A 26-year-old Chinese male was admitted to our hospital due to breathing-related chest pain on the left for 4 days. He was in good health before, had no immunodeficiency diseases, and did not take any immunosuppressive agents. He was a software engineer, with no history of tourism and no history of contact with patients infected with Tropheryma whipplei. Physical examination was normal. The chest CT showed a thick-walled cavity in the left upper lung. Vascular convergence sign and local pleural thickening can be seen (shown in Figure 1). Blood routine test, C-reactive protein, erythrocyte sedimentation rate, procalcitonin, 1,3-beta-d-glucan assay, and endotoxin test were normal. Serological tests of Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella pneumoniae, respiratory viruses, and HIV were negative. Autoantibodies were all negative. Tuberculosis was suspected first, but tuberculin test was negative. In order to determine the cause of the disease, bronchoscopy was performed and showed normal bronchial mucosa. Bronchoalveolar lavage fluid (BALF) was analyzed by metagenomics next generation sequencing (mNGS). Tropheryma whipplei was detected and it was the only pathogen identified.
The patient was diagnosed with Tropheryma whipplei infection. He was treated with intravenous ceftriaxone (2 g, once daily) for 2 weeks. Then, he received oral administration of trimethoprim-sulfamethoxazole (0.96 g, twice daily). His chest pain was relieved one week after starting treatment. Six weeks after treatment, a follow-up chest CT scan showed that the pulmonary cavity disappeared, leaving only a little patchy infiltration. The pleural thickening was reversed (shown in Figure 2). The patient is still under treatment and follow-up.
Chest CT after 6 weeks of treatment, showing the cavity disappeared, leaving only a little patchy infiltration. The pleural thickening was improved.