Vancomycin-resistant enterococci

Vancomycin-resistant enterococci (VRE) are gaining much attention in the West, chiefly because of the lack of available antimicrobial therapy for VRE infections as most VRE are also resistant to drugs previously used to treat such diseases (e.g. aminoglycosides and ampicillin), the possibility that the vancomycin-resistant genes present in VRE can be transferred to methicillin-resistant Staphylococcus aureus (MRSA), and increasing reports of VRE and the trend towards endemicity in North America. There are three case reports and a study showing stool carriage of more than 10% from Singapore. One of the case reports is notable as the VRE isolated from the urinary tract is community-acquired. In Europe, there is a strong association between the use of avoparcin (a glycopeptide) in animal feeds and the emergence of VRE. Clonal dissemination resulting in nosocomial transmission is also demonstrated. Prior vancomycin use is a risk factor for the subsequent development of VRE bacteraemia. The laboratory plays an important role, namely, a) detection of VRE, and b) determination of susceptibilities of antimicrobials whereby possible therapeutic options may be instituted when antimicrobial intervention is indicated. There is a need to evaluate existing infection control measures against VRE to prevent it from becoming endemic in Singapore as had happened in North America.     

Vancomycin-resistant enterococci in intensive care hospital settings

Vancomycin-resistant enterococci (VRE) have recently emerged as a nosocomial pathogen and present an increasing threat to the treatment of severely ill patients in intensive-care hospital settings. We outline results of a study of the epidemiology of VRE transmission in ICUs and define a reproductive number R0; the number of secondary colonization cases induced by a single VRE-colonized patient in a VRE-free ICU, for VRE transmission. For VRE to become endemic requires R0 > 1. We estimate that in the absence of infection control measures R0 lies in the range 3-4 in defined ICU settings. Once infection control measures are included R0 = 0.6, suggesting that admission of VRE-colonized patients can stabilize endemic VRE.     

Vancomycin-resistant enterococcus

Vancomycin-resistant enterococcus (VRE) rapidly is becoming a significant cause of nosocomial infections. VRE lives in the environment (e.g., bedside tables, side rails, door knobs) for five to seven days, making transmission difficult to eliminate. Patients who are immunosuppressed or are receiving multiple antibiotics are particularly susceptible to developing VRE infections. Nursing management is the cornerstone of prevention and treatment. Nurses need to identify patients at risk, maintain isolation, and educate patients, family members, and other healthcare team members.     

Vancomycin-resistant Enterococcus faecium colonization in children

This paper describes the genomic structure of the human Prostaglandin F receptor gene (FP) with its exon-intron borders and 5' flanking sequences. Furthermore, the location of the gene has been localized to a very small region on 1p31.1 using FISH and radiation hybrids analysis. The PGF receptor (FP) is highly expressed in mouse tissues especially in the corpora lutea in ovaries and in the kidney. Recently, it has been shown that homozygous knockout-mice lacking the gene for this receptor are unable to deliver normal fetuses at term. It might be speculated that the lack of the FP gene has the same effect in human as in mouse. Mutation analysis in families with difficulties in parturition would therefore be of high interest. The results presented here provides data necessary for further investigations of the FP gene.     

Virulence of enterococci

Enterococci are commensal organisms well suited to survival in intestinal and vaginal tracts and the oral cavity. However, as for most bacteria described as causing human disease, enterococci also possess properties that can be ascribed roles in pathogenesis. The natural ability of enterococci to readily acquire, accumulate, and share extrachromosomal elements encoding virulence traits or antibiotic resistance genes lends advantages to their survival under unusual environmental stresses and in part explains their increasing importance as nosocomial pathogens. This review discusses the current understanding of enterococcal virulence relating to (i) adherence to host tissues, (ii) invasion and abscess formation, (iii) factors potentially relevant to modulation of host inflammatory responses, and (iv) potentially toxic secreted products. Aggregation substance, surface carbohydrates, or fibronectin-binding moieties may facilitate adherence to host tissues. Enterococcus faecalis appears to have the capacity to translocate across intact intestinal mucosa in models of antibiotic-induced superinfection. Extracellular toxins such as cytolysin can induce tissue damage as shown in an endophthalmitis model, increase mortality in combination with aggregation substance in an endocarditis model, and cause systemic toxicity in a murine peritonitis model. Finally, lipoteichoic acid, superoxide production, or pheromones and corresponding peptide inhibitors each may modulate local inflammatory reactions.     

