Prion diseases
The morphological picture is generally typical of subacute spongiform encephalopathies. Key nosologies from the material:
- Alpers' disease — a hereditary chronic encephalopathy affecting children and adolescents. Lasts about 8–12 months. When developing in utero, it leads to microcephaly and joint immobility. In the central nervous system, neurons die and glia proliferates (especially in the cortex of the occipital lobe, striatum, and Ammon's horn), while Purkinje cells disappear in the cerebellum. Extensive centrilobular necrosis forms in the liver.
- Spongiform myositis with prion inclusions (IBM) — manifests as slowly progressive muscle weakness and pain. Vacuoles containing spiral filaments with prion proteins (PrP), Aβ peptides, and apolipoprotein E appear in muscle fibers.
The risk group for prion infection includes pathologists, surgeons (medical and veterinary), as well as meat processing plant workers.
Malaria: Life cycle and pathogenesis
Malaria is an infection caused by the intracellular parasite Plasmodium. The causative agent for falciparum malaria is P. falciparum, for tertian malaria — P. vivax, quartan malaria — P. malariae, and ovale malaria — P. ovale.
The life cycle of plasmodium is divided into two phases:
- In the mosquito organism (sporogony): a female Anopheles mosquito ingests blood from an infected person containing gametocytes. In her stomach, they develop into sporozoites, which accumulate in the salivary glands.
- In the human organism (schizogony): sporozoites enter the blood during a bite. First, they invade the liver (tissue stage), where they multiply into merozoites. Then, merozoites enter the bloodstream and infect erythrocytes, feeding on hemoglobin. Hemoglobin residues are converted into a black pigment — hemozoin.
The destruction of erythrocytes causes the release of pyrogens, leading to a powerful attack of intermittent fever with chills. Massive hemolysis leads to suprahepatic jaundice and anemia. Hemmozoin is engulfed by macrophages, causing the spleen, liver, and bone marrow to turn a dark gray color.
Complications and clinical forms of malaria
Falciparum malaria is the most severe. Parasites secrete sequestrins that bind to ICAM-1 receptors on the vascular endothelium. Because of this, infected erythrocytes "stick" to capillary walls without reaching the spleen for destruction. This causes parasitic blood stasis, microthrombosis, and organ ischemia.
Complications of falciparum malaria:
- Cerebral ischemia with neuronal death and the formation of Dürck's granulomas (composed of glia and macrophages).
- Malarial coma and infectious-toxic shock (main causes of death).
- Acute kidney injury and pulmonary edema.
- Treatment with quinine can cause massive hemolysis with dark urine.
Interesting fact: people lacking the Duffy antigen on erythrocytes (common in people of African descent) and patients with hemoglobinopathies or G6PD deficiency have genetic resistance to malaria.
Amoebiasis
Caused by the protozoan Entamoeba histolytica, transmitted via the fecal-oral route. Cysts survive in the stomach due to their chitinous shell, and active trophozoites emerge from them in the intestine. Only 10% of infected individuals develop the disease (when infected with a virulent strain).
The amoeba secretes enzymes (hyaluronidase, cysteine proteinases) that dissolve the mucosa of the large intestine (most commonly the cecum and ascending colon). Deep ulcers with undermined, overhanging edges form. Purulent-hemorrhagic inflammation with necrosis develops. A characteristic clinical sign is frequent stool resembling "raspberry jelly" (mucus with blood).
Briefly: answers to topical questions
Which respiratory tract cells are the main target in respiratory syncytial infection?
In respiratory syncytial infection, the epithelium of the respiratory tract and alveolar ducts is affected. Focal epithelial necrosis, desquamation, and proliferation with the formation of syncytia or papillae develop. In early childhood, the lower respiratory tract is predominantly affected.
How are syncytia morphologically formed in respiratory syncytial infection?
Syncytia are formed as a result of the proliferation of the affected epithelium of the respiratory tract and alveolar ducts. Morphologically, they are giant cells containing large, pale, rounded nuclei. Clusters of the virus, appearing as small basophilic inclusions, are identified in the cytoplasm of these structures. The formation of such syncytia is a characteristic cytopathic effect of this pathogen.
