The history, transmission, and pathophysiology of tuberculosis

Cobit, Tuberculosis

Tuberculosis

Tuberculosis (TB) was revealed to be infectious in 1865 and the bacteria that cause the disease were acknowledged in 1882. Even supposing the bacteria and means of extend were recognized, a drug that could eradicate the bacteria was not discovered until 1943. In the interim, infected persons, who were able to come up with the money for the cost, were sent to sanatoriums and rest homes as treatment. With the breakthrough of streptomycin in 1943 and two other drugs effectual against the TB bacteria by 1952, the cure rate significantly increased and the death rate considerably decreased (Tuberculosis 2007: From Basic Science to Patient Care, 2007).

TB is a continual bacterial contagion caused by a germ called Mycobacterium tuberculosis that grows best in areas of the body that have lots of blood and oxygen. It multiplies through the air when a person with the disease coughs or sneezes. A person may build up contagion of TB when they draw in the air droplets from the person who's sick with the ailment. The disease more often than not contaminates the lungs but can infect other parts of the body counting the spine, brain or kidney. Treatment is often a success but usually takes a long process of about six to nine months of treatment.

Tuberculosis can be considered as either latent that means that you have the TB bacteria in your body, but your body's immune system fight the infection and try to keep it from turning into active TB and you don't have any symptoms of TB right now and can't spread the disease to others. It can also be considered as active that means that the TB bacteria are growing and causing symptoms. If your lungs are infected with active TB, it is easy to spread the disease to others. It is an old disease and has been identified by a lot of names including consumption, wasting disease, and white plague.

Pathophysiology

Tubercle bacilli at the start produce a primary infection, followed by a latent or dormant phase and, in some cases, by dynamic disease. Infectivity is not transmissible in the primary and latent phases (www.merck.com).Tuberculosistakes place when individuals breathe in bacteria that where cough out by infected persons. The organism is deliberate on the increase and puts up with the intracellular setting, where it may wait metabolically static for years before reactivation and infection. The most important determinant of the pathogenicity of tuberculosis is its capacity to break away from host defense mechanisms, including macrophages and delayed hypersensitivity responses.

Humans are the solitary known reservoir for Mycobacterium tuberculosis and TB is transmitted by airborne droplet nuclei. TB exposure occurs by sharing common airspace with an individual who is in the infectious stage of TB and when inhaled, droplet nuclei are deposited inside the terminal airspaces of the lung. Upon encountering the bacilli, macrophages consume and transfer the bacteria to regional lymph nodes and these bacilli may be killed by the immune system, may proliferate and cause primary TB, may turn out to be dormant and remain asymptomatic, or may reproduce after a latency period.

From then on, transportation of the infected macrophages to the regional lymph nodes takes place. Lymphohematogenous spreading of the mycobacteria to other lymph nodes, the kidney, epiphyses of long bones, vertebral bodies, juxtaependymal meninges nearby to the subarachnoid space, and, occasionally, to the apical posterior areas of the lungs. In addition, chemotactic causes released by the macrophages create a center of attention to circulating monocytes to the location of infection, leading to delineation of the monocytes into macrophages and ingestion of free bacilli. Logarithmic reproduction of the mycobacteria arises within the macrophage at the primary site of infectivity.

Diagnosis

Tuberculosis is diagnosed by a consideration of clinical presentation, tuberculin skin test using the Mantoux procedure, radiographic examination, bacteriology, direct staining and culture of sputum or other specimens for the presence of M. tuberculosis, molecular amplification and gene probes assist in rapid diagnosis. Definitive diagnosis of TB rests on isolation of M. tuberculosis from sputum, urine, biopsy material, CSF or other clinical specimens. A negative sputum test does not rule out a diagnosis of TB. Recovery and identification of mycobacteria from specimens has become more rapid with test procedures such as liquid medium systems and DNA probes (Communicable Diseases Section, Victorian Government Department of Human Services, 2005).

Tuberculin skin test (Mantoux test) which is a not detrimental test used to become aware of whether or not the TB germs are in the body. In some cases, you may be asked to have this analysis repeated at a later date. A chest x-ray is indispensable for excluding the existence of TB in the chest. It may also be essential to have follow-up chest x-rays at intervals for some three years following contact.

The most extensively used procedure for diagnosing tuberculosis is no more complicated than examining a suspected patient. Having a sputum sample under a microscope is one way to evaluate whether it contains TB mycobacteria. Even though this means diagnosis is not expensive and achievable even in isolated areas provided you have trained staff, there are serious limitations connected with this technique, as many people with active TB will not have adequate TB mycobacteria in their sputum, or indeed will have none at all. This is factual for patients suffering from extra-pulmonary TB and for patients co-infected with HIV.

