Cysticercosis

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University of Oklahoma Study Abroad Microbiology in Arezzo, Italy[1]

Image of Taenia solium. From: faculty.ccbcmd.edu [2]

Etiology/Bacteriology

Taxonomy

| Domain = Eukaryota | Phylum = Platyhelminthes | Class = Cestoda | Order = Cyclophyllidea | Family = Taeniidae | Genus = Taenia | species = T. solium

Description

Cysticercosis is an infectious disease that is caused by the larvae of Taenia solium. T. solium is a two-host zoonotic cestode whose adult stage consists of a 2-4 meter long tapeworm. The only known final host for this adult stage is humans, specifically in the small intestine. The intermediate host is the pig, so part of the T. solium life cycle takes place in that host prior to causing taeniasis in humans. Taeniasis is a parasitic infection caused by the presence of tapeworms in the intestine. A person with taeniasis is capable of infecting themselves or others with cysticercosis through fecal-oral transmission. Cysticercosis is transmitted by eating food or drinking water that is contaminated with T. solium eggs. 2-3 months after ingestion, the eggs develop into cysticerci, which are cysts formed by T. solium larvae. The location of the cysts throughout the body determines the symptoms that are demonstrated, diagnoses performed, and treatment used. If the cysts are located in the central nervous system, the infection is specifically called neurocysticercosis.

Cysticercosis is most prevalent in parts of Africa, Asia, Mexico, and Central and South America. However, it is a worldwide issue with about 50 million people having the infection. Because of its fecal-oral transmission, it is important to prevent consumption of contaminated food and water and practice proper hand washing techniques. If the parasite does infect a host, the host immune response will attempt to remove the infection through innate and adaptive responses. Inflammation is a key to the host immune response, yet it can hurt the host as much as it benefits it.

Pathogenesis

Transmission

Larvae of the tapeworm Taenia solium are what cause cysticercosis. If a person becomes contaminated with an adult tapeworm, an infection called taeniasis, they can shed T. solium eggs in their stool. These eggs must then be consumed through fecal-oral route transmission, which can occur by drinking water or eating food that is contaminated with T. solium eggs, or by putting a fecal contaminated object in one’s mouth. Due to this form of transmission, it is possible for autoinfection to occur. If a person has taeniasis, they can infect themselves with the T. solium eggs they shed and thus develop cysticercosis. (12)

Infectious dose, incubation, and colonization

The infectious dose required to cause cysticercosis is relatively unknown (15). The median incubation period for cysticercosis is estimated to be about 3.5 years (13) and can range from 10 days to 10 years (14). A person who has consumed T. solium may go for years without having any symptoms of infection. This is due to the fact that cysticerci often only cause symptoms when they are dying or become large enough to interfere with vital organs. (14) Furthermore, it normally takes 2-3 months for the eggs to develop into cysticerci (15).

Life cycle of Taenia solium. From: NCIB [3]

Upon consumption of T. solium eggs, the oncospheres hatch in the intestine and then penetrate the intestinal wall. T. solium contain sharp, spine hooks and four suckers that help them adhere to and penetrate the gut wall (17). They then migrate to skeletal muscle, the brain, eyes, subcutaneous tissues, and other places where they develop into cysticerci. (16)

Epidemiology

Taenia solium is prevalent in parts of Africa, Asia, Mexico, and Latin America where humans live in close proximity to pigs. This is because pigs are one of the hosts during the life cycle of this two-host parasite, while humans are the other host. When pigs eat T. solium eggs, the eggs develop into larvae and form cysts within the pig’s muscles and other tissues. Then, if humans consume undercooked or raw infected pork, they swallow these cysts. The larvae then come out of their cysts within the human gut and develop into adult tapeworms. Now, this person will shed T. solium eggs in their stool. At this point, if fecal-oral contamination occurs, cysticercosis will develop in whoever consumed the contaminated fecal matter. (12) It is clear that cysticercosis is spread by fecal-oral route, not the consumption of undercooked, infected pork meat.

Virulence factors

T. solium contains a number of virulence factors that allow it to survive amidst the host immune response. The oncospheres invade the host and are susceptible to antibody and complement responses, but by the time the host actually mounts an antibody response, the parasite begins to transform to the more resistant larval stage, called metacestode. During the larval stage, the parasite can evade complement-mediated destruction. This is achieved by a few different virulence factors including paramyosin, which is a protein that inhibits C1q; taeniaestatin, a proteinase, inhibits the classical and alternate pathways; and sulfated polysaccharides, which activate complement away from the parasite. The larval stage of T. solium also manipulates antibody production in such a way that the host produces antibody that cannot kill the mature metacestode, but instead provides a protein source to the parasite. Lastly, taeniaestatin may interfere with lymphocyte proliferation and macrophage functions; therefore, compromising the cellular immune response. (19)

References

[Sample reference] Takai, K., Sugai, A., Itoh, T., and Horikoshi, K. "Palaeococcus ferrophilus gen. nov., sp. nov., a barophilic, hyperthermophilic archaeon from a deep-sea hydrothermal vent chimney". International Journal of Systematic and Evolutionary Microbiology. 2000. Volume 50. p. 489-500.

Created by {Jordan Voth}, students of Tyrrell Conway at the University of Oklahoma.