Gas Gangrene Clostridial Myonecrosis

Almost every sample from soil and dusty surfaces has endospores of the gas gangrene bacillus, and the organism can frequently be recovered from cultures of wounds. Only rarely does contamination of a wound result in gas gangrene, however, because anaerobic conditions are necessary for the disease to develop. Primarily a disease of wartime, gas gangrene occurs mainly in neglected wounds with fragments of bone, foreign material, and extensive tissue damage, as might occur from schrapnel. Gas gangrene is highly unusual in peace time gunshot wounds, but it occurs occasionally in abdominal and other surgeries, especially in persons with underlying diseases.

Symptoms

Gas gangrene (figure 27.12) begins abruptly, with pain rapidly increasing in the infected wound. Increased swelling occurs in the area, and a thin, bloody or brownish fluid leaks from the wound. The fluid may have a frothy appearance due to gas formation by the organism. The overlying skin becomes stretched tight and mottled with black. The victim appears very ill and apprehensive, but remains quite alert until late in the illness when, near death, he or she becomes delirious and lapses into a coma.

Causative Agent

Several species of Clostridium can produce life-threatening gas gangrene when they invade injured muscle, but by far the most common offender is C. perfringens. These encapsulated Grampositive rods are shorter and fatter than C. tetani and usually do not exhibit spores in material from wounds or cultures.

Pathogenesis

Two main factors foster the development of gas gangrene: (1) the presence of dirt and dead tissue in the wound and

Gas Gangrene Pictures

Figure 27.12 Individual with Gas Gangrene (Clostridial Myonecrosis)

Fluid seeping from the involved area typically shows bits of muscle digested by Clostridium perfringens. Leukocytes are absent because the clostridial toxin kills them.

Figure 27.12 Individual with Gas Gangrene (Clostridial Myonecrosis)

Fluid seeping from the involved area typically shows bits of muscle digested by Clostridium perfringens. Leukocytes are absent because the clostridial toxin kills them.

702 Chapter 27 Wound Infections

Table 27.4 "Lockjaw" (Tetanus)

© Clostridium tetani spores from dust or dirt enter a wound.

@ In wounds sufficiently anaerobic, the spores germinate, vegetative bacteria release an exotoxin called tetanospasmin.

@ Tetanospasmin is carried to the central nervous system by motor nerve axons or by the bloodstream.

@ The toxin prevents any inhibitory neurons it reaches from functioning.

<5 The corresponding neurons, which cause muscles to contract, act unopposed by inhibitory neurons.

© The result is a sustained, painful cramplike muscle spasm.

Symptoms

Incubation period Causative agent

Pathogenesis

Epidemiology

Prevention and treatment

Restlessness, irritability, difficulty swallowing; muscle pain and spasm in jaw, abdomen, back, or entire body 3 days to 3 weeks; average 8 days Clostridium tetani, an anaerobic, spore-forming, Gram-positive rod Tetanus results from tetanospasmin, an exotoxin produced by the bacterium.The toxin is carried to brain and spinal cord by motor nerve axons or circulating blood; toxin acts against nerve cells that normally inhibit muscle contraction. Other nerves that normally cause muscle contraction then act unopposed, causing muscle spasms

Organisms common in soil; spores contaminate wounds, germinate in those having anaerobic conditions, particularly dirty or puncture wounds Immunization of children at ages 2 months, 4 months, 6 months, 18 months; booster dose at time of entering school and at 10-year intervals after that; tetanus immune globulin (TIG), cleaning wound.Treatment: metronidazole, tetanus antitoxin

(2) long delays before the wound gets medical attention. The toxin implicated in pathogenicity is a-toxin, an enzyme that attacks a vital component of host cell membranes called lecithin. Clostridium perfringens is unable to infect healthy tissue but grows readily in dead and poorly oxygenated tissue, releasing a-toxin. Growth is fostered by anaerobic conditions, as well as by the presence of growth factors and amino acids in dead tissue. Curiously, these infections are generally not ominous until they invade muscle. The toxin diffuses from the area of infection, killing leukocytes and tissue cells. Several enzymes produced by the pathogen, including collagenase and hyal-uronidase, break down macromolecules in the dead tissues to smaller ones, thereby promoting swelling. The organisms grow readily in the fluids of the dead tissue, producing hydrogen and carbon dioxide from fermentation of amino acids and muscle glycogen. These gases accumulate in the tissue and contribute to the rise in pressure, thereby fostering spread of the infection. Without prompt surgical treatment, massive amounts of a-toxin diffuse into the bloodstream and destroy red blood cells, tissue capillaries, and other structures throughout the body and cause death. The reason for the rapid onset of severe toxicity when muscle becomes involved is unclear. It is not reversed by administering antibody to a-toxin.

Epidemiology

Besides being widespread in soil, C. perfringens is present in the feces of many animals and humans, and in the vagina in from 1% to 9% of healthy women. Besides neglected battlefield

Nester-Anderson-Roberts: I IV. Infectious Diseases I 27. Wound Infections I I © The McGraw-Hill

Microbiology, A Human Companies, 2003

Perspective, Fourth Edition

27.3 Diseases Due to Anaerobic Bacterial Wound Infections 703

Table 27.5 Gas Gangrene (Clostridial Myonecrosis)

© Clostridium perfringens spores enter a wound having two essential characteristics: dead tissue and anaerobic conditions.

@ The spores germinate, and the vegetative bacteria multiplying in dead tissue produce a-toxin.

© a-toxin diffuses into normal tissue and kills it. The infection expands into the newly killed tissue, the bacteria utilizing amino acids and growth factors released from the tissue by bacterial enzymes.

@ Swelling and gas produced by fermenting amino acids and muscle glycogen aid rapid progress of the infection.

© Massive amounts of a-toxin are produced and diffuse into the bloodstream, destroying blood and other cells throughout the body.

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Responses

  • silke
    What is the causative agent of gas gangrene?
    3 years ago
  • Seredic Boffin
    What is the causative agent and the source of the gas in gas gangrene?
    2 years ago
  • frans
    What is the causative organism for gas gangrene?
    2 years ago
  • Roosa
    What are the causative agents for gas gangrene?
    1 year ago
  • Tess
    Which is causitive organism of gas gangrene?
    7 months ago
  • benjamin
    How does gas gangrene spread?
    4 months ago

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