Background and aim Creatinine assays are now standardised, however the effect of elevated glucose and ketoacids during acute diabetic ketoacidosis (DKA) on different Jaffe creatinine assays is unknown. We aim to assess this interference on different platforms using the Vitros enzymatic creatinine method as the gold standard. Methods Samples were collected from patients presenting to Emergency Department with DKA and analysed using 4 Jaffe assays (Architect, Roche, Beckman Coulter and Siemens) and 1 enzymatic assay (Vitros). Results Of the eighteen patients (12 M, 6F, age 32.1 ± 12.4 years), admission pH was 7.12 ± 0.16, HCO3 was 8.2 ± 4 mmol/L, glucose was 36.2 ± 13.8 mmol/L and capillary ketone was 5.7 ± 1.2 mmol/L. The average enzymatic creatinine value was 115.3 ± 64.2 μmol/L. All Jaffe creatinine results were significantly higher (p < 0.001), in order of magnitude: Architect (156.5 ± 64.7), Beckman (147.2 ± 69.1), Siemens (131.4 ± 57.7) and Roche (127.2 ± 57.5). Discussion Falsely elevated plasma creatinine results might delay the administration of intravenous potassium in DKA patients and clinicians need to be aware of this potential interference which appeared most marked on the Abbott platform. Creatinine assays are now standardised, however the effect of elevated glucose and ketoacids during acute diabetic ketoacidosis (DKA) on different Jaffe creatinine assays is unknown. We aim to assess this interference on different platforms using the Vitros enzymatic creatinine method as the gold standard. Samples were collected from patients presenting to Emergency Department with DKA and analysed using 4 Jaffe assays (Architect, Roche, Beckman Coulter and Siemens) and 1 enzymatic assay (Vitros). Of the eighteen patients (12 M, 6F, age 32.1 ± 12.4 years), admission pH was 7.12 ± 0.16, HCO3 was 8.2 ± 4 mmol/L, glucose was 36.2 ± 13.8 mmol/L and capillary ketone was 5.7 ± 1.2 mmol/L. The average enzymatic creatinine value was 115.3 ± 64.2 μmol/L. All Jaffe creatinine results were significantly higher (p < 0.001), in order of magnitude: Architect (156.5 ± 64.7), Beckman (147.2 ± 69.1), Siemens (131.4 ± 57.7) and Roche (127.2 ± 57.5). Falsely elevated plasma creatinine results might delay the administration of intravenous potassium in DKA patients and clinicians need to be aware of this potential interference which appeared most marked on the Abbott platform.

The Australian Group on Antimicrobial Resistance performs regular period-prevalence studies to monitor changes in antimicrobial resistance in selected enteric Gram-negative pathogens. The 2011 survey focussed on hospital-onset infections, examining isolates from all specimens presumed to be causing disease. In 2011, 1,827 Escherichia coli, 537 Klebsiella species and 269 Enterobacter species were tested using a commercial automated method (Vitek 2, BioMérieux) and results were analysed using Clinical and Laboratory Standards Institute breakpoints from January 2012. Of the key resistances, non-susceptibilty to the third-generation cephalosporin, ceftriaxone, was found in 9.6% of E. coli and 9.5%-12.1% of Klebsiella spp. Non-susceptibility rates to ciprofloxacin were 10.6% for E. coli, 0.0%-8.3% for Klebsiella spp. and 0.0%-5.0% in Enterobacter spp. Resistance rates to gentamicin were 8.6%, 2.9%-10.9%, and 0.0%-15.6% for the same 3 groups respectively. Eight strains, 5 Klebsiella spp. and 3 Enterobacter spp. were shown to harbour a carbapenemase (IMP-4).

