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Prevalence and risk factors for VRE colonisation in a tertiary hospital in Melbourne, Australia: a cross sectional study

Prevalence and risk factors for VRE colonisation in a tertiary hospital in Melbourne, Australia:... Background: Vancomycin-resistant Enterococcus (VRE) has been established as a significant health-care associated problem since its first isolation in Australia in 1994. In this study, we measured the point prevalence and identified risk factors associated with vanB VRE colonisation in a tertiary care hospital in Melbourne, Australia where VRE has been endemic for 15 years. Methods: A hospital-wide point prevalence survey was conducted on October 13, 2008 with colonisation detected using rectal swab culture. Patient’s demographic and medical information was collected through a review of medical records. Factors associated with VRE colonisation in univariate analysis were included in multivariate logistic regression model to adjust for confounding. Results: The prevalence of VRE colonisation on the day of screening was 17.5% (95% CI, 13.7 to 21.9). VRE was detected from patients in each ward with the prevalence ranging from 3% to 29%. Univariate analysis showed the use of any antibiotic, meropenem, ciprofloxacin, diarrhoea and longer length of hospital stay were associated with increased risk of VRE colonisation (p<0.05). However, age, sex, proximity to VRE positive cases, use of other antibiotics including cephalosporins, vancomycin were not associated with increased risk (P>0.05). Multivariate analysis showed the exposure to meropenem (p=0.004), age (≥65 years) (p=0.036) and length of stay ≥7 days (p<0.001) as independent predictors of VRE colonisation. Conclusion: Our study suggests that exposure to antibiotics may have been more important than recent cross transmission for a high prevalence of vanB VRE colonisation at our hospital. Keywords: VRE, Colonisation, Acquisition, Prevalence, Risk factors, Australia, VanB, Antibiotics Background in 1986 and subsequently worldwide [1]. In Australia, the The emergence and spread of vancomycin-resistant first case of VRE was reported in 1994 and by 1998 from Enterococcus (VRE) in health care settings has added all other major cities [2,3]. The predominant VRE genotype risks and complexities in patient management. VRE circulating in Australia is E. faecium vanB,incontrast to can cause a variety of health care-associated infections, the vanA genotype which is predominant in the United particularly bacteraemia and urinary tract infections. States and Europe [3,4]. Recent surveys have shown an in- Most enterococcal infections are caused by two species, crease in the prevalence of vancomycin resistance in cli- E. faecalis or E. faecium. VRE was first reported in Europe nical isolates of enterococci in Australia [5]. A VRE prevalence as high as 19.1% was reported during an out- break among hospital inpatients in Victoria [6]. Faecal co- * Correspondence: allen.cheng@monash.edu 1 lonisation with VRE in the community has been Department of Epidemiology and Preventive Medicine, Infectious Disease demonstrated in Australia but appears to be rare (preva- Epidemiology Unit, Monash University, Melbourne, Australia Infection Prevention and Healthcare Epidemiology Infectious Diseases and lence 0.2%) although the vanB gene appears to be common Microbiology Unit, Alfred Health, Melbourne, Australia in commensal bacteria including Clostridium spp [7-9]. Full list of author information is available at the end of the article © 2012 Karki et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 2 of 6 http://www.aricjournal.com/content/1/1/31 Previous studies have identified various risk factors for hospital admissions in patients that were found to be posi- VRE colonisation including advanced age, severe under- tive for VRE. lying illness, inter-hospital transfer, nursing home resi- At the time of the survey, our VRE policy recommended dency, extended hospitalization, specialized nutritional the screening of all ward patients where a new case of support, central venous catheterization, haematologic VRE infection or colonisation was detected. There were malignant tumours, solid organ allograft, chronic no systemic screening practices for patients in high risk haemodialysis, antibiotic exposure to vancomycin, third- areas or testing of diarrhoeal stools prior to this study. generation cephalosporins, metronidazole, antibiotics Patients with known VRE colonisation or infection were with anti-anaerobic activity, exposure to multiple anti- isolated in single rooms with a dedicated toilet if they had biotics and prolonged duration of antibiotic therapy faecal incontinence or diarrhoea. Healthcare workers were [10]. However, most of those studies involve high risk required to use gloves when entering the room, and gloves patients during outbreaks associated with vanA geno- and gown if contact with body fluids was anticipated. Hos- type. A previous study in Melbourne hospitals in 1998 pital floors were cleaned daily with 1000 part per million identified broad spectrum antibiotics as significant risk (ppm) sodium hypochlorite. factor for new colonisation with vanB VRE [11]. A nested case control (1:2) study was conducted to VRE colonisation can lead to infections which prolong identify risk factors associated with VRE colonisation. A hospital stay, increase the cost of care and increase mor- case was defined as a patient confirmed to be positive by bidity and mortality [12,13]. The identification of modifi- standard microbiological methods for VRE isolated from able risk factors may assist in identifying targets for rectal swabs taken for the point prevalence survey. A intervention to reduce the incidence of