Tuberculosis is one of the most frequent AIDS-defining illnesses and opportunistic infections in the United Kingdom, comprising 27% of all AIDS diagnoses in 2003. The Health Protection Agency estimates that 4% of HIV-positive people in the United Kingdom have tuberculosis, the majority of whom are from Africa.1 The incidence of tuberculosis in the general population has risen sharply over the past ten years.
Globally, tuberculosis is the most common serious HIV-related opportunistic infection. Approximately one third of the 40 million people living with HIV or AIDS worldwide are co-infected with tuberculosis. The vast majority live in sub-Saharan Africa and among this population, tuberculosis is a leading cause of illness and death. At the same time, countries that have a large HIV-infected population are having difficulty containing the spread of tuberculosis.
The onset of the AIDS epidemic saw a marked increase in the number of cases of tuberculosis worldwide because HIV and tuberculosis interact in a number of dangerous ways. For example, both infections affect the immune system in ways that can alter the natural course of either disease. As a result, HIV changes the symptoms and natural course of tuberculosis, leading to far more extrapulmonary disease. Co-infection complicates the medical management of both diseases, partly because there are interactions between the medications used to treat each disease.
Because of HIV's effect on the immune system, people with HIV are at least seven times more likely than HIV-negative people to develop primary tuberculosis within the first six months of M. tuberculosis infection. Vaccination has little effect on this risk.
People with HIV and latent tuberculosis are also far more likely to develop active disease, with an 8 to 10% chance of developing active disease each year, compared to a total lifetime reactivation risk of about 5% in the HIV-negative population.2 As damage to the immune system worsens, people with HIV are more likely to develop extrapulmonary tuberculosis.
Active tuberculosis has been shown to increase HIV viral load, which might be expected to accelerate loss of CD4 T-cells and disease progression.3 However, a more recent study of South African patients has suggested that high viral loads after a tuberculosis event may be due to pre-existing high viral load rather than tuberculosis itself.4 Viral load may remain elevated if the tuberculosis is not successfully treated, or may remain elevated in some people despite successful treatment.
Although antiretroviral therapy can substantially reduce the incidence of tuberculosis by 70 to 90%, recent studies have shown that most children and adults with HIV continue to have an elevated risk of contracting tuberculosis despite immune reconstitution.5 6 This elevated risk has been seen both in the UK7 and in Africa.8 9
Since effective antiretroviral therapy extends life expectancy, it is possible that the lifetime risk of developing tuberculosis may not be substantially reduced by HIV treatment. However, immune reconstitution removes some of the difficulties caused by HIV-related immunosuppression in terms of tuberculosis diagnosis.10
Antiretroviral therapy also reduces the incidence of TB at a population level among people living with HIV when a high level of access is achieved. A study in a South African township has shown that within three years of the introduction of ART new TB cases fell by 60% among people with HIV. By the end of the period 24% of all people with HIV and 90% of those eligible were receiving ART.11 Another South African study found that provision of both ART and isoniazid reduced the incidence of TB by 85% in a cohort of 2778 patients followed for just over three years, and that the effect of the combined intervention was significantly greater than the effect of either intervention alone on TB incidence.12