Journal of the New Zealand Medical Association, 23-August-2002, Vol 115 No 1160
Vancomycin-resistant enterococcal colonisation of hospitalised patients in Auckland
Simon Briggs, Arlo Upton, Mary Bilkey, Susan Taylor, Sally Roberts and David Holland
Vancomycin-resistant enterococci (VRE) were first reported in England and France in 1988.1,2 Since then, the prevalence of VRE colonisation and infection has increased markedly. In 2000, 26.3% of all enterococci associated with hospital-acquired infection in intensive care units in the USA were vancomycin resistant.3 This was an increase of 31% compared to the mean rate for the previous five years. In this article, the term VRE will refer to vancomycin-resistant Enterococcus faecalis and E. faecium, as these are the two species that result in the vast majority of infections caused by enterococci.
Patients at increased risk of colonisation or infection with VRE include the critically ill; those with severe underlying disease or immunosuppression (particularly renal failure, neutropenia and liver transplantation); those with prolonged hospital stay; and those who have received multiple antibiotics.4,5 A number of antibiotics, including vancomycin, cephalosporins and those with anaerobic activity, have been found to increase the risk of VRE colonisation and infection.5 It is thought that this increased risk may be due to the selective pressure exerted by these antibiotics on bowel flora, resulting in an increased susceptibility to colonisation with VRE and an increase in the number of these organisms once colonisation has occurred.6 Resistance in E. faecalis and E. faecium is almost entirely mediated by transferable plasmids containing the vanA or vanB genes.7
In February 2001, a VRE (E. faecium positive for the vanA gene) was isolated from the continuous ambulatory peritoneal dialysis (CAPD) fluid of an 80-year-old man with CAPD peritonitis. In the preceding months he had experienced several episodes of CAPD peritonitis, caused by a number of different organisms for which he received treatment with cephalosporins, vancomycin and gentamicin. This was the first clinical isolate of VRE from Auckland Hospital. As the number of patients colonised with VRE may be up to ten times higher than those with VRE infection5 the current study was undertaken to assess the rate of VRE colonisation in our hospitals.
From July to November 2001, faeces specimens submitted for Clostridium difficile toxin assay to the Microbiology Laboratories at Auckland and Middlemore Hospitals were examined for the presence of VRE. Following testing for C. difficile toxin, these faeces samples were frozen at -70°C. At weekly intervals the samples were thawed, inoculated onto the selective media bile aesculin azide agar containing 6 mg/L vancomycin (Fort Richard, Auckland) and incubated at 35°C for 48 hours. Gram stains were performed on any aesculin positive colonies; gram-positive cocci were subcultured onto sheep blood agar and incubated at 35°C for 24 hours. Colonies that were catalase negative, pyrrolidonyl aminopeptidase (PYR) positive, methyl-α-D-glucopyranoside (MGP) negative and motility negative were further identified with the Becton Dickinson BBL Crystal System (Becton, Dickinson and Company, Maryland, USA). Vancomycin minimum inhibitory concentrations (MIC) were performed on E. faecalis and E. faecium isolates by E-test (AB Biodisk, Solna, Sweden). Isolates with a vancomycin MIC > 4 mg/L were sent to the Institute of Environmental Science and Research (ESR), Porirua for confirmation of identification, antibiotic susceptibilities and for vanA/vanB gene detection. To ensure that freezing did not impair organism viability, four faeces specimens, negative for VRE, were ‘spiked’ with 1.5 x 107 colony-forming units of vancomycin-resistant E. faecalis reference strain ATCC 51299. These specimens were frozen at -70°C for one week before being thawed and inoculated onto agar as described above. VRE were isolated from all these specimens.
Faeces specimens from 608 adult and 78 paediatric inpatients at Auckland, Greenlane, National Womens’, Middlemore and Starship Hospitals were screened. Of the 686 patients, 388 were female and the median age was 63 years (range 3 weeks to 101 years). Of the adult patients (age > 15 years), 120 (20%) were considered to be at higher risk for VRE colonisation; these included patients from intensive care units (n=41) and the renal (n=42), haematology (n=27) and liver transplant (n=10) services. The other 488 adult patients were from a wide variety of services from the above hospitals. Of the 78 paediatric patients, 18 (23%) were from the haematology/oncology service or the intensive care unit.
VRE was isolated from two patients at Auckland Hospital, giving a colonisation rate of 0.5% (95% CI 0 to 1.2%) for this hospital and 0.3% (95% CI 0 to 0.7%) for all hospitals. No patients from the higher risk group (n=138) were found to have VRE colonisation. Both isolates were identified as E. faecalis; they were susceptible to ampicillin (MIC of 2 and 1 mg/L respectively), resistant to vancomycin (MIC > 256 mg/L), resistant to teicoplanin (MIC of 256 and > 256 mg/L respectively) and found to be of the vanA genotype.
Patient 1, a 63-year-old woman, was admitted with bowel obstruction secondary to adhesions from previous abdominal surgery as a child. Apart from asthma, she had no other medical history and had not received antibiotics in the previous year. Her last hospital admission had been in 1965. On the third day of her admission she was started on intravenous cefuroxime for pneumonia, and the faeces sample from which the VRE was isolated was sent four days later. As she had been in hospital for one week prior to the faeces sample being collected, patient-to-patient spread was considered. By the time the culture result was available, the patients who had shared her room had been discharged and so could not be tested. A second sample from the same patient also tested positive.
