Antibiotic resistant “superbugs” are a growing concern in all areas of health care. Methicillin Resistant Staphylococcus Aureus, or MRSA, is one of the deadliest. In a recent meta-analysis of 30 studies, the average mortality rate from MRSA infection was 36 percent.
Bacteria that are resistant to methicillin are also resistant to all other antibiotics in the beta-lactam class, which includes penicillin derivatives and cephalosporins. The only antibiotics available to kill MRSA are powerful and potentially toxic options such as vancomycin.
Most urinary tract infections (UTI) are caused by Escherichia coli. Staphylococcus aureus, both methicillin-resistant and methicillin-sensitive strains, are relatively rare. However, a study by Mayo Clinic showed that MRSA infections have almost tripled over the last decade. In 1997, only 3 per 1,000 urine cultures in their database were identified as MRSA. By 2007, the rate was 8 per 1,000.
Ordinary antibiotics are not only ineffective against MRSA, they can make the bacteria more virulent. There are two mechanisms for this effect: (1) the common antibiotics kill off other bacteria, clearing the way for MRSA to grow faster; (2) many antibiotics change the cellular chemistry of MRSA. The bacteria then increase production of Staphylococcal toxins, and switch on genes that cause MRSA to spread throughout the bloodstream. MRSA bacteria exposed to antibiotics also produce more of the molecules that cause adhesion to indwelling catheters.
Most antibiotics on the market today are derived from natural molecules that microbes produce, presumably to protect themselves from competition by other species. Genetic resistance to these antibiotics is to be expected; at least the microbe that produces the antibiotic must be resistant to it. Genetic material can be transferred from one species of bacteria to another in the form of plasmids and other sub-cellular units.
For natural options to prevent urinary tract infections, see