Melioidosis.

Melioidosis is a tropical bacterial infection caused by Burkholderia pseudomallei, a soil and water organism endemic in northern Australia, Southeast Asia, the Indian subcontinent, and increasingly Africa and the Americas. It causes pneumonia, abscesses, and septicemia and is responsible for an estimated 89,000 deaths per year worldwide. Most patients have diabetes as a predisposing condition.

Melioidosis is acquired by skin contact with contaminated soil or water (through cuts and abrasions), by inhaling aerosolized soil during storms, or by drinking contaminated water. Person-to-person transmission is extremely rare. Most cases occur in agricultural workers, soldiers, and travelers in endemic tropical regions, particularly during monsoon.

Person-to-person transmission of melioidosis is very rare. Documented cases include occasional perinatal transmission and laboratory-acquired infection from handling cultures. Standard hospital isolation precautions are sufficient for patients; close contacts are not at increased risk in everyday life.

Melioidosis can present in many ways. Most common are fever, cough, and pneumonia; many patients also develop skin abscesses, urinary symptoms, joint pain, or septic shock. Symptoms can develop over days to weeks. Diabetes, kidney disease, or recent travel to a tropical region with any of these symptoms should prompt testing for B. pseudomallei.

Melioidosis is endemic across northern Australia, Thailand, Vietnam, Laos, Cambodia, Malaysia, Indonesia, India, Bangladesh, and parts of southern China. Recent reports document cases in sub-Saharan Africa, the Caribbean, Central America, and the southern United States. The organism lives in soil and surface water year-round but cases peak during the wet season.

Diagnosis is made by culturing Burkholderia pseudomallei from blood, sputum, urine, pus, or other clinical specimens. Specialized selective media (Ashdown's medium) help recovery. Serology supports diagnosis but lacks specificity in endemic regions. Imaging detects pneumonia, splenic and hepatic abscesses, and prostatic abscess that are characteristic of the disease.

Treatment has two phases. The intensive phase uses intravenous ceftazidime or meropenem for 10-14 days or longer for severe disease. The eradication phase uses oral trimethoprim-sulfamethoxazole for 3-6 months to prevent relapse. Source control with abscess drainage and tight glycemic control are essential adjuncts. Standard antibiotics for ordinary pneumonia do not work against melioidosis.

Mortality depends on geography, presentation, and access to care. In northern Australia with intensive care, acute mortality is about 10%. In northeast Thailand, where presentation is often late, mortality is 30-40%. Septic shock at presentation carries 50% mortality or higher. Early diagnosis and prompt ceftazidime or meropenem therapy substantially improve survival.

Yes, with appropriate two-phase antibiotic treatment most patients can be cured. The intensive intravenous phase clears acute infection and the 3-6 month oral eradication phase prevents relapse. Relapse rates are 5-15% with full treatment and 25% or more with incomplete eradication. Long-term outcomes are good when underlying diabetes and other risks are also controlled.

Diabetes impairs neutrophil and macrophage function, both of which are critical for clearing B. pseudomallei. Hyperglycemia also raises tissue glucose available for bacterial growth. Diabetic patients have a 12-fold increased risk of melioidosis and worse outcomes. Tight glycemic control reduces both incidence and severity.

There is no licensed human vaccine for melioidosis as of 2026. Several candidate vaccines have shown promising results in animal models, and clinical trials are in progress. Prevention currently relies on reducing soil and water exposure, controlling diabetes, and rapidly diagnosing and treating any suspected case in endemic regions.

Burkholderia pseudomallei can persist intracellularly in macrophages for years to decades. Documented cases of latent reactivation include Vietnam-era veterans presenting with melioidosis 30 years after exposure. Reactivation typically follows immune compromise — new diabetes, malignancy, or immunosuppressive therapy. Lifelong awareness of melioidosis history is important.

Yes, although most US cases are travel-related, locally acquired cases have been documented in the Mississippi Gulf Coast and US territories such as Puerto Rico. The CDC issued an environmental health advisory in 2022 after locally acquired cases in Mississippi. Endemic areas may expand with climate change and increased monsoon-like rainfall in southern US states.

First-line intensive-phase antibiotics are ceftazidime or meropenem given intravenously. Trimethoprim-sulfamethoxazole is the first-line oral eradication drug for 3-6 months. Amoxicillin-clavulanate is a second-line eradication option. B. pseudomallei is resistant to penicillins, first-generation cephalosporins, gentamicin, polymyxins, rifampin, and macrolides — these antibiotics will not work.

Melioidosis presents in many ways — pneumonia, abscesses, sepsis, urinary tract infection — and can mimic tuberculosis, ordinary pneumonia, or cancer. Outside endemic regions, clinicians rarely consider it. Automated microbiology systems can misidentify the organism. Travel history and willingness to use selective culture media are essential for accurate diagnosis.

Yes, although melioidosis is much less common in children than in adults. Suppurative parotitis (parotid gland abscess) is a characteristic pediatric presentation, particularly in northern Thailand and Cambodia. Pediatric melioidosis is generally less severe than adult disease and has lower mortality with appropriate treatment.

Relapse occurs in 5-15% of patients within 1-2 years of completing full treatment. Risk is higher when the intensive or eradication phase is shortened, when adherence is poor, or when underlying conditions like diabetes are uncontrolled. Long-term follow-up at 3, 6, and 12 months after therapy is important to detect relapse early.

Whitmore disease is an older name for melioidosis, named after Captain Alfred Whitmore, the British pathologist who described the disease in Rangoon in 1911. The current name melioidosis comes from Greek meaning resembling distemper. Both names refer to the same infection caused by Burkholderia pseudomallei.

Total treatment lasts 3-7 months: 10-14 days of intravenous antibiotics (extended to 4-8 weeks for deep-seated or severe disease) followed by 3 months of oral trimethoprim-sulfamethoxazole for skin or lung disease, or 6 months for bone, joint, brain, or relapsed disease. Completing the full eradication phase is essential to prevent relapse.