Place of Poliomyelitis in Pediatric Infections
Within the study of pathology, poliomyelitis is a mandatory topic for medical students. To fully understand this disease, it is essential to know its etiology, causes, and the specific morphological changes occurring in the patient's body.
In addition to poliomyelitis, this group of infections includes chickenpox, measles, scarlet fever, pertussis, meningococcal and cytomegalovirus infections, and diphtheria. Because the provided material focuses primarily on diphtheria, its pathogenetic and morphological features are detailed below.
Pathogenesis and Effects of Diphtheria Toxin
If the patient has antitoxic immunity, the disease does not develop, but the person becomes a bacterial carrier. When the disease develops, the entire clinical and morphological picture is driven by the diphtheria exotoxin. The toxin acts primarily at the site of entry, and overall severity depends on the rate of its absorption into the systemic circulation.
There are three main directions of the toxin's impact on tissues:
- Cytopathic effect: the exotoxin triggers necrosis of epithelial cells directly at the site of infection entry.
- Vasoparalytic effect: pronounced vascular congestion occurs. Vascular permeability is compromised, leading to massive exudation of red blood cells and fibrinogen. Under the influence of tissue thromboplastin released from dead cells, fibrinogen transforms into fibrin. This forms the characteristic fibrinous membrane.
- Effect on nerve trunks: specific damage to the peripheral nervous system.
Pathology of Oropharyngeal Diphtheria
Oropharyngeal involvement is the most frequent location, accounting for 90 to 95% of all cases. Depending on clinical severity, three main forms are distinguished:
- Localized form. The inflammatory process does not extend beyond the tonsils. A diphtheritic variant of fibrinous inflammation develops, where the membrane is firmly fused to the underlying tissues. This dense fibrinous structure covering the necrotic zone creates an ideal environment for active bacterial replication, continuous exotoxin production, and subsequent entry into the blood.
- Disseminated form. Inflammation extends beyond the tonsils, affecting the palatal arches, uvula, and posterior pharyngeal wall. General intoxication symptoms become more pronounced. When fibrinous overlays are rejected, necrotic foci are exposed, which eventually become re-epithelized.
- Toxic form. Distinguished by marked edema not only of the oropharyngeal mucosa but also of the cervical adipose tissue. Lymph nodes are significantly enlarged, and general intoxication reaches critical levels.
Systemic Visceral Involvement
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 Damage) Most frequently manifests at the end of the first or beginning of the second week of the toxic form. Morphologically, it reveals profound cardiomyocyte dystrophy (primarily fatty), foci of muscle fiber necrosis, and lymphomacrophage infiltration of the interstitium. This complication is extremely severe and can cause fatal outcome due to acute heart failure.
Damage to Nerve Trunks Proceeds as parenchymatous neuritis. The morphological picture includes destruction of the myelin sheath, and in rarer cases, destruction of Schwann cells and the axon cylinders themselves. This condition usually develops at 3–7 weeks of illness, manifesting as peripheral paralysis of the trunk, limb, neck, diaphragmatic, and soft palate muscles.
Kidney and Adrenal Damage Against the background of severe intoxication, necrotizing nephrosis forms in the kidneys. Massive hemorrhages occur in the adrenal tissue, inevitably leading to acute adrenal insufficiency.
Respiratory Diphtheria and Late Complications
When the respiratory tract is affected, inflammation localizes predominantly in the laryngeal mucosa. Unlike oropharyngeal diphtheria, here the fibrinous membrane is loosely attached to the surface, leading to obstruction of the airway lumen and the clinical syndrome of croup.
If the inflammation extends lower—to the trachea and bronchial tree—it is diagnosed as descending croup. This life-threatening condition can lead to asphyxia (suffocation) and death, and is often complicated by secondary pneumonia. To save the patient during progressive asphyxia, emergency tracheostomy is performed. An important feature of this form is that systemic toxin effects are extremely rare here.
Specific Neurological and Cardiac Complications Aside from early paralysis, late cardiovascular disturbances manifesting 2–2.5 months after disease onset 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 is also life-threatening. However, if the patient successfully overcomes this critical period, the function of damaged neural structures fully recovers within 2–3 months.