Your activity: 104 p.v.
your limit has been reached. plz Donate us to allow your ip full access, Email:

Melioidosis: Epidemiology, clinical manifestations, and diagnosis

Melioidosis: Epidemiology, clinical manifestations, and diagnosis
Bart Currie, MBBS, FRACP
Nicholas M Anstey, MBBS, FRACP, PhD
Section Editor:
Daniel J Sexton, MD
Deputy Editor:
Allyson Bloom, MD
Literature review current through: Dec 2022. | This topic last updated: Aug 30, 2022.

INTRODUCTION — Melioidosis is an infection caused by the facultative intracellular gram-negative bacterium Burkholderia pseudomallei [1-4]. This organism is a widely distributed environmental saprophyte in soil and fresh surface water in endemic regions [5].

The epidemiology, clinical manifestations, and diagnosis of melioidosis will be presented here. The treatment and prognosis of this disease are discussed separately. (See "Melioidosis: Treatment and prevention".)


Geographic distribution

Historically endemic areas — Melioidosis occurs predominantly in Southeast Asia, northern Australia, South Asia (including India), and China (figure 1) [2,6-9]. The majority of diagnosed cases are from Thailand [10-13], Malaysia [14-17], Singapore [18-24], and northern Australia [25-27]. Cases are also reported from Papua New Guinea [28] and New Caledonia [29].

Northeastern Thailand and parts of northern Australia are "hyperendemic" for melioidosis [11,25], with seasonal peaks in the wet seasons. After 2010, there was an increase in incidence in northeastern Thailand, northern Australia, and South Asia [30-33].

Cases elsewhere globally — Melioidosis has been described outside the classic endemic regions. Many such cases are acquired by visitors to endemic areas, with symptoms arising after departure from the endemic area [34,35]. However, sporadic human or animal cases and occasional environmental isolates of B. pseudomallei have been increasingly described elsewhere, making the endemic boundaries of melioidosis less clear [8,9,36].

As an example, in the United States, melioidosis has been rare. Although most cases have been travel associated, several non-travel-associated cases have been reported, supporting the concept that B. pseudomallei is potentially endemic in the southern United States [37].

Endemicity in the Gulf Coast of the United States B. pseudomallei was identified in environmental samples (soil and water) from the Mississippi Gulf Coast region in July 2022 [38]. The environmental isolates were genetically linked to isolates cultured from two unrelated patients who lived in the area, had no history of travel, and presented with melioidosis in 2020 and 2022. This was the first confirmation that B. pseudomallei is endemic in the continental United States.

Bacterial genotyping of an earlier non-travel-associated case in Texas had supported the possibility that melioidosis may also be endemic there [39], as had a prediction model of the global presence of B. pseudomallei [40]. Nevertheless, environmental sampling from Texas has to date not recovered B. pseudomallei, so endemicity in that region of the Gulf Coast has yet to be confirmed.

Endemicity in Puerto Rico Although cases have rarely been reported from Puerto Rico, epidemiologic analysis and environmental sampling indicate that B. pseudomallei is endemic there [41]. Six cases of melioidosis were reported from eastern Puerto Rico between 1982 and 2012 [42]. During investigation of two of those cases, seropositivity to B. pseudomallei was identified in a subset of individuals who lived in proximity to the index patients, and B. pseudomallei was isolated from soil samples from a single site.

Sporadic non-travel-associated cases in the United States – Between March and July 2021, four non-travel-associated cases of melioidosis were described in patients from Georgia, Kansas, Texas, and Minnesota [43]. Genomic analysis suggested that an aromatherapy room spray product, which was manufactured in India and sold in the United States online and in stores between February and October, was the common source of exposure [44,45]. The B. pseudomallei isolates identified in this outbreak were most closely related to strains found in South Asia.

Previously, between 2008 and 2013, 34 cases of melioidosis were reported in the United States; only three did not have documented travel to an area endemic for melioidosis [46]. Despite extensive investigation, the source of the infection in these three cases could not be identified, but genomic analysis of B. pseudomallei from the patients suggested that the infecting bacteria were imported from Southeast Asia [47].

Cases suggestive of endemic infection have also been reported from Africa, Indian Ocean countries (such as Mauritius), the Middle East, the Caribbean, and Central and South America [48-52].

Despite better recognition and increased surveillance of infection, the full extent of global distribution of B. pseudomallei remains unclear, especially the extent to which melioidosis has spread beyond historical locations and the timing and modes of global spread [53]. Phylogenetic analysis of autochthonous cases from Madagascar and other isolates from a global dataset suggests spread of B. pseudomallei from Asia to Africa, with subsequent spread from West Africa to the Americas that was potentially linked to the slave trade [54,55]. Statistical modelling of clinical cases and environmental studies globally estimated that, in 2015, there may have been 165,000 melioidosis cases globally, with 89,000 deaths [40]. That study predicted that melioidosis was likely to be endemic in 34 countries that so far have had no confirmed cases. Targeted surveillance together with support for improved regional microbiology facilities are needed to reveal the accuracy of these predictions [56].

Transmission — Transmission of infection can occur via percutaneous inoculation, inhalation, aspiration, and occasionally ingestion.

Primary routes of transmission – The predominant mode of transmission is likely percutaneous inoculation during exposure to wet season soils or contaminated water [6,25,57]. Cases of pneumonia following presumptive inoculating skin injuries are well documented, suggesting that the organism can reach the lungs via the hematogenous route [25]. Inhalation (as described among soldiers in Vietnam exposed to dust raised by helicopter rotor blades) had previously been thought to be the primary route of acquisition [58-60].

During severe weather events such as tropical storms and cyclones, the primary mode of transmission may shift from inoculation to inhalation [61-64]. This is supported by observations that rainfall in the two weeks prior to onset of symptoms may be an independent risk factor for a pneumonic presentation, septic shock, and death, which are thought to be more likely with inhalational exposure [61]. Cases of melioidosis pneumonia that occurred at the time of the December 2004 tsunami in the Indian Ocean were associated largely with aspiration events, although inoculation of the organism in the setting of lacerations may have also occurred [62-64].

Ingestion of water contaminated with B. pseudomallei may also be a relatively important route of transmission, especially in endemic regions with unchlorinated water supplies [25,65,66]. Such transmission could explain the much higher rate of parotid and liver abscesses observed in parts of Southeast Asia compared with northern Australia [5,53,67].

Uncommon routes of transmission – Person-to-person transmission is extremely unusual, despite the large bacterial load in severely ill patients with bacteremic pulmonary melioidosis [5,68]. Mother-to-infant transmission during breastfeeding has been described in the setting of B. pseudomallei mastitis [2,69]. Sexual transmission has also been postulated as an uncommon route of transmission [70,71]. Laboratory-acquired infections and iatrogenic infections from contaminated hospital or surgical equipment occasionally occur [5,72-77]. Transmission through blood transfusion or organ donation has not been reported.

Transmission related to animal exposure is very rare; three possible cases have been described in Australia [77,78].

Risk factors

Exposure risk — In endemic areas, individuals who have environmental exposure to soil and water have a higher risk of exposure to and infection with B. pseudomallei. As an example, in a study of 1148 individuals with culture-confirmed melioidosis identified over 30 years in the Northern Territory of Australia, occupational or recreational exposure to soil or surface water was documented for 16 and 78 percent, respectively [79]. Relevant activities included gardening and landscaping. In a study of 204 patients with melioidosis in Thailand, 85 percent were rice farmers [80].

The risk of exposure and infection also varies by season. The majority of endemic clinical cases of melioidosis occur in the monsoonal wet seasons: 75 percent of cases in northeast Thailand (May to October) [81] and 81 percent of cases in the Northern Territory of Australia (November to April) [32]. Severe weather events (eg, monsoons or tropical cyclones) have been associated with local clusters of infection [79].

Comorbidities — Severe or fatal melioidosis most commonly occurs in individuals with specific comorbidities [26,32,79,80,82]. The most important risk factors for melioidosis are [11,32,57,80-84]:

Diabetes mellitus

Hazardous alcohol use

Chronic kidney disease

Chronic lung disease

In a study of 1148 individuals with culture-confirmed melioidosis identified over 30 years in the Northern Territory of Australia, these were the most common underlying conditions, reported in 45, 40, 27, and 12 percent of patients, respectively [79]. Although no single risk factor was associated with mortality, absence of any risk factor was associated with survival. Only 3 of 186 patients with no identified risk factor died; those with at least one risk factor were at least eight times more likely to die.