What intracellular inclusions are characteristic of cells infected with the respiratory syncytial virus?
Cells infected with the respiratory syncytial virus are characterized by the presence of specific small basophilic inclusions localized in the cytoplasm. These inclusions represent intracellular clusters of viral particles. This feature is detected in giant syncytial cells formed during the proliferation of the epithelium of the respiratory tract and alveolar ducts.
What macroscopic changes are observed in the lungs in severe respiratory syncytial bronchiolitis?
In respiratory syncytial infection, due to the obstruction of small bronchi and bronchioles, atelectasis, acute perifocal pulmonary emphysema, and focal serous pneumonia develop.
What microscopic changes develop in the bronchiolar wall during respiratory syncytial infection?
A complex of inflammatory and destructive changes develops in the bronchiolar wall:
- Necrosis and desquamation — focal death and shedding of the epithelium.
- Proliferation — epithelial overgrowth with the formation of syncytia or papillae.
- Edema — thickening of the bronchiolar wall.
Secretions containing inflammatory cells and desquamated epithelium accumulate in the lumen.
Which cells predominate in the inflammatory exudate in the alveoli during respiratory syncytial pneumonia?
Macrophages, neutrophils, and large cells forming syncytia are found in the inflammatory exudate during respiratory syncytial pneumonia. Marked diffuse lymphohistiocytic infiltration, characteristic of interstitial pneumonitis, develops in the interalveolar septa.
What is the morphological substrate for the development of bronchial obstruction syndrome in respiratory syncytial infection?
The morphological substrate of bronchial obstruction syndrome is the narrowing of the lumen of small bronchi and bronchioles. It is caused by wall edema, necrosis, death and desquamation of the epithelium, its proliferation, as well as impaired mucociliary clearance with the accumulation of secretions containing inflammatory cells and desquamated epithelium.
Which organs, besides the respiratory system, can be involved in the generalized form of respiratory syncytial infection?
When the infection generalizes, various internal organs and the nervous system can be involved in the pathological process:
- Internal organs — kidneys, liver, pancreas, and intestines (interstitial inflammation with papillary epithelial proliferations develops).
- Central nervous system — brain (meningoencephalitis may develop).
What are the main causes of death in young children with severe respiratory syncytial infection?
The main causes of death in young children with a severe course of the disease are pneumonia and severe pulmonary complications caused by secondary infection. Generalization of the infectious process with damage to internal organs can also be a cause of death.
How does the cellular composition of the infiltrate in respiratory syncytial infection differ from that in adenoviral infection?
In respiratory syncytial infection, macrophages, neutrophils, and large syncytial-forming cells are found in the alveolar exudate. In adenoviral infection, macrophages, lymphocytes, neutrophils, desquamated epithelium, and adenoviral cells are found in the alveoli. Lymphohistiocytic infiltration is observed in the interstitium in both infections.
For malaria: "Tropics adhere, three days rest" (falciparum malaria causes erythrocyte adhesion and stasis, whereas tertian malaria has a benign course with distinct attacks).
Class and exam questions
Why do organs turn black in malaria?
During the breakdown of hemoglobin by the plasmodium, the pigment hemomelanin is formed. It is phagocytosed by RES cells, accumulating in the spleen, liver, and bone marrow.
What are Dürck's granulomas?
These are accumulations of proliferating oligodendrogliocytes and macrophages in the brain, arising in response to ischemia in falciparum malaria.
What do ulcers look like in amebiasis?
They have undermined, slightly overhanging edges. The mucous membrane between the ulcers is usually preserved, but edematous and hyperemic.
What else to study on this topic
- Plasmodium development cycle: tissue and erythrocytic schizogony
- Mechanism of fever curve formation in malaria
- Pathogenesis of parasitic stasis and the role of ICAM-1 molecules
- Morphological changes of the spleen (acute and chronic stage)
- Human resistance factors to malaria
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