The HIV epidemic has had a dramatic impact on rates of tuberculosis (TB) and on TB control in populations where both infections are prevalent.1 HIV infection, in particular advanced HIV infection (AIDS), is more potent than any other risk factor for the progression to disease of recent or remotely acquired TB infection.2 It destroys or renders ineffectual the 2 immune cells most important to the containment of tubercle bacilli, macrophages and CD4 receptor bearing lymphocytes.3 Among people coinfected with Mycobacterium tuberculosis and HIV before availability of highly active antiretroviral therapy, the estimated risk of active TB relative to patients with no other known risk factor for active TB was 170.0 times greater for AIDS and 113.0 times greater for HIV infection without AIDS.2 Cases of reactivation TB attributable to HIV infection increase the risk of transmission of M. tuberculosis within the community, thereby constituting a second, indirect mechanism by which HIV increases TB morbidity.4
In Canada, dormant or latent TB infection is most common in 4 groups: foreign-born people from countries where TB is endemic, Aboriginals, the inner-city poor and homeless, and elderly people.5 Coinfection with HIV is common among inner-city people with a history of injection drug use,6 and recent data suggest that HIV/AIDS is increasing among Aboriginals6,7,8 and among foreign-born people from countries where TB is endemic.9 Treatment of latent TB infection reduces the risk of progression to active disease in people with HIV–TB coinfection.10,11
Patients with TB constitute an important “sentinel” population for HIV screening. In some African countries with high TB prevalence, the prevalence of HIV among TB patients exceeds 70%.12 In the United States, between 1985 and 1992, TB patients were 204–fold more likely to have AIDS than the general population.13 The benefits of identifying previously unrecognized HIV infection are substantial, in terms of both preventing future HIV transmission and providing antiretroviral therapy to affected patients.14 Knowledge of the HIV serostatus of TB patients may also influence the treatment of their TB.15 Even among those not receiving antiretroviral therapy there may be an increased risk of adverse reactions from anti-TB drugs.16 Because HIV-infected patients are at risk of peripheral neuropathy, coadministration of pyridoxine with isoniazid may be prudent. Some HIV-infected TB patients have reportedly experienced malabsorption of their anti-TB drugs, so measurement of serum drug levels may be necessary if there is a poor response to treatment.14
It is thus important to identify and treat active TB or latent TB infection in HIV-infected people (as outlined in Fig. 1 and Table 1) and HIV infection in those with TB (as in Table 2).
Health care providers, administrators and those involved in TB control should strive to promote coordinated care for patients with TB and HIV and to improve information-sharing between TB control programs and HIV/AIDS programs.
These recommendations were prepared by the authors for the Canadian Tuberculosis Committee. The recommendations have been approved by the Centre for Infectious Disease Prevention and Control, Population and Public Health Branch, Health Canada; the Canadian Thoracic Society of the Canadian Lung Association; and the Canadian Infectious Disease Society. They were first published in the Canada Communicable Disease Report.32
Acknowledgments
We thank members of the Centre for Infectious Disease Prevention and Control, Population and Public Health Branch, Health Canada, including the Canadian Tuberculosis Committee, as well as the Canadian Thoracic Society and the Canadian Infectious Disease Society, for their critical review and ultimate approval of these recommendations. We also thank Sue Falconer for secretarial assistance.
Footnotes
This article has been peer reviewed.
Contributors: Dr. Long prepared the initial draft of the article. Drs. Houston and Hershfield critically reviewed the article for revision.
Competing interests: None declared.
Correspondence to: Dr. Richard Long, Department of Medicine, University of Alberta Hospital, Rm. 2E4.21, Walter C. Mackenzie Health Sciences Centre, 8440–112 St., Edmonton AB T6G 2B7; fax 780 407-6384; richard.long@ualberta.ca
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