Other less common risk factors include malignancy, immunosuppressive therapy or conditions, especially high-dose glucocorticoids, rheumatic heart disease, congestive cardiac failure, and kava consumption [25,79,80]. Pulmonary hemosiderosis, chronic granulomatous disease, tuberculosis, and thalassemia have also been proposed as potential risk factors [80,85,86].

In patients with cystic fibrosis, B. pseudomallei can cause both colonization and pulmonary infections [87-90]. Patients with cystic fibrosis traveling to melioidosis endemic areas should be counseled about the possibility of infection with B. pseudomallei and that it can cause problems analogous to Burkholderia cepacia [91].

Children with melioidosis are less likely than adults to have identifiable risk factors [92-95]. One study from Malaysia reported that the risk of melioidosis was substantially higher among children with thalassemia major until universal iron chelation therapy was introduced [96].

INCUBATION PERIOD — The incubation period for acute melioidosis following inoculating injury ranges from 1 to 21 days (mean 4 to 9 days) [76,79,97]. The incubation period is likely influenced by the inoculating dose, mode of transmission, host risk factors, and variable virulence properties of the isolate [60,98]. Rapid onset of melioidosis (within 24 hours of inoculation) has been seen in the setting of presumed aspiration following near-drowning [99,100], as well as in a small number of patients with heavy environmental exposure [97].

Melioidosis can also uncommonly present as reactivation of latent infection years after the initial exposure. (See 'Spectrum and time course of infection' below.)


Spectrum and time course of infection — Serologic studies suggest that most infections with B. pseudomallei are asymptomatic or subclinical [101]; severe clinical disease occurs mainly in those with certain comorbidities [32,102-106]. (See 'Comorbidities' above.)

Among symptomatic individuals, most present with acute infection (within two months of diagnosis). In a study of 1148 individuals with culture-confirmed melioidosis identified over 30 years in the Northern Territory of Australia, 88 percent presented with acute infection, 9 percent with chronic infection, and 3 percent with reactivation of latent infection [79]. The observation that most cases present during the wet seasons, when the risk of exposure is highest, also suggests that most infections in endemic areas are acute [7,11,25,32,83,104] (see 'Exposure risk' above). However, in occasional cohorts, chronic infection is more common than acute [107].

The clinical presentation varies by time course of infection, although pneumonia is overall the most common manifestation of melioidosis:

Acute infection – The most common clinical manifestation of acute infection is pneumonia; other sites of infection include skin and soft tissue and the genitourinary tract (figure 2). Bacteremic spread of the organism can result in clinical manifestations involving virtually any site. Over half of all patients are bacteremic and up to a quarter can present with septic shock; overall mortality from melioidosis ranges from less than 10 to over 40 percent [30,79]. (See 'Common manifestations' below.)

Chronic infection – Of those with chronic melioidosis (symptoms persisting for longer than two months), the majority present with chronic pulmonary symptoms and signs that may mimic tuberculosis or with a non-healing skin ulcer or abscess [79] (see 'Pneumonia' below and 'Skin infection' below). Chronic infection is more indolent than acute infection and has been associated with a 6.5 times lower mortality rate (2 percent) [79].

Latent infection with (re)activation – Infection with B. pseudomallei can uncommonly be latent and subsequently activate, analogous to tuberculosis. As above, only 3 percent of over 1000 cases of melioidosis in northern Australia were thought to be reactivation of latent infection [79]. The longest reported latent period between exposure in an endemic region and the development of melioidosis in a nonendemic region is 29 years [108-111]. Although one case had suggested a 62-year latency period, subsequent genotyping of the bacterial isolate indicated that ascertainment of the timing of initial infection was incorrect and that the patient was likely infected through more recent travel [51].

Following the Vietnam War, approximately 225,000 returning military personnel were estimated to be at potential risk of reactivation of melioidosis [112]. Although occasional cases of B. pseudomallei (re)activation had been documented in Vietnam veterans, they were rare relative to the number of individuals exposed [59,108].

Impact of age on clinical presentation — Most cases of melioidosis occur in adults [113]. As an example, in a study of 1148 individuals with culture-confirmed melioidosis identified over 30 years in the Northern Territory of Australia, the median age was 50 years, and only 48 individuals (4 percent) were younger than 15 years of age [79].

The most common clinical presentations of B. pseudomallei infection are also distinct and generally less severe in children compared with adults [93,95]. In the study described above, children were more likely than adults to present with localized skin infection (58 versus 11 percent) and less likely to have bacteremia (15 versus 58 percent) [79]. Pneumonia occurs infrequently in children. In Southeast Asia, suppurative parotitis is a common presentation in childhood [92,93]. (See 'Parotitis' below.)

Although reported mortality rates in children are lower than in adults, mortality in neonates is exceptionally high (75 percent in one systematic review [114]).

Common manifestations

Pneumonia — Pneumonia is the most common clinical presentation of melioidosis in adults in almost all studies [2,15,22,113] and was reported in over half of the cases that occurred in the Northern Territory of Australia from 1989 to 2019 (figure 2) [79]. Patients with both acute and chronic infection present with pneumonia:

Acute presentation – Melioidosis can present similarly to acute community-acquired pneumonia, with high fever, cough, sputum, chills, rigors, and respiratory distress with or without shock [115]. Chest radiographic findings vary widely and may include discrete diffuse or patchy consolidation that is lobar or multilobar, necrotizing lesions, and pleural effusions (image 1 and image 2) [115-117]. Cavitation and abscesses with fluid levels can occur (picture 1). However, on initial chest radiograph, the infiltrates may be smaller and less extensive than would be expected in severely ill bacteremic patients. Mediastinal lymphadenopathy can occur, potentially linked to inhalational melioidosis, although melioidosis does not usually cause calcification.

Subacute or chronic presentation – Melioidosis can present similarly to tuberculosis, with chronic cough, purulent sputum production, hemoptysis, and night sweats. Imaging findings can also mimic tuberculosis with cavitating, nodular, or streaky infiltrates with fibrotic changes (image 3). Upper lobe consolidation is especially common in chronic melioidosis but can also often be seen in acute presentations. Some patients present with pleural effusion alone.

Skin infection — Skin infections are a relatively common site of localized infection (figure 2) [118]. Cutaneous melioidosis includes skin ulcers (picture 2) and abscesses, as well as pustules and furuncles, crusted erythematous lesions, and macular lesions (picture 3) [32,119]. Often, individuals are diagnosed after having failed to respond to other antibiotics targeted to typical skin pathogens.

Diffuse cellulitis is rare in studies from Australia [119], although it is more frequently reported in Asia [120]. Secondary skin infection characterized by multiple pustules due to systemic spread from a distant site has also been described, as has the uncommon spread of infection to subcutaneous tissues.

In an Australian series, cutaneous melioidosis is less likely to be associated with bacteremia than other forms and is more likely associated with a chronic presentation [79,119].

Genitourinary — Genitourinary melioidosis includes prostatic infection or abscess (image 4), kidney abscess, and urinary tract infection (figure 2). It presents with fever in association with suprapubic pain, dysuria, difficulty passing urine, or acute urinary retention requiring catheterization [121-123]. Diarrhea is a frequent additional complaint. On rectal exam, the prostate may be tender and boggy [123]. Prostatic abscess can also occur as a secondary manifestation in individuals who initially presented with a different site of involvement (eg, pneumonia).

Bacteremia — Bacteremia with B. pseudomallei can be primary (in the absence of a localized site of infection) or secondary (figure 2). In a study of 1148 individuals with culture-confirmed melioidosis identified over 30 years in the Northern Territory of Australia, bacteremia occurred in 633 (56 percent); 129 of those were cases of primary bacteremia without an evident focus of infection [79]. Such patients with primary bacteremia were commonly immunocompromised patients who presented with an acute febrile illness.

Less common sites of infection — Additional manifestations include bone and joint involvement, neurologic involvement, parenchymal abscesses, and parotitis. Rare foci of infection described in case reports or case series include mycotic aneurysms [32,124-129], mediastinal masses [32], pericardial collections (image 5) [10,26,130], and adrenal abscesses [26,131-133].

