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Mary D. Nettleman, MD, MS, MACP is the Chair of the Department of Medicine at Michigan State University. She is a graduate of Vanderbilt Medical School, and completed her residency in Internal Medicine and a fellowship in Infectious Diseases at Indiana University.
Dr. Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. He has a PhD in Microbiology (UT at Austin), and the MD (Univ. Texas Medical Branch, Galveston). He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications.
Enterococci are a group of gram-negative, round-shaped bacteria that commonly live in the gut, although they can cause infection anywhere in the body. They are resistant to several antibiotics, but in the past, physicians could rely on the drug vancomycin to effectively treat enterococcal infections. In recent decades, however, some enterococci have become resistant to vancomycin. The two main species that cause problems are vancomycin-resistant Enterococcus faecium and vancomycin-resistant Enterococcus faecalis, with E. faecium being the most common.
Vancomycin resistance is acquired when a sensitive Enterococcus acquires a special piece of DNA called a plasmid. The new strain is called vancomycin-resistant enterococci (VRE). One concern is that VRE appears able to transfer vancomycin resistance to unrelated bacteria such as MRSA (methicillin-resistant Staphylococcus aureus). In addition, VRE organisms are usually resistant to more than one antibiotic.
VRE can also be spread from person to person and are an increasing problem in hospitals and chronic-care facilities. Approximately 30% of all enterococcal infections are now caused by vancomycin-resistant strains (VRE).
VRE can exist in the body without causing infection, in which case a patient is said to be colonized with VRE. Colonization usually occurs in the bowel. If the number of VRE bacteria increases, they can invade the bloodstream or spread locally to cause an abdominal abscess or urinary infection. Once in the bloodstream, VRE can cause meningitis, pneumonia, or infection of a heart valve (endocarditis). VRE may also be introduced directly into an open sore or wound, causing a wound infection. The bacteria produce several substances, including proteases that help them break down the normal barriers between the gut tissue and the bloodstream.
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