TUBERCULOSIS

Tuberculosis. Primary, secondary and hematogenous tuberculosis. Morphological characteristics. Modern pathomorphosis tuberculosis.

Airborne respiratory infections.

TUBERCULOSIS

Etymologically, "mycobacterium" is derived from the Greek words ‘myces’ for fungus and ‘bakterium’ meaning small rod. The name "fungus" derives from the tendency of these microorganisms to spread diffusely over the surface of liquid medium in a mold like growth pattern.

According to the modern concept of clinical medicine, the term "Mycobacterium tuberculosis” which was discovered by the German scientist Robert Koch in the year 1882, unites the complex of four kinds of mycobacterium including: M. tuberculosis (MBT), M.bovis and its Bacilli Calmette-Guerin (BCG) variant, M.africanum and M.microti. There is a high degree of genetic relatedness in this group.

Mycobacterium tuberculosis is the major cause of tuberculosis in man. M.bovis and M.africanum can cause a disease clinically indistinguishable from classical tuberculosis. M.microti is not considered to be pathogenic for human beings but it can cause a disease resembling tuberculosis in rats. BCG strain is not а pathogenic for humans.

The given material about “Tuberculosis” in this textbook refers only to the disease caused by M. tuberculosis (MBT) or tubercle bacilli of Koch (BK), Typus humanus.

The natural reservoirs of MBT are – human, domestic and wild animals, birds.

MBT are slender, curved rods that are resistant (fast) to acids, alkalis, and dehydration. The cell wall contains complex waxes and glycolipids.

The MBT is not motile. The temperature borders or growth are between 29-42° C (optimum between 37-38° C). MBT is resistant to physical and chemical agents. MBT can endure very low temperatures and resist temperatures as high as 80° C for duration of 5 minutes.

MBT can survive for about 150 days in wet environment. When dry, MBT can cause TB in Guinea Pigs after an incubation period of 1 – 1.5 years. MBT in the lyophilized and frozen state has a viability of about 30 years.

MBT‘s viability is significantly reduced under intensive sunlight and under a high temperature environment. However, its viability remains significantly high when submitted to a damp and dark environment. MBT remains viable for several months when exposed outside host organism, especially in dark and damp rooms.

Mycobacterium tuberculosis

MBT has acid resistance (acid-fastness) that differ them from many other causative agents of the infection. Ziehl and Neelsen in 1883 developed a special method of MBT staining, based on acid-fastness of MBT.
A film preparation stained by carbol-fuchsine dye is decolorized by sulphuric acid and washing with water is processed by finish dyeing with methylene blue (Ziehl–Neelsen method).
In contrast to not acid-resisting bacteria MBT becomes apparent (having red color) at preservation of the coloring even after discoloration by acids and well stand out against blue background at microscopy. Ziehl–Neelsen method is still employed today.

Morphological changes of MBT. The morphology and the sizes of MBT are not constant, depending on the age of bacteria and, especially, on the condition of their environment and content of their nutrient medium.

The cord-factor. The lipids of the external membrane of MBT determine its virulence and formation of plait-like congestions (cord-factor) in nutrient medium. (

Koch noted about cord-factor in his initial report on the etiological agent of tuberculosis. First of all cord-factor related with virulence of M. tuberculosis. Formation of plait-like congestions was subsequently observed to occur among other mycobacterial species of lesser or having no virulence. Cord-factor was later identified as a highly unusual biological compound, trehalose 6,6-dimycolate, was observed to cause highly virulence, often lethal consequences when injected into experimental animals. However, the role of this compound in the pathogenesis of tuberculosis is unclear.

L-forms. One of the important features of MBT is its ability to produce L-forms The L-forms are characterized by reduced level of metabolism and weak virulence. Remaining viable L-forms can survive for a long time and produce anti-tubercular immunity.

The L-form differs from usual MBT by the expressed functional and morphological alterations. It has been discovered, that the transformation of MBT into the L-forms accelerated under long anti-bacterial therapy and under other factors, which inhibit the MBT growth, duplication and cell membrane formation.

It has been established, that L-forms can be found in the sputum of "MBT-negative" patients with destructive form of tuberculosis, capable, under the appropriate conditions, to be modified in rode-like variant which may cause reactivation of the tubercular process. Hence, elimination of MBT from cavities of such patients yet does not mean their sterilization from MBT.

MBT is resistant (tolerant) to many antibiotics. This property is connected first of all with highly hydrophobic cell surface, which serves as a physical barrier for chemical agents and antibiotics. The main reason of resistance is coded in the MBT genome.

MBT can become resistant to anti-tubercular drugs. Combined resistance of the MBT to several drugs considerably reduces efficiency of treatment of tuberculosis for last years.

As a result, the modern public health services deals not only with the dangerous infection of tuberculosis agent but also with the whole set of strains which are resistant against different drugs. In practice, for organizing of effective tuberculosis treatment, it is important not only to discover MBT, but in parallel (fast enough) to promptly determine its resistance – within two-three days in order to on time prescribe an effective chemotherapy.

During the late 80s of the last century a new method was discovered shortening the analysis process mentioned above. The new diagnostic test is based on selective amplification of nucleic acids (DNA or RNA) in vitro with the help of polymerase chain reaction (PCR).

This PCR method has a wide spectrum (the large opportunities) and serves as the base of exact DNA-diagnostics, which allows to identify any strain of MBT and to define the reason of the drug resistance.

The laboratory researches have shown that the occurrence of MBT resistance is connected with nucleotide replacements (mutations) in genes, encoding various enzymes, which directly influence with drugs.

Mutations in the gene katG, resulting in replacement of some amino acids in enzymes catalase and peroxidase are associated with resistance of some MTB strains to Isoniazid.

The resistance of MBT to Streptomycin is connected with missens mutation in a gene rpsL, coding S12 mitochondrial protein, or with nucleotide replacements in a gene rrs, coding 16S RNA.

The above submitted mutations in MBT genome are the only limited examples of formation of its resistance to anti-tuberculosis drugs. On this basis it is possible to make the following conclusion: introduction of new drugs in chemotherapy of tuberculosis leads to new mutations in МBT, resulting to resistance without exception of all used drugs and in this circumstance it is necessary to constantly take into consideration the tactics of tuberculosis treatment.

In spite of great advances in chemotherapy and immunology, tuberculosis still continues to be worldwide in distribution, more common in developing countries of Africa, Latin America and Asia.

