1. Describe succinctly the disease Gas gangrene

• Usually a complication of a crushing injury

• Infectious disease emergency

• Rapid onset of myonecrosis

• Gas production

• Sepsis

• Mortality in traumatic gas gangrene is >25%

• Incubation period is fewer than 3 days with rapid onset of symptoms

• Progression of toxemia and shock is rapid.

2.Describe the offending organism of this case, its morphologic, cultural characteristics  and their normal habitat.

• Caused by clostridium welchii

  • Exotoxin producing Clostridial species

  • Large gram positive bacilli, pleomorphic

  • Spore forming bacilli

  • Normally found in soil and GI tract and widely distributed in the environment

  • Thrives in the absence of oxygen

  • Breed in damaged tissue

3. What kinds of hosts are susceptible?

• Traumatic or post Surgical gas gangrene (Clostridium perfringens)

  • Direct inoculation

  • Normal host

  • Contamination may also occur from patient's faecal flora

• Spontaneous gas gangrene (Clostridium septicum)

  • Often in immune compromised host

  • Associated with hematological and GI malignancies

  • Drug abuse is a risk factor

4. How do these organisms gain access to humans?

Direct inoculation  into a  open wounds due to trauma, bullet wounds, and multiply along with facultative co infecting or colonizing organisms.

• Condition consisting of low oxidation reduction potential are necessary for C. perfringens sporulation, followed by rapid division. Gas gangrene is usually a mixed infection aerobic and anaerobic.

•  Presumably, the other facultative organisms assist in reducing the oxidative-reductive potential.

5. How do they invade and spread in humans?

Exotoxin, not bacterial proliferation, is responsible for rapid spread of infection.

• Primary toxicity

  • Exotoxin causes muscle destruction and creates an anaerobic environment conducive to further bacilli growth.

  • alpha toxin is produced by the growing C. perfringens, which kill muscle cells and inflammatory cells, alpha toxin's biologic activity is a lecithinase, causing necrosis, and hemolysis.

  • Beta and epsilon toxins are also necrotizing, and considered major toxins. Subsequently, new necrotic areas will foster growth and spread of the organisms.

  • Carbohydrate fermentation by C. perfringens is responsible for the gas production (crepitus).

• Secondary toxicity. Products of tissue breakdown cause secondary toxicity

  • CPK

  • Myoglobin

  • Potassium

6. What defenses humans have against these organisms?

• WBC's try to attack these organisms.

• We have no defense against toxins

7. How do these organisms able to overcome human defenses?

•  Inflammatory cells are killed along with muscle cells by alpha toxin.

8. What is the end result of this battle between organisms and humans?

Death occurs within about two days if the condition is not treated. Often have shock, jaundice, hemolysis and renal failure along with local findings.

• Local findings

  • Crepitance

  • Brawny edema

  • Fowl-smelling serosanguinous discharge

  • Skin discoloration

  • Cutaneous bullae

  • Ischemic appearing muscle tissue

  • Gas in soft tissue within fascial planes

• Systemic secondary to toxins

  • Fever or hypothermia.  Unlike many other infections, hypothermia, or just absence of fever can predominate the clinical course.

  • Tachycardia is frequently out of proportion to elevation of temperature that is, faster heart rates may not fit with a normal temperature.

  • Altered level of consciousness

  • Hemolytic anemia

  • Liver dysfunction

  • Hyperkalemia

  • Kidney dysfunction

  • Metabolic acidosis

  • Coagulopathy and thrombocytopenia

  • Myoglobinemia and Myoglobinuria

9. How do you diagnose this infection?

Rapid diagnosis is by 

• Clinical presentation

• Gram stain of bullae fluid or muscle tissue: Paucity of WBC with gram positive bacilli. Inflammatory cells are killed along with muscle cells by alpha toxin.

• Pathologic demonstration of myonecrosis : Myoglobinemia and Myoglobinuria

• Radiographs showing gas within fascial planes

• Microbiology culture

Non-specific findings

• CBC: Anemia hemolytic secondary to toxins

• LFT: Liver dysfunction

• Electrolytes: Hyperkalemia

• Renal panel: Kidney dysfunction

• ABG: Metabolic acidosis

• Coagulation panel: Coagulopathy and thrombocytopenia

10. What will be your therapeutic strategy?

• Surgical debridement is the definitive treatment: Emergency consult. Treatment may include fasciotomy, debridement, or amputation.

• Oxygen

• Hyperbaric oxygen:  may be helpful.

• IV fluids: Aggressive volume expansion

• Antibiotics : Treat mixed infection with Penicillin Sodium and Amino glycosides or Vancomycin.

• Tetanus toxoid

• Analgesics

11. How can you prevent it from spreading to others? Prevent its occurrence?

• Appropriate wound care at the time of injury

  • removal of dead tissue

  • copious irrigation

• Prophylactic antibiotics: Benzyl penicillin

The organism is not contagious and does not spread from person to person.

12. What are other clinical infections with these organisms?

Gall bladder with abdominal wall muscle involvement following surgery, uterus (endometrium) are other body sites can be infected by this organism to cause similar disease

13. What are the disease associated with other species of Clostridium?

• Tetanus

• Food poisoning: Botulism