A 44-year-old Caucasian man from Switzerland developed fever and productive cough, two weeks after returning from north-eastern Thailand, were he had stayed from December 2008 until February 2009. The general practitioner treated the patient for community-acquired pneumonia with amoxicillin-clavulanate for seven days. After initial improvement, the patient became febrile and dyspneic again.
On admission the patient was febrile (38.3°C), had a tachycardia of 130 beats/minute, a blood pressure of 120/78 mmHg, and a respiratory rate of 40/min.
Although the patient showed jugular venous distention, neither Kussmaul’s sign nor hepatomegaly or peripheral oedema were observed.
Laboratory tests revealed anaemia (hemoglobin 125 g/l, hematocrit 0.37), leucocytosis, (16.6 G/l; 80% neutrophils, 12% lymphocytes), elevated C-reactive protein (141 mg/l) and elevated B-type natriuretic peptide (208 ng/l). Laboratory screening for autoimmune diseases and vasculitis was negative. Electrocardiogram showed sinus tachycardia and low QRS voltage.
A chest radiograph showed bilateral pleural effusions and an enlarged cardiac silhouette. Computed tomography (CT) of the chest confirmed bilateral pleural effusions, with atelectasis of the inferior lobes, mediastinal lymphadenopathy and a prominent pericardial effusion. Abdominal CT showed a small intra-abdominal fluid collection.
Echocardiography confirmed a hemodynamic relevant pericardial effusion with diastolic compression of the right ventricle and a leftventricular ejection fraction of 55%. After pericardiocentesis and aspiration of 700 ml of a clear yellowish fluid the right ventricular function normalized, the leftventricular ejection fraction raised to 65%, and the QRS voltage normalized.
Pleural effusion (1.07 G/l leucocytes, 33% monocytes/macrophages, 54% lymphocytes, 13% polymorphonuclear neutrophil leucocytes; LDH 144 U/l with normal range of LDH in serum <265 U/l ,and with a pleural fluid/serum-quotient of 0.4 for LDH and 0.4 for total protein, respectively) was negative on Gram- and Ziehl-Neelsen stains and negative by Polymerase Chain Reaction Assay for Mycobacterium tuberculosis complex. Cultures remained negative for bacteria, including mycobacteria and fungi. Cultures of two sputum samples from the same day yielded normal upper respiratory tract flora. Four sets of blood cultures taken on four consecutive days remained sterile and urine was negative for Legionella antigen.
Pericardial effusion (1.4 G/l leucocytes, 58% monocytes/macrophages, 23% lymphocytes, 19% polymorphonuclear neutrophil leucocytes; pericardial fluid/serum-quotient of 0.6 for total protein content and of 2.3 for LDH activity, respectively) was negative on Ziehl-Neelsen stain and mycobacterial cultures remained negative. Two blood culture sets were inoculated with pericardial aspirate (10 ml volume per bottle), and a Gram-negative bacillus was isolated from both aerobic bottles after 35 hours of incubation in a BACTEC™ 9240 Blood Culture Analyzer (Becton Dickinson AG, Allschwil, Switzerland). Although identified as Burkholderia cepacia in a UNMIC/ID-62 panel of the Phoenix Automated Microbiology System (Becton Dickinson AG, Allschwil, Switzerland), diagnosis was regarded as tentative, since identification of B. cepacia by common automated identification instruments should be confirmed by molecular tests [3, 4]. Furthermore, pericardial effusion is an unusual location for occurrence of B. cepacia[3] and the isolate was unexpectedly sensitive to amoxicillin-clavulanate (MIC <= 4/2 mg/L). Analysis of the isolate by API 20NE biochemical test panel V7.0 (bioMérieux, Geneva, Switzerland) yielded Burkholderia pseudomallei (profile 1156577; 99.9%, ID, 1.0 T). Amplification and sequencing of a 500-bp fragment of the 16S rRNA gene by Fast MicroSeq 500 16S rDNA Bacterial Identification Kit and a PRISM 3130 Genetic Analyzer (Applied Biosystems, Foster City, CA, USA) with sequence analysis by MicroSeq ID Microbial Identification Software (Applied Biosystems, Foster City, CA, USA) confirmed the isolate as B. pseudomallei (DQ108392, 481-bp consensus length). Multilocus sequence typing (MLST) [5] of the isolate revealed the allelic profile 1/1/4/1/5/4/1, corresponding to B. pseudomallei sequence type 207, which has first been isolated from a patient in Thailand with invasive melioidosis in 2001 [6]. The isolate was sensitive to amoxicillin-clavulanate (2 μg/mL), ceftazidime (1.5 μg/mL), doxycycline (3 μg/mL) and trimethoprim-sulfamethoxazole (0.75/0.0375 μg/mL). Susceptibility testing was carried out by Etest (AB BIODISK, Sweden) and interpreted according to guidelines established by CLSI [7].
The patient received ceftazidime 2 g every 6 hours for 2 weeks followed by maintenance treatment for three months with doxycycline, trimethoprim-sulfamethoxazole and leucovorine. The patient fully recovered after four months and suffered no relapse in the two years follow-up.