Abstract
Background: Mycobacterium tuberculosis, the etiology of pulmonary and extra pulmonary tuberculosis is taunted to have predated the existence of mankind, and science has elucidated its presence in old Egyptian’ mummies, as it continues to evade current antibiotic treatments, wreck the havoc and decimate human populations. Presented here, are the Strengths, Weaknesses, Opportunities and Threats (SWOT) analysis of Mycobacterium tuberculosis, and the first proposal for the application of this innovative concept in the field of Tuberculosis research, to proffer holistic platform, focused knowledge, and strategies at undermining the prowess of the tubercle bacilli and overcoming its scourge. Materials and Methods: A systematic review was carried out to mine data on the strengths, the weaknesses, the opportunities and threats to M. tb, by review of several publications using meaningful theme and specific search phrases on the subject. Results: Strengths of Mycobacterium tuberculosis include: possession of abundant cell wall mycothiol; M. tb is highly contagious and requires low infectious dose (ID50) to establish infection; ability to specifically target and replicate in the host’ macrophages; ability to establish extrapulmonary multiorgan involvement; dual polymorphism i.e. existence in both an actively replicating form as well as or latent state; assumption of variable metabolic states; delayed seeding from the lungs of the replicating bacteria cells to the mediastinal lymph nodes; delayed macrophage apoptosis prior to bacterial growth and ultimate cellular necrosis; ability to shift to glyoxylate pathway during lipid metabolism in lieu of glucose during persistence phase in the host. Weaknesses of M. tuberculosis include: the requirement for growth of a membrane protein called Rv3671c during in vivo replication for survival in the acidic milieu of the macrophages and phagosome; M. tb is a fastidious slow growing bacterium with long generation time; establishment of productive infection in less than 10% of infected subjects; the bacterium is strictly an intracellular aerobic pathogen; and variable bacteria level of adenosine triphosphate. Opportunities harnessed by M. tb include: development and spread of resistant strains owing to inadequate and inappropriate drug treatment; limited efficacy and use of BCG Vaccine; MDR-TB is under-diagnosed in children; pathogenic synergy of coinfection of the Human Immunodeficiency Virus (HIV) and Mycobacterium tuberculosis (MTB); difficulty of TB screening in HIV-infected persons; immune status of the host; immigration; slow response of the cellular immune response to M. tbwhich enables constant endogenous reinfection of the host; anatomical vulnerability of the lungs; aerosols by inspired air is crucial for latent tuberculosis infection. Threats to M. tuberculosis include: the development and use of sensitive combination of microbiological tests as the gold-standard in HIV infected patients; annual TB test; selective isolation of TB patients by reintroduction of sanatoria; prioritizing genomic drug targets; sustenance of the global TB funds; development of potent vaccine; live imaging using computer tomography and positron electron tomography to characterize active TB in lesions; development and application of Infecton for imaging deep seated infections.
Highlights
Mycobacterium tuberculosis was discovered and described by Robert Koch on 24 March 1882, about 130 years ago, as the causative agent of tuberculosis (TB)
Once the organism is in the lungs, the bacteria are phagocytosed by macrophages, which migrate to the hylar lymph node and elicit a CD4 they usually produce immune cells (T-cells) mediated hypersensitivity response that forms small, hard, nodules called tubercles which are characteristics of tuberculosis and give the disease its name
In M. tuberculosis, the single malate synthase encoded by glcB is thought to play a key role in pathogenesis by imparting some degree of virulence to the bacteria. These findings demand further research into identifying and characterizing M. tuberculosis adhesins to elucidate their precise role in virulence establish the mechanisms behind their secretion and identify the receptors required for their association with the host cell surface
Summary
Mycobacterium tuberculosis was discovered and described by Robert Koch on 24 March 1882, about 130 years ago, as the causative agent of tuberculosis (TB). Advances in microscopic technique i.e., transmission electron microscope (TEM), scanning electron (SEM) and atomic force microcopy (AFM), have shown that the bacillus does not always manifest itself in the classical rod shape (Figure 1). They become shorter in older cultures, filamentous within macrophages and ovoid during starvation [1] and they may produce buds and branches in extensively drug resistance strains (XDR-TB). Once the organism is in the lungs, the bacteria are phagocytosed by macrophages, which migrate to the hylar lymph node and elicit a CD4 T-cell mediated hypersensitivity response that forms small, hard, nodules called tubercles which are characteristics of tuberculosis and give the disease its name. The WHO estimates that infected adults lose an average of 3 - 4 months of work while recuperating from TB disease and an average of 15 years of economic activity is lost from each adult TB death
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