VRE colonisation. control was defined as a patient confirmed to be nega- In this study, we measured the prevalence of VRE colon- tive for VRE colonisation on the same survey. For each isation in a hospital-wide point prevalence survey. We case, two unmatched controls were selected at random examined downstream risk factors for colonisation with from eligible patients. implications for VRE control policies, including antibiotic exposure and patient placement, in a tertiary referral hos- Microbiology pital in Melbourne, Australia where vanB VRE has been Rectal swabs were taken either by the patients them- endemic for many years. selves following instruction, or by nursing staff. The swabs were then plated onto bile aesculin media (BBL Enterococcosel agar, Cockeysville, MD) with vancomycin Methods 6 μg/mL and incubated at 37°C for up to 72 hours. En- Setting and study design terococci species were identified using the VITEK-2 sys- The Alfred hospital is a major tertiary teaching hospital tem (bioMérieux). Polymerase chain reaction was used in Melbourne, Australia with 427 beds. The hospital to detect the vanA or vanB genes as described previ- provides general services as well as broad range of spe- ously. [14] VRE colonisation was defined if an isolate of cialist care including referral services for trauma, cystic E. faecalis or E. faecium with vanA or vanB gene was fibrosis and heart/lung transplantation, HIV/AIDS, bone detected. Ribotyping of the isolates was performed using marrow transplantation as well as specialist intensive the Riboprinter Microbial Characterization system as care facilities. previously described [15,16]. We conducted a point prevalence survey on October 13, 2008 at the Alfred Hospital. All patients who were present Statistical methods in the hospital (including inpatients, patients in the emer- Standard statistical methods were used to summarize gency department, and day surgery but excluding psych- categorical and continuous measures and to compare iatry) at 8.00 a.m. were approached to participate. Patients proportions. Univariate analysis was performed to calcu- were provided with information sheets (including advice late unadjusted odds ratio. All variables with a p-value of about the potential consequences of VRE colonisation) and <0.2 in univariate analysis were included in the multiple verbal consent was obtained for participation. Patients were logistic regression model to examine independently asso- included irrespective of known VRE status. Patients were ciated risk factors for VRE colonisation. The association excluded if they were not able to consent, were for palliative was considered statistically significant if p<0.05. Statis- care only, had been discharged prior to being swabbed or tical analyses were performed using Stata statistical soft- they declined to participate. Single rectal swabs were pri- ware (Version 10; Stata Corp, College Station, Texas). marily taken by nursing staff. Clinical data collection included demographic details, bed location of all patients, Ethics antibiotic use (at least 12 hours before the collection of rec- As this VRE survey represented a quality assurance ac- tal swab in current admission), ICU exposure, and previous tivity, we did not obtain a formal ethical approval to Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 3 of 6 http://www.aricjournal.com/content/1/1/31 perform the point prevalence survey. However, we coun- TheprevalenceofVRE colonisation on theday of selled patients about the significance of VRE and pro- screening was 58 of 331 patients (17.5%, 95% CI, 13.7% vided written information, and obtained verbal consent to 21.9%). The proportion of patients colonised with to take rectal swabs from all patients and/or their rela- VRE was 3% in the emergency department and ranged tives. We obtained approval from the Alfred Health from 8% to 29% in inpatient wards. Of the 58 VRE iso- Human Research Ethics Committee and Monash Uni- lates, 57 were found to be Enterococcus faecium and one versity Human Research Ethics Committee to retrieve was Enterococcus faecalis. All the isolates were positive demographic and clinical information from the medical for vanB resistance genotype and no vanA resistance geno- records of patients for the case control study. type was detected. All together, 9 ribotypes were detected with the majority of isolates belonging to either of the two ribotypes (S-7, n=25, 43%; S-5, n=23, 39%). However, more Results than 1 ribotype was present in all wards where there was A total of 434 patients were present in hospital at the more than one VRE-colonised patient present. time of survey. Among the total, 331 (77%) were Of the total 58 patients found to be VRE colonised, 46 screened for VRE colonisation; 103 patients (23%) could (79.3%) were not previously known to be VRE colonised not be screened either due to refusal, discharge from and 12 (20.7%) were known to be previously colonised. hospital prior to the time of swabbing, patients not being A further 13 patients had a history of VRE colonisation present in the ward at the time of screening, or if the pa- but VRE was not detected on screening at the time of tient was for palliative care. the survey. Table 1 Factors associated with VRE detection in cases and controls (Univariate analysis) Variables Cases Controls Unadjusted OR P value Participants 58 116 - - Age ≥ 65 (years) 35 (60.3%) 56 (48.2%) 1.63 (0.82 to 3.26) 0.13 Male 36 (62.1%) 74 (63.8%) 0.92 (0.46 to 1.88) 0.82 Antibiotics Exposure to any antibiotic 45 (77.6%) 55 (47.4%) 3.83 (1.79 to 8.54) <0.001 Meropenem 8 (13.8%) 2 (1.7%) 9.12 (1.71 to 89.92) 0.001 Antibiotics other than meropenem 39 (67.2%) 54 (46.5%) 4.5 (2.06 to 10.71) 0.001 Vancomycin 13 (22.4%) 19 (16.38%) 1.47 (0.61 to 3.46) 