FORMS AND FEATURES OF PULMONARY TUBERCULOSIS*

Stage	Immune Reactivity	Clinicopathologic Features
Stage 1 (primary)
a. Initial infection	No immunity	Clinically inapparent nonspecific alveolitis
b. Initial infection	Developing immunity	Ghon's primary affection: isolated granulomatous reaction, most commonly in right upper lobe
 Primary lymphatic spread	Developing immunity	Lymphatic spread of infection to regional lymph nodes with respective granulomas: Ranke primary complex
Stage II (early postprimary generalization)
a. Lymphatic spread	Good	Isolated subpleural caseous granuloma, upper segments of right upper lobe
b. Bronchogenic spread	Intermediate	Acinar-nodular pulmonary tuberculosis with progressive caseous granulomas
b. Bronchogenic spread	Poor	Progressive caseous pneumonia without prominent granulomatous reaction
 Hematogenous spread	Intermediate	Systemic hematogenous caseous granulomas of different sizes (ie, different ages)
(late postprimary generalization)
d. Hematogenous spread	Nonimmune —> reactive	Miliary tuberculosis with systemic granulomas of uniform size (and age)
e. Hematogenous spread (also in early postprimary spread)	A-reactive	Miliary systemic necroses, tuberculosepsis acutissima, typhobacillosis Landouzy
Stage III (isolated organ tuberculosis)	High	Limited spread in isolated organs: cavernous pulmonary of renal tuberculosis, isolated tuberculomas (granulomas) in brain, spine, and other organs
Late generalization	High —> low	Local or systemic spread of isolated organ tuberculosis (lymphatic, bronchogenic, or hematogenous)

*The degree of immune reactivity (not resistance to disease) can be monitored by tuberculin skin testing; toxicity of tubercle bacteria is partly determined ird t.K tor."

The disease spreads in the body by various routes:

1. Local spread. This takes place by macrophages carrying the bacilli into the surrounding tissues.

2. Lymphatic spread. Tuberculosis is primarily an infection of lymphoid tissues. The bacilli may pass into lymphoid follicles ofpharynx, bronchi, intestines or regional lymph nodes resulting in regional tuberculous lymphadenitis which is typical of childhood infections. Primary complex is primary focus with lymphangitis and lymphadenitis.

3. Hematogenous spread. This occurs either as a result of tuberculous bacillemia because of the drainage of lymphatics into the venous system or due to caseous material escaping through ulcerated wall of a vein. This produces millet seed-sized lesions in

different organs of the body like lungs, liver, kidneys, bones and other tissues and is known as miliary tuberculosis.

Classification of tuberculosis. Tuberculosis is classified according to the clinical course into: tuberculosis of children and teenagers, tuberculosis of the lungs, tuberculosis of the other organs and systems.

There are 3 clinico-morphological types of tuberculosis:

1. Primary tuberculosis.

2. Secondary tuberculosis.

3. Hematogenic tuberculosis.

The most common pattern of human tuberculosis (TB) is pulmonary. The tuberculosis organism is inhaled into the alveolar spaces of the lung, but other tissues are also affected.

The main morphological characteristic of rnberculous is granuloma (rnbercle) formation in the affected areas. Each tubercle has an area of caseous tissue necrosis at its center. This is characterized by its homogeneity, and no ghost pattern of the original tissue structure remains. Viable mycobacteria are present within the necrotic debris.

Macroscopically, this necrotic tissue resembles cream cheese, hence its descriptive name caseous necrosis. The reason for the necrosis at the center of tubercles is uncertain, as it is not seen in the center of granulomas caused by other agents. A rnbercle is composed of activated macrophages with surrounding lymphoid cells and fibroblasts. The structure of a typical tuberculous granuloma is as follows: around the central area of caseous necrosis lies a collection of large, activated macrophages.

Histologically, this functional activation is manifest by the presence of bulky pale-staining granular cytoplasm, which is rich in endoplasmic reticulum. Because of a minimal resemblance to some epithelial cells, the term epithelioid cells was originally coined for these macrophages. Some of the activated macrophages cells fuse to form large multinucleate cells with many nuclei arranged around the periphery, and a large central cytoplasmic mass. In TB these giant macrophages are called Langhans’ cells. Around the zone of macrophages bordering the central caseous necrosis lies a collar of lymphocytes, reflecting the immunological response to the presence of mycobacteria.

As the tubercle persists, some fibroblasts appear within the lymphocyte collar and outside it. These are recruited by secretion of cytokines from the activated macrophages.

The outcome of tubercie formation depends on the balance between two conflicting sets of factors: those predisposing to extension of infection (ingestion of large numbers of highly virulent organisms, poor immune response) and those predisposing to containment, or healing and eradication of infection (ingestion of small numbers of poorly virulent organisms, good immune response, administration of appropriate antibiotics).

The outcomes of a granuloma may be:

1. The caseous material may undergo liquefaction and extend into surrounding soft tissues, discharging the contents on the surface. This is called cold abscess although there are no pus cells in it.

2. In tuberculosis of bones, joints, lymphnodes and epididymis, sinuses are formed and the sinus tracts are lined with tuberculous granulation tissue.

3. The adjacent granulomas may coalesce together enlarging the lesion which is surrounded by progressive fibrosis.

4. In granuloma enclosed by fibrous tissue, calcium salts may get deposited in the caseous material (dystrophic calcification) and sometimes the lesion may even get ossified over the years.

Pathogenesis: beginnings, clinical course and the consequences of illness depend on reactivity of organism. A value is important in pathogenesis belongs to support of virulence of agent in an organism, intercommunication between a hypersensitiveness and antituberculous immunity, specific defeat of tissues and development of caseouse (cheesy) necrosis. At the beginning of illness inflammation does not have characteristic signs, but in 2-3 weeks adopts specific granulomatous character. The permanent change of immunological reactions (hyperergy-immunity-hyperergy) lies in basis of undulating clinical course. Distinguish primary, hematogenic (after primary) and second clinic-morphological forms of tuberculosis.

Primary tuberculosis

It develops at the first hit of mycobacterium in an organism (child's or youth, rarer adult age). Thus, as a rule, the reaction of hypersensitiveness of immediate type develops with predominance of exudative-necrotic changes and inclination to generalization of infectious process.

Morphological expression of primary tuberculosis is a primary tubercular complex which consists of primary tubercular affect, lymphangitis and specific lymphadenitis.

A primary tubercular affect is a focus of specific inflammation which arises up in the place of primary accumulation of mycobacteris of tuberculosis. At the aerogenic way of infection a process appears subpleural, mainly in III, VIII, IX or the X segments more frequent of right lungs.

Macroscopically it is the focus of caseous necrosis of primrose of dense consistency by the sizes of hazel-nut, fibrinous inflammation develops on pleura.

Microscopically - at first acinous exudative pneumonia develops, later is focus of caseous pneumonia, which is limited a serous edema and lymphocytic infiltration with the next forming of tubercular granuloma. Exudate is quickly added necrosis. At an alimentary way of infection a primary affect is formed in lymphoid formations of lower department of jejunum or caecum with development of ulcer. A primary tubercular affect can also appear in tonsils (quinsy) or on the skin (ulcer of skin).

