Leprosy: causes and symptoms of the disease leprosy. Leprosy (leprosy): causes, symptoms and modern treatment methods Leprosy is treated in our time
Leprosy (leprosy), from Greek. lepros- scaly, rough, flaky ) - This is a chronic generalized disease characterized by specific granulomatous lesions of the ectoderm derivatives (skin, mucous membranes, peripheral nervous system) and pathological changes in internal organs.
History of discovery.
Leprosy is one of the oldest diseases known to mankind long before our era. detailed descriptions found in Egyptian papyri, Indian scriptures dating back to 1500 BC. It is known that it was widespread in China, Japan, and Persia. The spread of the disease was facilitated by the development of navigation and trade, as well as conquering campaigns - in the ancient sea it was the Phoenicians ( morbus phoenicicus) and Greeks ( elephantiasis graecorum), leprosy was brought to Europe by the legions of Rome. In Europe, the maximum spread of leprosy dates back to the 11th-13th centuries (wars, crusades, natural disasters, epidemics of other diseases), from where the disease spread to the New World (15th-16th centuries), Australia and Oceania (early 19th century). In most countries, the disease was equivalent to civil death with exclusion from society and disinheritance; the sick were either killed or expelled to desert places.
Expulsion of a patient with leprosy (leprosy).
The very biblical zaraath(leprosy) was a collective term denoting moral and physical uncleanness. To isolate the sick, xenodochias were organized back in Byzantium, in the Middle Ages they were replaced by leper colonies (created by the priest Lazarus - a person was placed in a coffin and a funeral service was held in the temple, leprosy was equated to death), the order of which resembled prisons, and escape was always punishable by death. However, draconian methods bore fruit. Since the 14th century. The incidence in Europe has decreased sharply, and leprosy now occurs in isolated outbreaks. Currently, there are from 2 to 13 million patients in the world, mainly in Third World countries. The largest number of patients is in Asia (India - 64%, China, Burma), Africa, South and Central America. In the territory former USSR The areas of the leprosy epidemic were the Baltic states, the mouths of the Volga, Danube, the Caucasus and Transcaucasia, and Central Asia. In these territories there are leper colonies (now the largest leper colony in the CIS is located in the Astrakhan region).
Pathogen - M. leprae was discovered by a Norwegian doctor G.A. Hansen in 1873 in scraping from the surface of the leproma.
Taxonomy.
Order - Actinomycetales
Family - Mycobacteriaceae
Genus - Mycobacterium
View - M. leprae
Morphology and tinctorial properties.
M. lepraeits morphological and tinctorial properties are similar to Mycobacterium tuberculosis. M. leprae has the shape of rods, straight or slightly curved with rounded ends, size 0.2-0.5×1-7 microns. Sometimes fine granularity is observed in the body of bacteria. Branching, segmented, coccoid, filamentous and club-shaped forms have been described. The smears contain intracellular parallel rows in the form of “packs of cigarettes”. Clusters of these groups form so-called “leprosy balls” (up to 200-300 bacterial cells in a cluster). They do not have flagella, do not form spores, and have a microcapsule. By chemical composition similar to M. tuberculosis- 3-layer cell wall, contains many fat-like substances: phosphatides, waxes (leprosin) and fatty acids (mycolic and leprosinic). Acid and alcohol resistant. Gram-positive. According to the Ziehl-Neelsen method, they are stained red. Dividing individuals have a transverse, non-coloring stripe.
Cultural properties.
Biochemical properties.
Recycle glycerin and glucose. Enzymes are isolated - peroxidase, cytochrome oxidase, alkaline phosphatase and specific- O-diphenoloxidase (DOPA oxidase), absent in other mycobacteria.
Antigenic structure.
Polysaccharide AGs are thermostable, group for mycobacteria;
Protein Ags are thermolabile, species-specific;
Glycolipids are species specific.
They have cross-reacting antigens with antigens of people of blood group 0 (I) Rh-.
Pathogenicity factors.
High lipid content;
Resistance.
Outside the human body, the pathogen quickly loses its viability, but in human corpses it can persist for a long time. Also remain viable after 10-12 years of storage at room temperature in 40% formaldehyde.
Epidemiology.
Anthroponosis.
The disease is slightly contagious.
