Lecture topic:

Lecture topic: "MAIN EVENTS AND FACTS IN THE HISTORY OF PHYSICS. GENERAL PATHOLOGY OF TUBERCULOSIS: ETIOLOGY, PATHOGENESIS, HISTOFUNCTIONAL CHARACTERISTICS. IMMUNOLOGY AND IMMUNOGENETICS.

lecturer: Dr. I. Y. Babaeva.

Tuberculosis

a common socially dependent infectious disease in which all organs and tissues of the human body can be affected. It is a disease that occurs during an infectious process as a result of the immune system defending the host against micro-organisms.

The epidemiological situation of tuberculosis worldwide

One third of the world's population is infected with

MBT.

More than 8.8 million new tuberculosis cases (141 per

100,000 population) are diagnosed each year.

More than 2 million people die from tuberculosis every year.

More than 95% of new cases and deaths occur in developing countries, with 75% are aged 15 - 54 years;

-More than 1 million deaths are attributed to HIV infection;

There is a high prevalence of multidrug-resistant tuberculosis.

THE GENERAL PATHOLOGY OF

TUBERCULOSIS

The family Mycobacteriaceae of the order Actinomycetales contains a single genus Mycobacterium, a group of obligate parasites. Mycobacteria (MB) are thin bacilliform cells with characteristic acid- and alcohol-resistance (at one of the growth stages), aerobic, immobile, and do not form spores. When stained with the Gram stain, they are weakly positive.

APPROACHES FOR CLASSIFYING MB:

1.In terms of speed and optimum growth temperature, pigment formation capacity;

2.In terms of clinically relevant complexes:

Causing tuberculosis, grouped into M. tuberculosis complex: M. tuberculosis, M. bovis, M. bovis BCG, M. africanum, M. microti, M. canettii, M. pinnipedii, M. caprae;

Non-tuberculosis MB group: M. avium complex; M. fortuitum complex; M. terrae complex; M. nonchromogenicum complex

MBT STABILITY

In the course of evolution, MBTs have developed various mechanisms to overcome or inactivate adverse environmental factors:

1.A strong cell wall.

2.Extensive metabolic capabilities.

3.Morphological plasticity, consisting in MBT transformation (formation of L-forms, dormant cells).

After MBT enters the lungs, the situation can develop according to 4 main patterns:

1.The primary host response may be sufficient to completely eliminate all MBT, thereby ruling out the possibility of TB disease.

2.In the case of rapid growth and multiplication of MBT, a disease known as primary TB develops.

3.In latent infection, the disease does not develop, but the MBs persist in the body in a so-called dormant state and their presence is only evident in the form of a positive skin reaction to tuberculin.

4.In some cases, MBT are able to move from a dormant state to a growth phase and the latent infection is replaced by a reactivation of the tuberculosis.

The process of infesting and parasitising the MF is as follows:

•Penetration of MBT into the MF without its activation;

•Suppressing the formation of the phagosomes or transforming them into an area that is comfortable for bacteria;

•Breakthrough from phagosomes into cytoplasm with inactivation of antimicrobial factors;

•Interference with cellular life;

•Decreased sensitivity of MF to activating T-lymphocyte signals;

•Reduced antigen-presenting function of MF and associated weakening of cytotoxic T-lymphocyte responses set up to destroy infected cells.

By penetrating the MF, the MBT activates a number of mechanisms that prevent the formation of the phagosome:

1.Producing ammonium, which alkalises the environment inside the phagosome.

2.Sulfolipid synthesis leading to the formation of a negative charge.

Pathogenetically, it is important that not all of the lung engulfed MBTs are removed from the lungs with surfactant drift and bronchial secretion - some of them develop in the interstitium, which is the bundle point for the formation of characteristic cell clusters - the granulomas.