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Botulism, gas gangrene, and clostridial gastrointestinal infections 

Botulism, gas gangrene, and clostridial gastrointestinal infections

Botulism, gas gangrene, and clostridial gastrointestinal infections

Dennis L. Stevens

, Michael J. Aldape

, and Amy E. Bryant



Botulism—information on five clinical forms.

Updated on 31 May 2012. The previous version of this content can be found here.
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date: 27 March 2017


Human botulism is caused by seven serological types of C. botulinum, which is ubiquitously distributed in the soil. Poisoning usually results from ingestion of preformed toxin in food, although this is rapidly inactivated at ordinary cooking temperatures, but it can also result from contaminated wounds. C. botulinum toxin binds irreversibly to the neuromuscular junction and is the most lethal known microbial toxin.

Clinical features, diagnosis, and treatment—there are five forms of clinical botulism: (1) foodborne botulism—ingestion of food contaminated by preformed toxin; (2) wound botulism—infection of a wound with Cl. botulinum and in vivo toxin production (3) infant botulism—ingestion of clostridial spores that colonize the gastrointestinal tract and release toxin; (4) adult enteric infectious botulism—similar to infant botulism; (5) inhalational botulism—considered a potential agent of bioterrorism. Clinical presentation is with symptoms suggesting gastrointestinal tract illness, followed by neurological symptoms including diplopia, blurred vision, dizziness, and difficulty with speech or swallowing, leading on to generalized flaccid paralysis. The diagnosis can be confirmed by testing for botulinum toxin in the patient’s serum, urine, or stomach contents, or in the suspect food. Treatment requires (1) supportive care—this, including mechanical ventilation, may be needed for many months until new synapses have developed; (2) antitoxin—this reduces case fatality and shortens the illness.

Gas gangrene

Gas gangrene is caused by C. perfringens (most commonly), C. histolyticum, C. novyii, C. sordellii, and C. septicum, which occur naturally in soil and in the gastrointestinal tracts of humans and animals. Common causes of the condition are severe trauma that interrupts the blood supply to the soft tissues (gunshot wounds, penetrating or crushing injuries) with contamination by dirt, vegetation, or clothing containing vegetative forms of clostridia or spores. Skin popping of black tar heroin is another recently recognized cause. The clostridia responsible elaborate a wide range of toxins with varying effects: the principle toxin of C. perfringens is α‎-toxin, a phospholipase C that cleaves phosphatidylcholine in eukaryotic cell membranes and activates neutrophils, platelets, and endothelial cells, causing obstruction of local blood flow.

Clinical features—severe and sudden pain is the most characteristic symptom. Infection progresses rapidly with local ecchymosis, blistering, massive swelling, and crepitus indicating gas in the tissue as progressive necrotizing soft-tissue infection destroys muscle, fascia, fat, and skin. Without rapid and appropriate treatment, bacteraemia, hypotension, and multiple organ failure ensue.

Diagnosis and treatment—diagnosis must be made on clinical grounds, although Gram stain of the wound discharge or tissue sample may be helpful. Treatment requires (1) early recognition and aggressive surgical debridement of devitalized tissue; (2) antimicrobials—most commonly penicillin and clindamycin (which suppresses α‎-toxin production); (3) anti-α‎-toxin serum. The benefit of hyperbaric oxygen (HBO) has not been proven in controlled trials. In an experimental model of gas gangrene, HBO did not improve the efficacy of clindamycin or penicillin.

Prevention—prophylactic antibiotic treatment reduces the risk, but this depends upon factors including the time interval between the injury and surgical debridement.

Particular forms of gas gangrene—(1) C. septicum can grow at ambient oxygen tensions, causing ‘spontaneous gas gangrene’ in normal tissues, most commonly when bacteria spread from a colonic adenocarcinoma to uninjured muscle. (2) C. sordellii causes haemoconcentration, leukaemoid reaction without fever, and gradually progressive shock that is fatal in 75 to 80% of patients. Women infected during parturition, after medical abortion, or following gynaecological surgery almost always die.

C. perfringens gastrointestinal infections

Food poisoning—if foods such as meat and heavy gravy infected with type A strains of C. perfringens are allowed to sit at room temperature, bacilli can multiply greatly. If the food is then inadequately heated before consumption, preformed heat labile enterotoxin, combined with toxin produced in the gut, causes self-limiting abdominal pain and diarrhoea, usually without fever or vomiting.

Necrotizing enterocolitis—C. perfringens type C β‎-toxin causes fulminating enterocolitis that destroys intestinal mucosa. Epidemic outbreaks occured in postwar Germany (Darmbrand) and New Guinea (enteritis necroticans, ‘pig bel’) following ingestion of contaminated food, or dramatic change from vegetarian to meat diets. Treatment consists of supportive care and antibiotics (usually benzylpenicillin). Complications, e.g. intestinal perforation, may require surgery, in which case mortality is high. A toxoid vaccine is protective and should be considered in areas of Papua New Guinea where the disease still occurs.

Acknowledgement: The authors acknowledge inclusion of material from the chapter in the previous edition by Dr H E Larson.

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