Prevalence of Clostridium sPP. in diarrhoeic and healthy dogs ...

Ann. Fac. Medic. Vet. di Parma (Vol. XXVII, 2007) pag. 143 - pag. 156can involve competition by bacteria for calories and essential nutrients, productionof harmful metabolites, and direct damage to the intestinal mucosa interfering withintestinal function. Histological changes in intestinal biopsies of partial villus atrophyand lymphocyte/plasma cell infiltrate are only present in 30% of cases, and often themucosal damage cannot be seen by conventional light microscopy [1].Dogs with and without signs of intestinal disease can harbour most of theenteric infectious agents [5]. In the case of clostridial pathogens, particularly importantare C. perfringens and C. difficile. The clinical documentation of C. perfringensand C. difficile as causes of diarrhoea in dogs is clouded by the presence of thesemicrorganims as a normal component of the indigenous intestinal microflora [6].Clostridium perfringensClostridium perfringens is a Gram-positive, anaerobic, spore-formingbacillus. This microrganism may be one of the most widespread pathogen, inhabitingthe gastrointestinal tract of human beings and animals as well as terrestrial andmarine environments [7]. It has been associated with outbreaks of acute, often severediarrhoea in humans, horses, dogs and cats. The elaboration of four major toxins,alpha (α), beta (β), iota (ι), and epsilon (ε), is the basis for typing the microrganisminto five toxigenic phenotypes (A, B, C, D and E).Each type may also express a subset of at least 10 other established toxins,including C. perfringens enterotoxin (CPE), a well-characterized virulence factorwhose production is co-regulated with sporulation [6]. Although all five types canharbour the enterotoxin gene (cpe), studies have shown that the overall frequency ofenterotoxigenic strains is relatively low (∼5%), with most strains belonging to typeA. Virtually all strains isolated from dogs are type A, with only one published reportdocumenting a type C infection in five cases of canine peracute lethal hemorrhagicenteritis [7]. Although several studies have shown an association between theimmunodetection of CPE in fecal specimens and canine diarrhoea, the pathogenesisof C. perfringens-associated diarrhoea in the dog is not fully understood, because CPEis also detected in up to 14% of non-diarrhoeic dogs. Isolation of nonenterotoxigenictype A strains from a diarrhoeic specimen does not preclude involvement in disease,because there is a plethora of other virulence factors that have not been evaluated. Oneof these virulence factors is the recently characterized C. perfringens β2 toxin, whichhas been associated with both necrotic enteritis in piglets and equine typhlocolitis.Clostridium perfringens is a part of the normal canine intestinal flora andis readily cultured from more than 80% of diarrhoeic and non-diarrhoeic dogs.Diarrhoeal diseases associated with C. perfringens in the dog have primarily beenattributed to CPE, which has been shown to induce fluid accumulation and diarrhoeain a canine model when administered orally or directly in the intestinal lumen[7]. Dogs with C. perfringens-associated diarrhoea frequently exhibit large-boweldiarrhoea characterized by increased frequency of bowel movements with tenesmus,fecal mucus and hematochezia; however, clinical signs of enteritis or enterocolitisare also commonly seen [6]. Despite the fact that CPE is detected in up to 34% ofdiarrhoeic dogs, the fact that it is also detected in 5% to 14% of non-diarrhoeic dogs146