1. The notion of primary tuberculous intoxication.
2. What is the primary tuberculous complex? List its components.
3. Variants in the course of primary tuberculosis.
4. Name forms of progression of primary tuberculosis with generalization of the process.
5. Main varieties of hematogenic tuberculosis.
6. What forms of postprimary tuberculosis do you know? Describe each of them.
7. Name complications, outcomes of postprimary tuberculosis and causes of death.
8. What are the peculiarities of modern tuberculosis? The notion of pathomorphosis of tuberculosis. Paraspecific responses in tuberculosis.
9. The notions of infection and morbidity (sickness) rates of tuberculosis.
Tuberculosis, primary tuberculous focus, lymphadenitis, phthisis, hematogenic tuberculosis, generalization, dissemination, hematogenic disseminated tuberculosis, postprimary tuberculosis, reinfection, fibrofocal tuberculosis, caseous pneumonia, fibrocavernous tuberculosis, pathomorphosis.
Sepsis(from Greek sepsis - «putrefaction») is a generalized infectious disease developing due to the presence of an infection focus in the organism. It has its own etiological, epidemiological, clinical, immunological and pathological characteristics.
The etiology of sepsis is various, it may be caused by different causative agents (staphylococci, streptococci, pneumococci, meningococci, blue pus bacilli, tuberculosis mycobacteria, typhoid bacilli, fungi and other agents except for viruses). Sepsis is not contagious, it cannot be reproduced experimentally. The clinical peculiarityof sepsis consists in the fact that irrespective of the character of the causative agent, the manifestations of the disease are similar due to generalization of infection and inadequate reaction of the organism to the causative agent. The course of the disease is not cyclic, as it is observed in many infections. Sepsis has no incubative period. The duration of the disease is different (from some days to several months and even years), that is why some forms of the disease may be defined, i.e. very acute, acute, subacute, chronic. Immunologic peculiarity of sepsis is that immunity is not produced, in the conditions of
increased reactivity the organism reacts to the causative agent inadequately, developing hyperergic reactions.
Pathological characteristics of sepsis are due to the fact that local and general disturbances in sepsis have no specific features as it is observed in many infections.
Sepsis is one of the most severe and frequent infections. The death rate in sepsis is very high. The incidence of sepsis has increased recently which is associated with the appearance of antibiotic-resistant strains of bacteria and administration of cytostatic preparations causing immune system insufficiency.
Sepsis is a special form of interaction of the macro- and microorganism, the influence of the causative agent and reaction to it are equally important. Hyperergic reaction of the organism and absence of immunity are responsible for infection generalization, acyclic course of the disease, general reactions, absence of ability to localize the infection.
Pathology. Both local and general changes can be noted in sepsis.
Local changes develop in the focus of infection (atrium) or at some distance. A septic focus (which is a focus of purulent inflammation) is formed. In some cases it is absent. The infection propagates from the focus through the lymph and blood vessels. Propagation of the infection through the lymph vessels causes lymphangitis, lyphothrombosis and lymphadenitis, that through the blood system (veins) causes
phlebitis and thrombophlebitis. Purulent thrombophlebitis with thrombus melting and thrombobacterial embolism is common. General changes in sepsis can be degenerative, inflammatory and hyperplastic. The degenerative changes develop in parenchymatous organs (liver, kidney, myocardium, muscles, central nervous system) and manifest by different types of dystrophy and necrobiosis frequently resulting in necrosis.
Inflammatory changes are represented by interstitial septic nephritis, hepatitis, myocarditis, acute polyp-ulcerative endocarditis with the tissue melting and tearing off of the valves, vasculitis accompanied by multiple hemorrhages. But hemorrhagic syndrome in sepsis is connected not only with vasculitis but also with intoxication, increased vascular permeability, anemia.
Hyperplastic processes in sepsis are observed mainly in the hemopoietic and lymphoid tissue. Bone marrow hyperplasia occurs in the flat bones. The yellow bone marrow becomes red, the amount of leukocytes in the blood increases, sometimes immature leukocytes are found. Leukemoid reaction develops. Lymphatic tissue hyperplasia causes enlargement of the lymphatic nodes, spleen, the latter becomes not only enlarged but also flabby, red on incision with abundant scraping of the pulp (septic spleen). Hyperplastic processes in histiocyte-macrophage system are the cause of the liver enlargement. Hemo-
lytic jaundice may result from hemolytic action of some bacterial toxins.