0.33 Teicoplanin 2 (3.4%) 2 (1.7%) 2.03 (0.14 to 28.63) 0.47 Any cephalosporin 19 (32.8%) 32 (27.6%) 1.27 (0.60 to 2.66) 0.47 Ceftriaxone 11 (18.9%) 24 (20.7%) 0.89 (0.36 to 2.11) 0.78 Cefotaxime 2 (3.4%) 0 - - Ceftazidime 5 (8.6%) 4 (3.4%) 2.64 (0.54 to 13.79) 0.14 Cefepime 1 (1.7%) 6 (5.2%) 0.32 (0.01 to 2.76) 0.27 Metronidazole 5 (8.6%) 19 (16.4%) 0.48 (0.13 to 1.43) 0.16 Ciprofloxacin 11 (18.9%) 9 (7.8%) 2.78 (0.96 to 8.11) 0.03 Ticarcillin-clavulanate 11 (18.9%) 12 (10.3%) 2.02 (0.74 to 5.41) 0.11 Ampicillin 1 (1.7%) 3 (2.6%) 0.66 (0.01 to 8.45) 0.72 Gentamicin 2 (3.4%) 9 (7.8%) 0.42 (0.04 to 2.16) 0.27 Piperacillin-tazobactam 5 (8.6%) 3 (2.6%) 3.55 (0.65 to 23.53) 0.07 Other factors ICU admission 18 (31.1%) 26 (22.4%) 1.55 (0.71 to 3.33) 0.21 Within 2 rooms of positive case 30 (62.5%) 54 (65.8%) 0.86 (0.38 to 1.94) 0.69 On same side as positive case 48 (82.8%) 83 (77.6%) 1.38 (0.57 to 3.53) 0.43 Diarrhoea 12 (21.1%) 11 (9.5%) 2.54 (0.94 to 6.85) 0.03 Length of stay (Median days) 11.5 (7–30) 6.0 (3–13) - <0.001 Length of stay ≥7 days 43 (74.2%) 43 (37.1%) 4.86 (2.30 to 10.51) <0.001 Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 4 of 6 http://www.aricjournal.com/content/1/1/31 Risk factors for VRE colonisation reported by previous studies conducted at Melbourne We compared the exposure to probable risk factors in hospitals [11,17-19]. This is also in contrast to previous 58 cases and 116 controls. studies demonstrating that VRE colonisation was Significantly higher proportions of cases had prior ex- restricted to particular high risk inpatient areas [11]. posure to one or more antibiotics (odds ratio (OR) 3.83, Our finding that 80% of the VRE colonised patients in 95% CI 1.79 to 8.54). Similarly, cases had a longer length the survey were newly detected cases demonstrates that of hospital stay compared to controls (P<0.001). Patients the previous screening strategy of surveying patients with VRE colonisation were more likely to have been ad- only on wards when a new clinical isolate of VRE was mitted for ≥7 days (OR 4.86, 95% CI 2.30 to 10.51). Uni- detected is inadequate. variate analyses identified prior exposure to any Prima facie, our results suggest that antibiotic selec- antibiotic (p <0.001), exposure to meropenem (p=0.001), tion pressures appear to play a larger role in determining ciprofloxacin (p=0.03), diarrhoea (p=0.03) as associated VRE colonisation than cross-transmission at our institu- with the detection of VRE colonisation (Table 1). How- tion. Exposure to antibiotics, particularly meropenem, ever, the prior use of vancomycin (p=0.33), ticarcillin- was strongly associated with VRE colonisation; this is clavulanate (p=0.11), pipericillin-tazobactam (p=0.07), consistent with previous studies suggesting that anti- metronidazole (p=0.16) and any cephalosporins were not biotic regimens with activity against anaerobic bacteria associated with colonisation status. Proximity to other are potent risk factors in the development of VRE VRE positive cases either in same side of the ward or [20-22]. The vanB gene is known to be present in com- located within next 2 rooms was not associated with mensal enteric bacteria such as Clostridium, and trans- VRE colonisation (p>0.05) (Table 1). mission of this gene to E. faecium has been In a multivariate logistic regression model, exposure to demonstrated in vivo [23]. In other studies, a variety of meropenem (adjusted OR; 12.24, 95% CI 2.24 to 66.77), other antibiotics have been implicated as risk factors for age ≥ 65years (adjusted OR 2.19, 95% CI 1.05 to 4.58) VRE colonisation, including vancomycin, metronidazole, and length of stay ≥7 days (adjusted OR 4.69, 95% CI piperacillin-tazobactam, ticarcillin-clavulanate and third 2.25 to 9.73) were independently associated with VRE generation cephalosporins [24-26]. However, our analysis colonisation (Table 2). After adjusting for age ≥ 65years, comparing meropenem and non-meropenem antibiotic length of stay ≥7 days and exposure to meropenem, ex- use with no antibiotic use showed the exposure to anti- posure to any antibiotic other than meropenem (com- biotics other than meropenem is also associated with pared to patients that did not receive any antibiotics) VRE colonisation. Thus, our study may have been under- was independently associated with VRE colonisation powered to detect differences at the level of individual (adjusted OR 2.95, 95% CI 1.27 to 6.88). In total, 16 antibiotics other than meropenem. (9.2%) patients in case–control study were from emer- We found ambiguous evidence regarding the extent of gency department and short stay units. A sensitivity ana- cross transmission of VRE, which has been shown to be lysis excluding the patients in these units did not alter important in previous studies [27,28]. We did not find any of the above effects, significantly. proximity to other VRE colonised patients to be a risk fac- tor for VRE detection. However, this does not exclude the Discussion possibility of cross transmission contributing to endem- We conducted a hospital-wide point prevalence survey icity, as transmission may have occurred prior to the time to measure the prevalence of VRE, as our previous sur- of the survey and would not be detected with frequent pa- veillance activities were targeted to patients felt to be at tient movements. Conversely, the finding that ribotyping risk and therefore may have resulted in selection biases. only demonstrated two large clones of VRE in patients In this survey, we confirmed that vanB VRE is endemic does not necessarily implicate extensive cross transmis- in inpatients at our hospital. We found a lower preva- sion. If transmission was significant, we would expect a lence in short stay areas, such as the emergency de- lower diversity among