Vancomycin-resistant Enterococcus: Difference between revisions
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<br>Vancomycin resistant Enterococcus was isolated in Europe in the late 1980s. However the use of Vancomycin began clinical use in the 1950s but was not wide spread until 1970s. Vancomycin works by inhibiting cell wall formation in gram positive bacteria and by this mechanism. Between each cell wall is a chain of amino acids that a cross linking enzyme recognizes and connects the carbohydrate chains. Vancomycin recognizes the two D alanine at the top of each chain and binds to them. The cross-linking enzyme can then not work properly and the cell wall would not from. For resistant bacteria, instead of have two D-alanine the last D-alanine has been replaced with D-lactate. This does not allow for vancomycin to bind properly and lets the cross-linking enzyme to properly form the cross links (figure 2).<br> | <br>Vancomycin resistant Enterococcus was isolated in Europe in the late 1980s. However the use of Vancomycin began clinical use in the 1950s but was not wide spread until 1970s. Vancomycin works by inhibiting cell wall formation in gram positive bacteria and by this mechanism. Between each cell wall is a chain of amino acids that a cross linking enzyme recognizes and connects the carbohydrate chains. Vancomycin recognizes the two D alanine at the top of each chain and binds to them. The cross-linking enzyme can then not work properly and the cell wall would not from. For resistant bacteria, instead of have two D-alanine the last D-alanine has been replaced with D-lactate. This does not allow for vancomycin to bind properly and lets the cross-linking enzyme to properly form the cross links (figure 2).<br> | ||
[[Image:plasmid.jpeg|thumb|300px|right|Figure 3. A vancomycin resistant bacteria sharing vanB gene with a vancomycin sensitive bacteria from the CDC.]] | [[Image:plasmid.jpeg|thumb|300px|right|Figure 3. A vancomycin resistant bacteria sharing vanB gene with a vancomycin sensitive bacteria from the CDC.]] | ||
<br>There are three types of clinically studied vancomycin resistant genes, vanA, vanB, and vanC. The highest resistance to vancomycin is vanA and continues decreasing with vanB then vanC. While vanB is still highly resistant to vancoymcin it is highly susceptible to teicoplanin. The last operon, vanC, has very low resistance to vancomycin and teicoplanin but this property is not transferable to other species. The resistance is transferred through a plasmid from an already resistant bacteria to a sensitive bacteria. Due to enterococcus capability of easily transferring DNA to other bacteria, this can prove troublesome for hospitals and health care centers.<br> | [[Image:flav.gif|thumb|300px|right|Figure 4. Chemical structure of Flavophospholipol from chemBlink.]] | ||
<br>There are three types of clinically studied vancomycin resistant genes, vanA, vanB, and vanC. The highest resistance to vancomycin is vanA and continues decreasing with vanB then vanC. While vanB is still highly resistant to vancoymcin it is highly susceptible to teicoplanin. The last operon, vanC, has very low resistance to vancomycin and teicoplanin but this property is not transferable to other species. The resistance is transferred through a plasmid from an already resistant bacteria to a sensitive bacteria. Due to enterococcus capability of easily transferring DNA to other bacteria, this can prove troublesome for hospitals and health care centers. There have been studies to find out if there could be a way to hinder the genetic transfer of these operons. Flavophospholipol (figure 4) <br> | |||
==Contamination in Hospitals== | ==Contamination in Hospitals== | ||
Revision as of 16:53, 12 May 2011
Introduction
By [Evan Baum]
Enterococci are a group of bacterial that are rod-shape, gram positive bacteria that can live within the digestive tract of humans. There, the aid in the digestion of food, but cause infections in other places of the body. Enterococci are very resilient organisms, the can be found not only in intestinal tract but in soil, water, and food. They are able to live in temperatures ranging from 10-45 C and pH ranges from 4.8 to 9.6.
Vancomycin-resistant Entercoccus (VRE) (figure 1) is a bacterial strain of Enterococcus that has acquired resistance to the antibiotic vancomycin through the uptake of a plasmid that has the resistance. VRE can be resistant to not just vancomycin, it can be resistant to other antibiotics commonly used for Enterococcus infections such as aminoglycosides, and ampicillin . VRE is a major concern to hospitals. Healthcare workers can carry the bacteria and pass it along to patients. VRE is most associated with nosocomial infections, making up about 30% of all enterococcus infections in hospitals. Healthy people can bring VRE into the hospital where it can then infect patients. This bacteria is very dangerous towards immunocompromised individuals. With VRE's aptitude for passing on it's genes to other bacteria, this strain is very capable of transferring it's resistance to lethal infections such as MRSA.
Vancomycin Resistance
Vancomycin resistant Enterococcus was isolated in Europe in the late 1980s. However the use of Vancomycin began clinical use in the 1950s but was not wide spread until 1970s. Vancomycin works by inhibiting cell wall formation in gram positive bacteria and by this mechanism. Between each cell wall is a chain of amino acids that a cross linking enzyme recognizes and connects the carbohydrate chains. Vancomycin recognizes the two D alanine at the top of each chain and binds to them. The cross-linking enzyme can then not work properly and the cell wall would not from. For resistant bacteria, instead of have two D-alanine the last D-alanine has been replaced with D-lactate. This does not allow for vancomycin to bind properly and lets the cross-linking enzyme to properly form the cross links (figure 2).
