Morphological changes in measles
Although the topic of the article is stated as scarlet fever, within the study of childhood infections, it is important to understand the pathogenesis of viral conditions such as measles. Changes in measles infection affect several body systems, forming a characteristic pathomorphological picture.
Skin involvement at the sites of specific rashes is characterized by marked hyperemia of the microvasculature. Lymphocytic and histiocytic infiltrates form around the vessels. Diapedetic hemorrhages are noted, later becoming sites of hemosiderin accumulation. Cellular vacuolization and the appearance of specific giant multinucleated epithelial structures are observed in the epidermis itself.
Reaction of the lymphatic system manifests as follicular hyperplasia in the lymph nodes. The most important diagnostic (pathognomonic) criterion is the detection of Warthin–Finkeldey giant multinucleated cells in the lymphoid tissue.
Changes in the respiratory organs begin with the development of serous-catarrhal pharyngitis and tracheitis. As the process progresses, the inflammation extends downward, involving the bronchial tree and alveoli. Specific measles pneumonia is interstitial: the inflammatory process localizes in the interalveolar septa and peribronchial tissue. The epithelium of the bronchial mucosa undergoes squamous metaplasia. Microscopically, macrophage-lymphocyte infiltrates, hyaline membranes, and giant cells are identified in the alveoli. If a secondary bacterial flora joins the viral process, severe necrotizing purulent bronchitis develops.
Complications and outcomes of measles infection
Complications can be triggered directly by the measles virus itself or by a secondary bacterial infection. Inflammatory processes are localized in various systems:
- Respiratory system: formation of laryngotracheobronchitis and pneumonia.
- Gastrointestinal tract: development of stomatitis, enteritis, or colitis.
- Central nervous system: onset of encephalitis and meningitis.
- Visual organs: keratitis, blepharitis, conjunctivitis.
In severely weakened children, an extremely severe specific complication may develop — noma (progressive moist gangrene of the soft tissues of the maxillofacial region). With timely therapy, the outcome of the disease is favorable, but emaciated patients retain the risk of a fatal outcome.
Pathological anatomy of mumps
Mumps (commonly known as epidemic parotitis) is caused by an RNA-containing paramyxovirus transmitted via airborne droplets. The virus has a tropism for glandular tissues (parotid and pancreas, testes) and the nervous system. Primary replication occurs in the epithelial cells of the respiratory tract and lymph nodes.
Morphological picture:
- Parotid glands: the process is usually bilateral. The glands are markedly enlarged and acquire a doughy consistency. At the microscopic level, marked edema and diffuse infiltration of the interstitium by plasma cells and lymphocytes are visible. The excretory ducts are compressed, with cellular debris and neutrophils accumulating inside them.
- Testicles (orchitis): the tissue becomes edematous, infiltrated by mononuclear cells, and punctate hemorrhages occur. Due to severe swelling in a confined space, blood flow is disrupted, leading to testicular infarctions. Outcome: sclerosis, atrophy, and male infertility.
- Pancreas: foci of necrosis appear, surrounded by clusters of leukocytes.
- Brain: during the development of viral encephalitis, foci of demyelination and perivascular lymphoglial cuffs are formed.
Infectious mononucleosis and poliomyelitis
Infectious mononucleosis is an anthroponotic disease caused by the Epstein–Barr virus (EBV), predominantly affecting adolescents and young adults. The virus is transmitted via saliva, invades the nasopharyngeal epithelium, and then infects B lymphocytes, causing their polyclonal activation.
Pathomorphology of mononucleosis:
- Blood: pronounced lymphocytosis (up to 18,000/µL) with the appearance of atypical T lymphocytes.
- Lymph nodes and spleen: marked hyperplasia of paracortical T-zones due to atypical lymphocytes. Splenomegaly can be so massive that there is a risk of spontaneous capsule rupture with fatal hemorrhage.
- Liver: moderate hepatomegaly, portal tracts infiltrated by atypical cells, micro-necroses are possible.
