Because of slow growth of mycobacteria, use of rapid tests to identify them is strongly recommended; rapid tests are widely used as an advanced diagnostic tool in clinical laboratories (1,2). These tests are particularly useful for diagnosing extrapulmonary mycobacterioses and identifying unusual mycobacteria as etiologic agents (3). Commercial probes are frequently used for rapid and specific identification of mycobacteria, especially Mycobacterium tuberculosis complex. However, cross-reactivity of DNA probes between mycobacterial species could result in incorrect diagnosis and treatment of patients (4,5). Misidentification could be a problem if a newly described species, such as M. kumamotonense (6), were an etiologic agent of a disease.
In July 2006, we obtained a fine-needle, puncture aspiration biopsy specimen from a cervical lymph node of a 30-year-old man at Doce de Octubre Hospital (Madrid, Spain). The patient was a recent immigrant from Paraguay and was HIV positive (C2 stage of infection). A biopsy specimen from a cervical lymph node showed necrotizing granulomatous lymphadenopathy. A computed tomographic scan showed cervico-thoraco-abdominal, multiple cervical, supraclavicular, axillar, paratracheal, and mediastinal lymphadenopathies. The patient had a CD4 cell count of 219 cells/mm3 and an HIV viral load of 197,181 copies/mL.
The aspiration sample was positive for acid-fast bacilli by fluorescent staining. The clinical isolate (designated 1369) obtained from the aspirate sample was grown in liquid media (MGIT Diagnostic Kit; Becton Dickinson Diagnostics, Sparks, MD, USA) and identified as M. tuberculosis complex by using the AccuProbe System (bioMérieux, Marcy l'Etoile, France).
A diagnosis of lymphoid tuberculosis was made, and the patient was treated with isoniazid, rifampin, ethambutol, and pyrazinamide. After 1 month, rifampin was withdrawn because of a cutaneous exanthem. Three months later, the clinical status of the patient had improved, fever had disappeared, and sizes of cervical and axillary lymph nodes had decreased. Treatment with tenofovir, emtricitabine, and lopinavir/ritonavir was started. Two weeks later, an immune reconstitution syndrome and adenopathies developed, but these resolved in 1 month.
Five months after treatment was started, susceptibility testing in a reference laboratory showed that isolate 1369 was M. kumamotonense. The isolate showed 100% identity with the 16S rRNA gene sequence of M. kumamotonense (GenBank accession no. AB239925). Results of PCR restriction analysis of heat shock protein 65 gene (7) (http://app.chuv.ch/prasite/index.html) were consistent with those for M. kumamotonense. The isolate was susceptible to ethambutol, rifampin, cycloserine, and ethionamide and resistant to isoniazid, streptomycin, pyrazinamide, and kanamycin.
http://www.cdc.gov/eid/content/16/7/1178.htm
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