1. Classification: superkingdom Procaryota, kingdom Bacteria, section Scotobacteria, class Bacterias, order Actinomycetalis, gr. VI. Actinomycetes and related microbes, Mycobacteriaceae, p. Mycobacterium, M. leprae.

2. Morphology: Gr+, stick, straight or slightly curved. Leprosy balls (“a pack of cigarettes”) form inside the cells. Acid-resistant.

3. Power type: chemoorganotroph, AER

4. Biological properties:

a) are not cultivated on artificial nutrient media

5. AG structure: group-specific polysaccharide and protein AG

6. Pathogenicity factors and pathogenesis:

The structures of cell membranes provide acid resistance, antiphagocytic properties, adjuvant properties, cause HRT (mycolic acids, CS waxes, arabinogalactan, trehalose mycolate - cord factor).

Introduction into the skin and mucous membranes VDP ® enter the nerve endings, lymphatic and circulatory systems ® slowly disseminate.

7. Clinical manifestations: Forms: lepromatous (the most severe), tuberculoid. Hypopigmentation or areas of redness (leprida) with loss of sensitivity, neuritis with uneven thickening of nerve trunks, positive skin smears for acid resistance of MB.

8. Immunity: In patients with leprosy, a CIO defect is detected. The extent of his damage is reflected by the Mitsuda reaction (with lepromine).

9. Epidemiology. Anthroponotic infection. The source is a sick person. LPC – prolonged contact with the patient.

10. Prevention: There is no vaccine.

11. Treatment: sulfone drugs, anti-tuberculosis drugs (rifampicin), desensitizing agents and biostimulants.

Material: scrapings from affected areas of skin and mucous membranes.

1. Bacterioscopy: Ziehl-Neelsen smear. In a positive case, the intracellular location of mycobacteria is in the form of clusters of red rods (“a pack of cigars”), coccobacilli and balls.

2. Biotest: on armadillos (lepromas are formed in the tissues - multiple nodules)

3. Allergy test with lepromin. Two days after administration - erythema and a small papule. Typical for patients with tuberculoid leprosy.

Mycobacterium leprosy

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. Mycobacterium 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 (“a pack of cigars”). Acid-resistant, stained red using the Ziehl-Neelsen method. Mycobacteria leprosy cannot be cultivated on artificial nutrient media. In 1960, an experimental model was created with infection of white mice in the footpads, in 1967 - infection of thymusectomized mice, and in 1971 - armadillos, in which typical granulomas (lepromas) are formed at the site of injection of Mycobacterium leprosy, and with intravenous infection develops a generalized process with the proliferation of mycobacteria in the 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 commonly 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).

Laboratory diagnostics. It is carried out using the bacterioscopic method. Examine scrapings from affected areas of the skin and mucous membranes. Smears are stained according to Ziehl-Neelsen. In positive cases, characteristically arranged Mycobacterium leprosy of a typical shape is found.

Prevention and treatment. There is no specific prevention of leprosy.

A set of treatment and preventive measures is carried out in specialized institutions - leper colonies and outpatient clinics. To treat leprosy, sulfone drugs (dapsone, diacetylsulfone, selusulfone, etc.), as well as anti-tuberculosis drugs (rifampicin, etc.) along with desensitizing agents and biostimulants are used.

The genus Mycobacterium includes more than 50 species and subspecies of mycobacteria - pathogenic, opportunistic and saprophytic, widespread in nature. At least 25 of them play an important role in human pathology, being causative agents of tuberculosis, mycobacteriosis and leprosy. Some types of mycobacteria are combined into complexes. For example, M. bovis complex includes M. bovis, BCG and M. africanum; M. avium complex (MAC) includes M. avium and M. intracellulare, etc. This is especially important for practical diagnosis and identification of mycobacteria using special research methods.

Leprosy pathogens microbiology

Leprosy- anthroponotic mycobacteriosis with a predominantly aerosol mechanism of infection, characterized by a long incubation period, a chronic course with granulomatous damage to the peripheral nervous system, skin, mucous membranes, musculoskeletal system and internal organs.

Leprosy- one of the oldest diseases, which has found a gloomy reflection in the literary monuments of many peoples of India (XV-X centuries BC), Egypt (“kushtra” in the Ebers Papyri, XIII-X centuries BC), China ( “Nei Ching Su Wen”, V century BC), etc. Trade relations and military campaigns contributed to the spread of the disease (“leprosy”) to the European continent (V-III centuries BC, called “ satyriasis" or "leontiasis", according to Aristotle), to the countries of South and Central America (XVI-XVIII centuries AD).

Most Full description leprosy given in the works of S. Aritaios (2nd century) and Claudius Galenus (2nd century), who identified the main signs of the disease in the form of thickening of the ears, lion-like face, mutilations, etc. The term “lepra” comes from the Greek translation of the biblical name of the disease “zaraath” "(3rd century BC), which in Europe was known as "elephantiasis".

Pathogen illnesses isolated from a patient by the Norwegian researcher Gerhard Hansen (l874), the staining method was developed by A. Neisser (1879). In 1919, K. Mitsuda proposed the lepromine test, which has important clinical and epidemiological significance. In 1943 G.H. Faget established the anti-leprosy activity of sulfone drugs, which are still the main means of treating leprosy. Important milestones in the study of leprosy were the development of S.S. Shepard (1960) method of laboratory cultivation of Mycobacterium leprosy in mice and modeling by W.F. Kirchheimer and E. Storrs (1971) Infections on armadillos.

In 1953. The WHO Expert Committee on Leprosy was created, and in 1979 leprosy was included in the WHO Program for the Control of Tropical Diseases. The implementation of a number of preventive measures (the creation of leper colonies to isolate “lepers”, etc.), changes in socio-economic conditions and other factors led to the X-XIII centuries. a decrease in the incidence of leprosy in European countries, but until the mid-80s of the 20th century. it remained high (about 12 per 10,000 inhabitants) in the countries of Asia and Africa, where there were about 12 million patients. After the development of new approaches to the treatment of patients by the WHO scientific group on leprosy, the incidence of leprosy in the world began to decline rapidly, and the implementation of the Global Strategy for the Elimination of Leprosy (GSEL) adopted at the 44th WHA in May 1991 ensured by the beginning of the 21st century. reducing the global incidence of leprosy by more than 89% and bringing it to 1.4 per 10,000 inhabitants.
Pathogen- Mycobacterium leprae Hansen, 1874 belongs to the genus Mycobacterium, family Mycobacteriaceae.

M. leprae- gram-positive straight or slightly curved rod with rounded ends, 1-7 µm long and 0.2-0.5 µm in diameter. Filamentous, coccoid, branched and dumbbell-shaped forms of bacteria are known. When stained according to Ziehl-Neelsen M. leprae turn red. In the cells of affected tissues, M. leprae is found in the form of clusters (“globi”), where the pathogens are located in parallel (“cigar packs”).

