It seems like MRSA is
everywhere lately, but how does a mild-mannered bacterium become an antibiotic-deflecting superbug? Where did it come from? Is there any kryptonite to defeat it?
MRSA stands for Methicillin-Resistant
Staphylococcus Aureus, but let's forget about the "Methicillin-Resistant" for now.
Staphylococcus aureus, or
Staph, is a Gram-positive spherical bacterium that appears in clusters. It's considered "Gram-positive" because unlike some other bacteria,
Staph has a peptidoglycan cell wall that absorbs Gram stain, turning it blue-violet.
In some people,
Staph can colonize the nasal passages and even the skin. Often, this isn't a problem, but under certain circumstances,
Staph can multiply, produce enterotoxins, and invade cells and structures, causing anything from food poisioning and skin infections to pneumonia and toxic shock syndrome. This
page is a great resource to learn more about bacteriology and
Staph's pathogenicity.
It turns out that the peptidoglycan cell wall is important. It protects the bacterium's internal machinery from the outside world. Methicillin, a beta-lactam antibiotic (named for its chemical structure), inhibits enzymes that are crucial in cell wall synthesis. By inactivating the enzymes, methicillin effectively turns the bacterium's cell wall into Swiss cheese, causing it to die.
So where does the "Methicillin-Resistant" fit in?
Think survival of the fittest. Like every other organism in the world, bacteria evolve, albeit at a faster pace. Where it take humans about 25 years to reproduce, it only takes bacteria about 20 minutes. Each time bacteria reproduce, there's a chance for a mutation that might have no effect, be detrimental, or convey an advantage. In a certain way, antibiotics "drive" mutations toward one direction.
Imagine trillions of bacteria all over the world, constantly reproducing. In the presence of an antibiotic, many will stop reproducing and die. However, a random genetic difference that protects a bacterium from the antibiotic in some way would provide it with a survival advantage. These bacteria would survive and reproduce, and in turn, the "fittest" bacteria in each new generation would survive to reproduce again. By exposing bacteria to antibiotics repeatedly, we inadvertently select for the bacteria with the strongest resistance over and over again, until the bacteria becomes "immune" to the antibiotic.
Some bacteria have evolved to produce an enzyme that actually breaks down the antibiotic before it can affect the cell wall. Other bacteria, like MRSA, have altered proteins that still function in cell wall synthesis, but no longer bind methicillin.
Are we doomed?
Not quite. Just because methicillin doesn't work against MRSA, doesn't mean that other drugs like vancomycin (some resistance reported), linezolid (Zyvox), daptomycin (Cubicin) and tigecycline (Tygacil) are ineffective. Although free registration is required, this Medscape
article is a great way to learn more about the clinical treatment of MRSA.
They key to preventing antibiotic resistance is prescribing/using antibiotics judiciously. Indiscriminate use is what got us into this mess in the first place. There are also steps you can take to decrease your chances of contracting MRSA. Check out these
guidelines from the CDC. In the meantime,
go wash your hands!
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