Oh my. Recessive genes in eukaryotes and prokaryotes...who woulda thunk it?!
Oh my. Recessive genes in eukaryotes and prokaryotes...who woulda thunk it?!
Recessive? Sounds more like a total time-out than it does recess.
Maybe if more Giardia got invites to the prom, the sex-drive would kick in.
A couple billion years seems like an awfully long preadolescence.
Proof that you don't lose it just because you don't use it.
Sort of like these recessive genes...
Vancomycin Immunity
This antibiotic binds to the cell wall of a microbe and prevents it from forming successfully. Like the opposite of penicillin (which breaks the completed wall down), this one acts as a sabotaged building block and doesn't let it form in the first place.Bacterial populations usually respond to penicillin by developing beta-lactamases, enzymes that destroy the chemical before it takes effect. Vancomycin, however, becomes highly toxic to germ organelles when broken down--an apparent catch-22! If the germ doesn't break it down, it incorporates poison into its cell wall and dies; if it does break it down, it creates poisonous by-products and dies anyway.
So, we have a "damned if you do, damned if you don't" drug on our hands, something that should be able to take out any nasties we aim it at. So, we aimed and we fired, and time passed, this new selective pressure had been introduced into the microbial world in Doctors' surgeries and hospitals across the western world.
This tale, however, would have a sting in it's tail, it showed us that we were in a chemical arms race with foes much much smaller and much much dumber than us.
A mere 30 years after vancomycin had started being used, a bizarre, multi-part anti-vancomycin system sprung forth in enterococci and other bacteria.
No less than 5 genes are involved in this contrived monstrosity of a defense. VanR and VanS produce enzymes that detect the presence of the antibiotic in the bacterium. Once activated, those enzymes activate VanA, which activates, in turn, several genes with subfunctions that (A) prevent vancomycin from being incorporated in the cell wall, (B) break it down, and (C) catalyze its toxic byproducts into harmless remnants.
This by no means stopped with vancomycin, several antibiotics have now become innefective in the hospitals against many infectious bacteria.
A particularly nasty one is MRSA, or methicillin-resistant Staphylococcus aureus, which luckily for us at the moment, is still vulnerable to the above vancomycin. MRSA strains first appeared in the late 1970s and currently 40-50 percent of SA isolated from U.S. hospitals are resistant to methicillin. These infections are treated with the powerful antibiotic vancomycin. Scientists hypothesize that the strains of SA most likely to evolve resistance to vancomycin are the MRSA.
Scientists expect strains of the bacterium Staphylococcus aureus (SA) that are fully resistant to the antibiotic vancomycin to evolve soon. Vancomycin-resistant Staphylococcus aureus (VRSA) is the term used to describe these strains. The expected emergence of VRSA is alarming because vancomycin is the only antibiotic that is effective against MRSA, strains of SA that are resistant to the antibiotic methicillin (MRSA).
Although VRSA—strains of SA that are fully resistant to vancomycin—do not currently exist, medical workers have recently isolated strains of SA that are four times more resistant to vancomycin than SA strains found previously. Because infections due to these strains do not respond to the usual doses of vancomycin, many physicians and other experts incorrectly refer to them as VRSA. They should be described as SA strains with intermediate resistance to vancomycin. Infections due to these strains can be cured using higher doses of vancomycin.