The Australian Group on Antimicrobial Resistance performs regular period-prevalence studies to monitor changes in antimicrobial resistance in selected enteric Gram-negative pathogens. The 2012 survey focussed on community-onset infections, examining isolates from urinary tract infections from patients presenting to outpatient clinics, emergency departments or to community practitioners. In 2012, 2,025 Escherichia coli, 538 Klebsiella species and 239 Enterobacter species were tested using a commercial automated method (Vitek 2, BioMérieux) and results were analysed using Clinical and Laboratory Standards Institute breakpoints from January 2012. Of the key resistances, non-susceptibility to the third-generation cephalosporin, ceftriaxone, was found in 4.2% of E. coli and 4.6%-6.9% of Klebsiella spp. Non-susceptibility rates to ciprofloxacin were 6.9% for E. coli, 0.0%-3.5% for Klebsiella spp. and 0.8%-1.9% in Enterobacter spp, and resistance rates to piperacillin-tazobactam were 1.7%, 0.7%-9.2%, and 8.8%-11.4% for the same 3 groups respectively. Only 1 Enterobacter cloacae was shown to harbour a carbapenemase (IMP-4).

The Australian Group on Antimicrobial Resistance (AGAR) performs regular period-prevalence studies to monitor changes in antimicrobial resistance in selected enteric Gram-negative pathogens. The 2010 survey focussed on community-onset infections, examining isolates from urinary tract infections from patients presenting to outpatient clinics, emergency departments or to community practitioners. Two thousand and ninety-two Escherichia coli, 578 Klebsiella species and 268 Enterobacter species were tested using a commercial automated method (Vitek 2, BioMérieux) and results were analysed using Clinical and Laboratory Standards Institute breakpoints from January 2012. Of the key resistances, non-susceptibility to the third-generation cephalosporin, ceftriaxone, was found in 3.2% of E. coli and 3.2%-4.0% of Klebsiella spp. Non-susceptibility rates to ciprofloxacin were 5.4% for E. coli, 1.0%-2.3% for Klebsiella spp., and 2.5%-6.6% in Enterobacter spp, and resistance rates to piperacillin-tazobactam were 2.8%, 3.2%-6.9%, and 16.8%-18.0% for the same 3 groups respectively. Only 3 strains, 2 Klebsiella spp. and 1 Enterobacter spp, were shown to harbour a carbapenemase (IMP-4).

AIM (1) Investigate incidence, magnitude and bacterial diversity of bacteraemia due to flossing compared with scaling and root planing (SRP) and (2) Identify any associations with clinical parameters. MATERIALS AND METHODS Full-mouth flossing and single quadrant SRP were performed at separate visits for 30 patients with chronic periodontitis. Baseline blood samples and at 30 s and 10 min. after completion of flossing, 5 min. after initiation of SRP and 30 s and 10 min. after completion of SRP were obtained. Total bacteraemia and viridans streptococcal bacteraemia (VSB) were investigated. RESULTS Total bacteraemia incidence was 30% for flossing and 43.3% for SRP (no significant difference; p = 0.21). Flossing and SRP caused the same incidence of VSB (26.7%). Flossing caused a higher mean magnitude of total bacteraemia than SRP (7.4 ± 16.2 CFU/ml versus 2 ± 3.4 CFU/ml), but the difference was not significant (p = 0.2). Flossing caused a higher mean magnitude of VSB than SRP (1.2 ± 1.6 CFU/ml versus 0.4 ± 0.2 CFU/ml), but the difference was not significant (p = 0.09). Viridans streptococci comprised 11.4% of flossing bacteraemia isolates and 7.6% in SRP. No correlations were found between clinical parameters and incidence or magnitude of bacteraemia following flossing. Gingival inflammation was significantly associated with incidence of total bacteraemia (p = 0.01) and VSB (p = 0.001) following SRP. No correlations were found for any parameter and magnitude of total bacteraemia or VSB following SRP. CONCLUSIONS No differences were found between flossing and SRP in the incidence or magnitude of total bacteraemia or VSB. This finding is important in the ongoing re-evaluation of antibiotic prophylaxis to prevent infective endocarditis.

Changes to antibiotic prophylaxis guidelines for the prevention of infective endocarditis (IE) have occurred in part due to similar incidences of bacteraemia caused by oral hygiene procedures as compared with dental treatments for which antibiotic prophylaxis has traditionally been provided. Viridans streptococci are important pathogens in IE. However, there is little evidence available comparing the magnitude of bacteraemia caused by oral hygiene activities with that caused by periodontal treatment. The aims of this study were to investigate the incidence and magnitude of viridans streptococcal bacteraemia (VSB) due to flossing as compared with scaling and root planing (SRP) in the same individual.

