Measlesis an acute highly contagious infectious disease characterized by catarrhal inflammation of the mucous membranes of the upper respiratory tract, conjunctiva and spotted papular eruption on the skin.

Etiology and pathogenesis. The causative agent of measles is an RNA-containing virus transmitted by air droplets. The virus enters the upper respiratory tract and eye conjunctiva. It causes degenerative changes in the epithelium of the mucous membrane and enters the blood, which is accompanied by short viremia resulting in dissemination of the virus in the lymphoid tissue, which in turn causes immune reconstruction. Viremia becomes more marked and prolonged, the eruption appears. When the eruption disappears, the virus cannot be found in the organism. The duration of the disease is 2—3 weeks. The disease produces stable immunity.

Pathology. Catarrhal inflammation develops in the mucous membrane of the mouth, trachea, bronchi, conjunctiva. The mucous membrane is swollen, plethoric, the mucous secretion is increased, which is

accompanied by rhinitis, cough, lacrimation. Severe cases are accompanied by necroses, the mucous membrane becomes dull, grayish-yellow, small lumps are seen on its surface. The edema and necrosis of the laryngeal mucosa can cause reflex spasm of its muscles with asphyxia development (so called false croup).

Measles is characterized by metaplasia of mucosa epithelium into multi-layer squamous epithelium observed in early periods (5th—6th days of the disease) which decreases the barrier function of the epithelium. Metaplasia is associated with local vitamin A deficiency. Viremia and generalization of the process result in enanthema and exanthema. Enanthema is noted on the mucous membrane of the cheeks against the lesser lower molars. It looks like whitish spots called Belsky-Filatov-Koplik spots which develop before the eruption on the skin. They are of great diagnostic significance. Exanthema in the form of large-spot papular eruption first appears on the skin behind the ears, then on the face, neck, body, inner surface of the extremities.

Complications. The prominent place is occupied by lesions of the bronchi and lungs connected with secondary viral and bacterial infections. The disease involves internal membrane of the bronchi (endobronchitis), middle layer (mesobronchitis), and external layer (peribronchitis). Panbronchitis can often be necrotic or purulent necrotic.

On incision, the involved lungs look like gray-yellow foci resembling tuberculosis ones. Such panbronchitis is the source of bronchoectasis, lung abscess, purulent pleurisy. The involvement of peribronchial lung parenchyma causes the development of peribronchial pneumonia and chronic disease of the lungs resulting in pneumosclerosis.

Moist gangrene of the soft tissue of the face (noma) is rarely observed at present.

The death of the patients with measles is associated with pulmonary complications and asphyxia in false croup. Modern seroprophylaxis and vaccination have resulted in considerable reduction of the frequency of illness and death rate.

Mumps.Mumps virus causes a transient inflammation of the parotid glands and rarely of the testes, pancreas and central nervous system. Mumps viruses are spread by air droplets and multiply within upper respiratory epithelial cells, salivary glands, and T-cells in lymph nodes. A transient viremia spreads the mumps virus to other glands and the central nervous system via the choroid plexus.

Pathology. In mumps (parotitis), which is bilateral in 70% of cases, affected glands are enlarged, have a soft consistency, and are moist, glistening, and reddish brown on cut-section.

Microscopically, the gland interstitium is edematous and diffusely infiltrated by histiocytes, lymphocytes, and plasmocytes that compress acini and ducts.

Neutrophils and necrotic debris may fill the ductal lumen and cause focal damage to the ductal epithelium.

In mumps orchitis, testicular edema, mononuclear cell infiltration, and focal hemorrhages has been revealed.

Complications: atrophy of testis with azoospermia development, serous meningitis and meningoencephalitis.

The death of the patients with mumps is associated with central nervous system involvement.

Infectious mononucleosis (Epstein-Barr virus), (Filatov's disease)is a benign, self-limited lympho-proliferative disease caused by EBV, a gamma-group herpesvirus. Infectious mononucleosis is characterized by fever, generalized lymphadenopathy, splenomegaly, sore throat, and the appearance in the blood of atypical activated T-lymphocytes (mononucleosis cells). Some patients develop hepatitis, meningoencephalitis, and pneumonitis. EBV is transmitted by close human contact, frequently with the saliva during kissing.

