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THE MERCK MANUAL MEDICAL LIBRARY: The Merck Manual of Diagnosis and Therapy
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Bacteria can be classified by their need and tolerance for O2:

  • Facultative bacteria, which grow in the presence or absence of O2
  • Microaerophilic bacteria, which tolerate low O2 concentrations but grow better anaerobically or with > 10% CO2
  • Obligate anaerobic bacteria, which are intolerant of O2

Obligate anaerobes replicate at sites with low oxidation-reduction potential (eg, necrotic, devascularized tissue). Obligate anaerobes have been categorized based on their O2 tolerance: strict anaerobes grow in 0.4% O2; moderate anaerobes grow in 0.8 to 2.5% O2; and aerotolerant anaerobes grow in 2.5% O2. The obligate anaerobes that commonly cause infection can tolerate atmospheric O2 for at least 8 h and frequently for up to 72 h.

Obligate anaerobes are major components of the normal microflora on mucous membranes, especially of the mouth, lower GI tract, and vagina; these anaerobes cause disease when normal mucosal barriers break down.

Gram-negative anaerobes and some of the infections they cause include

  • Bacteroides (most common): Intra-abdominal infections
  • Fusobacterium: Abscesses, wound infections, and pulmonary and intracranial infections
  • Porphyromonas: Aspiration pneumonia and periodontitis
  • Prevotella: Intra-abdominal and soft-tissue infections

Gram-positive anaerobes and some of the infections they cause include

  • Actinomyces: Head, neck, abdominal, and pelvic infections and aspiration pneumonia
  • Clostridium: Gas gangrene due to C. perfringens, food poisoning due to C. perfringens type A, botulism due to C. botulinum, tetanus due to C. tetani, and C. difficile–induced diarrhea (pseudomembranous colitis)
  • Peptostreptococcus: Oral, respiratory, and intra-abdominal infections
  • Propionibacterium: Foreign body infections (eg, in a cerebrospinal fluid shunt, prosthetic joint, or cardiac device)

Anaerobic infections are typically suppurative, causing abscess formation and tissue necrosis (often the result of thrombophlebitis, gas formation, or both). Many anaerobes produce tissue-destructive enzymes as well as some of the most potent paralytic toxins known.

Clues to anaerobic infection include

  • Polymicrobial results on Gram stain or culture
  • Gas in pus or infected tissues
  • Foul odor of pus or infected tissues
  • Necrotic infected tissues
  • Site of infection near mucosa where anaerobic microflora normally reside

Testing: Specimens for anaerobic culture should be obtained by aspiration or biopsy from normally sterile sites. Delivery to the laboratory should be prompt, and transport devices should provide an O2-free atmosphere of carbon dioxide, hydrogen, and nitrogen. Swabs are best transported in an anaerobically sterilized, semisolid medium such as Cary-Blair transport medium.

Clostridia

Clostridia are spore-forming, gram-positive bacilli present widely in dust, soil, and vegetation and as normal flora in mammalian GI tracts.

Nearly 100 Clostridium sp have been identified, but only 25 to 30 commonly cause human or animal disease.

Pathophysiology

The pathogenic species produce tissue-destructive and neural exotoxins that are responsible for disease manifestations. Clostridia may become pathogenic when tissue O2 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 street drugs. Serious noninfectious disease can occur after ingestion of home-canned foods in which clostridia have produced toxins.

Selected Conditions Associated With Clostridial Infections

Condition

Agent

Toxin

Soft-tissue infection: Crepitant cellulitis, myositis, clostridial myonecrosis

C. perfringens

α-Toxin (others)
Hemolysis

C. perfringens

Phospholipase C
    α-Toxin
Muscle necrosis

C. perfringens

θ-Toxin
Enteric diseases    
Food poisoning

C. perfringens type A

Enterotoxin

Enteritis necroticans

C. perfringens type C

β-Toxin

Antibiotic-associated colitis

C. difficile Possibly toxin A or B*

Neutropenic enterocolitis

C. septicum (others)

Unknown, possibly β-toxin

Colorectal cancer

C. septicum  
Hemolysis by septicolysine C. septicum δ-Toxin
Tissue necrosis C. septicum α-Toxin
DNA lysis by DNase C. septicum β-Toxin
Hyaluronan lysis by hyaluronilase C. septicum γ-Toxin
Neurologic syndromes    

Tetanus

C. tetani Tetanospasmin

Botulism

C. botulinum Botulinal toxins A–G
Abdominal infections: Cholecystitis, peritonitis, ruptured appendix, bowel perforation, neutropenic enterocolitis

C. perfringens , C. ramosum (many others)

β-Toxin
*Requires further study.

Diseases Caused by Clostridia

Diseases caused by clostridia include

  • Botulism (due to C. botulinum)
  • C. difficile–induced colitis
  • Gastroenteritis
  • Soft-tissue infections
  • Tetanus (due to C. tetani)
  • Enteritis necroticans (due to C. perfringens type C)
  • Neutropenic enterocolitis (due to C. septicum)

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. Tissue necrosis can be caused by C. septicum. 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.

Last full review/revision August 2009 by Joseph R. Lentino, MD, PhD

Content last modified August 2009

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