Ocular Cysticercosis

Updated: Aug 25, 2016
  • Author: Jean Deschênes, MD, FRCSC; Chief Editor: Hampton Roy, Sr, MD  more...
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Overview

Background

Cysticercus cellulosae, the larval form of the pork tapeworm Taenia solium, is the causative organism of cysticercosis, in which humans are the intermediate hosts in the life cycle. Cysticercus cellulosae may become encysted in various bodily tissues, usually the eyes, central nervous system (CNS), and subcutaneous tissues. An immunologic reaction with fairly intense inflammatory signs and symptoms may be produced, and the surrounding structures may be compressed.

Ocular cysticercosis may be extraocular (in the subconjunctival or orbital tissues) or intraocular (in the vitreous, subre­tinal space, or anterior chamber). [1, 2, 3, 4, 5, 6, 7]

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Pathophysiology

Humans are the intermediate hosts for T solium, and pigs are the definitive hosts. [8] A tapeworm larval cyst (cysticercus) is ingested with poorly-cooked infected pork; the larva escapes the cyst and passes to the small intestine, where it attaches to the mucosa with scolex suckers. Egg-containing proglottids develop as the worm matures in 3-4 months. The adult worm may live in the small intestine for as long as 25 years without symptoms (taeniasis) and pass gravid proglottids intermittently with the feces. Eggs extruded from the proglottid contaminate and persist on vegetation, where pigs consume them. T solium embryos penetrate the gastrointestinal mucosa of the animal host and are then hematogenously disseminated to peripheral tissues with the resultant formation of larval cysts (cysticerci).

Human cysticercosis occurs when T solium eggs are ingested via fecal-oral transmission from a tapeworm host. The human then becomes an accidental intermediate host. These oncospheres (primary larvae) penetrate the intestinal mucosa and enter the circulatory system. Hematogenous spread to neural, muscular, and ocular tissues occurs. Within these tissues, the oncospheres develop into secondary larvae (ie, the cysticerci).

The incubation period may vary from months to years. The host inflammatory response to cysticerci depends on the parasite's ability to evade host immunity; therefore, inflammation is restricted to degenerating cysts whose ability to evade host defenses is faltering. Lack of inflammation occurs with both healthy cysticerci (active disease) and those that have involuted (inactive disease). Upon involution, cysts undergo granulomatous change and exhibit calcification.

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Epidemiology

Frequency

United States

The incidence in the United States is increasing secondary to increased immigration from endemic areas, increased travel to endemic areas, and improved serologic testing and availability of diagnostic imaging. An estimated 1000 new cases per year are diagnosed in the United States.

International

Cysticercosis affects an estimated 50 million people worldwide. Ocular cysticercosis is endemic in tropical areas, such as sub-Saharan Africa, India, and East Asia. Other endemic areas include Mexico and Latin America. The reported incidence of ocular involvement varies from 10-30% in endemic areas. Some European studies report a higher incidence of ocular cysticercosis than neurocysticercosis. In Western countries, [9] the most common site of involvement in ocular cysticercosis is subretinal. In India, both intraocular cysticercosis and extraocular cysticercosis is observed with almost equal frequency.

Mortality/Morbidity

Cysticercosis may cause significant visual loss, especially if the cyst is located intraocularly or is compressing the optic nerve.

Race

The incidence is more common in the Asian and Latin American populations, in which cysticercosis is endemic.

Sex

There is no specific sex predilection.

Age

Orbital cysticercosis most frequently affects individuals aged 10-30 years. [10]

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