Leprosy of nose

Leprosy is a generalized, slightly contagious infectious disease characterized by skin damage, visible mucous membranes, peripheral nervous system and internal organs.

Hereditary transmission or congenital diseases do not exist. The only source of infection is a sick person, especially a lepromatous type of leprosy.

[1], [2], [3], [4], [5], [6],

Epidemiology of nasal leprosy

Leprosy is one of the oldest diseases known to mankind. It spread throughout the world from India, Persia, Abyssinia to Egypt, in which it was widely spread in 1300 BC. E. In Europe, leprosy spread during the time of the Crusades, to America, mainly to the Central and Southern, it was brought by Spanish and Portuguese mariners in the late fifteenth and early sixteenth centuries, and then the number of diseases increased due to the massive importation of Negro slaves from Africa. In Australia and Oceania, leprosy was imported by emigrants from China and India. In Russia, the disease has penetrated several ways: on the coast of the Black and Azov Seas - from Greece, the Caspian and Aral - from Central Asia, the Caucasus and the Transcaucasus - from Iran and Turkey, to the Baltics - from Germany and Scandinavia, to the Far East and Siberia - from China.

Leprosy is known since ancient times. Thus, in India, but the texts of the Rigveda ("The Book of Anthems" - a collection of predominantly religious hymns that arose among the Aryan tribes in the era of their migration to India), the leprosy was already familiar in the 7th century. BC. E. The first mention of leprosy in Japan dates back to the 8th century. BC. E. The "zaraath" mentioned in the Bible, according to NA Torsuyev (1952), was a collective term for the designation of physical and moral "impurity". Lepra appears in the works of Straboia, Plutarch, Halsna, Celsus, Pliny and others under various names (elephantiasis graecorum, leontina, leontiasis, satiris, etc.).

In past centuries, the disease leprosy was equated with civil death: the patients were expelled from society, they were deprived of the nature of inheritance, they were often killed. Then, in connection with the successes in the study of leprosy and the development of civilized society, the patients were placed in certain settlements (leprosariums), where they were provided with medical care and provided appropriate care.

According to WHO (1960), the total number of leprosy patients around the world is approximately 10-12 million. Apparently, by the year 2000 this number has not significantly decreased.

[7], [8], [9], [10], [11],

Cause of Leprosy Nose

The causative agent of leprosy is acid-fast mycobacterium (M. Leprae) - gram-positive rod very similar to MBT, obligate intracellular parasite, discovered in 1871-1873. The Norwegian scientist G. Hansen and studied in more detail in 1879 by A. Neisser (1855-1916) - an outstanding German dermatologist and venereologist, one of the founders of the doctrine of gonorrhea, leprosy and syphilis. The size of the rods varies from 1 to 8 μm in length and from 0.2 to 0.5 μm in thickness.

Inoculation and infection occurs with prolonged and close contact with a sick leprosy. Children are the most susceptible to leprosy. Immunity is relative. With the often repeated massive superinfection - an additional (repeated) infection of the patient in the context of an incomplete infectious process - the disease can occur against the background of the existing natural and acquired immunity. After the discovery of the causative agent of leprosy, the largest achievement in modern leprology was the discovery in 1916 of the Japanese leprologist K. Mitsuda of a substance contained in a microbe called lepromina. This substance, obtained by the extraction method from crushed lepromatous tissues and rendered harmless, injected intradermically to healthy adults, causes a positive lepromatous reaction in 80% of cases, while in the vast majority of infected this reaction does not occur.

[12], [13]

Pathogenesis of nasal leprosy

The entrance gates for infection are the skin and only occasionally - the mucous membrane of the upper respiratory tract and gastrointestinal tract. Clinical observations have shown that allergy and immunosuppressive conditions contribute to leprosy infection. The infected mycobacteria, passing through the dermal and mucous barriers, penetrate into the nerve endings, then into the lymphatic and blood capillaries and slowly disseminate, without usually causing any reactions at the site of introduction. With good macroorganism resistance, in most cases, the inserted sticks die without causing a disease. In other cases, the latent form of leprosy develops, which, depending on the resistance of the organism, can remain in this state throughout the life of the infected person. With less resistance, the abortive form of leprosy appears, manifested in the form of limited eruptions, which may disappear after a while. With insufficient resistance of the organism, depending on its degree, either a relatively benign tuberculoid leprosy develops, or the disease takes a severe malignant character with the formation of lepromatous granulomas containing an innumerable amount of mycobacteria (lepromatous leprosy). Intermediate position between the two types of leprosy is occupied by undifferentiated leprosy, which develops in persons with unstable resistance to infection, manifested by usual lymphocytic infiltration. This type of lepra exists for 4-5 years, then depending on the general state of the body it can develop into a severe lepromatous form or regress to a tuberculoid type.

Pathological anatomy of the nasal leprosy

With leprosy, there are three main types of histological changes: lepromatous, tuberculoid and undifferentiated. With the tuberculoid type, the pathological process develops in the skin and in the peripheral nerves, and with lepromatous, various internal organs, eyes, mucous membranes of the upper respiratory tract, etc. Are also affected. Granuloma of tuberculoid leprosy is typical, but not specific. It is formed by foci of epithelioid cells with an admixture of giant, surrounded by a lymphocytic shaft. In the lepromatous type, a specific granuloma appears, for which there is a presence of large "leprosy cells" (Virchov cells) with vacuolated protoplasm and a mass of intracellular compact clusters of rods. With an undifferentiated type of leprosy, the affected areas consist of lymphocytes with a small admixture of histiocytes and fibroblasts, occasionally there are single plasmatic and mast cells. Infiltrate is located predominantly perineurally; nerve branches are subjected to ascending degenerative and destructive changes, which leads to atrophy and destruction of innervated tissues.

