Epidemiology and transmission of cysticercosis
Author
A Clinton White, Jr, MD, FACP, FIDSA Section Editor
Peter F Weller, MD, FACP Deputy Editor
Elinor L Baron, MD, DTMH
Last literature review version 16.3: September 2008*|*This topic last updated: August 29, 2008*(More)
INTRODUCTION*—*Cysticercosis is caused by the larval stage of the tapeworm Taenia solium; clinical syndromes include neurocysticercosis (NCC) and extraneural cysticercosis. In endemic areas NCC is an important cause of adult-onset seizures [1-4] .
The epidemiology and transmission of cysticercosis will be reviewed here. The clinical manifestations, diagnosis, treatment, and prevention of cysticercosis and the life cycle of T. solium are discussed separately. (See "Clinical manifestations and diagnosis of cysticercosis" and see "Treatment and prevention of cysticercosis" and see "Intestinal tapeworms").
EPIDEMIOLOGY*—*Approximately 50 million people worldwide are estimated to have cysticercosis infection, although estimates are probably low since many infections are subclinical and there are relatively few population based data on prevalence [5,6] . Cysticercosis is endemic in many regions of Central and South America, sub-Saharan Africa, India, and Asia [1-4,7] . The prevalence of cysticercosis varies within these countries and is often higher in rural or periurban areas where pigs are raised and sanitary conditions are suboptimal [1-4,7] . In some such communities the rate of epilepsy approaches 3 percent, and 25 to 40 percent of these cases have evidence of cysticercosis [2-4] .
Individuals with cysticercosis also present for medical attention outside of endemic areas, particularly where there are significant numbers of immigrants [8-10] . In a prospective study of 1800 patients presenting with seizures to 11 US emergency departments over a two-year period, neurocysticercosis was the etiologic agent in about 2 percent of cases [9] . Neurocysticercosis was observed more frequently in emergency departments of Los Angeles, Phoenix, and Albuquerque (5.7 percent), which had a higher proportion of immigrant Hispanic patients than the other hospitals. Travelers to endemic areas represent another source of cysticercosis, although such infection accounts for a minority of cases in the United States [9,11] .
Individuals with no history of pork consumption or travel to endemic areas can also develop NCC. In a report of four cases in an Orthodox Jewish community (whose dietary laws strictly prohibit consumption of pork), for example, infection was transmitted by domestic workers who had recently emigrated from Latin American countries where T. solium is endemic [12] . Epidemiologic studies have demonstrated tight clustering in households; household contacts of patients with neurocysticercosis have a three-fold higher risk of positive serology for cysticercosis in comparison with controls [13] .
LIFE CYCLE AND TRANSMISSION*—*Cysticercosis is transmitted by ingestion of T. solium eggs shed in the stool of a human tapeworm carrier (show figure 1). Following ingestion, embryos (oncospheres) hatch in the small intestine, invade the bowel wall and disseminate hematogenously to brain, striated muscles, liver, and/or other tissues. Over a period of three to eight weeks, tissue cysticerci develop; these consist of membranous walls filled with fluid and protoscolices (composed of rudimentary bodies and heads with suckers and hooks). Localization of cysts to the brain results in neurocysticercosis; humans with cysticercosis are incidental dead end hosts.
Humans become T. solium tapeworm carriers by ingesting undercooked pork containing cysticerci in muscle tissue. Once ingested, the protoscolices are released from the cysts and attach to the human small intestine by their suckers and hooks. Subsequently, maturation into an adult tapeworm occurs over a period of two to four months. Adult tapeworms can reside in the small intestine for years; they may develop up to 7 m in length with each proglottid segment containing 50,000 to 100,000 eggs.
About 5 to 40 percent of patients with cysticercosis are tapeworm carriers, and most individuals with intestinal tapeworm infection do not develop symptomatic cysticercosis [14] . However, human tapeworm carriers are at risk for fecal-oral autoinoculation of eggs and subsequent development of cysticercosis. It has also been postulated that human tapeworm carriers may ingest eggs from proglottids carried from the small intestine into the stomach by reverse peristalsis, although this mechanism has not been proven.
Pigs acquire infection through ingestion of food or water contaminated by infected human feces. Rates of transmission are high in rural communities where pigs roam free and human fecal contamination of soil is common. Pig-to-pig transmission also occurs, although the magnitude and effect of this transmission on rates of human infection is not fully understood [15] .
A common misconception is that cysticercosis is acquired by eating pork. However, as the above life cycle illustrates, ingestion of infected pork only causes adult tapeworm infestation (taeniasis), because infected pork contains the larval cysts that develop into adult worms in human intestine, but does not contain the eggs that cause cysticercosis [16] .
Transmission of cysticercosis was previously thought to occur by indirect means such as by the ingestion of produce irrigated with water contaminated with human feces containing T. solium eggs. However, epidemiological evidence suggests that the most common source of infective eggs is an asymptomatic household tapeworm carrier [17,18] . Therefore, cysticercosis should be viewed as a disease largely transmitted from person to person, with infected pigs as perpetuators of infection.
The taenia life cycle is discussed in further detail separately. (See "Intestinal tapeworms" section on Taeniasis).
SUMMARY Cysticercosis is caused by the larval stage of the tapeworm Taenia solium. (See "Introduction" above). Approximately 50 million people worldwide are estimated to have cysticercosis infection, which is endemic in many regions of Central and South America, sub-Saharan Africa, India, and Asia. The prevalence of cysticercosis varies and is often higher in rural or periurban areas, especially where pigs are raised and where sanitary conditions are suboptimal. (See "Epidemiology" above). The most common source of infective eggs is an asymptomatic household tapeworm carrier. Household contacts of patients with neurocysticercosis have a three-fold higher risk of positive serology for cysticercosis, in comparison with controls. (See "Epidemiology" above). Cysticercosis is transmitted by ingestion of T. solium eggs shed in the stool of a human tapeworm carrier. Following ingestion, embryos (oncospheres) hatch in the small intestine, invade the bowel wall and disseminate hematogenously to brain, striated muscles, liver, and/or other tissues. (See "Life cycle and transmission" above). Humans become T. solium tapeworm carriers by ingesting undercooked pork containing cysticerci in muscle tissue. About 5 to 40 percent of patients with cysticercosis are tapeworm carriers, and most individuals with intestinal tapeworm infection do not develop symptomatic cysticercosis. (See "Life cycle and transmission" above). A common misconception is that one can acquire neurocysticercosis by eating pork. However, ingestion of infected pork causes adult tapeworm infestation (taeniasis) but not cysticercosis. This is because infected pork contains the larval cysts that develop into adult worms in human intestine, but does not contain the eggs that cause cysticercosis. (See "Life cycle and transmission" above).
ACKNOWLEDGMENT*—*The editorial staff at UpToDate, Inc. would like to acknowledge Drs. Peter Weller and Karin Leder, who contributed to an earlier version of this topic review.
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) on the matter - one school of thought would discourage eating carnivorous fish; the other school of thought would permit all 'creatures of the ocean'.
