LAUSR

A 64-year-old patient was admitted to a hospital for increasing dyspnea, angina, and peripheral edema. On examination, pleural as well as pericardial effusion and tachycardic atrial fibrillation were diagnosed. The patient had been healthy so far, he was not on any medication. Blood tests showed increased levels of proBNP (3197 pg/ml), troponin T (263 ng/ml), leucocytes (16.3 t/μl), CRP (98.4 mg/l), and liver enzymes (GPT 126U/l, g-GT 125U/l). Cardiac decompensation due to atrial fibrillation and infectious disease was diagnosed and pleuracentesis obtaining 2 L of clear fluid was performed without pathological, bacteriological, and histological findings. Due to increasing pericardial effusion (PE) with beginning hemodynamical relevance, the patient was referred to our hospital for pericardiocentesis and further workup. Echocardiography showed a large pericardial effusion (3.8 cm, Fig. 1) with beginning swinging heart and fibrous deposits. Via pericardiocentesis, 1550 ml of serous fluid were obtained. A pigtail catheter remained for further drainage. Pathological examination showed cell-rich fluid as in inflammatory pericarditis. Bacteriological and cytological tests did not show a specific pathology, especially no bacterial growth. During the next 5 days, the patient converted spontaneously to sinus rhythm. Via pigtail catheter, about 100 ml of fluid was aspirated daily from the pericardium. Due to the development of fever and the aspirated fluid turning yellowish, the pigtail catheter was removed suspecting bacterial superinfection. Repeatedly, pericardial fluid as well as blood cultures was sent to the lab for testing. Blood cultures remained negative, but in the pericardial fluid, bacteria identified via matrix-assisted laser desorption/ionization timeof-flight mass spectrometry (MALDI TOF–MS) as Burkholderia mallei or Burkholderia pseudomallei were found, both belonging to the risk group 3 of bacterial agents. The two species are closely related and could not be reliable differentiated via the applied method. Therefore, material was sent for species identification and antimicrobial susceptibility testing to the Bundeswehr Institute of Microbiology, Munich, Germany, specialized in highly pathogenic bacteria. Local health authorities were informed. The specialized lab in Munich confirmed via molecular methods (realtime PCR, target genes fliC und 16S-SNP) the identification of Burkholderia pseudomallei. Whole genome sequencing and in silico MLST genotyping revealed the sequence type ST289, described in Southeast Asia before (Thailand, Malaysia, Singapore). Antimicrobial susceptibility testing showed susceptibility towards the substances typically used for B. pseudomallei therapy (minimal inhibitory concentration values: ceftazidime:1.0 μg/ml—susceptible, increased exposure; meropenem: 0.25 μg/ml—susceptible, doxycyclin: 0.25 μg/ml—susceptible, increased exposure, cotrimoxazole: 0.0625/1.1875 μg/ml—susceptible, increased exposure). In the further course of the hospital stay, the pericardial effusion was increasing consistently, so that another pericardiocentesis with drainage had to be performed (Fig. 2). Melioidosis, or Whitmore’s disease (in German “Pseudorotz”), is an infectious disease that can infect humans or animals. The disease is caused by the bacterium Burkholderia pseudomallei [1, 2] which is on the list of potential biological weapons, classified as category B tier 1 select agent by US CDC. It is endemic in tropical climates, especially in Southeast Asia and northern Australia. The bacteria causing melioidosis are found in contaminated water and soil as well as on fruits and vegetables. It is spread to humans and animals through direct contact with the contaminated * Tiefenbacher CP [email protected]