Source of infection - a sick man. Bacteria are released from the patient through the skin, when coughing, sneezing, even when talking. There are reports of the pathogen being excreted in seminal fluid, feces, urine, and tears.
Leprosy is characterized by prolonged incubation period- 3-5 and even up to 20-30 years, so events with which they could associate the infection disappear from the patient’s memory.
MechanismAnd transmission routes infections are not fully understood due to the difficulty of studying them. It is believed that infection occurs through direct, long-term and close household contacts (direct and indirect), as well as through airborne droplets. Old writers call leprosy a disease of domestic cohabitation. The possibility of intrauterine infection has been proven, but children separated from sick parents after birth do not get sick. There is an assumption that blood-sucking insects (fleas, lice, bedbugs, mosquitoes) may play a role in the spread of leprosy.
Entrance gate:It is believed that the pathogen enters the human body through damaged skin and mucous membranes.
The leading role in the spread belongs to socio-economic factors - unfavorable living and living conditions: overcrowding, poor sanitary standards, low living standards.
Persons in contact with sick people are not dangerous to others.
Pathogenesis and clinical manifestations.
Features of the disease are determined by the following properties of the pathogen:
Slow reproduction (incubation period up to 20 years) and chronic course;
Damage to the nervous system leads to disability;
Optimum temperature below 37 0 C, therefore, cooled tissues are affected;
Causes immunological tolerance in people with lepromatous form, and such patients become the main source of infection.
M. lepraepenetrates the nerve endings, and from there into the lymphatic and blood capillaries, without causing visible lesions at the site of penetration. In most cases, the pathogen dies and is eliminated, or the disease is latent and does not manifest itself throughout life. The manifestation of the disease directly depends on the state of resistance factors. With minor deviations, an abortive infection develops in the form of limited granulomatous rashes (sometimes they can disappear spontaneously).
Classification of leprosy (Ridley-Jopling):
1. TT type - individuals with good immunity develop a relatively benign tuberculoid form. It is characterized by the formation of granulomas from epithelioid and giant cells, surrounded by a lymphocyte shaft, on the skin and mucous membranes, as well as damage to peripheral nerves; internal organs are less often affected. The skin elements of the rash (single slightly pigmented spots, papular rashes, plaques located asymmetrically) gradually resolve, leaving local anesthesia, atrophy (hair does not grow, sweat glands do not function). Damage to peripheral nerves leads to impaired sensitivity, and damage to large trunks leads to paresis, paralysis, finger contracture, and trophic ulcers.
2. LL type - considered unfavorable and severe lepromatous form with the formation of granulomas containing “leprosy cells” (Virchow cells), plasma cells, lymphocytes, fibroblasts. The course is malignant. The main cellular element of granuloma is the macrophage. Incomplete phagocytosis is characteristic - in such cells M. leprae multiply and accumulate in large quantities. This form is the most dangerous for others (tubercular leprosy), since in patients the pathogen is contained in leprosy, organs and tissues, and on the nasal mucosa. The disease begins with the appearance of red spots on the skin of the shoulders, thighs, and buttocks. The spots at first have no sharp boundaries, later they acquire a “rusty color” (devil’s marks - when pierced, they do not bleed and are painless). For a long time, the spots remain unchanged, but more often turn into infiltrates or lepromas. Their size ranges from millet grain to hazelnut. Color blue-brown. With diffuse infiltration, a “lion's face” (facies leonina) is formed - wrinkles and folds deepen, the nose thickens, the cheeks, lips and chin take on a lobed appearance. Eye damage is also common, leading to blurred vision and blindness. In the later stages of leprosy, the patient develops multiple lepromas, eyebrows and eyelashes fall out, fingers become deformed, and paresis and paralysis occur. Lepromas can ulcerate to form an ulcer with dense, steep edges and sanguineous discharge. Lepromas of the nasal septum are not uncommon, causing perforations and deformations. If lepromas form in the larynx, hoarseness, aphonia, and suffocation may occur. Infiltrates can merge and then the hands and feet take on a pillow-like appearance. The course of the disease is slow and long-term with periodic exacerbations under any stress (cold, pregnancy, surgery).
