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Chamberlain College of Nursing Mycobacterium Tuberculosis Discussion


Using your pathogen from the last two weeks, research and describe the ideal growth conditions of your pathogen. What terms learned this week would describe its ideal growth conditions? What is the nutritional mode of your microorganism? What are the host cells for your pathogen?

week 1

Mycobacterium tuberculosis (MTB) is an acid-fast bacillus-shaped bacterium that infects lung alveoli and is the causative agent of tuberculosis – a disease that is currently known as a global challenge. Tuberculosis may remain latent in approximately 90% of the individuals, and active disease is considered to be a failure of CD4 T-cell-mediated immunity (Korb et al., 2016). MTB infection is established via inhalation of infected droplets from sick individuals and results in symptoms like bloody cough and apnea. MTB is recognized by pattern recognition receptors (PPR) located in macrophages and dendritic cells (DC) – which results in MTB engulfment. Although modified phagosomes within macrophages are classical reservoirs for MTB replication, macrophages, are also the main cell responsible for MTB clearance (Korb et al., 2016). Infected macrophages elicit a strong initial response against MTB via TLR-2 signaling. Chronic TLR-2 signaling, however, may impair proper immunity, and may even hide MTB from T-cell recognition – thus, contributing to this pathogen’s known latency status (Korb et al., 2016). Additionally, alveolar macrophages enter the lung interstitium after MTB engulfment, which results in the establishment of the site of infection. MTB may also prevent apoptosis within macrophage’s phagosomes, which also contributes to MTB’s latency (Korb et al., 2016).

last week 2

Mycobacterium tuberculosis has an outer membrane, which is functionally identical to that observed in gram-negative bacteria but not structurally (Delougu, Sali. & Fadda, 2013). It consists of an asymmetric lipid bilayer in which the outer leaflet is composed of glycolipids and waxy structures, and the inner layer is composed of mycolic acids (Delougu, Sali. & Fadda, 2013). There is a periplasmic space between the outer and the inner membranes – a place where a thin layer of peptidoglycan is located (Delougu, Sali. & Fadda, 2013). This cell wall structure provides M. tuberculosis a strong, impermeable barrier against drugs – thus contributing to its virulence (Delougu, Sali. & Fadda, 2013). M. tuberculosis is phagocytized by local lung macrophages. Still, it may remain latent within them due to the secretion of ESX1 – a required protein so that M. tuberculosis can translocate from the phagosome into the cytosol of the infected hosts (Delougu, Sali. & Fadda, 2013). Researchers consider that elucidating the ESX systems was one of the main advancements regarding tuberculosis etiopathogenesis (Delougu, Sali. & Fadda, 2013).


Delogu, G., Sali, M., & Fadda, G. (2013). The biology of mycobacterium tuberculosis

infection. Mediterranean journal of hematology and infectious diseases, 5(1), e2013070. 


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