HIV infection is caused by RNA-containing retroviruses of the first and second types, possessing reverse transcriptase. The main core proteins of the virion - p24, p18, p15 - are the main antigens. The envelope contains the glycoprotein gp160, consisting of the supramembrane part gp120 and the transmembrane part gp41.

Stages of development of HIV infection

1.Specific interaction of viral envelope proteins with gp120-mediated receptors,

2.Specific penetration of the virus into the cell by endocytosis and stripping of the virus

3. DNA synthesis on a viral RNA template with the participation of reverse transcriptase

The source of infection is a person, the routes of transmission are sexual, parenteral, transplacental.

Pathogenesis includes several processes. The affinity of gp120 with CD4 lymphocyte receptors has been established. Target cells of HIV are primarily T-helpers, macrophages. Monocytes, astrocytes, endothelial cells.

Stages of HIV infection

1.Early acute

2. Chronic

3. Progression

Morphological manifestations of HIV

Persistent generalized lymphadenopathy, lymph node changes. The latter are manifested at the beginning of the hyperplasia of the cortical layer and the appearance of lymphoid follicles in the medullary layer, the germinal centers increase. All immunocompetent cells in the node are actively dividing by mitosis. The number of T-lymphoblasts, reticular cells increases, B-cells are activated.

Then the so-called fragmentation of the follicles occurs. Characterized by hypertrophy of vascular endothelial cells, active phagocytosis of erythrocytes, the appearance of giant cells.

Even later, follicular atrophy, erasure of the lymph node structure, hyalinosis of follicular centers, as well as destruction of dendritic cells are observed.

At the end, the lymph node is represented almost entirely exclusively by the stroma, the sinuses are overflowing with various cells, expanded.

In parallel, atrophic changes in all lymphoid organs develop. Other organs change to a lesser extent, in particular, the development of encephalitis and foci of demyelination is characteristic in the central nervous system. Atrophy of the testicles and seminiferous tubules is possible.

The terminal stage of HIV infection is AIDS.

Secondary infectious complications in AIDS

Tuberculosis

Pneumocystosis

Mycoplasmosis

Chlamydia

Of the tumors, Kaposi's sarcoma and GM lymphoma are more common. Also common cases of severe cryptogenic meningoencephalitis. + characteristic accidental involution of the thymus with aggravation of immunodeficiency

93... Neurospeed. The nature of the lesions and the features of morphological changes.

94. Sepsis. Modern concepts of etiology. Clinical and morphological forms.

Sepsis is a common infectious disease associated with the focus of infection in the body. Etiology - the presence of the pathogen in the body - staphylococcus, pneumococcus, mycobacterium. Pseudomonas aeruginosa, etc. Sepsis does not possess the property of contagiousness.

Local and general changes in sepsis do not give specific features. The main link in the pathogenesis of sepsis is bacteremia. Modern theories say. That the main predisposing factor in the development of sepsis is not a feature of the microbe, but the features of the reactivity of the macroorganism at the moment.

Sepsis morphology

Local changes develop both in the focus of introduction and beyond, a septic focus = a focus of purulent inflammation, may be absent. The infection spreads hematogenously and lymphogenically, which leads to lymphangitis, lymphadenitis, lymphothrombosis, phlebitis, thrombophlebitis. Possible bacterial embolism.

The presence of dystrophies and necrosis in the parenchymal organs is characteristic. Inflammatory processes are represented by interstitial varieanto-interstitial nephritis, hepatitis, myocarditis, etc. Hyperplasia is observed in the elements of the immune and hematopoietic tissues, in the liver.

Classification

By etiology

Pneumococcal

Gonococcal

Pseudomonas aeruginosa

Colibacillary

Others, etc

By the nature of the entrance gate

Therapeutic

Tonsillogenic

Surgical

Uterine

Otogenic

Odontogenic,

Umbilical

Cryptogenic

By clinical and morphological forms

Septicmia (toxicosis, hyperergia, fever, absence of purulent metastases, rapid course)

Septicopyemia (purulent processes in the entrance gate, bacterial embolism, abscesses in organs and tissues)

Septic endocarditis

Chroniosepsis (long-term non-healing primary septal focus and extensive suppuration)

83. HOSPITAL INFECTIONS: etiology, main morphological manifestations, outcomes, significance. Basic concepts of epidemiology. Hospital infection - diseases or complications, the development of which is associated with infection of the patient, which occurred during his stay in a surgical hospital. Hospital (nosocomial) infection remains the most important problem of surgery, despite the constant improvement of aseptic and antiseptic methods. Interestingly, since the discovery of antibiotics, when it seemed that the problem of fighting the infection was resolved, and until now, the frequency of purulent complications in surgery has decreased very slightly. Hospital infection has a number of characteristic features: Pathogens are resistant to major antibiotics and antiseptic agents. This is due to the passage of microflora in a surgical hospital, where there are low concentrations of antimicrobial agents in the air, on surfaces, in the body of patients. Pathogens are usually conditionally pathogenic microorganisms, most often - staphylococcus, Klebsiella, Escherichia coli, proteus vulgaris, etc. It occurs in patients who are weakened as a result of illness or surgery, often a superinfection. Often there are massive lesions by one strain of the microorganism, manifested by a similar clinical picture of the disease (complications). From the presented characteristics, it is clear that the complications that arise are severe, their treatment and prevention are difficult. The main measures for the prevention of nosocomial infection: Reducing the preoperative bed-day. Taking into account the peculiarities of filling the wards during hospitalization (patients with approximately the same length of stay in the hospital should be in the same ward). Early discharge with supervision at home. Change of antiseptics and antibiotics used in the department. Rational prescription of antibiotics. It is desirable to close surgical hospitals for ventilation (1 month per year). This measure is mandatory for purulent departments and in the event of an outbreak of hospital infection. Epidemiology (epi - on; demos - people;) is a general medical science that studies the patterns of occurrence and spread of diseases of various etiologies in order to develop preventive measures. The subject of study is a set of cases of a disease in a certain territory at a certain time among a certain group of the population. The object of the epidemiology of infectious diseases is the epidemic process, the patterns of its development and forms of manifestation. The subject of epidemiology is: the process of the emergence and spread of any pathological conditions among people (in the population); the state of health (the impossibility of the emergence and spread of pathological conditions). History of Epidemiology. Hippocrates (460-370 BC) The first theory of the cause is considered to be the founder of the science of epidemiology - the penetration of miasms located in space or in soil, in particular, in swampy places. The second living disease agent is "Contagium vivum". Fracastoro (1478-1553) Contagionist hypothesis during the Renaissance. The studies of L. Pasteur (1822-1895), R. Koch (1843-1910) and their many students determined not only the triumph of the contagionist theory, but also led to the development of many practical measures in the fight against infectious diseases (modern diagnosis of diseases, the use of disinfection, development and introduction into widespread practice of specific prophylaxis with the help of vaccines and serums, etc.) The English doctor is known for his investigation of the causes of the cholera epidemic in the 19th century.

84.THE MOST IMPORTANT UROGENITAL INFECTIONS Mycoplasmosis. A characteristic cytological characteristic is the giant cell transformation of the affected cells with the appearance of vacuoles along the periphery of the cytoplasm, perinuclear or large vacuoles, which give the cytoplasm a foamy or optically empty appearance. PIC-positive pathogens are found in vacuoles. Subsequently, the affected cells undergo necrosis. Inflammatory infiltration consists of lymphocytes, macrophages, and a small number of leukocytes. Mycoplasmas can be adsorbed on erythrocytes, thereby causing the transformation of their antigenic structure, which is accompanied by hemolysis of erythrocytes, leading to anemia and jaundice. Mycoplasmas have a tropism for epithelial cells and vascular endothelium. Therefore, mycoplasmosis is accompanied by vasculitis and hemorrhagic syndrome. Chlamydia. The pathogen (Chlamydia trachomatis) stains SHIK positively. It has two forms: elementary (infectious) bodies, smaller and reticular Halberdstedter-Provachek larger-initial ones. Chlamydia is an anthropozoonosis, widespread among animals, birds, and fish. Infection occurs by an ascending, descending route or from the focus of infection in the endometrium, as well as by a hematogenous route. Herpes simplex. Distinguish between acute and chronic herpes with exacerbations, as well as limited(localized) and generalized. Etiology. Causative agent herpes simplex is a type 1 and 2 DNA virus that is virulent to humans. Damage to the skin, mucous membranes and ophthalmic herpes is often caused by infection with the herpes virus type 1, genital type 2. Pathogenesis. The source of infection is a sick person or a virus carrier. The transmission of infection is carried out by contact. The penetration of the virus in the area of ​​the entrance gate during contact or airborne infection is accompanied by damage to the epithelium of the skin or mucous membrane with subsequent development regional lymphadenitis and hematogenous spread of the virus with viremia and viruria. The hematogenous spread of the virus is promoted by its adsorption on the surface of erythrocytes and the absorption of leukocytes by macrophages by the type of incomplete phagocytosis. Viremia occurs not only with generalized, but also with localized forms of herpes. The herpes virus has a high neurotropicity and therefore can be for a long time persist in nerve tissue without causing any painful manifestations. In chronic forms of herpes, which are found mainly in adults, exacerbation of the infection is associated with provoking moments - hypothermia, other infectious diseases. Pathological anatomy.A common form localized herpes is a lesion of the epithelium. There is swelling, redness with the gradual formation of a vesicle or many small vesicles with serous or serous-gcorrhagic contents, surrounded by a zone of edema and hyperemia. Trauma causes the formation of erosion or sores. When the vesicles dry up, a crust forms, which then disappears. Microscopically, balloon dystrophy with death of epithelial cells and accumulation of serous exudate in the epidermis is found in the epithelium. The dermis is edematous, its vessels are sharply full-blooded, there are lymphohistiocytic infiltrates in the perivascular tissue. Numerous giant cells are located along the periphery of the vesicles. In the nuclei of epithelial cells, intranuclear basophilic inclusions, surrounded by a zone of enlightenment, - corpuscles(according to the author who established the connection of inclusions with the herpes virus). Electron microscopy in the nuclei of affected cells can reveal the capsids of the virus, which from the nucleus, as the viral particles mature, enter the cytoplasm and are enclosed in vacuoles here. When the cell dies, viruses are released. The prognosis is favorable, however, cases with the addition of generalization of the process and a lethal outcome are possible.

