TUBERCLOSIS (туберкулез)

PRIMARY, HEMATOGENOUS, SECONDARY TUBERCULOSIS.

SEPSIS

TUBERCULOSIS

- A chronic infectious disease which can affect all organs of the human body, but more often the lungs.

CAUSATIVE AGENT OF TUBERCULOSIS

Four types of mycobacteria: 1.Mycobacterium tuberculosis2. Bovine (Mycobacterium bovis), 3.Bird (Mycobacterium avium), 4.M intracellulare complexes (or MAC) cold-blooded.

For human pathogens are the first two types.

Mycobacterium tuberculosis

Colorize Tsil-Neelsen

TUBERCULOSIS Epidemiology

Infection source: ill people and animals (mainly cattle).

Ways of infection contamination:- aerogenous (thus the special role is played by airborne and dust infections),- alimentary (with food),- contact, i.e. through the injured skin, mucous membranes,- transplacentary (seldom).

TUBERCULOSIS

Morphological classification: • primary tuberculosis; • hematogenous tuberculosis; • secondary tuberculosis.

PRIMARY TUBERCULOSIS

Primary tuberculosis complex:

1. primary affect (focus of specific lesion);2. tuberculous lymphadenitis (specific inflammation in regional lymph node); 3.tuberculous lymphangitis (specific  inflammation of lymph vessels).

PRIMARY TUBERCULOSISPrimary tuberculosis complex:

Tuberculous ulcer of intestine

Tuberculous ulcer of intestine

Tuberculous ulcer of intestine

Тuberculous lymphadenitis

TUBERCULOSIS

Primary tuberculosis complex:

TUBERCULOSIS

Tuberculous inflammation is composed of three types of tissue reactions, defined immunological status of the body: alterative, exudative, proliferative.

TUBERCULOSIS

Morphological substrate of tuberculosis - pockets of various sizes (from milliary to tuberculoma 2-4 cm in diameter or more), subject to caseous (curd) necrosis without melting or encapsulation of exposed melt to form a cavity - the cavity in different organs and ulcers on mucous membranes.

Тuberculous granuloma

Тuberculous granuloma

Тuberculous granulomas

PRIMARY TUBERCULOSIS

Variants of course:

1. attenuation of the primary tuberculosis foci and the healing of the primary focus; 2. progression of primary tuberculosis with generalization of the process;3. chronic course.

Encapsulation of the primary focus

PRIMARY TUBERCULOSIS

Forms of progression:

- hematogenous;- lymphogenous;- growth of primary affect;- mixed.

PRIMARY TUBERCULOSIS

Hematogenous form of progression developed when mycobacteriae enter the blood from the primary affect or caseous-modified lymph nodes and disseminate in the organism.

Tuberculosis of tongue

Tuberculosis of the thyroid gland

Tuberculosis of the thyroid gland

Tuberculosis of the thyroid gland

PRIMARY TUBERCULOSIS

Lymphogenous form of progression (generalization) – involvment of bronchial, bifurcative, paratraheal, suprar and subclavian, cervical and other lymph nodes. Lymphatic nodes are hyperplastic, enlarged in diameter by 1 - 5 cm, they have a caseous focus.

PRIMARY TUBERCULOSIS

Growth of primary affect – it is more severe progression form and is characterized by caseous necrosis of perifocal inflammation zone. Primary acinar tuberculosis focus transforms into lobular, then into segmental, lobar (development of lobar caseous pneumonia or primary pulmonary cavern).

PRIMARY TUBERCULOSIS

Mixed form of progression:

develops in weak patients after acute infections, in avitaminosis, hunger and oth.It is characterized by large primary focus, caseous bronchoadenitis, sometime with resolution of necrotic mass and fistula formation. In both lungs there are multiple tuberculosis foci.

PRIMARY TUBERCULOSIS

Outcomes of progression:

in negative cases death due to common generalization of process and tuberculosis meningitis;

in positive cases progression stops: exudative inflammation transform into proliferative, focus is encapsulated and calcificated.

PRIMARY TUBERCULOSIS

Peculiarities of primary chronic tuberculosis of lungs:

1) total caseous necrosis of lymph nodes;2) inclination to generalization with metastatic foci of extra pulmonary tuberculosis formation;3) hematogenous generalization of infection is accompanied with tuberculosis inflammation of serous coats (Tuberculosis polyserosiris – Plevritis, pericarditis) and activity of process in lymph nodes.

