The peculiarities of viral diseases
1. Being highly contagious, viruses cause epidemics and pandemic.
2. The variety of viruses determines the lesion of specific cells due to the virus trophism. The character of the cell receptors determines trophism.
3. The duration of the disease depends both on the type of the virus and the reactivity of the macroorganism and can be acute, chronic, slow.
4. The morphological manifestations of cell-virus interrelations are:
a) Cytolytic effect of the virus on the cell (influenza).
b) Formation of inclusions in the cell (influenza, adenovirus infection).
c) Integration of the virus and the cell genome without considerable destruction of the cell (hepatitis B, HIV infection).
d) Proliferation of target cells (smallpox).
e) Giant-cell transformations (measles).
Acute respiratory viral infection (ARVI)
The term denotes a group of acute inflammatory diseases caused by pneumotropic viruses (Influenza, parainfluenza, adenovirus infection, respiratory sincitial virus, rhinovirus, reovirus).
Influenza
Influenza is a disease characterized by abrupt onset, fever, sore throat, headache, muscle pains, and acute toxic state. Dry cough and nasal discharge are present but usually are overshadowed by systemic symptoms. In uncomplicated cases the illness lasts a few days, but pulmonary complications such as influenza pneumonia and secondary bacterial infection of the lung may complicate and prolong course.
Influenza viruses are highly contagious and afflict people of all ages and have 3 types:
a) Influenza A virus, the most common cause of viral pneumonia in adults, infects animals and man and produces pandemics.
b) Influenza B virus is apparently restricted to man, causes epidemics, and is associated with Reye’s syndrome in children and pneumonitis and croup in infants.
c) Influenza C virus causes sporadic upper respiratory infections, but not epidemic influenza. Influenza has significant mortality and morbidity, and may have long-term sequelae.
Patients with viral influenza during the third trimester of pregnancy, the aged, and persons with valvular heart disease or chronic bronchopulmonary disease all have increased susceptibility to bacterial superinfection. Superinfection usually occurs 1 to 5 days after the onset of the viral illness, while the patient appears to be getting well.
At present differential diagnosis of ARVI is not difficult. Immunomorphological study with antisera to the definite strain of viruses is performed in the smears from the mucous membrane of the upper respiratory tract or in the tissue (if it is autopsy material). In this case bright fluorescence is seen under the microscope.
Influenza viruses are transmitted by aerosols generated by coughing and sneezing.
The incubation period is 2 - 4 days.
The virus invades the bronchial and alveolar epithelium and endotheliocytes of the capillaries and multiplies there causing primary viremia. The epithelial cells die, the virus leaves them and invades ones more the bronchial and alveolar epithelium. At this stage acute bronchitis or tracheitis develops. These are the first clinical signs of the disease.
The development of the virus in the cells causes degeneration, necrosis and desquamation of the bronchial epithelium, which in turn causes secondary viremia.
Its manifestations are vasoparalytic action (plethora, stasis, hemorrhage) and immune-depressive action (phagocytosis inhibition, chemotaxis, etc.), which contributes secondary (often bacterial) infection.
Morphology
Clinical-morphological forms of influenza
1. Slight influenza is characterized by the lesion in mucosa of the upper respiratory tract (edema, hyperemia, serous inflammation). Laringitis, tracheitis and bronchitis occur. These are microcolonies of the virus; they also can be determined with immunomorphological method. The duration of the disease is 5 - 6 days with following convalescence.
2. Mild influenza is characterized by involvement of the pathological processes in mucosa of the bronchi, bronchioles and lungs.
The histopathologic features include a necrotizing tracheitis and bronchitis; diffuse hemorrhagic necrotizing pneumonitis with pulmonary edema.
Ciliated epithelial cells are destroyed and goblet cells and mucous glands disrupted. Individual cells show pycnosis of the nuclei and loss of cilia.
Interstitial pneumonia develops. Interalveolar septa are thickened due to proliferation with lymphocytes and macrophages.
Bronchioles become thickened, distended, and infiltrated with mononuclear cells. There is often severe inflammatory edema, and a fluid exudate in the alveolar spaces has a hyaline membrane appearance.
