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Lepra of the nose
Last reviewed: 05.07.2025

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Leprosy is a generalized, low-contagious infectious disease characterized by lesions of the skin, visible mucous membranes, peripheral nervous system and internal organs.
There is no hereditary transmission or congenital diseases. The only source of infection is a sick person, especially one suffering from the lepromatous type of leprosy.
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, where it became widespread in 1300 BC. Leprosy spread to Europe during the Crusades, to America, mainly to Central and South America, it was brought by Spanish and Portuguese sailors in the late 15th - early 16th centuries, and then the number of diseases increased due to the mass import of black slaves from Africa. Leprosy was brought to Australia and Oceania by immigrants from China and India. The disease penetrated Russia in several ways: to the coast of the Black and Azov Seas - from Greece, the Caspian and Aral Seas - from Central Asia, to the Caucasus and Transcaucasia - from Iran and Turkey, to the Baltic States - from Germany and Scandinavia, to the Far East and Siberia - from China.
Leprosy has been known since ancient times. Thus, in India, according to the texts of the Rigveda (the "Book of Hymns" - a collection of mainly religious hymns that arose among the Aryan tribes during the era of their migration to India), leprosy was already known in the 7th century BC. The first mention of leprosy in Japan dates back to the 8th century BC. According to N.A. Torsuev (1952), "zaraath" (leprosy) mentioned in the Bible was a collective term for physical and moral "impurity". Leprosy appears in the works of Straboius, Plutarch, Halsne, Celsus, Pliny and others under various names (elephantiasis graecorum, leontina, leontiasis, satiris, etc.).
In past centuries, leprosy was considered a civil death: patients were expelled from society, deprived of the right to inherit, and often killed. Then, due to advances in the study of leprosy and the development of civilized society, patients began to be placed in certain settlements (leprosariums), where they were given medical care and appropriate care.
According to WHO (1960), the total number of people with leprosy worldwide is approximately 10-12 million. Apparently, by 2000 this number had not decreased significantly.
Cause of nasal leprosy
The causative agent of leprosy is acid-fast mycobacterium (M. leprae) - a gram-positive rod, very similar to MBT, an obligate intracellular parasite, discovered in 1871-1873 by 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 theory 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 occur with prolonged and close contact with a patient with leprosy. Children are most susceptible to leprosy. Immunity is relative. With frequently repeated massive superinfection - additional (repeated) infection of the patient in the conditions of an incomplete infectious process - the disease can occur against the background of existing natural and acquired immunity. After the discovery of the causative agent of leprosy, the greatest achievement in modern leprology was the discovery in 1916 by the Japanese leprologist K. Mitsuda of a substance contained in the microbe, called lepromin. This substance, obtained by extraction from crushed lepromatous tissues and neutralized, injected intradermally into healthy adults, causes a positive lepromatous reaction in 80% of cases, while in the vast majority of infected people this reaction does not occur.
Pathogenesis of nasal leprosy
The entry points for the infection are the skin and, rarely, the mucous membrane of the upper respiratory tract and the gastrointestinal tract. Clinical observations have shown that allergies and immunosuppressive conditions contribute to leprosy infection. Mycobacteria that enter the body, having passed through the skin and mucous barriers, penetrate the nerve endings, then the lymphatic and blood capillaries and slowly disseminate, usually without causing any reactions at the site of introduction. With good resistance of the macroorganism, in most cases the introduced bacilli die without causing disease. In other cases, a latent form of leprosy develops, which, depending on the resistance of the body, can remain in this state throughout the life of the infected person. With less resistance, an abortive form of leprosy occurs, manifested in the form of limited rashes that can disappear after some time. If the body's resistance is insufficient, depending on its degree, either a relatively benign tuberculoid leprosy develops, or the disease takes on a severe malignant character with the formation of lepromatous granulomas containing countless mycobacteria (lepromatous leprosy). An intermediate position between the two types of leprosy is occupied by undifferentiated leprosy, which develops in people with unstable resistance to infection, manifested by normal lymphocytic infiltration. This type of leprosy exists for 4-5 years, then, depending on the general condition of the body, it can develop into a severe lepromatous form or regress into a tuberculoid type.
Pathological anatomy of nasal leprosy
In leprosy, there are three main types of histological changes: lepromatous, tuberculoid, and undifferentiated. In the tuberculoid type, the pathological process develops in the skin and peripheral nerves, while in the lepromatous type, various internal organs, eyes, mucous membranes of the upper respiratory tract, etc. are also affected. The granuloma of tuberculoid leprosy is typical but not specific. It is formed by foci of epithelioid cells with an admixture of giant cells, surrounded by a lymphocytic ridge. In the lepromatous type, a specific granuloma occurs, which is characterized by the presence of large "leprosy cells" (Virchow's cells) with vacuolated protoplasm and a mass of intracellular compact clusters of rods. In the undifferentiated type of leprosy, the affected areas consist of lymphocytes with a small admixture of histiocytes and fibroblasts, and occasional single plasma and mast cells are found. The infiltrate is located predominantly perineurally; nerve branches undergo ascending degenerative and destructive changes, which leads to atrophy and destruction of the tissues they innervate.
