Herd Health: Clostridial enteritis in neonatal pigs - the causes and treatment

Thursday, October 1, 2009

By the end of the 1990s, another cause of baby pig scours was emerging. At first Clostridium difficile took the lead, but C. difficile was quickly overtaken by Clostridium perfringens type A

by S. ERNEST SANFORD

I can't pinpoint exactly when I realized E. coli scours in baby pigs had decreased to such an extent that it was much less a major problem in the farrowing room in most of our barns. 

But I do know that, by the 1990s, there was considerably less E. coli scours in baby pigs than in previous decades. Work by researchers to identify virulence mechanisms of E. coli, development of efficacious vaccines, more targeted diets by feed company nutritionists, improved management techniques by producers – all contributed to significantly reducing baby pig E. coli scours from the huge problem it had been in earlier times.

Most of our coccidiosis problems were under control and, for the most part, wouldn't resurface for another decade, when Baycox was removed from the Canadian marketplace. Sure, we had a resurgence of E. coli scours in the late 1990s, but those were post-weaning E. coli in nursery room pigs and quite a different story.

What I do recall is that, by the end of the '90s and swinging into the new millennium, another cause of baby pigs scours was emerging – Clostridial enteritis. At first Clostridium difficile took the lead, but C. difficile was quickly overtaken by Clostridium perfringens type A.

Clostridium perfringens type C
Before I get into C. perfringens type A, I must make reference to C. perfringens type C.  C. perfringens type C used to be a major cause of neonatal diarrhea throughout most of the U.S. Midwest from the 1970s to the 1990s, but then decreased significantly in frequency and consequently in importance over the last decade or so.

Clostridium perfringens type C had never been a significant cause of diarrhea in Canada.  I spent years trying to find it in Ontario and only sporadically could I suspect that it was even possibly involved in neonatal piglet scours. I don't recall ever conclusively diagnosing C. perfringens type C enteritis in pigs in the nearly 20 years I spent as a pathologist in Ontario's diagnostic laboratory system.

Clostridium perfringens type A
Clostridium perfringens type A is ubiquitous in the environment and in the intestinal tract of domestic animals and humans. It aggressively colonizes the pig's intestines soon after birth and can be found there throughout the pig's life.

Nevertheless, it is believed to cause enteritis by production of a toxin, clostridial beta 2 toxin (CPB2). Several trials, however, have shown that both diarrheic and nondiarrheic pigs have CPB2, the main differences being that diarrheic pigs more consistently have CPB2 and have higher amounts of it. About 50 per cent of normal, asymptomatic pigs have CPB2. And 80-90 per cent of diarrheic pigs have CPB2, indicating a positive association between C. perfringens type A CPB2 toxin-producers and diarrhea in piglets.     

The dose of toxin is also important; the higher the dose the more likely to be contributing to the diarrhea. CPB2 toxin is believed to stimulate increased intraluminal fluids, thus producing a secretory diarrhea and mild inflammation of villus tips. The toxin's presence is diagnosed by PCR in intestinal tissue samples.

Rectal swabs and histology are insufficient for initial confirmatory diagnosis. Rectal swabs can be used to monitor clinical cases after the initial diagnosis. Reports of herds that have experienced outbreaks of C. perfringens type A diarrhea range anywhere from a low of 20 per cent to as high as 65 per cent or greater with an indication that more than 50 per cent of herds have at some time or other had to combat C. perfringens type A in the last decade.

C. perfringens type A results in about two to five per cent pre-weaning mortality, so not a massive mortality picture, but it remains a nagging, persistent and frustrating problem in affected farrowing rooms. It is interesting to note that researchers are usually unable to produce disease or even see lesions experimentally with C. perfringens type A.

Clinical signs are fairly non-specific, consisting of creamy to pasty feces, usually within 48 hours of birth and lasting for a few to five days with some growth compromise. Gross lesions may be completely absent or necropsy may reveal flaccid, thin-walled, gassy or watery small intestinal contents and pasty colonic contents. Intestines may appear normal histologically or have superficial villus tip necrosis, fibrin, inflammatory cells in villus tips, or simply mild congestion. Abundant intraluminal bacteria are seen.

Large numbers of C. perfringens type A bacteria are cultured, expressing genotype CPB2.  Diagnosis depends on isolation of the organism and demonstration of the CPB2 toxin.

