Pseudomembranous Colitis (Clostridium Difficile Infection): Risks and Treatment Strategies
While Clostridioides difficile (formerly Clostridium difficile) is the primary organism behind PMC, it's not the only one. Other pathogens have occasionally been found to cause similar colonic inflammation and pseudomembrane formation [1], [3]. But C. difficile is the most common and clinically relevant.
The process starts with antibiotics. These medications while useful for treating bacterial infections can disrupt the balance of normal colonic flora in the gut. This gives C. difficile – often present in small amounts in the intestines – the opportunity to flourish [2], [7], [9]. Spores that were once dormant now find an environment ripe for growth.
C. difficile produces two potent toxins, toxin A (TcdA) and toxin B (TcdB). These toxins bind to cells lining the colon, damaging them and setting off a cascade of inflammation. In severe cases the body's immune response and cell damage leads to the hallmark pseudomembranes seen in PMC [5].
Not all antibiotic therapy is created equal, but broad spectrum agents like clindamycin, cephalosporins and fluoroquinolones are often implicated. These drugs wipe out a wide range of gut flora making room for C. difficile to flourish [10].
PMC symptoms often start during or shortly after antibiotics:
These symptoms can overlap with other conditions but the timing, especially after antibiotics, is a key clue.
PMC doesn't affect everyone the same way. While some people have mild diarrhea others can spiral into severe colitis and complications like:
These cases need urgent medical attention.
Healthcare providers consider PMC when a patient on antibiotics develops sudden or worsening diarrhea, so rapid diagnosis is key. But diagnosing it isn't always easy.
Metronidazole: Metronidazole is used for mild to moderate PMC. It's effective, cheap and oral [1], [8]. But it's being replaced by other treatments due to higher relapse rates and slower symptom resolution.
Vancomycin: Oral vancomycin is now the go to for severe or complicated C. difficile infections. It stays in the gut (where it's needed) without being absorbed into the bloodstream so it targets the infection locally.
PMC relapses so recurrent Clostridioides difficile infection is common. Some patients may need extended vancomycin tapers, fidaxomicin (a newer antibiotic) or even fecal microbiota transplantation (FMT).
FMT involves restoring healthy gut bacteria by transplanting stool from a donor—a treatment that's showing promising results in recurrent Clostridioides difficile infection cases [4].
One of the best ways to prevent PMC is smart antibiotic prescribing. Avoiding unnecessary prescriptions especially broad spectrum antibiotics can help preserve the natural gut microbiome and prevent C. difficile overgrowth.
Hospitals and healthcare facilities also have a role to play by enforcing infection control measures such as hand hygiene and isolation protocols to limit the spread of C. difficile spores.
Pseudomembranous colitis is more than just a complication of antibiotic use—it's a serious gastrointestinal illness that needs timely diagnosis and treatment. Understanding the underlying disruption of gut microbiota and toxin production is key to managing and preventing this condition. As we learn more about PMC the emphasis remains on prevention through good antibiotic stewardship and early intervention when symptoms occur.
[1] Surawicz, C. M., & McFarland, L. V. (1999). Pseudomembranous colitis: causes and cures. Digestion, 60(2), 91–100. https://doi.org/10.1159/000007633
[2] Janoir C. (2016). Virulence factors of Clostridium difficile and their role during infection. Anaerobe, 37, 13–24. https://doi.org/10.1016/j.anaerobe.2015.10.009
[3] Tang, D. M., Urrunaga, N. H., & von Rosenvinge, E. C. (2016). Pseudomembranous colitis: Not always Clostridium difficile. Cleveland Clinic journal of medicine, 83(5), 361–366. https://doi.org/10.3949/ccjm.83a.14183
[4] Surawicz, C. M., & McFarland, L. V. (2000). Pseudomembranous Colitis Caused by C. difficile. Current treatment options in gastroenterology, 3(3), 203–210. https://doi.org/10.1007/s11938-000-0023-x
[5] Castagliuolo, I., & LaMont, J. T. (1999). Pathophysiology, diagnosis and treatment of Clostridium difficile infection. The Keio journal of medicine, 48(4), 169–174. https://doi.org/10.2302/kjm.48.169
[6] Farooq, P. D., Urrunaga, N. H., Tang, D. M., & von Rosenvinge, E. C. (2015). Pseudomembranous colitis. Disease-a-month : DM, 61(5), 181–206. https://doi.org/10.1016/j.disamonth.2015.01.006
[7] Trnka, Y. M., & Lamont, J. T. (1984). Clostridium difficile colitis. Advances in internal medicine, 29, 85–107. https://pubmed.ncbi.nlm.nih.gov/6369936/
[8] Brar, H. S., & Surawicz, C. M. (2000). Pseudomembranous colitis: an update. Canadian journal of gastroenterology = Journal canadien de gastroenterologie, 14(1), 51–56. https://doi.org/10.1155/2000/324025
[9] Counihan, T. C., & Roberts, P. L. (1993). Pseudomembranous colitis. The Surgical clinics of North America, 73(5), 1063–1074. https://doi.org/10.1016/s0039-6109(16)46141-4
[10] Weymann L. H. (1982). Colitis caused by Clostridium difficile: a review. The American journal of medical technology, 48(11), 927–934. https://pubmed.ncbi.nlm.nih.gov/6758571/
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