How bad are mrsa infections staphylococcus aureus treatment natural

Some of the Staphylococcus aureus, just by random chance, wasn’t as harmed by the antibiotics as others. Those organisms survived, multiplied and created more Staphylococcus aureus just like them –- resistant to antibiotics. Over time, these clever bugs became so resistant, that our arsenal of antibiotics just doesn’t work anymore. These new bugs are called “Methicillin Resistant Staphylococcus aureus” or MRSA. In 1961, the first MRSA bacteria were identified. Since then the strain is resistant not just to methicillin but to amoxicillin, penicillin, oxacillin, and many other antibiotics. MRSA Infections Today

It is estimated that about 5% of people in the U.S. are colonized with MRSA (meaning, the MRSA is on their skin or in their nose, but they are not “infected” -– they are just carrying the bacteria around).

People who are colonized have a higher risk of getting a MRSA infection -– for example, if a MRSA colonized person has an operation and the MRSA bacteria on his skin get into the wound, there could be a big problem.

In 2005, there were 368,600 hospital stays for MRSA infection. This was triple the number of MRSA infections in 2000 and 10 times the number from 1995. Around 60% of all “Staph” infections in hospitals are now MRSA infections. Overall, MRSA is estimated to make up about 8% of all hospital acquired infections. How Big Is The MRSA Infection Problem?

The global situation of MRSA is a bit harder to get a handle on. In Europe, the problem doesn’t seem quite as bad as in the U.S., partly because of differences in the prescribing of antibioitics and partly because of control measures that have been put in place (such as mandatory MRSA screening for all patients in some settings). That said, an epidemic is still brewing and as MRSA travels from the U.S. to Europe, expect to see the rates increase there too. How Did This Happen?

There are several reasons we have a MRSA problem today. The most basic reason is that the Staph bacteria has developed resistance to methicillin and other antibiotics. Why? Antibiotic resistance evolves through selective pressure and random mutations. While the bacteria are replicating, a portion of those reproduced (by chance) may be mutants and able to survive even in the presence of antibiotics. Those that survive may be fit enough to go on to reproduce and cause illness. There is also a lot of data that overuse of antibiotics for decades has contributed to the problem. Because we overused antibiotics for decades. For example, antibiotics are often prescribed for viruses (like when people have the cold or the flu), this causes strain on the bacteria. When exposed to the antibiotics, some bacteria naturally are “hardier” than others. These bacteria survive (especially when the patients don’t take their full dose of antibiotics). They survive, reproduce and create resistant offspring. Continue the cycle for a couple of decades and a new strain of bacteria appears that is resistant to the antibiotic.

But it is not only the misuse of medications that is the problem, there is a lot of misuse of antibiotics in the animal industry. Those antibiotics end up in food and in the water supply, providing a low dose of antibiotics that helps create resistant bacteria. What Does the Future Hold?

More of the same, lots more. There are no signs that MRSA and other infections are on the wane. As soon as one infection gets under control, it seems there are two to replace. While MRSA remains a huge concern (with no signs of slowing), two more superbugs are already poised to dethrone it: C. Diff. and A. Baumannii.

Invasive Methicillin-Resistant Staphylococcus aureus Infections in the United States. R. Monina Klevens, Melissa A. Morrison, Joelle Nadle, Susan Petit, Ken Gershman, Susan Ray, Lee H. Harrison, Ruth Lynfield, Ghinwa Dumyati, John M. Townes, Allen S. Craig, Elizabeth R. Zell, Gregory E. Fosheim, Linda K. McDougal, Roberta B. Carey, Scott K. Fridkin, and for the Active Bacterial Core surveillance (ABCs) MRSA Investigators. JAMA. 2007;298(15):1763-1771.