Mycobacterium Tuberculosis
The causative agent of tuberculosis, resides primarily in human macrophages. Discuss the mechanisms by which this organism resists the potent antibacterial activities of macrophages to establish and maintain an infection.
Tuberculosis is one of the most serious infections in the world, killing almost 3 million people worldwide annually. Thus, it is important to understand how this mycobacterium is pathogenic and the defence mechanisms it has in order to try and manage this potentially fatal disease. Mycobacterium tuberculosis, the causative agent of tuberculosis is a pathogen that can infect its host for decades without causing clinical disease, only to reactivate when host immunity is compromised. Recent work has begun to outline the complexity of this host-pathogen interaction and to reveal how the homeostatic balance between the two is achieved.
Normal Physiology of Macrophages
Macrophages, produced by the division of monocytes, are white blood cells within tissues; essentially, an immuno-defence mechanism. Macrophages are vital to the regulation of immune responses and the development of inflammation. After insult, macrophages normally become active to remove debris. Macrophages function in innate natural immunity by destroying microbes and in acquired immunity as an antigen-presenting cell.
During phagocytosis, macrophages are activated to destroy (consume) the bacteria devouring many times their own body mass in bacteria, essentially killing them with the macrophage’s acid-filled vacuoles. The ingested pathogen becomes trapped in a phagosome, which fuses with lysosome; from this enzymes and toxic peroxides digest and kill the pathogen. However, some advance pathogens such as Mycobacterium Tuberculosis have become resistant to the immune-defence mechanisms of the macrophage.
Structure of Mycobacterium Tuberculosis
Mycobacterium Tuberculosis is a gram positive, rod-shaped bacteria.(Reece, 2011, pp 579) M. Tuberculosis has the
Tuberculosis is one of the most serious infections in the world, killing almost 3 million people worldwide annually. Thus, it is important to understand how this mycobacterium is pathogenic and the defence mechanisms it has in order to try and manage this potentially fatal disease. Mycobacterium tuberculosis, the causative agent of tuberculosis is a pathogen that can infect its host for decades without causing clinical disease, only to reactivate when host immunity is compromised. Recent work has begun to outline the complexity of this host-pathogen interaction and to reveal how the homeostatic balance between the two is achieved.
Normal Physiology of Macrophages
Macrophages, produced by the division of monocytes, are white blood cells within tissues; essentially, an immuno-defence mechanism. Macrophages are vital to the regulation of immune responses and the development of inflammation. After insult, macrophages normally become active to remove debris. Macrophages function in innate natural immunity by destroying microbes and in acquired immunity as an antigen-presenting cell.
During phagocytosis, macrophages are activated to destroy (consume) the bacteria devouring many times their own body mass in bacteria, essentially killing them with the macrophage’s acid-filled vacuoles. The ingested pathogen becomes trapped in a phagosome, which fuses with lysosome; from this enzymes and toxic peroxides digest and kill the pathogen. However, some advance pathogens such as Mycobacterium Tuberculosis have become resistant to the immune-defence mechanisms of the macrophage.
Structure of Mycobacterium Tuberculosis
Mycobacterium Tuberculosis is a gram positive, rod-shaped bacteria.(Reece, 2011, pp 579) M. Tuberculosis has the
References: Huynh K.K et al; ‘A Delicate Dance: Host Response to Mycobacteria’ Current Opinion in Immunology, Vol 23,2011, pp 464-472 Sheff, B; ‘Mycobacterium Tuberculosis’, Nursing, vol 33 (11), November 2003, pp 75 Brighenti, S, Lerm, M; ‘How Mycobacterium Tuberculosis Manipulates Innate and Adaptive Immunity- New Views of an Old Topic’ 2012, Understanding Tuberculosis: Analyzing the Origin of Mycobacterium Tuberculosis Pathogenicity, pp 207-234. Goering V.G. et al, 2008; Mim’s Medical Microbiology, 4th Edn, Elsevier Reece,J.B et al, 2011; Campbell Biology, 9th Edn, Pearson, Kumar, V et al, 2010; Robbins and Cotran Pathologic Basis of Disease, 8th edn, Saunders, Philadelphia Brooks, G.F et al, 2010; Jawetz, Melnick & Adelberg’s Medical Microbiology, 25th edn, McGraw Hill, USA. Ralph, A, Kelly, P, Krause, V; ‘What’s New in Tb?’, Australian Family Physician, vol 38, no. 8, August 2009, pp. 578-583