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How do I get infected by C. difficile?

C. difficile infection typically requires two factors: the ingestion of spores via the fecal-oral route and the disruption of healthy microbiota (6).

Spore Spreading

C. difficile can be released into the environment in spore form by individuals who are infected or colonized. Spores can be transmitted between patients via common environmental surfaces (medical equipment, hospital surfaces, and even hospital pet therapy dogs) or the contaminated hands of healthcare personnel (6). Once C. difficile spores reach the intestine, they germinate into the vegetative form of the bacterium, which is capable of producing toxins but is also able to be targeted with to antimicrobial treatments (6).

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Most cases of C. difficile in the United States are associated with in- or outpatient contact in a healthcare setting (7, 8). However, 3% of healthy adults and almost 10% of hospitalized adults or long-term residents of care facilities are reported to be C. difficile carriers, which are colonized by the bacteria but are asymptomatic (9, 10). Community cases, which are defined by lack of hospitalization or antibiotic use within 12-weeks of C. difficile infection diagnosis, make up an increasing number of reported cases (11). Exposure to retail food products and domestic animals has been hypothesized to be a potential source of C. difficile in community cases (12), as this bacterium is widely present in nature (water, soil, food products, domestic and farm animals) (13).

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Gut Microbiota Disruption

The gut contains an extensive ecosystem of microorganisms (~10^11 bacteria per gram of intestinal content) that plays an important protective role in our health – this is referred to as the gut microbiota. Antibiotic use can kill these “good” protective bacteria allowing C. difficile spores to germinate, multiply, and produce toxins (14). The toxins released by C. difficile damage the surface of the intestine (14), causing diarrhea, abdominal pain, and fever, as well as more severe symptoms (5).

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References

5.         McDonald LC, Gerding DN, Johnson S, Bakken JS, Carroll KC, Coffin SE, et al. Clinical Practice Guidelines for Clostridium difficile Infection in Adults and Children: 2017 Update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA). Clin Infect Dis. 2018;66(7):e1-e48.

6.         Loo VG, Bourgault A-M, Poirier L, Lamothe F, Michaud S, Turgeon N, et al. Host and Pathogen Factors for Clostridium difficile Infection and Colonization. New England Journal of Medicine. 2011;365(18):1693-703.

7.         Chitnis AS, Holzbauer SM, Belflower RM, Winston LG, Bamberg WM, Lyons C, et al. Epidemiology of community-associated Clostridium difficile infection, 2009 through 2011. JAMA Intern Med. 2013;173(14):1359-67.

8.         Jury LA, Sitzlar B, Kundrapu S, Cadnum JL, Summers KM, Muganda CP, et al. Outpatient healthcare settings and transmission of Clostridium difficile. PloS One. 2013;8(7):e70175-e.

9.         Zacharioudakis IM, Zervou FN, Pliakos EE, Ziakas PD, Mylonakis E. Colonization with toxinogenic C. difficile upon hospital admission, and risk of infection: a systematic review and meta-analysis. Am J Gastroenterol. 2015;110(3):381-90; quiz 91.

10.       Riggs MM, Sethi AK, Zabarsky TF, Eckstein EC, Jump RL, Donskey CJ. Asymptomatic carriers are a potential source for transmission of epidemic and nonepidemic Clostridium difficile strains among long-term care facility residents. Clin Infect Dis. 2007;45(8):992-8.

11.       Guh AY, Mu Y, Winston LG, Johnston H, Olson D, Farley MM, et al. Trends in U.S. Burden of Clostridioides difficile Infection and Outcomes. New England Journal of Medicine. 2020;382(14):1320-30.

12.       Gould LH, Limbago B. Clostridium difficile in food and domestic animals: a new foodborne pathogen? Clin Infect Dis. 2010;51(5):577-82.

13.       Bauer MP, Kuijper EJ. Potential sources of Clostridium difficile in human infection. Infect Dis Clin North Am. 2015;29(1):29-35.

14.       Britton RA, Young VB. Role of the intestinal microbiota in resistance to colonization by Clostridium difficile. Gastroenterology. 2014;146(6):1547-53.

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