Septic arthritis or osteomyelitis — Bone and joint involvement is a relatively uncommon initial presentation of melioidosis (picture 4) [10,32,57,134,135]. Septic arthritis and osteomyelitis can also occur as a secondary manifestation in individuals who initially presented with a different site of involvement (eg, pneumonia).

In a retrospective review of 50 patients with B. pseudomallei septic arthritis or osteomyelitis in Australia, the lower limbs were the most commonly affected site, although cases occurred in the upper limbs, vertebra, and pelvis as well [136]. Twenty-eight percent of lower limb septic arthritis cases had accompanying osteomyelitis.

Neurologic involvement — Melioidosis can rarely cause encephalomyelitis (ie, meningoencephalitis) and meningitis, cerebral abscesses, myelitis, and epidural abscess. The type of neurologic manifestation may vary geographically. Encephalomyelitis due to melioidosis accounts for approximately 4 percent of melioidosis cases in northern Australia but is rarely described elsewhere; in Southeast Asia, cerebral abscess secondary to bacteremic seeding is the more common neurologic manifestation [53,137].

Encephalomyelitis associated with melioidosis primarily involves the brainstem; brainstem abscesses can also occur. Patients can present with unilateral upper motor neuron limb weakness, cerebellar signs, cranial nerve palsies (particularly VI, VII nerve palsy and bulbar palsy), or flaccid paraparesis [138,139]. Most have normal or near-normal consciousness on initial presentation. Cerebrospinal fluid (CSF) analysis demonstrates a predominantly monocytic pleocytosis (with white blood cell counts ranging from 30 to 775), elevated protein, and normal or slightly decreased glucose [138,139]. Culture of CSF is often negative. (See 'Culture' below.)

Computed tomography (CT) of the brain is typically normal in patients with encephalomyelitis associated with melioidosis; however, magnetic resonance imaging (MRI) usually reveals dramatic changes with extensive increased T2-weighted signal intensity in the brainstem (image 6). In the setting of flaccid paraparesis, similar changes may be observed in the spinal cord [139].

That melioidosis encephalomyelitis appears mostly restricted to cases in Australia may reflect regional genotypic differences between B. pseudomallei strains [140]. Animal studies suggest that brainstem infection can result from direct nerve root translocation of the bacteria from the nasal passages [141]. Similar nerve root translocation from skin sources has also been posited [95].

Abscesses within organs — Abscesses in internal organs are well recognized, especially in the spleen (where they are often multifocal), kidney, prostate (image 4), and liver (image 7) [10,26,57]. Fevers, chills, and rigors with and without hypotension are common, but localizing symptoms are often absent.

Parotitis — Suppurative parotitis is a common presentation of melioidosis in children in Thailand and Cambodia, accounting for up to 40 percent of cases among Thai children [92,93,142]. Children present with parotid pain accompanied by swelling and tenderness. Parotitis is far less common in Australia. Ingestion of water contaminated with B. pseudomallei may at least in part explain the higher rates of parotitis seen in parts of Southeast Asia [53,67].

True colonization is very uncommon — Patients with chronic lung disease and infection with B. pseudomallei who are not adequately treated may have residual respiratory infection following resolution of overt signs of disease. The majority of such cases manifest at least low-grade lung infection or disease elsewhere, and there is a significant risk of subsequent invasive disease [91,97,143]. With appropriate treatment, persisting infection is exceptionally uncommon, but true colonization with avirulent B. pseudomallei resulting from gene reduction has been described [144,145]. Therefore, isolation of B. pseudomallei from any clinical specimen generally warrants treatment.

Differential diagnosis — The differential diagnosis of melioidosis is broad and depends on the presenting features. As examples, acute pneumonia due to melioidosis could present similarly to other causes of community-acquired pneumonia (both bacterial and viral), chronic pulmonary infection often mimics tuberculosis, and skin involvement could be mistaken for staphylococcal or streptococcal skin and soft tissue infections. Multiple distinct sites of infection (eg, abscesses in multiple organs) should raise the possibility of Staphylococcus aureus or causes of other bacterial sepsis and disseminated infection.

The microbiologic differential diagnoses of clinical syndromes that have been associated with melioidosis are discussed elsewhere:

(See "Epidemiology, pathogenesis, and microbiology of community-acquired pneumonia in adults", section on 'Microbiology'.)

(See "Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis", section on 'Microbiology' and "Skin lesions in the returning traveler".)

(See "Acute bacterial prostatitis", section on 'Microbiology'.)

(See "Gram-negative bacillary bacteremia in adults", section on 'Microbiology'.)

(See "Clinical manifestations and complications of pulmonary tuberculosis", section on 'Differential diagnosis'.)


Clinical suspicion and diagnostic evaluation — The approach to diagnosis of melioidosis demonstrates the importance of the residence and travel history in the workup of infectious syndromes:

In endemic regions, melioidosis should be routinely considered part of the differential diagnosis of acute or chronic pneumonia, ulcerated or purulent skin lesions, undifferentiated sepsis, and prostatic abscesses; it should also be suspected as a potential cause of bone or joint infection, encephalomyelitis involving the brainstem and/or spinal cord, and cerebral or visceral abscesses. (See 'Historically endemic areas' above and 'Common manifestations' above.)

Outside of endemic regions, melioidosis should be suspected in individuals who present with one of these syndromes and have a history of travel to an endemic area or are from areas where cases are being increasingly reported, particularly if evaluation or treatment for other causes has not been informative. (See 'Cases elsewhere globally' above.)

The possibility of chronic melioidosis or, more rarely, (re)activation of latent melioidosis should also be considered in individuals with exposure to endemic areas who are being evaluated for suspected pulmonary tuberculosis.

For all such presentations, suspicion for melioidosis should be heightened in individuals with comorbidities that increase the likelihood of symptomatic infection, such as diabetes mellitus, hazardous alcohol use, and chronic kidney or lung disease. (See 'Comorbidities' above.)

When the possibility of melioidosis is suspected, we collect specimens from the following sites for microscopy and culture, the latter of which is the primary method of diagnosis [146] (see 'Culture' below):


Sputum (or other deep respiratory specimen)


Throat swab

Rectal swab

Swab from any ulcer or skin lesion

Pus/fluid from any drainable abscess or collection

Cerebrospinal fluid (CSF) from individuals with evidence of encephalitis or meningitis (although culture yield of CSF is low)

The likelihood of diagnosing melioidosis is maximized if appropriate clinical samples are obtained from symptomatic at-risk patients from a variety of sites and are sent to the microbiology laboratory for microscopy and culture. In the Northern Territory of Australia, a hyperendemic region, all cultures from blood, sputum, urine, and purulent drainage collected in both primary care clinics and hospitals during the wet season, when melioidosis cases peak, are routinely processed for B. pseudomallei detection [79].

B. pseudomallei grows readily in standard blood cultures, but in cultures from nonsterile sites, it can be overgrown by other organisms, including normal flora. Thus, use of selective media can be helpful to enhance organism recovery from those sites. Timely transport of specimens is important as organism viability decreases with low temperatures and desiccation [146]. If possible, sputum and swabs from skin lesions, throat, and rectum should be plated or inoculated directly onto selective media. The clinical laboratory should be made aware of the suspicion for melioidosis when specimens are submitted, particularly in nonendemic areas.

Serology is not generally useful in the diagnosis of melioidosis because of poor performance and lack of clear thresholds for diagnosis. (See 'Limited role of serology' below.)

Additional imaging to evaluate for other sites of infection — Most patients with suspected melioidosis who presented with pulmonary symptoms or sepsis will have already had chest imaging; we also perform chest radiograph in all other patients with suspected melioidosis. We also routinely perform computed tomographic (CT) scan of the abdomen and pelvis in all adult patients with confirmed or suspected melioidosis, if not already done, to evaluate for asymptomatic abscesses in the prostate (image 4), spleen, liver (image 7), and kidneys [25,116,123]. In children and adult females who are not systemically ill, abdominal ultrasound is a reasonable alternative to CT scan to avoid radiation exposure.