individual wards; however, we partment (3%) and the short stay unit, but prevalence found that in all wards with at least two VRE colonised was 8-29% in other inpatient areas. This is higher than patients had at least two ribotypes. We did not have access to pulsed field gel electrophoresis, regarded as the gold standard for epidemiological investigations of VRE [29]. Table 2 Factors associated with VRE detection in cases The purpose of this study was to examine “down- and controls (multivariate analysis) stream” exposures that had implications for VRE control Risk factor Adjusted OR (95% CI) p value policies, rather than patient-specific “upstream” risk fac- Meropenem 12.24 (2.24 to 66.77) 0.004 tors that are not modifiable. However, we did find older Age (≥65 years) 2.19 (1.05 to 4.58) 0.036 age and longer length of stay in hospital as independent Length of stay ≥7 days 4.69 (2.25 to 9.73) <0.001 predictor of VRE colonisation. This is reflected in the Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 5 of 6 http://www.aricjournal.com/content/1/1/31 low colonisation rate in patients with a short length of Author details Department of Epidemiology and Preventive Medicine, Infectious Disease stay, including emergency and short stay units. Epidemiology Unit, Monash University, Melbourne, Australia. Infection A strength of this study is that we conducted a Control, Eastern Health, Melbourne, Australia. Infection Prevention and hospital-wide survey including a broad range of patients, Healthcare Epidemiology Infectious Diseases and Microbiology Unit, Alfred Health, Melbourne, Australia. Infection Control Consultancy, Melbourne, thus minimizing selection biases [30]. A limitation of Australia. this cross-sectional study is that we were not able to de- termine the timing of acquisition of VRE in the patients Received: 11 July 2012 Accepted: 1 October 2012 Published: 8 October 2012 identified as being colonised; therefore, patients may have acquired VRE in the remote past, with antibiotic References use merely amplifying existing colonisation. In addition, 1. Uttley AH, Collins CH, Naidoo J, George RC: Vancomycin-resistant we do not have data on patient co-morbidities, previous enterococci. Lancet 1988, 1:57–58. invasive procedures, and indwelling devices, which may 2. Kamarulzaman A, Tosolini FA, Boquest AL, Geddes JE, Richards MJ: Vancomycin-resistant Enterococcus faecium in a liver transplant patient. have confounded our findings. We chose to perform rec- Aust NZ J Med 1995, 25:560. tal swabs due to practical reasons but previous studies 3. 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Ballard SA, Pertile KK, Lim M, Johnson PD, Grayson ML: Molecular that of new acquisition of VRE (whether by endogenous characterization of vanB elements in naturally occurring gut anaerobes. generation or exogenous exposure) and amplification of Antimicrob Agents Chemother 2005, 49:1688–1694. 8. Padiglione AA, Grabsch EA, Olden D, Hellard M, Sinclair MI, Fairley CK, existing low level colonisation by antibiotics [34]. Grayson ML: Fecal colonisation with vancomycin-resistant enterococci in Australia. Emerg Infect Dis 2000, 6:534–536. 9. Graham M, Ballard SA, Grabsch EA, Johnson PD, Grayson ML: High rates of Conclusions fecal carriage of nonenterococcal vanB in both children and adults. The endemic and high prevalence of vanB VRE in our set- Antimicrob Agents Chemother 2008, 52:1195–1197. 10. DeLisle S, Perl TM: Vancomycin-resistant enterococci: a road map on how ting mayhavebeenmaintainedby higherexposuretoanti- to prevent the emergence and transmission of antimicrobial resistance. biotics. Although cross transmission remains a possibility Chest 2003, 123:504S–518S. and is supported by predominance of two large clones of 11. Padiglione AA, Wolfe R, Grabsch EA, Olden D, Pearson SH, Franklin C, Spelman D, Mayall B, Johnson PDR, Grayson ML: Risk factors for new VRE, colonisation status did not appear to be associated detection of vancomycin-resistant enterococci in acute-care hospitals with proximity to other colonised patients. Our data sug- that employ strict infection control procedures. Antimicrob Agents gest that antibiotic stewardship efforts may be more effect- Chemother 2003, 47:2492–2498. 12. Joels CS, Matthews BD, Sigmon LB, Hasan R, Lohr CE, Kercher KW, Norton J, ive in reducing the spread of VRE in our hospital. Sing RF, Heniford BT: Clinical characteristics and outcomes of surgical patients with vancomycin-resistant enterococcal infections. Am Surg Competing interests 2003, 69:514–519. The authors declare that they have no competing interests. 13. DiazGranados CA, Zimmer SM, Klein M, Jernigan JA: Comparison of mortality associated with vancomycin-resistant and vancomycin- susceptible enterococcal bloodstream infections: a meta-analysis. Clin Authors’ contributions Infect Dis 2005, 41:327–333. The point prevalence study was designed by GH, LH, GL, PB, SB, RK, DS. The 14. Dutka-Malen S, Evers S, Courvalin P: Detection of glycopeptide resistance study was primarily co-ordinated by LH with support from GH, LH, GL, PB, SB, genotypes and identification to the species level of clinically relevant RK, including identifying patients, co-ordinating swab collection and enterococci by PCR. J Clin Microbiol 1995, 33:1434. collecting data on cases. DS oversaw microbiological testing and typing. LH 15. Bruce J: Automated system rapidly identifies and characterizes and KW managed the data and performed the initial analysis of cases. AC microorganisms in food. Food Technol 1996, 50:77–81. and SK designed and analysed the case control study with assistance from 16. Price CS, Huynh H, Paule S, Hollis RJ, Noskin GA, Pfaller MA, Peterson LR: JK and DS. SK collected the data on controls and drafted the manuscript. All Comparison of an automated ribotyping system to restriction authors interpreted the results and revised the manuscript. endonuclease analysis and pulsed-field gel electrophoresis for differentiating vancomycin-resistant Enterococcus faecium isolates. J Clin Acknowledgements Microbiol 2002, 40:1858–1861. We thank ward staff at the Alfred Hospital for assisting in this survey, 17. 