In M. leprae thermostable polysaccharide and thermolabile protein highly specific antigens, about 20 less specific antigens and a number of enzyme systems involved in bacterial reproduction are described. Killed M. leprae have the unique ability to activate cellular immune responses without the addition of adjuvants.
Outside the body, leprae can persist in humans for 1-7 days.

The causative agent of leprosy. Taxonomy. Characteristic

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.

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 case of 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, which contains lepromin A, is used. A preliminary test is carried out using a lepromin test. Development of genetically engineered vaccines, vaccines using specific antigens from M. leprae.

3. Causative agent of leprosy

In 1874, the Norwegian researcher G. Hansen described the causative agent of the disease - Mycobacterium leprae

Mycobacteria leprosy have polymorphism. Among typical individuals, there are long, short and thin cells, as well as larger, swollen, curved, branched, segmented, degenerative (breaking up into grains). The spherical forms are surrounded by a shell, some of these balls contain a large number of rods and small coccoid formations

In terms of the chemical composition, Mycobacterium leprosy is similar to Mycobacterium tuberculosis. The amount of lipids in them ranges from 9.7 to 18.6%. In addition to mycolic acid, they contain leprosic hydroxy acid, free fatty acids, wax (leprosin), alcohols, and polysaccharides.

Cultivation. The causative agent of leprosy does not grow on nutrient media used for growing Mycobacterium tuberculosis. Some successes in cultivating Mycobacterium leprosy were obtained as a result of introducing infectious material into the paw of mice, where they multiply for 230 - 30 days.

In 1971, English scientists managed to develop a completely satisfactory method for cultivating mycobacteria leprosy in the body of armadillos (armadillos). In animals, after infection with pathological material taken from people with leprosy, typical granulomas are formed in huge quantities. Armadillos have a relatively low body temperature (30 - 35 ° C), with it, cellular immunity against Mycobacterium leprosy is suppressed. The introduction of pieces of leprosy in colloidal sacs into the abdominal cavity of animals causes the formation of a wide variety of forms of Mycobacterium leprosy (acid-compliant, capsular, granular, coccal, spore-like, rod-shaped, filamentous, L-form), which similar to fungal mycelium.

Enzymatic properties have been poorly studied. Their research is hampered by the unresolved problem of cultivating M. leprae on nutrient media.

Toxin formation. Toxin production has not been established for Mycobacterium leprosy. They probably produce endotoxins and allergenic substances. The difficulty of studying this issue is due to the fact that for more than 100 years no experimental animal sensitive to Mycobacterium leprosy has been found.

Antigenic structure and classification not developed.

Resistance. Very high. Mycobacterium leprosy persists in human corpses for a long time. Outside the human body, their viability is quickly lost.

Pathogenicity for animals. Leprosy-like diseases of rats, buffaloes, and some species of birds are known, which differ significantly from human leprosy. Experimental animals become infected relatively easily after irradiation and removal of the thymus gland.

M. leprae is pathogenic only to humans. Leprosy in rats caused by Mycobacterium lepraemurium has been studied in some detail (Stefansky V.K., 1903). The disease in rats occurs chronically with damage to the lymph nodes, skin, internal organs, the formation of infiltrates, ulcerations, and hair loss. For the treatment of leprosy in rats, anti-tuberculosis drugs turned out to be more effective. This gives reason to believe that Mycobacterium leprae is genetically closer to tuberculosis and paratuberculosis pathogens. As stated above, Mycobacterium leprae has been shown to be virulent for armadillos, which develop typical granulomatous lesions.

Pathogenesis of the disease in humans. The source of infection is a sick person. The causative agent of leprosy is transmitted by airborne droplets, through the nasopharynx, damaged skin, and objects. However, infection occurs mainly through close and prolonged contact between healthy individuals and leprosy patients.

Mycobacterium leprosy, having penetrated the body through the skin and mucous membranes, invades the cells of various tissues and organs, then penetrates the lymphatic and blood vessels and gradually disseminates. When the body's resistance is high, mycobacteria leprosy mostly die. In some cases, infection leads to the development of a latent form of leprosy, which, depending on the body’s resistance, can continue throughout life and, as a rule, ends with the death of the pathogen. However, under unfavorable working and living conditions for such people, the latent form becomes active and is accompanied by the development of the disease . The incubation period lasts from 3 - 5 to 20 - 35 years. The disease is chronic.

According to clinical manifestations, leprosy is divided into three types: lepromatous, tuberculoid, undifferentiated

1. Lepromatous type characterized by minimal body resistance to the presence, reproduction and spread of the pathogen, as well as the constant presence of Mycobacterium leprosy in the affected areas. Lepromine test negative

2. Tuberculoid type is characterized by the body's high resistance to the reproduction and spread of Mycobacterium leprosy. Mycobacteria are not found in affected areas or are found in small quantities only during the period of a reactive state. An allergy test is usually positive

3. Undifferentiated type(unspecified group) is characterized by varying body resistance with a tendency towards resistance. Microscopic examination does not always reveal Mycobacterium leprosy. Allergy tests are negative or weakly positive

Immunity. Not studied deeply enough. The blood of patients contains complement-fixing antibodies. During the course of the disease, an allergic condition develops. The mechanism of immunity in leprosy is similar to the mechanism of immunity in tuberculosis.

In individuals with high resistance, mycobacteria leprosy are phagocytosed by histiocytes, in which they are relatively quickly destroyed. In such cases, leprosy takes on a benign tuberculoid form.

In individuals with low resistance, mycobacteria leprosy multiply in large numbers even in phagocytes (incomplete phagocytosis). The pathogen spreads throughout the body. Such patients develop a severe lepromatous form of the disease.

With an undifferentiated type of leprosy, resistance can vary from high to low. Relatively benign lesions can exist for years, but if the body's resistance decreases, the disease becomes a lepromatous form with a high content of mycobacteria in tissues and organs. When immunity is strengthened, the clinical picture of the disease takes on the tuberculoid type.

Immunity in leprosy is associated with the general condition of the macroorganism. In most cases, leprosy is common among low-income populations with a low cultural level. Children are most susceptible to leprosy. In some cases, they become infected as a result of contact with sick parents

Laboratory diagnostics. For research, a scraping is taken from the nasal mucosa (on both sides of the septum), the contents of leprosy skin nodes, sputum, discharge from ulcers, and blood is examined during fever. The main method for diagnosing leprosy is microscopic examination. Staining of smears is done according to Ziehl-Nielsen.

In some cases, a biopsy of leprosy areas and puncture of the lymph nodes are performed. Mycobacteria leprosy are located in clusters in the form of packs of cigars, and in preparations from nasal mucus - like red balls

To differentiate leprosy from tuberculosis, guinea pigs are infected with a suspension of pathological material in a 0.8% sodium chloride solution. In the presence of tuberculosis lesions, animals quite often get sick and die. Guinea pigs are immune to Mycobacterium leprosy

The Mitsuda allergy test is considered positive if, after 48–72 hours, erythema and a small papule (early reaction) appear at the site of injection of 0.1 ml of lepromin (a suspension of a leprosy node, ground in a mortar and boiled for a long time). By the end of the first week, they completely disappear or a late reaction appears, in which after 10-14 days a nodule forms at the injection site, reaching 1-2 cm by the 30th day and necrotizing in the center.

