Tuberculosis (TB) is a disease which was first isolated by Robert Koch, a German physician in 1882. It is an infectious disease which mostly affects the lungs but it can cause effects to other bodily organs. The causative parasite for Tuberculosis is a bacterium that takes the shape of a rod (measuring two to four micrometers in length and 0.2 to 0.5 micrometers in width), non-motile, and fairly large, called Mycobacterium tuberculosis. The parasite is of the Actinomycetes relationship. The bacterium’s physiology of a 15-20 hour generation time has been thought to result to its virulence. The cell wall is however, due to the presence of concentration of lipids, thought to be the main contributor for the virulence of the bacterium. The bacteria possesses a characteristic of resistance to attack from oxygen radicals among other agents like oxygen radicals, cationic reagents and lysozomes in the phagocytic granules due to, as thought, the lipids-alpha branched type-in the cell wall. They may also render the bacterium unlikely of attack by complement deposition in serum (Todar, 2008).
In the mycobacterium family is also the mycobacterium bovis which is the bacteria responsible for causing atypical tuberculosis. They are known as colonizers due to their living together with other bacteria in human bodies, and although they do not cause disease they may cause an illness which is clinically like typical tuberculosis. It is usually difficult to diagnose the types of illnesses that are caused by the atypical mycobacterium since they require repetitive attention by medicines and a period of about 1 and 1 and a half to two years for dosage. Atypical mycobacterium was the often cause of tuberculosis in children but chances have decreased because most of the milk fed to children is now pasteurized. Extrapulmonary TB may develop as a result of the consumption of unpasteurized milk by humans. A disease that is similar to TB and that prevails in people suffering from AIDS is caused by Mycobacterium avium. Leprosy is caused by a similar genus mycobacterium leprae. A human being is the only reservoir for mycobacterium tuberculosis where as the bovis type can reside in cows and humans but is rare in humans (Todar, 2008).
How the disease is passed on
During the breathing process, very small particles in the air carrying infected sputum from a sick person may be taken in. The infected person may have taken out the said sputum via normal processes like shouting, coughing, sneezing (majority cause), or spitting. People who are nearby can then pick these bacteria into their lungs through inhalation. A diameter of five micrometers is the tendency size for most effective droplet nuclei, which may be produced also through coughing and talking (Todar, 2008). A person who is about 10 feet away may be affected by inhaling the particles, and this forms the initial stage for the takeoff. The second stage involves the multiplication of the bacteria which happens in a virtually unrestricted way in macrophages that are un-activated. The microphages may burst due to the continued multiplication of the bacteria, which (bursting) can take effect at up to about 21 days from the first stage. More macrophages may emanate from the peripheral blood, but cannot destroy the bacteria since they are inactivated after the phagocyte of the bacteria. In the third stage, the lymphocytes-specifically the T-cells-which are beginning to infiltrate will recognize the mycobacterium antigens in the context of MHC molecules. The macrophages are activated due to IFN-gamma interferon’s liberation. Cytokines’ liberation and activation of the T-cells may also occur. The mycobacterium will not be controlled by AMI-antibody mediated immune if it is intracellular, whereas this immune may not kill it complementary if it is intracellular (the actual state), owing to much of the present lipids. The host at this stage will produce a vigorous cell-mediated immune (CMI) response, which makes the individual tuberculin-positive. In addition, Todar (2008) observes that the formation of tuberculosis starts at the third stage. The semi-solid or “cheesy” consistency of the mycobacterium is the characteristic of the tubercles, and owing to low pH and anoxic environment, the mycobacterium cannot multiply within the tubercles but will persist within them for extended periods. The mycobacterium uses the inactivated or poorly activated macrophages among the many that surround the tubercle during the fourth stage. The tubercle will grow as a result of the mycobacterium using these inactivated macrophages. Spreading of the bacterium to other areas will occur if arteries and bronchi are invaded by the tubercle which is growing. This may result to formation of milliary tuberculosis-millet seed-sized metastasizing tubercles (extrapulmonary tuberculosis), which may end up with the formation of secondary lessons. A characteristic with the fifth stage is the liquefaction-that leads to more growth of the bacterium which then starts to multiply extracellularly-of the tubercles caseous center whose reason is unknown. The walls of the bronchi may then rapture, letting the bacterium spread to other areas. Small percentage of the mycobacterium will mostly develop to the advanced stages and small percentages of the mycobacterium infections will result into diseases. This is because the host will begin to resist the effects of the mycobacterium or the infections.
Although the mycobacterium tuberculosis lacks classic bacteria virulence factors like fimbriae, capsules, and toxins; virulence has been contributed to physiological properties of the bacterium such as the following (Todar, 2008);
- Mycobacterium tuberculosis can counteract the toxic effects of reactive oxygen intermediates produced during phagocytosis.
- The ability of the mycobacterium tuberculosis to grow intracellularly is an effective way to attack the immune system of the host
- The mycobacterium tuberculosis possesses special cell entry mechanism which enables it to directly bind to the mannose receptors of the macrophages or indirectly through certain complement receptors or Fc receptors.
Drinking un-pasteurized milk may lead to transmission of the atypical bacteria.
After inhalation of the tuberculosis bacteria, a local lung infection-pneumonia may formerly be the result. Hilar lymph nodes near the heart organ are usually swelled.
Tuberculosis in its first stage is referred to as primary tuberculosis and here neither spreading of the bacteria does not occur nor does development of symptoms occur (Schiffman, 2008). The body’s immune system may succeed by rendering the bacteria inactive by forming scar tissues around the bacteria. Thus the spread of bacteria is hampered. The body may further react by depositing calcium from the blood stream onto the scar; a condition called calcification and causes the scar and the lymph nodes to harden. X-ray examination may reveal these scars as round marbles called a granuloma. They are easily differentiated from cancerous infection indicators by the evidence of the calcium on x-ray examination.