3. Occupies an intermediate position undifferentiated a form found in people with unstable immunity. It occurs with damage to peripheral nerves and mild skin manifestations. Over time (3-5 years), this type transforms into tuberculoid or lepromatous.
4. In addition, borderline tuberculoid, borderline and borderline lepromatous forms are distinguished.
Immunity.
Natural resistance is high. As a result of contacts with sick people, not everyone gets sick (no more than 1-2 out of every 100 contacts). However, all factors that contribute to weakened immunity increase the risk of disease. There are many cases where family members of a patient who lived with them from the very beginning of the disease remained healthy for a long time, which may indicate the formation of immunity in those in contact with patients. This is also confirmed in very rare cases of leprosy by doctors, service personnel leper colonies - in rare cases, when the rules established there were violated, and contact with patients went beyond the boundaries of official relations.
The more frequent incidence of the disease in children is most likely due to the imperfection of their immune system.
During the course of the disease, changes in immunocompetent cells occur: the number of T-lymphocytes decreases, their activity decreases - as a result, the ability to respond to pathogen antigens is lost (the formation of split tolerance to M. leprae). Humoral immunity is not impaired - antibodies to Mycobacterium leprosy are found in high titers in the blood serum of patients, but they do not play a protective role.
It is used to determine the activity of the immune system of patients, for diagnostic purposes, as well as to determine the effectiveness of treatment. Mitsuda's test- skin test with lepromin. Lepromin- autoclaved or boiled suspension of lepromatous tissue. 0.1 ml is administered intradermally. The standard lepromin preparation contains 100 million mycobacteria of leprosy per 1.0 ml. The reaction is positive in healthy people and in patients with tuberculoid form. Negative - in the lepromatous form, which indicates a sharp decrease in immunity. There is an early reaction (48 hours) - hyperemia, a small papule and a late reaction, which appears after 2-4 weeks in the form of a tubercle, nodule, sometimes with necrosis.
Microbiological diagnostics.
Material under study - scraping of the nasal mucosa (on both sides of the septum), contents of leprosy nodes, sputum, discharge from ulcers, punctates lymph nodes, pieces of organs, blood (during fever).
1. Bacterioscopic method (basic) .
2. Biological method.
3. Allergological method - Mitsuda test to determine the ability to respond to an immune response.
4. Molecular biological method - PCR, DNA hybridization.
Prevention and treatment.
SpecificThere is no prevention (an experimental vaccine has been created) and no treatment.
The main measures of nonspecific prevention:
Early identification of patients and their isolation in a leper colony, where they remain until cured;
Observation of the patient's family members and their examination for the first 10 years - 2 times a year, then - 1 time a year;
Newborn children are immediately isolated from their sick mother and fed artificially, then healthy children are raised in an orphanage at a leper colony;
Preventive administration of the BCG vaccine is used to the population of those areas where leprosy is common.
A huge amount has been tried to treat leprosy. in various ways, including gold preparations(gold in various compounds kills acid-fast bacteria) - crizolgan, solganol, sanacrisin; replanting of plant and animal tissues to stimulate the immune system (potassium iodide).
Has long been used chaulmugra oil, extracted from tropical legumes. The oil contains unsaturated fatty acids, which affect the level of lipase in the blood, which destroys the cell membrane of bacteria.
Currently, the main means of treating leprosy are:
Sulfone drugs (DDS/dapsone - 4,4-diaminodiphenylsulfone, etc.);
Rifampicin, clofazimine, fluoroquinolones (ofloxacin);
Anti-tuberculosis drugs (ftivazide, tibon);
Chaulmugra oil and its preparations (migrol, intileprol).
The drugs of choice are: dapsone, rifampicin and clofazimine, used alone or in combination.
Treatment is complex, long courses and sometimes lifelong.
Despite the fact that this disease was previously considered incurable and deadly, modern medicine has medicines to treat leprosy. With the help of antibiotics, you can get rid of the disease in a few months.
The causative agent of leprosy is the bacterium Mycobacterium leprae. It multiplies very slowly in the human body. The science of microbiology studies it. The causative agent of the disease is similar to Mycobacterium tuberculosis. In microbiology, Mycobacterium leprae was discovered in 1874.
Another name for leprosy is Hansen's disease (after the scientist who discovered the bacterium Mycobacterium leprae).