To diagnose leprosy, the complement fixation reaction and the indirect hemagglutination reaction are used.

Treatment. Until 1982, standard treatment for all forms of leprosy was dapsone (4,4-diaminodiphenylsulfone, DDS) monotherapy. Unfortunately, the increasing number of cases of leprosy caused by dapsone-resistant strains of leprosy bacilli has led to the need for the introduction of complex therapy based on the use of dapsone, rifampicin and clofazimine.

Treating leprosy requires much more than the use of antimicrobial agents. It is often necessary to correct deformities, prevent blindness and further prevent anesthesia of the limbs, treat reactive conditions and pay attention to the social, psychological and spiritual state of the patient.

Prevention. Patients with leprosy who secrete bacilli are isolated in a leper colony until clinical cure with constant monitoring. Patients who do not excrete microorganisms are treated on an outpatient basis. A systematic epidemiological survey of endemic foci is being carried out. Family members of a person with leprosy are subjected to a special medical examination at least once a year. Children born to mothers with leprosy are separated from them and fed artificially. Healthy children whose parents are sick with leprosy are placed in orphanages or given to relatives to raise and are examined at least 2 times a year.

A live attenuated vaccine against M. leprae has not been developed, but BCG vaccine appears to protect against leprosy in regions where it protects against tuberculosis, suggesting that such protection is induced by common mycobacterial antigens.

In principle, the incidence of leprosy can be controlled by chemoprophylaxis with acedapson (DADDS), a long-acting analogue of dapsone, but due to the increasing prevalence of dapsone resistance, such prophylaxis is not recommended.

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Taxonomy: family Mycobacteriaceae, division Firmicutes, genus Mycobacterium, M. leprae.

Pathogen properties:

Morphology: Gram-positive rod, straight or slightly curved, with pointed or thickened ends. Good Ziehl-Neelsen staining. Leprosy balls (“a pack of cigarettes”) form inside the cells. Acid-resistant.

Cultural properties: do not grow on nutrient media

AG structure: group-specific polysaccharide and protein antigen

Epidemiology. Anthroponotic infection. The source is a sick person. The transmission route is contact, airborne.

Pathogenesis: Once in the body, bacteria penetrate into the nerve endings, and from there into the lymphatic and blood capillaries. The pathogen dies and is eliminated; the disease may be latent. The likelihood of developing leprosy depends on the status of resistance factors.

Clinic: The incubation period is 4-6 years. There are 5 forms of the disease: polar tuberculoid, borderline tuberculoid, undifferentiated, borderline lepromatous and polar lepromatous.

Tuberculoid: proliferation of granulation tissue in the skin and mucous membranes.

Undifferentiated: skin rashes, nerve damage

Lepromatous: red-brown infiltrates on the face and distal parts of the extremities, loss of eyebrows and eyelashes, eye lesions, lymph nodes are enlarged in volume.

Immunity: In patients with leprosy, a CIO defect is detected. The extent of his damage is reflected by the Mitsuda reaction (with lepromine).

Material: scrapings from affected areas of the skin and mucous membranes, puncture of lymph nodes 1. Bacterioscopy: Ziehl-Neelsen smear. In a positive case, the intracellular location of mycobacteria is in the form of clusters of red rods (“a pack of cigars”), coccobacilli and balls. 2. Biotest: on armadillos (lepromas are formed in the tissues - multiple nodules) 3. Allergy test with lepromin. Two days after administration - erythema and a small papule. Typical for patients with tuberculoid leprosy.

Prevention: There is no vaccine.

Treatment: chemotherapy, sulfone drugs, anti-tuberculosis drugs (rifampicin), desensitizing agents and biostimulants.

73. Pseudomonas aeruginosa – Pseudomonas aeruginosa. Role in human pathology. Toxin formation and pathogenicity. Etiology and pathogenesis. Laboratory diagnosis.

Taxonomy: genus Pseudomonas, family Pseudomonadaceae, division Gracilicutes, pathogen Pseudomonas aeruginosa

Pathogen properties:

Morphology: Gram-negative, straight rods, arranged singly, in pairs or in short chains. Mobile. They do not form spores and have pili (fimbriae). Under certain conditions, they can produce capsule-like extracellular mucus of a polysaccharide nature.

Cultural properties: obligate aerobes that grow well on simple nutrient media. A distinctive feature is the limited need for nutrients. The formation of mucus is a characteristic feature of virulent strains. In liquid media it is a grayish-silver film. On dense media there are small convex S-colonies, the phenomenon of rainbow lysis.

Biochemical properties: low saccharolytic activity: does not ferment glucose and other carbohydrates. Reduces nitrates into nitrites, has proteolytic activity: liquefies gelatin.

Antigenic properties: O- and H-antigens.

Toxin formation and pathogenicity: Exotoxin A suppresses protein synthesis. The effect is manifested in a general toxic effect, edema, necrosis, arterial hypotension with collapse, metabolic acidosis, etc.

Exoenzyme S– pathological processes in the lungs.

Cytotoxin- development of neutropenia.

Hemolysin- necrotic lesions.

Endotoxin-pyrogenic reaction, stimulates inflammation

Neuramidase- disrupts the metabolic processes of substances containing neuraminic acids (connective tissue)

Proteolytic enzymes: elastase breaks down elastin, casein, hemoglobin, fibrin; alkaline protease hydrolyzes proteins.

Epidemiology: The source is a sick person. Mechanisms of infection: contact, respiratory, blood, fecal-oral.

Pathogenesis: penetrate damaged tissue. Inoculate a wound or burn surface. They reproduce. Local processes (infection of the urinary tract, skin, respiratory tract). Bacteremia. Sepsis.

Clinic: wound infections, burn disease, meningitis, urinary tract infections, skin infections, eye diseases, sepsis.

Immunity. In the blood serum of healthy people and those who have recovered from the disease, there are antitoxic and antibacterial antibodies, however, these antibodies are type-specific and their role in protecting against recurrent diseases has been little studied.

Microbiological diagnostics. Material for research: blood, pus and wound discharge, urine, sputum. The main diagnostic method is bacteriological examination of clinical material, which allows not only to identify the pathogen, but also to determine the sensitivity of bacteria to antimicrobial drugs. When identifying, growth on agar, a positive cytochrome oxidase test, and detection of thermophilicity (growth at 42C) are taken into account. Serotyping is used for intraspecific identification of bacteria.

The serological research method is aimed at detecting specific antibodies to rod antigens (usually exotoxin A and LPS) using RSC, RPGA.

