A 50-yr-old man visited our hospital because of intermittent fever associated with cough, sputum, generalized myalgia and general weakness for about four weeks. He had lived in Indonesia for twenty years for business, and visited a local hospital in Indonesia and was treated for typhoid fever without improvement of symptoms. He was previously healthy and had no history of diabetes. Initial chest radiograph and computed tomography (CT) images showed multiple satellite nodules in the left lower and upper lobes, and judging from that roentgenographic examination, tuberculosis was the most probable diagnosis (Fig. 1). Bronchoscopy showed no endobronchial lesion and washing cytology and culture were also negative. We prescribed moxifloxacin but his symptoms showed no improvement. Three months later we rechecked chest radiograph and CT findings, and found new infiltration in the left lower lobe and improvement of lesions in the left upper and lower lobes (Fig. 2). So he was admitted to our hospital for further evaluation. On physical examination initial body temperature was 38C and there was no other abnormal finding. Laboratory findings included white blood cell count of 5,240/microL and hemoglobin value of 11.6 g/dL. Hepatic function and renal function were normal. IgA was 227 mg/dL (normal range: 90-400 mg/dL) and anti-neutrophilic cytoplasmic antibodies with cytoplasmic staining pattern (CANCA) was negative.
Bronchoscopy was done once more and no endobronchial lesion was found. However, secretion was seen in left lower lobe, so washing cytology and culture was done. Cytology was negative but a species of bacteria grew on blood agar media (Fig. 3). It was Gram-negative, non-spore forming and showed as a safety pin shaped organism on microscopic examination (Fig. 4). By biochemical examination of API20NE strip and VITEK GNI card (BioMerieux, Inc., Hazelwood, U.S.A.), the organism was identified as Burkholderia pseudomallei. On DNA sequencing of 16S ribosomal RNA, it was compatible with B. pseudomallei with 100% homology and formed a characteristic rugose colony on blood agar.
We prescribed ceftazidime 2 g intravenously every 8 hr and he did not complain of intermittent fever any more. The cough, sputum and general condition improved slowly. After one week of intravenous ceftazidime, he was discharged with oral amoxicillin-clavulanate (750 mg every 8 hr). One month later the cough and sputum were almost disappeared but his general weakness persisted although it was also improving.
Four months later we rechecked chest CT to show an improvement of infiltration in left lower lobe. He said his condition was as good as his previous state before suffering from melioidosis. One month later, we stopped administrating oral antibiotics to him, which resulted in him taking amoxicillin-clavulanate for total five months.