Melioidosis is a severe disease that can be difficult to diagnose because of its diverse clinical manifestations and a lack of adequate diagnostic capabilities for suspected cases. There is broad interest in improving detection and diagnosis of this disease not only in melioidosis-endemic regions but also outside these regions because melioidosis may be underreported and poses a potential bioterrorism challenge for public health authorities. Therefore, a workshop of academic, government, and private sector personnel from around the world was convened to discuss the current state of melioidosis diagnostics, diagnostic needs, and future directions.

Combining an antistaphylococcal β-lactam with vancomycin may shorten the duration of MRSA bacteremia. Further trials with a larger sample size and objective clinically relevant end points are warranted. Australian New Zealand Clinical Trials Registry: ACTRN12610000940077 (www.anzctr.org.au).

We report an almost 1.7-fold proportional increase in C. glabrata candidaemia (26.7% versus 16% in 2004) in Australia. Antifungal resistance was generally uncommon, but azole resistance (16.7% of isolates) amongst C. tropicalis may be emerging.

Pediatric melioidosis commonly manifests as localized cutaneous disease in immunocompetent hosts. The disease can be fatal, especially in individuals with risk factors for disease. Melioidosis with encephalomyelitis can result in severe residual disability. Prompt diagnosis requires a high index of clinical suspicion in endemic areas.

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We report the results of typings, for immunoglobulin G allotypes, of 5392 Native Americans from ten samples, the typings having been performed over the last 20 years. Four cultural groups are represented: the Pimans-Pima and Papago; the Puebloans-Zuni and Hopi; the Pai-Walapai; and the Athabascans-Apache and Navajo. The haplotype Gm1;21 has the highest frequency in each population while Gm1,2;21 is polymorphic in all except the Hopi. The Mongoloid marker Gm1;11,13 is found primarily in the Athabascans. The Caucasian haplotype Gm3;5,11,13 is found at polymorphic frequencies in several of the populations but its frequency is very low or absent among nonadmixed individuals. Although Nei's standard genetic distance analysis demonstrates genetic similarity at the Gm and Km loci, the heterogeneity that does exist is consistent both with what is known about the prehistory of Native Americans and traditional cultural categories. When the current Gm distributions are analyzed with respect to the three-migration hypothesis, there are three distinct Gm distributions for the postulated migrants: Gm1;21 and Gm1,2;21 for the Paleo-Indians 16,000 to 40,000 years ago; Gm1;21, Gm1,2;21, and Gm1;11,13 for the second wave of Na-Dene hunters 12,000 to 14,000 years ago; and Gm1;21 and Gm1;11,13 for the Eskimo-Aleut migration 9,000 years ago. The Pimans, Puebloans, and the Pai are descendents of the Paleo-Indians while the Apache and Navajo are the contemporary populations related to the Na-Dene. Finally, the Gm distribution in Amerindians is found to be consistent with a hypothesis of one migration of Paleo-Indians to South American, while the most likely homeland for the three ancestral populations is found to be in northeastern Asia.

Objective: To compare the unprecedented 91 cases of melioidosis in the Top End of the Northern Territory of Australia from 1 October 2009 to 30 September 2010 with the 540 cases in the preceding 20 years and postulate reasons for this year of very high melioidosis incidence. Design, setting and participants: Review of prospectively collected data on all patients with culture‐confirmed melioidosis at Royal Darwin Hospital, the Top End's tertiary referral centre, since 1 October 1989. Main outcome measures: Population‐based annual incidence of melioidosis; differences in epidemiology, clinical presentations and outcomes for 2009–2010 compared with the preceding 20 years. Results: In 2009–2010, the estimated population‐based incidence of melioidosis was 50.2 cases per 100 000 in the Top End population overall, and 102.4 cases per 100 000 in the Top End Indigenous population. The proportion of patients acquiring melioidosis in the Darwin urban area increased from 49% in 1989–2009 to 65% in 2009–2010 (OR, 1.96; 95% CI, 1.20–3.19). Among the 49 Indigenous Australian patients with melioidosis in 2009–2010, 63% acquired the infection in Darwin, compared with 35% of Indigenous patients in the previous 20 years (OR, 3.17; 95% CI, 1.62–6.24). Conclusions: In 2009–2010, the Top End had the highest annual incidence of melioidosis documented from anywhere to date. The prominent increase in cases in Darwin was associated with above average rainfall in Darwin during December 2009 to February 2010. The increase in the proportion of Indigenous Australians who acquired melioidosis in Darwin may reflect movement of some Indigenous people into Darwin from remote communities.