Treatment: antibiotics (cephalosporins, β-lactams, aminoglycosides). Severe forms - plasma from blood immunized with a polyvalent corpuscular Pseudomonas aeruginosa vaccine. For local treatment: antipseudomonal heterologous immunoglobulin. For the treatment of purulent skin infections and burns - Pseudomonas aeruginosa bacteriophage.

Prevention: specific – sterilization, disinfection, antiseptics. Control over contamination of the external environment. Nonspecific – immunomodulators. Passive specific immunization with hyperimmune plasma. To create active immunity, vaccines (polyvalent corpuscular Pseudomonas aeruginosa vaccine, Staphyloproteus-Pseudomonas aeruginosa vaccine.

Herpesviruses, classification. The causative agents of chickenpox and herpes zoster, cytomegaly. Pathogenesis. Laboratory diagnosis. Treatment, prevention. The role of herpes viruses in the occurrence of malignant tumors.

Taxonomy: Family Herpesviridae. Subfamilies: Alphaherpesviruses, Betaherpesviruses, Gammaherpesviruses

· Alphaherpesviruses: genus Simplexvirus (herpes viruses types 1 and 2) and genus Varicellovirus (herpes virus type 3)

· Betaherpesviruses: genus Cytomegalovirus (type 5) and genus Roseolovirus (herpes viruses 6A, 6B and 7 types)

· Gammaherpesviruses: genus Lymphocryptovirus (type 4)

Herpes virus type 3.

Epidemiology: The reservoir of the pathogen is a sick person; the virus is transmitted by airborne droplets and contact.

Pathogenesis: the pathogen multiplies in the epithelium of the mucous membrane of the upper respiratory tract, then disseminates through the lymph and bloodstream into the skin. Shingles develops as a result of reactivation of the virus in the sensitive nodes of persons who have had chickenpox.

Clinic: Chicken pox- incubation period 14 days. It manifests itself as an acute infectious disease, accompanied by fever and papular-vesicular rash on the skin and mucous membranes. During the period of convalescence, the vesicles dry out with the formation of crumbs and healing without the formation of defects.

Shingles- characterized by rashes along the sensory nerves in the form of fuzzy pinkish spots. After 24 hours, the rash transforms into groups of painful vesicles surrounded by a clear demarcation zone. The lesions are localized on the chest. Lesions disappear within 2-4 weeks, but pain may persist for weeks to months

Microbiological diagnostics: Microscopy of smears according to Romanovsky-Giemsa. Isolation of the pathogen on cultures of human embryonic fibroblasts. Detection of virus Ag in the fluid of vesicles by immunodiffusion with precipitating sera and determination of the increase in antibody titers in paired sera.

Treatment: anti-itch medications, analgesics, acyclovir

Prevention: gamma globulin from the serum of patients who have had herpes zoster.

Herpes virus type 5.

Epidemiology: reservoir is a sick person. The pathogen is transmitted through the placenta, by contact, during feeding, through blood transfusions, and through sexual intercourse.

Pathogenesis: It affects almost all organs and tissues, causing either asymptomatic carriage or clinically pronounced conditions. With transplacental infection, damage to the liver, spleen, eyes, central nervous system, and respiratory tract is observed

Clinic: The infection most often occurs subclinically, in rare cases severe illness is observed, often with a fatal outcome. The acute form is characterized by damage to many internal organs, including the brain, kidneys, liver, and hematopoietic organs.

Microbiological diagnostics: microscopy of smears according to Romanovsky-Giemsa. Isolation is carried out by infecting fibroblast cultures. In express diagnostics, virus Ag is determined by RIF and DNA hybridization. Determination of circulating antibodies is carried out using the RSK, RPGA, RN methods with paired sera.

Treatment: agents that inhibit viral DNA synthesis

Prevention: live virus in the form of a monovaccine or divaccine (in combination with a vaccine against rubella virus)

Leprosy (leprosy) is the same disease, which also has many other names: Hansen's disease, hanseniosis, elephantiasis graecorum, lepra orientalis, lepra arabum, satyriasis, Crimean disease, Crimean disease, Phoenician disease, mournful disease, St. Lazarus disease, lazy death etc. Leprosy is a chronic infectious disease, a type of granulomatous disease. The causative agent of leprosy is Mycobacterium leprae.

In 2008, a second causative agent of leprosy was identified - Mycobacterium lepromatosis. The disease occurs with damage to the skin, peripheral nerves, anterior parts of the eyes and the mucous membrane of the upper respiratory tract. Mycobacteria are transmitted from a sick person to a healthy person through damaged skin and mucous membranes of the respiratory system. The disease develops through frequent contact with patients who are not receiving treatment.

In the Russian Federation, leprosy is rare. Cases of the disease are reported in countries in South America, Africa and Asia. According to WHO, in 2016, more than 170 thousand patients were registered living in 145 countries. In total, more than 10 million patients with leprosy are registered in the world.

Timely diagnosis of the disease and adequate treatment lead to complete recovery. Otherwise, patients remain deeply disabled for life.

Rice. 1. Lepers - this is what people with leprosy were called in ancient times.

Case history of leprosy

Leprosy has been known since ancient times. Information about the disease was recorded already in the 15th - 10th centuries BC. Leprosy is mentioned in the Bible and the Ebers papyri. Hippocrates described the disease. In ancient times, leprosy was rampant in the east. The widespread spread of the disease was noted in the Middle Ages. At the beginning of the 13th century, epidemics began in Europe. Presumably the disease was brought to this territory by the Crusaders. The deformation of appearance and deformity of leprosy patients caused disgust and fear. Such patients were called “lepers.” They were turned into real outcasts. In order to prevent the spread of infection, many places of settlement for “lepers” were created - leper colonies, where patients were kept until the end of their lives. The first leprosariums were located within the monasteries and contributed to the non-spread of infection, acting as quarantine institutions. In the middle of the 13th century, there were about 19 thousand leper colonies in Europe. Despite the fact that leprosy has been known since ancient times, the causative agent of the disease was discovered by Gerhard Hansen only in 1873. In 1948, the French journalist Raoul Follero founded the Order of Charity, and in 1966 the Federation of European Antileprozoal Associations. January 30th is Leprosy Rights Day.

Henry XIV, Louis XI, the Byzantine Emperor Constantine, and the impressionist artist Paul Gauguin suffered from leprosy.

Rice. 2. Patients with leprosy (“lepers”) were expelled from settlements in ancient times.

Prevalence of the disease

Leprosy is common mainly in countries with tropical climates. The maximum number of patients is recorded in countries such as Brazil, India, Burma, Indonesia, the Philippines, Nepal, Tanzania and the Republic of Congo.

Leprosy in Russia

In the territory of the former USSR, leprosy was recorded in the Lower Volga region, the Far East, Karakalpakia, the North Caucasus, Kazakhstan and the Baltic states. IN modern Russia The disease is rare - isolated cases annually. In total, there are about 700 patients who live in 4 leper colonies located in Astrakhan, Tver, Moscow region and Krasnodar Territory.

Rice. 3. Consequences of leprosy. Loss of fingers.