Confirming the diagnosis

Culture — Growth of B. pseudomallei from culture of any site is diagnostic of melioidosis [146]. Although prolonged “colonization” of the airways can occur in occasional situations, it is still likely reflective of a low-grade infection. (See 'True colonization is very uncommon' above.)

Blood cultures are positive for B. pseudomallei in 40 to 70 percent of individuals with melioidosis [118]. The organism grows in a wide range of commercially available blood culture media. With automated blood culture systems, almost all B. pseudomallei-positive specimens are detected within 48 hours [147]. However, such systems are less sensitive than conventional broth cultures; in one study, sensitivity for B. pseudomallei in blood culture was 74 percent for the automated system versus 90 percent with conventional culture, in which bacterial growth was detected by visualization [148].

B. pseudomallei grows well on MacConkey, blood, and chocolate agars. Using Ashdown agar, which contains gentamicin, or Ashdown liquid transport broth, which contains colistin, allows selective growth of B. pseudomallei and thus enhances recovery from sites where normal flora would have otherwise grown [149]. Alternative selective culture media have also been evaluated [150], but Ashdown remains the most commonly used in endemic areas.

Once an organism grows, identification of B. pseudomallei can be made by combining the commercial API 20NE or 20E biochemical kit with a simple screening system. This screening system includes Gram stain, the oxidase reaction, typical growth characteristics, and resistance to certain antibiotics [151,152]. B. pseudomallei is an oxidase-positive, non-lactose-fermenting, Gram-negative bacillus. Concerns have been raised about the low sensitivity of some biochemical tests and the potential for some commercial automated biochemical identification systems to misidentify the organism as other species, such as Burkholderia cepaciaBacillus spp, and Pseudomonas spp [6,153-157]. However, polymerase chain reaction (PCR) is being increasingly used for confirmation of bacterial isolates cultured from clinical samples [154], as is matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) [158]. Nevertheless, misidentification (eg, as Burkholderia thailandensis) has also been reported with MALDI-TOF MS [45]. With larger database profiles, B. pseudomallei is less frequently incorrectly identified as other Burkholderia species [159].

In patients with encephalomyelitis, culture of CSF is often negative; in such cases, the diagnosis is made by culture of B. pseudomallei from other sites in an individual with CSF leukocytosis and consistent findings on imaging. (See 'Neurologic involvement' above.)

When there is high suspicion for melioidosis but cultures are negative for B. pseudomallei, we recommend repeating cultures from potential foci of infection in addition to further imaging as clinically indicated based on presentation, and serial serology (see 'Limited role of serology' below). In rare circumstances, such as some cases of possible neurologic melioidosis, we make a presumptive diagnosis based on clinical suspicion despite negative cultures and treat as melioidosis, while acknowledging that isolation of B. pseudomallei on culture is required for a confirmed diagnosis.

Microscopy — Gram stain of sputum or purulent drainage from abscesses may demonstrate gram-negative bacilli. B. pseudomallei often has a characteristic bipolar staining with a "safety pin" appearance, particularly when the stain is performed from cultured isolates rather than directly from a clinical specimen (picture 5). However, the Gram stain appearance alone is not sufficient for diagnosis [118].

Limited role of serology — Serologic testing is not a reliable method of diagnosis. The indirect hemagglutination test (IHAT) and other serologic tests are available, but their utility remains limited, particularly in endemic areas [160,161].

Both sensitivity and specificity of IHAT are suboptimal [118,146]. In one study of patients with culture-confirmed melioidosis, serology was only positive at the time of presentation in approximately half, and approximately a quarter of those with longitudinal serologic testing did not seroconvert [162]. Conversely, significant background rates of antibodies to B. pseudomallei occur in healthy individuals in endemic areas, and there is no standardized threshold for titers suggestive of active infection [1,106,163]. Accuracy varies widely across different assays.

Several new enzyme-linked immunosorbent assays (ELISAs) targeting specific antigens, such as hemolysin co-regulated protein 1 (Hcp1) and O-polysaccharide (OPS), are being evaluated [164].

Other techniques — A variety of other antigen- and DNA-detection techniques have been used to increase the diagnostic yield, the rapidity of establishing a diagnosis, or to confirm isolate identity. However, most of these techniques are not yet commercially available [152,163,165-171].

Rapid immunofluorescence microscopy of pus, sputum, and urine has been useful in Thailand [172].

PCR has been evaluated but has historically not been sufficiently sensitive or specific for direct detection from clinical samples (eg, blood) [168,173,174]. It is being used more frequently to identify isolates that have grown on culture. (See 'Culture' above.)

A lateral flow immunoassay targeting capsular polysaccharide antigen shows promise for the rapid diagnosis of melioidosis directly from clinical samples and is also useful for confirming culture isolate identity [175-177].


Bacterial cause – Melioidosis is an infection caused by the facultative intracellular gram-negative bacterium Burkholderia pseudomallei. (See 'Introduction' above and 'Culture' above and 'Microscopy' above.)

Geographic distribution – Melioidosis occurs predominantly in the historically endemic regions: Southeast Asia, northern Australia, South Asia (including India), and China. Northeastern Thailand and parts of northern Australia are "hyperendemic," with seasonal peaks in the wet seasons. It has also occurred in non-travelers in other tropical and subtropical locations, such as Africa and the Americas (including Puerto Rico and the Gulf Coast of the United States), where the organism has been found in environmental samples. Elsewhere, infections primarily occur in travelers to endemic areas. (See 'Geographic distribution' above.)

TransmissionB. pseudomallei is transmitted predominantly through percutaneous exposure to wet season soils or contaminated water. During severe weather events, inhalation may be the primary mode of transmission. Ingestion of unchlorinated water supplies is another potential route. Person-to-person transmission is highly unusual. (See 'Transmission' above and 'Exposure risk' above.)

Spectrum of illness – Most B. pseudomallei infections are likely asymptomatic or subclinical. Most symptomatic infections present acutely and are associated with significant morbidity (figure 2). Severe clinical disease occurs mainly in adults with certain comorbidities (diabetes mellitus, hazardous alcohol use, chronic kidney and lung disease). (See 'Spectrum and time course of infection' above and 'Comorbidities' above and 'Impact of age on clinical presentation' above.)

Clinical features – Pneumonia is the most common clinical presentation of both acute (image 1 and image 2) and chronic (image 3) melioidosis in adults (figure 2). Skin infections, including ulcers (picture 2), abscesses, and macular lesions (picture 3), are also common. Genitourinary infection consists mainly of prostatic abscesses. Overall, bacteremia occurs in around half of cases, and septic shock in up to a quarter. (See 'Common manifestations' above.)

Less commonly, melioidosis can also present with a variety of clinical manifestations, including bone and joint infection, neurologic infection, and abscesses in visceral organs, generally due to bacteremic spread (figure 2). (See 'Less common sites of infection' above.)

Diagnostic evaluation – When melioidosis is suspected (consistent clinical syndromes in residents of or travelers from endemic areas), we suggest sending blood, sputum, urine, and throat and rectal swabs for microscopy and culture. We also send pus or swabs from any ulcer or skin lesions, drainable abscesses, and, in individuals with central nervous system abnormalities, cerebrospinal fluid (CSF). The laboratory should be notified of the clinical suspicion for melioidosis. We also obtain abdominal imaging to identify additional sites of infection. (See 'Clinical suspicion and diagnostic evaluation' above and 'Additional imaging to evaluate for other sites of infection' above.)

Microbiologic diagnosis – Growth of B. pseudomallei from culture of any site is diagnostic of melioidosis. On microscopy, the gram-negative bacillus often has a characteristic bipolar staining with a "safety pin" appearance. Serologic testing is not a reliable method of diagnosis, and other techniques are not widely available. (See 'Confirming the diagnosis' above.)

