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Clostridium difficile is a nosocomial pathogen identified as the cause of antibiotic associated diarrhea and colitis. In this study, we have documented the lysogeny of a C. difficile bacteriophage in hamsters during C. difficile infection. The lysogens isolated from the hamsters were toxin typed and their phage integration site was confirmed by PCR. Through toxin ELISA it was found that the toxin production in the in vivo isolated lysogens was affected due to ΦCD119 lysogenization as in the case of in vitro isolated ΦCD119 lysogens. Together our findings indicate that a baceriophage can lysogenize its C. difficile host even during the infection process and highlights the importance of lysogeny of C. difficile phages as an evolutionary adaptation for survival.

Toxigenic Clostridium difficile is the major cause of antimicrobial agent-associated pseudomembranous colitis and is the etiological agent of approximately 30% of cases of nonspecific colitis and diarrhea (without colitis) induced by antimicrobial agents. In addition, C. difficile has been implicated in certain intestinal diseases not related to prior antimicrobial administration. C. difficile has been reported to be one of the most common enteropathogens isolated from stool specimens submitted to hospital laboratories. Thus, diagnosis of C. difficile-associated intestinal disease should now be routinely performed in diagnostic clinical laboratories. The diagnosis of C. difficile-associated intestinal disease relies on the demonstration of either the organism or the toxin(s) in stool specimens or antibody response in serum to the toxin(s). Several selective medium are available for the recovery of C. difficile from stool specimens. The toxin(s) of C. difficile can be demonstrated using a variety of techniques, including biological assays as well as immunological assays. This article will review the techniques currently available to aid in the diagnosis of C. difficile-associated intestinal disease.

Recent studies have shown that a toxin of Clostridium difficile is implicated as the cause of virtually all cases of antimicrobial agent-associated pseudomembranous colitis (PMC), 1 and of approximately one-fifth of cases of antimicrobial agent-associated diarrhea without colonic pseudomembrane. 1,2 Occasionally, PMC or diarrhea not related to antimicrobial exposure has also been attributed to C. diflicile . 2–6 A variety of modes of therapy for antimicrobialassociated diarrhea (AAD) have been employed including vancomycin, metronidazole, tetracycline, bacitracin, anion-binding resins, antiperistaltic agents, corticosteroids, and an oral Lactobacillus preparation. Although assessment of the efficacy of treatment is complicated by the variable course of AAD, 7,8 available data are sufficient to permit a rational approach.

Antimicrobial agent-induced ileocecitis of laboratory animals and colitis of man share common features. The significance of a newly described toxin in these two entities, the apparent source of the toxin (Clostridium d�(fldile) and characteristics of the toxin are reviewed. Methods of toxin detection, isolation and rapid identification of C. dfJicile, and possible modes of therapy for antimicrobial agent-associated colitis of man are discussed. Am. J. Clin. Nuir. 32: 251-257, 1979. Diarrhea associated with the use of certain antimicrobial agents is a well-recognized problem in clinical medicine. The severity of this diarrhea ranges from a mild, self-limited process to a ful.minant necrotizing or pseu- domembranous colitis (PMC). Clindamycin (perhaps because ofits utility in the treatment of anaerobic infections, and its popularity with the clinician) is the most intensively studied of the several antimicrobial agents capable of producing PMC. Hypotheses proposed for the etiology of dlindamycin colitis have been summarized in a recent review of antimicrobial agent-asso- ciated diarrhea (1); they include the devel- opment of a localized Shwartzman reaction, alterations of protein synthesis in the gut mucosa, increases in the quantity of primary bile salts in the colon as a consequence of antibiotic-induced alterations in gastrointcs- tinal flora, viral-induced necrosis of cobonic mucosa, vascular compromise ofthe intestine, and suppression of the normal gut flora, thereby permitting the proliferation of an antibiotic-resistant, toxin-producing bacte- rium.

Clostridium difficile has been shown to be a cause of antimicrobial agent-associated diarrhea and colitis. The source from which this organism gains access to the gastrointestinal tract is not known. Cultures of the hospital environments of six of eight patients whose fecal cultures were positive for C. difficile yielded this organism, whereas cultures of control hospital sites were almost invariably negative. These data suggest that hospital environmental contamination may be a potential source of infection. Further studies are needed to determine the role of various possible sources of C. difficile in human diarrheal disease.

Clostridium difficile was recovered from a variety of environmental sites in three hospital rooms occupied by a patient who had colitis due to this organism.C. difficile was detected for 40 days after the patient was moved from one of these rooms. These findings suggest that the contaminated hospital environment may be a clinically significant reservoir forC. difficile and that this organism may be a nosocomial pathogen. Isolation of patients and adequate decontamination of rooms may be needed to minimize risk to other patients.

VANCOMYCIN given by mouth is effective for the treatment of pseudomembranous colitis,1 2 3 4 a disease now known to be caused by an exotoxin of Clostridium difficile.5 6 7 8 Only one relapse of colitis after treatment with vancomycin has been reported.9 This report documents the relapse of colitis in three patients after discontinuation of treatment with vancomycin by mouth. Case Reports Pertinent clinical data appear in Table 1. Pseudomembranous colitis and relapse of colitis in Cases 1 and 2 were documented by sigmoidoscopy and rectal biopsy, according to established criteria.10 The initial episode of colitis in Case 3 was revealed by air-contrast barium enema, . . .

C. difficile (CD) and its cytotoxin (C) has been demonstrated to be responsible for antimicrobial induced diarrhea (AID) and pseudomembranous colitis. We determined the incidence and manifestations of CD and C in 3 groups (Gp) of children with suspected acute or chronic AID (Gp 1), children with chronic diarrhea prior to antimicrobial therapy (Gp II) and control children without diarrhea (Gp III). Antibiotics (n of patients) used in Gp I include: lincomycin (1), clindamycin (1), ampicillin (4), amoxicillin (1), in Gp II inciude penicillin (2), metronidazole (1), amoxicillin (2), ampicillin (2), Six of 6 patients in Gp I had mild proctocolitis confirmed by rectal biopsy without pseudomembranes on proctosigmoidoscopy. All 7 patients in Gp I became asymptomatic within 6 weeks of discontinuing antimicrobial therapy except 1 patient who received oral vancomycin (V) and became asymptomatic during V therapy but diarrhea recurred after V therany with stool culture + for CD and C for up to 6 months. Children may become chronic carriers of CD; the presence of CD and C can be used to distinguish acute/chronic colitis related to antimicrobial therapy from other causes of colitis in children.