The causative agent of leprosy. Microbiology

Despite the fact that leprosy has been known since ancient times, the causative agent of the disease was first discovered by the Norwegian scientist Gerhard Hansen only in 1873.

Taxonomy of the pathogen

The cause of leprosy turned out to be a bacterium (bacillus) belonging to the Mycobacteriacea family, called Mycobacterium Leprae hominis(Hansen's bacillus, Hansen's bacillus).

In 2008, a second type of bacteria was discovered that causes leprosy - Mycobacterium lepromatosis. These bacteria have been found to cause diffuse lepromatous leprosy, prevalent mainly in the Caribbean. The disease is characterized by extensive ulcerations on the skin, damage to nerves and internal organs.

The structure of the causative agent of leprosy

Mycobacterium leprosy is similar to tuberculosis bacilli in a number of ways.

Rice. 4. Mycobacteria leprosy are cylindrical, straight or slightly curved.

Pathogenicity factors

The virulence factor of Mycobacterium Leprae is the phosphatide fraction, which is part of the cell wall lipids.

Antigens of the causative agent of leprosy

The microcapsule of the leprosy bacterium has antigenic properties. Two antigens have been identified: heat-stable and heat-labile. The heat-stable antigen (polysaccharide) is common to all mycobacteria; the heat-labile antigen (protein) is highly specific for leprosy mycobacteria.

Pathogen genome

The genome of the causative agent of leprosy was first deciphered in 2001. It consists of 3,268,203 nucleotide base pairs. Genetics from the University of Tübingen (Germany) have proven that the genome of Mycobacterium leprae has not changed over the past 500 years.

Reproduction

Mycobacterium leprosy reproduces by transverse fission. The process of reproduction occurs only in the cytoplasm of tissue cells.

Sustainability

In the external environment, leprosy pathogens exhibit increased resistance, but at the same time their virulent properties are quickly lost.

Microscopy

According to Ziehl-Neelsen, mycobacteria leprae are stained pink (Gram-positive, acid-fast). In recent years, the technique of staining smears using the Marcinowski method has become widespread.

Cultivation

It is not possible to grow Mycobacterium Leprae on artificial media. For cultivation, special media are used that contain human serum. In vitro, lineages of isolated mycobacteria are maintained in armadillos and on the paws of infected mice.

Rice. 5. The causative agents of leprosy (Mycobacterium Leprae) are located singly or in clusters, reminiscent of cigarette packs or balloons.

Epidemiology

Leprosy is a low-contagious disease. When infected, the disease develops in 10 - 20% of cases. There is a high natural resistance to leprosy infection. A strong immune system guarantees that a person will not get leprosy.

Risk group

Those at high risk for leprosy include those living in endemic areas. There is a high risk of getting sick among armadillo hunters, those who make crafts from the animals' shells, and when eating animal meat. Living in unsanitary conditions, malnutrition, alcoholism, hard physical labor, and diseases that weaken the immune system contribute to the disease. Leprosy is common in economically underdeveloped countries among the poorest segments of the population.

Source of infection

The reservoir and source of leprosy pathogens is a sick person and the armadillo animal. A person becomes infected from an animal through scratches received while hunting or by eating meat. Armadillos live in Central and South America and belong to the class of mammals. Every year, up to 150 people become ill with leprosy in the United States. All of them either hunted armadillos, or ate their meat, or made fakes from the armor of the animals.

How is leprosy transmitted?

Airborne droplets and contact are the main routes of transmission. The disease is not transmitted in utero.

• A sick person who is not undergoing treatment spreads Mycobacterium leprosy by coughing and sneezing. When talking, bacteria spread within a radius of up to 1.5 meters.
• Somewhat less frequently, pathogens enter the human body by contact through microcracks, scratches, wounds or scratches. The patient's belongings are also a factor in the transmission of infection. Mycobacterium leprosy in patients during periods of exacerbation is found in urine, tears, semen, urethral discharge, blood and breast milk.

Rice. 6. The photo shows an armadillo. The animal has a shell consisting of horny scutes, movably connected to each other.

Pathogenesis

Leprosy pathogens enter the human body through the mucous membrane of the upper respiratory tract and damaged skin. The full picture of the disease develops after an incubation period of years or decades. The penetration of Mycobacterium leprosy into the human body causes disease only in 10 - 20% of cases.

Lepromatous granulomas

Mycobacteria affect the skin, mucous membranes, superficially located peripheral nerves and internal organs, where granulomas form. In the lepromatous type of leprosy, granulomas consist of foamy macrophages stuffed with mycobacteria. Clusters of granulomas form lepromas. In the tuberculoid type of leprosy, granulomas consist of epithelioid cells and contain a small number of pathogens.

Rice. 7. Patients with leprosy. Lepromatous granulomas are visible on the face and neck.

Lepromatous neuritis

Leprosy affects the peripheral nervous system. There is a pronounced tropism of pathogens for lemmocytes - Schwann cells, located along the axons of nerve cells (long process), which perform supporting and trophic functions. Inflammation of peripheral nerves and associated neurological disorders develop more quickly in the tuberculoid type. In lepromatous leprosy, peripheral nerves are affected late. Lepromatous neuritis has an ascending nature. Gradually, the nerve fibers are destroyed and replaced by connective tissue. Damage to peripheral nerves leads to the development of motor and trophic disorders.

Rice. 8. Damage to peripheral nerves. Claw-shaped brush.

Damage to internal organs

More pronounced inflammation of internal organs is observed in the lepromatous type of leprosy. In the mucous membrane of the upper respiratory tract, lymph nodes, liver, spleen, testicles, adrenal glands, kidneys, heart, lungs, granulomas appear, consisting of macrophages filled with a huge number of leprosy pathogens.

Types of leprosy

Depending on the degree of immunological reactivity (cellular immunity), the patient develops one or another type of leprosy.

• Tuberculoid type of leprosy(most favorable) is formed in individuals with a high degree of immunological reactivity. The disease is less dangerous for others. The course is not severe, with primary damage to the skin and peripheral nerves. The rashes on the skin look like small papules and are accompanied by anesthesia. The infiltrates contain a small number of pathogens.
• Lepromatous type of leprosy is formed in individuals with a low degree of immunological reactivity. Antibodies produced during illness do not protect the body from infection. The disease affects the skin and mucous membranes, nerve trunks, lymph nodes and internal organs. Leproma infiltrates contain a huge number of mycobacteria. Over time, lepromas disintegrate. The resulting ulcers heal slowly. The lepromatous type of leprosy may have blurred and atypical forms.
• Undifferentiated type of leprosy develops when the type of immunological activity has not yet been formed in patients. With a favorable course, the tuberculoid type of leprosy develops in the future; with a low degree of immunological reactivity, the lepromatous type of leprosy develops.

Rice. 9. Tuberculoid (photo on the left) and lepromatous (photo on the right) type of leprosy.

Classification of the disease

There are three types (forms) of leprosy:

• lepromatous type,
• tuberculoid type,
• undifferentiated or borderline type.

