Remember Me
Or use your Academic/Social account:


Or use your Academic/Social account:


You have just completed your registration at OpenAire.

Before you can login to the site, you will need to activate your account. An e-mail will be sent to you with the proper instructions.


Please note that this site is currently undergoing Beta testing.
Any new content you create is not guaranteed to be present to the final version of the site upon release.

Thank you for your patience,
OpenAire Dev Team.

Close This Message


Verify Password:
Verify E-mail:
*All Fields Are Required.
Please Verify You Are Human:
fbtwitterlinkedinvimeoflicker grey 14rssslideshare1
Elmer, Gary W.; Vega, Rosario; Mohutsky, Michael A.; McFarland, Lynne V. (2011)
Publisher: Microbial Ecology in Health and Disease
Journal: Microbial Ecology in Health and Disease
Languages: English
Types: Article

Classified by OpenAIRE into

mesheuropmc: biochemical phenomena, metabolism, and nutrition
The etiology of C. difficile infection is primarily through contact of the pathogen to an intestinal milieu perturbed by exposure to antimicrobials. We have evaluated the relative abilities of 14 widely used antimicrobials to initiate a terminal infection in a modified hamster model of C. difficile disease. Animals were exposed to a highly toxinogenic strain of C. difficile for 10 days and were dosed with antibiotics for 5 days. Our results showed that orally administered clindamycin, amoxicillin, amoxicillin:clavulanate, and ampicillin initiated early onset disease that occurred during the 5 days of antibiotic dosing. Parenterally administered imipenem and ceftriaxone initiated disease within the first 2 days of dosing. Late onset disease (1–5 days after cessation of dosing) occurred in animals receiving the oral drugs, erythromycin, clarithromycin, and ciprofloxacin and in animals receiving parenterally administered piperacillin, piperacillin:tazobactam, ampicillin:sulbactam, and ciprofloxacin. No symptoms or C. difficile toxin A was evident in metronidazole treated, vancomycin treated or control animals not receiving antibiotics. Cecal antibiotic levels were below the MIC values for C. difficile but resulted in a perturbed intestinal microflora as evidenced by elevated cecal weights. This hamster model may be a useful model to study antibiotics relative to their risk of initiating early or late onset C. difficile disease in humans.
  • The results below are discovered through our pilot algorithms. Let us know how we are doing!

