Melioidosis in Asia‐Pacific Nations: Expanding Boundaries but Unknowns Remain

1.

Summary.

• Melioidosis is endemic in many regions of the Asia‐Pacific.

• The endemic boundaries of melioidosis remain unclear, but are likely expanding.

• With increasing diabetes, an ageing population and global climate change, rates of melioidosis are predicted to increase.

2.

The 2025 surge of cases of melioidosis in north Queensland, Australia, is a timely reminder for clinicians in the Asia‐Pacific region to be vigilant for this enigmatic tropical infection [1]. Referred to as “the great mimicker”, over half of all cases of melioidosis present as community‐acquired pneumonia, with a spectrum from chronic infection resembling tuberculosis (under 10% of all cases) to rapidly progressive multi‐lobar pneumonia (up to 20% of all cases) with septic shock and high mortality [2].

Following the first description of melioidosis in 1912 from Myanmar, progressive recognition of endemicity occurred through Southeast Asia, northern Australia, south Asia, and China [3]. The last decade has seen both unmasking of endemic foci in Africa and the Americas and evidence of more recent spread to new locations, including the southern USA [4]. Nevertheless, the boundaries of endemicity of melioidosis remain far from well‐defined [5]. Among Pacific nations, Guam, Fiji, and New Caledonia are endemic for melioidosis although cases are uncommon, and Yap had a cluster of 7 cases, all fatal, between 2013 and 2016 [6]. Timor Leste was considered likely to be endemic for melioidosis, but this was only established after introduction of new laboratory capacity enabled culture confirmation of three cases in 2022 [7].

Sequencing geolocated isolates of the causative soil and water sapronotic bacterium, Burkholderia pseudomallei , has provided important insights. Firstly, it is now clear that B. pseudomallei originated in Australia and subsequently spread to Southeast Asia, likely during the last Ice Age when land bridges connected Australia to the island of New Guinea and joined up islands in the Indo‐Malay Archipelago [8]. Secondly, molecular clock analyses place the spread of B. pseudomallei from Southeast Asia to Africa at around 2000 years ago, with subsequent more recent spread to the Americas linked in time to the centuries of the slave trade [9]. Thirdly, there is contemporary spread occurring in the Americas and elsewhere, potentially linked to severe weather events such as hurricanes, cyclones, and typhoons and likely to be increased by global climate change [2, 4]. This may explain the finding from bacterial genotyping that there have been at least three recent occasions where strains of B. pseudomallei have entered northern Australia from Asia and become established and spread locally [1, 10]. Nevertheless, the actual mode of spread back to Australia from Asia remains to be elucidated, with alternative possibilities including migratory birds and importation of contaminated plants or products.

Recognition that B. pseudomallei sometimes behaves like an opportunistic pathogen in humans is important, with host clinical risk factors being the most influential factor determining whether disease occurs after infection and its subsequent severity and outcome [11]. Seroprevalence studies suggest that the vast majority of those exposed to and infected with B. pseudomallei do not develop melioidosis (i.e., clinical disease). Only around 20% of cases have no identified clinical risk factor and fatal disease is rare in such cases provided there is timely diagnosis and access to the specific antibiotics required and to state‐of‐the‐art intensive care management. Diabetes is the standout risk factor, being present in around 40%–60% of all cases [2, 12]. The massive increase in diabetes rates globally and especially in the Asia‐Pacific region portends melioidosis becoming increasingly common. Apart from the other known clinical risk factors such as chronic kidney and lung disease, hazardous alcohol use, and immunosuppressive therapy (especially corticosteroids), older age is an independent risk factor for melioidosis, therefore making the ageing populations in Asia another driver of likely future rises in case numbers. As with infection with B. cepacia , for those with cystic fibrosis, infection with B. pseudomallei is a special concern, with advice to avoid travel to melioidosis‐endemic locations or at least minimise activities that may result in exposure to B. pseudomallei. Why diabetes is such a magnet for melioidosis remains to be fully elucidated, although the complex immunopathogenesis of this intracellular bacterium does have parallels with tuberculosis [2].