Each type of leprosy goes through 4 stages in its development:

• progressive stage,
• stationary stage,
• regressive stage,
• stage of residual changes.

Incubation period

The average incubation period for leprosy is 3 - 6 years. The possible range of latent period duration is from 3 to 35 years. The prodromal period does not have specific symptoms and is often not recorded. The onset of the disease is imperceptible. At first, weakness and malaise appear. The patient becomes lethargic and overwhelmed. Some of them experience numbness in their fingers and toes.

Lepromatous type. Signs and symptoms

The lepromatous type of leprosy is characterized by the development of various elements of skin lesions - fuzzy spots, plaques, infiltrates and nodes. When the disease occurs, the mucous membranes and internal organs are involved in the pathological process quite early, and the nervous system quite late. This type of leprosy is difficult to treat. A huge number of pathogens are localized in the elements of skin lesions. The lepromine reaction is negative due to the developed anergy.

Leprosy skin lesions

The disease most often affects the skin of the face, ears, wrists, elbows, knees and buttocks. Lepromas appear extremely rarely on the scalp, inner parts of the eyelids, armpits, elbows and popliteal fossae.

Spots and plaques

At the beginning of the disease, barely noticeable, blurred, reddish spots appear on the skin, transforming into plaques. Plaques do not have clear boundaries. Over time, as a result of the development of vascular paresis and hemosiderosis, spots and plaques acquire a brown or copper (rusty) tint. Due to increased sebum secretion, their surface becomes smooth, shiny, glossy (greasy). Enlarged excretory ducts of sweat glands and vellus hair follicles in the area of ​​infiltrates give the skin an “orange peel” appearance. Over time, sweating decreases and stops altogether. Sensitivity in the affected areas is not impaired. After 3 - 5 years, spots and plaques transform into lepromas.

Lepromas

Initially, lepromas resemble small single or multiple dense nodules ranging in size from 1 - 2 mm to 2 - 3 cm, painless, with a greasy surface, sharply demarcated from the surrounding tissues, and contain many leprosy pathogens. Over time, the tubercles transform into powerful infiltrates - nodes. Lepromas are dermal and hypodermal.

Hypodermal lepromas are located under the dermis (the skin itself) and at first the diseases are detected only by palpation. When they reach the dermis they become visible to the eye.

Dermal lepromas At first they look like oval-shaped papules, gradually turning into tubercles that have a reddish-rusty color, with a glossy surface, and rise above the surface of the skin.

Sometimes lepromas resolve. A pigmented spot remains in their place. Sometimes lepromas ulcerate. The formation of ulcers occurs from the center. They have steep, steep, raised edges. The bottom of the ulcers is covered with a yellowish-gray coating. Ulcers can merge to form extensive ulcerative surfaces. The bloody discharge contains a huge number of mycobacteria (up to 1 billion per 1 cm3). Gradually the ulcers scar. In their place, a sunken (sometimes keloid) scar remains. When ulceration of deep-lying lepromas occurs, joints and small bones are involved in the pathological process, which are destroyed and fall off (mutilatio), leading to deformities and disfigurement.

Signs and symptoms of leprosy affecting the face

Diffuse infiltration of facial skin leads to deepening of natural wrinkles and folds. The brow ridges begin to protrude sharply forward. The earlobes are growing. The nose, lips, cheeks and chin thicken. They take on a lobed appearance and a fierce expression, reminiscent of a “lion's face” (fades leonina).

Rice. 10. Photos of people suffering from leprosy. Multiple lepromas are visible on the skin of the face.

Signs and symptoms of leprosy with nasal lesions

The nasal mucosa is always affected in leprosy and long before the skin is affected. Rhinitis and nosebleeds are the first signs of leprosy. The nasal mucosa turns red and swells, then small erosions appear and massive crusts form, which leads to difficulty breathing. A picture of leprosy rhinitis develops.

Leprosy ulceration leads to destruction of the nasal septum. First, the tip of the nose rises upward, then the nose sinks (“saddle nose”).

Mycobacterium leprosy is detected in mucosal staples. Especially many pathogens are localized in the mucous membrane of the cartilaginous part of the septum.

Rice. 11. People suffering from lepromatous leprosy were called lepers. The photo shows patients whose faces are disfigured by leprosy.

Signs and symptoms of leprosy in the mouth

In severe leprosy, damage to the mucous membrane of the oral cavity and larynx is noted. The soft and hard palate, the back of the tongue and the red border of the lips are affected.

Rice. 12. With leprosy, the earlobes grow.

Signs and symptoms of leprosy in the eyes

With lepromatous leprosy, the organs of vision are often affected: the episclera becomes inflamed (episcleritis), the cornea of ​​the eye (focal keratitis), the iris (iridocyclitis), the outer layer of the eye (conjunctivitis), clouding of the lens is noted, and the edges of the eyelids become inflamed.

The appearance of lepromas on the surface of the iris leads to disruption of accommodation and deformation of the pupil. Lepronose keratitis and iridocyclitis without treatment lead to complete loss of vision. When the edges of the eyelids become inflamed, eyelashes fall out. Leprosy keratitis is characterized by the absence of discharge and mild symptoms of inflammation.

Rice. 13. Damage to the organs of vision due to leprosy.

Damage to hair and nails due to leprosy

After 3 - 5 years from the onset of the disease, hair loss is observed in areas of infiltration. Hair falls out from the eyebrows, eyelashes, beard and mustache areas. On the eyebrows, hair begins to fall out from the outer edge. In areas of infiltration, vellus hair loss is noted.

Nails with leprosy lose their shine, become dull, thickened, brittle, and acquire a grayish tint.

Rice. 14. As a result of trophic disorders in leprosy, mutilation (rejection) of the hands and feet develops.

Signs and symptoms of leprosy affecting internal organs

In lepromatous leprosy, damage to internal organs is noted.

• The liver and spleen increase in size and become denser. Many millet-like lepromas appear in the tissues of these organs. Chronic hepatitis develops.
• All groups of lymph nodes (except for the thoracic and mesenteric ones) are enlarged. They acquire a dense consistency, are mobile and painless.
• Leprosy affects the endocrine glands. A person ages quickly. Women experience menstrual irregularities and early menopause. In men, the testicles (orchitis) and appendages (epididymitis) are affected. Testicular function decreases. The sclerotic process leads to azospermia. Gynecomastia and infantilism develop. Potency decreases to the point of impotence.

Rice. 15. With atrophy of the circular muscles, the eyes do not close completely.

Signs and symptoms of leprosy affecting the nervous system

In leprosy, the peripheral nervous system is affected late. This is due to the high resistance of the axial cylinders to lepromatous infection. Basically, patients develop symmetrical polyneuritis. Nerve trunks affected by infection thicken, become dense and smooth, and are easily palpated.

In areas of development of leprosy infiltrates, sensitivity remains for a long time, but over time it is lost until complete anesthesia is achieved, which leads to frequent burns and damage that patients do not notice. Its causes are compression of the nerves by cellular infiltrates.

