Melioidosis masquerading as other tropical diseases: Diagnostic lessons from three challenging cases

Introduction

Melioidosis was first described by Whitmore ¹ and Krishnaswami. ² It is increasingly recognised as a major cause of community-acquired sepsis and focal infections in Southeast Asia and northern Australia. Once considered rare, the disease is now estimated to cause approximately 165,000 serious infections and 89,000 deaths annually worldwide. ³ It can present with a bewildering range of manifestations, from pneumonia and septicaemia to chronic localised infections that closely resemble tuberculosis, septic arthritis, or malignancy.^4,5 We report a series of three culture-confirmed cases of melioidosis, each illustrating uncommon and diagnostically challenging presentations: (i) false-positive scrub typhus serology, (ii) polymicrobial infection with Klebsiella pneumoniae, and (iii) chronic monoarthritis mimicking tuberculosis.

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Table 1.

Baseline investigation of all the cases.

Laboratory parameters	Case 1	Case 2	Case 3	Reference value
Hb (g/L)	94	108	128	120–170
Leucocytes (109/L)	19.1	13.1	14.8	4–11
Platelets (109/L)	142	149	163	150–450
Urea (mmol/L)	7.16	6.0	12.99	2.16–7.16
Creatinine (µmol/L).	97	150	230	53–115
Random blood sugar (mmol/L)	4.44	6.77	26.96	<7.8
HbA1C (%)	11	–	10.1	4%–5.6%
Bilirubin (µmol/L)	39.0	9.6	8.7	17.1
SGOT (µkat/L)	1.37	1.59	0.40	0.17–0.58
SGPT (µkat/L)	0.97	0.70	0.32	0.17–0.75
Albumin (g/dL)	2.8	2.9	3.5	3.5–5.2

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Figure 1.

Computed tomography (CT) thoracic scan of case 2 showing multifocal ground glass opacity and patchy consolidation, along with centrilobular nodules and tree-in-bud appearance.

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Figure 2.

Chest radiograph of case 3 showing patchy infiltrates in both perihilar and basal zones.

Case report 1

A 51-year old male, diabetic and chronic alcoholic, presented with fever for three months, which was intermittent, high-grade, and associated with chills and rigours. He was admitted to another hospital twice and was given an antibiotic course, but despite that, he persisted with fever. He also complained of swelling and pain in his left knee and bilateral lower leg swelling for over 10 days.

On examination, he had a tachycardia (120 beats/min) and hypotension (70/50 mmHg) with neutrophilic leucocytosis, thrombocytopenia, and mildly deranged liver function tests (Table 1). Echocardiography showed global left ventricular hypokinesia and severe systolic dysfunction. He was initially started on piperacillin/tazobactam and dual inotropic support. Knee aspiration showed leucocytosis, but the Cartridge-Based Nucleic Acid Amplification Test and Adenosine Deaminase ruled out tuberculosis. Blood culture and knee aspirate culture, which arrived later, showed a growth of Burkholderia pseudomallei; hence, meropenem was added for 14 days, with the patient showing consistent improvement. He was then gradually removed from inotropic support and showed good symptomatic improvement; his fever and knee swelling had subsided. Repeat echocardiography then showed normal left ventricular systolic function. Our patient was put on trimethoprim-sulphamethoxazole for prolonged eradication phase treatment.

Case report 2

A 45-year-old female presented with fever for one week, which was intermittent, low-grade, but not associated with chills and rigours, and had a cough with whitish sputum.

On examination, she had a tachycardia (121 beats/min) but was normotensive (blood pressure 110/80 mmHg), and not hypoxic (SpO₂ 94%). She had bilateral extensive wheezing with crepitations localised to infra-scapular areas. She was initially started on cefperazone/sulbactam. Further workup showed enzyme-linked immunosorbent assay immunoglobulin IgM to be positive for scrub typhus, and azithromycin and doxycycline were added. CT thoracic scan showed multifocal ground glass opacity and patchy consolidation, along with centrilobular nodules and tree-in-bud appearance (Fig. 1). On the third day, despite all these antibiotics, she developed worsening breathlessness and desaturation, and developed hypoxaemic respiratory failure, but she did not tolerate continuous positive airway pressurisation. During endotracheal intubation, her blood pressure dropped, requiring inotropic support. A significantly elevated neutrophilic leucocytosis was now seen compared to baseline. Meropenem was thus added. Later that day, blood cultures returned positive for Burkholderia pseudomallei, and trimethoprim-sulphamethoxazole was then also added. Despite this, on the fifth day, her condition deteriorated, needing high-dose multiple inotropic support. Desaturation despite a F_iO₂ of 100% persisted, but the relatives decided to take the patient home against medical advice.

