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Vancomycin Resistant Enterococcus (VRE) Essay

Vancomycin Resistant Enteroccus (VRE) Free Essay Example

Introduction

Vancomycin-resistant enterococcus was discovered in 1985.Vancomycin-resistant enterococcus (VRE) is a group of bacterial species of the genus Enterococcus that is resistant to the antibiotic vancomycin. Enterococci are basically enteric gram-positive coccoid shaped bacteria.

VRE can be found in the digestive and urinary tracts of some humans and it is particularly dangerous to immunocompromised individuals. VRE species have an enhanced ability to pass resistant genes to other bacteria. While infection of healthy individuals is uncommon, it is possible that they could be colonized with newly-resistant bacteria (Vancomycin-resistant enterococcus n.d).

Classification

According to Iwen, currently 14 species of enterooocci have been recovered from humans. Enterococcus faecalis accounts for 80 to 90% of enterococcal infections from all sources, with E. faecium responsible for a majority of the rest. The number of other species is generally less than 5%, although this may be higher, since methods to identify enterococci other than E. faecalis and E. faecium, are not widely used by clinical laboratories. In a study conducted at University Hospital evaluating enterococcal isolates recovered from blood cultures over eight years, E. faecalis was responsible for 68.5%, E. faecium for 26.2%, and the other enterococci for 5.3%. In this study, resistance was most evident with E.faecium, which was also responsible for all cases of vancomycin resistance. Nationally, resistance to vancomycin also occurs most frequently with E.faecium, even though other species of enterococci have become resistant. Intrinsic low-level vancomycin resistance occurs with E. casseliflavus and E. gallinarum, generally the most common faecium enterococcal species detected. These VRE species are found as normal stool flora and are not usually considered clinically significant even though sporadic blood stream infections have been detected in severely immunocompromised patients. Six phenotypes of vancomycin resistance, termed VanA, VanB, VanC, VanD, VanE, and VanG, have been described. Of these, only Van-A, Van-B and Van-C have been seen in general clinical practice so far.

  • vanA strains

It shows high-level vancomycin resistance and resistance to teicoplanin.

  •  vanB strains

vanB strains have variable resistance to vancomycin (MICs of 4 to >128 mcg per ml) and susceptibility to teicoplanin.

  • vanC strains

vanC strains show intrinsic resistance to low-levels of vancomycin and susceptibility to teicoplanin. These vanC enterococci which include E. casseliflavus and E.gallinarum can be differentiated from other enterococci since they are usually positive for motility. It is important for the laboratorian to distinguish these motile species from the other enterococci which show high-level vancomycin resistance, since the former are not considered an epidemiological threat for nosocomial transfer and are usually susceptible to standard therapies.

Diseases Caused by VRE

VRE are common only in patients who have been in hospital for long periods, those who have been fed by naso-gastric tube and those who have received certain antibiotics (especially vancomycin, teicoplanin or cephalosporins). However VRE are sometimes found in the faeces of people who have never been in hospital or recently been given antibiotics.

VRE cause the same range of infection as other enterococci: they are not more or less likely to cause illness than vancomycin-sensitive enterococci. Illness due to VRE is very rare in normal healthy people, hence family members and household contacts of patients with VRE are not at any risk and normal social hygiene should prevent them acquiring the organism.

Outbreaks within hospitals of VRE infection have been reported mainly from renal dialysis, transplant, hematology and intensive care units. VRE are becoming more common in hospitals world-wide. The number of UK hospitals sending VRE to the Reference Laboratory in London rose from one in 1988, to 18 in 1993 and to 47 in 1995. In the USA, between 1989 and 1993 there was a 20-fold increase in the proportion of enterococci resistant to vancomycin with a 14% rate seen on intensive care units. There is currently no sign that this trend can be reversed. A number of different strains of VRE are contributing to the increase both in the UK and abroad (Vancomycin-resistant enterococci 2007).

Infections commonly caused by enterococci include urinary tract infections, endocarditis, bacteremia, catheter-related infections, wound infections, and intra-abdominal and pelvic infections. Many infecting strains originate from the patient’s intestinal flora. From here, they can spread and cause urinary tract infection, intra-abdominal infection, and surgical wound infection. Bacteremia may result with subsequent seeding of more distant sites. For example, genitourinary tract infection or instrumentation often precedes the onset of enterococcal endocarditis. Meningitis, pleural space infections, and skin and soft-tissue infections have also been reported.