  1. White NJ. Melioidosis. Lancet 2003; 361:1715.
  2. Cheng AC, Currie BJ. Melioidosis: epidemiology, pathophysiology, and management. Clin Microbiol Rev 2005; 18:383.
  3. Wiersinga WJ, Currie BJ, Peacock SJ. Melioidosis. N Engl J Med 2012; 367:1035.
  4. Wiersinga WJ, Virk HS, Torres AG, et al. Melioidosis. Nat Rev Dis Primers 2018; 4:17107.
  5. Dance DA. Ecology of Burkholderia pseudomallei and the interactions between environmental Burkholderia spp. and human-animal hosts. Acta Trop 2000; 74:159.
  6. Dance DB. Melioidosis. Reviews Med Microbiol 1990; 1:143.
  7. Dance DA. Melioidosis: the tip of the iceberg? Clin Microbiol Rev 1991; 4:52.
  8. Dance DA. Melioidosis as an emerging global problem. Acta Trop 2000; 74:115.
  9. Currie BJ, Dance DA, Cheng AC. The global distribution of Burkholderia pseudomallei and melioidosis: an update. Trans R Soc Trop Med Hyg 2008; 102 Suppl 1:S1.
  10. Punyagupta S. Melioidosis. Review of 686 cases and presentation of a new clinical classification. In: Melioidosis, Punyagupta S, Sirisanthana T, Stapatayavong B (Eds), Bangkok Medical Publisher, Bangkok 1989.
  11. Chaowagul W, White NJ, Dance DA, et al. Melioidosis: a major cause of community-acquired septicemia in northeastern Thailand. J Infect Dis 1989; 159:890.
  12. Vuddhakul V, Tharavichitkul P, Na-Ngam N, et al. Epidemiology of Burkholderia pseudomallei in Thailand. Am J Trop Med Hyg 1999; 60:458.
  13. Leelarasamee A. Melioidosis in Southeast Asia. Acta Trop 2000; 74:129.
  14. Puthucheary SD, Lin HP, Yap PK. Acute septicaemic melioidosis: a report of seven cases. Trop Geogr Med 1981; 33:19.
  15. Puthucheary SD, Parasakthi N, Lee MK. Septicaemic melioidosis: a review of 50 cases from Malaysia. Trans R Soc Trop Med Hyg 1992; 86:683.
  16. Vadivelu J, Puthucheary SD, Mifsud A, et al. Ribotyping and DNA macrorestriction analysis of isolates of Burkholderia pseudomallei from cases of melioidosis in Malaysia. Trans R Soc Trop Med Hyg 1997; 91:358.
  17. Hassan MR, Pani SP, Peng NP, et al. Incidence, risk factors and clinical epidemiology of melioidosis: a complex socio-ecological emerging infectious disease in the Alor Setar region of Kedah, Malaysia. BMC Infect Dis 2010; 10:302.
  18. Chan KW, Jayaratnam FJ, Teo SK. Acute septicaemic melioidosis. A report of three fatal cases. Singapore Med J 1985; 26:382.
  19. Tan AL, Ang BS, Ong YY. Melioidosis: epidemiology and antibiogram of cases in Singapore. Singapore Med J 1990; 31:335.
  20. Yap EH, Chan YC, Goh KT, et al. Sudden unexplained death syndrome--a new manifestation in melioidosis? Epidemiol Infect 1991; 107:577.
  21. Yap EH, Thong TW, Tan AL, et al. Comparison of Pseudomonas pseudomallei from humans, animals, soil and water by restriction endonuclease analysis. Singapore Med J 1995; 36:60.
  22. Singapore Committee on Epidemic Diseases: Melioidosis in Singapore. Epidemiological News Bulletin 1995; 21:69.
  23. Lim MK, Tan EH, Soh CS, Chang TL. Burkholderia pseudomallei infection in the Singapore Armed Forces from 1987 to 1994--an epidemiological review. Ann Acad Med Singapore 1997; 26:13.
  24. Lo TJ, Ang LW, James L, Goh KT. Melioidosis in a tropical city state, Singapore. Emerg Infect Dis 2009; 15:1645.
  25. Currie BJ, Fisher DA, Howard DM, et al. The epidemiology of melioidosis in Australia and Papua New Guinea. Acta Trop 2000; 74:121.
  26. Currie BJ, Fisher DA, Howard DM, et al. Endemic melioidosis in tropical northern Australia: a 10-year prospective study and review of the literature. Clin Infect Dis 2000; 31:981.
  27. Malczewski AB, Oman KM, Norton RE, Ketheesan N. Clinical presentation of melioidosis in Queensland, Australia. Trans R Soc Trop Med Hyg 2005; 99:856.
  28. Warner J, Learoyd D, Pelowa D, et al. Melioidosis in the Western Province of Papua New Guinea. In: Annual Scientific Meeting, Medical Society of Papua New Guinea, Port Moresby 1998.
  29. Le Hello S, Currie BJ, Godoy D, et al. Melioidosis in New Caledonia. Emerg Infect Dis 2005; 11:1607.
  30. Limmathurotsakul D, Wongratanacheewin S, Teerawattanasook N, et al. Increasing incidence of human melioidosis in Northeast Thailand. Am J Trop Med Hyg 2010; 82:1113.
  31. Saravu K, Mukhopadhyay C, Vishwanath S, et al. Melioidosis in southern India: epidemiological and clinical profile. Southeast Asian J Trop Med Public Health 2010; 41:401.
  32. Currie BJ, Ward L, Cheng AC. The epidemiology and clinical spectrum of melioidosis: 540 cases from the 20 year Darwin prospective study. PLoS Negl Trop Dis 2010; 4:e900.
  33. Mohapatra PR, Mishra B. Burden of melioidosis in India and South Asia: Challenges and ways forward. Lancet Reg Health Southeast Asia 2022; 2:100004.
  34. Saïdani N, Griffiths K, Million M, et al. Melioidosis as a travel-associated infection: Case report and review of the literature. Travel Med Infect Dis 2015; 13:367.
  35. Dan M. Melioidosis in Travelers: Review of the Literature. J Travel Med 2015; 22:410.
  36. Dance DA. Editorial commentary: melioidosis in Puerto Rico: the iceberg slowly emerges. Clin Infect Dis 2015; 60:251.
  37. Currie BJ. Melioidosis and Burkholderia pseudomallei : progress in epidemiology, diagnosis, treatment and vaccination. Curr Opin Infect Dis 2022; 35:517.
  38. Melioidosis Locally Endemic in Areas of the Mississippi Gulf Coast after Burkholderia pseudomallei Isolated in Soil and Water and Linked to Two Cases – Mississippi, 2020 and 2022. July 27, 2022. (Accessed on August 01, 2022).
  39. Cossaboom CM, Marinova-Petkova A, Strysko J, et al. Melioidosis in a Resident of Texas with No Recent Travel History, United States. Emerg Infect Dis 2020; 26:1295.
  40. Limmathurotsakul D, Golding N, Dance DA, et al. Predicted global distribution of Burkholderia pseudomallei and burden of melioidosis. Nat Microbiol 2016; 1:15008.
  41. Hall CM, Jaramillo S, Jimenez R, et al. Burkholderia pseudomallei, the causative agent of melioidosis, is rare but ecologically established and widely dispersed in the environment in Puerto Rico. PLoS Negl Trop Dis 2019; 13:e0007727.
  42. Doker TJ, Sharp TM, Rivera-Garcia B, et al. Contact investigation of melioidosis cases reveals regional endemicity in Puerto Rico. Clin Infect Dis 2015; 60:243.
  43. Centers for Disease Control and Prevention. Statement on Melioidosis Cases, August 2021. (Accessed on August 18, 2021).
  44. Centers for Disease Control and Prevention. Source Implicated in Fatal Case in Georgia: CDC Health Alert Network. Multistate Outbreak of Non-travel Associated Burkholderia pseudomallei Infections (Melioidosis) in Four Patients: Georgia, Kansas, Minnesota, and Texas–2021. (Accessed on November 09, 2021).
  45. Gee JE, Bower WA, Kunkel A, et al. Multistate Outbreak of Melioidosis Associated with Imported Aromatherapy Spray. N Engl J Med 2022; 386:861.
  46. Benoit TJ, Blaney DD, Gee JE, et al. Melioidosis Cases and Selected Reports of Occupational Exposures to Burkholderia pseudomallei--United States, 2008-2013. MMWR Surveill Summ 2015; 64:1.