Symptoms and clinical course of nasal leprosy

There are three periods - the initial period, the peak period and the terminal period.

In the initial period, the patient periodically experiences a feeling of nasal congestion, a decrease in the severity of the sense of smell. The mucous membrane of the nose is pale, dry, covered with densely coalesced yellowish-brownish crusts with an unpleasant odor, but different from ozonous and sclerotic. When they are removed, the nasal mucosa begins to bleed. The arising rhinitis is resistant to any kind of treatment and can be accompanied by leprosy lesions in other areas of the body. On anatomical formations of the nasal cavity, lepromatous nodules arise, which merge, ulcerate and become covered with bloody yellowish-brown crusts.

In the period of height, pronounced atrophy of the nasal mucosa and other anatomical formations of the nasal cavity is caused by the defeat of trophic nerves. Nasal cavities widen and are covered with hard-to-separate crusts. Lepromes evolve in the direction of scarring, as a result of which the nasal passages and nostrils become stenotic. At the same time, new lepromatous eruptions occur, which leads to a variegated picture of lesions that are at different stages of development. The anterior paranasal sinuses remain intact, sometimes one can observe a nodular thickening of the nose pyramid.

In the terminal period of the development of the lepromatous process, in the absence of appropriate treatment, skin lesions occur in the nose and adjacent areas of the face with complete simultaneous destruction of the internal formations of the nasal cavity and its disfigurement. Simultaneously, there are signs of damage to the peripheral nervous system: of all sensitivities, only tactile remains; neurotrophic lesions determine the atrophy of the skin, muscles and skeleton in the residual stage of the facial leprosy.

The evolution of leprosy depends on many factors, and first of all on timely and correct treatment. The period from infection to the appearance of lesions of the skin or mucous membrane can last from 2 to 8 years. In most cases, in the absence of treatment, the disease continues to progress for 30 to 40 years, causing damage to the internal organs. Toxins of leprosy infection have a pronounced neurotropic property. They diffuse along the nerve trunks in the direction of the nerve nodes and centers and cause severe irreversible damage to the nervous system.

The diagnosis is based on the epidemics, described above the clinical picture, the biopsy data and the bacteriological examination. Differentiate leprosy from lupus, which is characterized by the absence of a violation of the sensitivity of affected areas, from tertiary syphilis (positive serological reactions and a short period of development), rhinoscleromas (cicatricial changes, absence of cutaneous and neurological lesions), leishmaniasis (nodular rashes, absence of Gensen's rod), from atrophic rhinitis and ozena (lack of leprom and wand Gensen).

Treatment of nasal leprosy

Prior to the discovery of sulfonic drugs, and then antibiotics, leprosy was considered an incurable disease. In 1943, an American leprologist G.Faget discovered the effectiveness of sulfonamides in the treatment of leprosy in combination with thiourea compounds. Currently, along with solesulfone for the treatment of lepra, sulfonamides dapsone (sulfonylbis) and sulfamethoxypyridazine are used, as well as an antibiotic from the group of ansamycins rifamycin. In addition, streptomycin, cortisone, ACTH, vitamins A, B1, B12 C, D2 are used. It is advisable to designate a milky-vegetable diet. Locally sometimes apply cryosurgical methods, vitaminized oils, ointments containing sulfonic and antibiotic drugs. Functional and cosmetic surgical treatment is carried out only a few years after the disappearance of mycobacterium leprosy in the affected areas. The treatment is carried out for a long time in special facilities for patients with leprosy - leprosoria, where the patients are temporarily. Particular attention is paid to newborns in mothers, patients with leprosy. They are immediately separated and placed in special institutions where the preventive treatment and vaccination of BCG is carried out according to the instructions. Healed patients become socially valuable citizens.

Prevention of nasal leprosy

Measures to prevent leprosy are determined by the relevant regulations of the Ministry of Health and the instructions of the sanitary and epidemiological service of the country. There are individual and social (social) precautionary measures. Individual prophylaxis consists mainly in observing personal hygiene measures, in particular in respecting the appropriate requirements for keeping the body clean, linen, clothes, shelter, preventing the use of substandard, infected and unadjusted products. Observance of caution when visiting leprosariums and communicating with sick leprosy. Medical workers in foci of leprosy should use gauze masks and gloves when taking a biopsy, surgical interventions, when examining patients, especially when examining the upper respiratory tract, taking a scraping from the affected mucous membranes. Public prevention is as follows:

1. early active detection and treatment of patients;
2. Preventive treatment of people aged 2 to 60 years who had prolonged contact with a leprosy patient (sulfon drugs, duration of treatment from 6 months to 3 years);
3. conducting periodic population examinations in zones endemic to leprosy to identify early forms of the disease;
4. spansernoe observation of family members of the patient leprosy (if necessary - quarterly laboratory studies, the duration of observation of 3 to 10 years).