Symptoms and clinical course of nasal leprosy
There are three periods: initial, peak and terminal.
In the initial period, the patient periodically experiences a feeling of nasal congestion and decreased olfactory acuity. The nasal mucosa is pale, dry, covered with tightly fused yellowish-brown crusts with an unpleasant odor, but different from ozenous and sclerotic. When they are removed, the nasal mucosa begins to bleed. The resulting runny nose is resistant to any treatment and may be accompanied by leprosy lesions in other areas of the body. Lepromatous nodules appear on the anatomical structures of the nasal cavity, which merge, ulcerate and become covered with bloody yellowish-brown crusts.
During the peak period, pronounced atrophy of the nasal mucosa and other anatomical structures of the nasal cavity develops, caused by damage to the trophic nerves. The nasal cavities expand and become covered with crusts that are difficult to separate. Lepromas evolve towards scarring, as a result of which the nasal passages and nostrils become stenotic. At the same time, new lepromatous eruptions appear, which leads to a motley picture of lesions at different stages of development. The anterior paranasal sinuses remain intact, and sometimes some nodular thickening of the nasal pyramid can be observed.
In the terminal period of the development of the lepromatous process, in the absence of appropriate treatment, skin lesions occur in the area of the nose and adjacent areas of the face with complete simultaneous destruction of the internal structures of the nasal cavity and its disfigurement. At the same time, signs of damage to the peripheral nervous system appear: of all types of sensitivity, only tactile sensitivity is preserved; neurotrophic lesions cause atrophy of the skin, muscles and skeletal system in the residual stage of facial leprosy.
The evolution of leprosy depends on many factors, and above all on timely and correct treatment. The period from infection to the appearance of skin or mucous membrane lesions can last from 2 to 8 years. In most cases, without treatment, the disease continues to progress for 30 to 40 years, causing damage to internal organs. Leprosy infection toxins 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 epidemiological history, the clinical picture described above, biopsy data and bacteriological examination. Leprosy is differentiated from lupus, which is characterized by the absence of sensitivity disorders in the affected areas, from tertiary syphilis (positive serological reactions and a short period of development), rhinoscleroma (scarring, absence of skin and neurological lesions), leishmaniasis (nodular rash, absence of Hensen's bacillus), from atrophic rhinitis and ozena (absence of leprosy and Hensen's bacillus).
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Treatment of nasal leprosy
Before the discovery of sulfone drugs and then antibiotics, leprosy was considered an incurable disease. In 1943, American leprologist G. Faget discovered the effectiveness of sulfonamides in the treatment of leprosy in combination with thiourea compounds. Currently, along with solusulfone, sulfonamides dapsone (sulfonylbis) and sulfamethoxypyridazine, as well as an antibiotic from the ansamycin group, rifamycin, are used to treat leprosy. In addition, streptomycin, cortisone, ACTH, vitamins A, B1, B12 C, D2 are used. It is advisable to prescribe a dairy-vegetable diet. Cryosurgical methods, vitaminized oils, ointments containing sulfone and antibiotic drugs are sometimes used locally. Functional and cosmetic surgical treatment is carried out only several years after the disappearance of the lepra mycobacterium in the affected areas. Treatment is carried out over a long period of time in special institutions for patients with leprosy - leprosariums, where patients are temporarily located. Particular attention is paid to newborns of mothers with leprosy. They are immediately separated and placed in special institutions, where preventive treatment and BCG vaccination are carried out as provided for by the relevant instructions. Cured patients become socially full-fledged citizens.
Drugs
Prevention of nasal leprosy
Leprosy prevention measures are determined by the relevant regulations of the Ministry of Health and the instructions of the country's sanitary and anti-epidemic service. A distinction is made between individual and public (social) preventive measures. Individual prevention consists mainly of observing personal hygiene measures, in particular, observing the relevant requirements for keeping the body, linen, clothing, and home clean, and not allowing the consumption of low-quality, infected, and improperly cooked foods. Caution is required when visiting leprosariums and communicating with leprosy patients. Healthcare workers in leprosy hotbeds should use gauze masks and gloves when taking biopsies, performing surgical interventions, and examining patients, especially when examining the upper respiratory tract and taking scrapings from affected mucous membranes. Public prevention consists of the following:
- early active identification and treatment of patients;
- preventive treatment of persons aged 2 to 60 years who have had prolonged contact with a patient with leprosy (sulfone drugs; duration of treatment from 6 months to 3 years);
- conducting periodic examinations of the population in areas endemic for leprosy to detect early forms of the disease;
- outpatient monitoring of family members of a patient with leprosy (if necessary, quarterly laboratory tests; duration of observation from 3 to 10 years).