Gas gangrene

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Gas gangrene is a bacterial infection that produces gas in tissues in gangrene. It is a deadly form of gangrene usually caused by Clostridium perfringens bacteria. It is a medical emergency.

Myonecrosis is a condition of necrotic damage, specifically to muscle tissue. It is often seen in infections with Clostridium perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis via specific exotoxins. These microorganisms are opportunistic and generally enter the body via significant skin breakage. In wartime particularly, the unhygienic conditions and frequent gross injuries meant that gangrenous infection of soil-borne bacteria was particularly prevalent. Indeed mankind has long suffered the ill-effects of gangrenous infections throughout history. Other causes of myonecrosis include ischemic necrosis, caused by vascular blockage (e.g. diabetes type II), tumours that block or hoard blood supply and disseminated intravascular coagulation (DIC) or other thromboses.

Gas gangrene is caused by exotoxin-producing Clostridial species (most often Clostridium perfringens), which is mostly found in soil but also found as normal gut flora, and other anaerobes (e.g. Bacteroides and anaerobic streptococci). Staphylococcus aureus and Vibrio vulnificus can cause similar infections.

Gas gangrene causes very painful swelling. The skin turns pale to brownish-red. If you press on the swollen area with your fingers, you may feel gas as a crackly sensation. The edges of the infected area grow so quickly that changes can be seen over a few minutes. The area may be completely destroyed.

Tissue and fluid cultures and Gram stain of fluid to test for Clostridium bacteria can be done. Blood cultures can be done to determine the bacteria causing the infection.

Any significantly massive infection is a medical emergency. In cases of gangrene, the infection is so severe by the time that a diagnosis is made that countering the bacterial load is impossible even with the strongest available antibiotics, for example gentamycin and vancomycin. Antibiotics alone are not effective because they don’t penetrate ischemic muscles enough to be effective. However, penicillin is given as an adjuvant treatment to surgery. There are two major reasons for this; current antibiotics only prevent replication of bacteria and the production of toxins continues in pre-existing bacteria. Also, the extent of injury caused by the infection may leave the muscle tissues so damaged that the body will never be able to replace the lost structures (including vasculature).

Often the only available cure is amputation, which physically removes the source of infection. Understandably this is not the favoured option unless circumstances are particularly dire. In addition to surgery and antibiotics, hyperbaric oxygen therapy (HBOT) is used and acts to inhibit the growth of and kill the anaerobic C. perfringens.

Clean any skin injury thoroughly. Watching for signs of infection (such as redness, pain, drainage, or swelling around a wound), and consulting health care provider promptly if these occur can help prevent gas gangrene.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Gas gangrene is caused by exotoxin-producing Clostridial species (most often Clostridium perfringens), which is mostly found in soil but also found as normal gut flora, and other anaerobes (e.g. Bacteroides and anaerobic streptococci). Staphylococcus aureus and Vibrio vulnificus can cause similar infections.

Clostridium is found most everywhere. The exotoxin is commonly found in C. perfringens type A strain and is known as alpha toxin. These environmental bacteria may enter the muscle through a wound and go on to proliferate in necrotic tissue and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time.

A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen and 16.1% oxygen was reported in one clinical case.^[1]

Myonecrosis differs slightly from other types of necrosis. While the underlying causes are almost identical, the type of affected tissue (namely muscle tissue) is significantly more important for the patient’s general health. Superficial necrosis is unsightly, and can lead to unattractive scarring but otherwise does not affect the patient’s likelihood of survival nor physical capability to the same extent. Conversely, massive myonecrosis will likely result in the loss of movement of the entire region. If the necrotic damage is allowed to continue throughout an affected limb then often that entire limb is lost permanently.

Soil-borne anaerobes are particularly well adapted to surviving harsh conditions. Often there is a scarcity of nutrition and the presence of numerous other species competing for resources. Changes in pH and temperature are often significant also. Competing bacteria often also possess the ability to create exotoxins that assist them in competing with other microbes in their natural environment. When such bacteria are able to enter a living host, they encounter a vast supply of nutrients, warm conditions and an abundance of water. This enables the microbes to rapidly proliferate, far in excess of the immune system‘s capability to defend, particularly as prokaryotic bacteria possess a far greater capacity for multiplication than the host’s immune system. The combination of bacterial load and ability to multiply is the basis for the microbes’ ability to cause massive infection. Alongside such rapid proliferation is a corresponding mass production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is produced by C. perfringens and is responsible for the disease manifestations. This exotoxin is known as alpha toxin.^[2]

Following a massive infection, gross injury and depletion of the host’s immune capability results in system wide sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory cytokines and the distribution of bacterial toxins. Massive infection is likely to result in death from a combination of system wide septic shock and the unintentionally damaging effects of the immune response. In animals, disability and distress caused by all of these factors markedly increases the chance of predation.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Clostridium perfringens (formerly known as C. welchii, or Bacillus welchii) is a Gram-positive, rod-shaped, anaerobic, spore-forming bacterium of the genus Clostridium.^[1] C. perfringens is everpresent in nature and can be found as a normal component of decaying vegetation, marine sediment, the intestinal tract of humans and other vertebrates, insects, and soil. It has the shortest reported generation time of any organism at 6.3 minutes in thioglycollate medium.^[2]

C. perfringens is the third most common cause of food poisoning in the United Kingdom and the United States though it can sometimes be ingested and cause no harm.

