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Introduction
Mycobacterium tuberculosis (Mt) is the organism that is responsible for causing tuberculosis (TB). This disease that existed as from the Neolithic era has been a quagmire to the medical field scientists even after the identification of the causative agent. This paper discusses M. tuberculosis with special focus on its structure and physiology, pathogenesis, epidemiology of the disease, treatment and prevention of the infection. Mycobacterium tuberculosis is a challenging bacterium due to its drug resistant tendencies that makes tuberculosis to continue spreading thus prompting for research into a vaccine or drugs that can overcome drug the resistance characteristic of the organism.
Structure and physiology of M. tuberculosis
Mycobacterium tuberculosis is classified as follows: Bacteria; Actinobacteria; Actinobacteridae; Actinomycetales; Corynebacterineae; Mycobacteriaceae; Mycobacterium; Mycobacterium tuberculosis complex (ExPaSy Proteomics Server, para 1). The organism is an acid-fast bacillus (rod-shaped). Its cell wall contains myoacid that is responsible for its acid-fast characteristic and the cell wall also makes it impenetrable to oral fluids since it is highly hydrophobic (due to it glycolipids and lipids). M. tuberculosis is barely affected by alkaline or acidic environment in addition to its resistance to complement lysis. The growth of M. tuberculosis is very slow and it takes up to 12 hours to replicate. In addition, the tubercle bacilli flourish in oxygen rich tissues since they are obligate aerobes. It is for this reason that the bacterium mainly infects the upper lobes of the lungs.
Pathogenesis and epidemiology
Human beings are the only known natural reservoirs of M. tuberculosis. The cell wall of Mt has neither extoxins nor endotoxins and its multiplication occurs in a phagosome. The phagosome avoids fusion with lysosome and thereby enzymatic degradation through production of exported repetitive protein. Two kinds of lesions are developed depending on the response from the host as well as the presence of Mt. Since the first site of infection is mainly the lungs, an exudative lesion occurs here (mostly lower in the lobes) as an acute inflammatory response.
A Ghon complex is an exudative lesion from both the parenchyma and lymph nodes. Other than the primary lesions located in the lower lobes of the lungs, the well oxygenated apices harbor the reactivation lesions. Reactivation lesions can also be located in the brain or bones since they are also well activated. The secondary lesion contains tubercle bacilli encapsulated by epithelioid cells and the lesion is known as a granulomatous lesion.
After the initial infection in the lungs, Mt can spread to other parts via erosion of tubercle or dissemination. The tubercle usually empties into the bronchus and spreads the disease agent to the rest of the lungs and the infection can be spread to other people through expectoration. The infection can also spread to the gastrointestinal tract following swallowing. The organism is capable of disseminating through the bloodstream and consequent spread to other parts of the body.
According to Mazurek et al., (para 7), it is estimated that up to 9 million new M. tuberculosis infections occur every year. In addition, an approximate 2 billion people have latent Mt infection. With about 3 million deaths resulting from Mt infections occurring every year, Mt is classified as the microbial agent that causes most deaths. Mt is passed from one person to the other through respiratory aerosol thus initial infection occurs in the lungs. Mt infections and TB cases are predominant in developing countries with up to 90% of the cases occurring in these nations. Moreover, a new TB infection arises every second (eMedicinehealth, para 14).
In the United States, active tuberculosis is 4.2 cases in 1000,000 persons according to 2008 estimates which reduced to 3.8 cases in 100, 000 persons in 2009. As of 2000, the prevalence rate of latent tuberculosis infection in the U.S. was 4.2 percent (Mazurek et al., para 8).
Diagnosis, treatment and prevention
Mycobacterium tuberculosis is diagnosed using a number of tests with chest x-ray being a leading diagnostic test to detect abnormalities in the lungs. A Mantoux (tuberculin) skin test is an immunologic test is also a common Mt test which tests the infection even when symptoms are absent. Interferon gamma release assays (IGRA) have also been developed to detect Mt. According to Mazurek et al (para 5), IGRAS detect sensitization to M. tuberculosis by measuring IFN-y release in response to antigens representing M. tuberculosis.
One of the already approved IGRA test is the QuantiFERON-TB Gold test. Sputum test is a confirmatory test for TB since the test detects the acid-fast bacilli. A culture of body secretions (including sputum) detects M. tuberculosis through growth of mycobacterium and the culture takes up to 12 weeks.
M. tuberculosis usually exhibits drug resistance hence multiple drugs are used in the treatment of the disease. Isoniazid had been the most common drug. To treat pulmonary TB, a combination of INH, rifampin and pyrazinamide is used with pyrazinamide running for 2 months whereas INH and rifampin are continued for 6 months. Ethambutol is a fourth drug that is used for up to 12 months in cases where there is INH resistance or in immmunocompromised patients.
It is notable that once the patient initiates treatment, the sputum is rendered noninfectious in 2-3 weeks. As a preventive measure, an attenuated vaccine has been produced from M. bovis but this confers partial resistance only and it cannot protect against infection. It is therefore advisable that other than using the vaccine as a prevention strategy, all milk should be pasteurized before consumption as this is helpful in avoiding intestinal tuberculosis. To improve host resistance to the organism, improved nutrition as well as housing is advocated for. Moreover, medical personnel can avoid Mt infection through sterile isolation procedures as well as using masks when handling the organism.
Since M. tuberculosis has continued to exhibit multiple drug resistance, it has become increasingly hard to treat TB. There is certainly need for new vaccines that can be used to completely control the infection whereas new drugs need to be developed to overcome multiple drug resistance. With detection of drug resistance genes in the Mt genome, it is expected that drugs that target the resistance genes will be developed as a new approach to preventing and treating TB. There are also prospects in development of recombinant vaccines in place of attenuated vaccine. While considering new prevention and treatment strategies, it is important to consider the effects of the new developments on immunocompromised persons since they are more prone to M. tuberculosis infection (Smith, p. 495).
Conclusion
Mycobacterium tuberculosis is one of the challenging microbial agents as it leads to a drug resistant infection known as tuberculosis. The acid fast bacillus primarily infects the lungs forming lesions as the organism multiplies in phagosomes. With one third of the worlds population being infected by this highly virulent organism that leads to many deaths, there is need to enhance diagnosis, treatment and prevention of the infection.
Multiple drug resistance must be countered by targeting drug resistance genes while recombinant vaccines should be developed to ensure that TB spread is effectively prevented. It will also be helpful to enhance host immunity through improved diet and housing as a way of preventing infection and disease. Without such measures, M. tuberculosis infection, disease and deaths thereof will continue plaguing human beings even in the 21st century.
Works Cited:
eMedicinehealth. Tuberculosis. 2010. Web.
ExPaSy Proteomics Server. HAMAP: Mycobacterium tuberculosis complete proteome. 2010. Web.
Mazurek, Gerald H., Jereb, John and Vernon, Andrew et al. Updated guidelines for using interferon gamma release assays to detect mycobacterium tuberculosis infection United States, 2010. CDC. Recommendations and Reports, 59(RR05):1-25.
Smith, Issar. Mycobacterium tuberculosis pathogenesis and molecular determinants of virulence. Clinical Microbiology Reviews, 13(3); 2003: 463-496. Web.
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