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BACKGROUND: This randomized clinical trial compares the incidence of wound infection after vascular surgery in patients who received prophylaxis using the same antibiotic as either a single-dose or a multiple-dose regimen (until the lines/ drain tubes were removed, but not for more than 5 days). METHODS: Each of the 302 patients who entered the study received ticarcillin 3.0 g/clavulanate 0.1 g (Timentin) intravenously immediately after the induction of anesthesia. Patients randomized to the multiple-dose group received an average of 14.3 doses (range 9 to 20). RESULTS: The incidence of wound infections was 18% (28 of 153) for patients in the single-dose group and 10% (15 of 149) for patients in the multiple-dose group (P = 0.04; relative risk estimate = 2.00, 95% confidence interval = -1.02 to 3.92). CONCLUSIONS: A multiple-dose antibiotic regimen, rather than single-dose therapy, provides optimal prophylaxis against wound infection for patients undergoing vascular surgery. Am J Surg. 1998; 175:87-90. [C] 1998 by Excerpta Medica, Inc.

The Australian Group on Antimicrobial Resistance (AGAR) performs regular multicentre period prevalence studies to monitor changes in antimicrobial resistance. In 2011, 29 laboratories in Australia participated in the national surveillance of Staphylococcus aureusresistance. The survey only included unique isolates from clinical specimens collected ≥48h after hospital admission. MRSA accounted for 30.3% of S. aureusisolates. MRSA resistance to ciprofloxacin, erythromycin, tetracycline, trimethoprim/sulfamethoxazole, gentamicin and clindamycin (constitutive resistance) varied considerably between regions. Resistance to non-β-lactam antimicrobials was uncommon in MSSA, with the exception of erythromycin. Regional variation in resistance was due to the differential distribution of MRSA clones between regions. The proportion of S. aureusgenetically characterised as healthcare-associated MRSA (HA-MRSA) was significantly lower in this survey (18.2%) compared with the 2005 survey (24.2%) (P<0.0001). Although four HA-MRSA clones were characterised, 98.8% of HA-MRSA were classified as either ST22-MRSA-IV [2B] (EMRSA-15) or ST239-MRSA-III [3A] (Aus-2/3 EMRSA). Multiclonal community-associated MRSA (CA-MRSA) increased markedly from 6.5% in 2005 to 11.7% of all S. aureusin 2011 (P<0.0001). Although the proportion of MRSA resistant to non-β-lactam antimicrobials has decreased nationally, the proportion of S. aureusthat are MRSA has remained stable. This is primarily due to non-multiresistant CA-MRSA becoming more common in Australian hospitals at the expense of the long-established multiresistant ST239-MRSA-III [3A] (Aus-2/3 EMRSA). Given hospital outbreaks of CA-MRSA are thought to be extremely rare, it is most likely that patients colonised at admission with CA-MRSA have become infected with the colonising strain during their hospital stay.

ABSTRACTWe report the molecular epidemiology of 27 clinical multidrug-resistant Staphylococcus epidermidis(MDRSE) isolates collected between 2003 and 2007 in an Australian teaching hospital. The dominant genotype (sequence type 2 [ST2]) accounted for 85% of the isolates tested and was indistinguishable from an MDRSE genotype identified in European hospitals, which may indicate that highly adaptable health care-associated genotypes of S. epidermidishave emerged and disseminated worldwide in the health care setting.

ABSTRACTClonal complex 59 (CC59) community-associated methicillin-resistant Staphylococcus aureus(CA-MRSA) strains were characterized using pulsed-field gel electrophoresis, spatyping, multilocus sequence typing, diagnostic DNA microarrays, and PCRs targeting staphylococcal cassette chromosome mec(SCCmec) elements and Panton-Valentine leukocidin (PVL). Six distinct groups within CC59 were characterized. At least seven different variants of SCCmecelements were identified (IVa [2B], IVb [2B], IVd [2B], IV variant [2B], IVa [2B&5], V variant [5C2], and V [5C2&5]). (The structural type is indicated by a Roman numeral, with a lowercase letter indicating the subtype, and the ccrcomplex and the meccomplex are indicated by an Arabic numeral and an uppercase letter, respectively. Where there is an extra ccrelement, this is indicated by “&” and an Arabic numeral designating the ccrtype.) The first group is similar to the American sequence type 59 (ST59) MRSA-IV CA-MRSA strain USA1000. The second group includes a PVL-negative ST87 strain with an SCCmecelement of subtype IVb (2B). The third group comprises PVL-variable ST59 MRSA-IV strains harboring multiple SCCmecIV subtypes. PVL-negative ST59 MRSA strains with multiple or composite SCCmecelements (IVa [2B&5]) form the fourth group. Group 5 corresponds to the internationally known “Taiwan clone,” a PVL-positive strain with a variant SCCmecelement (V [5C2&5]). This strain proved to be the most common CC59 MRSA strain isolated in Western Australia. Finally, group 6 encompasses the ST59 MRSA-V variant (5C2). The differentiation of CC59 into groups and strains indicates a rapid evolution and spread of SCCmecelements. Observed differences between groups of strains as well as intrastrain variability within a group facilitate the tracing of their spread.

