Epidemiology of Experimental Enterocecitis Due to Clostridium dlfficile

He, Larson; Ab, Price; Sp, Borriello

doi:10.1093/infdis/142.3.408

Cited by 78 publications

(31 citation statements)

References 21 publications

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“…Diet contributed to the development of antibiotic-associated diarrhea in hamsters in one study, and intestinal pH may be a factor.24 C. digicile toxin production can be altered in vivo by feeding different diets.23 Diets high in fat can affect both cell-mediated and humoral i m m~n i t y , l~.~~.~~ and diets high in cholesterol can alter membrane fl~idity.~ The high-fat, highcholesterol diet may cause alterations in the microbial populations in the intestine similar to the alterations caused by certain antibiotics that increase susceptibility to C. dijicile disease. 20,22 In the present studies, no significant differences in the cecal microbial flora were observed between the atherogenic and control diet groups (data not shown).…”

Section: Discussioncontrasting

confidence: 53%

Clostridium difficile Infection in Hamsters Fed an Atherogenic Diet

et al. 1995

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Abstract. Diarrhea and unexpected death were encountered in a group of young Syrian hamsters (Mesocricetus auratus) used for hyperlipoproteinemia and atherosclerosis research. The animals were fed an atherogenic diet containing 18% saturated fat and 0.366% cholesterol. Mortality began 45 days after hamsters were placed on this atherogenic diet. The atherogenic studies were aborted at 74 days because of high mortality. Toxigenic Clostridium dzjicile was isolated from animals found dead or euthanatized because of illness. Signs observed were unexpected death and acute liquid diarrhea. Characteristic pathologic changes were necrosis and hemorrhage of the intestinal mucosa with acute inflammation. Hepatic lipidosis was a consistent finding presumed to be associated with the consumption of the atherogenic diet. The study was repeated by placing 23 hamsters on the atherogenic diet and 10 hamsters on the control diet. In animals fed the atherogenic diet, the average time to mortality differed between studies, but clinical signs, gross and histologic lesions, culture findings, and toxin results in both atherogenic diet groups were similar. C. dzfiile was not isolated from the feeds. No antibiotics were found in the atherogenic diet. The results from these studies suggest that hamsters fed an atherogenic diet have increased susceptibility to disease caused by C. dzflcile as compared with hamsters fed a normal fat and cholesterol diet.

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Section: Discussioncontrasting

confidence: 53%

Clostridium difficile Infection in Hamsters Fed an Atherogenic Diet

et al. 1995

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“…All the animals were housed individually in sterile isolator cages with sterilised food and bedding (Larson et al,, 1980); 5 days later they were killed and their caecal contents were harvested and diluted 20-fold w/v in sterile distilled water. The caecal material obtained from the untreated hamsters was pooled and a portion was centrifuged at 12 000 rpm for 30 min and filtered through a 0.20-pm membrane filter.…”

Section: Growth Of C Dificile In Faecal Emulsions Derivedfrom Patienmentioning

confidence: 99%

“…There is much evidence to imply that a stable normal gut flora acts as a natural barrier to infection with C. dzficile (Bowden et al, 1981;Wilson et al, 1981;Borriello and Barclay, 1984;Schwan et al, 1984), and that infection with C. dzficile generally requires recent or current antimicrobial therapy to disrupt the gut flora and create an intestinal environment conducive to growth of C. dzficile and production of its toxins. In the Syrian hamster model of PMC, disease is induced by the administration of antibiotics which disrupt the normal gut flora and subsequent exposure to pathogenic strains of C. dzficile; neither antibiotic treatment nor exposure to C. dzficile alone is sufficient to produce disease if animals are housed in protected (i.e., C. dzficile-free) environments (Larson et al, 1980). Many attempts have been made to identify the individual components of the faecal flora that are antagonistic to C. dzficile in vitro (Rolfe et al,198 1 ; Borriello, 1982 Received 19 Jul.…”

Section: Introductionmentioning

confidence: 99%

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An in-vitro model of colonisation resistance to Clostridium difficile infection

Borriello¹,

Barclay²

1986

Journal of Medical Microbiology

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123

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Summary.To investigate the importance of the normal gut flora in preventing the establishment of Clostridium dzficile in vivo we have developed an in-vitro test system based on growth in faecal emulsions. Growth of C. dzficile and cytotoxin production are inhibited in faecal emulsions from healthy adults, but not in sterilised emulsions; the importance of viable bacteria in the inhibitory system is evident. Generally, faecal emulsions derived from infants, children and geriatric patients were less inhibitory than those from healthy adults. Those from bottle-fed infants were significantly less inhibitory than those from breast-fed infants. Decreased levels of cytotoxin in the latter group were attributed to the acidic pH of the stools. With the different patient groups studied, faecal samples not inhibitory to C. dzficile in vitro were obtained from 21% of patients with antibiotic-associated diarrhoea, 33% of those taking antibiotics but who did not have diarrhoea, 18.7% of those with diarrhoea unassociated with antibiotics, and 79% of those with C. dzficile-mediated diarrhoea. In some cases inhibition was due to low faecalpH, as in some infants, and in others to other filterable substances. The degree of inhibition could not be linked to specific volatile fatty acids or enzymes.

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“…Environmental contamination has been suggested as a significant factor in the transmission of C. dificile (Fekety et al, 1980;Larson et al, 1980). Survival of C. dificile in an aerobic environment is possible because this obligate anaerobe can form aerotolerant spores; there are reports that C. dzficile can survive for > 5 months in aerobic conditions (Kim et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

Recovery of spores of Clostridium difficile altered by heat or alkali

Kamiya

Yamakawa²,

Ogura³

et al. 1989

Journal of Medical Microbiology

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Summary. The effect of heating or alkali-treatment on spore recovery in ordinary growth medium was examined for four strains of Clostridium dificile. Heating spores at 80°C for 10 min produced 95-50-99-95% decreases in the recovery rates. Treatment with 0.1 N NaOH for 15 rnin produced 99-47 and 99.83% decreases in spore recovery rates for two of the four strains. The influence of either addition of lysozyme after treatment with sodium thioglycollate (thioglycollate-lysozyme method) or addition of sodium taurocholate (taurocholate method) on recovery of heat-or alkali-treated C. dificile spores was also examined. Viable spores of all strains altered by heating at 90°C or 100°C for 10 min could not be recovered at all by the taurocholate method. Nor did this method allow recovery of alkali-altered spores treated with >0-2 N NaOH for 15 min. On the other hand, 10-47% of altered spores heated at 90°C for 10 min were recovered by the thioglycollate-lysozyme method, and alkali-altered spores treated with 0.1-0.3 N NaOH for 15 min were as completely recovered by this method as untreated spores. These results indicate that the thioglycollate-lysozyme method is more effective than the taurocholate method for recovery of the heat-or alkali-altered C. dificile spores.

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Epidemiology of Experimental Enterocecitis Due to Clostridium dlfficile

Cited by 78 publications

References 21 publications

Clostridium difficile Infection in Hamsters Fed an Atherogenic Diet

Clostridium difficile Infection in Hamsters Fed an Atherogenic Diet

An in-vitro model of colonisation resistance to Clostridium difficile infection

Recovery of spores of Clostridium difficile altered by heat or alkali

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