Clostridium difficile

Although immediate reactions of anaphylaxis, bronchospasm, and urticaria have been reported, most commonly patients exhibiting an adverse reaction develop a maculopapular rash, usually after several days of therapy. They may also develop fever and eosinophilia (80,219). Cefoperazone (34) and ceftriaxone (39), having greater biUary excretion than other cephalosporins, are associated with an increased risk of diarrhea, which may be caused by selection of cytotoxin producing stains of Clostridium difficile (219). 

M ribosomal protection Neisseria, Mycoplasma, Ureaplasma, Haemophilus, Campylobacter, Clostridium, Enterococcus, Staphylococcus, Streptococcus Gardnerella, Kingella, Eikenella, Veillonella, Tusobacterium, Peptostreptococcus Clostridium difficile. Streptococcus pneumoniae... 

Important members of this toxin family are Clostridium difficile toxins A and B, which are implicated in antibiotics-associated diarrhea and pseudomembranous colitis. The large clostridial cytotoxins are single-chain toxins with molecular masses of 250-308 kDa. The enzyme domain is located at the N terminus. The toxins are taken up from an acidic endosomal compartment. They glucosylate RhoA at Thr37 also, Rac and Cdc42 are substrates. Other members of this toxin family such as Clostridium sordellii lethal toxin possess a different substrate specificity and modify Rac but not Rho. In addition, Ras subfamily proteins (e.g., Ras, Ral, and Rap) are modified. As for C3, they are widely used as tools to study Rho functions [2] [4]. 

Vancomycin (Vancocin) acts against susceptible gram-positive bacteria by inhibiting bacterial cell wall synthesis and increasing cell wall permeability. This drug is used in the treatment of serious gram-positive infections that do not respond to treatment with other anti-infectives. It also may be used in treating anti-infective-associated pseudomembranous colitis caused by Clostridium difficile. 

D Ari L, WA Barker (1985) p-cresol formation by cell-free extracts of Clostridium difficile. Arch Microbiol 143 311-312. 

Liyanage H, S Kashket, M Young, ER Kashket (2001) Clostridium beijerinckii and Clostridium difficile detoxify methylglyoxal by a novel mechanism involving glycerol dehydrogenase. Appl Environ Microbiol 67 2004-2010. 

Martin, A. J., Collins, C. J., Ruddy, R., Drudy, D., Hannan, M. M., and Kyne, L. (2008). Simultaneous control of norovirus and Clostridium difficile outbreaks due to enhanced infection prevention and control measures. /. Hosp. Infect. 68,180-181. 

Weber, D. J., Rutala, W. A., Miller, M. B., Huslage, K., and Sickbert-Bennett, E. (2010). Role of hospital surfaces in the transmission of emerging health care-associated pathogens Norovirus, Clostridium difficile, and Acinetobacter species. Am. ]. Infect. Control 38, S25-S33. 

Bacteria are likely precipitants in many other cases including Escherichia coli, Salmonella species, Shigella species, Vibrio cholerae, and Clostridium difficile. The term dysentery has often been used to describe some of these bacterial infections when associated with serious occurrences of bloody diarrhea. Additionally, acute diarrheal conditions can be prompted by parasites-protozoa such as Entamoeba histolytica, Microsporidium, Giardia lamblia, and Cryptosporidium parvum. Most of these infectious agents can be causes of traveler s diarrhea, a common malady alflicting travelers worldwide. It usually occurs during or just after travel subsequent to the ingestion of fecally-contaminated food or water. It has an abrupt onset but usually subsides within 2 to 3 days. 

Stool testing for ova and parasites may identify Clostridium difficile and amoeba as possible causes of diarrhea rather than IBS. 

Nosocomial Clostridium difficile-associated diarrhea (CDAD) is almost always associated with antimicrobial use therefore, we should avoid unnecessary and inappropriate antibiotic therapy. Almost all antibiotics except aminoglycosides have been associated with CDAD. 

Stoddart B, Wilcox MH. Clostridium difficile. Curr Opin Infect Dis 2002 15 513-518. 

It has been postulated that Chlamydia may produce a heat shock protein that causes tissue damage through a delayed hypersensitivity reaction. C. trachomatis may also possess DNA evidence of toxin-like genes that code for high-molecular-weight proteins with structures similar to Clostridium difficile cytotoxins, enabling inhibition of immune activation. This may explain the observation of a chronic C. trachomatis infection in subclinical PID. 

Hecht G, C Pothoulakis, JT LaMont, JL Madara. (1988). Clostridium difficile toxin A perturbs cytoskeletal structure and tight junction permeability of cultured human intestinal epithelial monolayers. J Clin Invest 82 1516-1524. 

Cartmill,T. D. Orr, K. Freeman, R. Sisson, P. R. Lightfoot,N. F. Nosocomial infection with Clostridium difficile investigated by pyrolysis mass spectrometry. J. Med. Microbiol. 1992,37, 352-356. 

O Neill, G. L. Brazier, J. S. Magee, J. T. Duerden, B. I. A comparison of PCR ribotyping and pyrolysis mass spectrometry for typing clinical isolates of Clostridium difficile. Anaerobe 1996, 2, 211-215. 

Kyne, L. Merry, C. O Connell, B. Harrington, R Keane, C. O Neill, D. Simultaneous outbreaks of two strains of toxigenic Clostridium difficile in a general hospital. J. Hosp. Infect. 1998,38,101-112. 

Inhibition of ENR FabK is appropriate for either a narrow spectrum against Streptococci and Clostridium difficile since it is an essential target for these species, or a broader spectrum in combination with a FabI inhibitor since some bacteria such as E. faecalis share both isoforms. 

Diarrhea Enteric infections Escherichia coli Cryptosporidium Shigella Vibrio cholerae Clostridium difficile Salmonella... 

Lima AA, Innes DJ Jr, Chadee K, Lyerly DM, Wilkins TD, Guerrant RL Clostridium difficile toxin A. Interactions with mucus and early sequential histopathologic effects in rabbit small intestine. Lab Invest 1989 61 419 125. 

Eichel-Streiber C, Warfolomeow I, Knautz D, Sauerborn M, Hadding U Morphological changes in adherent cells induced by Clostridium difficile toxins. Biochem Soc Trans 1991 19 1154-1160. 

Krivan HC, Clark GF, Smith DF, Wilkins TD Cell surface binding site for Clostridium difficile enterotoxin Evidence for a glycoconjugate containing the sequence Gal alpha l-3Galbeta l-4GlcNAc. Infect Immun 1986 53 573-581. 

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