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Nosocomial diarrhoea due to Clostridium difficile.

PURPOSE OF REVIEW: The purpose of this review is to summarize recent developments in the diagnosis, epidemiology, treatment and prevention of nosocomial diarrhoea due to Clostridium difficile. RECENT FINDINGS: Twenty-five years after its discovery, the diagnosis of C. difficile-associated diarrhoea is still problematic with laboratories trying to reconcile the time and expense of the diagnostic process. Newer molecular techniques may offer hope. With the introduction of new antibiotics into clinical practice, confusion has arisen about the risk they pose for C. difficile-associated diarrhoea. Strains of C. difficile that fail to produce an active toxin A are an emerging problem and good molecular epidemiology is required to determine whether highly infectious clones exist. Little progress has been made in the treatment of recurrent C. difficile-associated diarrhoea; however, the development of a vaccine is imminent. More effort is being made to rid the hospital environment of C. difficile through infection-control procedures or changes in antibiotic-prescribing policies. SUMMARY: C. difficile continues to be a major nosocomial infection in many health-care institutions throughout the world. Strategies that reduce exposure to the organism or to antibiotics will have an impact on rates of C. difficile-associated diarrhoea.

Anti-Bacterial Agents↗

Increasing hospitalization and death possibly due to Clostridium difficile diarrheal disease.

This study calculated yearly estimated national hospital discharge (1985 to 1994) and age-adjusted death rates (1980 to 1992) due to bacterial, viral, protozoal, and ill-defined enteric pathogens. Infant and young child hospitalization (but not death) rates in each category increased more than 50% during 1990 to 1994. Age-adjusted death and hospitalization rates due to enteric bacterial infections and hospitalizations due to enteric viral infections have increased since 1988. The increases in hospitalization and death rates from enteric bacterial infections were due to a more than eightfold increase in rates for specified enteric bacterial infections that were uncoded during this period (ICD9 00849). To identify bacterial agents responsible for most of these infections, hospital discharges and outpatient claims (coded with more detail after 1992) were examined for New Mexico's Lovelace Health Systems for 1993 to 1996. Of diseases due to uncoded enteric pathogens, 73% were due to Clostridium difficile infection. Also, 88% of Washington State death certificates (1985 to 1996) coded to unspecified enteric pathogen infections (ICD0084) listed C. difficile infection.

Clostridioides difficile↗

Comparison of selective media for optimal recovery of Clostridium difficile from diarrhoeal stools.

Five selective media were compared for their efficacy in the recovery of C. difficile from stool specimens. Of 341 diarrhoeic stool samples, 38 (11%) yielded C. difficile. Eighty per cent of the isolates were detected on modified taurocholate cycloserine cefoxitin fructose agar (MTCCFA) and 73 per cent were detected on taurocholate cycloserine cefoxitin fructose agar (TCCFA). MTCCFA was also found superior to the other four media as it supported better growth of C. difficile colonies, by effectively suppressing the competing microflora. These results suggest that the recovery rate of C. difficile could be enhanced when routine media, incorporated with taurocholate and lower concentration of cycloserine and cefoxitin, is used for the isolation of C. difficile from diarrhoeic stool.

Clostridioides difficile↗

Antibiotic associated diarrhoea and enterocolitis.

C. difficile is the major aetiological agent of AAD and PMC and results from overgrowth of C. difficile already present endogenously or of newly acquired exogenous organisms after suppression of competing gut flora. C. difficile produces two kinds of toxins A and B. These toxins attack the colonic mucosa which becomes necrotic with the formation in fulminating cases of an exudative pseudomembrane. Toxigenic and non-toxigenic strains of C. difficile may be present together in an individual suffering from AAD. There is substantial variation among strains with respect to the quantity of lethal toxin produced. There are several strategies available for the investigation of C. difficile associated disease. Detection of toxins by neutralization with C. sordelli antitoxin is an easy, simple and sensitive method. Methods to deal effectively with silent carriers are not known because the routine administration of antibiotic treatment in an attempt to eradicate the carrier state would in fact boomerang by promoting C. difficile associated enteric disease rather than eliminating C. difficile.

Adult↗