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Gastroenteritis and Enterocolitis Quiz

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A hospitalised patient develops profuse diarrhoea and abdominal cramping several days after completing a course of broad-spectrum antibiotics. Which mechanism best explains the development of this condition?

A Loss of normal gut flora allowing toxigenic Clostridioides difficile overgrowth ✓
B Immune-mediated destruction of enterocytes triggered by antibiotic hypersensitivity
C Direct invasion of the intestinal mucosa by antibiotic-resistant bacteria causing inflammation
D Antibiotic-induced increase in colonic motility leading to reduced water absorption
E Direct damage to the intestinal epithelium by the antibiotic causing inflammation

The answer is A: Loss of normal gut flora allowing toxigenic Clostridioides difficile overgrowth

Explanation

Why A is correct

See Clostridium difficile. Option A is correct. The healthy large bowel is home to a huge community of bacteria, the gut microbiota (also called normal flora), and these organisms compete with harmful species and hold them in check. Broad-spectrum antibiotics kill many of these protective bacteria as well as the target infection. The antibiotic-induced change in gut flora is the dominant predisposing factor, and the antibiotics with the highest risk include cephalosporins, ampicillin and amoxicillin, clindamycin and fluoroquinolones. This leaves room for Clostridioides difficile, a spore-forming bacterium, to multiply. It secretes two toxins, an enterotoxin (toxin A) and a cytotoxin (toxin B), which damage the lining of the colon and cause fluid loss and inflammation. The result is diarrhoea and cramping, sometimes with bloody stool, typically beginning 5 to 10 days after starting antibiotics, though it can occur on the first day or up to 2 months later. In severe cases the colon shows pseudomembranes, plaques that are easily dislodged. Treatment is with oral fidaxomicin or vancomycin. A reminder is that antibiotics plus diarrhoea in hospital means think Clostridioides difficile.

Trigger: broad-spectrum antibiotics kill the protective gut bacteria.
High-risk drugs: cephalosporins, ampicillin and amoxicillin, clindamycin and fluoroquinolones.
Mechanism: Clostridioides difficile multiplies and releases toxins that damage the colon lining.
Treatment: oral fidaxomicin or vancomycin.

Why the other options are incorrect

B. Immune-mediated destruction of enterocytes triggered by antibiotic hypersensitivity: Antibiotic hypersensitivity causes problems such as rash, fever or anaphylaxis, not a colitis that follows the course of antibiotics. Immune destruction of enterocytes (the cells lining the bowel) is a feature of conditions such as coeliac disease. It would be the answer for a drug allergy.
C. Direct invasion of the intestinal mucosa by antibiotic-resistant bacteria causing inflammation: Clostridioides difficile disease is caused mainly by toxins acting on the lining of the colon, not by bacteria invading the bowel wall. Invasion by resistant bacteria would describe an invasive bacterial dysentery. The link to antibiotics is the loss of normal flora, not the resistance of an invader.
D. Antibiotic-induced increase in colonic motility leading to reduced water absorption: Antibiotic-induced increased motility can cause loose stool with some drugs, but it does not explain this hospital presentation of profuse diarrhoea and cramping days after a broad-spectrum course, where loss of protective flora allows Clostridioides difficile to overgrow. This option is off-target because it describes a drug effect rather than the infectious colitis asked for.
E. Direct damage to the intestinal epithelium by the antibiotic causing inflammation: Clostridioides difficile colitis is caused by toxins released after the organism overgrows, not by the antibiotic itself directly injuring the bowel. Direct epithelial injury would describe a toxic drug effect rather than the infectious mechanism asked for.

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More questions from this set. Start the quiz to answer them and see each explanation.

1
Which description best characterises Campylobacter jejuni as a cause of gastroenteritis?
2
A university student develops sudden onset vomiting, watery diarrhoea and low‑grade fever after an outbreak of illness in shared accommodation. Which of the following best explains both the high transmissibility and the usual management approach of the most likely causative pathogen?

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