85. Syphilis: definition, cause, routes of infection, clinical and morphological forms, morphological manifestations, outcomes. Congenital syphilis.

Causative agent: Treponema pallidum. At the site of penetration on the mucous membrane, there is a primary focus (the epithelium is lifted by the serous exudate accumulated under it, then it is rejected and ulceration occurs at this place; productive inflammation develops at the bottom and edges with rather thick lymphoplasmacytic infiltrates and a small admixture of neutrophilic leukocytes). In these areas, there are many blood vessels on the side of which there is a loosening of the walls and proliferation of the endothelium, as well as adventitia cells. Macro: lesion like a red speck, later a papule; after 15-30 days - a flat ulcer (hard chancre) with a diameter of 1-2 cm with a bottom and walls of a cartilage-like consistency with a smooth surface and scanty discharge. Further - healing without treatment. Simultaneously with hard chancre - lymphogenous generalization with damage to the lymph nodes (more often regional). Primary focus and lymphadenitis - primary syphilis(syphilis may end at this stage).

More often without treatment - secondary syphilis... Typical is not lymph, but hematogenous generalization (15-30 days after the healing of the ulcer). First of all, foci of inflammation appear in the skin and mucous membranes: edema, plethora, lymphoplasmacytic infiltrates with an admixture of giant multinucleated cells. Macro: in the skin of various types of lesions (syphilides), mainly roseola (pink spots of the skin and mucous membranes, especially the mouth and larynx, not rising above the surface) and papules (bulging over the surrounding unchanged skin, copper-red, often around hair follicles ); on the palms and soles m. excessive keratinization. The liver (hepatitis) and joints are affected from the internal organs.

In case of progress - tertiary syphilis(more often after 3-4 years). Typical formation of gummas (resemble whitish or pinkish tumor nodes). In places of the greatest severity of gummy inflammation in the bee, pancreas, lungs and other organs, it ends in diffuse sclerosis (cirrhosis). Characterized by the involvement of the middle layer (mesaortitis) and adventitia of the aorta, especially its thoracic region. Perhaps the involvement of bones and joints with the development of periostitis, osteomyelitis and osteochondritis, as well as other organs (b. Testes - orchitis).

Neurosyphilis - vascular damage, meningitis and gum. Early - damage to the meninges, blood vessels and brain matter with a predominance of exudative reactions (within 5 years from the moment of infection). Late - damage to nerve cells, nerve fibers and glia (after more than 5 years).

10-15 years after infection - widespread atrophy with a significant decrease in organ weight in combination with expansion of the ventricles. Ganglion cells vacuolize, small areas of necrosis are possible. This is combined with an increase in glial cells and its fibers, hemosiderin deposition, and pulpy nerve fibers disappear in the cortex. Dystrophic changes predominantly involve the pyramidal tract and the posterior columns of the spinal cord. The pia mater becomes whitish, grows together with the surface of the brain and the dura mater. Depending on the localization of the maximum changes, there are different names for diseases: with the main lesion of the GM - progressive paralysis, the spinal cord - dorsal tabes.

85. Syphilis: definition, cause, routes of infection, clinical and morphological forms, morphological manifestations, outcomes. Congenital syphilis.

The causative agent is treponema pallidum,

Penetration: through the damaged epithelium from / epidermis Route of infection: sexual, vertical, very rarely - household, professional Acquired with - three periods, congenital - without periodization.

Incubation period ~ 3 weeks Epithelium - LS - LU - blood 1st syphilis = sensitization, 2nd - nt, generalization, 3rd - hzt, local PA lesions:

1st... at the site of penetration (PCh, PG, mouth, fingers) - papule (shortly), then - ulcer = hard chancre = 1st syphilitic complex, heals on its own after 2-3 months, a scar remains macro - edges are even, cartilaginous consistency, bottom " lacquered ”, smooth micro - necrosis, infiltrate - lymphoid and pL cells, few np and epithelioid cells, many treponemas, in the vessels - endothelial proliferation (!) 1st syph affect = ulcer + LN region + nearest LN, follicular hyperplasia in LU proliferation of vascular endothelium, sclerosis 2nd... 6-10 weeks after infection, generalization is mainly with blood! Syphiloids appear - roseola, papules and pustules (Zinz does not name the latter). common to them - focal edema of the skin and skin, loosening of the epithelium, hyperemia, inflammation of the infiltrate, necrosis of the walls, contain many treponemas; lasts 3-6 weeks LU - enlarged, edema, hyperplasia, foci of necrosis. treponema 3rd. 3-6 years after infection, chronic interstitial inflammation, gum xp diff int inflammation - in the liver, lungs, aorta, testes. Infiltrates: lymphoid and pl cells, in the vessels - endarteritis and lymphangitis. Next - syphilitic sclerosis! gum = granulomas, in the liver, skin, soft tissues Visceral s. - defeat internal org, in the 3rd period

Heart - gummy / chronic interstitial inflammation, outcome - cardiosclerosis Arteries - often the aorta (affected to the descending part) - mesaortitis - infiltration, Pirogov-Langhans cells, destruction of elasticity, outcome - syphilitic aortic aneurysm, syphilitic aortic defect with valve lesions. sometimes defeat coronary art Neurosyphilis- defeat in n with-me, more often in the 3rd period gummy form - gummas of different size (millet - pigeon's egg), sometimes diffusely simple form - inflammation of the infiltration of the brain and membranes of the lesion - obliterating endarteritis, endophlebitis -> softening mosaic progress paralysis - late manifestation - the mind of the GM mass, atrophy of the subcortical structures and cerebellum, inflammation, dystrophy, necrosis of the nc, demyelination, inflammation of the MR, in the sp brain - damage to the posterior and side of the cords dorsal tabes - late manifestation - damage to the posterior cord, inflammation of the MR

Congenital with- syphilis stillborn premature babies (cynz does not distinguish this) - early with - late with

C m / r: miscarriage at the 6th month of the macerated fetus, the cause of death - toxic d-e treponema R c - manifests itself in the 1st month of life. edema of the fetus with delayed intra / morning development, hepatosplenomegaly, hyperplasia (!!!) of the placenta pemphigus sif (pemphigoid) - palms and feet, blisters with ser / g contents, red rim, at the base - infiltration of skin diffusion - palms of the foot around the mouth, buttocks, thighs, elbows, knees, syphrhinitis, Wegner's osteochondritis - pore tubule of bones stenosis of the gastrointestinal tract; brown (silicon) liver, dense, hc-lfc inf-I lungs - fibrous (white) pneumonia affecting the central nervous system P s - manifests itself at the age of 4 years Hutchison's triad : bad teeth (shape, size), deafness, keratitis, Dubois abscesses in the thymus, surrounded by a shaft of epithelioid cells, filled with ser w with nf and lfc, it is important: the placenta should reach 2 kg in case of sif m! (n - 600 g) infiltration, villous hyperplasia, sometimes abscesses

86.DISEASES OF THE Uterine Cervix. The most common pathology is pseudo-erosion (ectopia) cervix. In the presence of inflammation in the vaginal part of the cervix (ectocervix), squamous epithelium may be damaged with the development of true erosion... After 1-2 weeks, its surface is covered with glandular epithelium and forms acquired pseudo-erosion... In this case, the growth of the epithelium in depth is observed with the formation of branching glandular passages. Such changes are indicated as endocervicosis. It can also develop with persistence of congenital pseudo-erosion (displacement of the border between the flat and glandular epithelium), as well as with ectropione(eversion of the mucous membrane of the cervical canal as a result of trauma received during childbirth or abortion). In the future, it is possible to heal pseudo-erosion with the replacement of the glandular epithelium with a stratified squamous epithelium. In this case, sometimes there is a violation of the proliferation process with the development of dysplasia ( intraepithelial neoplasia). There are 3 degrees of dysplasia. Mild dysplasia characterized by a slight increase in the thickness of the basal layer and an increase in the number of mitoses. At moderate dysplasia the number of mitoses increases, atypical mitoses appear. The changes cover half of the formation thickness. In the future, there is a progressive loss of differentiation, until the entire layer is replaced by immature atypical cells. severe dysplasia /pak in situ. In 40% of cases, this form becomes invasive cancer within 3 months. up to 20 years. Infiltrative cervical cancer more often squamous cell, less often adenocarcinoma, occasionally glandular squamous cell.

87.DISHORMONAL ENDOMETRIC DISEASES. Diseases of the body of the uterus are of a dyshormonal nature and are more often associated with hyperestrogenism. Increased proliferation, as well as impaired endometrial rejection in the desquamation phase, lead to the development of hyperplastic processes. Thickening of the basal layer of the endometrium is indicated as basal hyperplasia. In the future, the thickened basal layer can be stretched and lengthened, which leads to the formation endometrial polyp. Endometrial glandular hyperplasia develops more often around menopause, as well as with anovulatory cycles in young women. It is characterized by increased proliferation of the glands and a violation of their cyclic changes. Cystic changes in the glands are often noted ( glandular cystic hyperplasia). With acute hyperestrogenism, there is active form glandular hyperplasia, characterized by an increase in the number of glandular structures, sometimes with a large number of mitoses. With prolonged exposure to low doses of estrogen (which can occur in postmenopausal women) develops resting form characterized by pronounced cystic changes in the glands and low mitotic activity. Atypical glandular hyperplasia (adenomatosis) characterized by an increase in the number and pronounced convergence of glands ("back to back"), changes in their structure with budding and papilla formation, as well as atypia of cells; is a precancerous condition. The most common endometrial cancer is adenocarcinoma. Dichormonal hyperplastic processes also include fibroids (leiomyoma) uterus, diagnosed more often at the age of 35 to 45 years. In the myometrium, dense, well-delimited, often multiple nodes are formed, having a fibrous structure in the cut. Histologically, various thicknesses, randomly located bundles of muscle fibers, separated by layers of connective tissue expressed in varying degrees, are visible. If there are endometrial areas in the tumor, it is designated as adenomyoma... After the onset of menopause, in most cases, the tumor undergoes regressive changes up to the complete disappearance of the muscle component. Endometriosis of the body of the uterus is also a common disease. adenomyosis. With this form of endometriosis, cyclical changes in the endometrium of ectopic foci are much less common, because their source seems to be the basal layer of the endometrium, which is less sensitive to the effects of hormones. Endometriosis- a common disease, character. the appearance of areas of the endometrium in an unusual place. Allocate genital and extragenital endometriosis. Genital endometriosis It is subdivided into internal, which develops in the myometrium (adenomyosis), isthmus and cervix, and external, the most frequent variant of which is ovarian endometriosis (less often there is damage to the fallopian tubes, sacro-uterine and wide uterine ligaments, peritoneum of the utero-rectal cavity). At extragenital endometriosis ectopic areas of the endometrium are found in the bladder, intestines, kidneys, lungs, and other organs outside the reproductive system. In areas of endometriosis, cyclical changes develop (as in normal endometrium) with intermittent bleeding in the desquamation phase. This leads to the formation of cysts filled with a densely brown viscous fluid (chocolate cysts), as well as hemorrhages, followed by the formation and formation of scars and adhesions between organs. Endometriosis can cause pain, dysmenorrhea, and infertility.