Vancomycin resistant enterococci

Enterococci are normal intestinal flora in humans. Among enterococci, Enterococcus faecalis and Enterococcus faecium are frequently isolated and can become nosocomial pathogens in hospitals, especially in intensive care units and oncology wards. Recently, vancomycin-resistant enterococci (VRE) such as E. faecalis and E. faecium have caused a serious problem of hospital-acquired infections in Europe and the USA. VRE also has another aspect as a cause of community-acquired infections. Especially, avoparcin which had been used to enhance growth of food animals is documented as associated with the spread of VRE in European countries. In Japan, there have only been a few of reports about VRE so far. However, there evidence that VRE might become prevalent in many hospitals in Japan. In fact, we have already isolated another highly vancomycin-resistant E. faecium (VCM:MIC > 128 micrograms/ml) from a hospitalized diabetic patient. We should pay a careful attention to VRE and perform the following control measures: 1)re-education and re-training about hospital infection control procedures, 2) prudent use of vancomycin in clinical settings, 3)accurate report of VRE in clinical laboratories, and 4) good communications and collaborations among physicians, nurses and other health care personnel and laboratory technicians. We should learn more from countries in which VRE are already prevalent, and pursue further investigations, to prevent the spread of VRE in Japan.     

Controlling vancomycin-resistant enterococci

After controlling an epidemic of vanB-type vancomycin-resistant Enterococcus faecium (VRE), we contained a subsequent vanA E faecium outbreak by using prospective laboratory-based surveillance, placing patients with VRE in private rooms, requiring the use of both gowns and gloves by all personnel entering the patients' rooms, and conducting prevalence surveys of patients on affected wards.     

Selective isolation of vancomycin-resistant enterococci

Broth formulations of two media selective for enterococci, Enterococcel, M-Enterococcosel broths were supplemented with 6 micrograms of vancomycin per ml and evaluated for isolation of vancomycin-resistant enterococci (VRE). Each broth was challenged with various concentrations of Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, and vancomycin-susceptible and vancomycin-resistant enterococci and with 193 perianal specimens obtained from patients at risk in our institution for VRE colonization. Both the Enterococcosel and M-Enterococcus broths with vancomycin detected as few as 1 to 9 CFU of VRE while inhibiting growth of the other organisms tested. Enterococcus faecium organisms (MIC, > 256 micrograms/ml) were recovered from 66 perianal swab cultures in the enterococcosel-vancomycin broth, and VRE were recovered from 62 perianal swab cultures in the M-Enterococcus-vancomycin broth. Enterococcosel-vancomycin broth detected VRE in perianal specimens 48 h earlier than did M-Enterococcus-vancomycin broth. Enterococcosel broth with 6 micrograms of vancomycin per ml can be used for the rapid and selective isolation of VRE from surveillance specimens.     

Vancomycin-resistant Enterococcus faecium infections in the ICU and quinupristin/dalfopristin

The incidence of vancomycin resistance among enterococci, and Enterococcus faecium in particular, has increased sharply in the last few years. This shift toward infection with resistant Gram-positive organisms is thought to be the consequence of certain features specific to the intensive care setting: a high concentration of severely compromised patients; continued use of indwelling devices and invasive procedures; and widespread, empiric use of antimicrobial agents directed against Gram-negative bacilli. Measures that can be taken to prevent the development of bacterial resistance in the ICU include strict adherence to infection control policies and asepsis, and rational use of antibiotics. Current antimicrobial regimens for serious enterococcal infections consist of a combination of ampicillin, penicillin G, or vancomycin plus streptomycin or gentamicin. High levels of resistances among some enterococcal isolates, however, may render these strategies ineffective. A new agent, quinupristin/dalfopristin (RP 59500), has demonstrated encouraging in vitro activity against vancomycin-resistant E. faecium. Initial clinical reports, though limited, are similarly promising. Although phase III clinical trials with RP 59500 are not completed, the agent is available through an emergency-use program for patients with severe Gram-positive infections who cannot tolerate or do not respond to all other clinically appropriate antibiotics.     

Gene transfer, gentamicin resistance and enterococci

1. Intravenous administration of the ganglionic nicotinic receptor agonist DMPP (1,1-dimethyl-4-phenylpiperazinium iodide) into urethane-anaesthetized rats evoked dose-dependent increases in mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). 2. The ganglionic nicotinic receptor antagonists pentolinium and hexamethonium either alone or combined did not inhibit the increase in RSNA and MAP evoked by 50 to 200 micrograms kg-1 doses of DMPP. The increase in renal sympathetic nerve activity evoked by DMPP occurred as a brief burst in firing. 3. The increase in MAP, but not RSNA, evoked by DMPP in the presence of pentolinium was inhibited by the selective alpha 1-adrenergic receptor antagonist prazosin. 4. The non-selective alpha-adrenoceptor and NPY receptor antagonist benextramine also inhibited the increase in MAP without inhibiting the increase in RSNA. Surprisingly, the combination of benextramine and pentolinium, or benextramine and hexamethonium, completely blocked the DMPP-evoked increase in RSNA and thus the increase in MAP. 5. The uptake1 antagonist desipramine combined with pentolinium did not affect the DMPP-evoked increases in MAP or RSNA when compared to the responses evoked in the presence of pentolinium alone. 6. Adding the selective M1 muscarinic receptor antagonist telenzepine to pentolinium and prazosin did not inhibit the increase in RSNA evoked by a 100 micrograms kg-1 dose of DMPP. 7. While the DMPP-evoked increase in MAP in the presence of ganglionic nicotinic receptor antagonists is primarily dependent upon activation of alpha 1-adrenoceptors, the increase in RSNA occurs via activation of ganglionic nicotinic receptors and activation of a mechanism susceptible to blockade by benextramine.     

