A 57-year-old man from a rural area in southern Taiwan presented after five days of progressive generalized weakness, unsteady gait, worsening dyspnea, chronic dry cough, and urinary frequency without dysuria. He reported two months of poor appetite and significant unintentional weight loss. His medical history included poorly controlled type 2 diabetes mellitus (HbA1c 9%), chronic alcohol use, benign prostatic hyperplasia, and malnutrition (BMI 16.8 kg/m2). He had frequent occupational exposure to soil and surface water.
On arrival he was drowsy and hemodynamically unstable with hypotension (96/66 mmHg), tachycardia (137 beats/min), and hypoxemia (SpO2 90% on a non-rebreather mask at 12 L/min). Distal extremities were cool with cyanotic discoloration but no frank necrosis. Initial labs showed leukocytopenia with a left shift (WBC 1,050/µL; band forms 8%), thrombocytopenia (35,000/µL), acute kidney injury (creatinine 2.29 mg/dL), elevated lactate (4.33 mmol/L), markedly raised transaminases (AST 615 IU/L; ALT 144 IU/L), hypoalbuminemia (2.08 g/dL), prolonged PT/INR (PT 15.1 s; INR 1.57), and an elevated D-dimer (4.53 mg/L FEU). C-reactive protein exceeded 160 mg/L.
Chest computed tomography revealed a 2.6-cm cavitary lesion in the right upper lobe with bilateral pulmonary infiltrates. Whole-body CT identified hypodense lesions suspicious for abscesses in the liver (segment VII), right kidney (1.5 cm), and prostate.
Two independently collected blood-culture specimens obtained at admission and a prostatic abscess aspirate subsequently yielded Burkholderia pseudomallei. Laboratory recognition included characteristic colony morphology and bipolar Gram staining, adjunctive matrix-assisted laser desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry, and final identification by VITEK 2 in a Taiwan CDC–authorized laboratory. Antimicrobial susceptibility testing, interpreted using historical CLSI-based criteria, showed susceptibility to trimethoprim-sulfamethoxazole (TMP-SMX), ceftazidime, and imipenem.
Empiric therapy was initially ceftriaxone plus levofloxacin for presumed severe community-acquired pneumonia, escalated to ertapenem on hospital day 1 and meropenem on day 2 during clinical deterioration. TMP-SMX was added after culture results supported melioidosis, but recurrent hyperkalemia and renal dysfunction prevented continued TMP-SMX and required alternative eradication regimens.
The patient required medical intensive care unit admission for septic shock and acute hypoxemic respiratory failure. He was intubated and mechanically ventilated, received vasopressor support (norepinephrine, with a transient vasopressin infusion), and underwent continuous venovenous hemofiltration (CVVH) for refractory metabolic acidosis and oliguria. CVVH was discontinued on hospital day 6 as renal and metabolic status improved. Mechanical ventilation was discontinued on day 20, and vasopressors were tapered off by day 7.
Meropenem was administered for an extended inpatient course (approximately 48 cumulative days across two treatment periods). Meropenem was briefly replaced by cefoperazone-sulbactam with inhaled colistin on day 14 because of concerns for a nosocomial carbapenem-resistant pathogen but was later resumed and continued through discharge.
Digital cyanosis was present on admission and progressively worsened during the first hospital week, evolving into dry gangrene of multiple fingers and toes. Transthoracic echocardiography revealed no valvular vegetations. Vascular imaging showed no large-vessel occlusion or peripheral arterial disease. A comprehensive autoimmune and vasculitis workup including anticardiolipin antibodies, anti-β2-glycoprotein I IgG, proteinase 3 and myeloperoxidase ANCA, and an extended myositis panel was unremarkable.
The symmetric acral distribution in the absence of major-vessel obstruction and the setting of septic shock with laboratory evidence of coagulopathy were clinically consistent with symmetrical peripheral gangrene (SPG), a phenomenon associated with microvascular thrombosis and disseminated intravascular coagulation in severe sepsis.
Image-guided drainage of the prostatic abscess was performed on hospital day 9. The aspirate cultured B. pseudomallei with the same susceptibility profile as the blood isolates, supporting hematogenous dissemination and confirming the prostate as a focus of infection. Drainage provided surgical source control and was considered an important component of the successful management strategy.
TMP-SMX was initiated after culture identification but discontinued within eight days because of hyperkalemia. An oral TMP-SMX rechallenge on day 39 was again stopped after three days for recurrent hyperkalemia and worsening renal function. Because TMP-SMX could not be tolerated, the patient was transitioned at discharge to an alternative eradication regimen of doxycycline plus amoxicillin-clavulanate for six months.
Molecular confirmation of the organism was not performed; the authors noted this as a limitation despite concordant culture results and phenotypic identification across specimens.
After discharge, gangrenous digits developed secondary infection. Three months post-discharge, the right index finger showed swelling and purulent discharge; cultures grew Pseudomonas aeruginosa and later methicillin-resistant Staphylococcus aureus (MRSA). Bone scintigraphy suggested osteomyelitis of the right second digit. Four months after discharge the right index finger was amputated to the middle phalanx and the left third and fourth fingers were amputated. Histopathology showed gangrenous necrosis with suppurative inflammation in skin, soft tissue, and bone. Persistent infection in nonviable tissue necessitated further amputation and sequestrectomy of the right third and fourth fingers three months later, with histopathology confirming necrotic bone and sequestrum.
Bilateral toe gangrene progressed to spontaneous auto-amputation without surgical intervention. At approximately 17 months after discharge and 11 months after completion of eradication therapy there was no evidence of recurrent melioidosis. The patient continued rehabilitation and counseling for strict glycemic control and alcohol cessation.
This case demonstrates fulminant disseminated melioidosis with bacteremia, cavitary pneumonia, multiple visceral abscesses, septic shock, multi-organ failure, and rare development of symmetrical peripheral gangrene (SPG). Host risk factors—poorly controlled diabetes mellitus, chronic alcohol use, and malnutrition—likely increased susceptibility and disease severity. Prostatic abscess was an important, clinically relevant focus that required drainage for source control.
Microbiological identification used phenotypic and mass spectrometry methods with concordant isolates from multiple sites; however, molecular confirmation was not performed. Early administration of meropenem, prompt intensive organ support, and timely source control were credited as factors contributing to survival despite the severity of illness.
SPG in this case developed without large-vessel occlusion and in the context of shock-related coagulopathy, thrombocytopenia, and markedly elevated D-dimer, findings compatible with sepsis-associated microvascular thrombosis and disseminated intravascular coagulation. The precise mechanism linking melioidosis and severe acral ischemia remains incompletely understood.
Key clinical lessons include the importance of early recognition of melioidosis in endemic settings, aggressive supportive care and appropriate antimicrobial therapy, vigilance for occult foci such as the prostate in men, and early recognition of peripheral ischemia. Even with survival, patients may experience significant long-term functional disability requiring reconstructive or amputative surgery and prolonged rehabilitation.