Case report 3

A 62-year old male with co-morbidity of type 2 diabetes and hypertension on irregular medication presented with complaints of low-grade, intermittent fever, and cough with expectoration for two days with central non-radiating chest pain in the central chest for two days.

On initial examination, he had a normal heart rate of 88 beats/min and was normotensive (110/70 mmHg) with bilateral infrascapular and interscapular crepitations. An electrocardiogram showed a normal sinus rhythm, and 2D echocardiography showed normal left ventricular systolic function. He had a neutrophilic leucocytosis (Table 1) chest radiography showed patchy infiltrates in bilateral perihilar and basal zones (Fig. 2). He was diagnosed as having a community-acquired pneumonia. He had been started on ceftriaxone, but the next day, within hours of admission, his chest pain worsened with evident breathlessness. Auscultation now revealed extensive crepitations in all lung fields; although his saturation was 98% on room air, he developed bradycardia the next day with an unrecordable blood pressure, followed by cardiac arrest. Despite cardio-pulmonary resuscitation according to protocol and endotracheal intubation, no improvement was sustained. A sputum culture later was reported with Klebsiella pneumoniae, and blood culture subsequently, after death, was also reported as showing Burkholderia pseudomallei.

Discussion

Melioidosis is considered endemic to Australia and Southeast Asian countries. In India, it is common in the southern states of Tamil Nadu and Kerala; a few reported cases have also occurred in the northeastern states.^6,7,8 Inoculation, inhalation, and ingestion are the three common modes of acquiring this infection. ⁹ One study reported that intense rain and wind are significant risk factors for the development of pneumonia through the inhalational route, contrary to the previous belief that pneumonia happens secondarily through the haematogenous route. Our second and third cases presented during the northeast monsoon season. ¹⁰ Male gender, diabetes mellitus, renal disease, and alcohol intake are common risk factors across various cases studied so far.^11,12

Pneumonia is more common during the winter months. The most common presentation was pneumonia seen in up to half the patients, followed by genitourinary and skin infections. Rare manifestations include musculoskeletal and neurological melioidosis. ¹³ Our first case had a fever for 3 months and was admitted twice to other hospitals. Arriving at a correct diagnosis is often difficult, and sometimes, repeating blood cultures is necessary. ¹⁴

Scrub typhus is more common than melioidosis in India, but the latter may exist concurrently, which requires specific therapy. Furthermore, up to 50% of cases of melioidosis may show false positivity for scrub typhus serology. ¹⁵

Tuberculosis is, however, the most common co-infection encountered with melioidosis. Co-infection with Klebsiella pneumoniae has not heretofore been reported; all co-infections give a poorer prognosis. ¹⁵

Ceftazidime is a first-line agent, widely used and known to reduce mortality. ¹⁶ However, carbapenems have been used as a first-line alternative, particularly in patients with severe disease. ¹⁷ They benefit from reduced release of endotoxins, ¹⁸ and demonstrate a post-antibiotic effect. ¹⁹ Furthermore, it is considered a popular agent of choice due to its broad spectrum; since melioidosis is a great mimicker, this is a wise empirical choice.

The spectrum of melioidosis is large, from pneumonia, the commonest manifestation, to arthritis, the least common. A high index of suspicion and in-depth knowledge about melioidosis are needed both to arrive at an earlier diagnosis and to review antibiotic coverage and reduce mortality. Melioidosis may present with diverse and deceptive clinical features, including false-positive serology for other tropical infections, polymicrobial co-infection, and chronic focal disease resembling tuberculosis. Awareness of these presentations is essential in endemic areas to avoid misdiagnosis and ensure timely, appropriate management.