TDK conference 2010

Transmissible gastroenteritis (TGE) of pigs is an enteric disease caused by a porcine coronavirus. It can affect animals of any age but is most commonly affecting younger animals. TGEV belongs to the Coronaviridae family, which constitutes enveloped viruses with an unusually large single stranded RNA genome (up to 28-30 kilobases) of positive orientation. Although the virus can infect pigs at any age, the clinical signs are less pronounced in adults. Piglets however, especially during the first week of life develop devastating intestinal infections. Hallmark clinical signs are mainly vomiting and diarrhea. Mortality rate in piglets without maternal immunity can reach 100%.

TGE was among one of the most important swine diseases until the mid 1980’s. Then a deletion mutant, namely the porcine respiratory coronavirus (PRCV) with no or very limited pathogenicity emerged and spread around the world. The widespread PRCV infection led to the gradual disappearance of TGE, due to the cross-protective immunity induced by the new virus.

Recently more and more cases of piglet diarrhea with an unclear aetiology have been reported. This study is a summary of such a case, where TGEV genome was detected by polymerase chain reaction (PCR) in a swine herd. In this case it was pigs at the age of weaning that were showing signs of diarrhea. Other viral, bacterial or parasitic infections were excluded by appropriate laboratory investigations, but a parallel presence of PRCV in the affected animals was detected.

The re-emergence of TGEV was confirmed by sequencing the PCR generated amplicons (targeting the spike, S gene). Apart from the deletion at the site of the S gene the genome sequences were identical in PRCV and TGEV cases. The reason for the re-emergence of the pathogenic coronavirus is not fully understood. But based on the widespread presence of porcine circoviruses, which are well known for their immunosuppressive nature, it was speculated and later confirmed by serological tests that there is a decreased cross protection between PRCV and TGEV. This decrease in cross protection could be in the background of the TGEV induced clinical problems.