Specific tubercular lymphangitis is inflammation of divert lymphatic vessels from a primary affect to the regional lymphatic node, which is characterized lymphocytic infiltration of wall with formation of tubercular granuloma.

Tubercular lymphadenitis is specific granulomatosis inflammation of regional (bronchopulmonary, bronchial, bifurcative) lymphatic nodes with quickly growth of caseous necrosis.

Three variants of clinical course of primary tubercular complex are possible:

1) cicatrization; 2) progress; 3) chronic clinical course.

Cicatrization of primary complex regardless of it localization begins from resorption of perifocal inflammation. Exudation inflammation changes productive, a bank from epithelial cells appears, and in subsequent connective tissue membrane. Caseous necrotic masses are dehydrated and a lime is put aside in them, than fossilization became. From the giant cells of resorption of necrotic masses the plates of bones appear the way of metaplasia with red marrow. Such fossilizated and ossified focuses of primary affect are healed obtained the name of focus of Gona. Parallel there is a sclerosis after motion of lymphangitis, and also sclerosis and fossilization of the initially staggered lymphatic nodes. In place of tubercular ulcer in a bowel a scar appears also. In the focus of Gona mycobacteris are saved for ten years which predetermines unsterile immunity.

Progress of primary tuberculosis can have four varieties: growth of primary affect, hematogenic, lymphogenic and a mixed form.

Growth of primary affect is the heaviest form of progress of primary tuberculosis. Essence consists in that arises up round primary caseous pneumonia, as it is known, not productive inflammation, but exudation. The fresh areas of exudative inflammation are quickly added necrosis and meet between it self - partial caseous pneumonia develops (fleeting pulmonary consumptions). Necrotic masses can dissolve in addition, and a primary pulmonary cavity takes place in them.

Hematogenic is a form of progress that arises up at the hit of mycobacteris from a primary affect or from caseous lymphadenitis in the circulatory system bloodstream, later they settle in preliminary sensitized tissues of organs with development of humps by sizes from miliary (miliary tuberculosis) to large, size from pea (macrofocal form of hematogenic spreading). In cases of favorable motion such focus are in bones, bodies of vertebrae, privy parts, kidneys encapsulated and others like that, in that number in top of lungs (focus of Simon). Development of tubercular eptomeningitis is dangerous.

Lymphogenic is the form of progress of primary tuberculosis that is characterized by gradual involvement in the process of all new lymphatic nodes: bronchial, bifurcational, paratracheal, submaxillary and others like that, with development in them of caseous necrosis. Especially dangerous is tubercular bronchadenitis, when lymphatic nodes squeeze clearance of bronchial tubes, or necrotic process passes to the tissue of mediastinum, sometimes with formation offistulas. At primary intestinal tuberculosis development of tubercular mesenteric lymphadenitis is possible.

The mixed form of progress of primary tuberculosis most often develops at the persons impaired by infections, operations, by starvation and others like that.

Death at the time of progress of primary tuberculosis mainly comes from tubercular meningitis, peritonitis or generalizated defeat of internal organs. At timely treatment focuses are encapsulated, but they can be the source of development of hematogenic tuberculosis.

Chronic motion of primary tuberculosis is observed in such cases: - a primary affect heals over, and in lymphostasis complex processes of cicatrization are changing with Acuteening yet; - at formation of primary pulmonary cavity and development of primary pulmonary consumptions. It causes sensitizing of organism. As a reply to it there are paraspecific displays in internal organs: diffuse or node proliferation of lymphocytes and macrophages, hyperplasia of organs of hemogenic, fibrinoid change of connecting tissues, arterioles, disproteinosis sometimes amyloidosis. Paraspecific reaction in joints at the cours of clinic of primary tuberculosis is known under the name of rheumatism of Ponse.

Hematogenic tuberculosis arises up at persons, who clinically got better from primary tuberculosis, but at them an infection is saved in the not fully healed focuses, there are focuses of the hematogenic sifting out and the stored is promoted sensitiveness to the tuberculin on a background the produced immunity to mycobacteria. At unfavorable terms (trauma, inflammation, avitaminosis, stress and others like that) an infection from the focus of inflammation in place screening, or latently running across lymphadenitis gets to the circulatory system bloodstream. The features of this form of tuberculosis are: predominance of productive reactions of tissues (formation of granuloma); - inclination is expressed to hematogenic generalization; it is a defeat of different organs and tissues. Select three varieties of hematogenic tuberculosis: 1) generalization, 2) hematogenic with the overwhelming damage of lungs, 3) hematogenic, from mainly by extrapulmonary damages.

Generalized hematogenic tuberculosis is the heaviest form. It arises out of focuses of screening, which arose up in different organs in the period of progress of primary tuberculosis and did not prove long time. Inflammation shows up development of plural humps in the internal organs with predominance of necrosis above exudation and prolypheration (quick as fulminant tubercular sepsis), or miliary humps with predominance of productive reaction (acute general miliary tuberculosis). They are often completed development of meningitis. Sometimes there is macrofocal general tuberculosis which is characterized by formation of large focuses of specific inflammation in different organs.

Hematogenic tuberculosis with the overwhelming defeat of lungs arises up as a result of their infecting from the focuses of screening, which mainly take place in privy parts or lymphatic nodes. Because mycobacteria act with the flow of blood the defeat of lungs is always bilateral, reflect. Acute and chronic forms distinguish. At the time of presence of little humps it we speak about miliary tuberculosis, at the time of presence of large - macrofocal. Chronic macrofocal or hematogenic-disseminated tuberculosis occurres at adults and characterized by followings signs: - mainly corticoplevural localization of focuses in both lungs; it is predominance of productive reaction; it is development of reticulated pneumofibrosis and emphysema of lungs; it is presence of the pressed cavities; it is hypertrophy of right ventricle of heart; it is presence of extrapulmonary tubercular focus. At chronic motion often there is scarring of humps, development of emphysema, cavity and, as a result, hypertension of small circle of circulation of blood with development of pulmonary heart.

Hematogenic tuberculosis form mainly develops a extrapulmonary defeat from focuses - screening, by bringing in the agent into one or other organ of hematogenic way in a period of the primary infecting. It can be acute and chronic. Distinguish the followings forms: osteoarticular, with the defeat of cerebrum, urogenital system, skin. A osteoarticular form is presented by tubercular spondilosis, coxitis, gonitis. Scoliosis, kyphoscoliosis, lordoscoliosis often develops. In a cerebrum tubercular leptomeningitis or tuberculomas develop in large hemispheres or cerebellum. Tuberculosis of the urogenital system shows up interstitial tubercular nephrite, inflammation of testicle and his additions, prostatitis, vesiculitis at men and endometritis and adnexitis at women. Tuberculosis of privy parts often ends with sterility.