General morphology of the infectious process. Pathomorphosis of infectious diseases. Viral infections: influenza, measles. Viral hemorrhagic fever with renal syndrome (hemorrhagic nephroso-nephritis). HIV infection.

1. General clinical and morphological characteristics of the infectious process.

Infectious process - various options for the interaction of microbes and a macroorganism, manifested in the corresponding clinical and morphological symptoms and various changes in laboratory and immunological

technical indicators.

Forms of infectious diseases: asymptomatic carriage, erased abortive forms (in vaccinated), localized forms, generalized (septic) forms; acute, subacute, chronic, slow (HIV infection, multiple sclerosis) and latent infections.

Koch's postulates: 1) microbes should be constantly detected in the lesions in this infectious disease in humans; 2) microbes must be isolated in a pure culture on an artificial nutrient medium; 3) the introduction of these microbes should cause a similar disease in experimental animals; 4) microbes should be released from lesions in experimental animals.

General pathomorphology of infectious diseases.

1) The presence of an entrance gate and a primary infectious focus with the development in it of an inflammatory reaction of varying severity (primary affect), the formation of a primary infectious complex (primary infectious focus, lymphangitis, lymphadenitis).

2) General morphological changes: skin rashes, vasculitis, hyperplasia of hematopoietic tissue, dystrophic and inflammatory changes in internal organs.

3) Development of immunomorphological processes: hyperplasia of the lymph nodes (lymphadenitis), spleen, tonsils, intestinal lymphoid apparatus, hyperplasia of hematopoietic tissue in the bone marrow. At the same time, reactive centers appear in the lymphoid follicles, antibody-forming plasma cells accumulate, the macrophage apparatus is activated, with some infections granulomas of a specific structure are formed. Immunopathological reactions can develop, in the first place, very immunocomplex lesions of the vessels of the microvasculature, autoantibodies are formed.

4) In addition to the immune system, during infectious processes, the endocrine system is also activated with stimulation of the hypothalamic-pituitary-adrenal system. This activation is of a nonspecific nature and underlies the development of a general adaptation syndrome, which contributes to the restructuring of the body during an infectious process.

2. Pathomorphosis of infectious diseases.

Pathomorphosis is a persistent change in the clinical and morphological picture of diseases, including infectious diseases. Biological pathomorphosis of infectious diseases: the appearance in nature of new mutant strains of pathogens or a periodic change of already known strains. The clearest examples of this process are the widespread occurrence in nature and primarily among the human population of the human immunodeficiency virus and prions (Creutzfeldt-Jakob disease, kuru, mad cow disease, scrapie in sheep).

Therapeutic pathomorphosis of infectious diseases: the emergence and widespread distribution of drug-resistant strains of microbes, an increase in chronic forms of infections and hence the predominance of sclerosis and atrophy processes in the pathomorphological picture of infectious diseases over severe destructive changes, an increase in allergic reactions. Natural antagonists of viruses are endosymbiontic bacteria, which secrete RNA and DNases that dissolve virion nucleic acids. The disappearance (or suppression) of normal endosymbiontic bacteria under the influence of antibiotics has led to the fact that a person has lost his natural antiviral "defenders". At the same time, viruses were able to persist in the human body, moving to the rank of slow viral infections. One example of this is believed to be the HIV pandemic.

The causative agent is the RNA virus of three main serovars (A, B, C), which has a pronounced ability to mutate and has a pronounced tropism in the epithelium of the upper respiratory tract and vascular endothelium. In addition to humans, cows, horses, pigs, and birds are ill with influenza. The routes of entry are the mucous membrane of the upper respiratory tract and the conjunctiva of the eyes. The main pathogenic effect of the influenza virus is cytopathic and vasoparalytic action, which is accompanied in severe cases of the disease by severe intoxication.

Clinical and anatomical forms of influenza: mild, moderate and severe. The severe form usually occurs in young children and the elderly, with immunodeficiencies, with a combination of A2 influenza with adenoviruses and RS viruses. In a mild form, the inflammatory process is limited to damage to the nasal mucosa, larynx, trachea and main bronchi. With flu of moderate severity, the lesion spreads to the small bronchi, bronchioles and alveoli, where serous-hemorrhagic inflammation develops. A severe form of influenza is characterized by a pronounced general intoxication, a confluent serous-hemorrhagic pneumonia with toxic hemorrhagic edema and the formation of hyaline membranes (respiratory distress syndrome) develops in the lungs. In 1918-1920, 500 million people of the planet were ill with the flu - "Spanish flu", 20 million of whom died. The severe course of influenza and its spread in the form of a pandemic was caused by the recent First World War. The cause of death was toxic hemorrhagic pulmonary edema. In some patients with severe influenza, severe secondary bacterial bronchopneumonia with ulcerative necrotic lesions of the larynx and trachea develop as a complication. They are caused by secondary immunodeficiency caused by the cytopathic effect of the virus on macrophages. As a result of intoxication and severe generalized circulatory disorders, the development of influenza encephalitis and serous meningitis is possible. Children have widespread petechial hemorrhages in the mucous membranes and skin, and they may have laryngeal edema with asphyxia (false croup). In half of the cases of influenza in the elderly, death occurs from acute cardiovascular failure, including in 25% of cases death occurs from myocardial infarction, in 20% of cases of pulmonary edema, the same percentage dies from PE.

Acute highly contagious viral infectious disease, predominantly of childhood, characterized by catarrhal inflammation of the mucous membranes of the upper respiratory tract, conjunctiva of the eyes and maculopapular rash of the skin. Immunity after the transferred measles is persistent, lifelong. The causative agent of measles is an RNA virus. Penetrates into the body by airborne droplets through the conjunctiva of the eyes and the mucous membrane of the upper respiratory tract. During the period of viremia, the virus settles in the lymphoid organs, mucous membranes, lungs, skin, and brain. After the incubation period (several days), whitish spots of Filatov-Koplik (measles enanthem) appear on the mucous membrane of the cheeks near the small lower molars. The next day, a merging maculopapular rash develops on the skin of the trunk. In vaccinated children, measles is easy. In weakened and unvaccinated children, measles occurs with symptoms of severe intoxication. At the same time, interstitial measles giant cell pneumonia develops in the lungs, measles encephalitis can develop in the brain. If measles is not complicated by the addition of a secondary infection, then the disease usually ends with recovery. However, due to the pronounced immunosuppressive properties of the virus (not only macrophages, but also lymphocytes are affected), there is a high risk of developing secondary bacterial complications - post-crustal pneumonia, exacerbation of tuberculosis, wet gangrene of the soft tissues of the cheeks (noma).

VIRAL HEMORRHAGIC FEVER WITH RENAL SYNDROME

(HEMORRHAGIC NEPHROSIS-JADE).

Synonyms: Far Eastern hemorrhagic fever, Yaroslavl hemorrhagic fever, Ural hemorrhagic fever, Tula fever. It is a NON-CONTAGIOUS form of hemorrhagic fevers, i.e. not transmitted from person to person.

The causative agent is a recently isolated filterable virus from the hantavirus family. The most severe forms of the disease are caused by the Hantaan and Dobrova viruses, the milder ones are caused by the Puumala and Seoul viruses. The infection is a typical zooanthroponosis and is transmitted by field mice with their feces. The incidence is characterized by a distinct seasonality - autumn, when field mice begin to nest on human habitation.

The disease begins acutely with the appearance of fever, headache, pain in the lumbar region, hyperemia of the face and visible mucous membranes, thrombocytopenia, hematuria. Characterized by an abundant petechial rash on the skin; nosebleeds are possible. In the classical course of GPLS, 5 phases are distinguished - fever, hypotension, oliguria, polyuria and convalescence. Death of patients can occur on the first day from hypotension and shock or after a few days in a febrile period from acute renal failure. Lethality is 3-20%. The main pathomorphological changes are noted in the kidneys, where there is a picture of tubulo-interstitial hemorrhagic nephritis. Macroscopically, the kidneys are significantly increased in size, the cortex is anemic with hemorrhagic specks, the sharply full-blooded pyramids of the medulla are striking. Spotted hemorrhages on the surface of the calyces and pelvis. Histologically, the kidneys show plethora and stasis in the vessels of the pyramids. There are numerous hyaline casts in the lumen of the tubules, which leads to the expansion of the tubules due to the accumulation of urine in them. In the interstitial tissue of the medulla there are infiltrates of lymphocytes, histiocytes and plasma cells. The survivors develop nephrosclerosis in the kidneys.

HIV INFECTION.

1. ETIOLOGY AND EPIDEMIOLOGY.

The first information about this disease began to appear in the early 80s. Described immunodeficiency, which afflicted drug addicts and homosexuals. The viral etiology of the disease was proven by French researchers - Gallo and Montagnier. The infection is caused by two strains of the RNA virus: HIV-1 and HIV-2. HIV-1 is the main pathogen in North America, Europe and Central Africa. HIV-2 causes the disease mainly in West Africa. HIV infection in Russia began to spread at a rapid pace only since 1996, and this is due to an avalanche-like increase in injecting drug addicts. Since the average duration of the course of HIV infection until the stages when secondary infections begin to develop is 1-4 years, it is after this period of time that a sharp increase in infectious pathology among the population, especially tuberculosis, should be expected. Among all HIV-infected people in Russia, the number of drug addicts is 70-90%. According to forecasts, in the next millennium, the total number of people infected with HIV will be about 5 million people. In France, every 14th person is infected with HIV (7%).

