Taenia solium, Taenia asiatica, and Taenia saginata : Taeniasis and Cysticercosis

Epidemiology and Life Cycle

Taeniasis refers to intestinal infection with the human tapeworms T. saginata, T. asiatica, or T. solium (i.e., class Cestoidea in the phylum Platyhelminthes). T. saginata, the beef tapeworm, is endemic in Africa, Eastern Europe, Latin America, the Middle East, and much of Asia. The prevalence in endemic areas where cattle raising is common can exceed 90%. T. solium, the pork tapeworm, also has a worldwide geographic distribution, occurring in rural communities where raising pigs is a common practice. Highly endemic areas include Latin America, sub-Saharan Africa, India, and Southeast Asia. T. asiatica, closely related to T. saginata, also is endemic in much of Asia. Although the clinical presentation and adult worm morphology are similar to T. saginata, the intermediate host of T. asiatica is the pig. Local transmission of T. solium has been described in the US, although most cases involve infection with the larval stages (i.e., cysticercosis) and not intestinal taeniasis.

Infection with T. saginata is acquired by eating undercooked beef that contains cysticerci, which are larval forms of the parasite ( Fig. 280.2 ). On entering the small intestine, the larvae excyst and attach to the mucosal surface using 4 suckers on the anterior scolex ( Fig. 280.1 ). Proglottids form at the base of the scolex and enlarge as they extend distally, a process referred to as strobilization . These segments pass through the large intestine and are excreted in the feces or actively exit the host by independent motility. Adult T. saginata tapeworms, which can grow to a length of 10 m, can survive within the intestine of an infected person for up to 25 years, shedding 6–10 proglottids daily, each of which contains up to 80,000 eggs.

The incubation period from the time of infection to the passage of T. saginata segments is approximately 10 weeks. After the intermediate bovine host ingests eggs or proglottids, emerging embryos invade the intestinal mucosa and disseminate through the bloodstream to subcutaneous tissues, where they form cysticerci. The life cycle resumes when the definitive human host ingests undercooked beef containing larval cysts. Unlike T. solium, ingested T. saginata eggs do not form cysticerci in humans.

Intestinal infection with T. solium and T. asiatica follows ingestion of undercooked pork containing cysticerci ( Fig. 280.2 ). After degradation of the cyst wall, the scolex attaches to the duodenal mucosa and develops into an adult in 6–8 weeks. Pigs, the intermediate hosts, ingest eggs contained in human waste. The eggs hatch in the stomach and release embryos that penetrate the pig’s intestinal wall, and larval stages migrate through the bloodstream to muscle, subcutaneous tissues, or other organs. Humans complete the T. solium and T. asiatica life cycles by eating pork meat ( T. solium ) or viscera ( T. asiatica ) containing viable cysticerci.

Clinical Manifestations

Most people with T. saginata or T. asiatica infection are asymptomatic, but they become aware of tapeworm segments passing in feces. ^, The proglottids of T. saginata often are actively motile, and people may notice them moving. Mild intermittent gastrointestinal symptoms such as nausea and epigastric pain have been reported, as have vomiting, diarrhea, and intestinal obstruction. Migration of proglottids down the thigh can be associated with pruritus. Rarely, proglottid segments are vomited or migrate aberrantly, ultimately leading to appendicitis, cholecystitis, or colonic perforation.

People harboring intestinal T. solium frequently are asymptomatic, becoming aware of tapeworm infection only upon fecal passage of proglottids. The T. solium proglottid segments are less motile than those of T. saginata and usually do not migrate onto the perianal skin. Anal pruritus and urticaria have been described with heavy infections, which are sometimes associated with serum eosinophilia. Intestinal symptoms include nausea, abdominal pain, change in appetite, and diarrhea. However, frequent coinfection with other intestinal pathogens makes it difficult to ascribe these symptoms exclusively to taeniasis.

Laboratory Findings and Diagnostic Tests

A definitive diagnosis of intestinal taeniasis requires the identification of proglottids or ova excreted from an infected person. To distinguish T. saginata or T. asiatica from T. solium, proglottids can be pressed gently between glass slides and injected with India ink through the lateral pore to visualize the uterine branches under light microscopy ( Fig. 280.1 ). T. saginata has 15 or more primary uterine branches on each side of the central core, and T. solium usually has <13 per side. Unlike T. saginata and T. asiatica, the scolex of T. solium possesses two rows of rostellar hooks, which it uses along with four suckers to attach to the mucosa of the small intestine.

Because patients infected with adult T. solium are at additional risk for cysticercosis due to autoinfection, attempts should be made to discriminate between T. saginata or T. asiatica and T. solium infection. ^, Taenia eggs, which rarely are present in fecal samples, cannot be distinguished based on morphology. Visualization of the adult worm by endoscopy has been described. ^, Laboratory tests may reveal mild peripheral blood eosinophilia.

Coproantigen detection of Taenia- specific antigens by fecal enzyme immunoassay (EIA) is more sensitive than standard microscopy for detecting infection. ^, Immunodiagnostic and polymerase chain reaction (PCR)-based tests can detect Taenia antigens or DNA in feces and distinguish among the major species. These assays have been used primarily in research settings, and their role in the routine diagnosis of tapeworm infections has not been established. Serodiagnostic testing for Taenia infection is used primarily for diagnosing cysticercosis, particularly involving the central nervous system (CNS). Serologic tests that are specific for the T. solium tapeworm carriers also have been developed but are not available widely. ^,

Treatment

Antihelmintic drug therapy is recommended for all children found to harbor an intestinal tapeworm. Praziquantel, administered orally in a single dose (5–10 mg/kg), is the drug of choice for taeniasis. ^, In children with T. solium infection, even modest doses of praziquantel can occasionally trigger the destruction of occult CNS cysts, particularly those in the brain parenchyma, perhaps leading to seizures. Albendazole, although effective for treating cysticercosis, is not recommended routinely for the treatment of intestinal tapeworm infection. Niclosamide (not marketed in the US) and nitazoxanide can be used as alternatives. ^,

Effective treatment can be associated with the passage of intact or disintegrating proglottids for days. However, purgatives (e.g., polyethylene glycol) can hasten the process and help identify the passage of the scolex (as a test of cure). If the scolex is not identified, a second stool examination should be performed approximately 3 months after anthelmintic therapy, allowing time for regeneration of proglottids from the scolex. Because reinfection is common in endemic areas, repeated courses of therapy may be necessary for long-term control.