Since it was initially published, the groupthink hypothesis (Janis, 1972) has been one of the most widely cited con- tributions to the study of decision-making. Although it was originally conceived as a model of faulty decision- making by political policy-making groups, its applicability to other types of decision-making workgroups is readily apparent. Also apparent is its potential applicability to decision-making by juries. The antecedent conditions and symptoms of groupthink are elaborated, as they may apply to decision-making by juries and preventative strate- gies are discussed.

AIMS:The aims of this study were to (1) investigate the incidence of bacteraemia following flossing in subjects with chronic periodontitis or periodontal health; (2) identify the micro-organisms in detected bacteraemias; and (3) identify any patient or clinical factors associated with such bacteraemia. MATERIAL AND METHODS:Baseline blood samples were obtained from 30 individuals with chronic periodontitis (17 M:13 F, 29-75 years) and 30 with periodontal health (17 M:13 F, 28-71 years) following a non-invasive examination. Each subject's teeth were then flossed in a standardized manner and blood samples obtained 30 s and 10 min. after flossing cessation. Blood samples were cultured in a BACTEC system and positive samples subcultured for identification. RESULTS:Forty per cent of periodontitis subjects and 41% of periodontally healthy subjects tested positive for bacteraemia following flossing. Viridans streptococci, which are commonly implicated in infective endocarditis (IE), were isolated from 19% of positive subjects and accounted for 35% of microbial isolates. Twenty per cent of subjects had a detectable bacteraemia at 10 min. post-flossing. No patient or clinical factors were significantly associated with post-flossing bacteraemia. CONCLUSIONS:Dental flossing can produce bacteraemia in periodontally healthy and periodontally diseased individuals at a rate comparable with that caused by some dental treatments for which antibiotic prophylaxis is given to prevent IE.

AIM:To investigate rinsing with povidone-iodine on bacteraemia caused by ultrasonic scaling.MATERIAL AND METHODS:Sixty patients with gingivitis undertook a randomized, placebo-controlled trial in which 30 rinsed with 0.9% saline and 30 with 7.5% povidone-iodine for 2 min. before ultrasonic scaling of FDI teeth 31-35. Blood samples before and after 30 s and 2 min. of scaling were cultured by lysocentrifugation.RESULTS:Oral bacteraemia occurred in 33.3% of the saline group and 10% of the povidone-iodine group. Regression analysis showed that rinsing with povidone-iodine was approximately 80% more effective than rinsing with saline in reducing the occurrence of bacteraemia, with a statistically significant odds ratio (OR) of 0.189 (95% confidence intervals, OR=0.043-0.827). There were 24 oral bacterial isolates in the saline group and 3 in the povidone-iodine group. Viridans streptococci comprised 11 of the isolates in the saline group and none in the povidone-iodine group. Bacteraemia magnitude was 0.1 colony-forming units/ml in the povidone-iodine subjects and 0.1-0.7 CFU/ml in the saline group.CONCLUSIONS:Rinsing with 7.5% povidone-iodine reduced the incidence and magnitude of bacteraemia and eliminated viridans streptococci from such bacteraemia. Povidone-iodine rinsing may be helpful for ultrasonic scaling of gingivitis patients at risk of infective endocarditis.

Aim: To investigate whether chewing in patients with untreated chronic periodontitis or plaque-induced gingivitis causes bacteraemia of oral origin.Method: Twenty-one patients with untreated chronic periodontitis (32-75 years old) and 20 with plaque-induced gingivitis (26-54 years old) chewed a standard wax medium for 4 min. Blood samples were drawn before, during and 5 min. post-chewing. Aerobic and anaerobic Bactec system culturing was performed for 21 days and positive bottles were subcultured and isolates were identified to genus level. A full periodontal analysis was performed on all teeth and included probing depths, recession, attachment levels, bleeding on probing, mobility plaque index and gingival index. Radiographs were assessed for the severity of alveolar bone loss.Results: No bacteraemia of oral origin was detected in any patient. Skin contaminants (Staphylococcus epidermidis, Propionibacterium spp.) were detected in blood samples from three patients (two periodontitis; one gingivitis).Conclusion: Chewing did not cause bacteraemia in chronic periodontitis or plaque-induced gingivitis patients and may not be a risk factor for infective endocarditis in at-risk individuals with periodontal disease.

