Essay on Tuberculosis (TB)

Read this essay to learn about Tuberculosis. After reading this essay you will learn about: 1. History of Tuberculosis 2. Epidemiology of Tuberculosis 3. Transmission 4. Immunology 5. Prevention 6. Treatment.

Contents:

1. Essay on History of Tuberculosis
2. Essay on Epidemiology of Tuberculosis
3. Essay on Transmission of Tuberculosis
4. Essay on Immunology of Tuberculosis
5. Essay on Prevention of Tuberculosis
6. Essay on Treatment of Tuberculosis.

Essay on History of Tuberculosis:

Tuberculosis (TB) is a disease known since antiq­uity and evidence of spinal TB in the form of fossil bones dates back to around 8000 BC. TB occurred as an endemic disease among animals long before it affected humans. The first con­firmed instance of TB in humans was noted in the deformities of the skeletal and muscular remains of the Egyptian mummies of around 2400 BC.

However, it could not be determined whether the disease was due to M. bovis or M. tuberculosis. In the 1700s and early 1800s, TB prevalence peaked in Western Europe and the United States and was undoubtedly the largest cause of death. Hundred to 200 years later, it had spread in full force to Eastern Europe, Asia, Africa and South America.

Essay on Epidemiology of Tuberculosis:

In the late 1980s, TB began re-emerging and now globally, kills more than 2 million people each year. It is thought that as many as 2 billion people have been exposed to the TB bacillus and are therefore at risk of developing the active disease. According to WHO (1999), TB is known to be the largest cause of death of the human species.

There has been a resurgence of the disease over the last two decades with cur­rently eight million new cases and about 200,000 deaths annually. It is estimated that between 2000 and 2020, nearly one billion people will become infected, 200 million will acquire the disease and 35 million will die from TB (WHO, 2006), in con­trast to the 1.6 million deaths from TB in 2005. Both the highest number of deaths and the high­est mortality rate are in the Africa region. The two essential factors for the rapid spread of TB are; crowded living conditions, which favour airborne transmission and a population with little natural resistance.

TB in populations can be attributed to three distinct factors:

1. Infection of an individual in the community with tubercle bacilli within a given time pe­riod.

2. Development of the disease shortly after such infection.

3. The disease developing long after the origi­nal infection, owing to the reactivation of la­tent bacilli.

Today, TB is the leading cause of death world­wide from a single human pathogen, claiming more lives than diseases such as Human Immu­nodeficiency Virus/Acquired Immune deficiency Syndrome (HIV/AIDS), malaria, diarrhoea, leprosy and all the other tropical diseases combined. The pandemic of HIV/AIDS infection and the evidence of an associa­tion with TB, have caused marked increases in the incidence of the disease in some countries.

Because of its ability to destroy the immune system, HIV has emerged as the most significant risk factor for progression of dormant TB infection to clinical disease. The Global Programme on AIDS of the WHO estimated that in 1992 at least 13 million adults and 1 million children had been infected with HIV worldwide. The impact of HIV/AIDS infection on the TB situation is great­est in those populations where the prevalence of TB ‘infection in young adults is very high.

The number of cases worldwide is now in­creasing rapidly due to multi-drug resistant strains of M. tuberculosis as a result of patient non-com­pliance and also due to an increase in patients with HIV/AIDS.

About 450 000 multi-drug resistant tuber­culosis (MDR-TB) cases are estimated to occur every year; the highest rates are in countries of the former Soviet Union and China. There are a number of countries that have made remarkable progress in expanding population cov­erage with cure rates, whereas South Africa battles with more than 188 000 new TB cases per year.

South Africa is burdened by one of the worst TB epidemics in the world, with the disease rates more than double of those observed in other developing countries and up to 60 times higher than those currently seen in developed countries.

Current strategies for the control of TB cen­tres around treatment with multi-drug regimes based on the very effective combination of isoniazid (INH., Fig. 6.1a) and rifampicin (RIF., Fig. 6.1b). In endemic areas, the diagnosis and treat­ment of smear positive patients are emphasized in order to interrupt the spread of the disease within the community.

Obstacles to the success of this strategy are the difficulties of early diagnosis and operational problems associated with delivery of a treatment that involves administration of mul­tiple drugs over a period of at least six months.

Essay on Transmission of Tuberculosis:

The principal risk method of being infected with TB is by inhaling contaminated air containing microbes that cause this disease. TB microbes can be present in sufficient concentrations in the air to cause infections and the disease. Once in air, water evaporates from the surface of a particle, decreasing its size and concentrating its contents of microbes.

These par­ticle forms a droplet nuclei in which evaporation continues until the vapour pressure of the droplet equals to the atmospheric pressure. The droplet nuclei are very stable, settle very slowly and re­main suspended in the air for very long periods.

Droplet nuclei are produced when a patient with active pulmonary or laryngeal tuberculosis coughs, speaks, sneezes or sings. Coughing can produce 3000 infectious droplet nuclei, talking for 5 min­utes an equal number and sneezing can produce over a million particles with a diameter of less than 100 nm.

When inhaled, drop­let nuclei usually travel through the airway until they reach the alveoli. Larger particles that are deposited on the way are removed through nor­mal mechanism of airway clearance (Dannenberg, 1989).

