Necrotic enteritis due to simultaneous infection with Isospora suis and clostridia in newborn piglets and its prevention by early treatment with toltrazuril

In this study, 51 piglets originating from five different sows were included in the investigations. The animal source of all sows had a history of Clostridium perfringens type A (beta 2) infection. The piglets of three sows (n=31) were experimentally infected with Isospora suis within the first 4 h after birth and were randomly assigned to the treatment group or the sham-dosing group. The piglets of the two remaining sows (n=20) served as I. suisuninfected controls. Twelve hours post-infection, the animals in the treatment group (n=15) were treated with toltrazuril (20 mg/kg BW, Baycox (R) 5% suspension). During an observation period of 14 days faecal consistency, faecal oocyst counts, faecal germ counts, mortality, body weight development and clinical status were recorded. One piglet per study group and litter was necropsied, and intestinal tissue samples were taken for histopathological investigations and in situ hybridisation on study days (SDs) 3 and 14. I. suis-infected but untreated piglets showed clinical disease resulting in liquefaction of faeces and decreased body weight development. In 59.2% of the observations, I. suis-infected but untreated piglets showed abnormal faecal consistencies whereas only 12.0% or respectively 4.4% of the faecal samples had a pasty consistency in the I. suis-infected-treated or in the control animals. The mean body weight at the end of the study was 3.37 kg in the I. suis-infected but untreated piglets while the average body weight in the I. suis-infected-treated animals was calculated as 4.42 kg and the control animal's mean body weight was 4.45 kg. Moreover, mortality, occurring between SDs 8 and 14, in this study group was 38.5% (n=5), with 30.8% (n=4) died from necrotic enteritis. In contrast, no piglets died in the I. suis-uninfected control group or in the toltrazuril-treated study group. The results of this study corroborate the hypothesis that simultaneous infection with I. suis and C. perfringens type A soon after birth leads to distinct interactions between the two pathogens and result in an increase in clinical disease, mortality and metabolically active C. perfringens type A.