Desquamation of the alveolocytes lead to decrease of surfactant and development surfactant-depending atelectases in the lungs.
The duration of the disease is 3 -4 weeks.
3. Severe influenza is characterized by the complicated duration of disease and occurs by:
1. Severe toxicosis.
Besides serous hemorrhagic bronchitis and pneumonia, hemorrhagic lung edema may develop. Hemorrhage to the brain and internal organs develop.
The patients die on, the 4th - 5th day of hemorrhage to vital centres and of acute respiratory and cardiovascular insufficiency.
2. Pulmonary complications.
If bacterial superinfection occurs, the picture is indistinguishable from that of ordinary bronchopneumonia or lobar pneumonia.
Lungs are dark red and firm with interstitial emphysema (pink color) that may extend into the mediastinal tissue. Necrotic foci, abscesses are presence also. Lungs appear as (“large variegated (motley) influenza lung”).
Microscopically, there is pronounced sloughing of the bronchial epithelium into the bronchial lumens.
Encephalitis, serous meningitis, brain edema, trunk dislocation develop in the brain.
Obliterating bronchitis, bronchiolitis, bronchiectasis, pneumofibrosis and other chronic lung diseases develop.
Degeneration and inflammation in the nodes of the vagus and sympathetic nerves cause neuritis.
Myocarditis and pericarditis, as well as encephalitis, might be found as postmorten examination of fatal cases, but they are uncommon.
The death is caused by intoxication, cerebral hemorrhages, brain edema, brain trunk dislocation, pulmonary complications (pneumothorax, empyema), and cardiovascular and pulmonary insufficiency.
Paramyxoviruses
Paramyxoviruses (parainfluenza viruses, respiratory syncytial virus, measles virus, mumps virus) are important causes of respiratory disease in infants and young children.
Paramyxoviruses are spherical enveloped viruses that contain single-stranded RNA.
They are transmitted by inhalation of droplets of aerosols.
Parainfluenza viruses infection (Types l-4)
Type 3 parainfluenza is the most prevalent of the parainfluenzas, occurring endemically throughout the year.
Infants are especially susceptible.
Parainfluenza viruses are spread principally by direct contact or by large droplets (in contrast to the spread of influenza virus by inhalation of small droplets).
Replication is restricted to the respiratory tract and moderate intoxication.
The infection involves only the upper respiratory tract, except in some infants in whom the primary infection may also involve the larynx, trachea, and bronchioles.
The pathology of the disease resembles slight influenza.
The characteristic signs are tracheal and bronchial epithelium proliferation, appearance of polymorphic cells with one or several picnotic nuclei (multinucleated cells).
Edema in larynx may lead to development of the “false croup” and asphyxia.
Complications are secondary infection, bronchopneumonia, asphyxia, angina, sinusitis, and otitis.
Respiratory Syncytial Virus infection
The respiratory syncytial virus is the most common cause of viral pneumonia in children under 2 years of age and is a common cause of death in infants aged 1 to 6 months.
This agent accounts for about one-third of hospital admissions for pneumonia and for up to 90% of those admitted for bronchiolitis.
Susceptibility is also increased in elderly or immunocompromised patients.
In temperate climates of the northern hemisphere, annual epidemics occur in midwinter (January-March).
Histopathologic features include necrotizing bronchitis, bronchiolitis, and interstitial pneumonia.
The infiltrate is purely mononuclear (predominantly lymphocytes). In many cases irregular intracytoplasmic inclusion bodies are seen in alveolar and bronchiolar epithelial cells, but intranuclear inclusions are not present.
The death is caused by asphyxia and pulmonary complications.
Adenovirus infection
Adenovirus infection (AVI) is caused by DNA-containing adenovirus. This is characterized by invasion of the upper respiratory tract, lymphoid tissue of the intestine, abdominal lymphatic nodes as well as conjunctivitis.
Adenoviruses (subgroup B, types 4 and 7) are common causes of acute respiratory disease and adenovirus pneumonia in military recruits coming together for the first time for basic training.
Adenoviruses (subgroup C) are also important causes of chronic pulmonary disease in infants and young children.
The course may be slight and severe.