Pathology. The major alterations involve the blood, lymph nodes, spleen, liver, central nervous system. The peripheral blood shows absolute lymphocytosis with a total white cell count between 12 000 and 18 000 per microliter, more than 60% of which are lymphocytes. Many of these are large, atypical lymphocytes, characterized by an abundant cytoplasm containing multiple clear vacuolations and an oval, indented, or folded nucleus. The lymph nodes

are typically changed and enlarged throughout the body, principally in the posterior cervical, axillary, and groin regions. Microscopically, the lymphoid tissue is flooded by atypical lymphocytes, which occupy the paracortical areas. There is B-cell reaction too, with enlargement of follicles.

The spleen is enlarged in most cases, weighing between 300 and 500 gm. It is usually soft and fleshy, with a hyperemic cut surface. The microscopical changes are similar to those of the lymphatic. These spleens are especially vulnerable to rupture, possibly resulting in part from infiltration of the trabeculae and capsule by the lymphocytes.

Liver function is almost always transiently impaired to some degree, although hepatomegaly is at most moderate. Microscopically, atypical lymphocytes are seen in the portal areas and sinusoids; scattered, isolated cells or foci of parenchymal necrosis filled with lymphocytes are revealed.

Mononuclear infiltration appears in the lungs, endocardium, pericardium, myocardium, kidneys, pancreas, gastric mucosa striated muscles, skin. Causes of death are meningoencephalitis, peripheral paralysis of the respiration, rupture of spleen, secondary infections.

Diphtheriais an acute infectious disease characterized by fibrinous inflammation in the focus of primary fixation of the causative agent and general intoxication due to exotoxin absorption. The disease

is more common in children, at present the disease is more frequent in children over 7 years.

Etiology and pathogenesis. The causative agent of the disease is diphtheria bacillus. The primary source of infection is the bacilli-carrier, to the less degree the sick person. Diphtheria is a local infection as hematogenic propagation is not observed. The diphtheria bacillus multiplies in the area of the infection atrium on the mucous membranes and excretes exotoxin. The exotoxin causes local necrosis of the epithelium, paretic dilation of the vessels with disturbance of their permeability, edema of the tissues and release of fibrinogen from the vascular bed. A fibrous coat is formed on the surface of the damaged mucous membrane. Exotoxin affects cardiovascular, nervous systems and adrenal glands. This simultaneous damage causes hemodynamic disturbances in the organism, excretion of the exotoxin from the organism is accompanied by the damage of tubular epithelium of the kidneys.

Pathology. Local changes can be found in the mucous membrane of the fauces, tonsils, upper respiratory tract. Sometimes diphtheria of the conjunctiva, reproductive organs in girls and wounds are observed. In diphtheria of fauces, the tonsils are enlarged, the mucous membrane is plethoric, covered with dense whitish-yellow membranes. The soft tissue of the neck is swollen. In severe toxic forms, the edema is considerable and can involve the anterior surface of

the chest. The type of inflammation is diphtheritic. Diphtheria of the respiratory tract is characterized by croup inflammation of the larynx, trachea, bronchi with formation of fibrinous membranes which can be discharged at cough. Croup inflammation of the larynx in diphtheria is called true croup, propagation of the process in the small branches of the bronchial tree is called descending croup, which may be accompanied by development of focal pneumonia. Regional lymphatic nodes of the neck are considerably enlarged, plethoric, with yellowish-white necrotic foci or hemorrhages on incision. Toxic myocarditis develops in the heart. The cavities of the heart are dilated, the muscle is dull, flabby, variegated. Parietal thrombi can be observed. The changes of cardiomyocytes are characterized by fat degeneration and small foci of myolysis. Alterative and interstitial forms of myocarditis are distinguished. If myocarditis develops at the beginning of the 2nd week of the disease and the death is caused by acute cardiac failure, the condition is called early cardioplegia. Myocarditis results in cardiosclerosis development.