Essay on Immunology of Tuberculosis:

TB is a prototype infection that requires control by the cellular immune response. In the first few weeks the host has almost no immune defence against infection by the bacteria causing TB. Small inhalation inocula multiply freely in the alveolar space or within alveolar macrophages. Unre­strained bacterial multiplication proceeds until the development of tissue hypersensitivity and cellu­lar immunity intervene.

The organism causing TB adheres to alveolar macrophages via multiple complements and might be destroyed in the phagosome. The intracellular mecha­nisms for killing or inhibiting the growth of the bacteria in alveolar macrophages include the production of nitric oxide and reactive oxygen inter­mediates.

Alveolar macrophages can also partici­pate, in a broader context of cellular immunity, through the process of antigen presentation and recruitment of T-lymphocytes, which are the white blood cells produced in the bone marrow but which mature in the thymus. These cells are im­portant in the body’s defence against certain bac­teria and fungi.

Macrophages which are antigens are pro­cessed in phagosomes via Major Histocompatibil­ity Complex (MHC) class II molecules to CD4 T- lymphocytes which are the major effector cells in cell-mediated immunity. The antigens bind to T- cell receptors on the surface of the T-lymphocytes. These CD4 T-lymphocytes tend to polarize into either Th1 cells (these are essential in controlling intracellular pathogens), producing predominantly interferon gamma (IFN-y) and interleukin 2 (IL-2) or Th2 cells producing predominantly cytokines interleukin 4 (IL-4), interleukin 5 (IL-5), interleukin 6 (IL-6), interleukin 10 (IL-10) and interleukin 13 (IL-13).

In mice, immunity correlates with a Th1 response. Macrophages infected with M. tuberculosis secrete interleukin 12 (IL-12), which in­duces the secretion of IFN-y by CD4 cells and natu­ral killer cells. The IFN-y enhances the activation of macrophages and improves their ability to pre­vent the spread of M. tuberculosis.

However, M. tuberculosis is not defenceless. It can produce ammonia to counteract phagosomal acidification. Its lypogly can actively scavenge toxic radicals reduced against it by the macroph­age.

Essay on Prevention of Tuberculosis:

The outcome of mycobacterial infection depends on the host immune response. In most individu­als, infection with M. tuberculosis induces an im­mune response sufficient for the protection against progression to the primary disease.

Bacille Calmette-Guerin (BCC) vaccine repro­duces minimal infection but does not impose a disease risk. BCG vaccine, which is derived from a strain of M. bovis attenuated through years of serial passage in culture, was first used in 1921 to protect against tuberculosis in humans. Many BCG vaccines are currently administered to 100 million young children each year throughout the world.

These vaccines are derived from the original strain but vary in cul­tural characteristics and ability to induce sensiti­zation to tuberculin. There are differences in tech­niques and methods of producing them as well as various routes of vaccine administration.

Essay on Treatment of Tuberculosis:

Before effective drugs were available, half of the patients with active pulmonary TB died within 2 years, and only a quarter were cured. With the advent of anti-TB chemotherapy, protracted bed rest and lengthy isolation became unnecessary, and in theory at least, successful treatment was a reasonable goal in all adults.

Mycobacterium is naturally resistant to most com­mon antibiotics and chemotherapy agents. This is probably due to their highly hydrophobic cell en­velope acting as an efficient permeability barrier. Due to the discovery of the effective antlmycobacetrial agentsethambutol (EMB., Fig. 6.1c), INH, pyrazinamide (PZA., Fig. 6.1 d), RIF and strepto­mycin (STR., Fig. 6.1e) between 1950 and 1970s, and reduction in poverty, there was a drastic de­crease in the number of TB cases especially in developed countries, however, since 1980s, the number of TB cases throughout the world has been increasing rapidly due to the emergence of MDR- TB.

The MDR forms of the disease, defined as forms resistant to two or more existing TB-drugs, are often fatal and are difficult and expensive to treat. The situation has recently been complicated by the association of TB with HlV in sub-Saharan Africa and many developing countries. The situation is ex­acerbated by the increasing emergence of exten­sively drug-resistant (XDR).

Reliable treatment therapy for TB treatment takes a period of 6 – 9 months with first line drugs (EMB, INH, PZA, RIF and STR). In the case of ac­quired drug resistance only second-line drugs (capreomycin, cycloserine, kanamycin and ethionamide) can be used and these have signifi­cant side effects with approximately 50% cure rate.

The current therapies reduce the pulmonary bacterial burden but the treatment periods of 6 months for non-immune suppressed individuals and at least 9 months for immune suppressed patients are re­quired for reliable treatment efficacy.

However, floroquinolones such as ofloxacin, norfloxacin can be used which are safer than the above-mentioned second-line drugs but have the disadvantage of being very expensive. Emer­gence of drug-resistant mycobacterial strains is alarming these days.

This occurs when a single drug is given alone and when the viable bacterial population in the lesions is large. The occurrence of drug resistance is widely thought to be due to the overgrowth of sensitive organisms by mutant resistant bacilli present in wild strains before they were ever in contact with the drug concerned.

There have been no new anti- TB drugs introduced in the past 30 years. Thus, there is an urgent need to search for and develop new effective and affordable anti-TB drugs.