Incubation period ranges from 2 to 20 years, that is, symptoms of leprosy may appear 20 years after infection. On average, the disease makes itself felt after 3-10 years.
Kinds
There are 4 types of leprosy:
- lepromatous (black leprosy);
- tuberculoid (white leprosy);
- undifferentiated;
- mixed.
These varieties differ in the number and location of ulcers.
Lepromatous
This variety is characterized by the rapid proliferation of bacteria, which causes the formation of nodules (lepromas) or plaques with a scaly surface on the skin. The skin thickens and folds appear.
A characteristic symptom of the lepromatous form is the “lion's face”.
Leprosy has a complex course. Eyebrows fall out, facial features are distorted, facial expressions are disrupted, the back of the nose sinks, and earlobes grow.
With this type, not only the skin and nerves are affected, but also the lymph nodes, the mucous membrane of the eyes and internal organs. The first symptoms are:
- nasal congestion;
- nosebleeds;
- labored breathing;
- hoarseness, laryngitis;
The most commonly affected areas are the face, wrists, elbows, buttocks, knees, kidneys and genitals.
Black leprosy is the most contagious and dangerous as it can be fatal.
Tuberculoid
In this form, the skin and peripheral nerves are affected, the internal organs remain untouched.
Leprosy begins with the appearance of red or white spots on the skin with clear contours, sometimes covered with scales. Over time, they increase in size and rise above the surface of the skin; their middle, on the contrary, sinks. In this area, the hair turns white and falls out, the skin loses sensitivity.
Damage to the nerves leads to muscle atrophy, this is especially felt if the limbs are affected. Destructive changes in bones and joints occur.
Symptoms of tuberculoid leprosy may disappear on their own.
This type of disease is most often localized on the hands and feet.
Undifferentiated
There are no typical skin manifestations. Symptoms include polyneuritis with paralysis and ulceration of the limbs.
Mixed
This type includes features of lepromatous and tuberculoid leprosy.
Symptoms
The first signs appear on the skin. The color of the skin changes, nodules, spots, papules and bumps appear. Further, the mucous membranes of the mouth, eyes and nose are affected, as well as the nerves that are located on the surface of the skin. The sensitivity of nerve endings disappears.
The pathological anatomy of leprosy (pathological anatomy of the disease) looks like this: first of all, those areas of the skin that are constantly in contact with air (face and hands) are affected. The formations can be seen on the ears, elbows, wrists and buttocks.
In advanced cases, the deep layers of the skin are affected, the symptoms of leprosy look like this:
- skin ulcers, tissue necrosis;
- loss of eyebrows and eyelashes;
- rashes on the mucous membranes of the nose and mouth;
- deformation of the face or limbs due to nerve damage and tissue death;
- numbness of the limbs;
- vascular disorders;
- enlarged inguinal and axillary lymph nodes.
The patient experiences malaise and weakness. In later stages, the earlobes grow, nosebleeds often occur, and nasal breathing becomes difficult.
If a person untimely applies for medical care, then there is a high risk that he will have external deformities.
Leprosy bacteria are not capable of causing the death of fingers and do not lead to deformation of the appearance. Necrosis develops due to the addition of a secondary bacterial infection, which occurs due to injuries to the skin.
How is leprosy transmitted?
Leprosy is a rare disease, especially in cold climates, but nevertheless affects more than 11 million people worldwide. To avoid getting sick, you need to know how the disease is transmitted. Is leprosy contagious or not?
The causative agent of leprosy is transmitted through contact with the skin of a sick person, but infection can only be caused by prolonged contact. Leprosy can also be transmitted by airborne droplets if the saliva of a patient enters the respiratory tract of a healthy person.
The disease is common in Africa, Asia, Japan, Korea, Central and South America. Children are more susceptible to the bacterium Mycobacterium leprae than adults.
The risk group includes the following categories of the population:
- children;
- people with chronic, complicated infectious processes and diseases;
- patients suffering from alcoholism or drug addiction.
Which doctor treats leprosy?
If you suspect leprosy, you should contact a dermatologist and infectious disease specialist. Consultation with an ophthalmologist and neurologist may be necessary.
Diagnostics
It is impossible to make a diagnosis based on an external examination. The disease must be differentiated from erythema, syphilis, sarcoidosis and herpes zoster.