Patient 2, a 17-year-old man was admitted with a one-day history of fever, abdominal pain and diarrhoea. Eight weeks previously, he had returned from spending four weeks in London, Paris and Washington. He had not received antibiotics in the last year and had no previous hospital admissions. His faeces sample was obtained at the time of admission. As well as VRE, Campylobacter jejuni and two Aeromonas species were isolated from his faeces.
This is the first screening programme in New Zealand that has identified patients colonised with VRE. The two VRE colonised patients detected by our survey represent a rate of 0.3% for all hospitals in those patients who had a faeces sample submitted for C. difficile toxin assay (0.5 % for Auckland Hospital alone). Two previous studies looking at VRE colonisation in New Zealand, one from Auckland in 1996,8 and the other from Otago in 1997/98,9 failed to isolate any vancomycin-resistant E. faecalis or E. faecium in a total of 804 stool specimens. The route by which the identified two patients became colonised with VRE is unknown. The first patient may have been colonised with VRE prior to her admission or may have acquired the organism while in hospital; this could not be further established. The second patient must have been colonised prior to his admission to hospital, possibly during recent overseas travel.
While VRE are still rarely isolated in New Zealand hospitals, colonisation and infection may be increasing. The national reference laboratory, ESR, has received fifteen VRE isolates since 1996: one in 1996, one in 1998, five in 1999, two in 2000 and six in 2001, including those in this report (personal communication H. Heffernan, ESR). Of these 15 isolates, 13 were E. faecalis and 14 were positive for the vanA gene. Of interest was the isolation of another vancomycin-resistant E. faecalis (MIC > 256 mg/l, vanA genotype) from an axillary abscess of a 31-year-old woman with end stage renal failure at Middlemore Hospital two weeks after our screening programme had finished. This was the second VRE isolated at Middlemore Hospital. The patient usually received haemodialysis at home but for the two weeks prior to her admission had attended the hospital inpatient dialysis unit. Within the last year she had spent eighteen days in hospital and received several antibiotics.
As colonisation with VRE usually precedes infection, and the number of patients colonised may be significantly higher than those infected, periodic screening for VRE colonisation of high-risk patients has been recommended, even in the absence of cases of infection.4 Screening with stool culture or a rectal or perianal swab has been advocated.4,10 We chose to perform VRE screening on samples submitted for C. difficile toxin assay, as these specimens were already available to the laboratory and given the similar detection rate when compared to screening with a rectal swab.11 This method has been used previously, as there are many common risk factors for the development of C. difficile-associated diarrhoea and the acquisition of VRE colonisation.12
There appear to be two different patterns of VRE colonisation and infection in Europe and the USA. In Europe, rates of VRE colonisation in hospitals appear to be similar to those in the community13 and there is evidence that the widespread use of avoparcin (a glycopeptide antibiotic similar to vancomycin) as a growth promoter in the livestock industry has resulted in a large reservoir of vanA E. faecium in poultry and swine with transmission to humans.14 Avoparcin has been banned by the European Union since 1997. In the USA, where avoparcin has never been used, VRE have not been detected in community surveys and hospital spread of VRE is the usual pattern.6 The use of vancomycin in American hospitals is thought to be much higher than in Europe6 and may have provided a selective pressure in humans analogous to avoparcin use in animals.
The epidemiology of VRE in New Zealand is still in its early days. We may follow the European pattern, as avoparcin was used in this country until 2000 and our use of vancomycin and cephalosporins is probably more comparable to that of Europe than the USA. With the exception of one isolate, all of the VRE isolates received by ESR to date have been vanA enterococci (mainly E. faecalis), which is the genotype most common in Europe.
As the rate of VRE colonisation is likely to increase in New Zealand, we can expect an increase in the number of cases of VRE infection. Hospitals need to be prepared to limit the spread of VRE by implementing strategies, including admission surveillance of high risk patients, contact isolation of VRE colonised/infected patients, reduction of antibiotic pressure and staff education.5 Our current rate of colonisation does not warrant screening of all high-risk patients but the other measures are essential. Reduction of antibiotic selective pressure by judicious use is a responsibility of all medical practitioners. We intend to repeat this survey in one to two years to monitor colonisation rates and review our policies.
Author information: Simon Briggs, Microbiology Registrar, Auckland Hospital; Arlo Upton, Microbiology Registrar, Middlemore Hospital; Mary Bilkey, Technical Specialist, Microbiology Laboratory, Auckland Hospital; Susan Taylor, Clinical Microbiologist, Middlemore Hospital; Sally Roberts, Clinical Microbiologist, Auckland Hospital; David Holland, Clinical Microbiologist, Auckland Hospital
Acknowledgements: We acknowledge the assistance of Helen Heffernan, ESR, and the staff of the Microbiology Laboratories at Auckland and Middlemore Hospitals.
Correspondence: Simon Briggs, Infectious Diseases Registrar, Auckland Hospital, Park Road, Grafton, Auckland. Fax (09) 307 4940; email: firstname.lastname@example.org
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