Clostridium difficile and C perfringens Infections

C difficile may be found in low concentrations in the feces of as many as 10% of healthy horses. C difficile and C perfringens organisms may be present in soil or the environment and be ingested by horses. The factors that trigger disease are not well known, but it is presumed that some alteration in the normal flora permits excessive multiplication of the bacteria, which produce toxins capable of causing intestinal damage and systemic effects.

Predisposing factors that have been suggested include change in diet and antibiotic therapy. Other host factors that may determine whether disease develops include age, immunity, and presence or absence of intestinal receptors for the clostridial toxins. Recent antibiotic therapy is a common feature of the history of horses with C difficile–induced diarrhea. Certain antibiotics, notably macrolides and especially erythromycin ethylsuccinate, β-lactam antibiotics, and trimethoprim/sulfonamide, are more likely than others to be associated with C difficile colitis. Mares with foals that are being treated with erythromycin ethylsuccinate appear to be at high risk. Elimination of roughage from the diet before surgery is also reported to predispose to C difficile colitis. Acute diarrhea has been reproduced in healthy neonatal foals using C difficile spores and vegetative cell forms. Acute anterior enteritis (duodenitis-jejunitis, see Clostridia-associated Enterocolitis in Horses) has also been associated with C difficile in a case-control study.

C perfringens type A is believed to cause diarrhea by elaboration of an enterotoxin (CPE), which is released during sporulation and stimulates intestinal epithelial cells to secrete excess fluid into the lumen. A novel necrotizing toxin, called β2, produced by some strains of C perfringens, has recently been strongly associated with colitis in horses.

Foals and adult horses may be affected. Typically, there are signs of abdominal pain and diarrhea with or without blood. There may be abdominal distention, especially in cases of C difficile–induced diarrhea. Dehydration, toxemia, and shock may develop, and the mortality rate is variable. One or several animals on a farm may be affected. Horses with anterior enteritis have associated severe recurrent nasogastric reflux, fever, and malaise.

Clinical features of the disease are similar to those of acute salmonellosis (see Salmonellosis), Potomac horse fever (see Potomac Horse Fever), or monocytic ehrlichiosis. The identification of C perfringens as the cause of diarrhea in horses depends on demonstration of the presence of enterotoxin or the gene for CPE in the feces or intestinal fluid and the absence of other likely etiologic agents. Most C perfringens found in the intestine of horses lack the gene for CPE expression. Large numbers of C perfringens in anaerobic fecal culture of horses with diarrhea is not diagnostically significant. The diagnosis of C difficile diarrhea is suggested by a history of recent treatment with antibiotics and is supported by demonstration of the presence of C difficile toxin A and/or B in a freshly passed or frozen fecal sample submitted to a laboratory using a human ELISA validated in horses, with good sensitivity and specificity. The toxin gene may be identified by PCR ribotyping.

Steps may be taken to reduce the opportunity for C difficile infections in horses. Proper isolation procedures and infectious disease control should be applied to high-risk horses receiving antibiotics. The environmental load of C difficile spores may be reduced by surface disinfection with sporicidal disinfectants, and the spread may be reduced by hand washing and by isolation of infectious horses and foals. There are no control measures available for prevention of C perfringens–induced diarrhea. Oral metronidazole (15 mg/kg, tid) is recommended for treatment of either of these clostridial infections. Metronidazole might be teratogenic, so its use should be avoided if possible in pregnant mares.