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Lecture notes, cheat sheets
Dermatovenerology. Leprosy (most important)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 12. Leprosy Leprosy (synonyms: leprosy, Hansen's disease) is a chronic disease that usually affects the skin, mucous membranes of the upper respiratory tract and the peripheral nervous system. Currently, leprosy is most common in Africa, Asia and South America. In Russia, there are sporadic cases of the disease. Etiology. The causative agent is an acid-fast, rod-shaped bacterium belonging to the Mycobacterium family. The microorganism is stable in the external environment. It is still not possible to cultivate the pathogen in an artificial medium. Mycobacterium leprosy multiplies intensively only during laboratory infection in the tissues of an armadillo. The causative agent of leprosy is intracellular parasites of macrophages. A long incubation period is associated with a low growth rate of microorganisms. Pathogenesis. Leprosy is a mildly contagious, low-pathogenic disease. Subclinical infection is common. No more than a third of people are susceptible to leprosy. Relatives of patients become ill more often, which confirms a genetic predisposition to the disease. The main route of transmission is considered to be airborne. The entrance gate is the mucous membrane of the upper respiratory tract. Transepithelial penetration of pathogens is also possible. Accidental infection can occur through a tattoo, smallpox vaccination, or surgery. Men get sick 2-3 times more often than women. The resistance of the infected organism and the virulence of the pathogen determine the form of the disease. The hormonal background matters: the first manifestation may be shortly after puberty, during pregnancy or after childbirth. During these periods, new lesions may appear and old lesions become more active. Immunity in leprosy is cellular in nature, it is minimal in lepromatous and dimorphic leprosy and maximal in patients with tuberculoid leprosy. In cases where the shortest "slow incubation period" between inoculation and the appearance of an open lesion can be established, it is 2-3 years. It is assumed that minor infection stimulates cellular immunity, resulting in the development of the tuberculoid variant of the disease. Massive invasion puts pressure on the immune potential, resulting in the development of the lepromatous type. Clinic. There are several clinical forms of the disease. These are lepromatous leprosy, tuberculoid leprosy, borderline or dimorphic leprosy and undifferentiated leprosy. Lepromatous type. The most severe form. It is characterized by polymorphism of clinical manifestations, especially in the skin. In addition to the skin, the nasal mucosa, oral cavity, nasopharynx, larynx, sometimes trachea, lymph nodes, peripheral nerve trunks, organs of vision, hearing, urogenital, and sometimes internal organs are affected. The first manifestations of the disease are usually rounded or irregularly shaped erythematous spots with a shiny surface, which may be rusty in color. The most characteristic localization is the face, extensor surfaces of the hands, forearms, and legs. Symmetry of rashes is characteristic. In the future, infiltration appears, plaques with normal sensitivity or hyperesthesia are formed. Due to the increased function of the sebaceous glands, the surface of the plaques is oily and shiny. Sweating is reduced (later it disappears completely). After 3-5 years, eyebrows and vellus hair on the plaques fall out. Possible loss of mustache and beard. With diffuse infiltration of the facial skin, natural wrinkles and folds deepen, the brow ridges protrude sharply, the nose is thickened, the cheeks and lips have a lobed appearance. Usually the scalp, elbow and popliteal fossae, and armpits are not affected. In the area of infiltrates, single or multiple tubercles and nodes (lepromas) are formed, sharply demarcated, painless. They can be dermal and hypodermal (at first they are detected only on palpation), their consistency is densely elastic. In the future, nodes and tubercles sluggishly, without pronounced inflammatory phenomena, ulcerate. Similar rashes can appear on intact skin. On the mucous membranes, as well as on the skin, the process can begin with the development of individual lepromas or diffuse lepromatous infiltration. All this leads to the formation of scars and deformities. Often the spleen is enlarged, there may be damage to the liver, kidneys, lungs, orchiepididymitis often manifests in