Diagnosis of leprosy includes laboratory and bacterioscopic studies, namely:
- scraping of skin or mucous membrane;
- puncture of lymph nodes;
- reaction to lepromin (to determine the form of leprosy);
- tests with histamine and nicotinic acid.
Treatment
Leprosy is treated in specialized medical and preventive institutions - leper colonies. Patients with this diagnosis should undergo therapy in isolation from other people. In developed countries, patients with leprosy are no longer admitted to such institutions.
There are 4 leper colonies in Russia.
Treatment of leprosy is a complex process. The sooner a person goes to the hospital, the higher the chances of curing the disease.
The result of treatment depends on the stage of leprosy and the correctness of the treatment regimen. Recovery takes from 6 months to a year. If the patient has a severe stage of leprosy, then treatment is longer.
The basis of drug therapy is antibiotics, NSAIDs and special drugs for leprosy. The type and regimen of antibacterial therapy is prescribed by the doctor individually for each patient.
Drug treatment:
- anti-leprosy drugs (Prothionamide, Pyrazinamide, Clofazimine, sulfone drugs Dapsone, Sulfetron and Dimocyfon);
- antibiotics (Rifampicin, Dapsone, Clarithromycin, Ofloxacin);
- anti-inflammatory drugs (prednisolone and acetylsalicylic acid);
- immunomodulators (Thimogen, Levomizol).
Treatment must be comprehensive. The course can be supplemented with hepatoprotectors, iron supplements, vitamin complexes and BCG vaccination.
The drug Dapsone inhibits the development of the disease.
Sulfone drugs are indispensable for preventing the development of complications, but they cannot be used in the following cases:
- diseases of the liver, hematopoietic organs and kidneys;
- heart defects;
- gastroenteritis;
- organic diseases of the nervous system.
Thalidomide, a sedative-hypnotic drug that suppresses the immune system, can be used to treat leprosy. It eliminates the symptoms of the disease.
In addition to medications, physiotherapeutic procedures and therapeutic exercises. The main goal of exercise therapy is to prevent the development of neuritis, contractures and amyotrophies.
Some patients require the help of a psychotherapist.
Complications
The consequences depend on the type of leprosy, its location and the timeliness of treatment. A person may experience the following complications:
- plantar ulcers;
- keratitis, laryngitis;
- chronic nosebleeds due to nasal deformity;
- corneal ulcer, lagophthalmos, glaucoma, blindness;
- distortion of appearance, facial deformation, mutation of phalanges, twisting of limbs;
- renal failure;
- erectile dysfunction and infertility in men.
A patient with leprosy loses sensitivity and is therefore often injured, causing him appearance becomes even more unattractive.
If the patient does not seek medical help, necrotizing vasculitis develops, therefore death inevitable.
Prevention
Preventive measures:
- strengthening immunity;
- balanced diet;
- improving quality of life;
- prevention of infectious and inflammatory diseases;
- conducting healthy image life.
Leprosy is a completely curable disease, but only those who seek diagnosis and treatment in time have a chance of recovery. We must not forget that this disease has a high probability of disability and death.