In the nervous system, the changes are localized in the peripheral nerves and vegetative ganglia. Parenchymatous neuritis with myelin decomposition develops. Disturbance of blood circulation, degenerative changes of the nervous cells are observed in the nervous ganglia. The changes manifest 1.5—2 months

later in the form of late paralysis of the soft palate, diaphragm, heart, in the damage of the glossopharyngeal, diaphragmatic and vagus nerves. Hemorrhages, degeneration and necrosis of the cells are observed in the medullary layer of the adrenal glands, foci of necrosis and disappearance of lipids are seen in the cortical layer. Necrotic nephrosis and massive necroses of the cortical layer in the severe cases of toxic diphtheria are observed in the kidneys.

Complications in diphtheria of the respiratory tract are caused by intubation or tracheotomy which can result in decubitus. Secondary infection in decubitus causes purulent perichondritis of the cartilages of the larynx, phlegmon, purulent mediasti-nitis. At present administration of antibiotics prevents these complications.

Death is caused by asphyxia (spasm of the larynx in true croup or occlusion of the respiratory tract with fibrinous membranes) or by accompanying pneumonia and purulent complications. The death may be caused by early cardioplegia in myocarditis and late cardioplegia or paralysis of the diaphragm due to parenchymatous neuritis when antitoxic serum is not administered in time.

Scarlet feveris one of the forms of streptococcal infection, it is an acute infectious disease accompanied by local inflammatory changes mainly in the fauces and typical generalized rash. The disease is common in children under 16, but it can also be observed in the adults.

Etiology and pathogenesis. The causative agent is beta-hemolytic streptococcus of group A of different serological types. The patients are infected through air droplets, but the disease can also be transmitted through personal belongings and foodstuffs (mainly milk). Pathogenesis of scarlet fever is complicated. Streptococcus causes inflammatory process in the site of the primary fixation (tonsils, skin, lungs) which is accompanied by regional lymphadenitis. This is called primary scarlatinal affect and primary scarlatinal complex. The course of the disease is divided into two periods, toxic and infectious allergic ones.

Pathology. Acute plethora («burning faucet») which involves the mucous membrane of the oral cavity and pharynx is observed, the tongue is raspberry-colored. The tonsils are enlarged, juicy, bright-red (catarrhal angina followed by necrotic angina). Necrosis may involve the soft palate, pharynx, auditory tube (Eustachian tube), middle ear, it can pass from the lymphatic nodes to the subcutaneous fat of the neck. Rejection of the necrotic masses results in ulcers. Cervical lymphatic nodes are plethoric, juicy, enlarged, with foci of necrosis and marked myeloid infiltration. The general changes depending on toxemia are first of all rash. It appears during the first two days of the disease, looking like small bright red dots. It covers all the surface of the body, excluding the nasolabial triangle, which is clearly seen against the bright red background of the skin of the face.

Degenerative changes and interstitial lymphohistiocyte infiltrates are noted in the liver, myocardium and kidneys. B-zone hyperplasia with plasmatization as well as myeloid metaplasia are observed in the spleen and lymphoid tissue of the intestine. In severe septic scarlet fever, the process in the site of the affect is of generalized purulent necrotic character with formation of a retropharyngeal abscess, otitis and purulent osteomyelitis of the temporal bone, purulent necrotic lymphadenitis, neck phlegmon. Septicopyemia with purulent metastases in the organs develops in most severe cases.

The second period may develop on the 3rd—5th week of the disease. The second period begins with moderate catarrh angina. The most significant is development of acute or chronic glomerulonephritis with possible nephrosclerosis development. Skin rash, vasculitis, serous arthritis, verrucous endocarditis can be observed.

The complications depend on purulent necrotic changes, e.g. on development of chronic otitis with hearing reduction or (in the second period) on chronic disease of the kidneys.

The death is caused by toxemia or septic complications.