The increasing prevalence of multiple-antibiotic resistant bacteria is a major public health problem. Recent summits have been held by the New South Wales and Victorian governments to develop strategies to combat this threat within the public hospital system. Papers in this issue of Pathology remind us, however, that the problem with multiple-antibiotic resistant bacteria is not confined to hospitals. The increasing importance of communityacquired methicillin-resistant Staphylococcus aureus (MRSA) and an apparent increase in serious infection due to such strains is highlighted. The emergence of methicillin resistance in S. aureus isolates recovered from non-hospitalised patients (community MRSA) is a worldwide phenomenon. Unlike typical hospital strains of MRSA, community strains are often non-multiresistant (defined as resistant to (3 non-blactam antibiotics). Following their first appearance among intravenous drug users in the late 1980s, epidemics of community MRSA have moved beyond the original demographic groups. In Australia, such isolates first appeared in Western Australia in the early 1990s, initially in patients from remote areas of the Kimberly and Gold Fields regions, but soon became the predominant ‘type’ of MRSA strains in Perth, with subsequent spread to the eastern states in the late 1990s. Here, isolates were initially recovered from Polynesian visitors or migrants, with molecular typing studies confirming that these strains were identical to those responsible for epidemics in New Zealand and the Pacific Islands. Today, community MRSA strains have been seen in all ethnic groups, particularly in Sydney and Brisbane, and have been increasingly recovered from patients in rural communities and in the indigenous population. Importantly, strains of MRSA have also been introduced into Australia from further afield. In particular, epidemic MRSA (EMRSA)-15 and EMRSA-16 strains from the United Kingdom are increasingly reported in Australia, probably introduced by British healthcare workers. If the British experience is anything to go by, this is of particular concern, as these initially community strains appear to be persistent colonisers and spread readily once introduced into nursing homes and hospitals; they have become the predominant MRSA strains in UK hospitals within only a few years. The paper by Gosbell and co-workers highlights the complexity in epidemiology of MRSA in Australia, which becomes readily apparent when isolates are genotyped using methods such as multilocus sequencing. Interestingly, there was a diverse range of genotypes: of 16 patients with community MRSA bacteraemia in western Sydney, half were infected with a nosocomial strain (the UK EMRSA15 strain), only three were infected with an Oceania strain, and the remaining with Western Australian or Queensland strains. Most of the patients had risk factors for infection. Unfortunately the Staphylococcal Reference Facility at Liverpool Hospital has now had its government funding withdrawn, severely compromising the ability of researchers in eastern Australia to conduct such studies in the future. Community strains of MRSA possess the mecA gene complex and hence are resistant to all currently available blactam agents. Whilst typically susceptible to other drug classes such as the aminoglycosides, macrolides, tetracyclines, sulphonamides and quinolones (EMRSA-15 strains are quinolone resistant), resistance to these agents may be readily acquired, so that laboratory testing is essential to guide therapy. However, there is no standardisation of which non-b-lactams should be incorporated into antimicrobial testing algorithms for these organisms, and data regarding the relative therapeutic efficacy of these agents for treating the spectrum of infections caused by community MRSA are incomplete. Gosbell presents the results of time-kill and disc synergy studies on an Oceania phage type strain, and recommends that clindamycin, cotrimoxazole or doxycycline could be used for treatment of mild to moderate infections such as boils and cellulitis. Certainly, clindamycin has become the treatment of choice for such community MRSA infections in many centres. The study by Pimentel and Lum is a useful reminder for laboratories to be vigilant in detecting inducible clindamycin resistance (ICR) in S. aureus strains, which appear resistant to erythromycin but susceptible to clindamycin (i.e., dissociative resistance). In their evaluation of the ‘D-test’, ICR was recognised in all 100 isolates with dissociative macrolide and lincosamide resistance. Vancomycin remains the mainstay of therapy for bacteraemia and other serious invasive infections with MRSA, whether community or hospital acquired. Increasing reports of MRSA with reduced susceptibility to vancomycin (so-called ‘VISA’ strains) in Australia, including in non-multiresistant strains, underscores the need for accurate and timely determination of antimicrobial susceptibility by laboratories. Whilst most commonly cause skin and soft tissue infections, community MRSA are increasingly responsible for serious life-threatening invasive infections. Multiple Pathology (June 2006) 38(3), pp. 199–200

