Protozoal infections: Amoebiasis and Toxoplasmosis
In amoebiasis, the pathological process is localized in the wall of the large intestine, where inflammation, necrosis, and ulceration develop. Intestinal complications (ulcer perforation with peritonitis) and extraintestinal manifestations pose a danger. The pathogen can enter the liver via branches of the portal vein (v. portae) (in 40% of cases), causing amoebic hepatitis and abscesses, or be carried hematogenously to the lungs.
Toxoplasmosis is an anthropozoonosis caused by Toxoplasma gondii. Sexual reproduction of the parasite occurs in the body of felids, while asexual reproduction occurs in intermediate hosts (including humans). Infection occurs via alimentary (the main route), contact, or transplacental routes. Inside macrophages, the pathogen undergoes a stage of incomplete phagocytosis and schizogony, destroying cells and disseminating throughout the body. During chronic infection, true cysts form in the brain and muscles. The congenital form depends on the time of infection:
- 1st trimester: severe generalized process, often leading to fetal death.
- 2nd trimester: microcephaly, gliosis, calcification, microphthalmia with cataract.
- 3rd trimester: subacute meningoencephalitis, retinitis.
Tissue helminthiases: Trichinosis
Causative agent — Trichinella spiralis. Humans are infected alimentarily through insufficiently cooked meat of wild or domestic animals. Pathogenesis includes three stages:
- Intestinal: release and invasion into the mucosa.
- Migratory: females give birth to larvae, which are disseminated via lymph and blood.
- Muscular: by the 18th day, larvae invade skeletal muscles, where they become encapsulated (can persist for up to 40 years).
The disease proceeds through enzymatic-toxic, immunological (violent allergic reaction, vasculitis), and immunopathological phases. In severe cases, myocarditis, pneumonia, and meningoencephalitis develop.
Cystic helminthiases: Echinococcosis and Cysticercosis
Echinococcosis is caused by the larval stages of cestodes (Echinococcus granulosus and E. multilocularis). Definitive hosts are canids, which shed oncospheres. In humans (intermediate hosts), oncospheres penetrate the intestinal wall and settle in the liver or lungs, transforming into larval cysts. These cysts grow for decades, compressing tissues. A fibrous capsule forms around them, which may calcify. Cyst rupture threatens with anaphylactic shock and dissemination (secondary echinococcosis).
Cysticercosis is caused by Cysticercus cellulosae, the bladder worm of the pork tapeworm (Taenia solium). Infection occurs via the fecal-oral route. Larvae are frequently localized in the brain and eyes, causing seizures and vision loss. Pathogenesis includes the stages of a viable parasite, death (the most toxic phase with pronounced serofibrinous inflammation), and residual changes (calcification).
Tropical infections: Leprosy
Leprosy (Hansen's disease) is a chronic infection caused by Mycobacterium leprae. It affects the skin, peripheral nerves, and internal organs. The disease has low contagiousness and is transmitted by contact and airborne droplets from an infected person. Mycobacteria invade through the nasopharynx or damaged skin (without a primary affect), then migrate into nerve endings, the lymphatic and blood streams. In the majority of infected individuals, the process is arrested by the immune system.
To memorize the triad of toxoplasmosis in lymph nodes: HHR — Hyperplasia (follicular), Granulomas, Sinus dilation.
Class and exam questions
What is the difference between a definitive host and an intermediate host using toxoplasmosis as an example?
In the definitive host (cats), sexual reproduction of the pathogen takes place with the release of oocysts. In the intermediate host (humans, other animals), asexual reproduction occurs with the formation of tissue cysts.
Which stage of cysticercosis is accompanied by the most pronounced inflammation?
Stage of parasite death. The dying cysticerci release a maximum amount of toxic substances, causing severe sensitization and serofibrinous inflammation.
Why is the rupture of an echinococcal cyst dangerous?
Rupture leads to the spilling of toxic fluid, causing severe anaphylactic shock, as well as dissemination of the peritoneum or pleura with scolexes, leading to the development of multiple secondary echinococcosis.
What else to study on this topic
- Morphological differences of various forms of toxoplasmosis
- Pathogenesis of fibrous capsule formation in trichinosis
- Mechanisms of parasite evasion from the immune response
- Alveococcosis: features of invasive growth and metastasis
- Pathological anatomy of the nervous system in leprosy
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