Extensively Drug-Resistant Mycobacterium tuberculosis, India

Emerging Infectious Diseases • www.cdc.gov/eid • Vol. 13, No. 9, September 2007 1429 niazid chemoprophylaxis due to resistance of the infecting organism. Decreased susceptibility to isoniazid among M. kansasii isolates is common (7,8), and this microorganism is naturally resistant to pyrazinamide (9). This pattern of resistance is a serious obstacle for the use of these drugs in monotherapy or when combined with rifampin in the prevention of lung disease caused by M. kansasii (10). The source of the infection in this patient is unknown. In a large series of infectious diseases associated with infl iximab therapy, nontuberculous mycobacteria were isolated in 9% of the patients who had mycobacterial diseases (2). As in our patient, these infections developed shortly after initiation of treatment with infl iximab, which suggests that reactivation of a latent infection is the most probable origin of the disease. Although a mildly positive tuberculin skin test result can be observed in patients infected with atypical mycobacteria, the strong reaction seen in this patient suggests a latent infection with M. tuberculosis (10). We could speculate on the possibility of a double infection with M. tuberculosis (contracted through household contacts with his father) and M. kansasii through environmental exposure. In this scenario, isoniazid chemoprophylaxis could have prevented the former but not the latter. In summary, failure of isoniazid chemoprophylaxis can be anticipated in patients who initiate treatment with infl iximab and who have latent infections due to M. kansasii. Despite routine antituberculous chemoprophylaxis, patients receiving infl iximab therapy should be carefully evaluated for lung infection caused by atypical mycobacteria.