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Vancomycin is a powerful antibiotic derived from Nocardia Orientalis. It is used against most gram-positive bacteria including Streptococci, Corynebacteria, Clostridia, Listeria, and Bacillus species. The only current microorganism with resistance to Vancomycin is VRE.

When coming into contact with Vancomycin, microorganisms are killed when their ability to perform bacterial cell wall synthesis is stopped. However, Vancomycin also damages the bacterial cell membranes and interferes with RNA synthesis.

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 Tn1546 (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.

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