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The causative agent of leprosy (leprosy) - M. leprae was described by G. Hansen in 1973. Leprosy is a chronic infectious disease that occurs only in humans. The disease is characterized by generalization of the process, damage to the skin, mucous membranes, peripheral nerves and internal organs.Morphology, physiology
Mycobacteria leprae are straight or slightly curved rods. In the affected tissues, microorganisms are located inside the cells, forming dense spherical clusters - leprosy balls, in which the bacteria are closely adjacent to each other with their lateral surfaces (“pack of cigars”). Acid-resistant, stained red using the Ziehl-Neelsen method. Mycobacteria leprosy cannot be cultivated on artificial nutrient media. In 1960 it was created experimental model with infection of white mice in the paw pads, in 1967 - infection of thymusectomized mice, and in 1971 - of armadillos, in which typical granulomas (lepromas) are formed at the site of injection of Mycobacterium leprosy, and with intravenous infection a generalized process develops with the proliferation of mycobacteria in affected tissues.Antigens
Two antigens were isolated from leproma extract: a heat-stable polysaccharide (group for mycobacteria) and a heat-labile protein, highly specific for leprosy bacteria.Pathogenicity and pathogenesis
The virulence of M. leprae appears to be related to the same factors that have been described for M. tuberculosis. This is primarily due to the high lipid content of bacterial cells. The incubation period is from 3-5 years to 20-35 years. The disease develops slowly over many years. There are several clinical forms, of which the most severe and epidemically dangerous is lepromatous: multiple infiltrates-lepromas are formed on the face, forearms, and legs, which contain a huge number of pathogens. Subsequently, lepromas disintegrate with the formation of slowly healing ulcers. Skin, mucous membranes, lymph nodes, nerve trunks, and internal organs are affected. Another form is tuberculoid. It is clinically easier and less dangerous to others. In this form, the skin, nerve trunks and internal organs are less frequently affected. Skin rashes in the form of small papules are accompanied by anesthesia. In the lesions, pathogens are found in small quantities.Immunity
As the disease progresses, the number and activity of T-lymphocytes decreases and, as a result, the ability to respond to Mycobacterium leprosy antigens is lost. Mitsuda's reaction to the introduction of lepromin into the skin in patients with the lepromatous form, which occurs against the background of deep suppression of cellular immunity, is negative. In healthy individuals and in patients with tuberculoid leprosy, it is positive. Thus, this test reflects the severity of T-lymphocyte damage and is used as a prognostic test, characterizing the effect of treatment. Humoral immunity is not impaired. Antibodies to Mycobacterium leprosy are found in high titers in the blood of patients, but they do not have protective properties.Ecology and epidemiology
The natural reservoir and source of the causative agent of leprosy is a sick person. Leprosy is a low-contagious disease. Infection occurs through prolonged and close contact with a sick person. Currently, according to WHO, there are about 10-12 million leprosy patients in the world. The disease is distributed mainly along the shores of the southern seas and large bodies of water (India, countries of Central and Southern Africa).Leprosy (leprosy)
Leprosy is a primary chronic generalized infectious disease of humans, which is characterized by specific lesions of the skin, mucous membranes, peripheral nerves and internal organs. The causative agent of the disease is Mycobacterium leprae. In addition, leprosy in rats is caused by M. lepraemurium, which is morphologically and tinctorially very similar to human leprosy bacilli. There are two main clinical forms of the disease: tuberculoid and lepromatous. The latter has a more severe progressive course. The leper excretes the pathogen when coughing, sneezing and talking, since he is in large quantities located in the mucous membrane of the nasopharynx. Infection of people most often occurs through the varicose veins route through close contact with patients with leprosy. In the laboratory diagnosis of leprosy, a predominantly bacterioscopic research method is used, much less often a bioassay on mice and armadillos and an allergy test with lepromin. The material for the study is scrapings of the nasal mucosa, scarifications from the affected areas of the skin, especially the brow ridges, earlobes, chin, as well as biopsies of leprosy and lymphatic nodes. A scraping of the mucous membrane on both sides of the nasal septum is carried out with a metal spoon until a drop of blood appears. To apply a scarification, the skin at the site of the lesion is pinched with two fingers into a fold, along which a small incision 1-2 mm deep is made with a scalpel. The scraped material from the walls of the incision is transferred to a glass slide. The prepared smears are stained using the Ziehl-Neelsen method or the Semenovich-Martsinovsky method. When conducting histological studies of biopsy specimens, some of the sections are also stained with one of the indicated methods to identify mycobacteria. In smears, leprosy bacteria look like ruby-red straight or slightly bent rods with rounded ends. Microscopy of histological sections reveals their accumulations inside the cells, where the rods are arranged in parallel, resembling packs of cigars. This makes it possible to differentiate them from mycobacterium tuberculosis, which in its morphological and tinctorial properties are similar to the causative agent of leprosy. When leprosy materials are inoculated on media selective for mycobacteria, there is no growth. Guinea pigs are not sensitive to M leprae. A biological test is performed on mice (the Japanese dancing mouse is especially sensitive). A homogenate of the test material is injected into the hind footpad of animals, and immunological reactivity is reduced by introducing T-immunosuppressants. In positive cases, an infiltrate appears at the site of inoculation of the material after a few months, containing granulomas with mycobacteria located inside the cells. When armadillos (Armadyl) are infected, they develop typical multiple nodes (lepromas) in tissues and organs, where many leprosy bacteria are microscopically detected. The allergy test with lepromin is used mainly to differentiate lepromatous from tuberculoid forms of leprosy. The allergen is prepared from autoclaved homogenates of affected tissues containing a huge number of mycobacteria. Lepromin is administered intradermally in the middle third of the forearm in a volume of 0.1 ml. After 48 hours, in positive cases, a hyperemic spot or papule develops (Fernandez reaction). Much later (1-2 months) a hump may form, often with necrosis (Mitsuda reaction). In patients with the lepromatous form, the allergy test will be negative, while in patients with the tuberculoid form and in healthy people, the allergy test will be positive. So the lepromin test has no diagnostic value; it is used only to determine the clinical form of the disease and prognosis.Chronic granulomatous disease, affecting the mucous membranes and upper respiratory tract. pathways, peripheral nervous system, eyes.
