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Sudden death in sows caused by Clostridium perfringens

Jeremy Rogers, Senior Veterinary Officer, PIRSA, Murray Bridge, SA and Effie Lee, Veterinary Pathologist, Gribbles Veterinary Pathology, Glenside

Posted Flock & Herd August 2021


Clostridium perfringens may have caused the sudden death in three otherwise healthy sows about a week after farrowing. The sows had food in the stomach, purple discolouration of parts of the body and otherwise very few post-mortem changes, apart from rapid autolysis. These changes are highly suggestive and epsilon toxin was detected and C. perfringens was cultured from the bowel. However, post-mortem invasion by C. perfringens cannot be ruled out.

African and Classical Swine Fever tests were negative.


Over the past two months, three sows had been found dead in the farrowing pens about one week after farrowing. The sows had been eating normally, with normal litters, the evening prior. Bodies were noted to start decomposing more rapidly than usual, and be "blown up" quickly. Due to the inability of an interstate veterinarian to be able to visit, PIRSA was requested to attend and investigate.

An observation by the manager was that deaths seemed to occur when there had been a warm day, but cold night.


The carcass was bloated, with purple discolouration on parts, and some blood-stained foam from the nose and some blood from the rectum. Internally there was advanced autolysis, despite the cold weather and approximately eight hours after death. Blood-tinged fluid in the abdomen was noted, and an enlarged and friable liver and spleen, both darker in colour. Loops of small intestine were distended with gas, and there was some food material in the stomach. The brain appeared very soft, almost liquified.

Image of bloated dead pig carcass
Figure 1. Purple skin discolouration, rapid decomposition and "blown up" carcass. The unusual pattern on the skin is from pen flooring impressions.
Image of pig carcass with skin reflected
Figure 2. Rapid autolysis. Showing gas buildup in abdomen and bruising in inguinal area.
Image of pig carcass showing disdended bowels
Figure 3. Distended bowel loops, enlarged and friable spleen and liver. Fibrin tags from abdominal exudate on abdominal organs, rapid autolysis.


As mentioned, African and Classical Swine Fever tests were negative. C. perfringens was cultured from colon contents and epsilon toxin was detected from unfixed bowel samples submitted.

It was noted that there was autolysis in the organ tissues examined, with the greatest degree occurring in the liver and spleen. Occasional bacteria were detected within blood vessels, vascular channels or sinusoids in the absence of vascular changes or inflammatory reaction inferring either a peracute infection or post-mortem invaders, the latter being more likely in this case. Furthermore, tissue autolysis can promote overgrowth of post-mortem invaders such as the C. perfringens isolated on culture. Unfortunately, in this case, tissue autolysis compromises histological analysis and prevents assessment of ante-mortem damage to blood vessel endothelium typically associated with epsilon toxin (angiotoxin) liberated by C. perfringens type D or type B.

C. perfringens type B produces two highly lethal toxins, beta-toxin and epsilon-toxin. It is potentially the most virulent of all C. perfringens isolates but studies of its virulence genetics are limited (Sayeed 2010).

C. perfringens type B causes primarily enterotoxic haemorrhagic enteritis in young pigs resulting in enteritis, dysentery, toxaemia and high mortality. C. perfringens can be found in low numbers within intestines of healthy animals. Any alimentary conditions that disrupt resident microbial balance, including undigested fermentable carbohydrates or intestinal stasis, can contribute towards increased intestinal C. perfringens and epsilon toxin. Epsilon toxin crosses the damaged intestinal barrier and spreads via the circulation (toxaemia) to several organs, causing toxic shock and death (Popoff, 2011).


Although epsilon toxin producing C. perfringens type B has been reported in pigs, references to C. perfringens type D in pigs are difficult to find in the literature. Some older texts say that these deaths are "unsubstantiated". However, consultant veterinarians in the pig industry do say that cases occur and that vaccines intended for ruminants are beneficial. (B. Lloyd and T. Holyoake pers comm.)

This case suggests that C. perfringens type D may have caused sudden death in these sows as in other species. The history and post-mortem findings in this case are consistent with mortality due to C. perfringens type D infection:

I have only seen this presentation on one other occasion, in grower pigs. The reason why some pigs are affected, while others are not, is unknown.

C. perfringens produce many toxins that are commonly linked to various diseases in many mammalian species. In particular, the epsilon toxin is of veterinary concern for some large animals and vaccines of varying quality are available to combat epsilon enterotoxemia (Stiles et al., 2013). There is still a lot to learn regarding epsilon toxin, how it works and how to protect against it.


  1. Sameera Sayeed, Jihong Li, & Bruce A McClane (2010). Characterization of Virulence Plasmid Diversity among Clostridium perfringens Type B Isolates. Infection and Immunity 78:495-504
  2. Michael Popoff (2011). Epsilon toxin: a fascinating pore-forming toxin. Review article. The FEBS Journal 278:4602-4615 febs.onlinelibrary.wiley.com
  3. Bradley G. Stiles, Gillian Barth, Holger Barth & Michel R. Popoff (2013). Clostridium perfringens Epsilon Toxin: A Malevolent Molecule for Animals and Man? Review article. Toxins 5:2138-2160
  4. Dr Barry Lloyd, Consultant Pig Veterinarian, Gawler, SA. Pers comm.
  5. Dr Trish Holyoake, Specialist Pig veterinarian, Bendigo, Victoria. Pers comm.


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