- Central nervous system: brain tissue edema, accumulation of lymphoid elements around the vessels of the pia mater.
Poliomyelitis is briefly described in the provided source: it is an anthroponotic infection caused by an enterovirus (RNA-containing). It is transmitted via the alimentary route and specifically affects motor neurons of the central nervous system, leading to severe neurological deficits.
Briefly: answers to topical questions
What are the pathomorphological changes in the fauces and tonsils in scarlet fever?
Pathomorphological changes in the fauces and tonsils in scarlet fever are represented by a primary affect in the form of tonsillitis (angina), which sequentially goes through several stages.
- Initial stage — catarrhal inflammation of the fauces and tonsils mucosa with sharply demarcated hyperemia ("flaming fauces") and enanthema on the palate.
- End of the first day — progression to catarrhal-purulent and purulent-necrotic inflammation (follicular, lacunar, or necrotic tonsillitis develops).
- Outcome — upon rejection of necrotic tissues, ulcerative-necrotic tonsillitis is formed.
Which specific structures of the central nervous system are affected in poliomyelitis?
In poliomyelitis, motor neurons of the central nervous system are specifically affected.
- Anterior horns of the spinal cord — selective, rapid, and irreversible cell death occurs.
- Cervical and lumbar enlargements — the most frequent localization of motor neuron lesions (the process is mainly pronounced in the lumbar region).
The destruction of these structures leads to the development of peripheral (flaccid) pareses and paralyses with pronounced atrophy of the innervated muscles.
What is the character and pathogenesis of the skin rash in scarlet fever?
The skin rash (exanthema) in scarlet fever is monomorphic, finely punctate, maculopapular, and located on a hyperemic background. The pathogenesis of the rash is due to toxemia, which causes generalized microvessel vasculitis.
- Dermis — marked hyperemia, erythrocyte stasis, sludge, moderate perivascular edema, and the formation of lymphomacrophagic infiltrates are observed.
- Epidermis — becomes infiltrated with exudate, and cells undergo keratinization and necrosis.
In the resolution stage, skin desquamation develops, which is large-lamellar on the palms and soles due to the thick epithelial layer.
What late infectious-allergic complications develop in the second to third week of scarlet fever?
In the second to third week of scarlet fever, against the background of sensitization and molecular mimicry, late allergic and autoimmune complications develop.
- Acute glomerulonephritis — post-streptococcal kidney injury with fixation of immune complexes on the glomerular basement membrane.
- Myocarditis and/or endocarditis — heart damage of a rheumatic (allergic) nature.
- Arthritis (synovitis) — joint damage similar in mechanism to rheumatic disease.
- Rheumatic fever — a delayed consequence of streptococcal sensitization.
These complications are based on delayed-type hypersensitivity and cross-reactivity of antigens.
To memorize the pathognomonic sign of measles, use the association: "Measles = UV rays" (Warthin–Finkeldey cells). For mononucleosis: "Mono = one, but many lymph nodes, spleen, and liver are affected" (generalized lymphadenopathy, splenomegaly, hepatomegaly).
Class and exam questions
Which cells are a pathognomonic morphological sign of measles?
Warthin–Finkeldey giant multinucleated cells found in the hyperplastic follicles of lymph nodes.
What is the mechanism of infertility development in mumps?
The virus causes marked edema and mononuclear infiltration of the testicular tissue. This leads to vascular compression, impaired blood supply, parenchymal infarctions followed by sclerosis and atrophy.
What is noma and in which infection does it occur?
Noma is a moist gangrene of the soft tissues of the face that can develop as a severe specific complication of measles in severely debilitated children.
What else to study on this topic
- Mechanisms of formation of Pirogov-Langhans giant cells and Berezovsky-Sternberg cells (for differential diagnosis)
- Pathogenesis of polyclonal B-lymphocyte activation upon Epstein-Barr virus exposure
- Histological structure of interalveolar septa and hyaline membrane formation in interstitial pneumonias
- Comparative characteristics of serous-catarrhal and fibrinous inflammation of the respiratory tract
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