VirB8-like protein TraH is crucial for DNA transfer in Enterococcus faecalis
NCBI Bookshelf. Boston: Massachusetts Eye and Ear Infirmary; Nelson I. Agudelo Higuita and Mark M Huycke. Authors Nelson I. Agudelo Higuita 1 and Mark M Huycke 2. The continuing progress of modern medical care toward more intensive and invasive medical therapies for human disease has undoubtedly contributed to the increased prevalence of these remarkable opportunistic pathogens.
This trend has also been attributed to the increasing antibiotic resistance among clinical isolates of enterococci. The rapid spread of enterococci with resistance Enterococcus fekalis in der Prostata vancomycin VRE has been of particular concern.
Many healthcare-associated strains that are resistant to vancomycin also show resistance to penicillin, as well as high-level resistance HLR to aminoglycosides. Over the past two decades, Enterococcus faecium has emerged as a leading cause of multidrug-resistant enterococcal infection in the United States Hidron, et al.
Treating infections caused by this species can be difficult, and the magnitude of the problem is vast. Although they were often resistant to high-level aminoglycosides and some macrolides, healthcare-associated infections in these units due to E. Other enterococcal species are rarer causes of human infection, including E. In the following sections, the common human infections caused by enterococci are briefly described.
The epidemiology of antibiotic-resistant enterococci in healthcare settings is summarized, including the role of colonization pressure and host factors on the emergence of VRE in clinical settings. Finally, the current challenges facing clinicians who treat antibiotic-resistant enterococcal infections are reviewed. Enterococci can cause a variety of infections. For some of these, other microorganisms are also frequently isolated from the same site.
In those situations, it is often not clear whether the manifestations of infection are the result of enterococci, or whether these relatively avirulent and opportunistic organisms Enterococcus fekalis in der Prostata merely bystanders or are playing a minor role in the infection.
The most common type of enterococcal infection occurs in the urinary tract. Lower urinary tract infections such as cystitis, prostatitis, and epididymitis are frequently seen in older men.
However, enterococci are exceedingly uncommon as a cause of uncomplicated cystitis Enterococcus fekalis in der Prostata young women. Enterococcal urinary tract infections are more likely to be acquired in hospital or long-term care settings, and thus, are more likely to be resistant to Enterococcus fekalis in der Prostata antibiotics. Enterococci are often recovered from Enterococcus fekalis in der Prostata of intra-abdominal, pelvic, and soft tissue infections. They are almost always isolated as only one component of mixed microbial flora and rarely cause monomicrobial infection at these sites.
The importance of enterococci in wounds and abscesses has been debated at length. Drainage of abscesses and debridement of wounds are often essential adjuncts to antibiotic therapy for these infections. Peritonitis, an infection of the abdominal lining, should be considered separately from intra-abdominal or pelvic mixed aerobic-anaerobic infections.
This infection occurs most often in conjunction with liver cirrhosis or in patients who receive chronic peritoneal dialysis. Enterococci Enterococcus fekalis in der Prostata cause monomicrobial infection in these situations—although they occur far less commonly than Escherichia coli for spontaneous bacterial peritonitis or coagulase-negative staphylococci, and Staphylococcus aureus for dialysis-associated peritonitis. Finally, enterococci are frequently found in cultures from decubiti and foot ulcers, as well as in association with osteomyelitis in diabetics, but their role in infections at these sites is not clearly defined.
Bacteremia and endocarditis are the more common manifestations of infections due to enterococci. Enterococci are currently the second leading cause of healthcare-associated bacteremia Hidron, et al.
In the last few years, the source of a bacteremia is usually the genitourinary tract, although a bacteremia also often arises from intra-abdominal or biliary sources, indwelling central lines, or soft tissue infections.