Antibiotic resistance patterns of enterococci and occurrence of vancomycin-resistant enterococci in raw minced beef and pork in Germany

The food chain, especially raw minced meat, is thought to be responsible for an increase in the incidence of vancomycin-resistant enterococci (VRE) in human nosocomial infections. Therefore, 555 samples from 115 batches of minced beef and pork from a European Union-licensed meat-processing plant were screened for the occurrence of VRE. The processed meat came from 45 different slaughterhouses in Germany. Enterococci were isolated directly from Enterococcosel selective agar plates and also from Enterococcosel selective agar plates supplemented with 32 mg of vancomycin per liter. In addition, peptone broth was used in a preenrichment procedure, and samples were subsequently plated onto Enterococcosel agar containing vancomycin. To determine resistance, 209 isolates from 275 samples were tested with the glycopeptides vancomycin, teicoplanin, and avoparcin and 19 other antimicrobial substances by using a broth microdilution test. When the direct method was used, VRE were found in 3 of 555 samples (0.5%) at a concentration of 1.0 log CFU/g of minced meat. When the preenrichment procedure was used, 8% of the samples were VRE positive. Our findings indicate that there is a low incidence of VRE in minced meat in Germany. In addition, the resistance patterns of the VRE isolates obtained were different from the resistance patterns of clinical isolates. A connection between the occurrence of VRE in minced meat and nosocomial infections could not be demonstrated on the basis of our findings.     

Infections caused by multiresistant enterococci in Norway

During the last decade antimicrobial resistant pathogens have become a major medical problem. Internationally, multiresistant enterococci have increased nosocomial morbidity and mortality. Such strains are often resistant to ampicillin, aminoglycosides, and glycopeptides such as vancomycin. The spread of these strains has been shown to correlate to the use of antibiotics and the practice of suboptimal infection control within health care facilities. The current situation in Norwegian hospitals is presented, including the only six cases with infections and the three carriers of vancomycin resistant enterococci found to date. Surveillance in the hospitals shows that such strains are uncommon in non-infected patients. To maintain this favourable situation it is necessary to continue to practice effective methods of infection control and to employ sound antibiotic policies.     

Colonization with vancomycin-resistant enterococci in chronic hemodialysis patients

OBJECTIVE: To identify the prevalence of chorioaminionitis and unique risk factors for this disorder among adolescents under 18 years of age. METHODS: At their first prenatal visit we interviewed 352 adolescents who received prenatal care and delivered an infant at our institution between April 20, 1992, and November 10, 1994, to elicit information on demographic characteristics and behavioral risk factors. Retrospective chart review confirmed the presence of chorioamnionitis using accepted clinical criteria. We determined reproductive history, evidence of sexually transmitted disease, duration of labor, use of oxytocin, an internal uterine pressure monitor or conduction anesthesia, timing and duration of ruptured membranes, type of delivery, and infant birth weight from review of subjects' charts. Logistic regression analysis was used to develop adjusted odds ratios (ORs) and 95% confidence intervals (CIs) for risk factors of chorioaminionitis. RESULTS: Ten percent (34 of 352) of adolescents met the clinical definition for chorioamnionitis. Alcohol and tobacco use during pregnancy (OR 7.6; 95% CI 2.3, 25.8) and being married or living with a partner (OR 2.7; 95% CI 1.1, 6.5) were significantly associated with chorioamnionitis, as was conduction anesthesia (OR 4.1; 95% CI 1.1, 15.4), a second stage labor longer than 2 hours (OR 3.5; 95% CI 1.4, 8.5), and rupture of the membranes longer than 18 hours (OR 6.9; 95% CI 2.5, 18.9). Parity or preterm delivery did not differ significantly between those with or without chorioamnionitis. CONCLUSION: These data suggest that in addition to risk factors observed in adults, adolescents who concurrently use tobacco and alcohol during pregnancy, are married or living with a male partner, and have conduction anesthesia are at increased risk for chorioamnionitis.