Classification. A number of features are taken into account in classification: 1) etiology, 2) infection atrium (location of the focus), 3) clinico-morpho-logical.
According to the etiology, the following types of sepsis can be distinguished: streptococcal, staphylococcal, pneumococcal, gonococcal, pyocyanic, coli-bacillary, anthracic, tuberculous, syphilitic, mycotic.
Depending of the infection atrium (location of the septic focus) sepsis is classified as therapeutic (parainfection), tonsillar, surgical, uterine, otogenic, odontogenic, umbilical, cryptogenic. In cryptogenic (from Greek kryptos - secret) sepsis the infection atrium is absent. According to clinico-morphological features there are 4 clinico-anatomical forms of sepsis: septicemia, septicopyemia, septic (bacterial) endocarditis and chronic septicemia.
Septicemiais a form of sepsis characterized by pronounced toxicosis (high temperature, delirium), increased reactivity of the organism (hyperergy), absence of purulent metastases and rapid course. The disease is frequently associated with streptococcus. The autopsy does not reveal the focus of sepsis as it is absent or poorly pronounced (the atrium is not found). The skin and sclera are usually yellow (hemolytic jaundice), hemorrhagic syndrome is well pronounced (petechial rash, hemorrhages to the serous and mucous
membranes and internal organs). Hyperplasia of lymphoid and hemopoietic system is typical. The spleen is enlarged, with pulp scraping (septic spleen). The lymph nodes are also enlarged. Proliferation of lymphoid and reticular cells as well as accumulation of mature and immature blood cells are found in the spleen and lymph nodes. Increased hemopoiesis with formation of a large number of immature forms is noted in the bone marrow of the flat bones and in the diaphyses of the bones. The foci of extramedullary hemopoiesis appear. Interstitial inflammation develops in the parenchymal organs (heart, liver, kidneys). The stroma of the organs is edematous, infiltration with neutrophils, lymphocytes, histiocytes is noted. Septicemia is also characterized by increased vascular permeability, fibrinoid changes in the vessels, allergic vasculitis which is responsible for hemorrhagic syndrome.
Septicopyemiais a form of sepsis characterized by purulent process in the infection atrium and bacterial embolism with formation of abscesses in various organs and tissues. In contrast to septicemia, hyperergy signs are moderate, the course of the disease is not very acute. The disease is associated with staphylococcus and blue pus bacilli (Pseudomonas aeruginosa). Autopsy usually demonstrates a septic focus, mainly at the infection atrium, purulent lymphangitis and lymphadenitis, the tissue of the lymphatic node can be melted. Purulent thrombo-
phlebitis, the source of thrombobacterial embolism is found in the area of the focus. At first metastatic abscesses appear in the lungs, then in the liver, kidneys (pustular nephritis), subcutaneous fat, bone marrow (purulent osteomyelitis), synovial membranes (purulent arthritis), heart valves (acute septic polyp-ulcerative endocarditis). Besides, purulent pleuritis and pericarditis develop in the cases of lung abscess. In liver abscess, purulent peritonitis develops. Kidney abscesses are complicated with peri- and paranephritis, skin abscess is complicated with phlegmon.
Septic (bacterial) endocarditisis characterized by septic lesion of the heart valves. At present the most common causative agents of bacterial endocarditis is Staphylococcus albus, aureus.
Classification. Septic (bacterial) endocarditis is classified according to the character of the course and the background disease. According to the character of the disease there is acute, subacute, prolonged (chronic) septic endocarditis. The duration of acute septic endocarditis is about 2 weeks, subacute - 3 months, chronic - several months and even years. Depending on the presence of the background disease, septic endocarditis (especially subacute and acute) is divided into 2 types: 1) that developing on the changed (defective) valves (secondary septic endocarditis), 2) that in the intact valves (primary septic endocarditis described in 1949 by B.A. Chernogubov (Cherno-gubov's disease).