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Melbourne: Victorian Department of Health; 2008. http://www.health.vic.gov.au/ infectionprevention/downloads/vre-report.pdf, accessed June 10, 2012. 20. Al-Nassir WN, Sethi AK, Li YJ, Pultz MJ, Riggs MM, Donskey CJ: Both oral metronidazole and oral vancomycin promote persistent overgrowth of vancomycin-resistant enterococci during treatment of Clostridium difficile- associated disease. Antimicrob Agents Chemother 2008, 52:2403–2406. 21. Carmeli Y, Eliopoulos GM, Samore MH: Antecedent treatment with different antibiotic agents as a risk factor for vancomycin-resistant enterococcus. Emerg Infect Dis 2002, 8:802–807. 22. MacIntyre CR, Empson M, Boardman C, Sindhusake D, Lokan J, Brown GV: Risk factors for colonisation with vancomycin-resistant enterococci in a Melbourne hospital. Infect Control Hosp Epidemiol 2001, 22:624–629. 23. 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Byers KE, Anglim AM, Anneski CJ, Germanson TP, Gold HS, Durbin LJ, Simonton BM, Farr BM: A hospital epidemic of vancomycin-resistant Enterococcus: risk factors and control. Infect Control Hosp Epidemiol 2001, 22:140–147. 28. Zhou Q, Moore C, Eden S, Tong A, McGeer A: Factors associated with acquisition of vancomycin-resistant enterococci (VRE) in roommate contacts of patients colonised or infected with VRE in a tertiary care hospital. Infect Control Hosp Epidemiol 2008, 29:398–403. 29. Gordillo ME, Singh KV, Murray BE: Comparison of Ribotyping and Pulsed- Field Gel-Electrophoresis for Subspecies Differentiation of Strains of Enterococcus-Faecalis. J Clin Microbiol 1993, 31:1570–1574. 30. Cole SR, Platt RW, Schisterman EF, Chu HT, Westreich D, Richardson D, Poole C: Illustrating bias due to conditioning on a collider. Int J Epidemiol 2010, 39:417–420. 31. 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Infect Control Hosp Epidemiol 2001, and take full advantage of: 22:576–578. doi:10.1186/2047-2994-1-31 • Convenient online submission Cite this article as: Karki et al.: Prevalence and risk factors for VRE • Thorough peer review colonisation in a tertiary hospital in Melbourne, Australia: a cross • No space constraints or color figure charges sectional study. Antimicrobial Resistance and Infection Control 2012 1:31. • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Antimicrobial Resistance & Infection Control Springer Journals

Prevalence and risk factors for VRE colonisation in a tertiary hospital in Melbourne, Australia: a cross sectional study

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Springer Journals
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Copyright © 2012 by Karki et al.; licensee BioMed Central Ltd.
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Biomedicine; Medical Microbiology; Drug Resistance; Infectious Diseases
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2047-2994
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10.1186/2047-2994-1-31
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23039285
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Abstract

Background: Vancomycin-resistant Enterococcus (VRE) has been established as a significant health-care associated problem since its first isolation in Australia in 1994. In this study, we measured the point prevalence and identified risk factors associated with vanB VRE colonisation in a tertiary care hospital in Melbourne, Australia where VRE has been endemic for 15 years. Methods: A hospital-wide point prevalence survey was conducted on October 13, 2008 with colonisation detected using rectal swab culture. Patient’s demographic and medical information was collected through a review of medical records. Factors associated with VRE colonisation in univariate analysis were included in multivariate logistic regression model to adjust for confounding. Results: The prevalence of VRE colonisation on the day of screening was 17.5% (95% CI, 13.7 to 21.9). VRE was detected from patients in each ward with the prevalence ranging from 3% to 29%. Univariate analysis showed the use of any antibiotic, meropenem, ciprofloxacin, diarrhoea and longer length of hospital stay were associated with increased risk of VRE colonisation (p<0.05). However, age, sex, proximity to VRE positive cases, use of other antibiotics including cephalosporins, vancomycin were not associated with increased risk (P>0.05). Multivariate analysis showed the exposure to meropenem (p=0.004), age (≥65 years) (p=0.036) and length of stay ≥7 days (p<0.001) as independent predictors of VRE colonisation. Conclusion: Our study suggests that exposure to antibiotics may have been more important than recent cross transmission for a high prevalence of vanB VRE colonisation at our hospital. Keywords: VRE, Colonisation, Acquisition, Prevalence, Risk factors, Australia, VanB, Antibiotics Background in 1986 and subsequently worldwide [1]. In Australia, the The emergence and spread of vancomycin-resistant first case of VRE was reported in 1994 and by 1998 from Enterococcus (VRE) in health care settings has added all other major cities [2,3]. The predominant VRE genotype risks and complexities in patient management. VRE circulating in Australia is E. faecium vanB,incontrast to can cause a variety of health care-associated infections, the vanA genotype which is predominant in the United particularly bacteraemia and urinary tract