AbstractObjective:To demonstrate that nosocomial transmission of vancomycin-resistant enterococci (VRE) can be terminated and endemicity prevented despite widespread dissemination of an epidemic strain in a large tertiary-care referral hospital.Interventions:Two months after the index case was detected in the intensive care unit, 68 patients became either infected or colonized with an epidemic strain of vanB vancomycin-resistant Enterococcus faeciumdespite standard infection control procedures. The following additional interventions were then introduced to control the outbreak: (1) formation of a VRE executive group; (2) rapid laboratory identification (30 to 48 hours) using culture and polymerase chain reaction detection of vanA and vanBresistance genes; (3) mass screening of all hospitalized patients with isolation of carriers and cohorting of contacts; (4) environmental screening and increased cleaning; (5) electronic flagging of medical records of contacts; and (6) antibiotic restrictions (third-generation cephalosporins and vancomycin).Results:A total of 19,658 patient and 24,396 environmental swabs were processed between July and December 2001. One hundred sixty-nine patients in 23 wards were colonized with a single strain of vanB vancomycin-resistant E. faecium.Introducing additional control measures rapidly brought the outbreak under control. Hospital-wide screening found 39 previously unidentified colonized patients, with only 7 more nonsegregat-ed patients being detected in the next 2 months. The outbreak was terminated within 3 months at a cost of $2.7 million (Australian dollars).Conclusion:Despite widespread dissemination of VRE in a large acute care facility, eradication was achievable by a well-resourced, coordinated, multifaceted approach and was in accordance with good clinical governance.

ABSTRACTA real-time PCR assay previously developed for use on the Roche LightCycler platform was investigated as an alternative to culture for the direct detection of vancomycin-resistant enterococci (VRE) in clinical specimens. PCR primers and fluorescence resonance energy transfer hybridization probes specific for the vanAand vanBgenes were combined in a multiplex real-time PCR assay performed directly with fecal material obtained by rectal swabbing and with enrichment broth samples. DNA was prepared from the rectal swabs and enrichment broths with a commercially available DNA preparation column designed specifically for use with fecal specimens. One hundred eighty duplicate rectal swabs were obtained from 42 patients who were previously found to be positive for VRE and who were being monitored for carriage of VRE. Direct and enrichment broth cultures were performed with one swab, while PCR was performed with the other swab as well as any corresponding presumptive positive enrichment broth. In total, 100 specimens from 30 patients remained positive for VRE by at least one method. The multiplex real-time PCR was positive for 88 enrichment broths of rectal swabs from 27 patients but for only 45 rectal swabs from 15 patients. Direct culture was positive for VRE for only 43 specimens from 11 patients, while enrichment broth culture was positive for VRE for 75 specimens from 22 patients. Inhibition studies for the multiplex real-time PCR assay, performed by spiking the DNA extracts from 50 negative rectal swabs and the corresponding enrichment broths with between 1 and 10 CFU of a VanB Enterococcus faeciumstrain, detected inhibition rates of 55.1 and 10%, respectively. PCR performed directly with enrichment broths was found to be significantly more sensitive than enrichment broth culture (P< 0.025). Negative samples were identified significantly earlier by PCR than by culture alone.

Thirty five patients were transferred to Royal Perth Hospital (RPH) after the Bali bombings. The patients had severe burn injuries and were considered to be at high-risk of both the carriage and acquisition of multi-resistant organisms (MROs). Whilst seeking to protect the Bali patients with a comprehensive infection control response, we also sought to protect other high-risk patients from nosocomial acquisition of MROs. MROs were detected from 25 (82%) of the 29 Bali patients admitted to RPH. Bali patients were colonised, or infected, with one or more of the following MROs: multi-resistant Acinetobacter baumannii (MRAB) (19 patients), extended-spectrum β-lactamase (ESBL) producing Gram-negative bacteria (15 patients), vancomycin-resistant enterococci (VRE) (nine patients), multi-resistant Pseudomonas aeruginosa (MRPA) (six patients), multi-resistant Chryseobacterium sp. (four patients), and methicillin-resistant Staphylococcus aureus (MRSA) (three patients). Five Bali patients developed a total of eight bacteraemic episodes, with MRPA sepsis contributing to death in two patients. Since the Bali bombings horizontal transmission of Bali MROs has occurred in 41 non-Bali patients in RPH. MRPA has had the greatest clinical impact. Eight non-Bali patients developed a total of 11 bacteraemic episodes, with MRPA sepsis contributing to death in four patients. However, apart from MRPA, we have now controlled transmission of the other MROs in RPH. The emergency response to the Bali disaster required strong leadership, good communication and multi-disciplinary teamwork. The infection control strategy contributed to good outcomes for most Bali bombing patients. However, many patients within the Bali cohort were heavily colonised with MROs, and some developed invasive infection. Subsequent nosocomial transmission of these MROs to non-Bali patients has been a legacy of the Bali tragedy.

In April 1982, a patient infected with methicillin‐resistant Staphylococcus aureus(MRSA) was transferred to the Royal Perth Hospital from the Royal Darwin Hospital. Within three months, 19 patients and four staff members had become infected or colonized with MRSA. The outbreak was terminated only after all colonized inpatients were transferred to a separate isolation unit. After the outbreak, all new patients and new employees who had been in hospitals outside Western Australia in the previous 12 months were screened. From June 1, 1982, to June 30, 1984, 28 of the 649 patients (4.3%) screened on admission to the Royal Perth Hospital were found to be harbouring MRSA. During the same period only one of the 468 persons (0.2%) screened on application for employment at the Hospital was found to be colonized with MRSA. Since the policy of screening new patients and staff from hospitals outside Western Australia was introduced, no serious outbreak of MRSA has occurred.