Pathology. Pathological changes are observed in the heart, vessels, spleen, kidneys. The disease pathology has a number of peripheral signs. They are associated with thromboembolism, infarction, multiple hemorrhages. Main changes are observed in the valves, mainly isolated endocarditis. Polyp-ulcerative endocarditis develops on both sclerotic and intact valves. Large thromboembolic polyp-shaped plaques appear on sclerotic valves. The plaques are easily crumbled and are saturated with calcium which is characteristic for the disease. After removal of the plaques, ulcerative defects are seen in the sclerotic and deformed cusps of the valves. In some cases they are superficial, sometimes they disturb the integrity of the valve with formation of acute aneurysm or destruction of the cusps. Thrombotic plaques are located not only on the cusps but also on the parietal endocardium. When the aortic valves are injured, the disease involves the aortic intima. The spleen is enlarged due to prolonged pulp hyperplasia, there are infarcts in the organ. Immune-complex diffuse glomerulonephritis develops in the kidneys. Infarctions and post-infarction scars are frequently observed. Interstitial inflammatory processes, vasculitis, hemorrhages, infarctions are observed in different organs. The foci of softening and hemorrhages are observed in the brain due to vascular changes (vasculitis, aneurysm) and thromboembolism.
The so-called peripheral signs of septic endocarditis are: 1) petechial hemorrhages in the conjunctiva
near the internal angle of the lower eyelid (Lukin-Libman spots); 2) nodular thickening on the palm surface of the hand (Osier's nodes); 3) thickening of the nail phalanges («drum sticks»); 4) necrosis foci in the subcutaneous fat; 5) hemorrhages to the skin and subcutaneous fat (Jeinway's spots); 6) jaundice. At present only Osier's nodes are observed in all instances.
Thromboembolic complications are frequent, as the source of thromboembolism, thromboendocarditis, is most commonly localized in the left heart. Thromboembolism frequently becomes generalized and dominates in the clinical picture of the disease. These are the cases of thromboembolic syndrome. The embolisms give the rise to infarctions in the lungs, spleen, kidneys, retina, skin necrosis, gangrene of the extremities, intestine, foci of softening in the brain. In spite of the presence of streptococci in the thrombi, suppuration in the tissue is absent which suggests hyperergic reaction of the organism in septic endocarditis.
Chronic septicemiais characterized by the presence of a septic focus and generalized suppurations. These septic foci can be found in carious teeth, tonsils but more frequently they are large suppurations resulting from wounds. The pus and tissue decay products are sucked in and cause intoxication, increasing cachexia and amyloidosis development. Chronic septicemia is frequent in wartime. The
changes in the organs and tissues in chronic septicemia are mainly atrophic. Cachexia and dehydration are pronounced. Brown atrophy is found in the liver, myocardium, striated muscles.
Stages of individual work in classStudy and describe macrospecimens
Septic endometritis. Determine dimensions of the uterus and thickness of its wall, describe the state of the mucous membrane. What manifestations of sepsis (local or general) do these changes belong to and what are they called?
Pulmonary abscess. Describe the cavity in the lungs, the state of its walls. What clinical-anatomical form of sepsis does this preparation manifest?
Brain abscess. Describe the appearance of the cavity in the brain. What is the cavity filled with? What is the state of its walls? What is the source of infection? What is the name of this form of sepsis according to its infection atrium?
Apostematous nephritis.Describe the size of the kidney, presence of greyish-yellowish pus-containing microfoci on its surface and on section. What is the name of this form of sepsis according to its infection atrium?
Septic spleen. Describe the size of the organ, the state of its capsule, colour on section, presence of scraping. What is the name of such a spleen? What kinds of septic manifestations are they: general or local?
Ulcerous skin lesions in chroniosepsis. Describe ulcerous changes in the skin. List manifestations of chroniosepsis.
Polypous-ulcerous endocarditis. Describe the size of the heart, volume of its chambers, thickness of ventricular walls,
state of the valvular cusps and presence of fibrinous warty formations on them.