Intestinal colonization with resistant enterococcal strains is more common than clinical infection; for example, in Cleveland, VRE stool isolates outnumber clinical isolates by a factor of 10 in hospitals in which active VRE surveillance is performed. If infection occurs, it usually develops in those who are previously colonized. Colonized patients are a potential source for the spread of organisms to the hands of health care workers, the environment, and other patients. Antibiotic-selective pressure facilitates the spread of resistant enterococcal strains by promoting overgrowth of these strains in the intestinal tract. Enterococci can survive for long periods on environmental surfaces, contributing to their transmission. VRE have been isolated from all objects and sites in health care facilities.

For colonization development and infection with VRE, antimicrobial and non antimicrobial risk factors have been identified. Vancomycin use is associated with VRE colonization and infection, but prior exposure is not required for colonization. Third-generation cephalosporins, aminoglycosides, aztreonam, ciprofloxacin, imipenem, clindamycin, and metronidazole have been associated with VRE colonization. Non antimicrobial risk factors (e.g., increased duration of exposure to individuals colonized with VRE and close proximity to other colonized patients) increase the likelihood of VRE exposure.

Individuals at risk for colonization include critically ill patients who have received lengthy courses of antibiotics (particularly those in long-term care facilities), solid-organ transplant recipients and patients with hematologic malignancies, and health care workers. Unfortunately, spontaneous decolonization is uncommon, and antimicrobials are unlikely to eradicate VRE colonization. Identified risk factors for VRE bacteremia include prior intestinal colonization, prior long-term antibiotic use, and increased severity of illness, hematologic malignancy, bone marrow transplant, mucositis, and neutropenia, indwelling urinary catheters, corticosteroid treatment, chemotherapy, and parenteral nutrition (Fraser 2010).

Diagnosis

Enterococci have two types of resistance to vancomycin: acquired and intrinsic (natural). Some types of enterococci bacteria acquire the resistance when other bacteria come in contact with enterococci and share genetic information; scientists believe enterococci acquired the gene that resists vancomycin from bacteria in the digestive tract. Acquired resistance has been noted with two clinically important forms of enterococci: E. faecium and E. faecalis.

Of the dozen or so types of enterococci bacteria, some, such as E. gallinarum and E. casseliflavus, have an inherent, low-level resistance to vancomycin. These are very uncommon strains, however, and are of limited clinical significance.

If anyone has an enterococcal infection, it is crucial that his/her healthcare providers quickly identify the strain, so that they can determine how best to treat and prevent patient-to-patient transmission. The healthcare specialist firstly wants to know if the strain infecting the person is resistant to vancomycin and if so, is the resistance intrinsic or acquired? If the resistance is acquired, does the strain contain specific genes that can share resistance traits with other bacteria, thus making it able to spread disease? Different tests are available to make those diagnoses. Some healthcare practitioners, as part of their normal infection control procedures, will test the person for the presence of VRE to learn whether the person might be infected or colonized with the bacterium. This helps facilities know whether specific procedures should be used to reduce the potential spread of VRE (Anti microbial Resistance: Vancomycin-Resistant Enterococci 2009).

Treatment of VRE infections

There are two main problems when treating VRE infections. Firstly, the range of antibiotics available for treatment is very limited. Secondly, predicting the antibiotics to which the strain will be sensitive, and therefore appropriate for treatment, is difficult. Hence effective treatment may be delayed while waiting for laboratory results. A number of new antibiotics are under development although it is too soon to know whether any of these will be safe and effective enough against VRE for widespread use. The people which are found to be harmlessly colonized by VRE need no special treatment with antibiotics or antiseptics. Over a period of time many of these people become spontaneously clear of VRE (Vancomycin-resistant enterococcus 2007).

Prevention

It is very important to prevent the spread of VRE from one person to another. If you have VRE, or someone you are living or visiting with has VRE, it is important to follow these precautions (Vancomycin Resistant Enterococcus Aug 2009):

  • Wash your hands.

The most important way to prevent the spread of VRE is hand washing. The use of soap in pump dispensers with paper towels is the most effective way to remove organisms from your hands and prevent spread to others.

  • Environmental cleaning.

This bacterium can live for a long time on inorganic objects, so extra cleaning of personal things and equipment is very important. The bacterium is found in stool so toilets need special attention. They should be cleaned with bleach regularly and should not be shared with anyone.

  • Personal hygiene.

People with VRE must use proper toilet hygiene.

  • Equipment.

Equipments for personal use must be left in the home and should not be shared with other people.

  • Laundry and waste disposal.

The bacterium is destroyed during the normal laundering process and all garbage can be put out for regular pick-up.

  • Gloves and gowns.

Gloves and gowns are not required for routine visits in the home. If gloves are used for cleaning, they should be discarded after use. Good hand washing must be practices following glove removal. Any gowns used in direct care must be left in the client’s room and laundered with other personal items.

  • Client movement.

Clients with VRE should not be restricted from moving freely throughout their home and the community. If the client is incontinent of feces, proper diapering is essential.