The widespread over-use of antibiotics has spawned mutated forms of disease causing bacteria, often referred to as "superbugs." First released in 1958, the ability of vancomycin to treat life-threatening infection has declined as bacteria adapt to the threat of this antibiotic. Vancomycin resistance in superbugs spreads through the organism's ability to mutate and to share genetic material from other resistant bacterial strains. Some bacteria have become so resistant that no antibiotic is left to treat the resulting infection.
Staphylococcus aureus (S. aureus) is the infectious agent in a number of illnesses ranging from minor skin infections through to chronic bone infections, deadly cases of blood poisoning, and infections of the heart. The war against S. aureus was initially won with the development of antibiotics; however, some strains of these bacteria in turn developed a resistance to the most effective medication, methicillin. As methicillin resistant S. aureus (MRSA) spread in hospitals globally, these strains also developed genes giving them increased virulence. In the United States, MRSA was responsible for more deaths in 2005 than AIDS. MRSA was also responsible for more serious infections than bacterial pneumonia, influenza, or bacterial meningitis.
Older, less frequently used antibiotics became the new line of defense against superbugs like MRSA. While most antibiotics inhibit bacterial enzymes, vancomycin works by inhibiting cell wall synthesis so that the bacteria ruptures and dies. It was thought that bacteria would be less likely to develop vancomycin resistance because of this mode of action. Vancomycin was not only effective against S. aureus, but also against coagulase-negative staphylococcal strains that were resistant to penicillins and cephalosporins.
Vancomycin's increasing popularity for treatment of superbugs became its downfall. In the 1986, vancomycin resistance was identified in enterococcal abdominal infections. This resistance was due to a gene called vanA, which unfortunately was picked up by S. aureus, creating a strain of vancomycin resistance in S. aureus (VRSA). The first VRSA was reported in the United States in 2002. Additional modes of vancomycin resistance continue to be identified, raising the concern that these superbugs might begin to spread rapidly.
Risk factors for developing a vancomycin resistant infection include a prior MRSA infection and previous exposure to vancomycin. Most vancomycin resistant infections occur in patients who have recently had a major surgery, or who have serious diseases such as cancer, diabetes, or kidney failure. Some studies suggest that initial low dosages of vancomycin early in treatment may be associated with the emergence of resistant bacteria.