2. PATHOGENESIS.

Factors of HIV pathogenicity.

Having penetrated into the body, the virus selectively infects CD-4 + cells (T-helpers), to a lesser extent macrophages, monocytes, neurons, glial cells. The result of this is the development of severe immunodeficiency, predominantly of the cellular type, due to the fact that the rate of death of CD-4 cells under the influence of the virus exceeds their neoplasm in the lymphoid tissue. At the same time, the number of T-helpers in the blood progressively decreases and the Tx / Tc ratio decreases to 0.2-0.5 (normally 1.9-2.4). The immediate mechanism of destruction of T-helpers by the virus is apoptosis, which is stimulated by a specific membrane protein of the virus p120. It is important to note that not only virus-infected T-helpers, but also sterile T-helpers undergo apoptosis (Scheme 1). Hence, it follows that one of the ways of pathogenetic therapy of HIV infection is the search for means that block cell apoptosis at some of its stages.

Pathological anatomy of AIDS (HIV infection): Methodical recommendations / Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - M., 1989 .-- 18 p.

Compiled by: Academician of the USSR Academy of Medical Sciences prof. A.P. Avtsyn, academician of the USSR Academy of Medical Sciences prof. N.K. Permyakov, prof. I.A. Kazantseva, MD O.G. Parkhomenko

Instructions of the Ministry of Health of the USSR dated 20.03.89, No. 269-U

Pathological Anatomy of AIDS (HIV Infection): Guidelines

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Pathological anatomy of AIDS (HIV infection): Methodical recommendations / Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - 1989.

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/ Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - 1989.

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Pathological anatomy of AIDS (HIV infection): Methodical recommendations / Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - 1989.

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/ Avtsyn A.P., Permyakov N.K., Kazantseva I.A., Parkhomenko O.G. - 1989.

MINISTRY OF HEALTH OF THE USSR

PATHOLOGICAL ANATOMY OF AIDS (HIV infection)

SCIENTIFIC RESEARCH INSTITUTE OF HUMAN MORPHOLOGY AMS USSR ALL-UNION SCIENTIFIC-METHODOLOGICAL CENTER OF PATHOLOGICAL-ANATOMICAL SERVICE

INTRODUCTION

Acquired Immune Deficiency Syndrome (AIDS) is an infectious disease in which a severe defect in cellular immunity occurs in previously healthy people. First described in 1981. By 1987, the Centers for Disease Control (USA) had data on more than 50 thousand AIDS patients aged 28 days to 60 years. Currently, according to the WHO, in 144 countries of the world there are about 140 thousand such patients and from 5 to 10 million people infected with the pathogen of AIDS.

The causative agent of AIDS is the human T-lymphotropic virus, which belongs to the retrovirus family. It was abbreviated as HTlv - III (or Hiv), in Russian - HIV (human immunodeficiency virus), in contrast to HTlv - I, which causes T-cell lymphomas, and HTlv - II, which is the etiological factor of the so-called hair cell leukemia.

An ELISA test (enzyme linked immunosorbent assay) is used to identify people infected with the virus, which detects the presence of serum antibodies to HIV. It is believed that the ELISA test should be confirmed by a more specific test, immunoblotting. Serum antibodies to HIV were found in 90% of patients with AIDS and in 50% with a high risk of developing AIDS (homosexuals, drug addicts, prostitutes, people with a history of blood transfusions, children born to infected mothers).

Birion HIV is a spherical particle with a diameter of about 1000 A. Its core contains the genetic material, which is RNA. Birion is dressed with a membrane, from which protein particles protrude in the form. The first stage of cell infection

HIV, like any other virus, is the binding of a viral particle to a special component of the cell membrane (receptor). For HIV, such a receptor is a protein called the Cd 4 antigen, to which a glycoprotein (GP-120), a viral envelope protein, binds. Consequently, the distribution of Cd 4 determines the spectrum of cells and tissues affected by HIV, i.e. causes the tropism of the virus. These are, first of all, T4 - halper lymphocytes, which in AIDS practically disappear from the lymphocyte population.

In addition to T4 - halper lymphocytes, Cd 4 antigen contains about 40% of monocytes (macrophages), the so-called dendritic antigen - representing cells of lymphoid organs and skin, as well as 5% of all B-lymphocytes in the body. Some cells, in particular glial and neuroendocrine intestinal (enterochromaffin) cellular elements, become infected with HIV in culture, but Cd 4 cannot be detected in them. This is due to the fact that these cells contain traces of messenger RNA encoding the Cd 4 protein, i.e. they are capable of synthesizing this protein. It appears that a very small amount of the Cd 4 protein is needed to infect an HIV cell. HIV infection causes severe immunosuppression with a predisposition to so-called opportunistic infections and tumors (see below). Damage to the immune system primarily occurs as a result of infection and death of T4 - halper lymphocytes. However, with the selective elimination of T4 - lymphocytes, which are of paramount importance for the generation of a specific immune response, severe changes develop throughout the immune system. These changes are induced by opportunistic infections (especially herpes viruses) in immunosuppressive patients and are manifested by a decrease in delayed-type hypersensitivity reactions and the reaction of lymphocyte blast transformation to antigens and methogens, polyclonal B-cell activation, a decrease in hematoxin of monocytes / macrophages, a decrease in cytoxicity and nonspecific immune cells. It is likely that the full spectrum of diseases associated with HIV infection has not yet been conclusively established. However, it is already known that the causative agents of opportunistic infections in AIDS can be viruses, bacteria, fungi and protozoa, which persist in the human body with a normal immune system, without causing clinical and morphological manifestations of the disease. After infection of the body with HIV, these pathogens are activated and the disease can become generalized.

Tumors characteristic of AIDS are also present because their occurrence is associated with viruses of the Herpes group, primarily the cytomegalovirus (for example, Kaposi's sarcoma) and the Epstein-Barr virus (for example, malignant B-cell lymphomas). The development of tumors is explained by the fall of the antitumor resistance of the organism.

SYNDROMOLOGY OF AIDS

Currently, there are:

1. Fully developed AIDS, meeting the criteria of the North American disease registration system, with the presence of opportunistic infections and / or tumors.

2. AIDS - associated complex - AIDS without signs of opportunistic infections and / or tumors.

3. Syndrome of chronic lymphadenopathy: presence of lymphadenopathy in homosexual men for more than 3 months with the involvement of 2 or more areas (excluding inguinal).

The spectrum of diseases in patients infected with HIV is extremely wide; they can be subdivided into separate syndromes. Although many organs and systems are damaged in AIDS, most patients die as a result of diseases of the lungs or the central nervous system.

The clinical syndromes observed in AIDS can be grouped according to the organ system that is most often affected:

pulmonary syndrome;

neurological syndrome;

intestinal syndrome;

damage to the skin and mucous membranes;

lymphadenopathy;

fever of unknown origin;

retinal syndrome.

PULMONARY SYNDROME

Pulmonary syndrome in AIDS is clinically manifested by fever, dry cough, and poor ascultative data.

With bilateral lung damage and the predominance of interstitial pneumonia, one should think about the following etiological factors: Pneumocystis carinii pnemoniae, cytomegalovirus infection; Logionella species; Micobakterium avium intracellulare (atypical mycobacterial infection) and / or Micobacterium tuberculosis; Toxoplasma gondii; pathogenic fungi (candidiasis, shtomycosis, actinomycosis, coccidioidosis, histoplasmosis).

With bilateral lesions with predominant involvement of the alveoli, the following are most often found:

a) atypical or typical mycobacterial infection;

b) pulmonary form of Kaposi's sarcoma (especially if the process is accompanied by hemorrhagic pleural effusion);

c) bacterial (usually staphylococcal) pneumonia.

Pneumocystis pneumonia - the most common opportunistic infection in AIDS, occurs in 85% of patients. Microscopically, Pneumocystis pneumonia is characterized by a foamy eosinophilic exudate in the alveoli; the number of alveolar macrophages is usually small; rarely, foci of granulomatous inflammation are observed, in long-term current cases, interstitial pulmonary fibrosis develops, and calcifications may occur. The pathogen persists in the lung tissue for up to 5-6 weeks. Pneumocysts are found in lung tissue and bronchoalveolar lavage (BAL). With the help of silver impregnation according to Gomus, staining with toluidine blue or Giemsa, it is possible to reveal oval, round or collapsed pneumocysts in histological sections of imprints of lung tissue from BAL. The detection of foamy exudate in the BAL fluid is the basis for a presumptive diagnosis of Pneumocystis pneumonia. A rapid method for detecting pneumocysts is the method of fluorescent antibodies. The detection rate of pneumocysts in the study of transbronchial biopsy and BAL fluid is 65-10 ..... Cytomegalovirus infection - the most often detected in autopsy and microscopic examination, generalized opportunistic infection, including it affects the lungs. However, an intravital diagnosis of cytomegaly is rarely made. Large cells containing cytomegalovirus (with typical intranuclear inclusions) are unevenly distributed in the lung tissue, the inflammatory response is minimal or absent. In severe pulmonary infection, diffuse interstitial pneumonia, hyaline membranes, and even areas of lung tissue necrosis are observed. The detection of cytomegalovirus by the immunoperoxidase method using monoclonal antibodies in the BAL fluid is very effective, however, a positive result often indicates the carriage of the virus, rather than an active infection. With transbronchial biopsy, the detection rate of cytomegalovirus pneumonia is 50-85 %%.

Mycobacterial pneumonia, including atypical pneumonia, in AIDS may not be diagnosed due to a minimal and atypical tissue reaction. Disseminated pulmonary tuberculosis has been described only in drug addicts and residents of the island of Haiti. Atypical mycobacterial infection is characterized by accumulations of foamy (granular) macrophages with PIC - positive cytoplasm, in which mycobacteria are detected. Epithelioid cell granulomas are rare. In all cases of AIDS, histological specimens of lung tissue should be stained according to Ziehl-Nielsen to identify acid-fast flora. With transbronchial biopsy, atypical mycobacterial infection is detected in 62-87 %% of cases.

