Alexander A Padiglione

Risk Factors for New Detection of Vancomycin-Resistant Enterococci in Acute-Care Hospitals That Employ Strict Infection Control Procedures

ABSTRACT Accurate assessment of the risk factors for colonization with vancomycin-resistant enterococci (VRE) among high-risk patients is often confounded by nosocomial VRE transmission. We undertook a 15-month prospective cohort study of adults admitted to high-risk units (hematology, renal, transplant, and intensive care) in three teaching hospitals that used identical strict infection control and isolation procedures for VRE to minimize nosocomial spread. Rectal swab specimens for culture were regularly obtained, and the results were compared with patient demographic factors and antibiotic exposure data. Compliance with screening was defined as “optimal” (100% compliance) or “acceptable” (minor protocol violations were allowed, but a negative rectal swab specimen culture was required within 1 week of becoming colonized with VRE). Colonization with VRE was detected in 1.56% (66 of 4,215) of admissions (0.45% at admission and 0.83% after admission; the acquisition time was uncertain for 0.28%), representing 1.91% of patients. No patients developed infection with VRE. The subsequent rate of new acquisition of VRE was 1.4/1,000 patient days. Renal units had the highest rate (3.23/1,000 patient days; 95% confidence interval [CI], 1.54 to 6.77/1,000 patient days). vanB Enterococcus faecium was the most common species (71%), but other species included vanB Enterococcus faecalis (21%), vanA E. faecium (6%), and vanA E. faecalis (2%). The majority of isolates were nonclonal by pulsed-field gel electrophoresis analysis. Multivariate analysis of risk factors in patients with an acceptable screening suggested that being managed by a renal unit (hazard ratio [HR] compared to the results for patients managed in an intensive care unit, 4.6; 95% CI, 1.2 to 17.0 [P = 0.02]) and recent administration of either ticarcillin-clavulanic acid (HR, 3.6; 95% CI, 1.1 to 11.6 [P = 0.03]) or carbapenems (HR, 2.8; 95% CI, 1.0, 8.0 [P = 0.05]), but not vancomycin or broad-spectrum cephalosporins, were associated with acquisition of VRE. The relatively low rates of colonization with VRE, the polyclonal nature of most isolates, and the possible association with the use of broad-spectrum antibiotics are consistent with either the endogenous emergence of VRE or the amplification of previously undetectable colonization with VRE among high-risk patients managed under conditions in which the risk of nosocomial acquisition was minimized.

Candida in Burns: Risk Factors and Outcomes

Sepsis due to Candida is an uncommon but a significant cause of death in burns patients. Colonization is common, but consensus guidelines for prophylaxis and empirical therapy do not specifically include this cohort. Our aim was to define predictive factors for candidaemia in a burns unit, to guide protocols for prevention and early treatment. We conducted a 10-year review (July 1998–December 2007) of patients admitted to the Victorian Adult Burns Service, Melbourne, Australia. Of 1929 patients admitted with acute burn injury, 143 had Candida isolated at any site, most commonly Candida albicans. There were 12 episodes of candidaemia. Prior colonization was an important risk factor for candidaemia, and the risk increased substantially with the number of colonized sites; indeed 43% of patients colonized at more than three sites (and not on antifungals) developed candidaemia. Other risk factors were higher total burn surface area, higher full-thickness surface area, prolonged admission, number and duration of intensive care unit admissions, number of visits to the operating theatre, alcohol as a contributing factor to burn, prior treatment with total parenteral nutrition, or certain antibiotics (ceftriaxone, vancomycin, amikacin, co-trimoxazole). The attributable mortality of candidaemia was 15% (n = 2). Initiation of antifungal therapy was often delayed. Our results support early empirical antifungal therapy in septic burns patients who are colonized, before the results of cultures become known. The role of prophylactic antifungals is less clear, but should be strongly considered for patients colonized at multiple sites.

Pseudomonas aeruginosa bacteraemia in burns patients: Risk factors and outcomes

INTRODUCTION We aimed to identify the risk factors for, and outcomes of Pseudomonas aeruginosa bacteraemia in adult burns patients. METHOD All adult burns patients who developed a Gram-negative bacteraemia over a period of 7 years were included. Retrospective data analysed included patient demographics, organisms cultured, antibiotic susceptibility patterns, isolation of P. aeruginosa in non-blood isolates, treatment, length of stay and mortality. RESULTS Forty-three patients developed a Gram-negative bacteraemia over the study period, 12 of whom had Pseudomonas bacteraemia during the course of their admission. In eight patients (18.6%) P. aeruginosa was the first Gram-negative isolated. The only factor predicting P. aeruginosa bacteraemia as a first episode (compared to another Gram-negative) was prior isolation of Pseudomonas at other sites (wound sites, urine or sputum). Overall length of stay was less in patients who developed P. aeruginosa as a first episode, mainly because of increased mortality in this group. Prior non-blood isolates of P. aeruginosa could have correctly predicted the sensitivity pattern of the strain of P. aeruginosa organism in 75% of patients who did not receive appropriate initial antibiotics. CONCLUSION Prior colonisation with P. aeruginosa predicts P. aeruginosa in blood cultures, as opposed to other Gram-negative bacteria. Clinicians should have a high index of suspicion for P. aeruginosa bacteraemia where a septic burns patient has a prior history of non-blood P. aeruginosa cultures. Empirical antibiotic regimes based on the antibiotic-sensitivity patterns of previous non-blood P. aeruginosa isolates in each patient should be given at the time blood cultures are taken.