There are three types of clinically studied vancomycin resistant genes, vanA, vanB, and vanC. The highest resistance to vancomycin is vanA and continues decreasing with vanB then vanC. While vanB is still highly resistant to vancoymcin it is highly susceptible to teicoplanin. The last operon, vanC, has very low resistance to vancomycin and teicoplanin but this property is not transferable to other species. The resistance is transferred through a plasmid from an already resistant bacteria to a sensitive bacteria. Due to enterococcus capability of easily transferring DNA to other bacteria, this can prove troublesome for hospitals and health care centers. There have been studies to find out if there could be a way to hinder the genetic transfer of these operons. Flavophospholipol (figure 4)
Contamination in Hospitals
Hospitals are a breeding place for VRE. Nosocomial infections are very common in surgeries and is surprisingly is one of the top three pathogens isolated from patient's blood. VRE can cause peritonitis, urinary tract infections and endocarditis, bacteremia, meningitis, and can infect a number of medical devices. VRE is easily passed on from person to person or from contaminated services and medical equipment This can lead to complications through surgery and hospital stay. There are improvements as to what visitors and nurses wear when they are in the presence of ICU patients. There have always been masks but there has been research to bring cap and gown when visitors come to the ICU. This is to prevent the spread of germs such as VRE from coming in contact with patients whose immune systems are already compromised. In the event of a patient becoming infected with VRE there are steps that hospitals are beginning to take in order to minimize the exposure and mobility the virus has with other people and medical instruments. People who are constantly in contact with the patient like nurses and doctors have sets of gowns, masks, caps and equipment so they do not overlap with patients who are not infected with the bacteria. A stool sample should be taken to see if there is colonization of VRE in the patent. After there is contact with an infected patient, the clothes should be taken off before exiting and immediately wash hands with antiseptic soap. Hand washing with antiseptic soap is a major part of preventing the spread of VRE. The most common way patients become infected with the bacteria is through touching a contaminated surface. This can be greatly diminished with hand washing. Before seeing patients, especially ones in ICU, health care workers and visitors should wash hands before and after to greatly reduce the impact of bacteria.
Prevention and Treatment
As stated above there is a great stance for hand washing to prevent the spread of VRE. This is especially useful and a simple thing to help prevent further infections. Indirectly, this also helps to lessen the resistance gene from becoming more evolved towards vancomycin. The use of clean gowns, caps, and medical equipment also reduces the likelihood of infection, with the presence of sterilization there has been a decrease in the medical equipment infections.
However, if a patient does become infected there are a few ways to deal with the infection. Linezolid is an antibiotic that is commonly used in place of vancomycin. To properly clean a room, an arriving method is to use hydrogen peroxide vapor to clean the room in which there has been an uprising of VRE. New research, does show that Lactobacillus was used to help treat an infection of VRE in the intestinal tract of patients.
Conclusion
Prevention and treatment of VRE should be taken seriously due to it's ability to give up the resistance gene to other bacteria. MRSA is a highly infections bacteria that, if given a vancomycin resistance gene, would be immune to all known antibiotics today. With prevention and understanding there is a chance that VRE could become better understood and treated to prevent spread and lessen the chance resistance genes being transferred.
References
[Centers for Disease Control and Prevention. Recommendations for preventing the spread of vancomycin resistance: recommendations of the Hospital Infection Control Practices Advisory Committee (HICPAC). MMWR 1995;44(No. RR-12)]
[Courvali, Patrice. "Vancomycin Resistance in Gram-Positive Cocci." Oxford Journals. 2006. Web. <http://cid.oxfordjournals.org/content/42/Supplement_1/S25.full.pdf+html>.]
[Heiken, Esther. "The Role of Enterococcal Surface Protein in the Pathogenesis of Enterococcus Faecium Infections." (2009). Print.]
[Heiken, Esther. "The Role of Enterococcal Surface Protein in the Pathogenesis of Enterococcus Faecium Infections." Dec. 2009. Web. <http://igitur-archive.library.uu.nldissertations/2009-1130-200122/heikens.pdf>. ]
[Manley, KJ, MB Fraenkel, BC Mayall, and DA Power. "Probiotic Treatment of Vancomycin resistant Enterococci: a Randomised Controlled Trial." 2007. Web. <http://www.mja.com.au/public/issues/186_09_070507/man10966_fm.html>. ]
[Riedl, S., K. Ohlsen, G. Werner, W. Witte, and J. Hacker. 2000. Impact of flavophospholipol and vancomycin on conjugational transfer of vancomycin resistance plasmids. Antimicrob. Agents Chemother. 44:3189-3192.]
Edited by student of Joan Slonczewski for BIOL 238 Microbiology, 2011, Kenyon College.