NEUROLOGICAL SYNDROME

HIV is capable of primarily affecting the nervous system. In addition, opportunistic infections involving the central nervous system and malignant brain lymphomas are common. It is necessary to carry out differential diagnostics between these processes Pathological changes in the central nervous system in AIDS based on the materials of 153 deaths from AIDS Infections

Normal, metabolic encephalopathy, or nonspecific changes 23.6%

Progressive spinal symptoms can be caused by damage to the spinal cord: a) HIV itself; b) HIV in combination with herpes and / or cytomegalovirus infection (for the diagnosis, the material for detecting the virus should be obtained from the cerebrospinal fluid). Lesions of the peripheral nerves of the so-called. peripheral neuropathy can be caused by both HIV infection and complications of chemotherapy, especially with vincristine. Sometimes polypathy occurs due to autoimmune muscle damage by antisarcolemmal auto-antibodies. For encephalopathy caused directly by HIV, in the clinical relationship, personality changes, amnesia, social isolation, and progressive dementia are characteristic. Pathomorphological changes develop mainly in the white matter and in the subcortical structures, the cortex is relatively preserved. There is a correlation between the severity of dementia and the severity of pathomorphological changes in the brain. Macroscopically, the pathology of white matter and subcortical formations of the brain is characterized by areas of blanching and foci of softening.

Histologically, HIV encephalomyelitis can be characterized as subacute encephalitis with multinucleated cells, small or larger clusters of microglia (monocytes / macrophages), which are especially abundant in subcortical structures, including basal ganglia and semioval centers. These microglial nodules can also be found in the brain stem, cephalicis, spinal cord, and less often in the cerebral cortex. For HIV infection in the central nervous system, the formation of multinucleated cells of the symplast type is pathognomical, which can be located in isolation or in combination with microglial nodules and nodes. Microscopically, in addition, foci of demyelination, perivascular inflammatory infiltrates, macrophages containing brown pigment (siderophages) and (i.e. impregnated with iron salts) neurons are characteristic. Neuronal changes are nonspecific for HIV.

The characteristic manifestations of HIV encephalomyelitis include the vacuolation of the white matter. Vacuolar myelopathy with lesions of the lateral and posterior columns of the spinal cord is especially common, but not specific. During vacuolation, the white matter looks like a perforated one (this process is also called). In the differential diagnosis of HIV-encephalitis, it should be taken into account that microglial nodules are also characteristic of cytomegalovirus encephalitis, however, in the latter, the degree of dementia does not correlate with the severity of damage to the brain matter.

Progressive multifocal leukoencephalopathy (PML), characteristic of AIDS, was previously considered a very rare disease. It was first described in people with oncological lymphoproliferative diseases, especially with chronic lymphocytic leukemia, as well as in patients with sarcoidosis. It is believed that PLM is caused by slow viruses (not by HIV itself) and only in patients with severe immunity deficiency. Fixed macroscopic preparations with PML reveal multiple grayish foci in the white matter of the brain and spinal cord, which are slightly sunken and have a granular appearance. In lesions, viruses destroy oligodendroids, the nuclei of which can be moderately hyperchronic, with homogeneous chromatin. The nuclei of many of the astrocytes surrounding the focus are enlarged, polymorphic, very reminiscent of the early stage of neoplastic transformation. In half of the described cases, perivascular infiltrates from lymphocytes and plasma cells were encountered. The most common opportunistic infections in the central nervous system in AIDS are cytomegalovirus encephalitis, cryptococcosis, and toxiplasmosis. These infections differ from HIV encephalitis in the presence of the corresponding microorganisms and the absence of characteristic multinucleated cells.

Encephalitis caused by cytomegalovirus is characterized by the presence of foci of necrosis and specific large cells with a large basophilic intranuclear inclusion surrounded by a light rim and small cytoplasmic inclusions (cells resembling). These cells are usually mononuclear, but may have 2-3 nuclei each; typical inclusions distinguish them from multinucleated cells pathognomonic for HIV encephalitis.

Xyptococcosis (fungal infection) can cause massive damage to the brain substance with the development of foci of necrosis, macroscopically and in their consistency resembling jelly. The accumulation of rounded forms of the fungus is well detected in histological sections during the PIC reaction.

Toxoplasmosis of the brain is manifested by the development of foci of necrosis of various sizes against the background of severe microcirculation disorders and hemorrhages. Toxoplasmosis in histological sections can be detected by Giemsa staining, they are characterized by an arrangement in groups.

All of the listed causative agents of opportunistic reactions of the central nervous system can be identified by electron microscopic examination.

Pediatric encephalopathy with AIDS is characterized by the following features:

1. decrease in brain weight;

2.inflammatory infiltrates (diffuse, nzhel microglial nodules are more characteristic);

3. multinucleated cells, multinucleated giant cells;

4. calcifications of small vessels, perivascular infiltrates;

5 . changes in white matter: demyelization, proliferation of astrocytes (astrocytosis) with relative safety of axons; absence of vacuolar myelopathy;

6. rare association with opportunistic infections;

7. during electron microscopic examination in multinucleated giant cells, the so-called, represented by accumulations of mitochondria surrounded by lipid vacuoles is found (retrovirus particles are shown in mitochondria and outside them).

INTESTINAL SYNDROME

The syndrome of diarrhea and wasting associated with HIV infection was first described in the Republic of Uganda. The incidence of diarrhea in AIDS patients in the United States is between 30% and 50%, and in Africa and Haiti it is 70-90%. Diarrhea is usually caused by opportunistic infections, most often caused by the following pathogens: a) Shigella, Campylobakter, Blastocystis hominis; b) cryptosporidium; c) clostridia.

In addition, in AIDS, a disease resembling Sprue is described without an established etiology. In biopsies of the small intestine, flattening of the villi, necrosis and desquamation of the epithelium, signs of chronic inflammation are noted. It has not been finally established whether these changes are the primary manifestation of HIV infection or they are associated with another, as yet unverified pathogen.

Immunological and immunomorphological study of cells of infiltration of the mucous membrane of the small intestine in AIDS indicates a severe depletion (reduction) of the population of T-4 lymphocytes, a sharp decrease in the number of plasma cells containing Ig A. AIDS; they probably play an important role in the pathogenesis of enteropathy in AIDS and in the development of opportunistic infections as a result of local impairment of cell-mediated immunity.

Intestinal biopsy in AIDS patients is the second most frequent after lung biopsy; their information content in terms of the possibility of establishing a diagnosis of the pathological process characteristic of AIDS is about 40%.

The characteristic manifestations of AIDS include diarrhea and proctitis in homosexuals, the causative agents of which are the most common pathogenic microorganisms of the intestine, the most common pathogens, sexually transmitted diseases, as well as the occasional intestinal flora, to which this individual has idiosyncrasy.

In AIDS patients, the intestines are mainly affected by 4 infections; candidiasis, cytomegaly, mycobacteria (M. avium intracellulare) and cryptosporidiosis. Rarely, but still found in the intestines with AIDS, histoplasmosis, toxoplasmosis, pneumocystis infection, botryomycosis. Also, tuberculosis of the ileocecal zone, colon, stomach is rarely encountered. Opportunistic infections and intestinal tumors in AIDS differ from their counterparts in patients with pre-AIDS in particular prevalence and severity. Thus, cryptosporidiosis, previously known as a common cause of diarrhea in calves, causes severe diarrhea and can affect the biliary tract and liver in AIDS patients. With abdominal syndrome without diarrhea in AIDS patients, cytomegalovirus infection, cryptosporidiosis, as well as tumors: Kaposi's sarcoma and malignant lymphocyte are most often detected. Candidiasis in AIDS patients is often limited to the oral mucosa and esophagus, but the entire gastrointestinal tract may be affected.

Candidal ulcers are usually not deep; during the SHIK reaction, numerous filaments of pseudomycelium are revealed in their bottom.

Cytomegalovirus infection predominantly affects the large intestine, especially the blind intestine, but penetrating ulcers are also possible in the small intestine. Sometimes there is a mild gastritis, esophagitis, and occasionally cholecystitis. Macroscopically, the mucous membrane looks hyperemic with small whitish depressions, which are ulcers. Microscopically, inflammation is often absent; intestinal crypts in a special plate contain typical viral inclusions. Most of the cells infected with the virus are of mesenchymal origin.

In the small intestine, cytomegaly causes deep ulcers that reach the serous membrane and can perforate, with a more pronounced inflammatory response. Microscopically, granulation tissue with numerous plasma cells, lymphocytes, histiocytes is visible at the edges of the ulcer; in part of the latter, viral inclusions are determined. They can also be found in fibroblasts, smooth muscle cells, and endothelium. Cytomegalovirus infection may not be accompanied by mucosal ulceration and manifest itself as focal or segmental productive inflammation mimicking Crohn's disease.

Another common opportunistic infection of the gastrointestinal tract in AIDS patients is atypical microbacterial infection caused by M. avium intracellulare. This infection affects the small intestine. Macroscopically, the mucous membrane looks swollen, thickened. Microscopically, flattened villi are visible, shortened and expanded due to infiltration from histocytes. These histocytes are similar to those found in Whipple's disease. With the PIC reaction, abundant cytoplasm is determined in them. When staining for acid-fast microorganisms according to Ziel-Nielson, many mycobacteria are detected in histocytes. If the process is widespread, then the syndrome of impaired absorption is clinically determined in patients. The defeat of the small intestine is often combined with an increase in mesenteric lymph nodes. The large intestine with atypical mycobacterial infection involves secondary and moderate involvement. Colon biopsies appear almost normal, and only a few histocytes show acid-fast bacilli. Intestinal tuberculosis with AIDS can proceed without typical granulomatosis and manifest as changes that mimic nonspecific ulceration.

Cryptosporidiosis. Pathogens do not invade tissue, but stick to the surface of the epithelium of the small and large intestine. They can be seen with normal staining (hematoxylin and eosin) as small blue-stained structures. Several intestinal infections in AIDS patients can be combined.

Kaposi's sarcoma occurs in AIDS patients in the stomach and intestines quite often. In most cases, this is combined with skin lesions, but the intestine may be the only organ in which foci of Kaposi's sarcoma develop. The tumor is localized submucosally and is not usually diagnosed with a superficial biopsy.

Malignant lymphomas in AIDS occur in the stomach, small intestine, and colon. Their localization in the oral cavity and anal region is also characteristic. The most common are B-cell (lymphoblastic, immunoblastic) lymphosarcomas with a poor prognosis. Cases of lymphogranulomatosis with lesions of the gastrointestinal tract are also described.

