Mycobacterium tuberculosis is a respiratory pathogen that attacks the human lungs, causing a disease known as tuberculosis. Tuberculosis is among the major bacterial infectious diseases that cause death globally. The bacteria spread from one person to another through tiny droplets from sneezes and coughs. However, Mycobacterium tuberculosis invasion into the immune system is not the same as having an active tuberculosis infection. Mycobacterium tuberculosis invasion involves three stages that include exposure, latent and active tuberculosis disease. Mycobacterium tuberculosis is a unique and prevalent pathogen with different morphological structures, grain stain characteristics, virulence factors, susceptibility to antibiotics, symptoms, mechanisms of invasion into the immunes system, and interactions with the host that result in either tuberculosis disease or latent TB infection.
According to Smith (2003), Mycobacterium tuberculosis invasion into the immune system results in either active tuberculosis disease or latent infection. The bacteria attack the human lungs, but it has the potential of affecting other parts such as the brain, kidney, and spine. Even though there are worldwide tuberculosis vaccines and antituberculosis agents, the impact of mycobacterium bacteria is still prevalent and disastrous in different countries. Every year, approximately 2milion people die of mycobacterium tuberculosis infections, which demonstrates the need for more effective drugs and vaccines against tuberculosis. The article provides comprehensive information on the pathogen’s host interaction, enlightening the reader on how these bacteria evade host defences and cause tuberculosis infection. Understanding mycobacterium tuberculosis’s structure, mode of invasion, molecular determinants of virulence, and drug resistance is key to developing new antituberculosis agents and preventive measures against tuberculosis.
Mycobacterium tuberculosis belongs to the pathogenic bacteria species found in the genus of Actinomycetota and the family mycobacteriaceae. The bacteria is considered unique among the group of eukaryotic cells because of its adaptive cellular features that enable it to survive in the hostile environment of macrophages. These features include high lipid content on its cell wall and mycolic acid. Also, in the host cell, mycobacterium bacteria appear to be surrounded by a capsule outside the cell wall (Smith, 2003). Pathogen information of mycobacterium tuberculosis is related to the information covered in class on Cell Anatomy, where we learned the distinct Characteristics of prokaryote and eukaryotes cells. A eukaryotic cell is complex and relatively large as compared to prokaryotic cells. Unlike a eukaryotic cell which has a membrane-bound structure, a prokaryotic cell has a distinct cellular.
Based on morphology, Mycobacterium tuberculosis has a relatively large nonmotile rod-shaped structure that does not have retains dye and phospholipid outer membrane. The measurement of the rod-shaped structures ranges from 0.2-0.5 in width and 2-4 micrometres in length. The morphological structure of mycobacterium gradually grows from the time of invasion into the host to active tuberculosis infection. In addition, the rods appear to be wrapped together due to fatty acids in the cell wall. The structure of rods being wrapped together is similar to strands of cord that make up a rope and is therefore referred to as coding. According to Smith (2003), mycobacterium tuberculosis is a unique acid-fast Gram-positive pathogen with high my colic acid and lipid content on its cell wall. Since Mycobacterium tuberculosis is an acid-fast bacterium with a mycolic acid content, it cannot be detected using the gram stain technique. The cell wall of MTB has an unusual wavy coating due to high acid content, making it impervious to gram staining. For this reason, mycobacterium tuberculosis is stained using florescent stains or acid-fast stains that include auramine and Ziehl-Nielsen stain.
Mycobacterium tuberculosis virulence involves various factors that enable the bacteria to invade, reside within the host’s cells, and evade the bacterial defences of macrophages. The MTB’s cell wall structure is the primary virulence factor for the bacterium. The cell wall is enriched with complex lipids such as my colic acid that helps the pathogen resist the host’s hostile environment, resulting in the bacteria’s growth. The other virulence factor is the protein inhibiting antimicrobial effectors (Russell, 2001). Information on structural characteristics of MTB, Gram staining, and acid-fast staining relates to the knowledge obtained in class on differential staining techniques. We learned various staining methods in class, including gram staining, acid-fast staining, and fluorescent staining.
Susceptibility to Antibiotics
Isoniazid is one of the most effective antibiotics used to prevent and treat tuberculosis. It acts by killing mycobacterium tuberculosis. The drug is in the class of antituberculosis agents that work by killing MTB in the host cells. Isoniazid, also referred to as pyridine-4-cadohydrazide, is a prodrug that turns into a pharmacologically active form after administration. The drug is metabolized into an active using hydrazine that reduces mycobacterial ferric KatG peroxidase and reacts with oxygen to form an enzyme complex known as oxyferrous (Vilchèze et al., 2007). After activation, the drug works by inhibiting the synthesis of the lipid components, including mycolic acid, which is the main component of the bacteria. The structure of Isoniazid covalently bonds the NAD cofactor, resulting in a slow but tight-binding acid synthesis inhibitor.
One possible mycobacterial resistance to Isoniazid is the KatG gene encoding peroxide enzyme and mutations in IHHA, which plays an important role in turning the prodrug isoniazid into a pharmacologically active drug. Information on susceptibility to antibiotics relates to what we learned in class on the Pharmacological effect of Antibiotics and drug resistance. We learned that prodrugs are drugs that turn into a pharmacologically active form upon administration. Also, bacteria can change over time and become resistant to a certain type of drug, which calls for more research on antituberculosis to manage antimicrobial resistance.
Smith I. (2003). Mycobacterium tuberculosis pathogenesis and molecular determinants of virulence. Clinical microbiology reviews, 16(3), 463–496. https://doi.org/10.1128/CMR.16.3.463-496.2003
Vilchèze, C., & Jacobs, Jr, W. R. (2007). The mechanism of isoniazid killing: clarity through the scope of genetics. Annu. Rev. Microbiol., 61, 35-50.
Russell, D. G. (2001). Mycobacterium tuberculosis: here today, and here tomorrow. Nature reviews Molecular cell biology, 2(8), 569-578.