Enterococcal bacteremias, in contrast to bacteremias with S. The major issue when dealing with enterococcal bacteremia is the presence of endocarditis. The treatment of endocarditis can be more problematic than the treatment of bacteremia due to a noncardiac source. In some studies, E. These high rates likely reflect patients who are at risk for developing enterococcal bacteremia—older adults with multiple underlying diseases, which may include diabetes mellitus, malignancy, heart disease, transplantation, and prior surgery.
Endocarditis is one of the most serious enterococcal infections. Two drugs that exhibit synergistic killing are required for effective therapy. In the situations of VRE or high-level aminoglycoside-resistant enterococcal endocarditis, antibiotic treatment often fails, and surgery to remove the infected valve is essential. The initial source of bacteremia leading to endocarditis is usually the genitourinary or gastrointestinal GI tract.
Enterococcus fekalis in der Prostata involvement is much more common than right-sided involvement. Unlike Enterococcus fekalis in der Prostata previous small study Murdoch, et al.
The clinical picture of enterococcal endocarditis is usually one of subacute infection characterized by heart failure, rather than embolic events McDonald, et al. Other infections less commonly or rarely seen due to enterococci include meningitis, hematogenous osteomyelitis, septic arthritis, and pneumonia. The latter Enterococcus fekalis in der Prostata quite rare, even in association with ventilators, and has only been documented in severely debilitated or immunocompromised patients who receive broad-spectrum antibiotics.
There is no evidence that antibiotic-resistant isolates of enterococci, such as VRE, are more or less likely to cause these infections than antibiotic-susceptible isolates of enterococci.
In addition to being well-recognized colonizers of the GI tract of most animals and insects, these hardy bacteria are routinely recovered from beach sands, freshwater and marine water sediments, soil, and aquatic and terrestrial vegetation. Many studies correlate increasing concentrations of environmental enterococci with GI and dermatological illnesses.
As a result, the Environmental Enterococcus fekalis in der Prostata Agency recommends enterococci as indicator bacteria for fecal contamination for brackish and marine waters.
For more information, see Enterococci as indicators of environmental fecal contamination. It must be remembered, however, that enterococci also naturally fill ecological niches, independent of contamination from outside sources. The development of molecular identification and typing methods allows for the facile detection and tracking of enterococci at the strain level. Despite this progress, it remains urgent to more thoroughly define ecological reservoirs, understand host and bacterial traits that promote colonization, and clarify mechanisms for transmission that enhance the spread of multi-drug resistant enterococci.
Enterococci are normal flora in the GI tract of humans, along with most other animals and insects. Enterococci are also normal inhabitants of the genital tract, with E. The emergence of VRE as leading causes of hospital infection has led to studies that better define characteristics of colonization with this organism. Subsequent studies in both experimental animals and colonized patients have shown that the quantity of VRE found in stool increases several logs Enterococcus fekalis in der Prostata antibiotics with activity against GI anaerobes are administered Donskey, et al.
This phenomenon is believed to be predominantly conferred by the anaerobic intestinal microbiota for humans, this includes Clostridium cluster XIVaClostridium cluster IVand Bacteroides spp. Eckburg, et al. In the small intestine, one mechanism for colonization resistance arises, in part, by the induction of defensins, cryptdins, and lectins Enterococcus fekalis in der Prostata Paneth cells.
Finally, an intact epithelial barrier, coupled with physiological functions that include salivation, immunoglobulin A, peristalsis, and gastric acidity, also contribute to colonization resistance.
Breakdown in these ordinary activities, especially when coupled with the administration of broad-spectrum antibiotics, increases the risk for colonization and transmission of antibiotic-resistant enterococci, and thereby promotes infection by these opportunists Donskey C.
In previous years, the source of enterococcal infection for most patients was thought to be their own endogenous flora. However, the marked rise in healthcare-associated enterococcal infections in the s and s led to studies that clearly demonstrated the transmission of pathogenic enterococci among patients in hospital settings Boyce, et al.
