Expanding the Geographic Boundaries of Melioidosis in Queensland, Australia.

Melioidosis is an infectious disease caused by the bacterium Burkholderia pseudomallei. Although this environmental organism is endemic in certain regions of Australia, it is not considered endemic in Southern Queensland, where the last case was reported 21 years ago. We report a climate change-associated outbreak of melioidosis occurring during two La Niña events in a region previously considered nonendemic for B. pseudomallei. During a 15-month period, 14 cases of locally acquired melioidosis were identified. Twelve patients were adults (> 50 years), with diabetes mellitus the most common risk factor in 6 of 12 patients (50%). Eleven patients (79%) had direct exposure to floodwaters or the flooded environment. This study suggests an association between climate change and an increased incidence of melioidosis. In addition, this is the first report of environmental sampling and whole-genome analysis to prove endemicity and local acquisition in this region.

Epidemiology of neonatal early-onset sepsis in a geographically diverse Australian health district 2006-2016.

AIM: To describe the epidemiology of EOS including blood culture utilisation, across a large and geographically diverse Australian health district. BACKGROUND: Sepsis in the first three days of life remains a leading cause of death and morbidity. In high-income countries, group B Streptococcus (GBS) and Escherichia coli (E. coli) have dominated as causes of EOS for five decades. METHOD: An 11-year retrospective cohort study to determine the epidemiology of EOS. Incidence rates were calculated per 1000 live births. Logistic regression with linear temporal trend and covariates for potential effect modifiers were employed. Blood culture utilisation was determined by examining the rate of babies undergoing blood culture within 72 hours of birth. RESULTS: Among 93,584 live born babies, 65 had confirmed EOS (0.69/1000 live births); 22 term, 43 preterm. Across the 4 largest birth units, the proportion of babies having blood culture within 72 hours of birth varied from 1.9-5.1% for term and 21-35% for preterm babies. The annual change in the EOS rate was significant, OR 0.91 (95% CI, 0.84 to 0.99, p = 0.03). Group B Streptococcus was the most common cause of EOS in term neonates at 0.35/1000 live births (95% CI, 0.07-0.63) in 2006 and 0.1/1000 live births (95% CI, 0-0.2) in 2016. Escherichia coli was the most common cause in preterm babies at 3.4/1000 (95% CI, 0.11-6.76) in 2006 reducing significantly to 1.35/1000 live births (95% CI, -0.07-2.78) by 2016. CONCLUSIONS: Escherichia coli and GBS were the most common causes of EOS in preterm and term babies respectively. Rates of all cause term and preterm EOS declined significantly as did preterm sepsis due to E. coli. While rate of sepsis due to early-onset GBS declined, this did not reach significance. Given the high proportion of preterm babies undergoing blood culture, it is unlikely that any EOS events were missed.

Group B streptococcal screening, intrapartum antibiotic prophylaxis, and neonatal early-onset infection rates in an Australian local health district: 2006-2016.

BACKGROUND: Intrapartum antibiotic prophylaxis (IAP) to reduce the likelihood of neonatal early-onset group B streptococcal infection (EOGBS) has coincided with major reductions in incidence. While the decline has been largely ascribed to IAP following either universal screening or a risk-based approach to identify mothers whose babies may most benefit from IAP, there is lack of high quality evidence to support this view. AIMS: To describe management of maternal GBS colonisation in one local health district using universal screening and assess rates of EOGBS over time. METHODS: A retrospective cohort study was undertaken to describe compliance with GBS management, to determine the incidence of EOGBS and association between rates and maternal screening. Linking routinely collected maternity and pathology data, we explored temporal trends using logistic regression and covariates for potential effect modifiers. RESULTS: Our cohort included 62,281 women who had 92,055 pregnancies resulting in 93,584 live born babies. Screening occurred in 76% of pregnancies; 69% had a result recorded, 21.5% of those were positive for GBS. Prophylaxis was used by 79% of this group. Eighteen babies developed EOGBS, estimated incidence/1000 live births in 2006 and 2016 was 0.35 (95% CI, 0.07 to 0.63) and 0.1 (95% CI, 0 to 0.2) respectively. Seven of 10 term babies with EOGBS were born to mothers who screened negative. Data were unable to provide evidence of difference in rates of EOGBS between screened and unscreened pregnancies. We estimated the difference in EOGBS incidence from crude and weighted models to be 0 (95% CI, -0. 2 to 0.17) and -0.01 (95% CI, -0.13 to 0.10) /1000 live births respectively. CONCLUSION: No change was detected in rates of EOGBS over time and no difference in EOGBS in babies of screened and unscreened populations. Screening and prophylaxis rates were modest. Limitations of universal screening suggest alternatives be considered.