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Diphtheria and Childhood Infections

Q: What is the causative agent of diphtheria?

The causative agent of diphtheria is Corynebacterium diphtheriae. These are Gram-positive, non-motile, non-spore-forming pleomorphic rods. Based on biochemical properties, two main biovars are distinguished: Biovar gravis — enzymatically active, ferments starch;Biovar mitis — lacks amylase activity and does not ferment starch. A characteristic morphological feature of the pathogen is the presence of volutin (metachromatic) granules at the poles of the cell, giving the bacteria a club-like shape, as well as a specific arrangement in smears at angles to each other resembling Roman numerals or stacked fingers.

Diphtheria et Infectiones Infantum

For medical students2 min readUpdated 2026-10-10

This material covers childhood infections, focusing on the pathophysiology and morphology of diphtheria alongside other major infectious pathologies such as scarlet fever, measles, and pyogenic processes caused by staphylococci and streptococci.

Scarlet fever pathogenGroup A β-hemolytic Streptococcus

Measles pathogenRNA virus of the Paramyxoviridae family

Scarlet fever rashFine punctate rash; the nasolabial triangle remains pale (Circumoral pallor)

ComplicationGlomerulonephritis (immune-complex mediated, type III hypersensitivity)

Pyogenic and Anaerobic Infections

This group of pathologies is caused primarily by Gram-positive cocci possessing numerous virulence factors capable of provoking purulent inflammation.

Staphylococcal Infection Most commonly occurs in surgical or burn wounds. It can act as a nosocomial (opportunistic) infection, especially in patients with intravenous catheters, prosthetic heart valves, and intravenous drug users. Typical manifestations include:

Furuncles and carbuncles.
Suppurative hidradenitis.
Soft tissue and skin phlegmon (cellulitis).
Lung abscesses and bone abscesses (osteomyelitis).

Streptococcal Infection Affects the skin, oropharynx, lungs, and heart valves. Most pathogenic strains belong to the β-hemolytic type. Streptococci secrete a specific exotoxin that drives fever, rash, and vasculitis. Examples include erysipelas and pharyngitis. Pneumococci (a cause of pneumonia) and S. mutans (causing dental caries) occupy a special place.

Scarlet Fever: Pathogenesis and Morphology

Scarlet fever is an infectious disease primarily affecting children aged 3 to 15 years. It is transmitted via airborne droplets from a person infected with any form of streptococcal infection.

Mechanism of Development The portal of entry is the mucous membrane of the pharynx and tonsils (less commonly wounds or burns, leading to an atypical form). A primary affect (purulent-necrotic inflammation) develops at the site of entry. Marked hyperemia of the throat ("flamed throat") and a characteristic "strawberry tongue" are observed.

Infection spreads via two pathways:

Lymphogenic: formation of regional lymphadenitis and lymphangitis (primary infection complex).
Hematogenous (toxinemia): the toxin enters the bloodstream, causing microvessel vasculitis (stasis, sludging). This manifests as a fine punctate rash starting on the face (excluding the pale nasolabial triangle) and spreading to the trunk.

Pathological Anatomy Scarlet fever tonsillitis (angina) begins as catarrhal, progressing by the end of the first day to catarrhal-purulent and purulent-necrotic forms. When necrotic masses slough off, ulcers form. Lympho-macrophage infiltrates develop in the skin due to vasculitis, leading to epidermal necrosis. The resolution stage shows lamellar desquamation (especially on the palms and soles).

Complications of Scarlet Fever

Complications are divided into two large groups based on the timing of onset and pathogenesis.

Early (Pyogenic) Complications Occur from the end of the first week. Associated with the direct spread of the purulent process:

Retropharyngeal abscess and neck phlegmon.
Otitis media and temporal bone osteomyelitis.
Purulent meningitis, brain abscess.
Sepsis.

Late (Autoimmune) Complications Peak in the second to third week. They are driven by cross-reactivity of antibodies against streptococci with host tissues (sensitization).

Endomyocarditis.
Glomerulonephritis: a productive intracapillary process of immune-complex nature (a manifestation of type III/IV hypersensitivity). May progress to chronic form.

Measles: Clinical and Pathological Features

Measles is an epidemic disease caused by an RNA-containing paramyxovirus. Transmission occurs via airborne droplets. The virus exhibits hemolyzing and hemagglutinating activity.

Pathogenesis After penetrating the respiratory epithelium, the virus replicates and spreads to regional lymph nodes. Primary viremia develops, followed by secondary viremia by the end of the first week. Mucosal involvement presents as serous-catarrhal inflammation. The immune response leads to suppressed cell-mediated hypersensitivity reactions, causing temporary anergy and immunosuppression.