infections. States and Europe [3,4]. Recent surveys have shown an in- Most enterococcal infections are caused by two species, crease in the prevalence of vancomycin resistance in cli- E. faecalis or E. faecium. VRE was first reported in Europe nical isolates of enterococci in Australia [5]. A VRE prevalence as high as 19.1% was reported during an out- break among hospital inpatients in Victoria [6]. Faecal co- * Correspondence: allen.cheng@monash.edu 1 lonisation with VRE in the community has been Department of Epidemiology and Preventive Medicine, Infectious Disease demonstrated in Australia but appears to be rare (preva- Epidemiology Unit, Monash University, Melbourne, Australia Infection Prevention and Healthcare Epidemiology Infectious Diseases and lence 0.2%) although the vanB gene appears to be common Microbiology Unit, Alfred Health, Melbourne, Australia in commensal bacteria including Clostridium spp [7-9]. Full list of author information is available at the end of the article © 2012 Karki et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 2 of 6 http://www.aricjournal.com/content/1/1/31 Previous studies have identified various risk factors for hospital admissions in patients that were found to be posi- VRE colonisation including advanced age, severe under- tive for VRE. lying illness, inter-hospital transfer, nursing home resi- At the time of the survey, our VRE policy recommended dency, extended hospitalization, specialized nutritional the screening of all ward patients where a new case of support, central venous catheterization, haematologic VRE infection or colonisation was detected. There were malignant tumours, solid organ allograft, chronic no systemic screening practices for patients in high risk haemodialysis, antibiotic exposure to vancomycin, third- areas or testing of diarrhoeal stools prior to this study. generation cephalosporins, metronidazole, antibiotics Patients with known VRE colonisation or infection were with anti-anaerobic activity, exposure to multiple anti- isolated in single rooms with a dedicated toilet if they had biotics and prolonged duration of antibiotic therapy faecal incontinence or diarrhoea. Healthcare workers were [10]. However, most of those studies involve high risk required to use gloves when entering the room, and gloves patients during outbreaks associated with vanA geno- and gown if contact with body fluids was anticipated. Hos- type. A previous study in Melbourne hospitals in 1998 pital floors were cleaned daily with 1000 part per million identified broad spectrum antibiotics as significant risk (ppm) sodium hypochlorite. factor for new colonisation with vanB VRE [11]. A nested case control (1:2) study was conducted to VRE colonisation can lead to infections which prolong identify risk factors associated with VRE colonisation. A hospital stay, increase the cost of care and increase mor- case was defined as a patient confirmed to be positive by bidity and mortality [12,13]. The identification of modifi- standard microbiological methods for VRE isolated from able risk factors may assist in identifying targets for rectal swabs taken for the point prevalence survey. A intervention to reduce the incidence of VRE colonisation. control was defined as a patient confirmed to be nega- In this study, we measured the prevalence of VRE colon- tive for VRE colonisation on the same survey. For each isation in a hospital-wide point prevalence survey. We case, two unmatched controls were selected at random examined downstream risk factors for colonisation with from eligible patients. implications for VRE control policies, including antibiotic exposure and patient placement, in a tertiary referral hos- Microbiology pital in Melbourne, Australia where vanB VRE has been Rectal swabs were taken either by the patients them- endemic for many years. selves following instruction, or by nursing staff. The swabs were then plated onto bile aesculin media (BBL Enterococcosel agar, Cockeysville, MD) with vancomycin Methods 6 μg/mL and incubated at 37°C for up to 72 hours. En- Setting and study design terococci species were identified using the VITEK-2 sys- The Alfred hospital is a major tertiary teaching hospital tem (bioMérieux). Polymerase chain reaction was used in Melbourne, Australia with 427 beds. The hospital to detect the vanA or vanB genes as described previ- provides general services as well as broad range of spe- ously. [14] VRE colonisation was defined if an isolate of cialist care including referral services for trauma, cystic E. faecalis or E. faecium with vanA or vanB gene was fibrosis and heart/lung transplantation, HIV/AIDS, bone detected. Ribotyping of the isolates was performed using marrow transplantation as well as specialist intensive the Riboprinter Microbial Characterization system as care facilities. previously described [15,16]. We conducted a point prevalence survey on October 13, 2008 at the Alfred Hospital. All patients who were present Statistical methods in the hospital (including inpatients, patients in the emer- Standard statistical methods were used to summarize gency department, and day surgery but excluding psych- categorical and continuous measures and to compare iatry) at 8.00 a.m. were approached to participate. Patients proportions. Univariate analysis was performed to calcu- were provided with information sheets (including advice late unadjusted odds ratio. All variables with a p-value of about the potential consequences of VRE colonisation) and <0.2 in univariate analysis were included in the multiple verbal consent was obtained for participation. Patients were logistic regression model to examine independently asso- included irrespective of known VRE status. Patients were ciated risk factors for VRE colonisation. The association