Mycobacteria are a bacterial genus with about 100 representatives and correspond to the only genus within the family Mycobacteriaceae. With the Gram stain, the representatives of the genus can be poorly stained. The structure of their cell walls resembles the wall structure of Gram-positive bacteria.
The cell wall of mycobacteria is therefore not equipped with an outer membrane, but consists of multi-layered peptidoglycans. The DNA analysis of the genus confirms the association with the Gram-positive bacteria. Since they carry a high GC content within the DNA, they also belong to the Actinobacteria.
A human pathogenic species of Mycobacteriaceae represents the species Mycobacterium tuberculosis. The pathogen corresponds to the most important tuberculosis pathogen and can infect different animal species with tuberculosis in addition to humans.
Mycobacterium tuberculosis is in the form of a rod and is not capable of active movement. The acid-fast bacteria of the species carry a bacterial cell wall of arabinogalactan, mycolic acids and lipophilic cell wall components.
The individual members of the species measure up to five μm. The bacterium species occurs all over the world. It is estimated that every third person is infected with tuberculosis. Clusters occur in Third World countries.
Bacteria of the species Mycobacterium tuberculosis live aerobically. The representatives of the species need oxygen for their metabolism. This distinguishes them from anaerobes, which can also survive in an oxygen-free environment and use other substances for energy production in case of doubt.
The tuberculosis pathogen proliferates exclusively in an intracellular manner and preferably uses macrophages for propagation. Characteristically, the bacteria grow extremely slowly and divide at most every 15 hours. Weak disinfectants can resist the bacteria.
Within the macrophages, bacteria of the species Mycobacterium tuberculosis often survive for several years. Since macrophages are part of the immune system, they escape the defense system with macrophage colonization and are not attacked.
After years of latent infection, the infection usually returns to an active state. Triggering circumstances are usually stress factors or other immunosuppressive processes.
The bacteria have lipolytic and fatty synthesis enzymes. If in doubt, the bacteria are capable of living off their own fat layer in the cell wall. During infection, external cholesterol is produced in the hosts, which also serves as a nutrient for Mycobacterium tuberculosis. The waxy, fatty cell wall of the bacterial species protects against destruction by the immune system and disturbs the signal transduction. Therefore, a full immune response does not occur after infection.
In the inactive state, bacteria of the species Mycobacterium tuberculosis live off their own fat layer and do not divide. Even in this state, however, enzymes such as catalase are active and inactivate substances such as antibiotics to protect the bacterium.
By reading errors of the DNA increases the mutation rate of the bacteria. Even in the phase of latent infection, the bacterial species can develop resistance for this reason.
The transmission of the pathogen takes place aerogenically. This infection path corresponds to the droplet infection. However, there is also the possibility of oral transmission. For example, the consumption of infected meat or other animal proteins can cause an infection.
Bacteria of the species Mycobacterium tuberculosis are in any case pathogenic to humans. In the inactive phase, the infection does not produce any symptoms, but has already begun.
The bacterium Mycobacterium tuberculosis is a causative agent of tuberculosis. After the initial infection, the latency is up to eight weeks. After that, non-specific symptoms occur. In addition to fever and night sweats, weight loss and loss of appetite are characteristic early symptoms.
If a tuberculous primary complex develops, or a pulmonary course begins, come to the symptoms mentioned coughing fits, hemoptysis (hemoptysis), lymphadenopathy and dyspnea (shortness of breath) added.
The individual immune system and the number of transmitted pathogens determined during the infection on the course. People with a strong immune system develop organ manifestation in just five percent of all cases. If organ involvement occurs, this type of manifestation occurs within the first two years after primary infection. Immunodeficient patients are much more likely to have organ manifestations. Especially often, such a course has been observed in people with alcoholism, with diabetes, with pre-existing pneumoconiosis, malnutrition or lymphoma.
In addition, drug immunosuppression with substances such as cyclosporine and cytostatics may increase the risk of organ manifestations. Also worth mentioning in this context are acquired immune deficiencies such as HIV infections, congenital immune deficiencies and a high age, which affects the immune system in an age-physiological manner.
The tuberculosis caused by Mycobacterium tuberculosis shows clinically different courses and stages. Primary tuberculosis may be, for example, pulmonary tuberculosis, hilum lymphocytic tuberculosis, exudative pleurisy, miliary tuberculosis, or Landouzy sepsis. In post-primary tuberculosis, intestinal involvement, genitourinary tuberculosis, tuberculous meningitis, skin manifestations and bone and kidney manifestations are conceivable.
The treatment of tuberculosis is done with multiple combinations of different antibiotics. These tuberculostatics are given over several months. In recent years, the development of resistance of the bacterial genus Mycobacterium tuberculosis has made the treatment of those affected significantly more difficult. As far as possible within the treatment, it is important to reduce immunosuppressive factors and to use the immune system as a natural support, far away from medicines.Tags: