil-emulsion porcine parvovirus vaccine, and had developed high haemagglutination-inhibiting antibody levels to the virus, farrowed three successive litters each, a total of 74 piglets. Serum samples from these piglets were tested for haemagglutination-inhibiting antibody at birth, three and 17 days after birth, and at monthly intervals thereafter to study the decline of maternally-derived antibody. Regression curves were constructed from the data to show the projected pathway (mean and 95 per cent tolerance limits) of the decline of maternally-derived antibody. Approximately half the pigs still had positive titres of up to 1/160 at six months old, and traces of antibody were detected in a few pigs at nine months. Thus, even at the onset of breeding some gilts can have maternally-derived antibody which may interfere with their ability to develop active immunity to porcine parvovirus. From the same litters three groups of 12 pigs were selected randomly and were vaccinated with a single dose of the oil-emulsion vaccine at 70 days, 130 days or 190 days respectively. Despite the presence of moderate to high titres of maternally-derived antibody, especially in the younger pigs, all of those vaccinated showed strong and long lasting antibody responses to the vaccine. High serum antibody titres at the time of vaccination seemed to depress the response to the vaccine slightly but the effect was not statistically significant. These results have important implications for prevention of reproductive failure induced by porcine parvovirus.

An inactivated, oil-emulsion vaccine for the prevention of porcine parvovirus-induced reproductive failure.

Pig fetuses inoculated at 45 days gestation with virulent porcine parvovirus (PPV) were harvested 10 days later. Virus was extracted, inactivated with binary ethylenimine and the antigen suspension emulsified with mineral oil adjuvant. One dose of this vaccine, or two doses with a 14 day interval, stimulated high and long lasting serum antibody titres in gilts. Vaccination caused no clinical reactions and lesions at injection sites were minor. Vaccination of seronegative gilts at 40 days gestation caused no adverse effects on fetuses. Six gilts which had been vaccinated five to nine weeks before mating were challenged intravenously with live, virulent PPV at 40 days gestation. At 98 days gestation 78 out of 84 (93 per cent) fetuses were alive and normal and no evidence of PPV infection was found in the six dead (mummified) fetuses. In four unvaccinated gilts similarly challenged with PPV at 40 days gestation only five out of 51 (10 per cent) fetuses survived to 98 days gestation and the virus was detected in 41 of the 46 dead (mummified) fetuses. This vaccine appears to be safe and effective for prevention of PPV-induced fetal loss in gilts.

Virus-like particles associated with porcine epidemic diarrhoea.

Porcine epidemic diarrhoea type II was reproduced in experimental pigs of various ages by oral dosing with minced intestine from a naturally occurring case of the disease. Virus-like particles which probably represent an unidentified coronavirus were seen by electron microscopy in the faeces and intestinal epithelium of infected animals.