Deep sensitivity, periosteal and tendon reflexes are preserved.

When the central nervous system is damaged, neuroses and psychoses develop.

When the peripheral nervous system is damaged, patients with leprosy develop motor and trophic disorders, and sensitivity is impaired.

Trophic disorders:

• Skin pigmentation is disrupted.
• Trophic ulcers appear on the feet.
• Mutilation (rejection) of the hands and feet is noted. At first, the hands and feet become soft, like the legs of frogs or seals, and then spontaneously tear off. The hands and feet are shortened.
• The function of the sweat and sebaceous glands is impaired. Over time, hypofunction is replaced by a complete absence of sweating and sebum secretion. The skin becomes rough and further cracks.

Movement disorders:

• As a result of the predominance of flexor tone, contractures develop. The fingers and toes bend (claw-shaped hand, cauda equina).
• As a result of muscle atrophy, the interosseous spaces collapse. The hand becomes flattened and resembles a monkey's paw.
• With atrophy of the orbicularis muscles, the eyes cannot close completely (lagophthalmos).
• Damage to the facial nerve leads to atrophy of the facial muscles. The face becomes mask-like and takes on a sad expression.
• With the disease, paresis of the masticatory muscles develops.

Rice. 16. Consequences of leprosy. When the nervous system is damaged, contractures, muscle atrophy and trophic disorders develop.

Signs and symptoms of leprosy. Tuberculoid type

Tuberculoid leprosy is relatively benign and slow. The disease affects the skin and peripheral nerves. Internal organs are slightly affected. Cases of spontaneous regression are often observed. In most cases, the prognosis of the disease is favorable. Tuberculoid leprosy has a low degree of contagiousness.

Skin lesions

In the tuberculoid form of the disease, depigmented or reddish spots with central blanching and sharply defined boundaries appear on the skin. The spots increase in size over time, and their edges rise. Along the edges of the spots there are dense and flat papules, delimiting the damaged area from healthy skin. When spots merge on the skin, patterns of a bizarre ring-shaped configuration are formed. The central part of the spots undergoes depigmentation and atrophy, and fades over time. Within the affected area, there is no skin sensitivity, sweating and sebum secretion stops. The resulting injuries, damage and burns lead to the development of secondary flora.

Rice. 17. Tuberculoid leprosy.

Damage to the peripheral nerves develops in the same way as in the lepromatous form of the disease, but already in the first stages of the disease and more easily. The affected nerve trunks (usually the radial, ulnar, facial and parotid nerves) become painful over time, thicken and begin to be palpated. Contractures and muscle atrophy develop, causing the limbs and face to take on a characteristic appearance (mask-like face, claw-shaped hand, horse foot). The skin appendages are affected - the work of the sebaceous and sweat glands is disrupted, hair and eyelashes fall out, nails thicken and crumble. The lepromine reaction is sharply positive.

Rice. 18. Tuberculoid type of leprosy.

Undifferentiated type of leprosy

The undifferentiated (borderline) type of leprosy develops when the patient has not yet developed a type of immunological activity. With a favorable course, the tuberculoid type of leprosy subsequently develops; with a low degree of immunological reactivity, the lepromatous type of leprosy develops. The lepromine reaction, depending on the direction of the pathological process, can be negative or positive. The undifferentiated (borderline) type of leprosy combines the clinical manifestations of 2 main types of the disease, but with a milder course.

Rice. 19. The undifferentiated (borderline) type of leprosy develops in cases where the type of immunological activity has not yet formed.

Immunity in leprosy

Natural immunity in leprosy is cellular in nature. Macrophages are able to capture mycobacteria, but cannot digest them (incomplete immunity). The number and activity of T-lymphocytes (cells responsible for cellular immunity) decreases, and secondary immunodeficiency develops. Antibodies are produced in the blood of patients, but they do not protect the body from infection. Acquired immunity is weakly expressed. Persons with natural immunity do not develop leprosy even in close contact with patients.

Rice. 20. The disease leprosy. Serious consequences include contractures and rejection of the fingers.

Leprosy is a severe chronic infectious pathology caused by the mycobacterium Mycobacterium leprae hominis. The source of infection is a person with leprosy. Synonyms: leprosy, Hansen's disease, Phoenician anomaly, St. Lazarus disease and others.

There are approximately 11,000,000 people suffering from leprosy worldwide. From a medical and social point of view, leprosy is a serious disease.

Leprosy has been known since ancient times. It was mainly suffered in the countries of the Middle East. Even then, separate closed settlements were built for the sick, where the sick slowly died. There is a well-known case from the New Testament when Jesus healed a whole group of leper patients.

The prejudiced attitude of society towards patients with leprosy, who are subject to complete physical and social isolation, greatly complicates the problem of identifying cases of the disease and combating it. To this should be added the chronic nature of the disease and the lack of confidence that even after prolonged treatment it is possible to achieve complete liberation of the body from mycobacteria.

WHO drew attention to the problem of leprosy in the first decades of its existence. She was inspired by Raoul Follero, who dedicated himself to the fight against leprosy. In honor of Follero, WHO registered back in 1954, January 30, World Leprosy Day. This day should attract the attention of the international community to a comprehensive review and thorough understanding of the problem of leprosy in the world and the possibility of helping such patients.

Etiology, epidemiology of leprosy (leprosy)

Currently, leprosy is widespread in Africa, Southeast Asia, South America and Oceania. Extremely rare - in Europe and North America. The disease can develop at any age and has no racial restrictions. The concentration of leprosy patients in economically undeveloped countries and its connection with overpopulation is noted quite often. Exogenous high-risk factors play an important role in the spread of leprosy.

The exact method of transmission of the disease is unknown, but long-term observations of patients indicate infection through constant contact of a healthy person with a leprosy patient. There is no evidence regarding the transmission of the disease to humans from rodents, fleas, insects and others. An important factor persistent infection, as well as the inability to trace the source of infection in registered patients, is the fact that asymptomatic contact patients can spread mycobacteria from the nasal cavity long before they are diagnosed with leprosy. It is worth noting that mycobacteria leprosy can spread from lepromatous ulcers of treated patients, from mother's milk, and from skin appendages. Lepromatous mycobacteria can probably be transmitted by airborne droplets. They are in soil and water.

Symptoms, diagnosis of leprosy (leprosy)

The disease has a long incubation period, which can last from six months to several decades, more often – 5-7 years. It is asymptomatic. A long latent period is also possible, manifested mainly in general malaise, causeless weakness, chilliness, etc.

There are two polar forms (types) of leprosy - lepromatous and tuberculoid, as well asfour stages of the disease: progressive, stationary, regressive and the stage of residual effects. In addition, intermediate or dimorphic leprosy is possible.