PATHOLOGICAL CHANGES IN OTHER ORGANS.

Liver pathology in AIDS. The following pathological processes are most typical:

1.infection: atypical mycobacterial infection, cryptococcosis, cytomegalovirus infection and viral hepatitis B;

2. Kaposi's sarcoma;

3. nonspecific changes.

Atypical mycobacterial infection is characterized by accumulations of histocytes both along the portal tracts, as well as inside the lobules. If granulomas are formed, then they also consist of histiocytes, the lymphocytic reaction is weak or absent. Histocytes have a light granular cytoplasm, are SHIK-positive and can be confused with those of Upla disease. When staining according to Ziehl Nielson, M. Avium intracellulare is detected in these cells.

A cryptococcal infection can be severe in the entire liver. Fungi are detected in sinusoids (single or in the form of clusters), the inflammatory reaction is very weak.

Viral hepatitis B occurs in about 25% of AIDS cases. The diagnosis is confirmed by immunomorphological detection of the hepatitis B virus antigen.

Kaposi's sarcoma can primarily affect the liver; it is characterized by localization in the area of ​​the liver gates and along the portal tracts. Nonspecific liver changes in AIDS patients result from massive therapy with antibiotics, cytostatics and corticosteroids.

The defeat of the esophagus in AIDS patients is usually caused by candidiasis, cytomegaly, mycobacteria, herpes simplex virus. The skin and mucous membranes of the mouth, pharynx, and external genitals are often affected by Kaposi's sarcoma. Candida ulcers are also characteristic; necrotizing gingivitis, often herpetic; Herpes zoster; seborrheic dermatitis occurs.

Describe in AIDS and other skin syndromes: psoriasis, herpes, molluscum occultus (do not miss syphilis!). for Kaposi's sarcoma in AIDS patients, infiltrative-plaque pale red lesions are characteristic, which are located not only on the lower extremities, but also on the face, external genetics and other areas of the skin.

Knotty formations are rare. Gitsological examination reveals foci of chaotic antiogenesis with the formation of thin-walled vascular cavities, proliferation of spindle-shaped cells, lymphoid-plasma cell and macrorhagal infiltration, hemosiderosis, erythrophagia.

Retinal damage in AIDS can develop as a reaction to Pneumocystis antigen in Pneumocystis pneumonia or is caused by cytomegalovirus.

Heart pathology in AIDS.

In patients with AIDS, there is an epicardial form of Kaposi's sarcoma and lymphosarcoma; frequent hemorrhages in the pericardium, myocarditis and pericarditis caused by opportunistic viral-bacterial, fungal or protozoal infection. Chronic lymphohistiocytic () myocarditis was found in more than 50% of autopsies of those who died from AIDS.

Kidney pathology in AIDS.

Describe HIV-associated nephropathy. The most frequent morphological findings are focal segmental glomerulosclerosis with deposits of immune complexes in the glomeruli, tubular microcystosis, the so-called tubulo-interstitial nephritis. With electron microscopy, tubuloreticular structures resembling viral particles are detected in the endothelium of the glomeruli and cells of the stromal infiltrate. The kidneys do not decrease in size throughout the disease until the development of uremia. The disproportion of changes in the nephrons of the severity of interstitial fibrosis may explain the preservation of the normal size of the kidneys.

LYMPHADENOPATHY

Generalized lymphadenopathy may be the primary manifestation of AIDS. The response of the lymph nodes in AIDS is divided into several types, which are successive stages of a dynamic process, starting with hyperplasia and ending with atrophy. The following types of lymphadenopathy are distinguished:

1. follicular hyperplasia;

2. hypervascular follicular type;

3. mixed follicular type;

4. follicular involution with lymphoid depletion.

With follicular hyperplasia, the follicles are very large, irregular in shape, sometimes spreading to almost the entire node. Hyperplastic centers are surrounded by mantle zones, which often look discontinuous and lose the characteristic concentric arrangement of lymphocytes, the latter can penetrate into the germinal centers. As the follicles enlarge within the germinal centers, the number of centroblasts increases, numerous mitoses are visible. The study using monoclonal antibodies showed an increase in the subpolation of T8 suppressor lymphocytes. In the parafolicular sinuses, there are many monocytoid cells with a weakly eosinophilic cytoplasm. Electron microscopic and immunomorphological data show that dendritic cells and T-4 lymphocytes in germinal centers are infected with HIV, and viral RNA activation was found in them.

The paracortical zone is also usually hyperplastic, represented mainly by small lymphocytes, immunoblates, neutrophilic leukocytes are found.

A characteristic feature is a decrease in the ratio of T-halper and T-suppressor due to a decrease in the number of T4-halper lymphocytes.

The pathological picture is complemented by plasma cells, a large number of dilated and full-blooded vessels, hemophagocytic macrophages, small accumulations of polymorphonuclear leukocytes, multinucleated giant cells, similar to those found in viral infections, multinucleated immunoblasts.

The hypervascular follicular type of lymphadenopathy in AIDS patients is often associated with Kaposi's sarcoma; characterized by changes resembling angiofolicular hyperplasia. In the tissues of the lymph nodes, the number of plasma cells is increased, there are many small tree-like branching blood vessels; the spectrum of follicle changes is wide - from large ones with hyperplastic germinal centers to hyalinized ones.

The mixed follicular type of lymphadenopathy is characterized by the presence of both hyperplastic and involutive follicles with the colonization of the paracortical zone with plasma cells. These changes are frequent in the case of opportunistic infections. The reduction of T4-lymphocytes is characteristic.

Follicular involution with lymphoid depletion is characterized by the complete absence of various follicles and germinal centers. Two morphological variants of this stage are described: the first is characterized by a large number of immunoblasts, plasma cells and proliferating blood vessels (resembles angioimmunoblastic lymphadenopathy); the second - an almost complete reduction of lymphocytes, an abundance of non-phagocytic macrophages; the remaining lymphocytes are represented by T8 -suppressors.

Lymph nodes in AIDS can be massively defeated by various opportunistic infections, Kaposi's sarcoma, and malignant lymphomas. With opportunistic infections, granulomatous processes are frequent. Infections are extremely aggressive, generalize quickly, and are resistant to therapy.

With a rapid local enlargement of the lymph nodes in an AIDS patient, one should think about Kaposi's sarcoma or malignant lymphoma; the defeat of these tumors of the femoral, paraaortic, retroperitoneal lymph nodes is especially characteristic. Buboes are commonly seen in malignant lymphoma, tuberculosis, or atypical mycobacterial infection.

In case of fever of unknown origin with anemia, splenomegaly, impaired liver function in an AIDS patient, one should first of all think about disseminated atypical mycobacterial infection, as well as malignant lymphoma.

PRINCIPLES OF PATHOLOANATOMIC AIDS DIAGNOSTICS

Before, after, and during autopsy, AIDS can be suspected if the manifestations of opportunistic infections and tumors described above are present, especially if these processes are combined or generalized. In the case when the clinical diagnosis of AIDS in a patient during his lifetime was confirmed by the detection of antibodies to HIV in the blood serum, the interpretation of these autopsies, as a rule, does not cause difficulties. If AIDS was suspected by a combination of pathological processes only at the autopsy, at least 5 ml of blood from the femoral vein should be sent (with a special hand) to the appropriate regional laboratory. Blood is collected in a dry sterile test tube, closed with a rubber stopper, placed in a plastic bag, treated with 3-5% chloramine solution and placed in a container.

It is believed that the detection of serum HIV antibodies is possible up to 24 hours after death, but the study is complicated by hemolysis of cadaveric blood. Therefore, a negative result does not mean that there was no HIV infection in this case. At the same time, the pathological diagnosis of AIDS can only be made if it is confirmed by a test for antibodies to HIV.

In each case suspected of having AIDS, a careful comparison of clinical and anatomical and pathological data should be carried out. It should be remembered that opportunistic infections and Kaposi's sarcoma are not specific manifestations of HIV infection and can be observed with severe secondary immunity deficits of various origins, in particular those associated with prolonged use of antibiotics, cytostatics, corticosteroids or other drugs with immunosuppressive effects.

When formulating a pathological diagnosis in cases of confirmation of HIV infection, the head of the diagnosis should be indicated: AIDS (positive reaction to HIV antibodies in blood serum). Next, opportunistic infections and / or tumors are listed in a sequence that reflects the severity of the pathological process and its role in thanatogenesis.

The epicrisis should indicate which of the diseases played a role in the onset of death.

For example: the death of an AIDS patient (the presence of antibodies to HIV in the blood serum) followed from bilateral pneumocystis pneumonia (or Kaposi's sarcoma with damage to the skin, lymph nodes, lungs and intestines). If the diagnosis of AIDS is not confirmed serologically or there was no possibility to conduct a study, but the case is extremely suspicious of AIDS, then this should be indicated and justified in the pathological epicrisis.

For pathologic-histological examination in cases suspicious of AIDS, the brain should be taken (necessarily from the region of the subcortical ganglia and the white matter of the hemispheres), the spinal cord, lungs (even in the absence of macroscopically visible inflammatory changes), organs of the gastrointestinal tract (pieces from all parts of the intestine should be examined microscopically after careful macroscopy), organs of immunogenesis (bone marrow, thymus, lymph nodes, spleen), liver, kidneys, heart, if indicated - retina, skin, oral mucosa, external genitals. The pieces are placed in conventional fixatives (formalin, Carnoy's liquid, 80% alcohol, etc.).

It must be remembered that all AIDS infections tend to generalize and can proceed as sepsis. Therefore, in all cases of HIV confirmed in vivo or if AIDS is suspected, send blood from the heart cavity for bacteriological examination.

As noted above, the role of pathologic histological examination of diagnostic biopsies and surgical material (especially lymph nodes, skin, lungs, intestines) in identifying cases of the disease suspected of AIDS is very large.

If opportunistic infections and / or tumors characteristic of AIDS are found in biopsy specimens in persons under 60 years of age, the pathologist must indicate in his conclusion the need to examine the patient for HIV antibodies or inform the attending physician about it. Caution should be exercised when drawing up a report and avoid unnecessary overdiagnosis of AIDS, given that this can cause serious ethical problems for the relatives of the deceased and all persons in contact with him.

