ABSTRACT
Sulfamethoxazloe-trimethoprim is one of the most frequently used antibiotics in the treatment of Nocardia infection. However, in vitro studies have shown an increase in sulfonamide resistance among Nocardia species. Here, we present a case with a brain abscess caused by Nocardia farcinica in which the test results for drug susceptibility to sulfonamide conflicted with the actual clinical course. A 74-year-old woman with autoimmune hepatitis who has being treated with oral prednisolone (16 mg/day) was admitted because of headaches and fever. A CT scan and MRI revealed a brain abscess that had ruptured into the lateral ventricle. She was empirically treated with antibiotics, but her condition did not resolve. Therefore, the abscess was drained surgically. Gram and Kinyoun stains for pus revealed a modified acid-fast branching filamentous bacterium consistent with Nocardia species. The pathogen was identified as Nocardia farcinica based on its 16S rRNA sequence. Consequently, the patient was treated with sulfamethoxazole -trimethoprim and amikacin. However, susceptibility testing (broth microdilution method) showed that the strain was completely resistant to sulfamethoxazole-trimethoprim. We therefore changed the therapeutic regimen to imipenem-cilastatin and amikacin, but her symptoms worsened and the treatment was thought to have failed. She was then re-treated with sulfamethoxazole- trimethoprim, and her symptoms resolved. Some reports have suggested that interpreting the results of Nocardia susceptibility testing may be difficult especially the susceptibility of Nocardia to sulfamethoxazole-trimethoprim. The present case suggests a confliction between susceptibility testing and the clinical course of a patient with Nocardia infection.