Microscopy is also of incomplete use for becoming aware of TB in children, because they often do not bring into being sufficient amount sputum to make a reliable sample. Even in the best of hands, microscopy will only detect around half of all TB cases. A different technique, identified as culture, consists of incubating a sputum sample over a few weeks to observe whether it contains live TB mycobacteria. Although this is a more responsive process when performed correctly, it is unfortunately slow, as you need to pass the time at least around three weeks, and every now and then up to eight weeks, to be certain no mycobacteria are there. It is also logistically easier said than done, requiring incubators, an uninterrupted power supply, and skilled staff.

More present methods such as those relying on DNA tests, for instance, are excessively sophisticated to be used in poor settings, in particular where tuberculosis takes its heaviest toll. What we need is a straightforward test that tells you when you have active TB, which gives way results more or less instantaneously and can be used by any nurse or health worker even when far away from a laboratory. Until we have an uncomplicated dependable test, many TB patients will keep falling through the net and die untreated.

The need for a suitable diagnostic tool is all the more pressing considering tuberculosis is for the most part a curable disease. TB is treated with a combination of antibiotic drugs which were developed over 35 years ago. At around U.S.$15 to 20 per patient, the treatment course is cheap. To prevent the emergence of any resistance, the drugs should be taken in combination. It is therefore recommended that TB drugs are produced in fixed-dose combinations or different drugs combined in a single pill.

Strategies to Control TB

The cost-effectiveness of short-course drug therapy for TB has been central to the global promotion of directly observed treatment short course (DOTS) by the World Health Organization. However, the DOTS approach alone may not be sufficient to bring TB under control, and interest is growing in other methods, such as developing a more effective vaccine, treating latent TB infection, testing for TB drug resistance, treating HIV co-infection, and active case finding. It is not clear how money can be best allocated for TB control; although DOTS programs are a good value, their full cost may be greater in countries where a broader investment in the health sector is needed (Tuberculosis, Perspectives in Health, 2009).

Impact of Tuberculosis

TB is a disease of young people. This is due to the fact that the greatest predictor of disease due to TB is the amount of time that has passed since infection with TB, this risk being greatest within 5 years of first becoming infected with TB. Even in countries where TB is uncommon and most disease arises from remote infection, most individuals who will be infected become infected by the age of 20 years. The association of TB with youth makes this disease an important factor in the economy of many countries, which simultaneously experience a low gross national product and a high incidence of TB, because the disease affects the most economically productive sector of the economy.

As a result, an organized TB control program, unlike many other health-related activities, is a net contributor to economic development (Kaufmann and Hahn, 2003). Once infected with TB, women of reproductive age are more susceptible to developing active TB than men of the same age. As a result, in certain regions, young women ages 15 to 24 with TB outnumber young men of the same age with the disease.

Strategies to Prevent TB

Preventive measures BCG vaccination has limited application in developed countries where the incidence of TB is low. It is an effective vaccine in reducing TB meningitis and death in babies and children less than five years in countries of high TB prevalence. It is not recommended for general use in the Australian community but should be considered for specific high risk groups such as infants and young children traveling for extended periods to countries with a high incidence of TB (Communicable Diseases Section, Victorian Government Department of Human Services, 2005).

Prevention Cost

Bacille Calmette-Guerin (BCG) vaccine, a live attenuated preparation derived from Mycobacterium bovis, is given to approximately 75% of infants worldwide. It is estimated that the number of tuberculous meningitis and miliary TB cases prevented by BCG vaccination and calculated the cost of vaccination per TB case or death prevented and the cost per disability-adjusted life-year (DALY) gained. They used estimates of prevalence of smear-positive pulmonary TB, contact rate, and annual risk for infection by country to extrapolate numbers of cases and deaths prevented in children in the 5 years after vaccination. They calculated illness and deaths prevented by geographic region using estimates of BCG efficacy (73% against tuberculous meningitis and 77% against miliary TB) from the published literature and a cost estimate of $2-$3 per BCG dose (Journal Watch Infectious Diseases, 2006).

Reference List

Communicable Diseases Section, Victorian Government Department of Human Services, 2005. The Blue Book: Guidelines for Control and Infectious Diseases. Victoria, Melbourne: Communicable Diseases Section, Public Health Group.

Kaufmann, S.HE., & Helmut, H. (2003). Mycobacteria and TB. Basel, Switzerland: S. Karger AG.

Palomino, J.C., Leao, S.C., & Ritacco, V. (Eds.). (2007). Tuberculosis 2007: From Basic Science to Patient Care. BourcillierKamps.

Trunz BB et al. Effect of BCG vaccination on childhood tuberculous meningitis and miliary

Tuberculosis worldwide: A meta-analysis and assessment of cost-effectiveness. Lancet 2006 Apr 8; 367:1173-80.