Secondary or the reactivation tuberculosis may occur if the body’s immune system is not strong enough to prevent the breakage of the bacteria through the aforementioned scar tissue. The inability of the immune system to stop break through of the bacteria may result from several issues which may include but are not limited to old age, attack by other infections such as cancer, some medications such as those used to treat inflammatory bowel or arthritis disease, anti-cancer drugs, and cortisone medications. Pneumonia may re-occur when the bacterium breaks through. The most involved parts affected beyond the lungs are the brain lining, kidney, bones, and spinal cord.
Figures indicating that around ten to fifteen million people carry TB and that close to 22,000 new cases in a year have been produced (Schiffman, 2008). People with higher risk of being infected with the TB include those in nursing care hospitals or units, diabetics and HIV infected victims of some cancerous illnesses, alcoholics and drug addicts among others. This may be used as a preventative precaution by anyone who intends to put first-hand measures towards the prevention of attack by this disease.
The symptoms
Patients may only show symptoms after several months of initial infection. The following are symptoms indicating an active TB (Staszewski & Boulinier, 2004).
- General body weakness, tiredness, fever, coughing, and chest pains
- Coughing out a sputum
- Coughing out of sputum with blood or blood
- Shortage of breath
- Loss of weight
- Sweating at night
Vaccination and effects
Vaccination assists the bodies through production of antibodies when it is exposed to a dead or attenuated live parasite. The production of these antibodies is necessary to render the body protective from the targeted illness or disease in the future or at present. Other products with antigenic properties may be utilized in place of killed microorganisms or attenuated ones. An example of the products with antigenic properties is the red blood cells of a sheep. Many aspects of the evolutionary ecology of a particular disease like TB can be addressed when experimental exposure to controlled amounts of antigens is applied to natural populations (Grenfell, 1995). Production of the antibodies is known as humoral immune response. The spread of tuberculosis can be controlled through vaccination. It is believed to be important in areas with common cases of TB, unlike the United States. Vaccination with BCG-Bacille Calmette Guerin (mostly helping infants and children) does not remove the likelihood of being infected at adulthood on exposure to the bacteria, and this calls into question the effectiveness and the utility of this vaccine.
As observed by Grenfell (1995) selection pressure caused on the bacteria like TB and other parasites by a vaccination program may lead to the evolution of such parasites. There have been escaping mutants that display epitopes that are not recognizable by the immune systems of the vaccinated individuals which have arisen. A parasite may respond to counteract the vaccine (Virulence) and this has been linked to the life-history trait of the pathogens. The transmission rate is another theoretical development. Trade-offs between virulence and transmission may result in the evolution of higher virulence due to competition among parasite strains. According to Staszewski and Thierry (2004), the pathogens become fitter when their life-history traits undergo evolution.
Drug-resistant Tuberculosis
Certain populations in some countries are at a danger of exposure to tuberculosis that does not respond to treatment. Patients in Southeast Asia have been indicated to have a drug-resistant TB resistant to INH. The INH-resistance of TB may be as a result of presence of INH-like substances in the cough syrups in Southeast Asia. Proper Tuberculosis management can help avoid the resistance of TB to drugs. Prison populations are also at high risk of exposure to Drug-resistant TB. Doctors and health personnel should be warned and alert over bad prescription, inappropriate and inadequate dosage since they can increase the likelihood of resistance of tuberculosis to drugs. The case of drug-resistant TB reveals to us that the third world countries and extremely poor countries which do not have adequate access to good medicine are at a higher risk of TB infection than the developed world where the majority have access to proper medical care and attention. Third world countries as well as the poorest countries which have poor economies cannot support the best health systems and programs to counter the TB disease. Implications concerning the price of medication arise causing the poor to wait until the disease develops to complex forms and/or develops resistance to drugs as a result of compromised medical attention at a lower cost (Thierry, 2004). Furthermore, these countries do not have full access to recent methods and technology to care for the patients.
As noted by Schiffman (2008) there has been found out that tuberculosis can develop resistance to even at least two drugs introduced to patients first, namely INH and the Rifampin, and the extremely resistant types which also show resistance to drugs offered in the second-line dosage. These are referred to as Multi-drug resistant tuberculosis-MDR-TB and XDR-TB respectively. Countries reported to have common cases of the latter are those found in Asia and the former Soviet Union, although it is locatable in the rest of the parts of the world. Increased HIV disease in Africa has been linked to the development of multiple and extremely drug-resistant types of TB.
The resurgence of TB may be checked by control of HIV which increases the chances of patients contracting TB as an opportunistic infection because of the decreased body immune system. The danger of exposure to TB is, therefore, higher in the countries with higher figures of HIV infections than those with lower figures. Citizens in countries faced with extreme poverty and thus poor medical access due to partially/inadequately funded programs to counteract HIV are also at a higher level of danger of TB. Other constraints that make these people at a higher risk include inaccessibility to good food and child immunization programs. Good laboratories in all countries can help people detect drug-resistant types of TB and proper TB care can reduce or eliminate the development of drug resistance. Since the spread of Tuberculosis is closely tied to HIV infection, for example in Africa, it is important that the HIV and TB care be carried out hand in hand to curb the spread of TB (Schiffman, 2008).
References
- Grenfell, B. and Dobson, A.P. (1995) Ecology of Infectious Diseases in Natural Populations. Cambridge University Press
- Todar Kenneth. “Tuberculosis”. 2008.
- Schiffman George. “Tuberculosis” Schoenfield Leslie (ed). 2008. Web.
- Staszewski Vincent & Thierry Boulinier. Vaccination: A way to address questions in behavioral and population ecology? 2004. Trends in Parasitology. Vol.20 No.1