Secondary tuberculosis

Tuberculosis, which comes after carried out primary, on a background of certain, although unstable immunity. It is caused by repeated superinfection, or the revivification process in place of focal screening in lungs after primary tuberculosis. It is often drawn by the decline of resistance of organism. Features of the secondary tuberculosis: - localized only in lungs, - has intracapillary spreading from an apex to basis, - there is unspecific inflammation in lymphatic nodes, - a change of clinic-morphologic phases is the display of his clinic-morphologic forms.

Distinguish the followings clinic-morphologic forms of the secondary tuberculosis:

1) Acute focal;

2) fibrous-focal;

3) infiltrative

4) tuberculoma;

5) caseous pneumonia;

6) Acute cavernous;

7) fibrous-cavernous;

8) cirrotic.

Acute focal secondary tuberculosis begins with inflammation of bronchioles in the focuses of screening of primary tuberculosis, which take place in I and II segments, mainly right lungs. Bronchitis quickly passes to panbronchitis with spreading of specific inflammation on peribronchial pulmonary tissue. In the peribronchial develops caseous pneumonia which is limited epithelioid and limphoid cells, there are cells of Pirogova-Langhansa. Such morphological complex (Bronchitis, panbronchitis, caseous pneumonia) is one-sided which will not outgoing of I-II segments of lungs it is adopted the focus of reinfection of Abricosov, or by acute focal tuberculosis. At cicatrization of such focuses of caseous bronchopneumonia appear petrifications or focuses Ashoff-Pul.

Fibrous-focal tuberculosis is the phase of course of acute focal tuberculosis, which combines in it self, both manifestations of cicatrization (encapsulation, fossilization) and of alteration of acinous and nodose focuses of caseous pneumonia. Arises up in place of focuses of Ashoff-Pul, which feed a large weakness to acuteening. Thus, morphologically at the time of fibrous-focal tuberculosis there are focuses of Simon (encapsulated and petrificated focuses of screening of primary tuberculosis), focuses of Ashoff-Pul and cells of caseous pneumonia. The feature of focuses of Simon consists in that they always are petrificated and encapsulated (but do not contain ossificates, as a focus of Gon), take place symmetric in the apexes of lungs, considerably more little and there are partly petrificated focuses of Ashoff-Pul are encapsulated.

Infiltration tuberculosis arises up at progress of acute focal or acuteening of fibrous-focal. Unspecific perifocal inflammation occupies the considerable areas of pulmonary tissue round the insignificant focuses of caseous necrosis and goes out outside a particle and even segment, goes down below the projection of clavicle on a lung. Such roentgenologic picture was described by Asman and Redeker, and a focus was named a focal infiltration of Asman-Redeker. Unspecific inflammation can resolve and then the focus of defeat adopts character of fibrous-focal tuberculosis. However, it is known, three forms of evolution of іnfiltrative tuberculosis: it is a transition in tuberculoma, - caseous pneumonia, it is cavernous tuberculosis.

Roentgenologically tuberculoma reminds a tumour. Morphologically the focus of caseous necrosis is by sizes to 5 cm, which is restricted by a fibrous capsule. More frequent localized in I or II segments of upper particle of right lungs. Essence consists in the citrization of іnfiltrative tuberculosis unspecific perifocal inflammation resolves, and the focus of caseous necrosis became restricted by a capsule.

Caseous pneumonia arises up in cases of progress of іnfiltrative tuberculosis, when caseous changes begin to prevail above perifocal unspecific inflammation, quite often spreading on all particles of lungs. Mainly it develops at persons with low resistance of organism.

Acute cavernous tuberculosis is the result of the festering melting and dissolution of caseous masses in the focus of іnfiltration of Asmana-Redekera or tuberculoma. Necrotic masses are excreted with a mucous, and a cavity which has a round, oval or wrong form and connected with clearance of segmental bronchial tube appears in them place. Its internal wall is presented by caseous masses, and external - by packed through inflammation pulmonary tissue. This form of the secondary tuberculosis is dangerous by the bronchogenic semination of lungs, and also excretion of mycobacteria with mucous on outwardly.

Fibrous-cavernous tuberculosis arises up as a result of sclerose of external layer of sclerosed of cavity wall. It has chronic course and is called chronic pulmonary consumptions too. The wall of cavity is dense, morphologically distinguish three layers in it: 1) necrotic (pyogenous), rich in leucocytes; 2) tubercular granulation tissue; 3) connective tissue. Its internal surface is rough with crossings beams which show by themselves sclerosed vessels and bronchial tubes, and external - with the focuses of inflammation (depending on a tissue reaction) and bronchiectases. By bronchogenic way with mucous a process spreads on neighbouring areas or even on the second lung .

Cirrotic tuberculosis is the final phase of the secondary tuberculosis. It shows up in considerable development of connecting tissue, by the presence of chronic cavities, scars, emphysema, bronchiectases, sclerosis of vessels, accretions of pleurae, deformation of lungs.

Complications of tuberculosis are numerous: meningitis, pleurisy, pericarditis, abscesses, fistulas, perifocal inflammations, can develop at the time of primary tuberculosis; at the time of secondary tuberculosis - bleeding, pneumatothorax, empyema of pleura, amyloidosis of internal organs, development of pulmonary heart develop.

Death mainly is caused by the indicated complications, chronic insufficiency of pulmonary heart, uremia.

This is an acid fast stain of Mycobacterium tuberculosis (MTB). Note the red rods--hence the terminology for MTB in histologic sections or smears: acid fast bacilli.

Mycobacteria can also be stained with auramine and viewed with fluorescence microscopy, in which acid fast bacilli now appear as glowing yellow rods. This method is easier to use to screen for mycobacteria and is the method routinely used in sputum specimens sent to the laboratory.

This spleen shows a miliary pattern of granulomatous inflammation, with numerous small tan granulomas. This suggests a poor immune response. This patient had AIDS. The infection turned out to be Mycobacterium avium-intracellulare (MAI), also known as Mycobacterium avium-complex (MAC).

The lymph nodes in this mesentery, best seen at the left, are enlarged and have cut surfaces that appear yellow-tan. These nodes are filled with sheets of Mycobacterium avium-complex (MAC).

Here are numerous confluent granulomas in upper lung fields in a case of active pulmonary tuberculosis.

Grossly, a granuloma tends to be a focal lesion. Seen here in a hilar lymph node is a granuloma. Granulomas due to infectious agents such as mycobacteria are often described as "caseating" when they have prominent caseous necrosis.

Here are two pulmonary granulomas. Granulomatous inflammation typically consists of mixtures of cells including epithelioid macrophages, giant cells, lymphocytes, plasma cells, and fibroblasts. There may even be some neutrophils.