ANNEX 1

ORDER OF THE MINISTRY OF HEALTH OF THE USSR dated 20.03.89, No. 269-U (addition to the Directive of the Ministry of Health of the USSR dated 22.12.87, No. 460-U.

In order to streamline the system for collecting and transmitting information on registration of deaths from AIDS, a special registration of AIDS diagnostics cases is introduced during pathological or forensic examination of a corpse based on a combination of pathological changes confirmed by serological examination of cadaveric blood for antibodies to HIV. For each such case, the health care institution fills out (form No. 058 / y) and sends it to the territorial sanitary and epidemiological station at the place of registration.

In cases where, according to the results of a pathological or forensic autopsy of a corpse, a suspicion of AIDS arises, but the study of cadaveric blood for antibodies to HIV gave a negative result or it was not possible to carry it out, the institution must also notify the sanitary-epidemiological station about this. detection of a disease suspected of AIDS.

Information about this person is also entered in the journal, on a separate sheet for registering infectious diseases (form 060 / y). First Deputy Minister I.N. DENISOV

APPENDIX 2

COMPREHENSIVE PLAN OF MEASURES FOR BODIES AND INSTITUTIONS OF HEALTH CARE IN PROVIDING PATHOLOGOANATOMIC OPENINGS IN CASES OF AIDS.

1. Determination of the procedure for informing the superior health authority in the event of a corpse with an established (or suspected) AIDS diagnosis.

2. Allocation of the pathological department for the autopsy of those who died from AIDS.

3. Determination of the order of delivery of corpses to the pathological department, in which the autopsy will be performed.

4. Ensuring the delivery of corpses by special vehicles.

5. provision of a stock of disinfectants and protective suits, incl. gloves.

6. ensuring the direction of fixed samples of organs and tissues to the Institute of Human Morphology of the USSR Academy of Medical Sciences, which acts as a consultative and methodological center for the pathological anatomy of AIDS.

7. determination of the laboratory base for serological examination of cadaveric blood for antibodies to HIV.

8. Compliance with the anti-epidemic regime for pathogens of the II group of pathogenicity when working with biopsy and autopsy materials.

APPENDIX 3

PRECAUTIONS FOR PERSONS PERFORMING OPENINGS AND EXAMINATIONS OF BIOPSY (SURGICAL) MATERIAL FROM PATIENTS AND DEATH FROM AIDS, AND FUNERAL FUNERAL STAFF.

The AIDS virus (HIV) is assigned to the II pathogenicity group, along with the viruses listed in Appendix 8 (approved by the USSR Ministry of Health on June 29, 1978).

1. In case of AIDS or suspicion of it, a special tag with a warning inscription should be attached to the body of the deceased.

2. All personnel involved in the autopsy must wear a Type I suit: double gloves, arm ruffles, waterproof aprons, boots or galoshes, shoe covers. Instruments and surfaces contaminated during opening must be treated with a 3% chloramine solution. The discharge of waste water into the sewerage system is stopped. Rinse water is collected in buckets or other containers containing disinfected solutions. A rug moistened with a disinfectant solution is placed at the entrance to the sectional room.

3. When handling tissue material and body fluids or, if necessary, come into contact with surfaces that may be contaminated with them, wear rubber gloves.

4. Clothes used for opening, soaked in blood or other body fluids, must be placed in a waterproof bag with a warning sign. Contaminated material can also be placed in color-coded plastic bags designed to collect and dispose of infectious waste. Before removing the suit, wipe the oilcloth apron with a cotton swab, abundantly moistened with disinfectant solution, remove it, rolling it with the outside inward; remove the second pair of gloves and armbands; boots or galoshes are wiped from top to bottom with cotton swabs abundantly moistened with a disinfectant solution (a separate swab is used for each boot).

5. For the handling of all liquids in laboratories, only mechanical pipettes with a rubber bulb should be used. Pipetting by mouth is prohibited!

6. all skin lesions on the hands must be covered with an adhesive plaster or fingertips.

7. All procedures and handling of potentially infectious material should be performed carefully to avoid the formation of droplets and aerosols. In case of contamination of hands or other parts of the body with blood or other body fluids, they should be treated with a disinfectant solution or 70o alcohol. If there is a suspicion that the infected material has entered the mucous membranes, they are immediately treated with a 0.5% solution of potassium permanganate, the eyes are washed with a 1% solution of boric acid or a stream of water, or a few drops of a 1% solution of silver nitrate are instilled, a 1% solution of protargol is instilled into the nose, the mouth and throat are additionally rinsed with 70 ° alcohol or 0.05% potassium permanganate solution or 1% boric acid solution.

8. In case of accidental spraying of infected material and at the end of work, the working surfaces of laboratory barrels must be decontaminated with a 3% chloramine solution.

9. On sterile jars with the material sent for research (blood, biopsy or surgical material), warning labels must be made, for example; ... If the outer surface of the can is dirty, it must be wiped with an aqueous solution of sodium hypochlorite (5.25%) diluted 1:10 or 3% chloramine solution. During transportation, all cans with the material should be hermetically closed with a rubber stopper and rubber film (from gloves) and placed in a second container or tight bag, which must be carefully inspected to ensure that there is no mechanical damage. The outer surfaces of containers or bags are treated with a 3% chloramine solution. An accompanying document is attached to the parcel, which indicates the full name, age, diagnosis, date of taking the material, the nature of the material, the name and position of the medical worker sending the material. All materials are sent by express. The fixed autopsy material is stored in a specially designated room. The procedure for recording, storing, handling, dispensing and sending materials containing the AIDS virus (HIV) is carried out in accordance with those approved by the USSR Ministry of Health on 05/18/1979.

10. When handling potentially infectious material, wear protective clothing (gowns or suits), which must be removed before leaving the laboratory.

11. All personnel should wash their hands thoroughly after completing work, removing clothing and before leaving the laboratory (breakout room).

12. After the autopsy, the corpse is sprinkled with a disinfectant solution (3% solution of chloramine B or bleach), wrapped in a sheet soaked in a disinfectant solution, and placed in a metal coffin or wooden coffin lined with oilcloth. At the bottom, bleach is poured with a layer of at least 10 cm. The transportation of the corpse to the cemetery or crematorium is carried out by the evacuation team, accompanied by specialists from the Department of Especially Dangerous Infections of the Torrtorial SES.

13. Funeral home staff should be aware of the potential hazard and take appropriate precautions to prevent contact with the skin or mucous membranes of body fluids.

14. All potentially contaminated materials used for pathomorphological (cytological) studies must be decontaminated (see item 15) and only then sent for disposal.

15. Modes of disinfection during the current disinfection of various objects:

APPENDIX 4

HIV INACTIVATION

Laboratory studies show that the concentrations of disinfectants calculated to inactivate retroviruses are quite sufficient to inactivate HIV: 40% ethyl alcohol, 30% isopropyl alcohol, 1% lysol, 5% phenol, 2% formalin, 200 mg sodium hypochlorite.

The infectivity of the virus completely disappeared after incubation for 1 min with 0.5% sodium hypochlorite or 70% ethyl alcohol. A widely used fixing mixture of ethyl alcohol and acetone in a 1: 1 ratio completely inactivated HIV within 10 minutes.

The thermal stability of HIV has been compared with the thermal stability of other RNA-containing enveloped viruses. Incubation at 60 ° in the presence of 5% human albumin leads to the destruction of the virus within 20 minutes. The addition of a stabilizer (50% sucrose with 2 glycine at pH 7.0), used to prevent denaturation of some proteins during concentration and purification, lengthens the incubation time at the elevated temperature required to suppress HIV infectivity. It is important that even in the presence of stabilizing additives, HIV retains a sufficiently high thermal stability: heating at 60 ° for 1-3 hours completely inactivates it.

The rate of HIV inactivation in the culture fluid depends on the incubation temperature and the presence of human serum or plasma. The infectivity of the virus remains at 25 ° for 15 days, at 37 ° for 11 days. At room temperature, HIV remains infectious in a liquid medium or in a dried state for at least 4-7 days. This stability was demonstrated in vitro by keeping the virus-containing preparations under sterile conditions. And yet, these results indicate the ability of the virus to maintain biological activity for a long time in environmental objects. Inactivation of HIV in the presence of various disinfectants.

The time of HIV inactivation in the studied autopsy and biopsy material during its fixation depends on the volume of the tissue piece being examined. The order of fixation is as follows: cut pieces of organs no more than 1x1x0.5 cm in size are placed in fixing liquid in a clean container. A piece of cotton wool (gauze) is placed on the bottom. The volume of the fixing liquid should be 7-10 times the volume of the test material. Fixation time: 1-2 days or more at room temperature. The material is stored in a specially designated place.

HIV infection. Taxonomy, characteristics of pathogens. Laboratory diagnostics, prevention.

The human immunodeficiency virus causes HIV infection, resulting in the development of acquired immune deficiency syndrome.

The causative agent of HIV infection is a lymphotropic virus belonging to the family Retroviridae family Lentivirus.

Morphological properties: RNA virus. Spherical viral particle The envelope consists of a double lipid layer permeated with glycoproteins. The lipid membrane comes from the plasma membrane of the host cell in which the virus reproduces. The glycoprotein molecule consists of 2 subunits located on the surface of the virion and penetrating its lipid membrane.

The core of the virus is cone-shaped and consists of capsid proteins, a number of matrix proteins and protease proteins. The genome forms two strands of RNA, for the implementation of the process of reproduction, HIV has reverse transcriptase, or reverse transcriptase.

The genome of the virus consists of 3 major structural genes and 7 regulatory and functional genes. Functional genes perform regulatory functions and ensure the implementation of reproductive processes and the participation of the virus in the infectious process.

The virus mainly affects T- and B-lymphocytes, some cells of the monocytic series (macrophages, leukocytes), cells of the nervous system.

Cultural properties : on a cell culture of T-lymphocytes and human monocytes (in the presence of IL-2).

Antigenic structure: 2 types of virus - HIV-1 and HIV-2 HIV-1, has more than 10 genotypes (subtypes): A, B, C, D, E, F ..., differing in the amino acid composition of proteins.

HIV-1 is divided into 3 groups: M, N, O. Most isolates belong to group M, in which 10 subtypes are distinguished: A, B, C, D, F-l, F-2, G, H, I, K. Stability: Sensitive to physical and chemical factors, dies when heated. The virus can persist for a long time in a dried state, in dried blood.