Staphylococcus aureus bacteraemia (SAB) is common. Around 8000 cases occur per year in Australia, of which 60% are hospital- or healthcare-associated. Risk factors for SAB include injectable drug use, haemodialysis, indwelling vascular catheters and immunosuppression. Metastatic infection develops in up to one-third of patients with SAB, with joints and heart valves being the most commonly affected sites. Community-acquisition,persistent fever, positive blood cultures after 48 h of treatment and the presence of embolic lesions correlate with the presence of complicated SAB (i.e. high risk of endocarditis and/or other metastatic complications). All patients require careful clinical evaluation to exclude endocarditis and other metastatic foci. Echocardiography,preferably transoesophageal echocardiography, should be performed to exclude endocarditis. Most patients with SAB, and all with features of complicated SAB, require prolonged intravenous antibiotic therapy (at least 4 weeks), but a subgroup with good prognostic features may be suitable for shorter intravenous therapy (2 weeks). Penicillinase-resistant penicillins (e.g.flucloxacillin) are the agents of choice for SAB with methicillin-sensitive strains. Vancomycin or first-generation cephalosporins are alternatives but have lower antimicrobial activity than flucloxacillin. However, vancomycin remains the therapy of choice for SAB due to methicillin-resistant strains. Combination therapy with gentamicin may be useful for the first few days of treatment in selected patients, but otherwise there are few data to support the use of combination regimens in SAB. Newer agents such as linezolid and quinupristin/dalfopristin may have a role in selected patients, especially in SAB due to S. aureus strains with reduced susceptibility to vancomycin.

An annual survey of antimicrobial resistance in clinical isolates of Staphylococcus aureus was conducted in 21 Australian teaching hospital microbiology laboratories in eight major cities from 1989 to 1999. A total of 19,000 isolates were tested for susceptibility to 18 antimicrobials, with 3795 being methicillin-resistant (MRSA). Resistance to ciprofloxacin in MRSA increased from 4.9% to 75.9%. The proportion of MRSA resistant to erythromycin decreased significantly (99.0%-88.9%), as did that to trimethoprim (98.4%-82.4%) and to tetracycline (96.5%-80.1%). The proportion of MRSA isolated increased in Sydney, Melbourne, Canberra, Adelaide, Perth, and Darwin, but not in Brisbane. The proportion in Hobart peaked in 1994. MRSA in Perth were predominantly non-multiresistant (nmMRSA) throughout the survey (i.e., resistant to less than three of eight indicator antibiotics) due mainly to local strains that originated in the community. The proportion of nmMRSA increased to modest levels in the other cities. In eastern cities, this was due to the appearance of strains closely related to nmMRSA seen in other countries of the southwestern Pacific.

It is likely that many did not have a good death. In hospitals the pervasive ethos of healing and curing is not conducive to confronting death. Investigations and invasive procedures continue when palliative care is actually long overdue, and technology stubbornly defies death. When death is imminent, feelings of helplessness, guilt or failure are allayed by hiding reality behind closed curtains or abandoning the dying patient to a side room.