Giant cells are a "committee" of epithelioid macrophages. Seen here are two Langhans type giant cells in which the nuclei are lined up around the periphery of the cell. Additional pink epithelioid macrophages compose most of the rest of the granuloma.

This is a caseating granuloma. Epithelioid cells surround a central area of necrosis that appears irregular, amorphous, and pink. Grossly, areas of caseation appear cheese-like.

With a poor immune response to the agents producing granulomatous inflammation, there can be extensive spread of infection with the production of a "miliary" pattern of granulomas, as seen here in the lung of a patient with miliary tuberculosis. The 1 to 2 mm granulomas are scattered around like millet seeds (millet is a type of cereal grain).

Here is the gross appearance of a lung with tuberculosis. Scattered tan granulomas are present, mostly in the upper lung fields. Some of the larger granulomas have central caseation. Granulomatous disease of the lung grossly appears as irregularly sized rounded nodules that are firm and tan. Larger nodules may have central necrosis known as caseation--a process of necrosis that includes elements of both liquefactive and coagulative necrosis).

On closer inspection, the granulomas have areas of caseous necrosis. This is very extensive granulomatous disease. This pattern of multiple caseating granulomas primarily in the upper lobes is most characteristic of secondary (reactivation) tuberculosis. However, fungal granulomas (histoplasmosis, cryptococcosis, coccidioidomycosis) can mimic this pattern as well.

There is a small tan-yellow subpleural granuloma in the mid-lung field on the right. In the hilum is a small yellow tan granuloma in a hilar lymph node next to a bronchus. This is the "Ghon complex" that is the characteristic gross appearance with primary tuberculosis. In most persons, the granulomatous disease will not progress. Over time, the granulomas decrease in size and can calcify, leaving a focal calcified spot on a chest radiograph that suggests remote granulomatous disease.

The Ghon complex is seen here at closer range. Primary tuberculosis is the pattern seen with initial infection with tuberculosis in children. Reactivation, or secondary tuberculosis, is more typically seen in adults.

At high magnification, the granuloma demonstrates that the epithelioid macrophages are elongated with long, pale nuclei and pink cytoplasm. The macrophages organize into committees called giant cells. The typical giant cell for infectious granulomas is called a Langhans giant cell and has the nuclei lined up along one edge of the cell. The process of granulomatous inflammation takes place over months to years (did you ever hear of a committee action that was completed in a short time?)

туберкулома леге

Tuberculoma

интерстициал пневмон+сотовое легк

Milliar tuberculosis of the lung.

туб очаг легкого

Fibrous-focal tuberculosis.

абсцес леген-7

Cavernous tuberculosis.

Tuberculous lymphadenopathy.

The boy isemaciated, as is usual with patients with disseminated.

Tuberculous meningitis. Note the opacity of the leptomeninges covering the interpeduncular cistern. The pus tends to accumulate along the base of the brain in TB meningitis.

Acute viral respiratory infections

Among ARVI most often we observe influenza, parainfluenza, adenovirus and respiratory-syncytial infection.

Influenza (grippe, French. - to grab) is an acute viral disease of respiratory ways with spreading on the respiratory area of lungs, characterized by their catarrhal inflammation, primary and secondry virusemia, oppressing the protective systems of organism and expressed intoxication.

Etiology. An agent is pneumotropic RNA-containing viri of three conditioned serologic kinds of antigens A, (A1, A2), B, C. Antigenic tunic of virus is apt at changeability which causes development of the repeated epidemics.

Electron micrograph of influenza A virus.

Pathogenesis. With the drops of mucus of sick man, approximately on the2-3d day of illness, at the time of cough and sneeze virus gets on the epithelium of upper respiratory tracts and due to the presence of specific receptors of lipoglycoproteid tunic (capsid) is adsorbed by these cells. Such antigen of capsid, as neuraminidase dissolves the tunic of prismatic epithelium and an agent gets to the middle of cell of owner, and RNA - polymerase activates reproduction of virus. Reproduction of it takes place and in endothelium of capillaries, which draws primary virusemia. Characteristically is that virus, which submerged in an epithelium not only propagates oneself but also draws the cytolytic influence, causing necrosis and desquamation. Virus frees oneself, and populates all cell areas of respiratory ways, causing catarrhal inflammation. A characteristic feature is desquamation of epithelium by layers, and also presence in their cytoplasm of basophilous (microcolony of virus) and oxyphyle (focal destruction) of organelles. Violation of integrity of epithelium barrier of bronchial tubes, alveoli determines possibility of development of secondry virusemia. At this time such negative possibilities of virus, as a angiopathyc action (plethora, spasm, plasm- and haemorrhage) and oppressing protective forces of organism (phagocytosis of neutrophil, oppressing chemotaxis and phagocytosis of monocytes, development of allergy) show up most brightly. These properties of agent determine possibility of joining of the second infection, character of local and commons displays of illness.

Pathological anatomy. In motion illnesses, middle weight and heavy forms of influenza are easily possible.

Easy (ambulatory) form of influenza. It lasts for 5-6 days. It is characterized by catarrhal inflammation of mucus tunic of nose, pharynx, and larynges. It shows up hyperemia, increased formation of eyewater, and also by dystrophy, necrosis and exfoliation of epithelium.

Influenza of middle weight. Heavily flows at pectoral children, people of old age and patients with cardio-vascular pathology. It is characterized by distribution of catarrh on trachea, bronchioles and alveoli, often with the origin of focal necrosis of mucus tunic. Bronchopneumonia which can pass to protracted or chronic forms which develop in lungs. Sometimes cardiac insufficiency causes death.

Heavy form of influenza. Two variants are distinguished in its motion:

1 - with predominance of intoxication,

2 - with predominance of pulmonary complications.

The heavy form of influenza with predominance of intoxication has malignant fleeting character (patients perish in 4-6 days). On a section find out hemorrhagic tracheobronchitis and acinous bronchopneumonia, petechial hemorrhages in internal organs and cerebrum.

The heavy form of influenza with predominance of pulmonary complications also has malignant motion. On a background of expressed intoxication in respiratory tracts fibrinogenous- hemorrhagic inflammation develops with passing to mucus tunic of trachea and bronchial tubes with subsequent development of the necrotic phenomenon, and also focuses of abscess formation, hemorrhages in organ parenchyma. Lungs are enlarge in size, have the pied colouring on a cut (“large pied lung”).

Complications and causes of death. Patients die mainly from complications predefined by intoxication, damage of vascular bloodstream and joining of the secondary infection. Yes, intoxication causes dystrophy of cardiomyocytes, and dystrophy and necrobiosis of intramural nervous ganglions of heart can cause its stop. Stasis, hyaline blood clots are causes of cerebral edema with wedging of cerebellum tonsils into the large cervical opening, and also hemorrhages. Joining of bacterial infection which is predefined oppressing the immune system assists development of pneumonia complicated by an abscess, sometimes abscesses of cerebrum and festering meningoencephalitis.