  47. Stewart T, Engelthaler DM, Blaney DD, et al. Epidemiology and investigation of melioidosis, Southern Arizona. Emerg Infect Dis 2011; 17:1286.
  48. Miralles IS, Maciel Mdo C, Angelo MR, et al. Burkholderia pseudomallei: a case report of a human infection in Ceará, Brazil. Rev Inst Med Trop Sao Paulo 2004; 46:51.
  49. Rolim DB, Vilar DC, Sousa AQ, et al. Melioidosis, northeastern Brazil. Emerg Infect Dis 2005; 11:1458.
  50. Inglis TJ, Rolim DB, Sousa Ade Q. Melioidosis in the Americas. Am J Trop Med Hyg 2006; 75:947.
  51. Gee JE, Gulvik CA, Elrod MG, et al. Phylogeography of Burkholderia pseudomallei Isolates, Western Hemisphere. Emerg Infect Dis 2017; 23:1133.
  52. Birnie E, James A, Peters F, et al. Melioidosis in Africa: Time to Raise Awareness and Build Capacity for Its Detection, Diagnosis, and Treatment. Am J Trop Med Hyg 2022; 106:394.
  53. Currie BJ. Melioidosis: evolving concepts in epidemiology, pathogenesis, and treatment. Semin Respir Crit Care Med 2015; 36:111.
  54. Sarovich DS, Garin B, De Smet B, et al. Phylogenomic Analysis Reveals an Asian Origin for African Burkholderia pseudomallei and Further Supports Melioidosis Endemicity in Africa. mSphere 2016; 1.
  55. Chewapreecha C, Holden MT, Vehkala M, et al. Global and regional dissemination and evolution of Burkholderia pseudomallei. Nat Microbiol 2017; 2:16263.
  56. Currie BJ, Kaestli M. Epidemiology: A global picture of melioidosis. Nature 2016; 529:290.
  57. Leelarasamee A, Bovornkitti S. Melioidosis: review and update. Rev Infect Dis 1989; 11:413.
  58. Brundage WG, Thuss CJ Jr, Walden DC. Four fatal cases of melioidosis in U. S. soldiers in Vietnam. Bacteriologic and pathologic characteristics. Am J Trop Med Hyg 1968; 17:183.
  59. Mackowiak PA, Smith JW. Septicemic melioidosis. Occurrence following acute influenza A six years after exposure in Vietnam. JAMA 1978; 240:764.
  60. Howe C, Sampath A, Spotnitz M. The pseudomallei group: a review. J Infect Dis 1971; 124:598.
  61. Currie BJ, Jacups SP. Intensity of rainfall and severity of melioidosis, Australia. Emerg Infect Dis 2003; 9:1538.
  62. Chierakul W, Winothai W, Wattanawaitunechai C, et al. Melioidosis in 6 tsunami survivors in southern Thailand. Clin Infect Dis 2005; 41:982.
  63. Allworth AM. Tsunami lung: a necrotising pneumonia in survivors of the Asian tsunami. Med J Aust 2005; 182:364.
  64. Athan E, Allworth AM, Engler C, et al. Melioidosis in tsunami survivors. Emerg Infect Dis 2005; 11:1638.
  65. Cottew GS, Sutherland AK, Meehan JF. Melioidosis in sheep in Queensland. Aust Vet J 1952; :113.
  66. Ketterer PJ, Webster WR, Shield J, et al. Melioidosis in intensive piggeries in south eastern Queensland. Aust Vet J 1986; 63:146.
  67. Limmathurotsakul D, Kanoksil M, Wuthiekanun V, et al. Activities of daily living associated with acquisition of melioidosis in northeast Thailand: a matched case-control study. PLoS Negl Trop Dis 2013; 7:e2072.
  68. Kunakorn M, Jayanetra P, Tanphaichitra D. Man-to-man transmission of melioidosis. Lancet 1991; 337:1290.
  69. Ralph A, McBride J, Currie BJ. Transmission of Burkholderia pseudomallei via breast milk in northern Australia. Pediatr Infect Dis J 2004; 23:1169.
  70. Webling DD. Genito-urinary infections with Pseudomonas pseudomallei in Australian Aboriginals. Trans R Soc Trop Med Hyg 1980; 74:138.
  71. McCormick JB, Sexton DJ, McMurray JG, et al. Human-to-human transmission of Pseudomonas pseudomallei. Ann Intern Med 1975; 83:512.
  72. Green RN, Tuffnell PG. Laboratory acquired melioidosis. Am J Med 1968; 44:599.
  73. Ashdown LR. Nosocomial infection due to Pseudomonas pseudomallei: two cases and an epidemiologic study. Rev Infect Dis 1979; 1:891.
  74. Schlech WF 3rd, Turchik JB, Westlake RE Jr, et al. Laboratory-acquired infection with Pseudomonas pseudomallei (melioidosis). N Engl J Med 1981; 305:1133.
  75. Sookpranee M, Lumbiganon P, Puapermpoonsiri S, et al. Contamination of Savlon solution with Pseudomonas pseudomallei at Srinagarind Hospital. In: Melioidosis, Punyagupta S, Sirisanthana T, Stapatayavong B (Eds), Bangkok Medical Publisher, Bangkok 1989.
  76. Sookpranee M, Lumbiganon P, Boonma P. Nosocomial contamination of Pseudomonas pseudomallei in the patients at Srinagarind Hospital. In: Melioidosis, Punyagupta S, Sirisanthana T, Stapatayavong B (Eds), Bangkok Medical Publisher, Bangkok 1989.
  77. Choy JL, Mayo M, Janmaat A, Currie BJ. Animal melioidosis in Australia. Acta Trop 2000; 74:153.
  78. Stanton AT, Fletcher W. Melioidosis, John Bale and Danielson Ltd, London 1932. Vol 21.
  79. Currie BJ, Mayo M, Ward LM, et al. The Darwin Prospective Melioidosis Study: a 30-year prospective, observational investigation. Lancet Infect Dis 2021; 21:1737.
  80. Suputtamongkol Y, Chaowagul W, Chetchotisakd P, et al. Risk factors for melioidosis and bacteremic melioidosis. Clin Infect Dis 1999; 29:408.
  81. Suputtamongkol Y, Hall AJ, Dance DA, et al. The epidemiology of melioidosis in Ubon Ratchatani, northeast Thailand. Int J Epidemiol 1994; 23:1082.
  82. Currie BJ, Jacups SP, Cheng AC, et al. Melioidosis epidemiology and risk factors from a prospective whole-population study in northern Australia. Trop Med Int Health 2004; 9:1167.
  83. Guard RW, Khafagi FA, Brigden MC, Ashdown LR. Melioidosis in Far North Queensland. A clinical and epidemiological review of twenty cases. Am J Trop Med Hyg 1984; 33:467.
  84. Limmathurotsakul D, Chaowagul W, Chierakul W, et al. Risk factors for recurrent melioidosis in northeast Thailand. Clin Infect Dis 2006; 43:979.
  85. Ruchin P, Robinson J, Segasothy M, Morey F. Melioidosis in a patient with idiopathic pulmonary haemosiderosis resident in Central Australia. Aust N Z J Med 2000; 30:395.
  86. Tarlow MJ, Lloyd J. Melioidosis and chronic granulomatous disease. Proc R Soc Med 1971; 64:19.
  87. Dance DA, Smith MD, Aucken HM, Pitt TL. Imported melioidosis in England and Wales. Lancet 1999; 353:208.
  88. Visca P, Cazzola G, Petrucca A, Braggion C. Travel-associated Burkholderia pseudomallei infection (Melioidosis) in a patient with cystic fibrosis: a case report. Clin Infect Dis 2001; 32:E15.
  89. Holland DJ, Wesley A, Drinkovic D, Currie BJ. Cystic Fibrosis and Burkholderia pseudomallei Infection: An Emerging Problem? Clin Infect Dis 2002; 35:e138.
  90. O'Carroll MR, Kidd TJ, Coulter C, et al. Burkholderia pseudomallei: another emerging pathogen in cystic fibrosis. Thorax 2003; 58:1087.
  91. Geake JB, Reid DW, Currie BJ, et al. An international, multicentre evaluation and description of Burkholderia pseudomallei infection in cystic fibrosis. BMC Pulm Med 2015; 15:116.
  92. Dance DA, Davis TM, Wattanagoon Y, et al. Acute suppurative parotitis caused by Pseudomonas pseudomallei in children. J Infect Dis 1989; 159:654.
  93. Lumbiganon P, Viengnondha S. Clinical manifestations of melioidosis in children. Pediatr Infect Dis J 1995; 14:136.
