Tuberculosis and Human immunodeficiencv virus infection
Dr. Charoen Chuchottaworn M. D.
Central Chest Hospital,
Ministry of Public Health,
Nonthaburi, Thailand 11000.
Tuberculosis is an old disease which had long history with human being dated back to the Egyptian era. The advance of chemotherapy for tuberculosis in the past fifty years has given a chance to eliminate tuberculosis from the health problem. Unfortunately, an explosive epidemic of new emerging virus, Human Immunodeficiency virus type I (HIV), has burned out all the chance to eliminate tuberculosis. The interaction between tuberculosis and HIV infection are mutually related. From knowledge of basic pathogenesis of HIV infection, HIV attacks CD4 T lymphocyte which is the core cell of human body's immunity. The virus entered into the cells and survived from host immunity. The virus can multiply itself in lymphocyte and eventually destroys the hosted lymphocyte. The viruses which bursted out from destroyed hosted lymphocyte will infect other CD4 T lymphocytes again. This vicious cycle will repeat again and finally the number of CD4 T lymphocyte decreases down which means that body's immunity is deteriorated especially for cell mediated immunity. Infections which need cell mediated immunity for protection are easily to be occured such as infection with fungus, mycobacteria and many other intracellular organisms. Tuberculosis is one of the infection which need cell mediated immunity to prevent or protect infected persons to develop an active disease. So theoretically, pandemic of HIV infection must have obvious impacts on the epidemic of tuberculosis. And tuberculosis is the single most important opportunistic infection in HIV infected patients because it is the only disease in HIV infected patients which can transmit to healthy or immunocompromised persons and causes a disease. Co-epidemic of HIV infection and tuberculosis will deteriorate epidemic situation of both diseases.
Prevalence of HIV seropositive in tuberculous patients
Seroprevalence of HIV infection in tuberculosis patients in each geographic area is varied regarding to HIV epidemic rate. The reported HIV seroprevalence rate in tuberculosis patients was 0-50% in the United States. In the sub sahara countries, the higher seroprevalence could be seen which was 20-50%. In Thailand HIV seroprevalence varied from region to region. In the northern region which is higher HIV infection epidemic area, the HIV seroprevalence in tuberculosis was 20-40%. In southern region, the HIV seroprevalence rate was 17% and in Bangkok, the HIV seroprevalence was 15-25%.
Impact of HIV infection epidemic to tuberculosis epidemic
From the epidemiological study in pre-chemotherapentic era have shown that not every infected person with tubercle bacilli developed active tuberculosis disease. Nearly 10% of infected persons proved by tuberculin test had developed active disease and approximately 5% would developed disease in 5 years after infection. This figure has been change in HIV infected patients. Approximately break down rate to active tubcrculosis in HIV infected patients with tuberculin test positive was 7-10% per year or 50% in 10 years. In some studies which did not determine tuberculin reactivity of HIV infected patients has also shown a higher rate of reactivation as compare to the control patients. This means that more number of new tuberculosis patients will be occured from the pool of tuberculosis infected persons in population. In Thailand, the estimated number of HIV infected patients is 1 miuion in the year 2000. These are in the age group of 20-40 years old which had tuberculin test positive rate of 20% from the prevalence survey. So 200,000 HIV infected patients has already been infected with tuberculosis and these patients will develop to be new active tubcrculosis of 14,000-20,000 per year which will add up to the pool of active tuberculosis in this country.
For patients who have been infected with HIV before infected with tubercle bacilli, these patients will have rapid progression of tuberculosis instead of can be controlled by immunity. This rapid progression tuberculosis can be easily seen in nosocomial infections with tuberculosis in HIV infected patients. The available molecular technique of RFLP was used to prove nosocomial transmission. The transmission can occur not only by drug susceptible strains but also multidrug resistant strains. These rapid progression of recent infection of tuberculosis will increased the number of active tuberculosis cases. Eventhough the infectiousness of tuberculosis in HIV infected patients was the same as non-HIV infected patients. It is more likefy to have more transmission of infection in HIV infected patients because there is a more number active tuberculosis in HIV infected patients and these patients usually lived in a closed area or living-place such as intravenous drug abuses patients.
Impact of active tuberculosis on the course of HIV infection
Because tuberculosis is a potent immune stimulator and increases production of many cytokines such as tumor necrosis factors. These cytokines induce HIV replication in CD4 T-lymphocyte. So active tuberculosis in HIV infected patients stimulates replication of HIV and then accelerates the more deterioration of immune status. Other evidences which suggest that tuberculosis accelerate the deterioration of immune status are that tuberculosis was associated with CD4 T lymphocyte depression and treatment of tuberculosis restored CD4 T lymphocytes. Cohort of HIV infected patients with tuberculosis had higher rate of opportunistic infections and mortality rate than HIV infected patients without tuberculosis.
Impact of HIV infection on the course of tuberculosis
Many direct effects of HIV co-infection on tuberculosis patients could be observed. First of all, clinical presentations of tubereulosis in HIV infectcd patients are more "atypical" than in non-HIV infected patients and varied regarding to immune status of patients. These atypical features made tuberculosis was more difficult to diagnose. More extrapulmonary and disseminated disease could be seen. Laboratory technique had lower sensitivity and specificity in HIV infected patients. And because of these atypical features, patients usually had delayed diagnosis.
Tuberculosis patients who had HIV infection usually did not adhere to treatment even with short course regimen. This is an important problem bccause non-compliance patients created treatment failure and induced drug resistance. In clinical trials,it was easy to keep compliance rate under the trial condition but in routine practice, complianee usually
