THE LIFE AND TIMES OF NECROTIZING FASCIITIS (FLESH-EATING BACTERIA)
Georgia grad student Amy Copeland’s battle with flesh-eating bacteria was recently named one of CNN’s Top 10 Health Stories of 2012. Like many terms coined by the media, ‘flesh-eating bacteria’ isn’t entirely correct. Or even sort-of correct. The bacteria don’t eat human tissue at all, but rather secrete a variety of toxins that can kill skin, muscle, and other types of tissue. Let’s take a closer look at the facts. An infection with flesh-eating bacteria, which affects somewhere between 500 and 1000 Americans each year, produces a rare and very severe condition known by the medical community as necrotizing fasciitis (NF), in which the skin and underlying tissue are destroyed.
The term ‘necrotizing fasciitis’ was coined by the physician B. Wilson in 1952, and refers to tissue death (necrosis) that extends along the flat connective tissue (fascia) that surrounds muscle, fat, blood vessels, and nerves. NF is most commonly found in the arms, legs, and abdominal wall, and is fatal in about 25% of patients. It spreads very fast, in some cases up to 3 centimeters per hour. NF usually occurs in patients whose immune system is already compromised, and often follows surgery, infection, injury, or childbirth. Older age, obesity, alcohol abuse, and diabetes all raise the risk of developing NF.
NF is most commonly caused by a bacterial infection, though in rare cases it can be brought on by other organisms such as fungi. Many different types of bacteria can cause this illness, and often four or more types are present in the same infection. The most common strain, and the one typically referred to as the ‘flesh-eating bacteria,’ is Streptococcus pyogenes (pronounced strep-toe-cock-us pie-ah-jen-knees, or S. pyogenes, for short). In Latin, this tongue-twister means ‘pus-generating,’ a name that seems obvious if you’ve ever seen a picture of NF. S. pyogenes is the perpetrator of a host of other, more common infections, including strep throat, impetigo, cellulitis, and rheumatic fever. Worldwide, this single pathogen is responsible for about 700 million mild infections each year, about 650,000 of which go on to develop into severe, invasive infections like NF.
Another bacterial strain that is increasingly being found in NF is methicillin-resistant Staphylococcus aureus (pronounced staff-el-oh-cock-us or-ee-us, aka MRSA), the same antibiotic-resistant ‘superbug’ making headlines for running rampant in hospitals and other health care settings.
The vast majority of NF cases begin in an existing wound, where the bacteria are able to penetrate the outer layer of the skin. By expressing ‘virulence factors’ on the bacterium’s cell surface, S. pyogenes can delay and/or disable multiple parts of the body’s immune response. For example, in a normal situation, immune cells rush to the site of infection and phagocytose, or engulf, harmful pathogens. S. pyogenes, however, employs a variety of methods to not only avoid detection and phagocytosis by these cells, but to invade and kill them. The bacteria are able to persist inside the immune cell, even after the patient is treated with antibiotics. By evading the immune response, the bacteria can move deeper into the body, spreading into neighboring cells and tissues.
Pain signals a problem
The first symptom of NF is usually a red, hot, and swollen wound with severe pain that is much more intense than the appearance of the wound would suggest. By the time necrosis is present, the illness is already fairly advanced. Primary treatment of NF involves surgery to remove the damaged tissue (a process termed ‘debridement’), and is accompanied by amputation of one of more limbs to control the infection in about 25-50% of cases. Other treatment steps in addition to surgery include antibiotic treatment with the goal of preventing systemic infection, restoration of fluid imbalances in body that have resulted from the infection, and support of any failing organ systems.
Hope on the horizon?
With the mortality rate at a whopping 25%, current treatments for NF leave a lot to be desired. Many scientists are now working to develop better drugs, and others are searching for a vaccine to prevent the illnesses caused by S. pyogenes entirely. Several vaccines have been developed against a molecule called M protein that is expressed by S. pyogenes, and one has even successfully completed Phase I and Phase II clinical trials. Unfortunately, however, M protein vaccines have a major limitation. There are many diverse strains of S. pyogenes that exist – even within a single geographical region – each with slightly different versions of M protein. Current M protein vaccines don’t target all of the strains, rendering them an impractical solution. Additional vaccine candidates targeting other parts of the bacterium have been developed, and though they have not yet been tested in humans, they are protective against S. pyogenes in animal studies. Although still a long way off, the hope is that some day a vaccine, ideally administered to children, will be able to prevent S. pyogenes infections and NF in the first place.
In the meantime, since early recognition and treatment are key to survival, experts believe that education of healthcare professionals on the first signs of NF, which often mimics other, less severe infections, is an important step to reducing mortality and improving patient outcome.