Vancomycin is generally considered as the
last resort antibiotic, although recently Europe approved
quinupristin (on the market as Synercid) for bacteria who gained
resistance to vancomycin. The Columbia Encyclopedia (6th ed., 2000) stated that bacterial resistence to vancomycin is rare.
They are wrong. So, what is this substance, what does it do, what about resistance and its use and is this really "the end" regarding treatment of bacterial infections?
First of all, the
structure of vancomycin can be viewed at http://www-micro.msb.le.ac.uk/Tutorials/dfwt/vanc.gif, originally purified from
Streptomyces orientalis. It belongs to the
penicillin-family of antibiotics in its function to kill
Gram+ bacteria like staphylococci and enterococci who are resistant to ß-lactam antibiotics by interfering with the cell wall synthesis and causing damage to the cell membrane.
Cell wall biosynthesis is troubled because of the inhibition of cross-linking of
peptide chains (
peptidoglycan strands); it is not exactly clear how it messes with the already built
membrane. (
Teiresias, it does not interfer with RNA synthesis)
Vancomycin was first used about 40 years ago. But at that time, antibiotics more convenient in use and with less side effects were available (aka:
oral intake instead of
intravenous); it gained popularity in the eighties again when serious troubles with antibiotic resistance started to arise and the
purification process of vancomycin was improved.
It is/was (
...) used to treat
infections by bateria like
Stapylococcus aureus,
Clostridium difficile,
S. haemolyticus,
S. pneumoniae and
Enterococcus faecarium. However, they're getting resistant to vancomycin. Resistance in this case is defined as follows:
susceptible is <= 4 µg/ml, intermediate 8-16 µg/ml and
resistant >= 32 µg/ml (National Committee for Clinical Laboratory Standards in the USA). See also
VRE,
MRSA/
VISA.
Vancomycin resistance in VRE is located on a gene cluster similar to Tn
1546 (is a specialized
transposon and called an
integron). Ironically, it appears that resistance is promoted in tandem with the use of other antibiotics, due to the
selective advantage, but
synergistic activity with other antibiotics (
oxacillin) in a "
cocktail" is also documented. Thing to figure out is wich combinations are best in the long run.
In the case of vancomycin resistance, it originates with VRE (vancomycin resistant enterococci) in
livestock, mainly used in
Europe. The current
hypothesis is, that they got it because of the use of
avoparcin (=
glycopeptide antimicrobial drug used as a feed additive) in "sutherapeutic doses" (i.e. not enough to kill the bacteria). It promotes animal growth, but it's not known why and how, it just does, and that's what the
bio-industry wants. Researchers don't know how it emerged in the
hospitals in the US, or elsewhere in the world.
Bacteria are everywhere; the bacterial world can be imagined as one huge
multicellular organism passing on some of their genes to each other all the time. It is supposed that the MRSA got its resistance genes from the VRE: both like hospitals very much. Especially in the USA, antibiotics are widely used, ok, misused, to kill certain micro-organisms, hence providing the selective advantage for
survival and growth of VRE and MRSA (i.e.
Darwinism at work). When
patients who aquired a VRE infection in the hospital go home, they pass it on to family members etc.
Although it is quite alarming to know that there are bacteria out there resistant to about the 100 available antibiotics, it doesn't necessarily mean that
humans have lost the "war against bacterial infections". Like the quinupristin, new drugs are invented, although it is not clear if "we" can stay at least one step ahead of the bacteria. More important is the
control of
growth and
infection of the vancomycin resistant bacteria:
-
hygiene regulations properly implemented in hospitals;
- change in
prescription attitude by the medicals, aka the right antibiotic in the right dose for the target bacteria and not for viruses;
- patients who just have to finish an antibiotic
treatment, instead of halting a treatment by the time they start to feel well again;
- limited/restricted use of antibiotics in
agriculture;
- limited use (though I'd say a
ban) of antibacterial substances in
consumer goods. The even put antibiotics/antibacterial substances in certain toys "coz kids put the dirty stuff in their mouth", and some underwear "so you won't have the awful smell in your crotch" (no kidding! they are real ad slogans). Get real, most micro-organisms are good for you and help maintaining your
immune system.
On the other hand, these proposed regulations exist for at least five years, and nothing has been really put into practice, so maybe it is the end after all. Time will tell.
Part of the information in this write-up was collected from 8 sources, most of them found after a google search on vancomycin. A nice article about prevalence, sources and public health implications can be viewed at http://www.cdc.gov/ncidod/EID/vol3no3/mcdonald.htm.