Infectious Diseases in Clinical Practice:
Mycobacterium africanum Presenting as a Brain Mass
Bhanot, Nitin MD; Badem, Olga MD; Mathew, Liby MD; Haran, Mehandi MD
Maimonides Medical Center, Brooklyn, NY.
Address correspondence and reprint requests to Nitin Bhanot, MD, Division of Infectious Diseases, Maimonides Medical Center, 4802 10th Ave, Brooklyn, NY 11219. E-mail: firstname.lastname@example.org.
A 27-year-old woman, who had emigrated from Sierra Leone 5 years prior, presented with worsening headaches of 3-month duration. Magnetic resonance imaging of the brain revealed a lobulated mass lesion with central necrosis in the right parietal and occipital lobes. Biopsy was performed, and histopathology revealed multiple granulomas. Although acid-fast stain of the tissue was negative, gene probe showed Mycobacterium tuberculosis complex, and culture revealed Mycobacterium africanum. This species is rare in the United States, and to the best of our knowledge, this is the first reported case of M. africanum causing a brain mass.
A27-year-old woman, without a significant medical history, presented with daily continuous headaches of 6-month duration. There were no identifiable precipitating factors, and analgesics partially relieved the symptoms. The headaches had gradually become intolerable, and a day before presentation, the patient had a witnessed generalized tonic-clonic seizure, an event that prompted her to seek immediate medical care. The patient had a 10-lb weight loss in the previous 2 months and attributed it to poor eating habits. She denied loss of appetite, fevers, or night sweats. She had emigrated from Sierra Leone 5 years ago with her husband and 4-year-old child, who were both in good health. She had quit smoking 1 year previously and did not drink alcohol or use recreational drugs.
On physical examination, she had a temperature of 98.8°F orally, pulse rate of 80/min, blood pressure of 134/74mm Hg, and respiratory rate of 14/min. She was in distress from an excruciating headache. The remainder of the physical examination was unremarkable. The leukocyte count was 10,500/μL (neutrophils, 71.1%; lymphocytes, 21.7%; and eosinophils, 3.2%), hemoglobin level was 11.5g/dL, hematocrit level was 35.3, and platelet counts were 403,000/μL. Hepatic and renal function tests were within reference range.
Computed tomographic scan of the head revealed a lobulated parenchymal mass measuring 4.3 × 3.3 cm in the right parietal occipital region, with a right-to-left midline shift and surrounding reactive edema. Intravenous dexamethasone was administered, and MRI of the brain (Figs. 1 and 2), performed the same day, confirmed the computed tomographic findings. Computed tomographic scan of the chest, abdomen, and pelvis was obtained and showed mild bronchiectatic changes in the medial posterior left lower lobe and no other abnormalities.
Excisional biopsy of the brain lesion was performed.Frozen section revealed multiple granulomas suspicious for tuberculosis (Fig. 3). Treatment with isoniazid 300 mg daily, rifampin 600 mg daily, pyrazinamide 1000 mg daily, and ethambutol 800 mg daily was initiated. Dexamethasone was continued with gradual tapering. Acid-fast staining of the brain tissue was negative, but gene probe testing was positive for Mycobacterium tuberculosis complex by using the AccuProbe Culture Identification Test (Gen-Probe, San Diego, Calif). The culture grew Mycobacterium africanum on day 36 that was susceptible to isoniazid, rifampin, ethambutol, and pyrazinamide. Confirmation of M. africanum was done at the microbiology laboratory of the New York State Department of Health by a polymerase chain reaction-based genomic deletion assay (not commercially available). Although the patient had no respiratory complaints, culture of induced sputum also showed M. africanum.
The patient's symptoms improved on antituberculous therapy. Human immunodeficiency virus enzyme-linked immunosorbent assay was negative. The patient subsequently recalled having been in contact with her uncle, who was having pulmonary tuberculosis in Sierra Leone.
Mycobacterium africanum, initially described by Castetset al1 in 1968 in a patient from Senegal, is a common cause of tuberculosis in Africa.2 It has been rarely reported to cause disease in other parts of the world.3 Desmond et al4 reported 5 cases in the United States in 2004. Three of those patients were from Africa, but the other 2 had no history of travel to Africa or having being in contact with Africans with tuberculosis. Our case is, to the best of our knowledge, the first to reveal this manifestation of M. africanum infection. It adds to the small list of cases of M. africanum diagnosed and reported in the United States.
Although some authors have questioned the validity of M. africanum as a unique species because of its biochemical similarities with Mycobacterium bovis and M. tuberculosis,5 molecular and genotypic analyses have established a distinct identity of M. africanum as a separate member of the M. tuberculosis complex.6-8 Traditionally, M. africanum has been identified by phenotypic and biochemical tests.5 Newer tests such as spoligotyping and polymerase chain reaction are more rapid, convenient, and accurate methods of identification.6-8
Speciation of M. tuberculosis complex assumes importance for epidemiological and treatment purposes.7 The therapeutic implications are particularly significant for M. bovis because of its inherent resistance to pyrazinamide.7 Mycobacterium africanum, on the other hand, has susceptibility patterns similar to M. tuberculosis.9 Although some animal studies have suggested low virulence of M. africanum compared with M. tuberculosis, disease course and outcomes have been alike.3,9,10
Treatment of brain tuberculomas by medical therapy alone can be successful, and surgical intervention is recommended if the diagnosis is uncertain or in the event of failure to respond to antituberculous therapy.11-13 On antituberculous treatment, existing tuberculomas may paradoxically enlarge, and new granulomas may appear, despite adequate therapy.14,15 This phenomenon does not necessarily imply failure of therapy; immune-mediated mechanisms have been suggested as a cause. 16 Medical therapy should be continued, and steroids dose may improve symptoms and outcome.16 Surgical intervention, however, may be needed for lesions that continue to enlarge or persist or in the event of complications such as hydrocephalus.17
In view of advanced diagnostic modalities and increasing trends of immigration, clinicians and microbiologists should be alert to the potential of M. africanum to cause disease in the United States.
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