Vancomycin-resistant Enterococci Bloodstream Infections Research Articles

Vancomycin resistant enterococcus (VRE) bloodstream infections (BSI) in patients with malignant hematological disorders: Is the sick getting sicker?

Vancomycin resistant enterococcus (VRE) bloodstream infections (BSI) in patients with malignant hematological disorders: Is the sick getting sicker?

Efficacy of oral ramoplanin for inhibition of intestinal colonization by vancomycin-resistant enterococci in mice.

Ramoplanin is a glycolipodepsipeptide antibiotic with activity against gram-positive bacteria that is in clinical trials for prevention of vancomycin-resistant Enterococcus (VRE) bloodstream infections and treatment of Clostridium difficile diarrhea. Orally administered ramoplanin suppresses VRE intestinal colonization, but recurrences after discontinuation of treatment have frequently been observed. We used a mouse model to examine the efficacy of ramoplanin for inhibition of VRE colonization and evaluated the etiology of recurrences of colonization. Eight days of treatment with ramoplanin (100 microg/ml) in drinking water suppressed VRE to undetectable levels, but 100% of mice developed recurrent colonization; a higher dose of 500 microg/ml in water was associated with recurrent colonization in 50% of mice. Two of eight (25%) mice treated with the 100-microg/ml dose of ramoplanin had low levels of VRE in their cecal tissues on day 8 despite undetectable levels in stool and cecal contents. Mice that received prior ramoplanin treatment did not develop VRE overgrowth when challenged with 10(7) CFU of oral VRE 1, 2, or 4 days later. In communal cages, rapid cross-transmission and overgrowth of VRE was observed among clindamycin-treated mice; ramoplanin treatment effectively suppressed VRE overgrowth in such communal cages. Ramoplanin treatment promoted increased density of indigenous Enterobacteriaceae and overgrowth of an exogenously administered Klebsiella pneumoniae isolate. These results demonstrate the efficacy of ramoplanin for inhibition of VRE colonization and suggest that some recurrences occur due to reexpansion of organisms that persist within the lining of the colon. Ramoplanin treatment may be associated with overgrowth of gram-negative bacilli.

Emergence of resistance to chloramphenicol among vancomycin-resistant enterococcal (VRE) bloodstream isolates

Therapeutic options for vancomycin-resistant enterococcal (VRE) bloodstream infections are extremely limited. Chloramphenicol is effective when VRE isolates are susceptible to this agent. However, longitudinal trends in chloramphenicol-resistant VRE (CR-VRE) are unknown. The possible association between CR-VRE and antibiotic use has not been studied. We analyzed the antimicrobial susceptibility profiles of all VRE blood isolates from 1991–2000 at our institution. We performed a correlational study to examine the relationship between annual hospital-wide use of specific antibiotics and antibiotic classes and CR-VRE prevalence. During the 10-year study period, the prevalence of CR-VRE increased from 0 to 11% ( P<0.001, trend). CR-VRE prevalence was correlated only with chloramphenicol use ( P=0.05) and quinolone use ( P=0.01). If these trends continue, dependence on newer, more expensive agents will increase. The correlation between both chloramphenicol use and quinolone use and the prevalence of CR-VRE suggests that efforts to preserve the utility of chloramphenicol in VRE infections may depend on optimizing the use of these agents.

Ramoplanin: a novel antimicrobial agent with the potential to prevent vancomycin-resistant enterococcal infection in high-risk patients.

The prevention of vancomycin-resistant Enterococcus (VRE) colonization and infection continues to be a high priority for clinicians. An oral antimicrobial agent that reduces or eliminates VRE gastrointestinal colonization could be useful for preventing VRE infection in selected patients. Ramoplanin, a glycolipodepsipeptide, is the first in a new class of antimicrobials. It has excellent in vitro activity against vancomycin-resistant Enterococcus faecium and Enterococcus faecalis. It is orally administered, and not absorbed systemically. In clinical trials, VRE gastrointestinal colonization was reduced to undetectable levels in 80-90% of patients during receipt of ramoplanin. A randomized, double-blinded, placebo-controlled multicentre study is currently being conducted to determine whether ramoplanin will prevent VRE bloodstream infection in oncology patients who are neutropenic due to treatment for a haematological malignancy or a bone marrow/stem cell transplant.

