Clostridium difficile, an anaerobic, spore-forming, toxin-forming, gram-positive bacillus present in the bacterial flora of the colon is the principal cause of nosocomial diarrhoea in adults.
Aim: Assessment of favouring factors of Clostridium difficile infections as well as the interactions between them, in critically ill hospitalized patients undergoing complex medical and surgical treatments.
Material and Methods: A retrospective case-control study involving eighty patients admitted in the Intensive Care Unit (ICU) of the County Clinical Emergency Hospital Tîrgu-Mureş was conducted between January and October 2014. Patients aged eighteen years and over, who had undergone complex medical and surgical treatment, were divided into two subgroups. Group 1 included patients who developed diarrhoea but were not diagnosed as having a Clostridium difficile infection (CDI). Group 2 included patients who developed diarrhoea due to CDI as indicated by a positive culture and the expression of exotoxin. The assessed parameters were age, length of stay (LOS), antibiotic spectrum, association with proton pump inhibitors (PPI) or H2-receptor antagonists, immunological status, the presence or lack of gastrointestinal tract surgery.
Results: The mean age was 64.6 years with an average LOS of 10 days. Fifty-six percent of patients came to the ICU from internal medicine wards and forty-three percent from surgical wards. 20.5% of them were immunosuppressed. Co-association of ceftriaxone and pantoprazole significantly increased the risk of CDI compared to co-administration of any other antibiotic or pantoprazole (p=0.01). The odds ratio for Pantoprazole together with any antibiotic versus antibiotic therapy alone was significantly higher (p=0.018) with a sevenfold increase in the risk of positive exotoxin increase.
Conclusions: Antibiotic use is associated with “no risk to develop CDI” in the first five days of administration. PPIs associated therapy increased the risk of CDI in first seventy-two hours regardless of the antibiotic type, and contributes to an active expression of CD exotoxin.
If the inline PDF is not rendering correctly, you can download the PDF file here.
1. Walters PR Zuckerbraun BS. Clostridium difficile infection. Clinical Challenges and management strategies. Critical Care Nurse. 2014;34:2-35.
2. Barletta JF Sclar DA. Proton pump inhibitors increase the risk for hospital-acquired Clostridium difficile infection in critically ill patients. Crit Care. 2014;18:714.
3. Vindigni SM Surawicz CM. C. difficile Infection: Changing epidemiology and management paradigms. Clin Transl Gastroenterol. 2015;6e99 .
4. Miller BA Chen LF Sexton DJ Anderson DJ. Comparison of the burdens of hospital onset healthcare facility-associated Clostridium difficile infection and of healthcare-associated infection due to methicillin-resistant Staphylococcus aureus in community hospitals. Infect Control Hosp Epidemiol. 2011;32:387-90.
5. Vaishnavi C. Clinical spectrum & pathogenesis of Clostridium difficile associated diseases. Indian J Med Res. 2010; 131:487-99.
6. McDonald LC Killgore GE Thompson A et al. An epidemic toxin gene variant strain of Clostridium difficile. N Engl J Med. 2005;353:2433-41.
7. Vecchio AL Zacur GM. Clostridium difficile infection: an update on epidemiology risk factors and therapeutic options. Curr Opin Gastroenterol. 2012;28:1-9.
8. Biswal S. Proton pump inhibitors and risk for Clostridium difficile associated diarrhea. Biomed J. 2014;37:178-83.
9. Oake N Taljaard M Walraven C Wilson K Roth V Forster AJ. The effect of hospital-acquired Clostridium difficile infection on in-hospital mortality. Arch Intern Med. 2010;170:1804-10.
10. Poutanen SM Simor AE. Clostridium difficile associated diarrhea in adults. CMAJ. 2004;171:51-8.
11. Voth DE Ballard JD. Clostridium difficile toxins: Mechanisms of action and role in disease. Clin Microbiol Rev. 2005;18:247-63.
12. Donskey CJ. The role of the intestinal tract as a reservoir and source for transmission of nosocomial pathogens. Clin Infect Dis. 2004;39:219-26.
13. Pepin J Saheb N Coulombe MA et al. Emergence of fluoroquinolones as the predominant risk factor for Clostridium difficile-associated diarrhea: A cohort study during an epidemic in Quebec. Clin Infect Dis. 2005;41:1254-60.
14. Neal KR Scott HM Slack RCB Logan RFA. Omeprazole as a risk factor for campylobacter gastroenteritis: case control study. BMJ 1996;321:414-5.
15. Williams C. Occurrence and significance of gastric colonization during acid-inhibitory therapy. Best Pract Res Clin Gastroenterol. 2001;15:511-21.
16. Linsky A Gupta K Lawler EV Fonda JR Hermos JA. Proton pump inhibitors and risk for recurrent Clostridium difficile infection. Arch Intern Med. 2010;170:772-8.
17. Klingensmith ME Neville LL Delpire E Wolfe MM Soybel DI. Gastrin-mediated effects of omeprazole on rat colon mucosa. Surgery. 1999;126:272-8.
18. Liebensten Z Wenisch C Patruta S Parschalk B Daxbock F Garninger W. Omeprazole treatment diminishes intra- and extra-cellular neutrophil reactive oxygen production and bacterial activity. Crit Care Med. 2002;30:1118-22.
19. Dial S Delaney JAC Barkun AN Suissa S. Use of gastric acid-suppressive agents and the risk of communityacquired Clostridium difficile-associated disease. JAMA. 2005;294:2989-95.
20. MacLaren R Reynolds PM Allen RR. Histamine-2 Receptor Antagonists vs Proton Pump Inhibitors on Gastrointestinal Tract Hemmorhage and Infectious Complications in the Intensive Care Unit FREE. JAMA Intern Med. 2014;174:564-74.
21. Dubberke ER Reske KA Yan Y Olsen MA MacDonald LC Fraser VJ. Clostridium difficile-associated disease in a setting of endemicity: identification of novel risk factors. Clin Infect Dis. 2007;45:1543-9.