PRIMARY TUBERCULOSIS

Chronic primary tuberculosis arises in case of slowly progressive wavy course of specific process. It results in organism sensibilization: increase of it`s sensitivity to nonspecific agents and development of paraspecific reactions (diffuse and nodular proliferation of lymphocytes and macrophagocytes, fibrinoid changes in blood vessel wall, hyperplastic changes of hemopoietic tissue, disproteinosis, sometime amyloidosis.

HEMATOGENOUS TUBERCULOSIS

Arises and develops in organism after primary infection and healing, but in patients secondary foci or not full healed foci are kept in different organs and lymph nodes. Due to action of negative factors and hypersensitivity to tuberculosis latent process exacerbation arises.

Subvariants:1) generalized hematogenous tuberculosis;2) hematogenous tuberculosis with lungs lesion mainly;3) hematogenous tuberculosis with extrapulmonary lesions mainly.

HEMATOGENOUS TUBERCULOSIS

Generalized hematogenous tuberculosis is severe form of disease in which multiple tuberculosis tuberculum and

necrotic foci appear.

Depending on morphological substrate its 3 kinds are distinguished:

I. Acute tuberculosis sepsis (necrotic type),II. Acute general miliary tuberculosis,III. Acute general large focal tuberculosis .

HEMATOGENOUS TUBERCULOSIS

Hematogenous tuberculosis with lungs lesion mainly – most frequent form of pulmonary tuberculosis.

Variants: а) acute miliary lung tuberculosis;б) chronic miliary lung tuberculosis;в) chronic large focal tuberculosis of lungs.

HEMATOGENOUS TUBERCULOSIS

Chronic large focal tuberculosis of lungs is one of intermediate form of hematogenous tuberculosis with kept immunological features (appear in adult persons).

Main morphological signs: 1. symmetric damage of both lungs;2. mainly corticopleural localization of pathological process in lungs;3. predominance of proliferative reactions;4. development of diffuse net sclerosis;5. development of emphysema; 6. hypertrophy of right heart;7. absence of inclination to destruction;8. formation of caverns in the borderline zones of lungs and their symmetric localization;9. presence of extrapulmonary metastatic foci.

Generalized hematogenous tuberculosis

Hematogenous TUBERCULOSIS

Miliary tuberculosis of the lungs

Hematogenous tuberculosis, extrapulmonary lesions

Secondary tuberculosis

Formation of cavities in place of multiple

granulomas

Secondary tuberculosis

Forms of secondary tuberculosis of lungs: 1.acute focal tuberculosis; 2.fibrous focal tuberculosis; 3.infiltrative-pneumonic; 4.tuberculoma; 5.caseous pneumonia; 6.acute cavernous tuberculosis;7.fibrous cavernous tuberculosis; 8.cirrhotic tuberculosis.

Cavernous tuberculosis

Secondary tuberculosis

Secondary tuberculosis

Tuberculosis of the kidney

Tuberculosis of the kidney

TUBERCULOSIS

COMPLICATIONSIn primary tuberculosis: tuberculosis meningitis,

pleuritis, pericarditis, peritonitis.In tuberculosis of bones: sequesters, abscess,

deformations, fistula. In secondary tuberculosis complications are provided

by caverns: hemorrhage, rupture of wall and spreading into pleural cavity (empyema and pneumothorax).

Amyloidosis (complication of chronic purulent processes).

Tuberculosis complications: Amiloidosis

Tuberculosis complications: Amiloidosis

TUBERCULOSIS

Causes of death -the progression of a specific process, accompanied by severe intoxication and degeneration of parenchymal organs; swelling of the brain in the generalization of tuberculosis and miliary tuberculosis with tuberculous meningitis hydrocephalus in fibrosis in the soft meninges; -increasing with the development of renal failure, uremia with bilateral renal tuberculosis; -pulmonary bleeding from vascular wall cavity arrozirovannyh with the progression of pulmonary tuberculosis may be; -amyloid-lipoid nephrosis with progressive renal amyloidosis in general; chronic pulmonary heart disease, against which may develop acute pulmonary heart disease on the left type.

Office of Vitebsk region State service of medical forensic examinations. № 216 forensic examination of a corpse

FORENSIC MEDICAL DIAGNOSIS: Bilateral apical caseous pneumonia with abscess

formation. Focal tuberculosis more harmful lobe of right lung. MBT + (smear). Swelling of the brain. Serous pericarditis. Serous diffuse myocarditis. Sacral bedsore. Arterial hypertension: myocardial hypertrophy, the increase in the size and weight of the heart, not constrictive coronarosklerosis, diffuse small focal cardiosclerosis, arteriolonephrosklerosis. Atherosclerosis of the aorta (II Stage, 2 nd degree) and the base of the brain vessels. Steatosis. Liver fibrosis second degree.