Effectiveness of a multifaceted infection control policy in reducing vancomycin usage and vancomycin-resistant enterococci at a tertiary care cancer centre

We undertook a prospective cohort study to evaluate the role of a multifaceted infection control policy including the use of a ‘vancomycin order form,’ in decreasing the transmission of vancomycin-resistant enterococci (VRE). In January 1997, a multifaceted infection-control policy was implemented amongst patients admitted to the M. D. Anderson Cancer Center in whom neutropenic fever developed or who were found to be colonized or infected with VRE. As part of this programme, we initiated the use of a vancomycin order form to reduce the use of empirical vancomycin. The total incidence of VRE infections declined from 0.437/1000 patient days in 1996–97 to 0.229/1000 patient days in 1998–99 (P=0.008). The VRE bloodstream infections declined from 0.338/1000 patient days in 1996–97 to 0.181/1000 patient days in 1998–99 (P=0.027). Empiric vancomycin use decreased from 416g/1000 patient days in 1996–97 to 208g/1000 patient days in 1998–99 (P<0.001), resulting in a decreased vancomycin cost from $2561/1000 patient days in 1996–97 to $1195/1000 patient days in 1997–98 (P<0.001). We conclude that a multifaceted infection control policy incorporating the use of a vancomycin order form can effectively decrease the use of empirical vancomycin and can play a role in limiting the spread of VRE in an endemic setting.

Association between mucositis severity and vancomycin-resistant enterococcal bloodstream infection in hospitalized cancer patients.

To determine the role of mucositis severity in the development of vancomycin-resistant enterococcal (VRE) bloodstream infection (BSI). A tertiary-care university medical center. Hematology-oncology-unit inpatients. Patients with VRE BSI (case-patients) were compared with VRE-colonized (control) patients from September 1994 through August 1997. Oral mucositis severity was recorded on the day of VRE BSI for case-patients and on hospital day 22 (median day of hospitalization of case-patient VRE BSI) for controls. There were 19 case-patients and 31 controls. In univariate analysis, case-patients were significantly more likely than controls to have a higher mucositis severity score, diarrhea, or a higher severity of illness score. In multivariate analysis, only mucositis remained as an independent risk factor, and increasing mucositis score was significantly associated with VRE BSI. Mucositis severity was independently associated with an increasing risk for VRE BSI. Interventions to alter mucositis severity may help to prevent VRE BSI in hospitalized cancer patients.

Epidemiology and Mortality Risk of Vancomycin-Resistant Enterococcal Bloodstream Infections

Risk factors for vancomycin-resistant enterococcal (VRE) bloodstream infection (BSI) were studied at a tertiary-care hospital by comparing 46 patients with VRE-BSI with 46 randomly selected patients with vancomycin-susceptible enterococcal (VSE) BSI. Among patients with an enterococcal BSI, risk factors for mortality were determined. Independent risk factors for VRE-BSI were increasing APACHE II score (odds ratio [OR], 2.3/5-point increase; 95% confidence interval [CI], 1.4-3.9), receipt of vancomycin (OR, 11; 95% CI, 5.5-21), or diagnosis of hematologic malignancy (OR, 8.4; 95% CI, 3.9-18). After controlling for APACHE II score and gender, patients with VRE- versus VSE-BSI did not have a significantly elevated risk of mortality (OR, 3.3; 95% CI, 0.7-15). Five of 28 VRE blood isolates typed using pulsed-field gel electrophoresis had identical banding patterns. These data suggest that increasing severity of illness, underlying disease, and receipt of vancomycin are major risk factors for VRE-BSI.