  94. Edmond K, Currie B, Brewster D, Kilburn C. Pediatric melioidosis in tropical Australia. Pediatr Infect Dis J 1998; 17:77.
  95. McLeod C, Morris PS, Bauert PA, et al. Clinical presentation and medical management of melioidosis in children: a 24-year prospective study in the Northern Territory of Australia and review of the literature. Clin Infect Dis 2015; 60:21.
  96. Fong SM, Wong KJ, Fukushima M, Yeo TW. Thalassemia major is a major risk factor for pediatric melioidosis in Kota Kinabalu, Sabah, Malaysia. Clin Infect Dis 2015; 60:1802.
  97. Currie BJ, Fisher DA, Anstey NM, Jacups SP. Melioidosis: acute and chronic disease, relapse and re-activation. Trans R Soc Trop Med Hyg 2000; 94:301.
  98. Bovornkitti S, Leelarasamee A, Thamlikitkul V. Melioidosis. Arch Monaldi 1985; 40:203.
  99. Achana V, Silpapojakul K, Thininta W, Kalnaowakul S. Acute Pseudomonas pseudomallei pneumonia and septicemia following aspiration of contaminated water: a case report. Southeast Asian J Trop Med Public Health 1985; 16:500.
  100. Lee N, Wu JL, Lee CH, Tsai WC. Pseudomonas pseudomallei infection from drowning: the first reported case in Taiwan. J Clin Microbiol 1985; 22:352.
  101. Cheng AC, Wuthiekanun V, Limmathurotsakul D, et al. Intensity of exposure and incidence of melioidosis in Thai children. Trans R Soc Trop Med Hyg 2008; 102 Suppl 1:S37.
  103. Strauss JM, Alexander AD, Rapmund G, et al. Melioidosis in Malaysia. 3. Antibodies to Pseudomonas pseudomallei in the human population. Am J Trop Med Hyg 1969; 18:703.
  104. Ashdown LR, Guard RW. The prevalence of human melioidosis in Northern Queensland. Am J Trop Med Hyg 1984; 33:474.
  105. Kanaphun P, Thirawattanasuk N, Suputtamongkol Y, et al. Serology and carriage of Pseudomonas pseudomallei: a prospective study in 1000 hospitalized children in northeast Thailand. J Infect Dis 1993; 167:230.
  106. Wuthiekanun V, Chierakul W, Langa S, et al. Development of antibodies to Burkholderia pseudomallei during childhood in melioidosis-endemic northeast Thailand. Am J Trop Med Hyg 2006; 74:1074.
  107. Koshy M, Jagannati M, Ralph R, et al. Clinical Manifestations, Antimicrobial Drug Susceptibility Patterns, and Outcomes in Melioidosis Cases, India. Emerg Infect Dis 2019; 25:316.
  108. Chodimella U, Hoppes WL, Whalen S, et al. Septicemia and suppuration in a Vietnam veteran. Hosp Pract (1995) 1997; 32:219.
  109. Mays EE, Ricketts EA. Melioidosis: recrudescence associated with bronchogenic carcinoma twenty-six years following initial geographic exposure. Chest 1975; 68:261.
  110. Newland RC. Chronic melioidosis: a case in Sydney. Pathology 1969; 1:149.
  111. Kingston CW. Chronic or latent melioidosis. Med J Aust 1971; 2:618.
  112. Clayton AJ, Lisella RS, Martin DG. Melioidosis: a serological survey in military personnel. Mil Med 1973; 138:24.
  113. Birnie E, Virk HS, Savelkoel J, et al. Global burden of melioidosis in 2015: a systematic review and data synthesis. Lancet Infect Dis 2019; 19:892.
  114. Thatrimontrichai A, Maneenil G. Neonatal melioidosis: systematic review of the literature. Pediatr Infect Dis J 2012; 31:1195.
  115. Meumann EM, Cheng AC, Ward L, Currie BJ. Clinical features and epidemiology of melioidosis pneumonia: results from a 21-year study and review of the literature. Clin Infect Dis 2012; 54:362.
  116. Tan AP, Pui MH, Tan LK. Imaging patterns in melioidosis. Australas Radiol 1995; 39:260.
  117. Chong VF, Fan YF. The radiology of melioidosis. Australas Radiol 1996; 40:244.
  118. Gassiep I, Armstrong M, Norton R. Human Melioidosis. Clin Microbiol Rev 2020; 33.
  119. Gibney KB, Cheng AC, Currie BJ. Cutaneous melioidosis in the tropical top end of Australia: a prospective study and review of the literature. Clin Infect Dis 2008; 47:603.
  120. Zueter A, Yean CY, Abumarzouq M, et al. The epidemiology and clinical spectrum of melioidosis in a teaching hospital in a North-Eastern state of Malaysia: a fifteen-year review. BMC Infect Dis 2016; 16:333.
  121. Kan SK, Kay RW. Melioidosis presenting as prostatitis--a case report from Sabah. Trans R Soc Trop Med Hyg 1978; 72:522.
  122. Woo ML, Chan PS, French GL. A case of melioidosis presenting with prostatic abscess in Hong Kong. J Urol 1987; 137:120.
  123. Morse LP, Moller CC, Harvey E, et al. Prostatic abscess due to Burkholderia pseudomallei: 81 cases from a 19-year prospective melioidosis study. J Urol 2009; 182:542.
  124. Steinmetz I, Stosiek P, Hergenröther D, Bär W. Melioidosis causing a mycotic aneurysm. Lancet 1996; 347:1564.
  125. Lee SS, Liu YC, Wang JH, Wann SR. Mycotic aneurysm due to Burkholderia pseudomallei. Clin Infect Dis 1998; 26:1013.
  126. Torrens JK, McWhinney PH, Tompkins DS. A deadly thorn: a case of imported melioidosis. Lancet 1999; 353:1016.
  127. Low JG, Quek AM, Sin YK, Ang BS. Mycotic aneurysm due to Burkholderia pseudomallei infection: case reports and literature review. Clin Infect Dis 2005; 40:193.
  128. Anunnatsiri S, Chetchotisakd P, Kularbkaew C. Mycotic aneurysm in Northeast Thailand: the importance of Burkholderia pseudomallei as a causative pathogen. Clin Infect Dis 2008; 47:1436.
  129. Amezyane T, Lecoules S, Algayres JP. Mycotic iliac aneurysm associated with Burkholderia pseudomallei. Int J Infect Dis 2010; 14 Suppl 3:e381.
  130. Ruff MJ, Lamkin N Jr, Braun J, Barnwell P. Melioidosis complicated by pericarditis. Chest 1976; 69:227.
  131. Osteraas GR, Hardman JM, Bass JW, Wilson C. Neonatal melioidosis. Am J Dis Child 1971; 122:446.
  132. Weber DR, Douglass LE, Brundage WG, Stallkamp TC. Acute varieties of melioidosis occurring in U. S. soldiers in Vietnam. Am J Med 1969; 46:234.
  133. Lee SC, Ling TS, Chen JC, et al. Melioidosis with adrenal gland abscess. Am J Trop Med Hyg 1999; 61:34.
  134. Subhadrabandhu T, Prichasuk S, Sathapatayavongs B. Localised melioidotic osteomyelitis. J Bone Joint Surg Br 1995; 77:445.
  135. Popoff I, Nagamori J, Currie B. Melioidotic osteomyelitis in northern Australia. Aust N Z J Surg 1997; 67:692.
  136. Shetty RP, Mathew M, Smith J, et al. Management of melioidosis osteomyelitis and septic arthritis. Bone Joint J 2015; 97-B:277.
  137. Chadwick DR, Ang B, Sitoh YY, Lee CC. Cerebral melioidosis in Singapore: a review of five cases. Trans R Soc Trop Med Hyg 2002; 96:72.
  138. Woods ML 2nd, Currie BJ, Howard DM, et al. Neurological melioidosis: seven cases from the Northern Territory of Australia. Clin Infect Dis 1992; 15:163.
  139. Currie BJ, Fisher DA, Howard DM, Burrow JN. Neurological melioidosis. Acta Trop 2000; 74:145.
  140. Sarovich DS, Price EP, Webb JR, et al. Variable virulence factors in Burkholderia pseudomallei (melioidosis) associated with human disease. PLoS One 2014; 9:e91682.
  141. St John JA, Walkden H, Nazareth L, et al. Burkholderia pseudomallei Rapidly Infects the Brain Stem and Spinal Cord via the Trigeminal Nerve after Intranasal Inoculation. Infect Immun 2016; 84:2681.