Tissue the right upper lobe on the cut. 

SEPSIS

Sepsis is a generalized infection with immunosuppressive properties,

characterized by polyetiology and the acclivity

- of flow, which has some differences from other infectious diseases.

Etiological features of sepsis

Sepsis, polyetiologicaly has a variety of pathogens: Streptococcus, pneumococcus, meningococcus, Pseudomonas aeruginosa, Mycobacterium tuberculosis, fungi and other

microorganisms, but most often staphylococci, Klebsiella, Streptococcus and Pseudomonas

aeruginosa.

Epidemiological features of sepsisSepticemia is not contagious,

unless it takes place against a background of contagious infections (cavernous tuberculosis, typhoid, and others).

The clinical features of sepsisIn the course of the disease is not cyclical.

Regardless of the pathogen during monotonous. process:

1. very acute - acute (up to 2 or 3 days of lightning);

2. acute - up to 6 weeks; 3. subacute - more than 6 weeks (long); 4. chronically.

The clinical features of sepsis

Clinical signs of sepsis may be: -fever, chills, severe sweating; -tachypnea over 20 breaths per minute; -GNI disorder: insomnia, psychosis,

hallucinations; -hypotension, rapid pulse; -on the skin - petechial rash; -in the blood: anemia, leukocytosis, leukocyte shift

to the left, the increase in erythrocyte sedimentation rate;

-violation of diuresis: oliguria, anuria possible.

Immunological differences of sepsis: 

Fail to develop immunity.

Pathological differences of sepsis:  Local and general changes do not

have specific features, whereas other infections have

characteristic changes.

Pathological anatomy of sepsis

Local changes: Develop from the “entrance gate" of infection (septic focus).

From the septic focus infect the lymphatic and blood vessels throughout the body, getting into the bloodstream.In the case of spread through the lymphatic system arise

lymphangitis, lymphadenitis, may be lymphothrombose.In the case of distribution by the circulatory system occur phlebitis. Violation of the integrity of the endothelium of the veins leading to the formation of blood clots, often purulent.

Festering in the removal of a blood clot becomes an embolus - peddler of bacterial infection (thrombosebacteriamia

embolus).

Septic focus (septic endometritis). Atrium.

Septic focus. Phlegmonous-ulcerative appendicitis

а – infiltration of leukocytes,б – the destroyed mucosa.

в – in the lumen of the appendix pus.

Pneumonia with abscess formation. The lumen of the bronchus (a) and the cavity of many of the alveoli (b) are

filled with pus.

Thrombosebacteriamia embolism. Pustular or apostematose nephritis. On the left - in the context of

renal abscesses are seen. Right - on the surface of the kidney visible ulcers.

Bacterial thrombotic embolism - purulent nephritis. and - in the hearth of suppurative bacterial emboli are seen melting. b - the vessels

around the abscess rapidly expanded and more fulfilling.

Septic pulmonary infarction caused by thromboembolism.

Pathological anatomy of sepsis

General changes in the organs in sepsis:1. dystrophic,2. inflammatory,3. hyperplastic.Common degenerative changes occur in the

liver, kidneys, myocardium, muscle, central nervous system. Frequently degenerative changes go into necrobiotic that end necrosis.

General changes. Hyaline droplet degeneration of renal tubular epithelium.

General changes. Hydropic degeneration of renal tubular epithelium.

Balloon degeneration nephrotic. в- the large vacuoles, я - core, m - homogenized mitochondria.

General changes. Fatty degeneration of the myocardium.

Fatty liver. In the cytoplasm of hepatocytes visible droplets of fat.

Fatty degeneration of hepatocytes. The cytoplasm is filled with fat.

Hydropic degeneration of hepatocytes. в - on-site vacuole EPS m - modified mitochondria РБ - the remnants of

ribosomes.

Pathological anatomy of sepsis

Terms and inflammatory changesPresented mediate (interstitial) productive inflammation:Characterized by the presence of cellular infiltrate in the stroma of the organ.With the progression of interstitial inflammation occurs sclerosis and damaged parenchyma of the organ.At the heart valves may be polypus-ulcerative endocarditis. The valve is loose, pieces of it can come off and become an embolus.  Inflammatory changes are observed in the vessels - multiple vasculitis, it is one of the causes of hemorrhage.