Parainfluenza (para, grets. - near) is influenza -like illness which is caused by the virus of parainfluenza, characterized by the catarrh of respiratory tracts, moderate general intoxication and inflammation of conjunctiva and lymph nodes.

Etiology. Agent of parainfluenza is pneumotropic RNA-containing virus of I-IV types, family of Paramyxovirus.

Pathogenesis is similar to such at the time of influenza, but intoxication is expressed insignificantly. It is proved that the virus of parainfluenza has ability to reproduce itself not only in the epithelium of respiratory ways and endothelium of capillaries but also in the cells of ependyma of vascular interlacements of cerebrum. Like, virus of parainfluenza, as well as the one of influenza, is capable of repressing protective forces of organism.

Pathological anatomy. Illness which is caused by the virus of parainfluenza of I or II type morphologically corresponds to the clinic- morphological displays of easy form of influenza, but often there is an unreal croup, especially children have it, as a result of edema of larynx and pharynx. Virus of parainfluenza of III type damages bronchioles and alveoli with development of peribronchial pneumonia, and virus of IV type causes intoxication which is less expressed, than at the time of influenza. The feature of morphological changes of trachea, bronchial tubes and alveoli is proliferation of epithelium, with appearance of polymorphic cells which contain a few pyknotic nuclei.

Complications of parainfluenza are observed as a result of joining of the secondary bacterial infection. Bronchopneumonia, quinsy, sinusitis, otitis develop most often, eustachitis.

Death can be caused by asphyxia at the time of unreal croup or pulmonary complications.

Adenoviral infection is an acute respiratory infection, caused by adenovіri and characterized by the damage of respiratory ways, conjunctiva, lymphoid tissue of throat and pharynx, sometimes - intestines and lymph nodes of abdominal area.

Etiology. Adenovіri – is a group of DNA - containing viri.

Pathogenesis. Infection is passed by a respiratory way. Virus gets into the epithelium of the respiratory way, viral DNA is transformed in nuclei, where its reproduction is realized. The viral intranuclear includings draw the lytic action on a cell. The exit of agent from the lost cell predetermines intoxication. a generalization of process on other organs and tissues, and also joining of the secondary infection is possible.

Pathological anatomy. Morphological displays depend on weight of illness.

Easy form of adenoviral infection is characterized by acute catarrhal inflammation of upper respiratory tracts, conjunctiva and regional lymphadenitis. Adenoviral pneumonia often develops at children. Diagnostic signs are: presence of adenoviral cells (polynuclear), presence of the fuchsin-free including in the cytoplasm, nuclei are enlarged through the presence of including adenoviruses.

Adenovirus pneumonia

Heavy form can be conditioned by predominance of generalization of virus or predominance of the secondary bacterial infection. At the time of the generalization of infection there is reproduction of virus in epithelial cells of intestines, liver, kidneys, pancreas, ganglionic nerve cells of cerebrum. Adenoviral cells appear thus. At the time of predominance of the secondary bacterial infection, on a background a generalization of virus, suppuration and necrosis appear morphologically.

Complications are mainly caused by the secondary bacterial infection with development of otitis, sinusitis, quinsies, pneumonia.

Death is caused by suppurative processes in lungs, and also adenoviral pneumonias and defeats of cerebrum at the time of generalization of infection.

Adenovirus hepatitis

Respiratory syncytial infection is an acute infectious disease which is caused by respiratory syncytial virus.

Etiology. It is caused by the RNA containing virus of family of Paramyxoviridae, which is able to form in a culture of giant cells and syncytium.

Pathogenesis. It is similar to such at the time of parainfluenza and influenza. At the children of junior age the process begins from a defeat of lungs, and then passes to the bronchial tubes. At the children of senior age and adults it is restricted by upper respiratory tracts. Generalization of infection is possible.

This electron micrograph of respiratory syncytial virus (RSV).

Pathological anatomy. Morphologically illness shows up by laryngotracheobronchitis, by a bronchitis and bronchopneumonia. Histological proliferation of epithelium appears as papillae and layers which draw the obstruction of bronchial tubes with development of acute emphysema and atelectasis. In the time of inflammatory exudation there are a lot of large cells which form symplasts, often immunological alteration of organism takes place. In easy cases changes show up the serous catarrh of mucus tunic of upper respiratory tracts. A festering or festering-ulcerous catarrh develops rarer. At the time of generalization of infection cellular inflammatory infiltration and papillary excrescences of epithelium appear in intestines, pancreas, kidneys, in ependyma of cerebral ventricles.

Complications are mainly pulmonary as a result of joining of the secondary infection. In serious cases death is caused by pneumonia, generalization of infection.

Prion illnesses are caused by the modified proteins which do not have nucleic acids. The followings diseases belong to this group of illnesses take: kuru, which is associated with cannibalism; illness of Creytsfeldt - Yakob, which is related with transplantation of cornea; bovine porous encephalopathy which is so-called illness of cow rabies; atypical illness of Creytsfeldt - Yakob, which is passed to humanbeings with food products from animals, which are ill incow rabies.

Pathogenesis - the protracted latent period, permanent making progress motion, neurotropy, high lethality. Mіcrocystous regeneration of grey matter of cerebrum with surplus of hypertrophied astrocytusis is typical for prion illnesses and making progress death of neurons.

Measles

Measles is an acute highly contagious infectious disease which manifests itself by the catarrhal inflammation of overhead mycoses lay of respiratory tracts, conjunctiva, maculo-papulous eruption on skin.

Etiology and pathogenesis .The agent is a DNA-virus which is passed by respiratory way from a patient into mucous tunic of the upper respiratory tracts, eyes conjunctive of a healthy man, then gets to blood with the development of virusemia. Virus has an ability to reduce the barrier function of epithelium, phagocytic activity, represses the immune system.

Pathomorphology. In the mucous tunic edema, plethora, the secretion of mucus, lymphohistiocytic infiltration is promoted, sometimes in an epithelium there are vacuolar dystrophy, methaplasy, exfoliation and necrotic changes. Mucus becomes dingy, of grey-yellow color. Edema and necrosis of the mucous tunic of larynx brought to the development of unreal croup. In the consequence of virusemia thre is the appearance of enantem and exanthema. Enanthema is white spots of Bilshovskiy-Filatov-Coplic on mucous tunic of cheeks near small lower cheek-teeth. Exanthema is the large maculo-papulous eruption on the skin on face, neck, trunk, etc. At microscopic researches of the eruption we find edema, hyperemia, perivasculitis lymphohistiocytic infiltration in a papillary tunic, to the vacuolisation epidermis, sometimes parakeratosis. In the immune system there is the prolypheration with plasmatisation of B-dependent areas and multiplying of the centers of the reproduction of follicles. There are giant denuclearized macrophags. The lungs between alveolar partitions are infiltrated by lymphocytes, hystіocytes, plasmatic cells. The development of interstitial giant cells measles pneumonia is possible. The development of measles encephalitis in a cerebrum is possible.

