Infections difficile

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. 

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. 

Clindamycin 20-30 mg/kg per day in 3-4 doses (adult 300 mg four times daily or 450 mg three times daily) Nausea, diarrhea, C. difficile colitis, anorexia S Oral liquid has very poor taste only for pneumococcal infection... 

The incidence of community-associated C. difficile infection (defined as occurring in patients not hospitalized in the year prior to diagnosis) is increasing.36 In addition to antibiotic use, community-associated C. difficile cases are associated with the use of gastric acid suppressive agents (e.g., proton pump inhibitors and H2-receptor antagonists). 

Leukocytosis, hypoalbuminemia, and fecal leukocytes are nonspecific but suggestive of C. difficile infection. 

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. 

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. 

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. 

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

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. 

Brito GA, Sullivan GW, Ciesla WP Jr, Carper HT, Mandell GL, Guerrant RL Clostridium difficile toxin A alters in vitro-adherent neutrophil morphology and function. J Infect Dis 2002 185 1297-1306. 

Flegel WA, Muller F, Daubener W, Fischer HG, Hadding U, Northoff H Cytokine response by human monocytes to Clostridium difficile toxin A and toxin B. Infect Immun 1991 59 3659-3666. 

Alcantara C, Stenson WF, Steiner TS, Guerrant RL Role of inducible cyclooxygenase and prostaglandins in Clostridium difficile toxin A-induced secretion and inflammation in an animal model. J Infect Dis 2001 184 648-652. 

Cerquetti M, Luzzi I, Caprioli A, Sebastianel-li A, Mastrantonio P Role of Clostridium difficile in childhood diarrhea. Pediatr Infect Dis J 1995 14 598-603. 

Bouza E, Pelaez T, Alonso R, Catalan P, Munoz P, Creixems MR Second-look cytotoxicity An evaluation of culture plus cyto-toxin assay of Clostridium difficile isolates in the laboratory diagnosis of CDAD. J Hosp Infect 2001 48 233-237. 

Rifaximin Rifamycin Antibiotic Gut bacteria Enteric infection Diarrhea, infectious Hepatic encephalopathy Small intestine bacterial overgrowth Inflammatory bowel disease Colonic diverticular disease Irritable bowel syndrome Constipation Clostridium difficile infection Helicobacter pylori infection Colorectal surgery Bowel decontamination, selective Pancreatitis, acute Bacterial peritonitis, spontaneous Nonsteroidal anti-inflammatory drug enteropathy... 

Progress in defining new treatments for C. difficile infection has been hindered by the heterogeneous nature of hospital-acquired diarrhea, and in particular by whether colitis and/or pseudomembranous colitis is present in individual cases. Study groups have usually been poorly defined in this context, and given the spontaneous resolution of symptoms in a proportion of cases the true efficacy of treatment approaches often remains uncertain. Enthusiasm to explore new treatment possibilities for C. difficile has been largely fuelled by the apparently high relapse rate of conventional (metronidazole or vancomycin) treatment [138],... 

There is a consensus amongst published recommendations for the management of C. difficile infection [19-21], The most important first step in the treatment is cessation of the precipitating agent, most commonly antibiotics, if this is deemed to be medically appropriate. In mild disease, this is often sufficient for full recovery. In more... 

A randomized open trial, performed in patients with C. difficile pseudomembranous colitis, compared rifaximin (200 mg 3 times daily) to vancomycin (500 mg 2 times daily) and found the two drugs similarly effective [141]. The clearance of bacterial toxins was, however, more rapid with vancomycin. Further large double-blind clinical studies are needed to better define the role of rifaximin in the treatment of C. difficile infection. 

Zimmerman MJ, Bak A, Sutherland LR Review article Treatment of Clostridium difficile infection. Aliment Pharmacol Ther 1997 11 1003-1012. 

Wilcox MH, Spencer RC Clostridium difficile infection Responses, relapses and reinfections. J Hosp Infect 1992 22 85-92. 

Wenisch C, Parschalk B, Hasenhundl M, Hirschl AM, Graninger W Comparison of vancomycin, teicoplanin, metronidazole, and fusidic acid for the treatment of Clostridium difficile-associated diarrhea. Clin Infect Dis 1996 22 813-818. 

McFarland LV, Stamm WE Nosocomial Clostridium difficile infection (letter). N Engl J Med 1989 321 190. 

Barbut F, Petits JC Epidemiology of Clostridium difficile-associated infections. Clin Microbiol Infect 2001 7 405-410. 

Nelson DE, Auerbach SB, Baltch AL, Desjar-din E, Beck-Sague C, Rheal C, Smith RP, Jarvis WR Epidemic Clostridium difficile-associated diarrhea Role of second- and third-generation cephalosporins. Infect Control Hosp Epidemiol 1994 15 88-94. 

Dickinson et al. [27], in 1985, published a double-blind controlled trial on the use of oral vancomycin as an adjunctive therapy in acute exacerbations of idiopathic colitis. No significant difference was found between the two treatment groups with only a trend in favor of a superior efficacy of vancomycin. It is important to underline that 7 of the 40 patients enrolled had colonic CD and that none of them had C. difficile infection that could explain the action of vancomycin. Subsequently, intravenous metronidazole, in addition to steroids, was effective similar to placebo in inducing remission [28],... 

Infection with Helicobacter pylori is widely spread in the world and as many as 50% of the population is estimated to be infected, with the highest incidence in Asia and developing countries. The bacterial toxins of Helicobacter pylori damage the epithelial cells in the stomach and can in the long term lead to gastric atrophy (Pilotto 1996, Faisal et al. 1990, Pilotto et al. 1999). The consequential decrease in secretion of acid causes a higher gastric pH level which can increase the risk of enteric infections, for example, with Campylobacter and Clostridium difficile. 

Karjalainen, T., Bare, M. C., Collignon, A., Trolle, S., Boureau, H., Cotte-Laffitte, J., and Bourlioux, P. (1994). Cloning of a genetic determinant from Clostridium difficile involved in adherence to tissue culture cells and mucus. Infect. Immun. 62,4347- 355. 

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