Pathological anatomy of sepsis

Hyperplastic processes. Yellow marrow becomes red: in the blood increases the

number of immature white blood cells (leukemoid reaction).

There is hyperplasia of the lymph nodes, they increase in size with the advent of the reactive centers.

The spleen is flabby, is red and gives ample scraping the pulp (septic spleen).

Bacterial intoxication leads to an increase in the liver, jaundice may occur

Sepsis. Septic spleen. Abundant scraping the pulp.

Spleen with antigenic stimulation (hyper immunization).

Hyperplasia of lymph node and spleen. Visible accumulation of macrophages (macrophage

reaction).

Hyperplasia of the lymph node. Visible clusters plasmoblast stained Brochette pink.

Classification of sepsisTakes into account three features:etiology; the entrance gate; clinical and morphological. On the etiology distinguish streptococcal,

staphylococcal, pneumococcal, gonococcal, Pseudomonas, and other bacterias. The most common are staphylococcus and Pseudomonas aeruginosa.

Classification of sepsisDepending on the entrance gate. Prerequisite

for the development of sepsis is the formation of a septic focus.

Septic focus can be formed directly in the implementation of the pathogen. Such a center, and sepsis, is called the primary.

In other cases, the septic focus can evolve from a common source of infection (pneumonia with prolonged, chronic otitis, furunculosis). Such a septic focus, and sepsis, caused by them is called secondary. Secondary sepsis is a complication of infectious disease.

Localization of septic focus

pulmonary (most common in nosocomial infections associated with intubation);umbilical (primary focus is localized in the umbilical wound or umbilical vein);skin;urinogenous;tonsilogenny;mother (may be associated with criminal abortion, childbirth);otogenic (due to a primary septic focus in the ear due to exacerbation of chronic otitis media).cryptogenic.

Clinical and morphological forms of sepsis septicemia, pyosepticemia, bacterial endocarditis, hroniosepsis.

SepticemiaSepticemia - a form of sepsis, which is

characterized by: turbulent flow, expressed severe toxemia, often

develop bacterial (septic, toxic-infectious) shock;

the absence of suppurative focus (or he is small),purulent metastases;

takes place against a background of strong hyperergic reactions;

most often associated with streptococcal septicemia.

Pathological anatomy of septicemia No septic focus; hemolytic jaundice, icteric skin and sclera; hemorrhagic lesions (hemorrhagic syndrome); hyperplasia of lymphoid and hematopoietic tissues,

resulting in increased spleen, which is called "septic" (abundant scraping), lymph nodes increase, bone marrow hyperplasia (myelogram shift to the left).

in parenchymatous organs (liver, kidney, heart), an intermediate inflammation, increased vascular permeability of the tissue.

develop fibrinoid changes of vessel walls, allergic vasculitis.

Bacterial (septic, toxic-infectious) shock Bacterial shock can be defined as a condition

caused by microorganisms and their toxins, stimulates the activity of endogenous release of biological substances, leading to hypotension, disorders of central hemodynamics and microcirculation, dramatically reducing the oxygen in the tissue perfusion.

Bacterial shock

There are: - exotoxic shock (caused by gram-

positive flora, which has exotoxin) -endotoxic (lipopolysaccharide caused

by gram-negative microorganisms).

The pathogenesis of endotoxic shock, sepsis caused by gram-negative bacteria.

Aggravating factors of bacterial shockrough handling in the septic focus

(necrectomy, ligation with damage to granulation)

rapid intravenous administration of large doses of antibiotics that have antibacterial properties.

Pulmonary edema. In the alveoli visible filling of liquid, colored in pink.

Necrosis of renal tubular epithelium (necrotic nephrosis).

Syndrome Waterhouse-Friderichsen. On the left is normal, the increased right adrenal gland due to

extensive bleeding in meningococcal shock.

Purulent meningitis. a - a creamy exudate gives a dim view pia mater. в- in the accumulation of neutrophils in

subarachnoid space.

septicopyemia Septicopyemia - a form of sepsis, which is

characterized by: suppurative processes in the entrance of infection

and ulcers can be found in many tissues and organs (metastatic foci of inflammation). ;

hyperergic reaction is moderately expressed, and this form is not rapid flow;

caused by Staphylococcus aureus and Pseudomonas aeruginosa:

intoxication is often weak; gives a chronic sepsis.

