Mycobacterium Tuberculosis in Spinal Tuberculosis

Abstract

Even in an era of remarkable medical advances, there is an issue of why tuberculosis remains in the list of disastrous diseases, afflicting humans and causing suffering. There has not been a plausible answer to this, and it has been suggested that clinicians and medical scientists could presently not win the war against the tubercle bacilli. With regards to this issue, based on the authors' own clinical and research experiences, in this review, the available literature was revisited in order to address the raised questions and to provide recent information on characteristics of tubercle bacilli and possible ways to more effectively treat tuberculosis.

Keywords: Behavior; Cell envelops; Drug response; Morphology; Tissue pathology.

Fig. 1. Mycobacterial envelope structures. A complex cell wall includes a peptidoglycan layer linked to a chain of galactose polymers (arabinan). Arabinan forms ester links to mycolic acids, which form an outer bilayer with phenolic glycolipids. Outside the outer bilayer is a capsule of loosely associated phospholipids and phenolic glycolipids [13].

Fig. 2. Mycolic acids coat the cell wall of Mycobacterium tuberculosis.

Fig. 3. Cell wall chemical structure of Mycobacterium tuberculosis. The extreme hydrophobicity of bacillary cell wall prevents phagocytosis. 40% of total dry cell weight is lipid. This sketch does not represent the layering of cell wall. The role of the mycolic acid (membrane lipid) and its compounds are illustrated. True envelope structure will be illustrated separately in Fig. 2.

Fig. 4. Generation and destruction of reactive oxygen species (ROS). The autooxidation of flavin adenine dinucleotide (FAD) and the Fenton reaction occur spontaneously to produce superoxide and hydroxyl radicals, respectively. The other reactions require enzymes. FAD is a cofactor for a number of enzymes (for example, NADH dehydrogenase 2). Catalase and peroxidase do not produce ROS but detoxify hydrogen peroxide. NAD, nicotinic acid.

Fig. 5. Four of the 5 phases of phagocytosis: adherence, ingestion, digestion, and excretion. As the first step of phagocytosis, a phagocyte's pseudopod adheres to the surface of Mycobacterium tuberculosis and gradually wraps the mycobacterium entirely. The pseudopod wrapped mycobacterium is then brought inside the phagocyte, into a structure called a phagosome. Fusion of phagosomes with lysosomes enable the destruction of the phagocytosed pathogens. However, several microorganisms have evolved ways to defeat this process. Mycobacterium inhibits phagolysosomal fusion by the mycobacteria-produced sulfatides.