1. Slight AVI is characterized by acute rhinitis, laryngitis, tracheobronchitis, acute pharyngitis, conjunctivitis and regional lymphadenitis. Histopathologic features of adenovirus pneumonitis include necrotizing bronchitis and bronchiolitis, with necrosis and desquamation of the epithelium Sloughed epithelial cells are subsequently mixed with mononuclear cells, mucus, and cell debris, so that the damaged bronchiole resembles a thrombosed blood vessel. There is interstitial pneumonia, with areas of consolidation showing extensive necrosis, hemorrhage, edema, and mononuclear inflammatory infiltrate. Two distinctive types of intranuclear inclusions - smudge cells and Cowdry type A intranuclear inclusions - are scattered throughout the lesions but primarily involve bronchiolar epithelial cells and alveolar lining cells.
2. Severe AVI is caused by generalization of the virus and secondary infections. In generalized infection, the viruses multiply in the epithelium of the intestine (diarrhea), kidneys, liver, pancreas, ganglious cells of the brain with development of inflammation and hemorrhages. Secondary infection is characterized by suppuration and sepsis.
Complications: otitis, sinusitis, tonsillitis, pneumonia due to the secondary infection. The cause of death is pneumonia, sepsis.
Measles
Measles is 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 inhalation (air-droplets).
The virus enters the upper respiratory tract and eye conjunctiva.
Degenerative changes in the epithelium of the mucous membrane and hematogenous spread are accompanied by short viremia resulting in dissemination of the virus in the lymphoid tissue, which in turn causes immune reconstruction.
Viremia becomes more expressed and prolonged, the eruption appears. When the eruption disappears, the virus cannot be found in the organism.
Incubation period is 9-11 days. The duration of the disease is 2 - 3 weeks.
The disease produces stable immunity.
Morphology
Catarrhal inflammation in the mucous membrane of the mouth, trachea, bronchi, conjunctiva develops.
The mucous membrane is swollen, plethoric; the mucous secretion is increased, which is accompanied by rhinitis, cough, and lacrimation.
Severe cases are accompanied by necroses; the mucosa becomes dull, greyish-yellow; small lumps are seen on its surface.
The edema and necrosis of the laryngeal mucosa can develop reflex spasm of its muscles with asphyxia (so called “false croup”).
Measles is characterized by metaplasia of mucosa epithelium into multilayer squamous epithelium observed in early periods (5th - 6th days of the disease), which decreases the barrier function of the epithelium.
Varies from pure interstitial (viral) pneumonia to lobar (bacterial) pneumonia. There are often pathognomonic multinucleated giant cells (Warthin-Finkeldey cells), intranuclear and intracytoplasmic inclusions, and hyperplasia of distal bronchial cells. In immunocompromised patients measles pneumonia may occur without rash and is often fatal.
Viremia and generalization of the process result in enanthema and exanthema:
1. 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.
2. Exanthema in the form of large-spot papular eruption first appears on the skin behind the ears, then on the face, neck, body, and inner surface of the extremities.
Complicationsis accompanied with the secondary viral and bacterial infection.
Destructive (necrotic or purulent-necrotic) panbronchitis can occur.
The disease involves internal membrane of the bronchi (endobronchitis), middle layer (mesobronchitis), and external layer (peribronchitis).
On incision, the involved lungs look like grey-yellow foci resembling tuberculosis ones. Such panbronchitis is the source of bronchiectasis, lung abscess, and 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 disease 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 inhalation (air-droplets) and multiply within 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.
Morphology
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.
ACQUIRED IMMUNE DEFICIENCY SYNDROME (AIDS)
Etiology and pathogenesis
Human immunodeficiency virus (HIV) is the causative agent for AIDS.
HIV is a retrovirus that contains only RNA. HIV is a sexually transmitted disease.
Infection is aided by Langerhans cells in mucosal epithelial surfaces, which can become infected.
Infection is also aided by the presence of other sexually transmitted diseases that can produce mucosal ulceration and inflammation.
The CD4+ T-lymphocytes have surface receptors to which HIV can attach to promote entry into the cell. The infection extends to lymphoid tissues which contain follicular dendritic cells that can become infected and provide a reservoir for continuing infection of CD4+ T-lymphocytes.
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