excluded if they were not able to consent, were for palliative was considered statistically significant if p<0.05. Statis- care only, had been discharged prior to being swabbed or tical analyses were performed using Stata statistical soft- they declined to participate. Single rectal swabs were pri- ware (Version 10; Stata Corp, College Station, Texas). marily taken by nursing staff. Clinical data collection included demographic details, bed location of all patients, Ethics antibiotic use (at least 12 hours before the collection of rec- As this VRE survey represented a quality assurance ac- tal swab in current admission), ICU exposure, and previous tivity, we did not obtain a formal ethical approval to Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 3 of 6 http://www.aricjournal.com/content/1/1/31 perform the point prevalence survey. However, we coun- TheprevalenceofVRE colonisation on theday of selled patients about the significance of VRE and pro- screening was 58 of 331 patients (17.5%, 95% CI, 13.7% vided written information, and obtained verbal consent to 21.9%). The proportion of patients colonised with to take rectal swabs from all patients and/or their rela- VRE was 3% in the emergency department and ranged tives. We obtained approval from the Alfred Health from 8% to 29% in inpatient wards. Of the 58 VRE iso- Human Research Ethics Committee and Monash Uni- lates, 57 were found to be Enterococcus faecium and one versity Human Research Ethics Committee to retrieve was Enterococcus faecalis. All the isolates were positive demographic and clinical information from the medical for vanB resistance genotype and no vanA resistance geno- records of patients for the case control study. type was detected. All together, 9 ribotypes were detected with the majority of isolates belonging to either of the two ribotypes (S-7, n=25, 43%; S-5, n=23, 39%). However, more Results than 1 ribotype was present in all wards where there was A total of 434 patients were present in hospital at the more than one VRE-colonised patient present. time of survey. Among the total, 331 (77%) were Of the total 58 patients found to be VRE colonised, 46 screened for VRE colonisation; 103 patients (23%) could (79.3%) were not previously known to be VRE colonised not be screened either due to refusal, discharge from and 12 (20.7%) were known to be previously colonised. hospital prior to the time of swabbing, patients not being A further 13 patients had a history of VRE colonisation present in the ward at the time of screening, or if the pa- but VRE was not detected on screening at the time of tient was for palliative care. the survey. Table 1 Factors associated with VRE detection in cases and controls (Univariate analysis) Variables Cases Controls Unadjusted OR P value Participants 58 116 - - Age ≥ 65 (years) 35 (60.3%) 56 (48.2%) 1.63 (0.82 to 3.26) 0.13 Male 36 (62.1%) 74 (63.8%) 0.92 (0.46 to 1.88) 0.82 Antibiotics Exposure to any antibiotic 45 (77.6%) 55 (47.4%) 3.83 (1.79 to 8.54) <0.001 Meropenem 8 (13.8%) 2 (1.7%) 9.12 (1.71 to 89.92) 0.001 Antibiotics other than meropenem 39 (67.2%) 54 (46.5%) 4.5 (2.06 to 10.71) 0.001 Vancomycin 13 (22.4%) 19 (16.38%) 1.47 (0.61 to 3.46) 0.33 Teicoplanin 2 (3.4%) 2 (1.7%) 2.03 (0.14 to 28.63) 0.47 Any cephalosporin 19 (32.8%) 32 (27.6%) 1.27 (0.60 to 2.66) 0.47 Ceftriaxone 11 (18.9%) 24 (20.7%) 0.89 (0.36 to 2.11) 0.78 Cefotaxime 2 (3.4%) 0 - - Ceftazidime 5 (8.6%) 4 (3.4%) 2.64 (0.54 to 13.79) 0.14 Cefepime 1 (1.7%) 6 (5.2%) 0.32 (0.01 to 2.76) 0.27 Metronidazole 5 (8.6%) 19 (16.4%) 0.48 (0.13 to 1.43) 0.16 Ciprofloxacin 11 (18.9%) 9 (7.8%) 2.78 (0.96 to 8.11) 0.03 Ticarcillin-clavulanate 11 (18.9%) 12 (10.3%) 2.02 (0.74 to 5.41) 0.11 Ampicillin 1 (1.7%) 3 (2.6%) 0.66 (0.01 to 8.45) 0.72 Gentamicin 2 (3.4%) 9 (7.8%) 0.42 (0.04 to 2.16) 0.27 Piperacillin-tazobactam 5 (8.6%) 3 (2.6%) 3.55 (0.65 to 23.53) 0.07 Other factors ICU admission 18 (31.1%) 26 (22.4%) 1.55 (0.71 to 3.33) 0.21 Within 2 rooms of positive case 30 (62.5%) 54 (65.8%) 0.86 (0.38 to 1.94) 0.69 On same side as positive case 48 (82.8%) 83 (77.6%) 1.38 (0.57 to 3.53) 0.43 Diarrhoea 12 (21.1%) 11 (9.5%) 2.54 (0.94 to 6.85) 0.03 Length of stay (Median days) 11.5 (7–30) 6.0 (3–13) - <0.001 Length of stay ≥7 days 43 (74.2%) 43 (37.1%) 4.86 (2.30 to 10.51) <0.001 Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 4 of 6 http://www.aricjournal.com/content/1/1/31 Risk factors for VRE colonisation reported by previous studies conducted at Melbourne We compared the exposure to probable risk factors in hospitals [11,17-19]. This is also in contrast to previous 58 cases and 116 controls. studies demonstrating that VRE colonisation was Significantly higher proportions of cases had prior ex- restricted to particular high risk inpatient areas [11]. posure to one or more antibiotics (odds ratio (OR) 3.83, Our finding that 80% of the VRE colonised patients in 95% CI 1.79 to 8.54). Similarly, cases had a longer length the survey were newly detected cases demonstrates that of hospital stay compared to controls (P<0.001). Patients the previous screening strategy of surveying patients with VRE colonisation were more likely to have been ad- only on wards when a new clinical isolate of VRE was mitted for ≥7 days (OR 4.86, 95% CI 2.30 to 10.51). Uni- detected is inadequate. variate analyses identified prior exposure to any Prima facie, our results suggest that antibiotic selec- antibiotic (p <0.001), exposure to meropenem (p=0.001), tion pressures appear to play a larger role in determining ciprofloxacin (p=0.03), diarrhoea (p=0.03) as associated VRE colonisation than cross-transmission at our institu- with the detection of VRE colonisation (Table 1). How- tion. Exposure to antibiotics, particularly meropenem, ever, the prior use of