Meningococcal infectionis an acute infectious process which has three main forms: nasopharyngitis, purulent meningitis and meningococcemia. This is characterized by periodic epidemics, the disease is

more common in children under 5 years, but the disease may occur in persons of any age.

Etiology and pathogenesis. The causative agent is meningococcus.

Meningococcal nasopharyngitis is characterized by catarrhal inflammation of the mucous membranes with marked hyperemia, edema of the back of the pharynx and hyperplasia of lymphatic follicles. This form is of great epidemiological importance as clinical diagnosis is often difficult.

In meningococcal meningitis the pia mater is severely plethoric, saturated with dull serous exudate during the first days of the disease. By the end of the 2nd—3rd day the exudate becomes thicker, green-yellow, purulent. By the 5th—6th day it becomes denser due to fibrinous effusion. The process begins with basal surface and passes through the perivenous spaces to the convex surface mainly of anterior portion of the brain, locating there in the form of a yellow-green «cap». The purulent process involves the meninges of the spine.

The death may occur from the brain swelling with wedging of the cerebellum tonsils to the great foramen and strangulation of the oblong brain during the acute period, later the cause of death is meningoencephalitis, purulent ependymitis or general cerebral cachexia due to hydrocephalia and atrophy of the brain hemispheres during the following periods.

Meningococcemia is characterized by generalized damage of microcirculation, skin rash, changes in the joints, vascular membrane of the eyes, adrenal glands and kidneys. Changes in the serous layers of the pericardium are observed. If the patient dies during the first 24—48 hours, meningitis may be absent. The rash is hemorrhagic, star-like, located mainly on the buttocks, lower extremities, eye lids and scleras. There may be vesicles or dull dryish foci of necrosis in the center of the skin elements. Purulent arthritis is observed in the small joints of the extremities.

Focal necroses and hemorrhages or bilateral massive hemorrhages with the development of acute adrenal insufficiency (Waterhouse-Friderichsen syndrome) are noted in the adrenals. Necrosis of nephrothelium of the tubules (necrotic nephrosis) is observed in the kidneys. The changes of the microcirculation are characterized by vasculitis and necrosis.

The death of the patients is caused by bacterial shock, its severity is aggravated by hemorrhages to the adrenals, acute renal insufficiency is not so common (in the adults). When the course of the disease is prolonged, the death occurs from septicemia or purulent meningitis.

Stages of individual work in class Study and describe macrospecimens

Diphtheritic laryngotracheobronchitis. Describe the colour of the mucous coat and character of fibrinous films, name the kind of the inflammation, list complications and give definitions to such notions as «laryngeal diphtheria» and «descending croup».

Heart in diphtheria. Describe the size of the heart, state of its cavities, thickness of the myocardium, its colour; name the morphological changes which the myocardium develops in diphtheria; list possible complications, name their cause and outcome.

Morbillous laryngotracheobronchitis. Describe the appearance of the preparation, the colour of the laryngeal, tracheal and bronchial walls; explain what process causes this colour; name the causative agent of measles and describe the pathogenesis of necrotic bronchitis, list other morphological signs of bronchitis in measles,give examples of complications after necrotic bronchitis.

Purulent meningitis. Give characteristics of blood filling in the pia mater, state of the gyri and sulci, the appearance of the exudate; name the form of meningococcal infection, say when meningitis develops, list its outcomes.

Hydrocephaly. Describe the appearance of the brain, expressiveness of its gyri, volume of the lateral ventricular sinuses, thickness of the brain substance; name the pathological process in the cerebral hemispheres in hydrocephaly; list changes in the pia mater, say which of them are observed at the initial stages of the disease, list their etiology.

Henoch's angina. What changes have developed in the fauces? Describe the colour and blood filling of the tonsillar

mucosa; determine the mechanism of these changes; list possible complications, describe changes in regional lymph nodes.

Multiple bronchiectasia of lungs. Describe the appearance of the lung, state of the lumens in the bronchi, thickness of their walls, character of the exudate, pathogenesis of bronchiectasia, name the disease which results in such a complication, list its outcomes.

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