Tuberculosis & Antibiotic resistance Essay
Tuberculosis & Antibiotic resistance
Tuberculosis (TB), also known as consumption, is an infectious disease caused by the bacterium Mycobacterium tuberculosis (MTB). TB is the leading cause of death in the world among reported deaths caused by a bacterial infectious disease. The disease affects 1.8 billion people per year, which is equal to one-third of the entire world population (Todar).
Pulmonary tuberculosis accounts for the majority of the TB cases in the United States (Todar). Bovine tuberculosis is another infectious form of TB caused by the bacterium Mycobacterium bovis (Tortora, Funke, and Case 690). M. bovis is the etiologic agent of TB in cows and rarely in humans. Both cows and humans can serve as reservoirs. Humans can also be infected with M. bovis by the consumption of unpasteurized milk. This route of transmission can lead to the development of extrapulmonary TB, exemplified in history by bone infections that led to hunched backs (Todar).
M. bovis accounts for only 1% of TB cases in humans in the United States. Another bacterium associated with TB that forms in patients with the late stages of human immunodeficiency virus (HIV) is Mycobacterium avium-intrecellulare (Tortora, Funke, and Case 690). According to Todar, M. tuberculosis is a fairly large nonmotile rod-shaped bacterium distantly related to the Actinomycetes.
The rods are 2-4 micrometers in length and 0.2-0.5 um in width. Many non-pathogenic mycobacteria are components of the normal flora of humans, found most often in dry and oily locations. M. tuberculosis is an obligate aerobe. For this reason, in the classic case of tuberculosis, MTB complexes are always found in the well-aerated upper lobes of the lungs. The bacterium is a facultative intracellular parasite, usually of macrophages, and has a slow generation time, 15-20 hours, and a physiological characteristic that may contribute to its virulence. Todar also states that
the cell wall structure of M. tuberculosis deserves special attention because it is unique among procaryotes, and it is a major determinant of virulence for the bacterium. The cell wall complex contains peptidoglycan, but otherwise it is composed of complex lipids. Over 60% of the mycobacterial cell wall is lipid. The lipid fraction of MTB’s cell wall consists of three major components, mycolic acids, cord factor, and wax-D. Mycolic acids are unique alpha-branched lipids found in cell walls of Mycobacterium and Corynebacterium.
They make up 50% of the dry weight of the mycobacterial cell envelope. Mycolic acids are strong hydrophobic molecules that form a lipid shell around the organism and affect permeability properties at the cell surface. Mycolic Acids are thought to be a significant determinant of virulence in MTB. Probably, they prevent attack of the mycobacteria by cationic proteins, lysozyme, and oxygen radicals in the phagocytic granule. They also protect extracellular mycobacteria from complement deposition in serum (Todar). TB has many structural and physiological properties that have been recognized for their contribution to mycobacterial virulence and pathology (Todar).
According to Tortora, Funke, and Case, an important factor in the pathogenicity of the mycobacteria, rod-shaped bacteria with waxy outer coats (NIAID), probably is that the mycolic acids of the cell wall strongly stimulate an inflammatory response in the host. In the initial stage there are no symptoms of the disease but the infection is present when tubercle bacilli reach the aveoli of the lung and are ingested by macrophages and also some evade ingestion, and therefore, survive.
In stage two, the tubercle bacilli multiply in the macrophages causing a chemotactic response that brings additional macrophages and other defensive cells to the area forming a surrounding layer and in turn an early tubercle. The surrounding macrophages are not successful in destroying bacteria but release enzymes and cytokines that cause lung damaging inflammation. During stage three, symptoms of the disease appear as many macrophages die, releasing tubercle bacilli and forming a caseous center in then tubercle.
Many of the tubercle will remain dormant and serve as a basis for later reactivation of the disease. The disease may be arrested at this stage, and lesions become calcified. In stage four of infection, symptoms of the disease appear in some patients as a mature tubercle is formed. As the disease progresses the caseous center enlarges in a process called liquefaction. When the caseous center enlarges, an air-filled tuberculous cavity is formed in which the aerobic bacilli multiply outside of the macrophages.
In stage five, liquefaction continues until the tubercle ruptures, which allows bacilli to spill into a bronchiole and then disseminate throughout the lungs and into the circulatory and lymphatic systems. These five stages are how the disease progresses when the defenses of the body fail. In most healthy individuals, the infection is arrested, and fatal TB does not develop (Tortora, Funke, and Case 689).