Pseudomembranous enterocolitis

Pseudomembranous enterocolitis

Description, Causes and Risk Factors:

Enterocolitis with the formation and passage of pseudomembranous material in the stools; occurs most commonly as a sequel to antibiotic therapy; caused by a necrolytic exotoxin made by Clostridium difficile.

Pseudomembranous enterocolitis is a disease first recognized in the 1800's and thought to be related to poisons and irritants. Subsequently this disorder has been described in a variety of clinical settings including the postoperative state, after recent antibiotic therapy, debilitating illnesses such as uremia and congestive heart failure, obstruction of the colon, staphylococcal infection of the bowel and ischemia of the gut. These various clinical associations have led to multiple synonyms including postoperative enterocolitis, staphylococcal enterocolitis, antibiotic enterocolitis and, the original term, diphtheritic enterocolitis. Whether the term colitis or enterocolitis is used depends upon clinical, radiologic, surgical or pathologic localization. In approximately a third of the cases, the disease is confined to the colon.

Pseudomembranous enterocolitis can result in significant patient morbidity and mortality, especially if it is not diagnosed early. Overall mortality rates from 1.1% to 3.5% have been reported for patients with PMC. It is important for radiologists to be aware of this potentially life-threatening condition and its imaging characteristics because they may be the first to suggest the diagnosis.

Pseudomembranous enterocolitis usually caused by Clostridium difficile. Pseudomembranous enterocolitis can rarely be caused by other bacteria, eg Staphylococcus spp. or enterotoxigenic Clostridium perfringens, Campylobacter spp., Listeria spp. and Salmonella spp.

Pseudomembranous enterocolitis has emerged, particularly in recent years, as a major and very expensive healthcare problem. Spores formed by the organism are implicated in spread of infection and have implications for hygiene and prevention of infection. C. difficile is an anaerobic Gram-positive rod which secretes two types of toxin (A and B), which cause disruption to the barrier function of the colonic mucosa. They are cytotoxic to cells of the intestinal tract, B being about 1,000 times more potent than A. Transmission of infection is via an indirect fecal-oral route, through spores left on surfaces. The spores can survive for months and patients can become carriers. The risk of colonization increases with length of hospital stay.

C. difficile is classified into strains by polymerase chain reaction (PCR) ribotyping:

    Ribotype 001 is a common cause of C. difficile infection (CDI) in the UK.

  • C. difficile 027 (also known as: C. difficile NAP1/027 or C. difficile BI/NAP1/027) is associated with higher mortality, severity, and relapse rate.

  • C. difficile 078 has a higher incidence among community-acquired C. difficile infection (CA-CDI).


The clinical features of pseudomembranous enterocolitisinclude diarrhea, abdominal tenderness, fever, dehydration, and leukocytosis. Occasionally, patients with pseudomembranous enterocolitispresent with or progress to fulminant, life-threatening colitis. Such patients are acutely ill, with signs and symptoms of lethargy, fever, tachycardia, and abdominal pain, and may progress to toxic megacolon and colonic perforation resulting from full-thickness colonic necrosis.


Prior to the advent of tests to detect C. difficile toxins, the diagnosis was most often made by colonoscopy or sigmoidoscopy. The appearance of "pseudomembranes" on the mucosa of the colon or rectum is diagnostic of the condition. The pseudomembranes are composed of an exudate made of inflammatory debris, white blood cells, etc.

Although colonoscopy and sigmoidoscopy are still employed, stool testing for the presence of C. difficile toxins is now often the first-line diagnostic approach. Usually, only two toxins are tested for - toxin A and toxin B - but the organism produces several others. This test is not 100% accurate, with a considerable false-negative rate even with repeat testing.

Another, more recent two-step approach involves testing for the presence of C. difficile in the stool and then testing for toxin production. The first step is performed by testing for the presence of the C. difficile GDH (glutamate dehydrogenase) antigen. If the first step is positive, a second test, a PCR assay targeting the toxin genes, is performed.


Appropriate therapy for pseudomembranous enterocolitis has never been prospectively analyzed, but symptomatic therapy consisting of cessation of antibiotics, bowel rest and vigorous replacement of fluid and electrolytes losses (often huge) seems appropriate. Other supportive measures felt useful include oral lactobacilli, fecal enemas, and specific anti-staphylococcal therapy if stool Gram stain indicates their presence.

Other treatment options for pseudomembranous enterocolitis consist of oral administration of metronidazole or vancomycin, and most patients respond well within 3-4 days. In a study by Morris, medical therapy failed in 22% of patients prior to initiation of treatment with metronidazole or vancomycin, resulting in the need for surgical intervention. Today, pseudomembranous enterocolitis is essentially a "medical" disease with less than 1% of patients requiring surgery. However, in patients with a fulminant and toxic form of pseudomembranous enterocolitis who fail to respond to medical therapy, surgical intervention (usually partial colectomy with a temporary diverting ileostomy) can be lifesaving.

NOTE: The above information is educational purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.

DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.


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