Abstract

The mycobacterium tuberculosis species is responsible for thousands of deaths resulting from the tuberculosis disease. Owing to its relationship with this disease, the bacterium is a great source of concern among the academic field. The basic structure of the bacterium makes it an ideal cause of the disease. Further, the species has a waxy coating that makes it highly resistant to treatment because it makes the cells impervious. The bacterium that was first detected in 1882 can only reside within the human body thus limiting its survival rates. However, this means that it tends to attack the human body by concentrating on the lungs. Ideally, the bacterium has a high affinity for oxygen thus confining it to the upper parts of the lungs within the human body. The unique nature and structure of the bacterium unlike other species makes it an ideal subject of study.

Mycobacterium tuberculosis

Mycobacterium tuberculosis is a pathogen that is restricted to a particular condition and is a species in the mycobacteriaceae family (Ferguson & Rhoads, 2009). This pathogenic bacterium is the causative agent of dreaded Tuberculosis disease that affects thousands of people across the globe. According to Patil (2015), tuberculosis is an airborne disease that is highly contagious and comes about due to the mycobacterium tuberculosis bacterial infection. This bacterium was detected in 1882 for the first time by one Robert Koch (Agyeman & Ofori, 2017). Studies conducted over past decade have shown that mycobacterium tuberculosis depends on only human beings as its reservoir. This bacterium has a waxy coated wall on the surface of its cells. The waxy coating is present because of an acid known as mycolic acid (Saxena et al, 2014). This mycolic acid is a type of a fatty acid that covers the walls hence they cannot be digested. Further, the existence of this wall means that the lung cells cannot be able to fight the bacterium off. Cole et al, (1998) observes that the pathogenic bacterial species has a high affinity for oxygen. Immediately the pathogen gets to the lungs, it has a safe place to hide which is a strategic place for the disease to be initiated.

The nature of the bacterium and its high affinity for oxygen dictates its location within the human body. In addition, the fact that the bacterium can only survive within the human body limits its possibility of survival externally (Kamerbeek et al, 1997). The complexes of Mycobacterium tuberculosis are constantly located in the top area of the lobes of the lungs. This is because the bacterium requires oxygen for survival and the upper part of the lungs has sufficient air or oxygen. This bacterium is in most cases referred to as a pathogen which has the host as its inhabitant (Telenti et al, 1993). It is part of a makeup that consists of nine species at least. The species are: M. bovis, M. microti, M. mungi, M. tuberculosis sensu strictu, M. pinnipedii, M. africanum, M. canetti M. capraes and M. orygis. Studies have also observed that a number of Mycobacterium tuberculosis species only infect the specific population of humans by adjusting their structures (Smith, 2003).

The bacterium is also unique due to its ability to restructure and therefore improve its resistance to treatment. Consequently, the bacterium is stubbornly resistant to treatment (Russell, 2001). The mycolic acid makes it impossible for the cells to be affected by the Gram staining. The Gram staining is a practical method used to increase the difference in an image by a microscope. This means that the mycobacterium tuberculosis results come out as either positive or negative on the Gram staining result. The full DNA sequence of the bacterium has its initial publishing in 1998 (Smith, 2003). The sequence showed a striking large amount of ability to yield enzymes that lead to the break down and the build up of fats also known as lipids.

The transmission of the mycobacterium tuberculosis is very easy since it is remarkably impervious of being affected by chemicals and also drying.  It is not able to move hence it is non motile and it is not able to yield pores. It takes 15-20 hours for the bacterium to divide which is highly on the slow side because the tough walls of the cells makes it hard for necessary nutrients to pass through (Danelishvili et al, 2003). In contrast, other bacteria divide in minutes. Ultimately, the bacterium it is a rod-shaped small bacterium and is able to bear disinfectants that are not strong.

Conclusion

Mycobacterium tuberculosis is one of the most significant bacterial species for its role in causing the tuberculosis disease. Indeed, its basic structure is ideal for causing the deadly disease as evidenced by the high resistance it has on medications. The bacterium has a waxy coating on its cell surface that is rather unusual among bacteria of such species. This coating makes the cells impervious thus making it very hard to detect when taken through a Gram staining. Having being detected in 1882 for the first time, the bacterial species depends on human bodies as the only reservoir thus limiting its chances of survival outside of the body. However, the high affinity that the bacteria holds for oxygen means that is resides within the lungs of the human body and poses major concerns for human health. Within the lungs, the bacterial species maintains its position within the upper parts of the lungs that have high oxygen content. Overall, the fact that the bacterium causes tuberculosis makes it highly significant to study.

References

Agyeman, A. A., & Ofori-Asenso, R. (2017). Tuberculosis—an overview. Journal of Public Health and Emergency, 1(1).

Cole, S., Brosch, R., Parkhill, J., Garnier, T., Churcher, C., Harris, D., … & Tekaia, F. (1998). Erratum: Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence. Nature, 396(6707), 190.

Danelishvili, L., McGarvey, J., Li, Y. J., & Bermudez, L. E. (2003). Mycobacterium tuberculosis infection causes different levels of apoptosis and necrosis in human macrophages and alveolar epithelial cells. Cellular microbiology, 5(9), 649-660.

Ferguson, L. A., & Rhoads, J. (2009). Multidrug‐resistant and extensively drug‐resistant tuberculosis: The new face of an old disease. Journal of the American Academy of Nurse Practitioners, 21(11), 603-609.

Kamerbeek, J., Schouls, L. E. O., Kolk, A., Van Agterveld, M., Van Soolingen, D., Kuijper, S., … & Van Embden, J. (1997). Simultaneous detection and strain differentiation of Mycobacterium tuberculosis for diagnosis and epidemiology. Journal of clinical microbiology, 35(4), 907-914.

Patil, J. S. (2015). Current Treatment of Tuberculosis. J Pharmacovigil, 3, e143.

Russell, D. G. (2001). Mycobacterium tuberculosis: here today, and here tomorrow. Nature Reviews Molecular Cell Biology, 2(8), 569-586.

Saxena, P., Asthana, A. K., & Madan, M. (2014). Comparison of microscopy and PCR in detection of Mycobacterium tuberculosis. Journal of Microbiology and Infectious Diseases, 4(04).

Smith, I. (2003). Mycobacterium tuberculosis pathogenesis and molecular determinants of virulence. Clinical microbiology reviews, 16(3), 463-496.

Telenti, A., Imboden, P., Marchesi, F., Matter, L., Schopfer, K., Bodmer, T., … & Cole, S. (1993). Detection of rifampicin-resistance mutations in Mycobacterium tuberculosis. The Lancet, 341(8846), 647-651.

 
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