What causes leprosy (leprosy)?

Causes of Leprosy

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

M. leprae are acid- and alcohol-resistant gram-positive bacteria that look like straight or curved rods 1 to 7 μm long and 0.2-0.5 μm in diameter. They are practically no different from tuberculosis mycobacteria in size and tinctorial properties. They are immobile and do not form typical spores. As a rule, fragmented and granular forms are also found in human lesions, along with rod-shaped M. leprae that are homogeneously stained according to Ziehl-Neelsen. M. leprae are obligate intracellular parasites of the mononuclear phagocyte system that reproduce by transverse division into 2-3 daughter cells and form large clusters in the macrophage cytoplasm with a typical “cigarette pack” arrangement. In addition, pathogens can reproduce by budding and branching.

The ultrastructure of M. leprae does not differ fundamentally from that of other mycobacteria. Ultrathin sections of M. leprae reveal a fringed microcapsule 5-15 nm thick, consisting of mucopolysaccharides. The thin three-layer cell wall (an outer osmiophobic layer and two tightly adjacent osmiophilic layers with a total thickness of 8-20 nm) has pronounced rigidity: it is preserved 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 ("elementary Robertson membrane"). In the cytoplasm, 1-2 polymorphic mesosomes are usually found - invaginates of the plasma membrane, corresponding in some functions to the mitochondria of eukaryotic cells. In the cytosol of M. leprae there is a weakly expressed nucleoid, a small number of ribosomes, vacuoles, volutin inclusions of the homogeneous body type, and sometimes spore-like formations.

The pathogen is characterized by unusually slow growth, which is not typical for bacteria: the time of one division is 12 days.

Of the antigenic determinants, the most significant is the specific phenolic glycolipid (PGL-1). It contains 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% lipids, among which high-molecular mycolic acids predominate. A carbohydrate-free lipid (phthiocerol dimycocerosate) has also been 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% glycerol solution; they remain viable for several weeks when dried in various ways in shaded conditions. Direct ultraviolet radiation has a detrimental effect on them.

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Epidemiology of leprosy

The only proven source of infection in leprosy is a sick person. Most specialists admit both airborne and contact (percutaneous) routes of transmission of leprosy. Data from epidemiological studies indicate the predominant importance of the airborne route of transmission: usually, a sick person can serve as a source of infection when he develops extensive lesions of the mucous membrane of the nasopharynx, i.e. during the period of massive release of the pathogen into the environment through the respiratory tract. At the same time, registered cases of infection during surgical interventions, as well as during tattooing, confirm that infection with leprosy and penetration of the pathogen through damaged skin are possible.

Most people are relatively immune to leprosy. There is no racial predisposition or special resistance to leprosy. However, if we take into account the data of immunogenetics, we cannot deny the role of factors of genetically determined predisposition to leprosy within individual ethnic groups and populations, as evidenced by the fact that blood relatives are infected with leprosy 3-6 times more often than spouses from each other, since the genetic differences between the latter are more pronounced. It is known that the 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, a decrease in non-specific resistance, and general hygiene. The main indicator of immunoreactivity to M. leprae is the intradermal test for lepromin, proposed in 1919 by K. Mitsuda. Lepromin is a suspension of crushed and autoclaved leprosy of a patient, containing a huge amount of M. leprae (1 ml of standardized lepromin contains from 40 to 160 million bacterial bodies). When introducing 1.0 ml of this antigen intradermally into the inner surface of the forearm in patients with the lepromatous type of the disease and in an insignificant 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 the tuberculoid type of leprosy and most healthy people, it is positive, i.e. their relative natural immunity to leprosy is characterized by a fairly high intensity. Consequently, the lepromin test has no diagnostic value, but helps to establish the type of disease, and is also important for the prognosis. Lepromin-negative individuals from among contacts constitute a high-risk group for the disease, and the transformation of a negative lepromin test in a patient into a positive one indicates an increase in the intensity of specific cellular immunity to M. leprae antigens. The reaction to Mitsuda's lepromin develops 3-4 weeks after its administration (a tubercle, a nodule, sometimes with necrosis, appears).

Leprosy is a historically known human disease. There are a huge number of convincing scientific and literary descriptions indicating the high prevalence of leprosy up to pandemics in the past. Gradually, the level of its incidence decreased and reached the nature of endemic distribution, characteristic only of certain regions of the world. An important role in reducing the prevalence of leprosy is played by the World Health Organization, which took control of the fight against this disease as a public health problem. Thanks to the implementation of various WHO programs developed specifically for leprosy endemic countries, the lower epidemic threshold of the global incidence of leprosy, not exceeding 1 case per 10,000 people on Earth, was finally overcome.

Today, according to the latest WHO data, at the beginning of the 21st century, slightly more than 500,000 new patients with leprosy are registered annually in the world, mainly among the population of the countries of South America, Africa and Southeast Asia. Approximately the same number of patients are simultaneously undergoing treatment. The main endemic countries today are recognized as Brazil, Congo, Madagascar, Mozambique, India, Nepal and some others. In Russia, isolated patients with leprosy are only occasionally registered in certain regions (Lower Volga).

In the second half of the 20th century, leprosy patients were registered in almost all countries of the world. In 1980, their number, according to WHO estimates, was about 13 million people. However, after the WHO decided to provide combination therapy with three drugs (dapsone, rifampicin, clofazimine) to all patients and remove patients who had completed the full course of this treatment from the register, by 2000 the number of registered people decreased to 600-700 thousand people. At the same time, already in the 21st century, from 500 thousand to 800 thousand new cases of leprosy are registered annually, the problem of relapses is becoming increasingly urgent, and, as most experts believe, the problem of eliminating leprosy to isolated cases will last for decades. Currently, the countries most affected by leprosy are Southeast Asia (India, Indonesia, Myanmar), some African countries and Brazil.

In Ukraine, leprosy has never been widespread. The maximum number of registered patients (about 2,500 people) was noted in the early 1960s.

In the absence of a specific anti-leprosy vaccine, the BCG vaccine is recommended for the prevention of leprosy, but according to various authors, it protects against leprosy by only 20-70%. Chemoprophylaxis of leprosy is carried out in a number of countries. Preventive treatment with one of the sulfone series drugs for 6-12 months is prescribed to persons living together with a patient with leprosy (a bacterium excretor).

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