Special Considerations

Treatment of pregnant women with taeniasis can be complicated. Their newborn infant could be exposed to infected stool if treatment is deferred until after delivery. Data on the safety of praziquantel in the setting of pregnancy are insufficient. Niclosamide, which is not absorbed, is a potential alternative.

Prevention and Control

Thorough cooking of meat is a key measure for the prevention of infection with Taenia . Transmission of taeniasis can be reduced by improving sanitation and husbandry practices, along with strict inspection of pork or beef prior to sale or consumption. ^{, ,} Unfortunately, in many resource-poor countries, these practices are not economically feasible. Public health measures, such as sanitary disposal of human feces and restriction of cattle and pigs from land contaminated by human feces, also may prevent transmission. Freezing meat at −20°C kills cysticerci but often is not practical in endemic areas.

No vaccine for human T. saginata infection exists. Protection of calves from challenge infection has been achieved after immunization with an oncospheral adhesion protein.

Mass chemotherapy programs targeting communities where T. solium is highly endemic may reduce transmission from humans to pigs, thereby interrupting the natural life cycle of T. solium . ^{, ,} One intervention study demonstrated that the prevalence of human taeniasis was reduced from 4% to 1% within 10 months after treatment with niclosamide, and the seroprevalence of T. solium infection among pigs was reduced from 55% to 7%. These strategies will likely have long-term benefit only if education succeeds in reducing the behaviors that encourage the proliferation and transmission of the parasite within high-risk communities. Vaccination of pigs using recombinant T. solium proteins also has the potential to limit the burden of disease in the porcine host, reducing the prevalence of taeniasis and cysticercosis in humans. ^,

Epidemiology and Pathogenesis

The availability of brain imaging studies, especially computed tomography (CT) scans, has led to an increased appreciation of the significance of neurocysticercosis as a common cause of neurologic disease. Neurocysticercosis is prevalent in many areas of the world, including Latin America, the Caribbean, sub-Saharan Africa, India, Southeast Asia, China, and Indonesia. ^, In endemic areas worldwide, neurocysticercosis is responsible for almost 30% of epilepsy cases.

A community-based study in a highly endemic area from Peru showed that 40% of persons with epilepsy had CT or serologic evidence of neurocysticercosis. A meta-analysis of countries in Latin America estimated a neurocysticercosis prevalence of 32% among persons with epilepsy. Studies from Latin America also found that up to one-half of patients with adult-onset seizures had evidence of neurocysticercosis on imaging studies. Population-based surveys in Latin America and sub-Saharan Africa have documented CT abnormalities consistent with neurocysticercosis in up to 70% of people with seizures from rural communities. ^, Among patients with focal seizures in India, CT scans demonstrated lesions consistent with neurocysticercosis in 40%, including viable cysts, typical calcifications, or single enhancing CT lesions. ^, Similar data were reported for children with seizures and for patients from northern India. Although single enhancing CT lesions in this group were frequently attributed to other causes, excisional biopsies demonstrated histopathologic evidence of cysticercosis in most. Neurocysticercosis also has become recognized as a major public health problem throughout Asia. ^,

In the US, there are approximately 2000 hospitalizations for cysticercosis each year. Cases primarily occur among immigrants from endemic areas. One review identified 75 cases of locally transmitted cysticercosis in the US from 1954 to 2005. Neurocysticercosis also has been observed among long-term travelers to endemic areas. The economic burden of neurocysticercosis cases in nonendemic areas can be substantial.

Human cysticercosis follows ingestion of eggs excreted by a tapeworm-infected person, presumably by fecal–oral contamination. Neurocysticercosis is not acquired directly from eating pork, as illustrated by cases that have occurred in an Orthodox Jewish community in New York City, vegetarians in India, and a case of CNS disease in an infant. ^{, ,} However, tapeworm carriers can infect themselves by fecal–oral contamination, and both stages of the parasite (i.e., cysticercus and adult tapeworm) can be found in a single person.

After ingestion, eggs hatch and release oncospheres that invade the circulatory system and disseminate to somatic tissues where they mature into cysticerci. Cysticerci in skeletal and cardiac muscle, subcutaneous tissue, and lung usually spontaneously form granulomas, which calcify over time. However, most disease attributable to cysticercosis results from invasion of the CNS.

After tissue invasion, cysticerci reach their final size within a few weeks. Symptoms of neurologic disease, however, usually develop several years after infection. ^, Although the parasites secrete a variety of immunomodulatory compounds that can suppress the host’s inflammatory response, cysticerci degenerate over time and trigger a host inflammatory response mediated by a variety of cytokines, which is associated with disruption of the blood-brain barrier. Degradation of the parasite cyst occurs in stages. During the colloid stage, the cyst wall degenerates with invasion by inflammatory cells. The cysticercus eventually fibroses, and the cavity collapses (i.e., granular-nodular stage). The granulomatous cyst can calcify (i.e., calcified stage). It may be possible to detect remnants of the cysticercus (e.g., hooklets) in the calcified lesion.