vancomycin (p=0.33), ticarcillin- was strongly associated with VRE colonisation; this is clavulanate (p=0.11), pipericillin-tazobactam (p=0.07), consistent with previous studies suggesting that anti- metronidazole (p=0.16) and any cephalosporins were not biotic regimens with activity against anaerobic bacteria associated with colonisation status. Proximity to other are potent risk factors in the development of VRE VRE positive cases either in same side of the ward or [20-22]. The vanB gene is known to be present in com- located within next 2 rooms was not associated with mensal enteric bacteria such as Clostridium, and trans- VRE colonisation (p>0.05) (Table 1). mission of this gene to E. faecium has been In a multivariate logistic regression model, exposure to demonstrated in vivo [23]. In other studies, a variety of meropenem (adjusted OR; 12.24, 95% CI 2.24 to 66.77), other antibiotics have been implicated as risk factors for age ≥ 65years (adjusted OR 2.19, 95% CI 1.05 to 4.58) VRE colonisation, including vancomycin, metronidazole, and length of stay ≥7 days (adjusted OR 4.69, 95% CI piperacillin-tazobactam, ticarcillin-clavulanate and third 2.25 to 9.73) were independently associated with VRE generation cephalosporins [24-26]. However, our analysis colonisation (Table 2). After adjusting for age ≥ 65years, comparing meropenem and non-meropenem antibiotic length of stay ≥7 days and exposure to meropenem, ex- use with no antibiotic use showed the exposure to anti- posure to any antibiotic other than meropenem (com- biotics other than meropenem is also associated with pared to patients that did not receive any antibiotics) VRE colonisation. Thus, our study may have been under- was independently associated with VRE colonisation powered to detect differences at the level of individual (adjusted OR 2.95, 95% CI 1.27 to 6.88). In total, 16 antibiotics other than meropenem. (9.2%) patients in case–control study were from emer- We found ambiguous evidence regarding the extent of gency department and short stay units. A sensitivity ana- cross transmission of VRE, which has been shown to be lysis excluding the patients in these units did not alter important in previous studies [27,28]. We did not find any of the above effects, significantly. proximity to other VRE colonised patients to be a risk fac- tor for VRE detection. However, this does not exclude the Discussion possibility of cross transmission contributing to endem- We conducted a hospital-wide point prevalence survey icity, as transmission may have occurred prior to the time to measure the prevalence of VRE, as our previous sur- of the survey and would not be detected with frequent pa- veillance activities were targeted to patients felt to be at tient movements. Conversely, the finding that ribotyping risk and therefore may have resulted in selection biases. only demonstrated two large clones of VRE in patients In this survey, we confirmed that vanB VRE is endemic does not necessarily implicate extensive cross transmis- in inpatients at our hospital. We found a lower preva- sion. If transmission was significant, we would expect a lence in short stay areas, such as the emergency de- lower diversity among individual wards; however, we partment (3%) and the short stay unit, but prevalence found that in all wards with at least two VRE colonised was 8-29% in other inpatient areas. This is higher than patients had at least two ribotypes. We did not have access to pulsed field gel electrophoresis, regarded as the gold standard for epidemiological investigations of VRE [29]. Table 2 Factors associated with VRE detection in cases The purpose of this study was to examine “down- and controls (multivariate analysis) stream” exposures that had implications for VRE control Risk factor Adjusted OR (95% CI) p value policies, rather than patient-specific “upstream” risk fac- Meropenem 12.24 (2.24 to 66.77) 0.004 tors that are not modifiable. However, we did find older Age (≥65 years) 2.19 (1.05 to 4.58) 0.036 age and longer length of stay in hospital as independent Length of stay ≥7 days 4.69 (2.25 to 9.73) <0.001 predictor of VRE colonisation. This is reflected in the Karki et al. Antimicrobial Resistance and Infection Control 2012, 1:31 Page 5 of 6 http://www.aricjournal.com/content/1/1/31 low colonisation rate in patients with a short length of Author details Department of Epidemiology and Preventive Medicine, Infectious Disease stay, including emergency and short stay units. Epidemiology Unit, Monash University, Melbourne, Australia. Infection A strength of this study is that we conducted a Control, Eastern Health, Melbourne, Australia. Infection Prevention and hospital-wide survey including a broad range of patients, Healthcare Epidemiology Infectious Diseases and Microbiology Unit, Alfred Health, Melbourne, Australia. Infection Control Consultancy, Melbourne, thus minimizing selection biases [30]. 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Infect Control Hosp Epidemiol 2001, and take full advantage of: 22:576–578. doi:10.1186/2047-2994-1-31 • Convenient online submission Cite this article as: Karki et al.: Prevalence and risk factors for VRE • Thorough peer review colonisation in a tertiary hospital in Melbourne, Australia: a cross • No space constraints or color figure charges sectional study. Antimicrobial Resistance and Infection Control 2012 1:31. • Immediate publication on acceptance • Inclusion in PubMed, CAS, Scopus and Google Scholar • Research which is freely available for redistribution Submit your manuscript at www.biomedcentral.com/submit

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Antimicrobial Resistance & Infection ControlSpringer Journals

Published: Oct 8, 2012

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