Tuberculoid leprosy

Tuberculoid leprosy usually begins with the appearance of a clearly defined hypopigmented spot, within which hyperesthesia is noted. Subsequently, the spot enlarges, its edges rise, become roll-shaped with a ring-shaped or spiral pattern. The central part of the spot undergoes atrophy and sinks. Within this lesion, the skin is devoid of sensitivity, there are no sweat glands and hair follicles. Near the spot, thickened nerves innervating the affected areas are usually palpated. Nerve damage leads to muscle atrophy; The muscles of the hand are especially affected. Contractures of the hands and feet are common. Injuries and pressure lead to infections of the hands and feet, and neurotrophic ulcers form on the soles. In the future, mutilation of the phalanges is possible. When the facial nerve is damaged, lagophthalmos and resulting keratitis occur, as well as corneal ulcers, leading to blindness.

Lepromatous leprosy

Lepromatous leprosy is usually accompanied by extensive skin lesions that are symmetrical relative to the midline of the body. Lesions can be represented by spots, plaques, papules, nodes (lepromas). They have vague borders and a dense and convex center. The skin between the elements is thickened. The most commonly affected areas are the face, ears, wrists, elbows, buttocks and knees. Characteristic sign– loss of the outer third of the eyebrows. Late stages of the disease are characterized by so-called “lion face” (distortion of facial features and impaired facial expressions due to thickening of the skin), enlargement of the earlobes. The first symptoms of the disease are often nasal congestion, nosebleeds, and difficulty breathing. Complete obstruction of the nasal passages, laryngitis, and hoarseness are possible. Perforation of the nasal septum and deformation of the cartilages lead to retraction of the nasal bridge (saddle nose). Penetration of the pathogen into the anterior chamber of the eye leads to keratitis and iridocyclitis. The inguinal and axillary lymph nodes are enlarged, but not painful. In men, infiltration and sclerosis of testicular tissue lead to infertility. Gynecomastia often develops. Late stages of the disease are characterized by hypoesthesia of the peripheral limbs. Skin biopsy reveals diffuse granulomatous inflammation.

Immunity in leprosy is cellular in nature, it is maximum in patients with tuberculoid leprosy and minimal in lepromatous form. To assess the immune response and differential diagnosis between the two forms of the disease, a lepromin test is used. The reaction to an intradermally administered suspension of mycobacterium leprosy is positive in the tuberculoid form and negative in the lepromatous form.

Leprosy can be diagnosed by the presence of clinical symptoms of the disease. Confirmatory research methods are bacterioscopic and histological.

Treatment and prevention of leprosy (leprosy)

Treatment is a long-term course (up to 3-3.5 years) with the prescription of anti-leprosy drugs of the sulfone group (diaphenylsulfone, solusulfone, diucifone, etc.). The duration of the course is 6 months, the break in treatment is 1 month. Multibacterial leprosy requires initial treatment with rifampicin, dapsone, or clofazimine, followed by medicines sulfonic group. Evaluation of the effectiveness of treatment is controlled by bacterioscopic and histological research methods. Currently, there are 4 leper colonies in Russia (a place for detection, treatment, isolation, and prevention of leprosy): in Astrakhan, Krasnodar Territory, Sergiev Posad District of the Moscow Region, Stavropol Territory.

The main problem of WHO is the fight against leprosy at the level of primary prevention. Today, the main goal should be early diagnosis and effective drug therapy. Secondary prevention measures - identifying cases of the disease - are also important. This can be achieved through primary health care with the active participation of the entire population of a country where cases of leprosy have been reported. In places where leprosy is endemic, mass surveys of the population, sanitary and educational work among the population and doctors are carried out. In addition to the epidemiological situation, socio-economic factors are of great importance, which explains the widespread spread of the disease among the poorest populations in Asia and Africa. The health systems of these countries prioritize expanding services to identify and treat leprosy patients and ensure that modern treatment is available to all patients. Prevention of leprosy among medical personnel and other persons who, by the nature of their work, come into contact with patients, consists of strict adherence to sanitary and hygienic rules (frequent hand washing with soap, mandatory sanitation of microtraumas, etc.). Cases of infection of medical personnel are rare.

In general, the disease itself is caused by rod-shaped microorganisms - Mycobacterium leprae. They were discovered in 1874 by the Norwegian scientist G. Hansen. He worked at the hospital of St. Jorges (founded in the 15th century) in Bergen. It is now a museum and perhaps the best preserved leper colony in Northern Europe. The bacterium discovered by Hansen became the first pathogen known to mankind. These microorganisms have properties close to those of tuberculosis, but do not have the ability to multiply in nutrient media and often do not show themselves in any way for many years. So far, it has not been possible to obtain growth of the pathogen on a nutrient medium, as well as in tissue cultures. The microbe turned out to be quite picky and did not want to grow on the most delicious artificial media. Moreover, for a long time it was not possible to reproduce the picture of leprosy in experimental animals. To find out the patterns of development of this terrible disease, some doctors tried to infect themselves. However, these experiments did not lead to a positive result. For example, in 1844, even before the discovery of the causative agents of leprosy, 29-year-old Norwegian doctor Daniel Cornelius Danielsen experimented on himself: he injected himself with the blood of a leprosy patient and rubbed the pus of the patients into the scratches. But Danielsen did not develop the disease, just as leprosy did not develop in his two self-infected young colleagues. Then Danielsen cut out a piece of the leprosy tubercle from a leprosy patient and injected it under the skin of himself and his colleagues. But during 15 years of observation, until 1858, they did not have a trace of the disease; everyone remained completely healthy.

Then they began to think that Hansen’s bacilli, visible under a microscope, were non-viable, dead pathogens. However, in 1960, the American Shepard managed to infect mice with mycobacterium leprosy by injecting the pathogen into the sole of the paw. However, the characteristic picture of the disease and massive proliferation of bacteria were not observed. The search for a suitable experimental animal continued.

Next characteristic feature mycobacteria is their low growth rate (this, by the way, is characteristic of their entire family), which causes a very long (on average 5, sometimes up to 20 years) incubation period, as well as an almost 100% chronic course of the disease.

The pathogenicity of Mycobacterium leprae is associated with chemical composition cells, especially with lipid composition. They are responsible for the unusual cellular reactions of the body in response to the introduction of these rods. However, more on this later. Now is the time to move from theory to practice. We have already learned about the history, who causes this disease - we also know. Now we can consider the mechanism of infection and the processes that occur after this in the human body. Suffice it to say that the incubation period of the disease is often 15-20 years, which is due to the characteristic features of leprosy. By itself, it is not capable of causing tissue necrosis. This means that the activity of microorganisms must be activated by some external factors, for example, secondary bacterial infection, poor diet, contaminated water or poor living conditions.

A long incubation period and an equally long latent period often lead to the fact that when leprosy is diagnosed, treatment begins too late, since doctors experience objective problems with early diagnosis diseases. Currently, experts know two forms of leprosy:

lepromatous - the pathogen affects mainly the skin;

tuberculoid - for the most part the disease affects the peripheral nervous system.

Undefined or undifferentiated.