Infection occurs through percutaneous exposure, inhalation, aspiration, or ingestion of B. pseudomallei . The mode of infection is likely to have a major influence on clinical presentation, severity, and outcome for melioidosis [11]. Inhalation and aspiration are thought to be linked to rapidly progressive pneumonia (often with mediastinal lymphadenopathy) with systemic infection, septic shock, and higher mortality. The differential between cutaneous and inhalational melioidosis parallels that seen between cutaneous and inhalational anthrax, plague, and tularaemia, and the concern of inhalational melioidosis is the basis for B. pseudomallei being considered a Tier 1 select agent by the US Centers for Disease Control. In regions of Asia and Southeast Asia where rural populations have unchlorinated domestic water supplies, ingestion of B. pseudomallei from water contaminated with B. pseudomallei is thought to explain the high seropositivity rates and the most common presentation in children being parotid abscesses. This contrasts with northern Australia, where seropositivity is low and infections in children are rare, with skin ulcers/abscesses being the commonest childhood manifestation of melioidosis [13, 14].

What remains unknown is the relative contribution of the three main modes of infection, with recognition that even with percutaneous exposure there may be bacteraemic spread and multifocal pneumonia analogous to that seen with Staphylococcus aureus infection. What is clear is that pathogenesis varies by the occupational and recreational activities undertaken that result in melioidosis as well as by climate factors and geographical location. For instance, in northern Australia a link has been made between high pressure hosing and inhalational melioidosis presenting as pneumonia [13]. In addition, epidemiological studies in Singapore, Taiwan and northern Australia all support a shift from percutaneous inoculation to inhalation during severe weather events with heavy winds and rain, with consequent more pneumonia and higher mortality.

Diagnosis of melioidosis requires confirmation of culture of B. pseudomallei from a clinical sample such as blood, sputum, urine, and pus. This requires microbiology laboratory resources and, most importantly, access to blood cultures (around 50% of cases are bacteraemic). In patients with hilar or mediastinal lymphadenopathy, endobronchial ultrasound and biopsy may be needed, and in endemic areas it is important to collect fresh tissue for culture even if cancer is considered the most likely diagnosis (Figure 1). Identification of B. pseudomallei can be problematic for scientists not familiar with the organism, and it is therefore important to mention suspected melioidosis in the clinical notes accompanying the pathology request. Motile Gram‐negative bacilli that are oxidase‐positive and are susceptible to amoxycillin‐clavulanate but resistant to gentamicin and colistin can be presumptively identified as B. pseudomallei . Importantly, misidentification as B. cepacia complex or B. thailandensis can occur with automated biochemical testing and with MALDI‐TOF mass spectrometry respectively [2].

FIGURE 1.

CT scans from a patient with pulmonary melioidosis showing a pulmonary mass with background emphysema (A) and a necrotic subcarinal lymph node (B).

As for tuberculosis, therapy for melioidosis requires antibiotics for a prolonged period, unlike usual community‐acquired bacterial pneumonias. The therapy consists of an initial intensive phase of intravenous ceftazidime or meropenem, followed by an eradication phase of oral antibiotics, with trimethoprim/sulfamethoxazole preferred [2]. The duration of each phase is determined by the clinical foci and severity of infection, with usually a minimum of 2 weeks of intravenous therapy and a minimum of 3 months of subsequent eradication therapy. Acquired resistance to the standard antibiotics is rare but well recognised, as is relapsed melioidosis when therapy has not eradicated the infection, either because of inadequate duration or adherence or because of a persisting focus of infection that requires source control by surgery or drainage, such as empyema, organ abscesses and osteomyelitis.

Conflicts of Interest

The authors declare no conflicts of interest.

Currie B. J. and Meumann E. M., “Melioidosis in Asia‐Pacific Nations: Expanding Boundaries but Unknowns Remain,” Respirology 30, no. 10 (2025): 917–919, 10.1111/resp.70098.