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

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Ann. Fac. Medic. Vet. di Parma (Vol. XXVII, 2007) pag. 143 - pag. 156saggi ELISA e/o la ricerca delle relative sequenze geniche mediante reazioni diamplificazione genica, dovranno essere eseguite sui ceppi di C. perfringens e diC. difficile per poter valutare correttamente le implicazioni e il significatoepidemiologico di questi ritrovamenti nei campioni di feci di cani diarroici e non.AbstractThe purpose of this epidemiological study was to evaluate the prevalenceof Clostridium spp. among diarrhoeic and healthy dogs. Particular attention wasaddressed to C. perfringens and C. difficile isolation, since these microrganisms havebeen associated with acute and chronic large and small bowel diarrhoea, and acutehemorrhagic diarrhoeal syndrome in the dog.Some dogs were kennelled dogs, others belonged to students and staff ofthe Veterinary Faculty of Parma, and others were dogs admitted to the DidacticVeterinary Hospital.A total of 95 canine fecal samples (36 diarrhoeic and 59 non-diarrhoeic dogs),collected from July 2006 to March 2007, were analysed by culture assay. Sixty-two ofthe 95 fecal specimens (65.3%) were positive for one or more Clostridium spp. A totalof 89 different Clostridium strains were identified. The most common Clostridiumdetected was C. perfringens (15.7%), followed by C. bifermentans (13.5%),C. clostridiiforme (13.5%), C. fallax (12.4%), C. beijerinckii/butyricum (11.2%),C. difficile (11.2%), and C. septicum (9.0%). Other Clostridium species were isolatedin lower percentage, ranging from 2.3% to 1.0%.Relatively to C. perfringens isolation, 6 of the 14 positive fecal samples(42.9%) belonged to diarrhoeic dogs. In the case of C. difficile, the 80.0% (8 of 10) ofcanine fecal samples positive by culture assay belonged to dogs with enteritis.Further investigations (concerning, for example, the detection of toxinproduction by ELISA assays and/or the gene revelation by polymerase chain reactions)should be applied on C. perfringens and C. difficile strains to assess properly the fullimplications and the epidemiological meaning of these findings in fecal samples ofdiarrhoeic and non-diarrhoeic dogs.IntroductionThe development of microbiota of dogs begins at birth when the sterile foetusis colonized in the birth canal and by the immediate environment. The succession ofevents in bacterial colonization is similar in the human and canine intestine, with thevery first colonizers originating from the mother, followed by microbes benefitingfrom breast-feeeding and then drastically changing towards obligate anaerobes andheterogeneous flora as solid foods are introduced [10].The gastrointestinal tract of dogs is colonized by a variety of microrganisms.The number of microrganisms increases from approximately 10 2 -10 5 colony formingunits (CFU)/g in the proximal small intestine to 10 5 -10 9 CFU/g in the distal smallintestine, and then dramatically rises in the large intestine to approximately 10 10 -10 11 in the colon [1]. This quantitative proximal-distal gradient is accompanied144
Ann. Fac. Medic. Vet. di Parma (Vol. XXVII, 2007) pag. 143 - pag. 156by complex qualitative changes from a predominantly aerobic flora in the smallintestine to a predominantly anaerobic flora in the large intestine. There is a widevariation in the bacterial flora between normal individuals, and concentrations maybe affected by a variety of circumstances or behaviours, including environment, diet,scavenging and coprophagia. Increased numbers of bacteria in the small intestinecarry an increased risk of a harmful outcome. Whether this is manifest clinically willdepend on individual circumstances, including the composition of the diet whichbacteria can convert to potentially harmful metabolites. The nature of a host responseto the increased load could also be important, and this may involve stimulation ofimmunoglobulin and mucus production, suppression of potentially damaging cellmediated immune responses, a compensatory production of structural and functionalepithelial cell proteins, and increased epithelial cell turnover. The threshold betweenapparent normality and clinical disease may therefore differ between individuals andbe influenced by a delicate balance between the microflora and the host. Clinicaldisease associated with bacterial overgrowth is a very common problem in dogs andoccurs when this balance is tipped against the host [1].Primary enteric bacterial pathogens can also cause acute clinical diseasesince they possess virulence factors with adverse effect on the intestine. Adherenceto the surface or invasion of the mucosa facilitate long-term colonization by certainenteropathogens, predisposing to a carrier status or chronic disease, the outcomeprobably depending on expression of virulence determinants and the host response[1].Since dogs are carnivorous, the total length of their intestine in relation to thebody length is somewhat shorter and the motility slower than in humans. As a wholethe digestive tract of dog, however, resembles that of humans and the physiologyis similar in many ways. Like humans, dogs utilize intestinal microbiota in theirphysiology and both are homothermic mammals. The pH values in the differentcompartments of the digestive tract are also comparable to those of human, being thepH in the dog stomach 3, in duodenum and jejunum 6, in ileum 7.5, in colon 6.5 andin feces 6.2 [10].The main cultivable bacterial groups and most common findings in humansand dogs are similar, including clostridia, bacteroides, streptococci, coliforms,enterococci, lactobacilli and veillonellae with increasing counts towards the largeintestine [10]. Most intestinal pathogens cause similar clinical symptoms in dogs asin humans (C. difficile, multiresistant Gram-negatives, enterococci, staphylococci).The most common intestinal dysfunction in dogs is diarrhoea. Another commondisturbance, small intestinal bacterial overgrowth, composing of Escherichia coli,enterococci and clostridia is associated with raised serum folate, reduced serumvitamin B12 concentrations and altered mucosal permeability and function [10].In the most cases of bacterial overgrowth, the cause cannot be identified, buthost factors known to predispose to bacterial overgrowth include defective gastric acidsecretion, interference with normal motility or stasis, and defective local immunity[1]. Other factors, as a potentially stressful or contamined environment, diet andcoprophagia, may also play a role and could contribute to the relatively high numbersof bacteria reported in kennelled dogs [1]. The damaging consequences of overgrowth145
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Prevalence of Clostridium sPP. in diarrhoeic and healthy dogs ...

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