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Burkholderia pseudomallei is the causative agent of the high-mortality disease melioidosis. Although melioidosis is classified as a tropical disease, rare autochthonous cases have been reported from temperate climatic regions, with uncertainty as to whether B. pseudomallei is persistent in the local environment and whether specific genetic mechanisms facilitate the survival of B. pseudomallei outside the tropics. Sporadic cases of melioidosis occurred in a valley region (latitude 31.6°S) in southwest Western Australia, Australia, between 1966 and 1992. We report a new melioidosis cluster in the same region following high rainfall in January 2017. More than 20 animals died, and B. pseudomallei was isolated from four alpacas, a parrot, and three environmental samples taken from the farm where the alpacas resided. Epidemiological data and genomics revealed that two locations on the farm were the probable sources of the alpaca infections. We determined that B. pseudomallei isolates from the 2017 cluster belonged to sequence type 284 (ST-284), as did all isolates recovered from 1966 to 1992. Genomic analysis confirmed that the ST-284 isolates were clonal and contained conserved genomic islands and limited evidence of recombination. We identified protein-coding regions unique to these isolates that might influence the persistence of B. pseudomallei in this temperate region. We demonstrate the environmental persistence of B. pseudomallei in a temperate region for over 50 years, with limited genetic changes suggesting a latent state and with activation, potential aerosolization, and local dispersal following unusually high rainfall.IMPORTANCE Burkholderia pseudomallei is predominantly a tropical pathogen uncommonly found in the environment of temperate climatic regions. It is unclear if introduction into temperate regions is sporadic and temporary or if B. pseudomallei can persist in such environments. B. pseudomallei was identified in the environment of southwest Western Australia with melioidosis cases between 1966 and 1991. We report a new cluster with 23 animal fatalities in the same region from 2017, with B. pseudomallei again being recovered from the environment. Comparison of the isolates from the first and second clusters using genomics revealed a single sequence type, high clonality, and limited recombination, even though the time of recovery of the isolates spanned 51 years. This is a major contrast to the extensive genomic diversity seen in the tropics. Our data support the suggestion that B. pseudomallei has the ability to persist in nontropical environments, potentially in a latent state, and has the ability to activate following favorable conditions (rainfall) and then infect animals and humans.

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INTRODUCTION: Psoas abscess is a recognized but under-diagnosed complication of prosthetic hip joint infections. CASE REPORT: We report a case of a 68-year-old man with right and left hip arthroplasties performed 22 and 14 years ago, respectively, who presented with non-specific symptoms and was subsequently diagnosed with left psoas abscess on CT scan. Drainage of the psoas abscess was complicated by the formation of a discharging sinus connected to the left hip. He then developed an infected right thigh haematoma, which also formed a discharging sinus connecting to the right hip post-drainage. He was treated with bilateral two-stage revision total hip arthroplasties and multiple courses of prolonged antibacterial therapy. Both abscesses and hip joints cultured the same species of multi-sensitive Staphylococcus aureus. The causal link between the psoas abscess and the prosthetic hip infections is discussed, as well as the investigation and management. CONCLUSION: We recommend routine exploration of the iliopsoas bursa when revision of an infected total hip arthroplasty is performed to rule out intrapelvic spread of the infection [3]. There should be high index of suspicion of prosthetic hip infection in patients presenting with Psoas abscess and vice versa. A CT scan might be warranted to rule out concomitant infection in both these patients.

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Melioidosis, caused by the highly recombinogenic bacterium Burkholderia pseudomallei, is a disease with high mortality. Tracing the origin of melioidosis outbreaks and understanding how the bacterium spreads and persists in the environment are essential to protecting public and veterinary health and reducing mortality associated with outbreaks. We used whole-genome sequencing to compare isolates from a historical quarter-century outbreak that occurred between 1966 and 1991 in the Avon Valley, Western Australia, a region far outside the known range of B. pseudomallei endemicity. All Avon Valley outbreak isolates shared the same multilocus sequence type (ST-284), which has not been identified outside this region. We found substantial genetic diversity among isolates based on a comparison of genome-wide variants, with no clear correlation between genotypes and temporal, geographical or source data. We observed little evidence of recombination in the outbreak strains, indicating that genetic diversity among these isolates has primarily accrued by mutation. Phylogenomic analysis demonstrated that the isolates confidently grouped within the Australian B. pseudomallei clade, thereby ruling out introduction from a melioidosis-endemic region outside Australia. Collectively, our results point to B. pseudomallei ST-284 being present in the Avon Valley for longer than previously recognized, with its persistence and genomic diversity suggesting long-term, low-prevalence endemicity in this temperate region. Our findings provide a concerning demonstration of the potential for environmental persistence of B. pseudomallei far outside the conventional endemic regions. An expected increase in extreme weather events may reactivate latent B. pseudomallei populations in this region.

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Burkholderia pseudomallei was quickly identified from blood cultures collected from septicemic patients by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry analysis using an in-house reference library. This procedure reduced the time to definitive identification by more than 24 hours. This analysis is a useful addition to laboratory methods for early recognition of septicemic melioidosis in non-endemic settings.

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We report the first isolation in Australia of a hypervirulent epidemic strain of Clostridium difficile, PCR ribotype 027. It was isolated from a 43-year-old woman with a permanent ileostomy, who appears to have been infected while travelling in the United States. The isolate was positive for toxin A, toxin B and binary toxin, and resistant to fluoroquinolone antimicrobials, and had characteristic deletions in the tcdC gene. All diagnostic laboratories and health care facilities in Australia should now be on high alert for this organism.

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BACKGROUND AND OBJECTIVE: To investigate the association between serological evidence of past infections with common respiratory pathogens and lung function in members of an isolated community of Aborigines from tropical coastal north-western Australia. METHODS: FEV(1) and FVC were assessed by dry bellows spirometer. Serum IgG titres to 11 common respiratory pathogens were assayed. Smoking history was assessed by questionnaire. Reciprocal positive IgG titres were taken as >or=10 for all pathogens with the exception of Legionella spp. (>or=40) and Burkholderia pseudomallei (>or=20). Linear regression analysis examined associations between titres and lung function after adjustment for age, height, gender and smoking, separately for adults (age > 17 years) and children. RESULTS: An increased total number of positive IgG titres was significantly associated with reduced FEV(1) (P = 0.01) and FEV(1)/FVC ratio (P = 0.01) suggesting the presence of airflow obstruction. This association was independent of age, gender, height, weight and smoking status. CONCLUSIONS: The burden of past respiratory infections may be an important determinant of airway function in this Aboriginal community.

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