Clostridial diarrheas in piglets: A review.

Clostridium perfringens type C and Clostridioides difficile are the main enteric clostridial pathogens of swine and are both responsible for neonatal diarrhea in this species. The role of Clostridum perfringes type A is under discussion. History, clinical signs, gross lesions and histological findings are the basis for a presumptive diagnosis of C. perfringens type C or C. difficile infection. Confirmation is based upon detection of beta toxin of C. perfringens type C or toxin A/B of C. difficile, respectively, in intestinal contents or feces. Isolation of C. perfringens type C and/or C. difficile is highly suggestive of infection by these microorganisms but it is not enough to confirm a diagnosis as they may be found in the intestine of some healthy individuals. Diagnosis of C. perfringens type A-associated diarrhea is more challenging because the diagnostic criteria have not been well defined and the specific role of alpha toxin (encoded by all strains of this microorganism) and beta 2 toxin (produced by some type A strains) is not clear. The goal of this paper is to describe the main clostridial enteric diseases of piglets, including etiology, epidemiology, pathogenesis, clinical signs, pathology and diagnosis.

Characterization of the Maternally Derived Antibody Immunity against Rhdv-2 after Administration in Breeding Does of an Inactivated Vaccine.

Inactivated strain-specific vaccines have been successfully used to control rabbit haemorrhagic disease (RHD) caused by RHDV-2 in the rabbit industry. It is unknown whether and how vaccination of breeding does contributed to protect the population of young susceptible rabbit kits. The present study investigates whether the immunity against RHDV-2 produced by vaccination of breeding does is transmitted to their progeny and its dynamic once inherited by kits. For this purpose, New Zealand female rabbits of 8-9 weeks of age were allocated into 2 groups of 40 subjects each and bred during 6 reproductive cycles. The first experimental group was vaccinated with a commercially available inactivated vaccine against RHDV-2 whereas the second group was inoculated with PBS. Moreover, the present study was also meant to identify the mechanisms of transmission of that maternal immunity. For this reason, rabbit kits of vaccinated and non-vaccinated breeding does were cross-fostered before milk uptake. The RHDV-2 antibody response was monitored in the blood serum of breeding does and of their kits by competition ELISA (cELISA) and solid-phase ELISA (spELISA). Since it has been clearly demonstrated that cELISA positive rabbits are protected from RHD, we avoided the resorting of the challenge of the kits with RHDV-2. Results showed that RHDV-2 antibodies were inherited by kits up to one year from vaccination of breeding does. Once inherited, the maternally derived antibody response against RHDV-2 lasted at least until 28 days of life. Finally, the study also elucidated that the major contribution to the maternal derived immunity against RHDV-2 in kits was provided during gestation and probably transmitted through transplacental mechanisms although lactation provided a little contribution to it. The present study contributed to elucidate the characteristics of the maternal antibody immunity produced by vaccination and its mechanisms of transmission.