Interventions in order of significance and success for treatment and control of C. perfringens type A diarrhea are:
– Injectable tylosin, which seems to be the most effective treatment for C. perfringens type A diarrhea;
– Autogenous vaccination of sows;
– Feedback of feces and intestinal contents from affected baby pigs;
– And above all, excellent and vigorous sanitation with Virkon-S at 2X concentration or Synergize being the disinfectants of choice. Aggressive sanitation alone is sometimes sufficient to control C. perfringens type A scour without any of the other above interventions.

Other control measures include removal of plastic or rubber mats from the farrowing room creep areas and their replacement with disposable mats. Farrowing room floors are to be thoroughly dry prior to introduction of incoming sows. A survey of U.S. swine veterinarians done by Dr. Karen Lehe and reported at the American Association of Swine Veterinarians meeting in Dallas in March 2009 indicated that antibiotics given to late gestation and lactating sows, oral antibiotics to affected pigs, commercial vaccines, prebiotics and probiotics in sow feed were all of little value.

Clostridium difficile
Clostridium difficile has become fairly well known through numerous media reports of people being hospitalized because of C. difficile infection. C. difficile diarrhea is seen in piglets one to seven days of age. Scouring due to toxin-induced colitis could start almost immediately after birth. 

Gross lesions include moderate to severe mesocolonic edema where the folds of the colon become enveloped in copious amounts of soft, watery to gelatinous material (edema). Colonic contents are frequently pasty to watery and yellow, yet some affected piglets may be constipated. There are no significant lesions in the small intestines.

Diarrheic strains of C. difficile produce several toxins, of which toxinotype V is the one most frequently associated with disease in both piglets and people. Most piglets recover quickly, but are often left stunted as disrupted nursing by the sick piglets precipitates agalactia in the sows, resulting in inadequately nourished piglets when they recover from their bouts of diarrhea.

Weaning weights of affected piglets could be 400 grams to almost one kilogram below normal. Infection by the C. difficile bacterium is high in pigs (>90 per cent) but actual disease, though increasingly reported over the last two decades, appears to be much less common. 

Histological examination revealing inflammation in the colon, often with superficial mucosal necrosis and inflammatory cell exudates, supports a diagnosis of C. difficile enteritis. Since it is a normal resident of the gastrointestinal tract, isolation of the bacterium is, by itself, insufficient for a diagnosis. Detection of toxins in feces or colon by ELISA or PCR is used to aid in the diagnosis of C. difficile disease. The absence of mesosolonic edema can virtually rule out C. difficile disease in pigs. The presence of mesocolonic edema, however, is only indicative of disease in about 50 per cent of cases.

The bacterium is also a commonly reported cause of diarrhea in humans and there is growing concern that transfer from pigs or pork might be a source of infection in humans.

Toxinotype V is associated with disease in pigs and has also been demonstrated in people with disease.

Disease in people follows antibiotic therapy, which kills off competing bacteria and allows overgrowth of C. difficile. Antibiotic therapy, however, does not seem to be a trigger for C. difficile disease in pigs.

At this time, any claim for a zoonotic connection of C. difficile disease from pigs to people is tenuous to nonexistent. Canadian studies show 20 per cent of retail meat contaminated with C. difficile, with a higher incidence of contamination in the winter months.

In summary, the clostridial organisms, C. perfringens type A and C. difficile have become significant contributors to diarrhea in neonatal pigs over the last decade. Scours by either of these two bacteria can start soon after birth. Both organisms are normal inhabitants of the pig's intestines.

A toxin, CPB2, produced by C. perfringens type A is believed to be the direct cause of enteritis. Injectable tylosin or autogenous vaccination of the sow is the treatment most likely to succeed against C. perfringens type A. Sanitation, however, especially the use of Virkon-S at 2X concentration, or Synergize is recommended as a key preventive measure.

C. difficile is more variable in disease presentation than C. perfringens type A. Scours, which can occur in piglets from one to seven days old, are usually self-limiting but piglets are often left stunted. Diarrhea is associated with a toxin, toxinotype V, produced by the organism. Mesocolonic edema is a major, but not exclusive, feature of C. difficile disease in pigs. BP

S. Ernest Sanford, DVM, Dip. Path., Diplomate ACVP, is a swine specialist with Boehringer Ingelheim Vetmedica (Canada) in Burlington. Email:  ernest.sanford@boehringer-ingelheim.com