men, damage to the prostate gland, spermatic cords is possible. Characterized by lymphadenitis, periostitis (especially of the tibia, ulna, ribs), leading to fractures, fractures, deformities of the joints, shortening and deformation of the phalanges. The course of the disease is chronic, with exacerbations that are provoked by hormonal changes, surgical interventions, errors in therapy. During exacerbations, there is a rise in body temperature, an increase and soreness of the lymph nodes, brightness, disintegration of infiltrates, new rashes. The nervous system is affected relatively late - in the form of symmetrical polyneuritis. Gradually, infiltration of the entire nerve trunk occurs, as it develops, sensitivity is lost until complete anesthesia. In the later stages, there may be trophic and motor disorders. Tuberculoid form. The skin, peripheral nervous system, and rarely the internal organs are affected. The causative agent is detected by histological examination of organs, in skin scrapings. The causative agent is absent in the nasal mucosa. This form is characterized by a rash of small reddish-cyanotic flat polygonal papules. Often, merging, they form figures (discs, rings, half rings). A peripheral ridge is characteristic (the outer edge is, as it were, raised, clearly defined, more saturated in color, and the inner edge is "blurred", indistinctly passes into the central pale part of the lesion). There may be plaques, tubercles resembling a lupoma. Peeling, erythematous and depigmented rashes are possible. Reduced sensitivity in the elements of the rash and often around them. At first, mild hyperesthesia develops, then thermal, pain and tactile sensitivity sequentially disappear. Sweating decreases, then stops. Hair becomes dull and may fall out. Localization is asymmetric, in any area. Border leprosy. Immune reactivity in this form of the disease varies widely and changes under the influence of stress, infections, exhaustion. All this is reflected in the clinical manifestations of target tissues. Undifferentiated leprosy is an unstable clinical form in which the skin is affected, the spots (hypo- and hyperpigmented) are not sensitive to pain and temperature. The main feature is multiple nerve lesions. After a few years, this form becomes either tuberculoid or lepromatous. Diagnostics. The main signs are clinical changes in the skin. Caution should also be with a decrease and disappearance of sensitivity in certain areas of the skin, parasthesias, mild contractures of the 5th, 4th and 3rd fingers, beginning muscle atrophy, pasty hands and feet, persistent lesions of the nasal mucosa. Confirmatory methods are bacterioscopic and histological. For bacterioscopic examination in the lepromatous type, scrapings are taken from the nasal mucosa. Additionally, functional tests are carried out with histamine for sweating (weakly expressed), nicotinic acid (inflammation), mustard plaster (no reaction) and detection of sensitivity dissociation in the lesion. The lepromine test (intradermal injection of a suspension of leprosy mycobacteria obtained by homogenizing leprosy) is not diagnostic. It is carried out to assess the immune response and differential diagnosis of various types of leprosy: the test is positive in the tuberculoid variant and negative in the lepromatous variant (with dimorphic leprosy, both positive and negative results are possible). Treatment. Depending on the type of disease, treatment is carried out in a leper colony or at the place of residence (for minor skin manifestations of abacillary leprosy). Combination treatment, a course with the use of anti-leprosy drugs (diaphenylsulfone, solusulfone, diucifone and other sulfone derivatives): courses of 6 months with breaks of 1 month. For multibacterial leprosy, start with rifampicin or clofazimine and then move on to sulfones. In addition, solusulfone, benemycin, ethionamide, lampren can be used. The effectiveness of treatment is assessed based on the results of bacterioscopic control and histological examination. The average duration of therapy is 3-3,5 years. Prevention. General prevention consists of improving the standard of living of the population, early detection, isolation and treatment of patients. Contact persons are examined and observed for at least 7 years. Preventive chemotherapy with sulfones is carried out. Men who have been in contact with leprosy patients are not subject to conscription into the army. Author: Sitkalieva E.V. << Back: Lupus >> Forward: Eczema
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