BCG Vaccine
Introduction
Bacille Calmette Guerin (BCG) is the most common vaccine administered to combat tuberculosis disease in the world. (1) The vaccine contains a weakened live strain of Mycobacterium bovis, which is present in cows and shares a common ancestor with the human tubercule bacillus Mycobacterium tuberculosis (2). Similar to other vaccines, BCG creates the formation of antibodies from the harmless strain of Myobacterium bovis to help prevent tuberculosis, and the vaccine usually leaves a skin lesion or a scar (1). The efficacy of BCG vaccine varies from 0-80% depending on age, the type of BCG vaccine, and the population (1). Although BCG remains as the primary vaccine against tuberculosis, it has only produced variable amounts of success. Many factors, including recent findings that distinct BCG strains have very different biochemical characteristics due to mutations, have further complicated the issue (1). Researchers are currently searching for a more effective way to treat tuberculosis disease, but none has been found to date (1).
Origin
The origin of the Bacile Calmette Guerin virus began when Albert Calmette and Camille Guerin started working on Mycobacterium bovis in 1908. After the stain was attenuated 230 times over thirteen years, BCG was used as a vaccine to treat tuberculosis (1). The strain went through many unknown genetic changes as it became less virulent in animals. After the original success of the vaccine, it was distributed all around the world. However, as the vaccine underwent distribution, the newly distributed strains underwent distinct genetic changes (1). BCG strains continued to change as individual countries altered the strain to fit their own needs (3). Currently, there are seven strands that are administered throughout the world, but they differ in gene sequences and protein production (3).
Tuberculosis Function
Tuberculosis is almost always contracted through the air when the respiratory system ingests the bacteria Mycobacterium Tuberculosis. Once the bacteria enter the organism, Mycobacterium tuberculosis becomes implanted in alveoli and is usually ingested by nearby macrophages, although it can also be ingested by alveolar epithelial type II pneumocytes (4). When the bacteria enter the macrophage it is phagocytosed by macrophage mannose and occupies an endocytic vacuole called the phagosome (4). After the Mycobacterium tuberculosis becomes assimilated in the phagosome, it must avoid death from the macrophage’s phagolysosome. Mycobacterium tuberculosis has many mechanisms to combat this problem, which include stopping phagosome-lysosome fusion and recruiting RAB proteins to prevent phagosomal maturation and catalyze endosome trafficking (4). If the bacteria continue to grow in the lung, it can have varying effects depending on the strength of the organism’s immune system. Latent tuberculosis occurs when the organism has a strong immune system; in which case the infection cannot progress and remains dormant. However, if an organism has a weak immune system, the granulomatous focal lesions that prohibit the spread of bacteria liquefy and allow Mycobacterium tuberculosis to replicate and spread throughout the lungs (4). It is for this reason that other factors that slow the immune system such as HIV, sickness, and aging can bolster the effectiveness of Mycobacterium tuberculosis. Eventually, uncontrolled growth of Mycobacterium tuberculosis can lead to lung damage and eventually suffocation and death because of an organism’s lack of oxygen (4).
BCG'S response to Tuberculosis
Structural and Functional Differences of Mycobacterium tuberculosis and BCG
Problems with BCG
Conclusion and Potential New Treatments
References
1. 2. 3. 4. 5. 6. 7.
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Edited by Scott Treiman, student of Joan Slonczewski for BIOL 116 Information in Living Systems, 2013, Kenyon College.