Filatov - Koplik spots of measles

Histopathology of measles pneumonia. Giant cell.

Complications. The defeats of bronchial tubes and lungs are accompanied by the secondary bacterial infection by the development of endobronchitis, mesobronchitis, peribronchitis, sometimes of the necrotic or septic-necrotical panbronchitis, which can be the source of bronchiectasis, abscesses of lungs, festering pleurisy.

Death is caused by pulmonary complications, with asphyxia at the time of unreal croup.

Infectious mononucleosis

Infectious mononucleosis (illness of Filatov) is an acute infectious disease with the overwhelming damage of the lymphogistiocitar system.

Etiology and pathogenesis. An agent can be herpes-like virus of Epshtain-Bar. An infection spreads from a patient or virus carrier by a respiratory way, alimentary, contact, by transplacental ways. There is an inflammation of mucous tunic, and later viral-bacterial quinsy. The virus spreads by lymph and blood. In regional lymph nodes, liver, spleen, red marrow there is hystiomonoсytar, lymphoid prolypheration, atypical lymphocytes and mononuclear cells appear in peripheral blood.

Epstein-Barr Virus

Clinically illness can have typical and atypical motion of different degree of weight with the development of hepatosplenomegaly, hypogranulocytosis, thrombocytopenia, tonsillopharyngitis, and obstructive changes in respiratory tracts.

Pathomorphology. On the mycoses tunic of fauces, overhead respiratory tracts there are catarrhal changes, sometimes ulcer process. The glands of pharyngeal ring are enlarged, puffed up, plethoric; their tissues are of rather yellow, grey-red color with the grey-yellow cells of necrosis. Structure of the picture is fully effaced due to macrophagal, mononuclear, giant-cells infiltrations. Spleen is multiplied, a capsule is tense, and there is parenchyma of crimson color on a section. A liver is enlarged, in parenchyma there is infiltration by lymphoid, plasmatic, mononuclear cells. Soft brain-tunics are puffed up, plethoric, they are infiltrated by hystіocytes, mononuclear cells, meningoencephalitis can develop, poliomyelitis with the development of dystrophic changes in gangliose cells, perivascular hemorrhages. Mononuclear infiltrates are observed in lungs, in endo-, pericardium, interstitium, myocardium, kidneys, pancreas, mycoses tunic of the digestive system, endocrine glands.

Structure of the lymph node in infectious mononucleosis

Death is caused by the break of spleen, peripheral paralysis of breathing, secondary infection.

Diphtheria

Diphtheria (diphtheria is a rind, tape) is an acute infectious disease which is characterized by fibrinous inflammation of tissues in the hearth of the primary fixing of agent and general intoxication with the toxic defeat of the cardio-vascular and nervous systems, adrenal glands.

Etiology. An agent is a stick of diphtheria which belongs to the family of coryneforms. Mechanism of transmission is respiratory from carrier of bacterium, rarer from patients.

Pathogenesis. A diphtheria stick propagates itself in the area of gate of entrances: the mucous tunic of pharynx, pharyngeal tonsils, overhead respiratory tracts, sometimes privy parts at girls, wounds. In the process of vital functions a stick excrete exotoxin which has an ability to repress the biosynthesis of enzymes of respiratory cycle, that is why it paralyses the tissue breathing; to change cholinergic processes; to violate the synthesis of catecholamines with the accumulation of them in tissues.

Stained Corynebacterium cells. The "barred" appearance is due to the presence of polyphosphate inclusions called metachromatic granules.

Locally he draws necrosis of epithelium and the development of fibrinous inflammation, sucked into blood, damages heart, nervous system, adrenal glands, causes paresis and destruction of microcirculatory bloodstreams, and his excretion with urine is caused by the damage of nephrothelium of nephron canaliculars.

Pathomorphology. In connection with that pharynx, skin, tonsils, mycoses privy parts deported a multi-tuniced epithelium diphtheritic inflammation develops at them. They are covered with fibrinous tape which tissues necrotized under, saturated with fibrin and leucocytes. Tape long time torn away does not that create terms for suction of toxins, but consequently the origin of toxemia Regional gland begin to necrotize. Toxic (alterative, parenchimatous) and interstitial serous myocarditis develops in heart. Alterative myocarditis is characterized by fatty dystrophy of cardiac hystiocyte which are reason of heart cavity dilatation. If myocarditis on the 2-nd week of disease is drawn by death from acute cardiac insufficiency, in such cases, we speak about an early heart failure at diphtheria. The carried out myocarditis stimulates the development of cardiosclerosis.

фибрин в альвеол-микро

Fibrinous inflammation of the lung at the diphtheria.

Late heart, diaphragm, soft palate failures are conditioned by parenchimatous neuritis of glossopharyngeal, vagus, sympathetic nerve and diaphragm nerves, and also by dystrophic changes up to cytolysis III neck sympathetic nerve and nodose ganglion of vagus nerve mainly on the 1,5 month from the beginning of illness. In the medulla of adrenals we find out hemorrhages, dystrophy and necrosis of cells, in cortical tunic there is necrosis and disappearance of fat. A serious toxemia causes the development of necrotic nephrosis in kidneys.

Fibrinous inflammation at the diphtheria.

The separate form of diphtheria is considered diphtheria of respiratory tracts. The mucous tunic of aeriferous ways below vocal cords are mainly affected by croupous inflammation, although they can be possibly affected by diphtheritic. One everything depends on the depth of necrotic process through expression of action of exotoxin. The mucous tunic secrets much mucus, and consequently, fibrinous tape is quickly torn away, and toxemia at this form of diphtheria does not achieve high degree. However, tearing away of tape, edema of the mucous tunic can close the clearance of trachea and draw an asphyxia. Croupous inflammation of larynx at diphtheria got the name of a real croup, unlike the edema of mucus, which is observed at ARVI. Croupous inflammation can spread from trachea and bronchial tubes on bronchioles (descending croup), which can be accompanied by the development of focal pneumonia.

Complications at diphtheria of respiratory tracts are often linked with the tracheotomy and with the introduction of tracheotomy tube and presented by bedsores, septic perichondritis of cartilages of trachea, phlegmons , mediastenitis.

Death at diphtheria is mainly coused by untimely introduction of antitoxic whey from an early heart failure at myocarditis, late heart and diaphragm, acute adrenals insufficiency, asphyxia, acute kidney insufficiency, septic complications, chronic cardiac insufficiency failures from the development of cardiosclerosis.

