Antibiotic Resistance iff Evolution

It's in print now, and as my friend who works at a dictionary company tells me, having something acknowledged in print is what it takes.

Bacteria have been steadily evolving to evade the action of antibiotics and infections are becoming more difficult to fight.

For instance, the CDC said, in 1972, only 2 percent of Staphylococcus aureus bacteria infections were drug-resistant but in 2004, 63 percent were.

In a few cases, no available antibiotics can cure an infection, and many more resist methicillin, a later-generation type of antibiotic. [ref]

Yeah!

This is not just a science issue for me, this one is PERSONAL. And I'm sure I'm repeating myself now, so feel free to skip. I've got a (non-contagious) skin condition called hidradenitis suppurativa (HS). Part of this involves bacterial infections in my apocrine sweat glands, primarily caused by staphylococcus aureus (staph). Staph is actually very common, something like 80% of the population have it sitting passively on our skin, and it doesn't do anything bad to them, but in me it gets inside my sweat pores and my body overreacts. So killing the staph should help treat my HS.

Keflex (cefalexin) is in the class of antibiotics called cephalosporins, which are part of the larger group called β-lactams. All β-lactams act by messing with bacterias' cell walls. I think I was prescribed Keflex when in my teens and college a few times, but it hasn't worked for ages. Amoxicillin is another type of β-lactam, and it used to work on me when I was in college and grad school, but sometime around 2004 we realized that it wasn't really doing anything anymore.

In case you're curious (or even if you're not), the term "penicillin" actually refers to a category of antibiotics including the originally discovered penicillin, and various derivatives of it including amoxicillin and methicillin. The penicillins and the cephalosporins are related in that they're both β-lactams and both act by breaking bacterial cell walls. Methicillin isn't actually used today, though it has lent its name to methicillin resistant staphylococcus aureus (MRSA, resistant staph). MRSA is actually any staph that's resistant to the penicillins.

Waitasec, amoxicillin is a penicillin. Amoxicillin doesn't work on me. I have staph. Holy smokes, I have MRSA! But wait, amoxicillin used to work... *thinks* *lightbulb!* Holy darwinism, Batman, I've evolved MRSA under my skin! ...ick... Yeah. And to make matters worse, having that MR stand for "multiple resistant" might be a more accurate description, b/c you may recall (or skim upwards) Keflex isn't a penicillin, it's a cephalosporin. And that too used to work but now doesn't, so my pretty pretty staph evolved that during my lifetime too.

THIS is one of the top reasons why I get really REALLY pissed when people deny evolution.

What I use these days is Levaquin (levofloxacin), part of the category of fluroquinolones, which is part of the quinalones. Unlike β-lactams, quinalones act by messing with the DNA and DNA transcription of bacteria. Interestingly, the use of Levaquin reveals another interesting feature of my MRSA: the FDA does not recommend Leva for MRSA, but only for the methicillin suscpetible strains. There is widespread incidence of quinalone resistant staph, possibly by overusage in European livestock. And yet, the MRSA that are in me are not resistant to quinalones despite being resistant to multiple forms of β-lactams. I see this as more evidence that my MRSA have evolved within me, though I haven't confirmed this with my dermatologist.

*sigh* That's enough ranting for me. Maybe I should take some microbiology courses. ;)