Poliomyelitis and diphtheria: pathological anatomy

Place of poliomyelitis in the structure of childhood infections

As part of the study of pathological anatomy, poliomyelitis is included in the list of topics requiring mandatory mastery by students. For a full understanding of this disease, it is necessary to clearly know its etiology, causes of occurrence, and specific morphological changes taking place in the patient's body.

In addition to poliomyelitis, this group of infections includes chickenpox, measles, scarlet fever, pertussis, meningococcal and cytomegalovirus infections, as well as diphtheria. Since the provided material focuses primarily on diphtheria infection, its pathogenetic and morphological features are reviewed in detail below.

Pathogenesis and effects of diphtheria toxin

If the patient has antitoxic immunity, the disease itself does not develop, but the person becomes a bacterial carrier. In the event of disease onset, the entire clinical and morphological picture is driven by the action of the diphtheria toxin. The toxin exerts its primary action in the area of the portal of entry, and the overall severity of the condition directly depends on the intensity of its absorption into the systemic circulation.

There are three main directions of the toxin's impact on tissues:

Cytopathic effect: the exotoxin provokes epithelial cell necrosis directly at the site of infection introduction.
Vasoparalytic effect: pronounced congestion of blood vessels occurs. The permeability of the vascular wall is impaired, leading to massive exudation of erythrocytes and fibrinogen. Under the influence of tissue thrombokinase released from dead cells, fibrinogen transforms into fibrin. This is how the typical fibrinous membrane of the disease is formed.
Impact on nerve trunks: specific damage to the peripheral nervous system.

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Pathological anatomy of oropharyngeal diphtheria

Oropharyngeal involvement is the most frequent localization, accounting for 90 to 95% of all cases. Depending on the severity of the clinical course, three main forms are distinguished:

Localized form. The inflammatory process does not extend beyond the tonsils. A diphtheritic variant of fibrinous inflammation develops, in which the membrane is firmly fused to the underlying tissues. This dense fibrinous structure covering the necrosis zone creates an ideal environment for the active reproduction of bacteria, continuous production of exotoxin, and its subsequent entry into the blood.
Disseminated form. Inflammation extends beyond the boundaries of the tonsils, affecting the palatine arches, uvula, and posterior pharyngeal wall. Symptoms of general intoxication become more pronounced. When fibrinous deposits slough off, necrotic foci are exposed, which eventually become covered with new epithelium.
Toxic form. Characterized by the addition of pronounced edema of not only the oropharyngeal mucosa, but also the subcutaneous fat of the neck. Lymph nodes significantly increase in size, and general intoxication reaches critical values.

Systemic involvement of internal organs

The depth of internal organ damage in toxic diphtheria is directly proportional to the concentration of exotoxin in the blood. The most vulnerable target organs are the heart, peripheral nervous system, kidneys, and adrenal glands.

Myocarditis (heart involvement) Most often manifests at the end of the first or the beginning of the second week of the toxic form. Morphologically, deep dystrophy of cardiomyocytes (primarily fatty), foci of myocardial fiber necrosis, and lymphomacrophagal infiltration of the interstitium are revealed. This complication is extremely severe and can cause fatal outcome against the background of acute heart failure.

Nerve trunk involvement Proceeds as parenchymatous neuritis. The morphological picture includes destruction of the myelin sheath, and in rarer cases, destruction of Schwann cells and the axis cylinders themselves. This condition usually develops at 3–7 weeks of the disease, manifesting as peripheral paralysis of the muscles of the trunk, limbs, neck, diaphragm, and soft palate.

Kidney and adrenal involvement Against the background of severe intoxication, necrotic nephrosis forms in the kidneys. Massive hemorrhages occur in the adrenal tissue, which inevitably leads to the development of acute adrenal insufficiency.

Respiratory diphtheria and late complications

In respiratory tract involvement, inflammation is localized predominantly in the laryngeal mucosa. Unlike oropharyngeal diphtheria, here the fibrinous membrane easily separates from the surface, leading to obturation (blockage) of the respiratory lumen and the clinical picture of croup.

If the inflammation spreads further down — to the trachea and bronchial tree — descending croup is diagnosed. This life-threatening condition can lead to asphyxia (suffocation) and death, and is also frequently complicated by pneumonia. To save the patient during progressive asphyxia, an emergency tracheostomy is performed. An important feature of this form is that systemic effects of the toxin are extremely rare here.

Specific neurological and cardiac complications In addition to early paralyses, late cardiovascular disorders manifesting 2–2.5 months from the onset of the disease pose a particular danger. They are associated with toxic damage to the vagus nerve (n. vagus) and intramural cardiac ganglia, which can provoke sudden cardiac arrest. Paralysis of respiratory muscles and swallowing muscles are also life-threatening. However, if the patient successfully overcomes this critical period, the function of the damaged neural structures fully recovers within 2–3 months.

Briefly: answers to topical questions

What specific morphological changes occur in the central nervous system in poliomyelitis?

In poliomyelitis, the central nervous system undergoes predominant involvement of the gray matter of the anterior horns of the spinal cord with the death of motor neurons.

Macroscopic changes:

Meninges — hyperemia and edema.
Brain tissue — swollen, bulging above the meninges on cross-section.
Gray matter — the "butterfly" pattern is blurred and indistinct.
Anterior horns of the spinal cord — brownish petechial hemorrhages and small depressed areas of tissue softening.

Microscopic changes (maximally pronounced in the paralytic stage):

Localization — predominantly the gray matter of the anterior horns of the spinal cord, less frequently the posterior horns.
Foci of inflammation — polymorphonuclear leukocytes and microglia.
Neuronophagic nodules — form around necrotic motor neurons.
Glial nodules — form in the spinal cord tissue.

What is the etiology and main transmission routes of poliomyelitis?

Poliomyelitis is an anthroponotic infectious disease caused by an RNA-containing virus of the genus Enterovirus (Enterovirus).

Main characteristics of the pathogen and transmission routes:

Antigenic structure — three independent serotypes of poliovirus (I, II, and III) are distinguished.
Stability — the virus is highly resistant in the external environment, but is rapidly killed by boiling, ultraviolet radiation, contact with chlorine-containing disinfectants, and iodine.
Transmission route — infection is transmitted from person to person, most commonly via the alimentary route.

Class and exam questions

The main factor determining both clinical symptoms and morphological changes in tissues is the specific diphtheria toxin.

The heart is affected at the end of the 1st to the beginning of the 2nd week in the toxic form. Severe myocarditis develops, accompanied by fatty degeneration of cardiomyocytes, their necrosis, and cellular infiltration of the interstitium.

The heart is affected at the end of the first or beginning of the second week in the toxic form. Severe myocarditis develops with fatty degeneration of cardiomyocytes, their necrosis, and interstitial infiltration.

The fibrinous membrane formed in the larynx is loosely attached to the underlying tissues. Its easy detachment leads to mechanical obstruction (blockage) of the respiratory tract lumen, causing croup syndrome and asphyxia.

The fibrinous membrane formed in the larynx is loosely attached to the underlying tissues. Its easy detachment leads to mechanical obstruction of the respiratory tract, causing croup and asphyxia.

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What else to study on this topic

Etiology, pathogenesis, and morphological manifestations of chickenpox
Pathological anatomy and characteristic complications of measles
Clinical and morphological periods and changes in scarlet fever
Main clinical forms of meningococcal infection in children
Features of the pathogenesis and manifestations of pertussis
Clinical and morphological forms of cytomegalovirus infection (CMVI)

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