Taxonomy. family Mycobacteriaceae, genus Mycobocterium, species M. leprae.
Morphological and cultural properties: straight/curved stick with rounded ends. Gram-positive, they do not form spores or capsules, have a microcapsule, and do not have flagella. Acid and alcohol resistance, which causes Ziehl-Neelsen staining. Not cultivated on artificial nutrient media. It multiplies only in the cytoplasm of the cell by division and forms spherical clusters. A characteristic feature of leprosy cells belonging to macrophages is the presence of a pale nucleus and “foamy” cytoplasm. Does not form toxins.
Biochemical properties. They utilize glycerol and glucose and have a specific enzyme, O-diphenoloxidase. They have the ability to produce extracellular lipids. Aerobes by identifying OM enzymes on the membrane structures of the microorganism: peroxidases, cytochrome oxidase.
Antigenic structure. Pronounced ability to enhance cellular immune responses without the addition of adjuvants. A number of M. leprae antigens are common to all mycobacteria, including the vaccine strain BCG, which is used for the prevention of leprosy. A species-specific glycolipid containing a trisaccharide has been isolated from M. leprae. Antibodies to the glycolipid are detected only in patients with leprosy, which is used for the active identification of patients with leprosy when examining individuals using ELISA.
Pathogenesis, clinic: Anthroponosis. The reservoir, the source of the pathogen, is a sick person (when coughing, sneezing, it releases bacteria).
The main mechanism of infection is aerogenic, the route of transmission is airborne. The entrance gate is the mucous membrane of the upper respiratory tract and damaged skin. The pathogen spreads through the lymphohematogenous route, affecting cells of the skin and peripheral nervous system. The incubation period is from 3-5 years. With high resistance, polar resistance develops tuberculoid form of the disease(TT-type of leprosy), and with low resistance develops polar lepromatous form diseases (LL-type of leprosy).
Immunity: relative. In areas with massive infection, leprosy can be caused by existing natural or acquired immunity.
Microbiological diagnostics: Material for bacterioscopic examination: scrapings from the skin and mucous membranes of the nose, sputum, punctate lymph nodes. Smears are stained according to Ziehl-Neelsen. Highest value bacterioscopy of scrapings has LL-form, in which M. leprae is detected in all rashes in large quantities. At TT form M. leprae diseases are detected very rarely in scrapings, so the final role in diagnosing the disease is played by histological examination of biopsy samples of the skin and mucous membranes, which makes it possible to determine the structure of granulomas.
Serological diagnosis based on the detection of antibodies to phenolic glycolipid in ELISA. At LL-form diseases, antibodies are detected in 95% of cases, and in TT form- in 50% of cases. Currently, monoclonal antibodies have been obtained that make it possible to detect leprosy antigens in tissues, and PCR is being developed.
Of additional importance is the study of the patient’s immune status, including the lepromin test (lepromin A). In patients LL-shape the test is negative, and in patients TT form she is positive.
Treatment: Sulfone drugs: dapsone, solusulfone. Rifampicin, clofazimine and fluoroquinolones. Gene therapy methods.
Prevention: There is no specific prevention. To relatively enhance immunity, the BCG vaccine is used, integral part which is lepromin A. A preliminary test is carried out using a lepromin test. Development of genetically engineered vaccines, vaccines using specific antigens from M. leprae.
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