Antibiotic-associated

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]. 

As with all drugs, the specific side effects of the quinolones must be considered when they are chosen for treatment of bacterial infections [5]. Reactions of the gastrointestinal tract and the central neivous system are the most often observed adverse effects during therapy with quinolones. It should be underlined, however, that compared with many other antimicrobials, diarrhea is less frequently observed during quinolone treatment. Antibiotic-associated colitis has been observed rarely during quinolone therapy. Similarly, hypersensitivity reactions, as observed during therapy with penicillins and other (3-lactams, is less frequently caused by quinolones. Some other risks of quinolone therapy have been defined and must be considered if a drug from this class is chosen for treatment of bacterial infections. 

Additionally, with chronic hypoxia, normal hemoglobin and hematocrit values may represent relative anemia.12 Increased red blood cell production is a physiologic response to hypoxia however, this response may be blunted in CF and may result in symptoms of anemia despite normal lab values. Abnormal bleeding may also be observed as a result of vitamin K malabsorption or antibiotic-associated depletion of gastrointestinal flora and vitamin K synthesis. 

Repeated oral administration of an antibiotic that reaches very high concentrations within the GI lumen could have profound effects on intestinal flora [ 12,13]. As expected, rifaximin markedly reduced fecal bacterial counts during oral intake but the effect was short-lasting since the bacterial population recovered within 1-2 weeks from the end of treatment (table 4) [82], Most importantly, fungal colonization occurred very rarely. Indeed, Candida albicans, which has been implicated in the pathogenesis of antibiotic-associated diarrhea [82, 83], was isolated from the fecal samples of only 2 out of 10 patients given 1,200 mg of rifaximin daily [81] and in none of the volunteers taking 800 mg daily [82],... 

Surawicz CM Antibiotic-associated diarrhea and pseudomembranous colitis Are they less common with poorly absorbed antimicrobials Chemotherapy 2005 51(suppl 1 ) 81—89. 

Antibiotic-associated diarrhea Pseudomembranous colitis Clostridium difficile Rifaximin Clostridium difficile-assodated diarrhea... 

Diarrhea is a well-known complication of antibiotic therapy. Rates of antibiotic-associated diarrhea (AAD) vary from 5 to 25%. Some antibiotics are more likely to cause diarrhea than others, specifically, those that are broad spectrum and those that target anaerobic flora. This paper reviews the effects of antibiotics on the fecal flora as well as host factors which contribute to AAD. Clinical features and treatment of AAD are also described. Prevention of AAD rests on wise antibiotic policies, the use of probiotics and prevention of acquisition in the hospital setting. Data from clinical trials suggest that poorly absorbed antimicrobials might have a decreased risk of causing AAD and Clostridium difficile-associated disease, as concluded from studies of antibiotics used for preoperative bowel decontamination and poorly absorbed antibiotics used for traveler s diarrhea. Controlled trials would prove this but are not yet available. Probiotics may be a good adjunct to poorly absorbed antibiotics to minimize the risk of diarrhea associated with antibiotics. 

Bergogne-Berezin E Treatment and prevention of antibiotic associated diarrhea. Int J Antimicrob Agents 2000 16 521-526. 

Bartlett JG Antibiotic-associated diarrhea. Clin Infect Dis 1992 15 573-581. 

Surawicz CM, Elmer GW, Speelman P, McFarland LV, Chinn J, Van Belle G Prevention of antibiotic-associated diarrhea by Saccharo-myces boulardii. A prospective study. Gastroenterology 1989 96 981-998. 

Clausen MR, Bonnen H, Tvede M, Mortensen PB Colonic fermentation to short-chain fatty acids is decreased in antibiotic-associated diarrhea. Gastroenterology 1991 101 1497-1504. 

Danna PL, Urban C, Beilin E, Rahal JJ Role of Candida in pathogenesis of antibiotic-associated diarrhoea in elderly inpatients. Lancet 1991 337 511-514. 

Ponnuvel KM, Rajkumar R, Menon T, Sanka-ranarayanan VS Role of Candida in indirect pathogenesis of antibiotic associated diarrhoea in infants. Mycopathologia 1996 135 145— 147. 

Krause R, Schwab E, Bachhiesl D, Daxbock F, Wenisch C, Krejs GJ, Reisinger EC Role of Candida in antibiotic-associated diarrhea. J Infect Dis 2001 184 1065-1069. 

Wistrom J, Norrby SR, Myhre EB, Eriksson S, Granstrom G, Lagergren L, Englund G, Nord CE, Svenungsson B Frequency of antibiotic-associated diarrhoea in 2462 antibiotic-treated hospitalized patients A prospective study. J Antimicrob Chemother 2001 47 43-50. 

McFarland LV Epidemiology, risk factors and treatments for antibiotic-associated diarrhea. Dig Dis 1998 16 292-307. 

Arvola T, Laiho K, Torkkeli S, Mykkanen H, Salminen S, Maunula L, Isolauri E Prophylactic Lactobacillus GG reduces antibiotic-associated diarrhea in children with respiratory infections A randomized study. Pediatrics 1999 104 e64. 

G, Gasbarrini A Effect of Lactobacillus GG supplementation on antibiotic-associated gastrointestinal side effects during Helicobacter pylori eradication therapy A pilot study. Digestion 2001 63 1-7. 

Wunderlich PF, Braun L, Fumagalli I, D Apuz-zo V, Heim F, Karly M, Lodi R, Politta G, Vonbank F, Zeltner L Double-blind report on the efficacy of lactic-acid-producing Enterococcus SF68 in the prevention of antibiotic-associated diarrhoea and in the treatment of acute diarrhoea. J Int Med Res 1989 17 333-338. 

An antibiotic association was used in an Italian randomized controlled study in which metronidazole 250 mg... 

The answer is c. (Hardman, pp 996-997r 1145—1146. Ka tzung, p 8455 Metronidazole is often used to treat antibiotic-associated enterocolitis, especially when caused by C difficile. Vancomycin is no longer preferred because it induces selection of resistant staphylococci. Clindamycin is also associated with C difficile colitis, but in another way a higher percentage of patients taking this over other antibiotics develop antibiotic-associated enterocolitis. 

Clindamycin, which is active against Gram-positive aerobic organisms and Gram-negative anaerobes, may cause antibiotic-associated colitis. 

Treatment with antibacterial agents alters the normal flora of the colon and may permit overgrowth of Clostridia. Studies indicate that a toxin produced by Clostridium difficile is a primary cause of antibiotic-associated colitis. ... 

Oral Staphylococcal enterocolitis and antibiotic-associated pseudomembranous colitis produced by C. difficile. The parenteral product may also be given orally for these infections. Oral vancomycin is not effective for other types of infection. 

Vancomycin is not absorbed after oral administration and must be given intravenously. Oral administrations are used for intraluminal gastrointestinal infections such as antibiotic-associated pseudomembranous colitis produced by Clostridium difficile. Vancomycin is widely distributed in the body but does not cross the blood brain barrier and does not penetrate into bone. It is excreted mainly via the urine, resulting in accumulation in patients with renal insufficiency. Its elimination half-life is 4-11 hours but can increase to 6-10 days in renal failure. 

The spectrum of gastrointestinal tract infections (GTI) cover a wide spectrum from asymptomatic Helicobacter pylori gastritis to self-limiting viral gastroenteritis to food poisoning to bacterial enterocolitis to antibiotic-associated Clostridium difficile colitis to typhoid fever with sepsis and multi-organ failure. 

Antibiotic-associated colitis and other superinfections may result from altered bacterial balance. 

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