Introduction

• Although C. perfringens can be a normal commensual of the canine intestinal tract, it can under certain circumstances, become pathogenic and initiate chronic, acute or per acute (hemorrhagic) diarrhea. This is thought to depend on the biotype and ability of the organism to produce toxin.

Pathogenesis

Etiology

• There are 5 biotypes of C. perfringens Clostridium perfringens (A to E) based on the presence of toxin genes - alpha, beta, iota, and epsilon.
• All these biotypes can harbour the toxin gene CPE.
• Most studies have shown that biotype A is most common with 15% being biotype A + CPE.
• Unfortunately some normal dogs carry biotype A + CPE, so other as yet unknown virulence factors may be involved.

Predisposing factors

General

• Infection follows either: ingestion of food contaminated with enterotoxogenic C perfringens, or a change in the intestinal environment which results in C perfringens producing toxin. The latter might be due to antibiotic use, diet change, viral infection or EPI Exocrine pancreatic insufficiency.

Pathophysiology

• C. perfringens can be cultured in 80% of dogs with and without diarrhea.
• The ability of C. perfringens to adhere to the intestine may be associated with changes in the intestinal environment, loss of brush border enzymes or lysosomes.
• Presence of CPE genes is thought to be the deciding factor for inducing diarrhea. CPE is a small protein produced by the organism during sporulation and is released on lysis of the organism. CPE interacts with the tight junction proteins (occludins) altering tight junction structure and function. This leads to increased permeability and diarrhea. These changes appear to occur most often in the ileum or colon.

Diagnosis

Treatment

Outcomes