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Taenia solium - Life Cycle, Pathogenesis, Pathology, Host Immunity, Epidemiology, Reservoir, Transmission

Last Modified: January 27, 2023

Life Cycle of Taenia solium

The life cycle of Taenia solium is completed in two different hosts:

Intermediate hosts: Pig is an intermediate host where larval development takes place. Occasionally, man becomes the intermediate host.

Definitive host: Man is the definitive host of T. saginata as they harbor the adult tapeworm.

  • Infection of Taenia solium starts when humans consume raw or undercooked pig infested with Cysticercus cellulosae

  • the larvae are digested-free in the small intestine

  • once it comes in contact with the bile, the protoscolex evaginates to attach to the intestinal wall with the help of hooks and suckers

  • after adhering to the host intestinal wall, it produces a chain of segments from the caudal end of the scolex and eventually develops into an adult tapeworm within 62 to 72 days

  • eggs are fertilized within the sexually mature segments

  • these eggs are intermittently extruded from the segments into the intestinal lumen and passed along with the feces

  • sometimes, as the parasite matures, the terminal gravid proglottids separate in short chains of 5-6 from the end of the tapeworm and are expelled along with the feces

  • pigs acquire Taenia solium infection after consuming eggs or gravid proglottids passed in human feces

  • inside the cattle stomach, each gravid segments disintegrate to release 30,000 to 50,000 eggs

  • from each egg, a six-hooked embryo called an oncosphere emerges and adheres by penetrating the intestinal wall with their hooks

  • the larvae invade the mucosa and vessels of the submucosa within 24 to 72 hours and are carried via the lymphatic or circulatory system to muscles, brain, fats, visceral organs, and the tongue

  • these larvae lose their hooklets, enlarge and develop into a fluid-filled cyst called Cysticercus cellulosae within 9 weeks to 10 weeks

  • the Cysticercus bovis can remain viable (infectious) in the intermediate hosts for up to 8 weeks after which they die, disintegrate, and become fibrotic and calcified

  • if humans consume undercooked pig infested with Cysticercus bovis, the life cycle of Taenia solium continues

  • humans can also be infected in the same process as pigs by ingesting food, or drinking water, contaminated with feces from a person infected by the adult worms i.e. tapeworm eggs are ingested instead of the cysts

  • similar to infection in pigs, the larvae invade the mucosa and vessels of the submucosa, carried via the lymphatic or circulatory system to different tissues where they develop into cysts

  • in humans, most cysts are present in the Central Nervous System, skeletal muscles, eye, and sub-cutaneous tissues resulting in a condition called cysticercosis

Fig: T. solium lifecycle (Source: CDC)

Pathogeneis, Pathology of Taenia solium

Both adults and cysts i.e. Cysticercus cellulosae of Taenia solium are pathogenic to humans. The adult tapeworm is less pathogenic and occasionally may cause mild irritation or inflammation of the intestinal mucosa due to its armed scolex. The cysts on the other hand are highly pathogenic causing a serious disease known as cysticercosis.

Cysticercosis occurs after ingesting food, or drinking water, contaminated with feces from a person infected by the adult worms i.e. tapeworm eggs are ingested instead of the cysts. Most cysts, which can remain viable for a few years, occur in the skin, skeletal muscles, eye, and central nervous system.

In the brain, the cysts overcome the host defenses by secreting prostaglandins and other substances that inhibit the activation of the complement system as well production of cytokines. As a result, minimal host inflammation occurs around the live cysticercus- a minimal cellular reaction consisting of a few eosinophils and macrophages is found around the live cyst.

Once the cyst dies, it is densely surrounded by inflammatory cells such as leucocytes, multinucleated giant macrophages, and in rare cases foreign body giant cells. Calcification of dead Taenia solium cyst is completed within 5 years of infection.

Host Immunity of Taenia solium

Cysticercus cellulosae is able to induce the host immune response. Anti-cysticercus antibodies such as IgG antibodies are produced in serum, CSF, and saliva. Although these antibodies do not help in controlling the course of infection, they are responsible for protecting the host against subsequent re-infection by cysticerci.

Pathological lesions and damage to the host cells in cases of cysticerci are immunologically mediated and are caused by marked inflammatory response against the dead cysts.

Epidemiology of Taenia solium

Taenia solium is worldwide in distribution. It is most common in areas or countries with low socio-economic status, poor sanitation, and pork-eating communities.

This tapeworm is endemic to Central America, South America, South Africa, Southeast Asia, Eastern Europe, and China.

Reservoir, Source of Taenia solium

Both infected humans and pigs are the reservoirs of Taenia solium. Cysticercus cellulosae (cyst) and eggs of the tapeworm are the infective stages.

Transmission of Taenia solium

Taenia solium is transmitted by:

  • ingestion of food or water contaminated by eggs or cysts

  • endogenous autoinfection: poor personal hygiene may result in the anus-hand-mouth transfer of eggs or cysts

  • reverse peristalsis movements may throw back Taenia eggs into the duodenum where they hatch to cause autoinfection

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