The primary mode of spread from patient-to-patient occurs through the hands of healthcare workers Hayden, Transmission of enterococci from a healthcare Enterococcus fekalis in der Prostata hands to a patient may involve direct inoculation onto intravenous or urinary catheters.
A more likely mechanism, however, is that healthcare-associated strains colonize the GI tract of patients with reduced colonization resistance Donskey C. In this fashion, new strains become part of the patient's endogenous flora, which then serves as a springboard for infection. Acquired enterococcal strains carrying genes that encode antibiotic resistance can persist in the GI tract via selective pressure from broad-spectrum antibiotics frequently used in hospitalized patients Donskey, et al.
The spread of VRE has been noted between acute and long-term care settings and, although uncommon, into the community Moreno, et al. Frequent contact with healthcare providers and movement of colonized patients among different healthcare settings is undoubtedly responsible for these patterns of transmission.
The hospital environment appears to play an important role in the transmission of multidrug-resistant enterococci Hota, The dramatic rise of VRE in Enterococcus fekalis in der Prostata s led to investigations that highlighted the role of the environment in healthcare-associated infections.
However, environmental reservoirs for antibiotic-susceptible enterococci are not likely to be different from those for VRE. Thermometers and thermometer handles appear to be common surfaces involved in the transmission of VRE Livornese, Enterococcus fekalis in der Prostata.
A high concordance between strains occurring in the Enterococcus fekalis in der Prostata environment and those colonizing patients has been reported Bonilla, et al.
The healthcare environment is readily contaminated with VRE, with the highest densities found on medical devices such as blood pressure cuffs, intravenous fluid pumps, or stethoscopesgowns, bed rails, bedside tables, bed linens, urinals, and bedpans Bonilla, et al.
Not surprisingly, increased environmental contamination has been noted when colonized patients have diarrhea, and there is an increased density of VRE in stool following anti-anaerobic antibiotic use Donskey, et al.
Several studies have emphasized the tenacity with which enterococci remain viable on environmental surfaces Hota,and its subsequent transmission to the hands of healthcare workers. Finally, Enterococcus fekalis in der Prostata one controlled prospective study, environmental contamination with VRE was shown to be highly predictive of VRE acquisition Drees, et al. Many investigators have defined specific risk factors for GI colonization with antibiotic-resistant enterococci.
Drees et al. Drees, et al. Many of these patients are cared for in specialized units, and acquisition of GI colonization can be traced back to care within these units and other factors, as noted above. The vast majority of VRE-colonized Enterococcus fekalis in der Prostata do not develop symptomatic infections. The ratio of colonization to infection with VRE is estimated to be approximately Hayden, ; Slaughter, et al.
The risk for VRE infection, however, increases among certain patient groups. A number of risk factors for infection with VRE have also been reported as risk factors for bacteremia with high-level aminoglycoside-resistant enterococci, including chronic renal failure, ICU stay, prior antibiotic use including cephalosporinsbladder catheterization, expression of cytolysin as an enterococcal virulence determinant, and prolonged hospitalization Caballero-Granado, et al.
The majority of healthcare-acquired infections are caused by microorganisms that are resistant to at least one of the antibiotics most commonly used to treat these infections. This is especially true for infections due to VRE, where treatment options are particularly limited see below and Enterococcal infection. Therefore, measures that minimize the spread of these resistant organisms are essential.
Each healthcare facility needs a comprehensive infection control program that can decrease the transmission of VRE among patients. Specific policies should be based on the rates of resistance within the facility, and should be appropriate for the specific healthcare setting. For example, specific control measures within an acute care hospital setting may differ somewhat from those applicable to a long-term care setting.
The consensus opinion of experts highlight four interventions as being most important for controlling the spread of VRE in healthcare settings: i active periodic surveillance cultures or molecular testing of patients at highest risk for carriage; ii decontaminating the hands of healthcare workers using an antiseptic-containing preparation before and after all patient contact; iii adherence to barrier precautions i.