BackgroundSurgical site infections following coronary artery bypass graft (CABG) procedures pose substantial burden on patients and healthcare systems. This study aims to describe the incidence of surgical site infections and causative pathogens following CABG surgery over the period 2003–2012, and to identify risk factors for complex sternal site infections.MethodsRoutine computerised surveillance data were collected from three public hospitals in Queensland, Australia in which CABG surgery was performed between 2003 and 2012. Surgical site infection rates were calculated by types of infection (superficial/complex) and incision sites (sternal/harvest sites). Patient and procedural characteristics were evaluated as risk factors for complex sternal site infections using a logistic regression model.ResultsThere were 1,702 surgical site infections (518 at sternal sites and 1,184 at harvest sites) following 14,546 CABG procedures performed. Among 732 pathogens isolated, Methicillin-sensitive Staphylococcus aureus accounted for 28.3% of the isolates, Pseudomonas aeruginosa 18.3%, methicillin-resistant Staphylococcus aureus 14.6%, and Enterobacter species 6.7%. Proportions of Gram-negative bacteria elevated from 37.8% in 2003 to 61.8% in 2009, followed by a reduction to 42.4% in 2012. Crude rates of complex sternal site infections increased over the reporting period, ranging from 0.7% in 2004 to 2.6% in 2011. Two factors associated with increased risk of complex sternal site infections were identified: patients with an ASA (American Society of Anaesthesiologists) score of 4 or 5 (reference score of 3, OR 1.83, 95% CI 1.36-2.47) and absence of documentation of antibiotic prophylaxis (OR 2.03, 95% CI 1.12-3.69).ConclusionsCompared with previous studies, our data indicate the importance of Gram-negative organisms as causative agents for surgical site infections following CABG surgery. An increase in complex sternal site infection rates can be partially explained by the increasing proportion of patients with more severe underlying disease.

IgA nephropathy is the predominant primary GN in Queensland, and nephrotic syndrome the most common indication for a renal biopsy. While crescentic GN incidence has significantly increased with time, focal segmental glomerulosclerosis incidence has not shown any trend. Incidence of GN overall appears to increase with age. The annual rate of biopsy in this study appears lower than previously published in an Australian population.

Pertussis epidemics have displayed substantial spatial heterogeneity in countries with high socioeconomic conditions and high vaccine coverage. This study aims to investigate the relationship between pertussis risk and socio-environmental factors on the spatio-temporal variation underlying pertussis infection. We obtained daily case numbers of pertussis notifications from Queensland Health, Australia by postal area, for the period January 2006 to December 2012. A Bayesian spatio-temporal model was used to quantify the relationship between monthly pertussis incidence and socio-environmental factors. The socio-environmental factors included monthly mean minimum temperature (MIT), monthly mean vapour pressure (VAP), Queensland school calendar pattern (SCP), and socioeconomic index for area (SEIFA). An increase in pertussis incidence was observed from 2006 to 2010 and a slight decrease from 2011 to 2012. Spatial analyses showed pertussis incidence across Queensland postal area to be low and more spatially homogeneous during 2006-2008; incidence was higher and more spatially heterogeneous after 2009. The results also showed that the average decrease in monthly pertussis incidence was 3·1% [95% credible interval (CrI) 1·3-4·8] for each 1 °C increase in monthly MIT, while average increase in monthly pertussis incidences were 6·2% (95% CrI 0·4-12·4) and 2% (95% CrI 1-3) for SCP periods and for each 10-unit increase in SEIFA, respectively. This study demonstrated that pertussis transmission is significantly associated with MIT, SEIFA, and SCP. Mapping derived from this work highlights the potential for future investigation and areas for focusing future control strategies.

Objective: To describe the epidemiology and rates of all health care‐associated bloodstream infections (HA‐BSIs) and of specific HA‐BSI subsets in public hospitals in Queensland. Design and setting: Standardised HA‐BSI surveillance data were collected in 23 Queensland public hospitals, 2008–2012. Main outcome measures: HA‐BSIs were prospectively classified in terms of place of acquisition (inpatient, non‐inpatient); focus of infection (intravascular catheter‐associated, organ site focus, neutropenic sepsis, or unknown focus); and causative organisms. Inpatient HA‐BSI rates (per 10 000 patient‐days) were calculated. Results: There were 8092 HA‐BSIs and 9418 causative organisms reported. Inpatient HA‐BSIs accounted for 79% of all cases. The focus of infection in 2792 cases (35%) was an organ site, intravascular catheters in 2755 (34%; including 2240 central line catheters), neutropenic sepsis in 1063 (13%), and unknown in 1482 (18%). Five per cent (117 of 2240) of central line‐associated BSIs (CLABSIs) were attributable to intensive care units (ICUs). Eight groups of organisms provided 79% of causative agents: coagulase‐negative staphylococci (18%), Staphylococcus aureus (15%), Escherichia coli (11%), Pseudomonas species (9%), Klebsiella pneumoniae/oxytoca (8%), Enterococcus species (7%), Enterobacter species (6%), and Candida species (5%). The overall inpatient HA‐BSI rate was 6.0 per 10 000 patient‐days. The rates for important BSI subsets included: intravascular catheter‐associated BSIs, 1.9 per 10 000 patient‐days; S. aureus BSIs, 1.0 per 10 000 patient‐days; and methicillin‐resistant S. aureus BSIs, 0.3 per 10 000 patient‐days. Conclusions: The rate of HA‐BSIs in Queensland public hospitals is lower than reported by similar studies elsewhere. About one‐third of HA‐BSIs are attributable to intravascular catheters, predominantly central venous lines, but the vast majority of CLABSIs are contracted outside ICUs. Different sources of HA‐BSIs require different prevention strategies.