  142. Pagnarith Y, Kumar V, Thaipadungpanit J, et al. Emergence of pediatric melioidosis in Siem Reap, Cambodia. Am J Trop Med Hyg 2010; 82:1106.
  143. Jenney AW, Lum G, Fisher DA, Currie BJ. Antibiotic susceptibility of Burkholderia pseudomallei from tropical northern Australia and implications for therapy of melioidosis. Int J Antimicrob Agents 2001; 17:109.
  144. Price EP, Sarovich DS, Mayo M, et al. Within-host evolution of Burkholderia pseudomallei over a twelve-year chronic carriage infection. MBio 2013; 4.
  145. Pearson T, Sahl JW, Hepp CM, et al. Pathogen to commensal? Longitudinal within-host population dynamics, evolution, and adaptation during a chronic >16-year Burkholderia pseudomallei infection. PLoS Pathog 2020; 16:e1008298.
  146. Hoffmaster AR, AuCoin D, Baccam P, et al. Melioidosis diagnostic workshop, 2013. Emerg Infect Dis 2015; 21.
  147. Tiangpitayakorn C, Songsivilai S, Piyasangthong N, Dharakul T. Speed of detection of Burkholderia pseudomallei in blood cultures and its correlation with the clinical outcome. Am J Trop Med Hyg 1997; 57:96.
  148. Teerawattanasook N, Limmathurotsakul D, Day NPJ, Wuthiekanun V. Short report: Failure of Burkholderia pseudomallei to grow in an automated blood culture system. Am J Trop Med Hyg 2014; 91:1173.
  149. Ashdown LR. An improved screening technique for isolation of Pseudomonas pseudomallei from clinical specimens. Pathology 1979; 11:293.
  150. Peacock SJ, Chieng G, Cheng AC, et al. Comparison of Ashdown's medium, Burkholderia cepacia medium, and Burkholderia pseudomallei selective agar for clinical isolation of Burkholderia pseudomallei. J Clin Microbiol 2005; 43:5359.
  151. Dance DA, Wuthiekanun V, Naigowit P, White NJ. Identification of Pseudomonas pseudomallei in clinical practice: use of simple screening tests and API 20NE. J Clin Pathol 1989; 42:645.
  152. Steinmetz I, Reganzerowski A, Brenneke B, et al. Rapid identification of Burkholderia pseudomallei by latex agglutination based on an exopolysaccharide-specific monoclonal antibody. J Clin Microbiol 1999; 37:225.
  153. Glass MB, Popovic T. Preliminary evaluation of the API 20NE and RapID NF plus systems for rapid identification of Burkholderia pseudomallei and B. mallei. J Clin Microbiol 2005; 43:479.
  154. Inglis TJ, Merritt A, Chidlow G, et al. Comparison of diagnostic laboratory methods for identification of Burkholderia pseudomallei. J Clin Microbiol 2005; 43:2201.
  155. Lowe P, Engler C, Norton R. Comparison of automated and nonautomated systems for identification of Burkholderia pseudomallei. J Clin Microbiol 2002; 40:4625.
  156. Amornchai P, Chierakul W, Wuthiekanun V, et al. Accuracy of Burkholderia pseudomallei identification using the API 20NE system and a latex agglutination test. J Clin Microbiol 2007; 45:3774.
  157. Podin Y, Kaestli M, McMahon N, et al. Reliability of automated biochemical identification of Burkholderia pseudomallei is regionally dependent. J Clin Microbiol 2013; 51:3076.
  158. Cunningham SA, Patel R. Importance of using Bruker's security-relevant library for Biotyper identification of Burkholderia pseudomallei, Brucella species, and Francisella tularensis. J Clin Microbiol 2013; 51:1639.
  159. Suttisunhakul V, Pumpuang A, Ekchariyawat P, et al. Matrix-assisted laser desorption/ionization time-of-flight mass spectrometry for the identification of Burkholderia pseudomallei from Asia and Australia and differentiation between Burkholderia species. PLoS One 2017; 12:e0175294.
  160. Cheng AC, O'brien M, Freeman K, et al. Indirect hemagglutination assay in patients with melioidosis in northern Australia. Am J Trop Med Hyg 2006; 74:330.
  161. Pumpuang A, Dunachie SJ, Phokrai P, et al. Comparison of O-polysaccharide and hemolysin co-regulated protein as target antigens for serodiagnosis of melioidosis. PLoS Negl Trop Dis 2017; 11:e0005499.
  162. Harris PN, Ketheesan N, Owens L, Norton RE. Clinical features that affect indirect-hemagglutination-assay responses to Burkholderia pseudomallei. Clin Vaccine Immunol 2009; 16:924.
  163. Sirisinha S, Anuntagool N, Dharakul T, et al. Recent developments in laboratory diagnosis of melioidosis. Acta Trop 2000; 74:235.
  164. Pumpuang A, Phunpang R, Ekchariyawat P, et al. Distinct classes and subclasses of antibodies to hemolysin co-regulated protein 1 and O-polysaccharide and correlation with clinical characteristics of melioidosis patients. Sci Rep 2019; 9:13972.
  165. Zysk G, Splettstösser WD, Neubauer H. A review on melioidosis with special respect on molecular and immunological diagnostic techniques. Clin Lab 2000; 46:119.
  166. Anuntagool N, Naigowit P, Petkanchanapong V, et al. Monoclonal antibody-based rapid identification of Burkholderia pseudomallei in blood culture fluid from patients with community-acquired septicaemia. J Med Microbiol 2000; 49:1075.
  167. Samosornsuk N, Lulitanond A, Saenla N, et al. Short report: evaluation of a monoclonal antibody-based latex agglutination test for rapid diagnosis of septicemic melioidosis. Am J Trop Med Hyg 1999; 61:735.
  168. Haase A, Brennan M, Barrett S, et al. Evaluation of PCR for diagnosis of melioidosis. J Clin Microbiol 1998; 36:1039.
  169. Anuntagool A, Intachote P, Naigowit P, Sirisinha S. Rapid antigen detection assay for identification of Burkholderia (Pseudomonas) pseudomallei infection. J Clin Microbiol 1996; 34:975.
  170. Smith MD, Wuthiekanun V, Walsh AL, et al. Latex agglutination for rapid detection of Pseudomonas pseudomallei antigen in urine of patients with melioidosis. J Clin Pathol 1995; 48:174.
  171. Schully KL, Young CC, Mayo M, et al. Next-generation Diagnostics for Melioidosis: Evaluation of a Prototype i-STAT Cartridge to Detect Burkholderia pseudomallei Biomarkers. Clin Infect Dis 2019; 69:421.
  172. Wuthiekanun V, Desakorn V, Wongsuvan G, et al. Rapid immunofluorescence microscopy for diagnosis of melioidosis. Clin Diagn Lab Immunol 2005; 12:555.
  173. Meumann EM, Novak RT, Gal D, et al. Clinical evaluation of a type III secretion system real-time PCR assay for diagnosing melioidosis. J Clin Microbiol 2006; 44:3028.
  174. Chantratita N, Meumann E, Thanwisai A, et al. Loop-mediated isothermal amplification method targeting the TTS1 gene cluster for detection of Burkholderia pseudomallei and diagnosis of melioidosis. J Clin Microbiol 2008; 46:568.
  175. Houghton RL, Reed DE, Hubbard MA, et al. Development of a prototype lateral flow immunoassay (LFI) for the rapid diagnosis of melioidosis. PLoS Negl Trop Dis 2014; 8:e2727.
  176. Robertson G, Sorenson A, Govan B, et al. Rapid diagnostics for melioidosis: a comparative study of a novel lateral flow antigen detection assay. J Med Microbiol 2015; 64:845.
  177. Woods KL, Boutthasavong L, NicFhogartaigh C, et al. Evaluation of a Rapid Diagnostic Test for Detection of Burkholderia pseudomallei in the Lao People's Democratic Republic. J Clin Microbiol 2018; 56.
Topic 3146 Version 25.0