    • 1. Kelly CP, LaMont JT. Clostridium difficile infection. Ann Rev Med 1998; 49: 375 - 90.
    • 2. Gorbach SL, Bartlett JG. PM enterocolitis: A review of its diverse forms. J Infect Dis ;(Suppl) 1977; 135: S89 - 94.
    • 3. Fekety R, McFarland LV, Surawicz CM, Greenberg RN, Elmer GW, Mulligan ME. Recurrent Clostridium difficile diarrhea: Characteristics of and risk factors for patients enrolled in a prospective, randomized, double-blinded trial. Clin Infect Dis 1997; 24: 324 - 33.
    • 4. Tedesco FJ. Clindamycin and colitis: a review. J Infect Dis 1977; 135: S95 - 8.
    • 5. Bartlett JG, Chang TW, Gurwith M, Gorbach SL, Onderdonk AB. Antibiotic-associated-pseudomembraneous colitis due to toxin-producing Clostridia. N Engl J Med 1978; 298: 531 - 4.
    • 6. Gantz NM, Zawacki JK, Dickerson WJ, Bartlett JG. Pseudomembranous colitis associated with erythromycin. Annals of Internal Medicine 1979; 91: 866 - 7.
    • 7. Job ML, Jacobs NFJ. Drug-induced Clostridium difficile-associated disease. Drug Safety. 1997; 17: 37 - 46.
    • 8. Settle CD, Wilcox MH. Review article: antibiotic-induced Clostridium difficile infection. Aliment Pharmacol Ther 1996; 10: 835 - 41.
    • 9. Spencer RC. The role of antimicrobial agents in the aetiology of Clostridium difficile-associated disease. J Antimicrob Chemother. (suppl. C) 1998; 41: 21 - 7.
    • 10. Anand A, Bashey B, Mir T, Glatt AE. Epidemiology, clinical manifestations, and outcome of Clostridium difficile-associated diarrhea. Am J Gastroenterol 1994; 89: 519 - 23.
    • 11. Silva J, Fekety R, Werk C, et al. Inciting and etiologic agents of colitis. Rev Infect Dis 1984; 6: S214 - 21.
    • 12. Aronsson B, Mo¬® llby R, Nord CE. Antimicrobial agents and Clostridium difficile in acute enteric disease: Epidemiological data from Sweden, 1980 - 82. J Infect Dis 1985; 151: 476 - 81.
    • 13. de Lalla F, Privitera G, Ortisi G, et al. Third generation cephalosporins as a risk factor for Clostridium difficile-associated disease: a four-year survey in a general hospital. J Antimicrob Chemother 1989; 23: 623 - 31.
    • 14. Bignardi GE. Risk factors for Clostridium difficile infection. J Hosp Infect 1998; 40: 1 - 15.
    • 15. Ebright JR, Fekety R, Silva J, Wilson KH. Evaluation of eight cephalosporins in hamster colitis model. Antimicrob Agents Chemother 1981; 19: 980 - 6.
    • 16. Bartlett JG, Chang TW, Moon N, Onderdonk AB. Antibiotic-induced lethal enterocolitis in hamsters: studies with eleven agents and evidence to support the pathogenic role of toxin-producing Clostridia.. Am J Vet Res 1978; 39: 1525 - 30.
    • 17. Weinberg DS, Fernandes PB, Kao CC, Clark JM, Bonner DP, Sykes RB. Evaluation of aztreonam, cefoperazone, latamoxef and ceftazidime in the hamster colitis model. J Antimicrob Chemother 1986; 18: 729 - 45.
    • 18. Larson HE, Borriello SP. Quantitative study of antibiotic-induced susceptibility to Clostridium difficile enterocecitis in hamsters. Antimicrobial Agents & Chemotherapy 1990; 34: 1348 - 53.
    • 19. Torres JF, Lyerly DM, Hill JE, Monath TP. Evaluation of formalin-inactivated Clostridium difficile vaccines administered by parenteral and mucosal routes of immunization in hamsters. Infect Immun 1995; 63: 4619 - 27.
    • 20. Bongaerts GPA, Lyerly DM. Role of toxins A and B in the pathogenesis of Clostridium difficile disease. Microbial Pathogenesis 1994; 17: 1 - 12.
    • 21. Kink JA, Williams JA. Antibodies to recombinant Clostridium difficile toxins A and B are an effective treatment and prevent relapse of C. difficile-associated disease in a hamster model of infection. Infect Immun 1998; 66: 2018 - 25.
    • 22. McFarland LV, Mulligan ME, Kwok RY, Stamm WE. Nosocomial acquisition of Clostridium difficile infection. N Engl J Med 1989; 320: 204 - 10.
    • 23. Hirschhorn LR, Trnka Y, Onderdonk A, Lee M-LT, Platt R. Epidemiology of community-acquired Clostridium difficile-associated diarrhea. J Infect Dis 1994; 169: 127 - 33.
    • 24. Borriello SP. Pathogenesis of Clostridium difficile infection. J Antimicrob Chemother ;(suppl. C) 1998; 41: 13 - 9.
    • 25. Gerding DN, Olson MM, Peterson LR, et al. Clostridium difficile-associated diarrhea and colitis in adults. Archives of Internal Medicine 1986; 146: 95 - 100.
    • 26. Olson MM, Shanholtzer CJ, Jr Lee JT, Gerding DN. Ten years of prospective Clostridium difficile-associated disease surveillance and treatment at the Minneapolis VA Medical Center, 1982 - 1991. Infect Control Hosp Epidemiol 1994; 15: 371 - 81.
    • 27. McFarland LV. Giannella RA, editors. Gastroenterology Clinics of North America. Philadelphia: WB Saunders; 1993;Diarrhea acquired in the hospital. p. 563 - 577.
    • 28. Mitchell DK, Van R, Mason EH, Norris DM, Pickering LK. Prospective study of toxigenic Clostridium difficile in children given amoxicillin:clavulanate for otitis media. Pediatr Infect Dis J 1996; 15: 514 - 9.
    • 29. Salata RA, Gebhart RL, Palmer DL, et al. Pneumonia treated with imipenem:cilastatin. Am J Med 1985; 78: 104 - 9.
    • 30. Berkeley AS, Freedman K, Hirsch J, Ledger WJ. Imipenem: cilastatin in the treatment of obstetric and gynecologic infections. Am J Med 1985; 78: 79 - 84.
    • 31. James AH, Katz VL, Dotters DJ, Rogers RG. Clostridium difficile infection in obstetric and gynecologic patients. South Med J 1997; 90: 889 - 92.
    • 32. McFarland LV, Bauwens JE, Melcher SA, Surawicz CM, Greenberg RN, Elmer GW. Ciprofloxacin-associated Clostridium difficile disease. The Lancet 1995; 346: 977 - 8.
  • No related research data.
  • No similar publications.

Share - Bookmark

Cite this article

Collected from