Pathological anatomy septicopyemiaThere is a festering hotbed of lymphagenitis, lymphadenitis,

suppurative thrombophlebitis - a source of thromboembolism.

If thromboembolism of the veins of the systemic circulation, the first metastases occur in the pulmonary veins, and then in the organs of the systemic circulation: the spleen, liver, kidney, intestine, subcutaneous fat, bone marrow, synovial membranes, and heart valves (acute septic polypus-ulcerative endocarditis).

Hyperplastic processes are less pronounced than with septicemia. Found septic spleen, lymph nodes but can not be increased. No leukemoid reaction (myelogram and blood).

Mediate inflammatory reactions are mild or moderate.

Septic (bacterial) Endocarditis

This is a special form of sepsis, which is characterized by septic valvular heart disease.

Pathogens - staphylococcus, streptococcus, enterococcus.On the one hand for this disease is characterized by

hyperegic, as well as for septicemia, on the other side there is a septic focus on the valves of the heart, and the main damage is subjected to the cardiovascular system.

At present, it is shown that the disease is associated with circulating immune complexes in the body, containing the pathogen antigen and thus are the most toxic. Since the action of immune complexes associated increase in vascular permeability, vasculitis, etc.

Septic (bacterial) Endocarditis

By the nature of the flow divided into: Acute, up to 2 weeks; Subacute, up to 3 months; The protracted, lasting months or years.

Presence or absence of underlying disease are divided into:

Arising on intact valves - primary septic endocarditis (20-30% of cases).

Evolving in the modified (perverse) valves - secondary bacterial endocarditis (in 70-80% of cases, often against a background of rheumatic heart disease).

Pathological anatomy of septic endocarditis

Heart. In 75% of the cases affects the aortic valve (alone or in combination with mitral and others). On the valve there is polypous-ulcerative endocarditis. On the surface of the ulcer is formed thrombus. Often calcification occurs (post necrotic calcification).    The newly formed connective tissue deforms the wing valves and forms a heart defect. In the interstitial tissue infarction are found nodules (granulomas) develop myocarditis.

In the vascular system, particularly in the microvasculature are visible alterative, productive change: plazmorragiya and fibrinoid necrosis of endo-and perivasculities with the growth of connective tissue around the vessel. Inflammatory changes lead to the formation of aneurysms and their subsequent rupture. Especially dangerous aneurysm in the brain.

Septic pulpous-ulcerative endocarditis, the aortic valve.

Bacterial endocarditis. Are degraded vegetation, damaging the free edge of the mitral valve.

Pathological anatomy of septic endocarditis

The spleen is enlarged with infarcts of various limitations, as the spleen is affected first. Symptoms of hypersplenism: leucocytopenia, thrombocytopenia, and anemia.

Light struck a third of patients in the form of a heart attack (pulmonary embolism), pneumonia, pulmonary vasculitis, which manifests itself nonspecific pneumonia.

Kidneys. It often occurs as immunocomplex glomerulonephritis (hematuria, proteinuria. Cylindruria, hypertension, edema).

In the brain, heart attacks occur both on the grounds of thromboembolism and hemorrhage due to aneurysm rupture. In all patients, an infectious-toxic encephalopathia: headache, lethargy, and insomnia occurs.

Peripheral symptoms of septic endocarditis

The appearance of petechiae in the field squeezing of the skin. Petechiae in the conjunctiva of the eye from the inner corner of the

lower eyelid. Osler nodules (a manifestation of septic vasculitis) - painful thickening

on the palmar surface of the brush from the millet seed to a pea. Drumsticks (thickening of the phalanges) due to the soft tissues -

the proliferation of connective tissue, swelling of the periosteum. Hemorrhages in the skin (Janeway spots). Jaundice (hemolytic).

Frequent thromboembolic complications. If you take multiple thromboembolism in nature, this process is called thromboembolic syndrome.

Chroniosepsis Characterized by long-term healing septic focus.Outbreaks can be in carious teeth, tonsils, purulent

non-healing wounds.  Proceeds from long-term intoxication, which leads

to amyloidosis, and exhaustion. Changes in organs and tissues are atrophic in

nature. Patients can remain for a long time, a satisfactory

state of health. However, without proper treatment of the disease inevitably leads to death.

Amyloidosis of spleen (sago spleen).

Amyloidosis spleen. Much of the follicles replaced by amyloid.

Renal amyloidosis. Amyloid in the glomerular capillary.