A 32-year-old male, a diagnosed diabetic and on medical nutrition therapy since the past two years, presented to our outpatient clinic with a painful swelling over his forehead. The swelling had been progressively increasing in size over the past three months, and had partially ruptured two days before his arrival to our clinic. Five months earlier, he had suffered a head injury after a fall in the bathroom, at which time he had sustained a minor laceration involving the same portion of his forehead. The fall was followed immediately by a single episode of generalised tonic-clonic seizure lasting around one minute. He had not sought any medical help at that time, and had had no further seizures since then. He denied any constitutional symptoms such as fever or weight loss. There was no history of substance abuse.
Local examination revealed a tender, warm, cystic midline swelling with sero-purulent discharge on his forehead. Neurologic examination did not reveal any focal deficits. Review of cardiovascular, respiratory and gastro-intestinal systems was essentially normal.
Routine laboratory parameters including ESR (10 mm/hr) were unremarkable except for uncontrolled hyperglycaemia with glycosylated haemoglobin (HbAlc) levels at 9.0%. Cranial MRI confirmed the presence of a scalp collection (, ). The collection was seen to extend through a bony defect in the calvarium into the extradural space with hyperaemia over the adjacent meninges. A left frontal craniotomy was performed under general anaesthesia and the granulation tissue biopsied. Histopathologic examination showed dense fibrocollageneous tissue with infiltration by neutrophils forming microabscesses, surrounded by lymphocytes, histiocytes and areas of caseous necrosis with few palisading epithelioid cells, and dead bony spicules. Although staining for acid-fast bacilli was negative, tuberculosis was suspected based on the characteristic picture of caseating necrosis, the presence of diabetes – a known risk factor for tuberculosis, and the chronic nature of infection. Mantoux test performed was indeterminate with an induration of eight mm. Plain chest X-ray performed was normal, and revealed no stigmata of current or past tubercular infection. Initial culture reports of the pus were sterile. Although the clinical and histopathologic picture was compatible with a tubercular cold abscess, the absence of definitive evidence in the form of absence of acid fast bacilli in the biopsy, absence of radiographic signs of tuberculosis and indeterminate tuberculin skin test, prompted us to await the mycobacterial culture report. The patient was therefore treated with subcutaneous insulin and discharged with instructions to return after one month for follow-up of mycobacterial culture of the biopsy sample. In the event that the culture was positive, we planned to initiate antitubercular drugs in accordance with the DOTS regimen recommended in India. Unfortunately, the patient was subsequently lost for follow-up, returning only after another 11 months. In the interval, the swelling had persisted, now associated with a discharging sinus. Although he had not yet received anti-tubercular therapy in any form, he appeared relatively well. Systemic symptoms were once more conspicuous by their absence. The remarkable indolent nature of the swelling prompted us to review his previous medical records, which revealed that delayed cultures of pus and granulation tissue had grown B. pseudomallei, with a typical sensitivity to co-amoxiclav, ceftazidime, cotrimoxazole and meropenem. A repeat biopsy of the discharging sinus was performed and showed no evidence of tuberculosis. Moreover, mycobacterial culture of granulation tissue from the first biopsy remained sterile.
Figure 1 Contrast enhanced MRI brain (Tl sequence, coronal section) showing a well-defined fluid intensity lesion measuring 6.7x2.7x5.7 cm in the scalp in the left high fronto-parietal region (red arrow) with an iso-intense periphery, communicating with a similar (more ...)
Contrast enhanced MRI brain (Tl sequence, sagittal section) showing the same lesion. Note the contiguous meningeal enhancement in the frontal region (white arrow)
Having definitively ruled out tuberculosis, pharmacotherapy for melioidosis was initiated with parenteral co-amoxiclav (1.2 g IV q8h) for 14 days, followed by maintenance phase with oral cotrimoxazole (320/1600 mg PO ql2h) for 20 weeks. The patient made a rapid recovery with complete resolution of the discharging sinus and the underlying abscess. After more than a year of follow-up, the patient is healthy with no recurrences.