Morphological Manifestations

Enanthem: appears 1–2 days before the skin rash as whitish spots with a hyperemic halo.
Koplik spots: located on the buccal mucosa near the molar teeth (a key diagnostic sign). Specific giant epithelial cells are found within these lesions.
Exanthem: maculopapular rash with a strict centrifugal progression pattern (behind the ears $\rightarrow$ face $\rightarrow$ neck $\rightarrow$ trunk $\rightarrow$ extremities).

Mnemonic

Measles rash spread pattern: E-F-N-T-E (Ears, Face, Neck, Trunk, Extremities). The rash descends from top to bottom.

Frequently asked questions

What is the causative agent of diphtheria?

The causative agent of diphtheria is Corynebacterium diphtheriae. These are Gram-positive, non-motile, non-spore-forming pleomorphic rods. Based on biochemical properties, two main biovars are distinguished:

Biovar gravis — enzymatically active, ferments starch;
Biovar mitis — lacks amylase activity and does not ferment starch.

A characteristic morphological feature of the pathogen is the presence of volutin (metachromatic) granules at the poles of the cell, giving the bacteria a club-like shape, as well as a specific arrangement in smears at angles to each other resembling Roman numerals or stacked fingers.

What two types of fibrinous inflammation develop in diphtheria depending on necrosis depth and epithelium type?

Depending on the depth of necrosis and the thickness of the fibrinous membrane, croupous and diphtheritic inflammation are distinguished.

Feature	Croupous Inflammation	Diphtheritic Inflammation
Epithelium Type	Prismatic, cylindrical secretory	Stratified squamous or deeply damaged by necrosis
Tissue Adhesion	Loose	Firm
Depth of Necrosis	Superficial	Deep
Membrane Thickness	Thin	Thick, tightly bound to tissue
Sloughing	Easy, rapid, as a cast	Difficult, exposing an ulcerated surface

Croupous inflammation is typical for the larynx, trachea, and bronchi, posing a risk of lumen obstruction and asphyxia. Diphtheritic inflammation develops in the fauces, tonsils, and esophagus, leaving deep ulcers after the membrane is removed.

What pathomorphological changes in the heart are caused by the exotoxin in the toxic form of diphtheria?

The exotoxin causes diphtheria (infectious-toxic) myocarditis. Macroscopically, the heart becomes enlarged due to the dilation of all chambers and appears flabby. Microscopic changes include:

Focal eosinophilia — alteration in cardiomyocyte staining;
Dystrophy — hydropic and fatty changes;
Waxy degeneration — necrosis of muscle fibers and myofibrils leading to stromal collapse;
Interstitial inflammation — perivascular accumulation of serous exudate and small lymphoplasmacytic infiltrates.

If the patient survives, the organization of necrosis foci leads to reticular cardiosclerosis.

Which peripheral nerves are most frequently affected in diphtheritic polyneuropathy?

In diphtheritic polyneuropathy, cranial nerves and peripheral limb nerves are affected. In the early period, nerves located in the zone of maximal toxin concentration are involved:

Glossopharyngeal and vagus nerves (cranial nerves IX–X) — their damage causes paralysis of the soft palate, nasal voice, and swallowing disorders;
Ciliary nerve (n. ciliaris) — leads to accommodation paralysis;
Abducens nerve (n. abducens) — causes strabismus and ptosis.

Subsequently, a symmetrical peripheral polyneuropathy develops, predominated by motor disturbances, decreased deep tendon reflexes, and progressive muscle weakness in the extremities. In severe cases, diaphragmatic paralysis occurs.

What specific multinucleated giant cells are found in lymphoid tissue in measles?

In measles, specific multinucleated giant cells known as Warthin–Finkeldey cells are found in lymphoid tissue. Their presence is a pathognomonic sign of the disease. These cells form via the fusion of multiple epithelial and lymphoid cells due to the syncytium-forming action of the measles virus. They localize in lymph nodes amid follicular hyperplasia, as well as in the tonsils and intestinal lymphoid tissue. Unlike Langhans giant cells, they contain numerous nuclei and serve as a key morphological marker for the histological verification of measles infection.

What is the primary pathogenic factor of streptococcal infection?

Streptococci secrete an exotoxin that causes toxinemia, fever, systemic vasculitis, and a characteristic rash.

What cells are typical for the morphological picture of measles?

Specific giant epithelial cells are found in the affected areas (such as the enanthem).

What is the core mechanism of late scarlet fever complications?

They occur on weeks 2–3 and are autoimmune in nature, driven by cross-reacting antibodies leading to glomerulonephritis and endomyocarditis.

Go deeper

Pathogenesis of primary affect formation in streptococcal pharyngitis
Mechanisms of giant cell formation in measles infection
Immune-complex nature of glomerulonephritis in scarlet fever
Differentiating rashes across various childhood infections