Purulent and anaerobic infections
This group of pathologies is caused predominantly by Gram-positive cocci, which possess numerous virulence factors and are capable of provoking purulent inflammation.
Staphylococcal infection Most commonly occurs in surgical or burn wounds. Can act as a hospital-acquired (opportunistic) infection, especially in patients with intravenous catheters, prosthetic heart valves, and in intravenous drug users. Typical manifestations include:
- Furuncles and carbuncles.
- Purulent hidradenitis.
- Soft tissue and skin phlegmons.
- Abscesses in the lungs and bones (osteomyelitis).
Streptococcal infection Affects the skin, oropharynx, lungs, and heart valves. Most pathogenic strains belong to the beta-hemolytic type. Streptococcus secretes a specific exotoxin, which causes fever, rash, and vasculitis. Examples of such diseases include erysipelas and pharyngitis. A special place is occupied by pneumococci (the cause of pneumonia) and S. mutans, which causes dental caries.
Scarlet fever: pathogenesis and morphology
Scarlet fever is an infectious disease affecting primarily children aged 3 to 15 years. It is transmitted via airborne droplets from a person suffering from any form of streptococcal infection.
Mechanism of development The entry gate 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 fauces ("fiery red throat") and a specific "strawberry tongue" are observed.
The infection spreads via two pathways:
- Lymphogenic: formation of regional lymphadenitis and lymphangitis (primary infection complex).
- Hematogenous (toxinemia): the toxin enters the blood, causing microvascular vasculitis (stasis, sludging). This manifests as a punctate rash starting on the face (excluding the pale nasolabial triangle) and spreading down to the trunk.
Pathological anatomy Scarlet fever tonsillitis begins as catarrhal, but by the end of the first day transforms into catarrhal-purulent and purulent-necrotic forms. When the masses slough off, ulcers form. In the skin, lymphomacrophage infiltrates form due to vasculitis, leading to epidermal necrosis. In the resolution stage, lamellar desquamation is observed (especially on the palms and soles).
Complications of scarlet fever
Complications are divided into two large groups depending on the timing of onset and pathogenesis.
Early (purulent) complications Arise from the end of the first week. Associated with direct spread of the purulent process:
- Retropharyngeal abscess and neck phlegmon.
- Otitis media and osteomyelitis of the temporal bone.
- Purulent meningitis, brain abscess.
- Sepsis.
Late (autoimmune) complications Reach a peak in the second to third week. Their basis is a cross-reaction of antibodies against streptococcus with the body's tissues (sensitization).
- Endomyocarditis.
- Glomerulonephritis: a productive intracapillary process of immune complex nature (a manifestation of delayed-type hypersensitivity). May progress to a chronic form.
Measles: clinical course features
Measles is an epidemic disease caused by an RNA-containing paramyxovirus. Transmission occurs via airborne droplets. The virus exhibits hemolytic and hemagglutinating activity.
Pathogenesis After penetrating the respiratory epithelium, the virus replicates and reaches regional lymph nodes. Primary viremia develops, and by the end of the first week—secondary viremia. Mucosal involvement proceeds as serous-catarrhal inflammation. The immune response leads to a decrease in immediate-type hypersensitivity reactions, causing anergy and immunodeficiency.
Morphological manifestations
- Enanthem: appears 1–2 days before the skin rash. These are whitish spots with a hyperemic halo.
- Koplik's spots: localized on the buccal mucosa near the small molar teeth (a key diagnostic sign). Specific giant epithelial cells are found in the foci.
- Exanthem: maculopapular rash with a strict sequential appearance (behind the ears $\rightarrow$ face $\rightarrow$ neck $\rightarrow$ trunk $\rightarrow$ limbs).
Briefly: answers to topical questions
What is the causative agent of diphtheria?
The causative agent of diphtheria is the diphtheria corynebacterium (Corynebacterium diphtheriae). These are Gram-positive pleomorphic rods that are non-motile and spore-forming (Note: non-spore-forming). Depending 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 granules at the poles of the cell, giving the bacterium a club-like shape, as well as a specific arrangement in smears at an angle to each other in the form of Roman numerals or spread fingers.
What two types of fibrinous inflammation develop in diphtheria depending on the depth of necrosis and the type of epithelium?
Depending on the depth of necrosis and the thickness of the fibrinous film, croupous and diphtheritic inflammation are distinguished.
| Sign | Croupous inflammation | Diphtheritic inflammation |
|---|---|---|
| Type of epithelium | Prismatic, cylindrical secreting | Stratified squamous or deeply damaged by necrosis |
| Tissue attachment | Loose | Firm |
| Depth of necrosis | Superficial | Deep |
| Film thickness | Thin | Thick, tightly adhered to tissue |
| Sloughing | Easy, rapid, as a cast | Difficult, exposing an ulcerated surface |
Croupous inflammation is typical for the larynx, trachea, and bronchi, creating a threat of organ lumen obstruction and asphyxia. Diphtheritic inflammation develops in the fauces, tonsils, and esophagus, leaving deep ulcers after the film is removed.
What pathomorphological changes in the heart does the exotoxin cause 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 — altered staining of cardiomyocytes;
- Dystrophy — hydropic and fatty change;
- 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 diphtheria polyneuropathy?
In diphtheria polyneuropathy, cranial nerves and limb nerves are affected. In the early period, nerves located in the zone of maximum toxin concentration are involved:
- Glossopharyngeal and vagus nerves (cranial nerves IX–X) — their involvement causes soft palate paralysis, nasal voice, and swallowing disorders;
- Ciliary nerve (n. ciliaris) — leads to paralysis of accommodation;
- Abducens nerve (n. abducens) — causes strabismus and ptosis.
Subsequently, a symmetrical peripheral polyneuropathy develops with a predominance of motor disorders, decreased deep tendon reflexes, and progressive limb muscle weakness. In severe cases, diaphragmatic paralysis develops.
What specific multinucleated giant cells are found in lymphoid tissue in measles?
In measles, specific multinucleated giant Warthin–Finkeldey cells (Warthin–Finkeldey) are found in the lymphoid tissue. Their presence is a pathognomonic sign of this disease. These cells are formed as a result of the fusion of numerous epithelial and lymphoid cells under the syncytium-forming action of the measles virus. They are localized in lymph nodes against the background of follicular hyperplasia, as well as in the tonsils and intestinal lymphoid tissue. Unlike Pirogov–Langhans cells, they contain numerous nuclei and serve as a key morphological marker for the histological verification of measles infection.
Stages of the measles rash: E-F-N-T-L (Ears, Face, Neck, Trunk, Limbs). The rash spreads from top to bottom.
Class and exam questions
What is the main pathogenetic factor of streptococcal infection?
Streptococcus produces an exotoxin that causes toxemia, fever, systemic vasculitis, and a characteristic rash.
Which cells are typical for the morphological picture of measles?
Specific giant epithelial cells are found in the lesions (e.g., in the area of enanthema).
What is the essence of late complications of scarlet fever?
They appear in the 2nd–3rd week and are autoimmune in nature. Due to cross-reacting antibodies, glomerulonephritis and endomyocarditis develop.
What else to study on this topic
- Pathogenesis of the primary affect formation in streptococcal tonsillitis
- Mechanisms of giant cell formation in measles infection
- Immune complex nature of glomerulonephritis in scarlet fever
- Differences in rashes across various childhood infections
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