Scarlatina fever

Scarlatina fever (scarlatina fever ital. - red) is an acute streptococcus infectious disease which manifests itself in tonsillitis, typical eruption (exanthema) general intoxication.

Etiology. An agent is a beta- hemolytic streptococcus of group A and, that contains an erythrolysin toxin and allergen. An infection is transmitted by a patient with scarlatina fever, reconvalescentor, and also patients with other infections (tonsillitis, erysipeloid, pneumonia, and others like that) of streptococci by a respiratory way, rarer through objects and food (milk).

Pathogenesis of scarlatina fever is difficult and conditioned toxic, allergic and septic mutual relations of micro- and to macro organisms. In the place of the primary fixing of streptococcus, more frequent in tonsils, to the skin, there is a primary focus of inflammation (primary scarlatina fever affect) which spreads through of the circulatory system and lymphatic ways with the involvement in the process of regional gland. A primary affect, vasculitis and lymphadenitis, make a primary scarlatina fever complex. Localization of affect out of the tonsils is called an extrabuccal scarlatina fever. Exactly in this period (I period) the toxic phenomena of commons, which causes the defeat of the nervous, endocrine and cardio-vascular systems, eruption, manifestation due to the formation of antitoxic antibodies. It lasts for 7-9 days. On the 2-3 week of motion illnesses calms down to infectiously-allergic displays it and on the first plan the symptoms of allergic reaction come forward from the side of skin, joints, bloodstreams, kidneys, heart (II period). Allergic changes through activating of penetrating of barriers of tissues and vascular bloodstream, the invasions of streptococcus can promote in organs with the development of sepsis.

Pathomorphology. Every period of scarlatina fever has the characteristic manifestation. The degree of their expression determines the easy, middle and severe form of illness. The first period (allergization) manifests itself by catarrhal quinsy with the acute plethoric of tonsil and pharynx (blazing pharynx), which can often change into necrotic or even ulcerous. On a background hyperemic skin bright point purple-red eruption appears with the exfoliation of epithelium on the surfaces of bends of limbs, in exception of nasolabial triangle, which pale and expressly well-defined on the general red background of skin. Vasculitis of bloodstreams of skin lies in the basis of eruption. The manifestation of dystrophy is present in an epidermis, by the edema, and also necrosis of epidermis. Severe dystrophic changes develop in parenchimatous organs, interincompatible lympho- histiocytic infiltrates, disorders of blood circulation, hyperplasia of spleen is expressed.

Follicular tonsillitis

At the severe form of scarlatina they can entail death on the 2-3 day of disease. Septic complications mainly arise up on the second week of illness and show up activating of septic-necrotic process in a primary complex, to development of retropharyngeal abscess with erosion of bloodstreams of bloods and mortal bleeding, metastasis of pus into different organs.

The second period of scarlatina is not obligatory. It can develop on the 3-5 week of illness at presence of provoking factor - super cooling and begins from an easy catarrhal tonsillitis. The basic threatening manifestation of this period is a sub acute glomerulonephritis; there can be warty endocarditis, arthritics, vasculitis of skin, and consequently, an urticaria.

Complications: lymphadenitis, otitis, otogenic abscesses of cerebrum, endocarditis, glomerulonephritis, arthritis, defects of heart, cardiosclerosis.

Death is mainly caused by toxemia, festering-septic complications, kidney and cardiac insufficiency.

Meningococcal infection.

Meningococcal infection. An acute infectious disease more frequent in child's age with epidemic flashes, which is manifested in three forms: meningococcal nasopharyngitis, festering meningitis, meningococcal sepsis.

Etiology and pathogenesis. The agent is a meningococc. An infection is transported by a respiratory way from a patient or the transmitter of infection. The penetration of agent in the mucous tunic of nasopharynx causes the development of meningococcal nasopharyngіtis, and at hematogenic spreading and the penetration of him over the hematoencephalic barrier predetermines the development of festering meningitis. Meningococcal sepsis which is manifested by bacterial shock and is connected with the accumulation of endotoxin can develop at the violation of immunological reactivity. Thus paresis of shallow bloodstreams, stasis, thromboses, hemorrhages, necrosis, take place in internal organs.

Pathomorphology.

Meningococcal nasopharyngіtis manifests itself by the catarrhal inflammation of mucous tunics, with their hyperemia and hyperplasia of lymphatic follicles. This form is dangerous in an epidemiology aspect.

Meningococcal meningitis begins from a basal surface by the serose inflammation on the first days, and then passes on a hemisphere and in 2-3 days festering inflammation develops as rather yellow-green cap, the fibrinous inflammation joins in 5-6 days. Septic ependyma and pyocephalus, meningoencephalitis can develop. Making progress hydrocephaly and atrophy of brain can develop during the organization of fibrin.

Neisseria meningitidis

Meningococcemia is characterized by the generalized defeat of microcirculatory bloodstreams, hemorrhagic eruption on skin, mucous and serous tunics, in internal organs. Eruption on skin is mainly localized on buttocks, lower limbs, eyelids, sometimes on sclera there are cells of necrosis in the center of vesicles. Focuses of necrotizes and hemorrhages develop at adrenal glands, that predetermines the development of the acute adrenal insufficiency – the syndrome of Woterkhaus-Frideriksen, in kidneys –the necrosis of epithelium of nephron canaliculars is necrotic nephrosis, in bloodstreams there are vasculites, extravasations, necrotizes of wall.

Death is caused by the edema of brain in the first stage of illness or from a cerebral cachexy in the late terms of illness at the time of meningitis or from bacterial shock, acute adrenal insufficiency - at the time of meningococcal sepsis.

A whooping-cough

A whooping-cough is an acute infectious disease of children with the defeat of breathing organs and the development of typical fits of the spasmic coughing.

Etiology and pathogenesis. The agent - the stick of whooping-cough is transported to the mucous tunics of the upper respiratory tracts by a respiratory way from a patient. At the destruction of agent endotoxin cause the annoying of the nervous receptors of larynx which predetermines the fit of the spasmic coughing through difficult mechanisms; infant children have attacks of apnoea with the loss of consciousness and asphyxia.

Pathomorphology. The mucous tunic of respiratory tracts is plethoric, covered with mucus, lympho-plasmocytic infiltration, in lungs there are areas of atelectasis, hyperemia, interstitial emphysema, and spontaneous pneumothorax can develop. Piecemeal pneumonia develops at the infant children. In brain there are edemas, plethora and small extravasations. Breaks and ulcers on the bridle of tongue are typical.

Complications are predefined by the joining of the second infection and the development of panbronchitis, peribronchial pneumonia.

Death occurs rarely and mainly at infant children from asphyxia, pneumonia, spontaneous pneumothorax.