The prevalence of fecal colonization with VRE among residents of long-term-care facilities in Melbourne, Australia.

A point-prevalence survey performed among residents of eight nursing homes in Melbourne, Australia, found a rate of fecal VRE colonization of 3.1% (9/292; 95% confidence interval, 1.1-5.1), all vanB Enterococcusfaecium. This is a higher rate than in the general community (3.1% vs 0.2%). Many residents (16%) had been inpatients in acute-care hospitals in the previous 3 months.

Secondary bacterial infection and empirical antibiotic use in toxic epidermal necrolysis patients

The objective of this study was to determine rates of positive bacterial cultures in patients with extensive toxic epidermal necrolysis, the rate of bacteremia, whether empirical antibiotics had been commenced, and their effectiveness when commenced. The authors conducted a retrospective chart review of patients with extensive toxic epidermal necrolysis between January 2001 and December 2012 admitted to the Victorian Adult Burns Service, Melbourne, Australia, with respect to the amount of positive cultures, number and type of organisms identified, whether empirical antibiotics had been commenced, and whether antibiotics were effective against organisms cultured. A total of 27 patients were admitted over the study period of 11 years. Seventeen of these patients developed at least one positive bacterial culture. Patients who grew positive cultures had a longer length of stay in intensive care unit and in hospital overall compared with patients who did not grow positive cultures. Thirty-five positive cultures were collected overall, with empirical antibiotics commenced in 22 cases. In terms of sensitivity, antibiotics were appropriate in 19 cases. Four patients developed bacteremia, two of whom died. This study does not dispute the generally accepted practice of avoiding prophylactic antibiotics in toxic epidermal necrolysis patients, but in the context of a relatively low rate of bacteremia in this patient population, advises appropriate and targeted empirical antibiotic use where clinical infection is suspected.

Management of dengue in Australian travellers: a retrospective multicentre analysis

Objectives: To describe the epidemiology, clinical and laboratory features and outcomes of dengue in returned Australian travellers, applying the revised WHO dengue classification (2009) to this population.

Dengue fever in travellers: are we missing warning signs of severe dengue in a non-endemic setting?

Reprinted from World Health Organization. Dengue: guidelines for diagnosis, treatment, prevention and control. New edition 2009. Geneva: WHO, 2009. ALT 1⁄4 alanine aminotransferase. AST 1⁄4 aspartate aminotransferase. CNS 1⁄4 central nervous system. DSS 1⁄4 dengue shock syndrome. HCT 1⁄4 haematocrit. u W cases of dengue virus infection each year. Far North Queensland has experienced dengue epidemics, with deaths reported in outbreaks in 2004 and 2008e2009.

The heat is on: a case of hyperthermia-induced posterior reversible encephalopathy syndrome (PRES).

Severe burn injury remains a major burden on patients and a significant health issue for the society. Following severe burns, patients develop a systemic inflammatory response (SIRS) and hypermetabolic phenomena [1, 2]. This can lead to severe hyperthermia which is resistant to commonly employed treatments. Experimental and clinical studies suggest that the central nervous system is exceptionally sensitive to thermal damage [3, 4]. We present a case of posterior reversible encephalopathy syndrome (PRES) in the setting of prolonged and severe hyperthermia ([40 C) and burns. The possible mechanisms and functional consequences of hyperthermic brain injury in this patient are discussed.

Microbiology of wildfire victims differs significantly from routine burns patients: data from an Australian wildfire disaster.

The catastrophic wildfires of February 2009 in Victoria, Australia killed 173 people and hospitalised 18 adults with burns. We conducted a case-control study of wildfire victims (WFVs) compared to routine burns patients to assess early differences in bacteriology. Demographic, outcome and bacteriology data (for the first 72 h) were prospectively collected on all 18 WFVs, and compared to those of 36 RBPs matched 2:1 for age, gender, burns severity (total body surface area ≥20%) and ICU admission. We found that WFVs had more positive cultures overall (10/18 [56%] vs 7/36 [19%], p=0.04), and we cultured more Gram negative bacteria from wounds (11/13 [85%] vs 3/12 [25%], p=0.005). Although WFVs were more likely to culture Enterobacteriaceae (5/18 vs 2/36) and Aeromonas spp. (3/18 vs 1/36), and less likely to culture Staphylococcus aureus (2/18 vs 6/36), these differences were not statistically significant. Given the predominance of Gram negative organisms cultured from WFVs, our routine burn wound prophylaxis (intravenous cephazolin) would have been inadequate in the WFV group. We suggest that an alternative regimen of oxacillin/nafcillin/flucloxacillin plus gentamicin (or a fluoroquinolone if renal impairment present) may be more appropriate for burn wound prophylaxis in this complex group of patients.