ANZ Journal of SurgeryVolume 71, Issue 10 p. 563-563 Post-discharge surgical wound surveillance David H. Mitchell, David H. Mitchell Centre for Infectious Diseases, and Microbiology Westmead Hospital, Westmead, NSWSearch for more papers by this author David H. Mitchell, David H. Mitchell Centre for Infectious Diseases, and Microbiology Westmead Hospital, Westmead, NSWSearch for more papers by this author First published: 07 July 2008 https://doi.org/10.1046/j.1445-2197.2001.02214.xCitations: 2Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. REFERENCES 1 Olson M & Lee J. Continuous 10 year wound infection surveillance. Arch. Surg. 1990; 125: 794 – 803. 2 Kent P, McDonald M, Harris O, Mason T, Spelman D. Postdischarge surgical wound infection surveillance in a provincial hospital: Follow-up rates, validity of data and review of the literature. ANZ J. Surg. 2001; 71: 583 – 9. 3 Society for Hospital Epidemiology of America; Association for Practitioners in Infection Control; Surgical Infection Society. Consensus paper on the surveillance of surgical wound infection. Infect. Control Hosp. Epidemiol. 1992; 13: 599 – 605. 4 Murphy C & McLaws M-L. Methodologies used in surveillance of surgical wound infection and bacteremia in Australian hospitals. Am. J. Infect. Control 1999; 27: 474 – 81. 5 Holtz T & Wenzel R. Postdischarge surveillance for nosocomial wound infection: A brief review and commentary. Am. J. Infect. Control 1992; 20: 206 – 13. 6 Reimer K, Gleed C, Nicolle L. The impact of postdischarge surveillance on surgical wounds. Todays OR Nurse 1987; 9: 31 – 6. 7 Association for Professionals in Infection Control and Epidemiology. Infection Control and Applied Epidemiology. St Louis: Mosby, 1996. 8 Mitchell D, Swift G, Gilbert G. Surgical wound infection surveillance: The importance of infections that develop after hospital discharge. Aust. N.Z. J. Surg. 1999; 69: 117 – 20.DOI: 10.1046/j.1440-1622.1999.01500.x Citing Literature Volume71, Issue10October 2001Pages 563-563 ReferencesRelatedInformation

Background: The aim of this study was to evaluate two methods of post-discharge surgical wound surveillance and to compare the incidence and outcomes of wound infections that develop prior to patients' discharge with those that develop after hospital discharge.Methods: One thousand, three hundred and sixty inpatients who underwent major elective surgery in an 800-bed teaching hospital in western Sydney between February 1996 and July 1997 were followed prospectively. Pre-discharge wound surveillance was performed by clinical assessment by an independent researcher on the fifth (or later) postoperative day. Post-discharge wound surveillance was performed by a mail out of questionnaires completed independently by patients and surgeons.Results: Overall, 138 wound infections were diagnosed (incidence 10.1%), of which fewer than one-third (n = 44) were diagnosed before discharge (average 10.4 days postoperatively) and the remainder (n = 94) after discharge (average 20.6 days postoperatively). Seven hundred and eighty-two (57.5%) post-discharge survey forms were returned by patients and 680 (50.0%) by surgeons. When forms were returned by both surgeons and patients for the same wound (641 cases), there was substantial agreement in diagnosing infection or no infection (kappa = 0.73).Conclusions: The majority of nosocomial surgical wound infections develop after the patients' discharge from hospital. A post-discharge surveillance programme including self-reporting of infections by patients and return of questionnaires by patients and surgeons is feasible in an Australian hospital setting. However, such a programme is labour and resource intensive and strategies to increase return of questionnaires are required.

Multi-resistant Acinetobacter baumannii (MRAB) is an increasingly important cause of nosocomial outbreaks, particularly in intensive care units (ICUs). Over a 4-year period, more than 130 patients colonised or infected with MRAB were identified at our institution, with 90 per cent of cases from the adult ICU or neighbouring high-dependency wards. Most isolates were from wound or respiratory sites but 14.5 per cent came from sterile sites. Typing of isolates by pulsed-field gel electrophoresis (PFGE) showed that six distinct pulsotypes circulated during this period, including two strains that exhibited high-level carbapenem resistance. PFGE typing also helped direct infection control efforts, which included isolation/cohorting of cases, emphasis on handwashing and use of barrier precautions by staff, plus improved cleaning of the environment. Inappropriate prescribing of antibiotics, particularly third-generation cephalosporins and carbapenems, was reduced. Despite these measures, control of the outbreak was difficult. MRAB may become endemic in institutions, despite the use of recommended infection control measures. [AIC Aust Infect Control 1999; 4(2):12-15]