Clostridia are spore-forming, gram-positive, anaerobic bacilli present widely in dust, soil, and vegetation and as normal flora in mammalian gastrointestinal tracts. Pathogenic species produce tissue-destructive and neural exotoxins that contribute to disease manifestations.
(See also Overview of Anaerobic Bacteria.)
Nearly 100 Clostridium species have been identified, but only 25 to 30 commonly cause human or animal disease.
Pathophysiology of Clostridial Infections
The pathogenic species produce tissue-destructive and neural exotoxins that are responsible for disease manifestations. Clostridia may become pathogenic when tissue oxygen tension and pH are low. Such an anaerobic environment may develop in ischemic or devitalized tissue, as occurs in primary arterial insufficiency or after severe penetrating or crushing injuries. The deeper and more severe the wound, the more prone the patient is to clostridial infection, especially if there is even minimal contamination by foreign matter.
Clostridial disease can also occur after injection of illicit drugs.
Serious noninfectious disease can occur after ingestion of home-canned foods in which clostridia have produced toxins.
Diseases Caused by Clostridia
Diseases caused by clostridia (see table Selected Conditions Associated With Clostridial Infections) include
Botulism (due to C. botulinum)
Clostridioides (formerly, Clostridium) difficile–induced colitis
Tetanus (due to C. tetani)
Clostridial necrotizing enteritis (due to C. perfringens type C)
Neutropenic enterocolitis (typhlitis) (due to C. septicum)
Selected Conditions Associated With Clostridial Infections
Condition | Agent | Toxin |
|---|---|---|
Soft-tissue infection | ||
Crepitant cellulitis, myositis, clostridial myonecrosis, hemolysis | C. perfringens, others | Alpha-toxin (phospholipase C), theta-toxin, others |
Gas gangrene, tissue necrosis, hemolysis | C. septicum | |
Enteric diseases | ||
C. perfringens type A | Enterotoxin | |
Clostridial necrotizing enteritis (enteritis necroticans; pigbel) | C. perfringens type C | Beta-toxin |
Clostridioides difficile (formerly Clostridium difficile) | Toxin A or B or C. difficile binary toxin (CDT) | |
C. septicum, others | Unknown, possibly beta-toxin | |
C. septicum | — | |
Abdominal infections: Cholecystitis, peritonitis, ruptured appendix, bowel perforation | C. perfringens, C. ramosum, many others | Beta-toxin* |
Neurologic syndromes | ||
C. tetani | Tetanospasmin | |
C. botulinum | Botulinal toxins A–G and F/A Hybrid | |
* Beta-toxin is produced by C. perfringens type C, but most of these infections are caused by C. perfringens type A, which does not produce beta-toxin. | ||
The most frequent clostridial infection is minor, self-limited gastroenteritis, typically due to C. perfringens type A. Serious clostridial diseases are relatively rare but can be fatal.
Abdominal disorders, such as cholecystitis, peritonitis, ruptured appendix, and bowel perforation can involve C. perfringens, C. ramosum, and many others.
Muscle necrosis and soft-tissue infection, which is characterized by crepitant cellulitis, myositis, and clostridial myonecrosis, can be caused by C. perfringens.
Skin and tissue necrosis can be caused by bloodborne C. septicum from the colon.
Clostridia also appear as components of mixed flora in common mild wound infections; their role in such infections is unclear.
Hospital-acquired clostridial infection is increasing, particularly in postoperative and immunocompromised patients. Severe clostridial sepsis may complicate intestinal perforation and obstruction.
