What causes leprosy (leprosy)?

Causes of leprosy

The cause of leprosy is mycobacterium leprosy (Mycobacterium leprae), discovered in 1871 by the Norwegian doctor G. Hansen. According to the decision of the International Manila Conference on leprosy in 1931, the Hansen bacillus was assigned to the family Mycobactertaceae and named Mycobacterium leprae hominis. .

M. Leprae - acid and alcohol resistant Gram-positive bacteria, having the appearance of straight or curved sticks with a length of 1 to 7 microns, 0.2-0.5 microns in diameter, in size and tinctorial properties practically not different from mycobacterium tuberculosis, immobile, not forming typical disputes. As a rule, in the foci of lesions in humans, in addition to the rod-shaped M. Leprae, which are homogeneously stained according to the Ziehl-Nielsen, fragments and granular forms are also found. M. Leprae - obligate intracellular parasites of the mononuclear phagocyte system, multiplying by transverse division into 2-3 daughter cells and forming large clusters in the cytoplasm of a macrophage with a typical arrangement of the "cigarette in packs" type. In addition, it is possible to propagate pathogens by budding and branching.

The ultrastructure of M. Leprae has no fundamental differences from that of other mycobacteria. In ultra-thin sections, M. Leprae show a fimbriated microcapsule 5-15 nm in thickness, consisting of mucopolysaccharides. A thin three-layered cell wall (an outer osmiophobic layer and two osmiophilic layers densely adherent to each other with a total thickness of 8-20 nm) exhibits severe rigidity: it persists for a long time in the affected tissues even with complete lysis of the cytoplasm of M. Leprae ("shadow cells"). Next comes a three-layer lipoprotein cytoplasmic membrane ("Robertson's Elementary Membrane"). In the cytoplasm, usually one or two polymorphic mesosomes are present-invaginates of the plasma membrane, corresponding in some functions to the mitochondria of eukaryotic cells. In the cytosole of M. Leprae are located a weakly expressed nucleoid, a small amount of ribosomes, vacuoles, volutin. Inclusions of the type of homogeneous bodies, and sometimes sporopodal formations.

For the pathogen is characterized by unusually slow growth, not characteristic of bacteria: the time of one division is 12 days.

Of the antigenic determinants, the most specific phenolic glycolipid (PGL-1) is most significant. It includes a unique trisaccharide, on the basis of which attempts are being made to create a specific artificial antigen.

The cell wall of M. Leprae consists of 50% of lipids, among which high molecular weight mycolic acids predominate. A non-carbohydrate lipid (fthiocerol dimicozerosate) is also described, which differs from those of other mycobacteria. The ability of M. Leprae to secrete lipids has been established.

The pathogenicity factors of M. Leprae have not been studied.

M. Leprae survive for a long time at low temperatures and during storage. For example, in a 40% solution of glycerol; remain viable for several weeks when dried in various ways under shading conditions. Direct ultraviolet irradiation acts on them fatal.

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Epidemiology of leprosy

The only proven source of infection with leprosy is a sick person. Most specialists admit both airborne and percutaneous (percutaneous) transmission of leprosy. Data from epidemiological studies indicate the prevalent value of the airborne droplet transmission: usually the patient can serve as a source of infection in the development of his extensive lesions of the nasopharyngeal mucosa, i.e. In the period of massive excretion into the environment by the respiratory route. At the same time, registered cases of infection during surgical interventions. And also with a tattoo confirm that it is possible to contaminate leprosy and penetrate the pathogen through the damaged skin.

Most people are relatively unresponsive to leprosy. There is no racial predisposition or special resistance to leprosy. However, if you take into account the data of immunogenetics, you can not deny the role of factors of genetically determined predisposition to leprosy inside individual ethnoses and populations, which is indicated by a 3-6 times more frequent infection of leprosy blood relatives than the spouses from each other, because between the latter genetic differences are more pronounced . It is known that concordance for leprosy in monozygotic twins is almost three times higher than in dizygotic twins. Seasonality and climatic conditions have some significance in leprosy infection only in relation to the intensification of migration processes, the degree of professional contacts with sources of infection, the reduction of non-specific resistance, general hygiene. The main indicator of immunoreactivity for M. Leprae is the intradermal test for lepromine, proposed in 1919 by K. Mitsuda. Lepromin is a suspension of the grown and autoclaved leprom of the patient, containing a huge amount of M. Leprae (1 ml of standardized lepromine contains from 40 to 160 million bacterial bodies). When injected intradermically into the inner surface of the forearm OD ml of this antigen in patients with lepromatous type of disease and in a small part (up to 10-12%) of healthy individuals, the test is always negative (anergy, tolerance to M. Leprae). At the same time, in patients with tuberculoid type of leprosy and most healthy people, it is positive, i.e. Relative natural immunity to leprosy in them is characterized by a rather high intensity. Therefore, the lepromine test does not have diagnostic value, but it helps to establish the type of the disease, and it is also important for the prognosis. Lepromino-negative individuals from the number of contacts constitute a group of increased risk of the disease, and the transformation of a negative lepromine test in a positive patient indicates an increase in the intensity of specific cellular immunity to M. Leprae antigens . Reaction to lepromine Mitsuda develops 3-4 weeks after its appearance (there is a tubercle, a node, sometimes - with necrosis).

Leprosy is a historically known disease of man. There is a huge amount of convincing scientific and literary and artistic descriptions that testify to the prevalence of leprosy up to pandemics in the old days. Gradually the level of its morbidity declined and reached the character of endemic spread, characteristic only for certain regions of the world. An important role in reducing the prevalence of leprosy is played by the World Health Organization, which has taken control of the fight against this disease, as a public health problem. Through the implementation of various WHO programs developed specifically for endemic countries, the lower epidemic threshold of the global leprosy incidence, which does not exceed 1 case per 10,000 of the world's population, was finally overcome.

Today, according to the latest WHO data, at the beginning of the XXI century. In the world, a little more than 500,000 new leprosy patients are registered annually, mainly among the populations of South America, Africa and South-East Asia. Approximately the same number of patients is simultaneously on treatment. The main endemic countries today are Brazil, Congo, Madagascar, Mozambique, India, Nepal and some others. In Russia, single leprosy patients are only occasionally registered in certain regions (Lower Volga region).

In the second half of XX century. Patients with leprosy were registered practically in all countries of the world. In 1980, their number, according to WHO, was about 13 million people. However, after WHO decided to provide a combination therapy with three drugs (dapsone, rifampicin, clofazimine) for all patients, and taking into account patients who completed the full course of this treatment, by 2000 the number of registered patients decreased to 600-700 thousand people . At the same time already in the XXI century. Annually register from 500 thousand to 800 thousand new cases of leprosy, the problem of relapses becomes more urgent, and, as most experts believe, the problem of eliminating leprosy up to individual cases will last for another decades. Currently, the most affected leprosy is the countries of Southeast Asia (India, Indonesia, Myanmar), some countries in Africa and Brazil.

In Ukraine, leprosy has never been widespread. The maximum number of registered patients (about 2500 people) was noted in the early 60's.

In the absence of a specific antiepileptic vaccine for the prevention of leprosy, the BCG vaccine is recommended, but, according to different authors, it protects against leprosy only by 20-70%. In a number of countries, chemoprevention of leprosy is carried out. Preventive treatment with one of the sulfonic drugs for 6-12 months is prescribed for persons living together with a leprosy (bacterial) patient.

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