Pathogenicity factors, pathogenesis: The virus attaches to the lymphocyte, enters the cell and reproduces in the lymphocyte. As a result of the multiplication of HIV in the lymphocyte, the latter are destroyed or lose their functional properties. As a result of the multiplication of the virus in various cells, it accumulates in organs and tissues, and it is found in the blood, lymph, saliva, urine, sweat, and feces.

With HIV infection the number of T-4-lymphocytes decreases, the function of B-lymphocytes is disrupted, the function of natural killer cells is suppressed and the response to antigens is reduced and the production of complement, lymphokines and other factors regulating immune functions (IL) is disrupted, as a result of which dysfunction of the immune system occurs.

Clinic: the respiratory system is affected (pneumonia, bronchitis); Central nervous system (abscesses, meningitis); Gastrointestinal tract (diarrhea), malignant neoplasms (tumors of internal organs) occur.

HIV infection proceeds in several stages: 1) the incubation period, averaging 2-4 weeks; 2) the stage of primary manifestations, characterized at first by acute fever, diarrhea; the stage ends with an asymptomatic phase and persistence of the virus, restoration of well-being, however, HIV antibodies are determined in the blood, 3) the stage of secondary diseases, manifested by damage to the respiratory, nervous system. HIV infection ends with the last, 4th terminal stage - AIDS.

Microbiological diagnostics.

Virological and serological studies include methods for the determination of HIV antigens and antibodies . For this, ELISA, IB and PCR are used. The sera of HIV-1 and HIV-2 patients contain antibodies to all viral proteins. However, to confirm the diagnosis, antibodies to gp41, gpl20, gpl60, p24 proteins in HIV-1 and antibodies to gp36, gpl05, gpl40 proteins in HIV-2 are determined. HIV antibodies appear 2-4 weeks after infection and are detected at all stages of HIV.

Virus detection method in blood, lymphocytes. However, for any positive test, an IB reaction is set to confirm the results. PCR is also used, which is capable of detecting HIV infection in the incubation and early clinical period, but its sensitivity is somewhat lower than that of ELISA.

Clinical and serological diagnoses are confirmed by immunological studies if they indicate the presence of immunodeficiency in the examined patient.

Diagnostic enzyme-linked immunosorbent assay for the determination of antibodies to HIV - includes viral antigens adsorbed on a carrier, antibodies against human Ig. Used for AIDS serodiagnosis.

Treatment: the use of reverse transcriptase inhibitors acting in activated cells. The drugs are thymidine derivatives - azidothymidine and phosphazide.

Prophylaxis . Specific - no.

Herpes infection: taxonomy, characteristics of pathogens. Laboratory diagnostics. Specific prophylaxis and treatment.

HSV causes herpes infection, or herpes simplex, characterized by vesicular rashes on the skin, mucous membranes, damage to the central nervous system and internal organs, as well as lifelong carriage (persistence) and relapses of the disease.

Taxonomy. Family Herpesviridae. Genus Simplexvirus.

Structure. The HSV genome encodes about 80 proteins necessary for the reproduction of the virus and the interaction of the latter with the cells of the body and the immune response. HSV encodes 11 glycoproteins, which are attachment proteins (gB, gC, gD, gH), fusion proteins (gB), structural proteins, immune evasion proteins (gC, gE, gl).

The virus causes lytic infections of fibroblasts, epithelial cells, and latent infections of neurons.

Cultivation... For the cultivation of the virus, a chicken embryo is used (small dense plaques are formed on the envelope) and a cell culture, on which it causes a cytopathic effect in the form of the appearance of giant multinucleated cells with intranuclear inclusions.

Antigenic structure... The virus contains a number of antigens associated with both internal proteins and glycoproteins of the outer envelope. The latter are the main immunogens that induce the production of antibodies and cellular immunity. There are two serotypes: HSV type 1 and HSV type 2.

Resistance. The virus is unstable, sensitive to sunlight and UV rays.

Epidemiology. The source of the infection is a sick person.

HSV-1 and HSV-2 are transmitted mainly by contact (with vesicular fluid, saliva, sexual intercourse), through household items, less often by airborne droplets, through the placenta, at the birth of a child.

Both types of viruses can cause oral and genital herpes. HSV-1 often affects the mucous membranes of the mouth and pharynx, causing encephalitis, and HSV-2 - the genitals (genital herpes).

Pathogenesis... Distinguish between primary and recurrent herpes simplex. More often, the virus causes an asymptomatic or latent infection.

Primary infection. Vesicle - the manifestation of herpes simplex with degeneration of epithelial cells. The core of the vesicle is composed of multinucleated cells. Affected cell nuclei contain eosinophilic inclusions. After a while, the apex of the vesicle is opened, and an ulcer is formed, which soon becomes covered with a scab with the formation of a crust, followed by healing.

Bypassing the entrance gates of the epithelium, viruses pass through sensitive nerve endings with further movement of nucleocapsids along the axon to the body of the neuron in the sensitive ganglia. The reproduction of the virus in the neuron ends with its death. Some herpes viruses, reaching the ganglionic cells, can lead to the development of a latent infection in which neurons do not die, but contain a viral genome. Most people (70-90%) are lifelong carriers of the virus, which persists in the ganglia, causing a latent persistent infection in neurons.

Latent infection sensory neurons is a characteristic feature of the neurotropic herpesviruses HSV. In latently infected neurons, about 1% of the cells in the affected ganglion carry the viral genome.

Clinic. The incubation period is 2-12 days. The disease begins with the onset of itching in the affected areas, the appearance of edema and bubbles filled with fluid. HSV affects the skin (vesicles, eczema), mucous membranes of the mouth, pharynx (stomatitis) and intestines, liver (hepatitis), eyes (keratitis) and the central nervous system (encephalitis). Recurrent herpes is caused by the reactivation of a virus stored in the ganglia. It is characterized by repeated rashes and damage to organs and tissues.

Genital infection is the result of autoinoculation from other affected areas of the body; but the most common route of infection is sexual. The defeat manifests itself in the formation of a vesicle, which ulcerates rather quickly.

The herpes simplex virus enters during the passage of the newborn through the birth canal of the mother, causing neonatal herpes. Neonatal herpes is detected on the 6th day after childbirth. The virus disseminates into internal organs with the development of generalized sepsis.

Immunity. The main immunity is cellular. HRT is developing. NK cells play an important role in early antimicrobial defense. The organism of the affected person reacts to the glycoproteins of the virus, producing cytotoxic T-lymphocytes, as well as T-helpers, which activate B-lymphocytes, followed by the production of specific antibodies.

Glycoproteins cause the formation of virus neutralizing antibodies. Virus - neutralizing antibodies suppress the intercellular spread of viruses.

Microbiological diagnostics. Use the contents of herpetic vesicles, saliva, scrapings from the cornea of ​​the eyes, blood, cerebrospinal fluid. In stained smears, giant multinuclear cells, cells with enlarged cytoplasm and intranuclear inclusions are observed.

To isolate the virus, HeLa cells, Hep-2 cells, and human embryonic fibroblasts are infected with the test material.

Growth in cell culture is manifested by cell rounding with subsequent progressive damage to the entire cell culture. Chicken embryos are also infected, in which, after intracerebral infection, encephalitis develops. The isolated virus is identified in RIF and ELISA using monoclonal antibodies.

Serodiagnostics carried out with the help of RSK, RIF, ELISA and the neutralization reaction according to the increase in the patient's antibody titer. IB is also capable of detecting type-specific antibodies.

With express diagnostics in smears-prints from rashes, stained according to Romanovsky-Giemsa, giant multinucleated cells with intranuclear inclusions are revealed. To identify the virus, amplification of viral DNA genes in the PCR reaction is also used.

Treatment. For treatment, interferon preparations, interferon inducers and antiviral chemotherapy drugs (acyclovir, vidarabine) are used.

Prevention. Specific prophylaxis of recurrent herpes is carried out during the period of remission by repeated administration of inactivated culture herpes vaccine.

Morphology and structure of the human immunodeficiency virus (HIV)

Human immunodeficiency virus is a lymphotropic virus that causes HIV infection, ending with the development of AIDS, which is characterized by a predominant lesion of the immune system, a prolonged course, polymorphism of clinical manifestations, high mortality, a variety of natural routes of transmission (g.o. sexual and parenteral), a tendency to rapid epidemic spread.

HIV was discovered in 1983 by L. Montagnier and R. Gallo.

Family: Retroviridae, Genus: Lentivirus.

Morphology and structure of HIV.

HIV RNA virus. HIV virions are spherical, 100 nm in diameter. The outer shell of virions is formed by a double layer of lipids, permeated with glycoproteins - "thorns". The lipid membrane comes from the plasma membrane of the host cell in which the virus reproduces. The glycoprotein molecule consists of 2 subunits - gp 120- is located on the surface of the virion, gp 41- permeates the lipid layer. The formation of both proteins occurs with a non-covalent bond between them occurs when the protein of the outer shell of HIV-gp-161 is cut. The core is located under the outer shell of the virion. It has a conical or cylindrical shape and consists of capsid proteins p24 and p25, a number of matrix proteins (p6 and p11), protease proteins (p11 and p11). For reproduction, HIV has reverse transcriptase or revirtase. The HIV genome consists of: 1) 3 main structural genes: gag- encodes matrix, capsid, nucleocapsid proteins and protease proteins; pol - encodes reverse transcriptase; env- encodes gp120 and gp41. 2) 7 regulatory and functional genes: tat and rev - increase the rate of protein transcription, nef- controls the termination of HIV reproduction, vif- encodes a protein responsible for the budding of the virus from one cell and infecting another. They also include vpr, vpu, vpx- provide the implementation of the processes of reproduction and infection.

Core proteins and envelope glycoproteins (p161), which are characterized by a high level of antigenic variability, have antigenic properties.

There are 2 types of virus - HIV-1 and HIV-2, which differ in structural and antigenic characteristics, which determines the differences in the course of the disease.

The life cycle of HIV consists of 4 stages (adsorption, RNA release, RNA synthesis, assembly), which is realized in 1-2 days. The virus mainly affects lymphocytes, sometimes macrophages, leukocytes, dendritic cells, cells of the nervous system, because they contain the CD 4 receptor, with which the viral p120 interacts specifically.