Infections due to C. perfringens show evidence of tissue necrosis, bacteremia, emphysematous cholecystitis, and gas gangrene, which is also known as clostridial myonecrosis. The toxin involved in gas gangrene is known as α-toxin, which inserts into the plasma membrane of cells, producing gaps in the membrane that disrupt normal cellular function. C. perfringens can participate in polymicrobial anaerobic infections. Clostridium perfringens is commonly encountered in infections as a component of the normal flora. In this case, its role in disease is minor.

The action of C. perfringens on dead bodies is known to mortuary workers as tissue gas and can be halted only by embalming.

In the United Kingdom and United States, C. perfringens bacteria are the third most common cause of foodborne illness, with poorly prepared meat and poultry, or food properly prepared but left to stand too long, the main culprits in harboring the bacterium.^[3] The clostridium perfringens enterotoxin (CPE) mediating the disease is heat-labile (inactivated at 74 °C (165.2 °F)). It can be detected in contaminated food (if not heated properly), and feces.^[4] Incubation time is between six and 24 (commonly 10-12) hours after ingestion of contaminated food.

Since C. perfringens forms spores that can withstand cooking temperatures, if cooked food is let stand for long enough, germination can ensue and infective bacterial colonies develop. Symptoms typically include abdominal cramping, diarrhea; vomiting and fever are usual. The whole course usually resolves within 24 hours. Very rare, fatal cases of clostridial necrotizing enteritis (also known as pigbel) have been known to involve “Type C” strains of the organism, which produce a potently ulcerative β-toxin. This strain is most frequently encountered in Papua New Guinea.

Many cases of C. perfringens food poisoning likely remain subclinical, as antibodies to the toxin are common among the population. This has led to the conclusion that most of the population has experienced food poisoning due to C. perfringens.

Despite its potential dangers, C. perfringens is used as the leavening agent in salt rising bread. The baking process is thought to reduce the bacterial contamination, precluding negative effects.^[5]

Clostridium perfringens is the most common bacterial agent for gas gangrene, which is necrosis, putrefaction of tissues, and gas production. It is caused primarily by Clostridium perfringens alpha toxin. The gases form bubbles in muscle (crepitus) and the characteristic smell in decomposing tissue. After rapid and destructive local spread (which can take only hours), systemic spread of bacteria and bacterial toxins may cause death. This is a problem in major trauma and in military contexts. C. perfringens grows readily on blood agar plate in anaerobic conditions, and often produces a double zone of beta hemolysis.

Research published in 2014 suggested that a strain of C. perfringens might be implicated in multiple sclerosis (MS). Tests in mice found that a toxin made by a rare strain of C. perfringens caused MS-like damage in the brain, and earlier work had identified this strain of C. perfringens in a human with MS.^[6] MS patients were found to be ten times more immune-reactive to the epsilon toxin than healthy people.^[7]

C. perfringens can be diagnosed by Nagler’s reaction where the suspect organism is cultured on an egg yolk media plate. One side of the plate contains anti-alpha-toxin, while the other side does not. A streak of suspect organism is placed through both sides. An area of turbidity will form around the side that does not have the anti-alpha-toxin, indicating uninhibited lecithinase activity. Other tests/reactions: Catalase: Negative, Spot indole: Positive, Lecithinase: Positive, Lipase: Negative, Litmus Milk: Stormy Fermentation, Reverse CAMP plate: Positive, Gas Liquid Chromatography products: (Acetic, Butyric and Lactic Acids).

Clostridium perfringens infection must be differentiated from other causes of viral, bacterial, and parasitic gastroentritis.

8Small bowel diarrhea: watery, voluminous with less than 5 WBC/high power field

Large bowel diarrhea: Mucousy and/or bloody with less volume and more than 10 WBC/high power field
† It could be as high as 1000 based on patient’s immunity system.

The table below summarizes the findings that differentiate inflammatory causes of chronic diarrhea^{[8][9][10][11][11]}

On May 7, 2010, 42 residents and 12 staff members at a Louisiana state psychiatric hospital experienced vomiting, abdominal cramps, and diarrhea. Within 24 hours, three patients had died. The outbreak was linked to chicken which was cooked a day prior to being served and was not cooled down according to hospital guidelines. The outbreak affected 31% of the residents of the hospital and 69% of the staff who ate the chicken. It is unknown how many of the affected residents ate the chicken.^[12]

In May 2011, a man died after allegedly eating food contaminated with the bacteria on a transatlantic American Airlines flight. The man’s wife and daughter are suing American and LSG Sky Chefs, the German company that prepared the inflight food.^[13]

In December 2012, a 46-year-old woman died two days after eating a Christmas Day meal at a pub in Hornchurch, Essex, England. She was among about 30 people to fall ill after eating the meal. Samples taken from the victims contained C.perfringens. The hotel manager and the cook were jailed for offences arising from the incident.^[14]

In December 2014, 87 year old Bessie Scott died three days after eating a church potluck supper in Nackawic, New Brunswick, Canada. Over 30 other people reported signs of gastrointestinal illness, diarrhea and abdominal pain. The province’s acting chief medical officer says Clostridium perfringens is the bacteria that most likely caused the woman’s death.^[15]

• Clostridium perfringens genomes and related information at PATRIC, a Bioinformatics Resource Center funded by NIAID
• Pathema-Clostridium Resource

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• Coma
• Delirium
• Disfiguring or disabling permanent tissue damage
• Jaundice with liver damage
• Kidney failure
• Shock
• Spread of infection through the body (sepsis)
• Stupor

Gas gangrene usually begins suddenly and quickly gets worse. It is often deadly.

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