Taenia Solium (Pork Tapeworm) Infection and Cysticercosis
Presentation, diagnosis, and management of intestinal infection with the adult T. solium tapeworm are similar to those of T. saginata (beef tapeworm) infection. Adult T. solium range in size from 2 to 8 meters.
However, humans may also act as intermediate hosts for T. solium larvae if they ingest T. solium eggs from human excreta (see Figure: Taenia solium life cycle). Some experts postulate that if an adult tapeworm is present in the intestine, gravid proglottids (tapeworm segments) may be passed retrograde from the intestine to the stomach, where oncospheres (immature form of the parasite enclosed in an embryonic envelope) may hatch and migrate to subcutaneous tissue, muscle, viscera, and the central nervous system.
Adult tapeworms may reside in the small bowel for years. They reach 2 to 7 m in length and produce up to 1000 proglottids; each contains about 50,000 eggs.
Taenia solium life cycle
Taeniasis and cysticercosis occur worldwide. Cysticercosis is prevalent, and neurocysticercosis is a major cause of seizure disorders in Latin America. Cysticercosis is rare in Muslim countries. Infection in the US is most common among immigrants, but North Americans who have not traveled abroad have been infected by ingesting ova from immigrants harboring adult T. solium.
Rarely, zoonotic Taenia species other than T. solium cause neurocysticercosis.
Viable cysticerci (larval form) in most organs cause minimal or no tissue reaction, but dying cysts in the central nervous system, eye, or spinal cord can release antigens that elicit an intense tissue response. Thus, symptoms often do not appear for years after infection.
Infection in the brain (neurocysticercosis) may result in severe symptoms due to mass effect and inflammation induced by degeneration of cysticerci and release of antigens.
Depending on the location and number of cysticerci, patients with neurocysticercosis may present with seizures, signs of increased intracranial pressure, hydrocephalus, focal neurologic signs, altered mental status, or aseptic meningitis.
Cysticerci may also infect the spinal cord, muscles, subcutaneous tissues, and eyes.
Substantial secondary immunity develops after larval infection.
(See also guidelines for diagnosis and treatment of neurocysticercosis from the Infectious Diseases Society of America [IDSA] and the American Society of Tropical Medicine and Hygiene [ASTMH].)
Intestinal infection with adult T. solium worms can usually be diagnosed by microscopic examination of stool samples and identification of ova and/or proglottids. However, the ova are indistinguishable from those of T. saginata and T. asiatica. T. solium eggs are present in ≤ 50% of stool samples from patients with cysticercosis.
Neurocysticercosis is usually diagnosed when CT or MRI is done to evaluate neurologic symptoms. Scans may show solid nodules, cysticerci, calcified cysts, ring-enhancing lesions, or hydrocephalus. The Centers' for Disease Control and Prevention immunoblot assay (using a serum specimen) is highly specific and more sensitive than other enzyme immunoassays (particularly when > 2 central nervous system lesions are present; sensitivity is lower when only a single cyst is present).
Intestinal infection is treated with praziquantel 5 to 10 mg/kg orally as a single dose to eliminate adult worms. Praziquantel should be used with caution in patients who also have neurocysticercosis (including previously asymptomatic or unrecognized disease) because by killing cysts, praziquantel may trigger an inflammatory response associated with seizures or other symptoms.
Alternatively, a single 2-g dose of niclosamide (not available in the US) is given as 4 tablets (500 mg each) that are chewed one at a time and swallowed with a small amount of water. For children, the dose is 50 mg/kg (maximum 2 g) once.
Treatment of neurocysticercosis is complicated. Detailed clinical practice guidelines on the Diagnosis and Treatment of Neurocysticercosis were published by the Infectious Diseases Society of America and the American Society of Tropical Medicine and Hygiene in 2018.
The initial treatment goals for symptomatic neurocysticercosis are
Corticosteroids (prednisone up to 60 mg orally once/day or dexamethasone 12 to 24 mg orally once/day) are used to reduce inflammation and increased intracranial pressure. Recipients of prolonged corticosteroid therapy should be evaluated for concurrent latent tuberculosis and strongyloidiasis.
Conventional antiseizure drugs are given to patients who have seizures. These drugs can be used prophylactically in patients at high risk of seizures, particularly those who have multiple degenerating lesions with associated inflammation.
Neurosurgical intervention may be necessary for patients with increased intracranial pressure or intraventricular cysticerci.
Anthelmintic treatment of neurocysticercosis is complicated, and consultation with an expert is recommended. Choice of treatment depends on the location, number, viability, and size of cysticerci; stage of the disease; and clinical manifestations. Prior to anthelmintic treatment, an ophthalmologic examination should be done to exclude the presence of ocular cysticerci.
Not all patients respond to treatment, and not all patients must be treated (cysts may already be dead and calcified, or the potential inflammatory response to treatment may be worse than the disease, as in cysticercal encephalitis when patients have a large number of cysts and widespread brain inflammation).
When anthelmintic treatment is used, albendazole 7.5 mg/kg orally twice/day for 15 days appears to be more effective than the alternative, praziquantel 16.6 mg/kg orally 3 times a day for 15 days. The combination of albendazole plus praziquantel has been reported to result in a higher rate of radiographic resolution than albendazole alone in patients with more than 2 parenchymal cysts. Albendazole alone or in combination with praziquantel given for ≥ 30 days has been used to treat cysts in the subarachnoid space (racemose cysticercosis), which are less responsive to anthelmintic drugs. Patients receiving prolonged, high dose treatment with albendazole need to be monitored for bone marrow suppression and drug-related hepatitis. Neuroimaging is repeated at 6-month intervals until the findings have resolved.
Either prednisone or dexamethasone is started a few day before and continued during the course of anthelminthic administration to reduce the inflammation that occurs in response to dying cysts in the brain. Corticosteroids increase the cerebrospinal fluid (CSF) level of the active metabolite of albendazole but decrease the CSF level of praziquantel. Methotrexate has been used as a corticosteroid-sparing agent in patients requiring more than 2 weeks of anti-inflammatory therapy.
Neither albendazole nor praziquantel should be used in patients with ocular or spinal cord cysticerci due to potential adverse effects of the inflammatory response elicited by dying cysts.
The presence of intraventricular cysticerci is also a relative contraindication for anthelminthic drugs because the resulting inflammatory response elicited by the dying cysts can cause obstructive hydrocephalus.
Surgery may be necessary for obstructive hydrocephalus (due to intraventricular cysticerci including those in the 4th ventricle) or spinal or ocular cysticercosis. Intraventricular cysticerci are removed endoscopically when possible. Ventricular shunts may be needed to reduce increased intracranial pressure.
Intestinal T. solium infection can be prevented by cooking whole cuts of pork to ≥ 63° C (≥ 145° F) as measured with a food thermometer placed in the thickest part of the meat, then allowing the meat to rest for 3 minutes before carving or consuming. Ground pork should be cooked to ≥ 71° C (≥ 160° F). Ground pork does not require a rest period.
Identifying and treating carriers of adult T. solium is an important public health measure in preventing cysticercosis. In the US, transmission has occurred when people who were infected in endemic areas had adult T. solium in their intestines, then contaminated food with their stool. It is very important that food handlers from endemic areas be taught and adhere to good handwashing practices.
When traveling to endemic areas with poor sanitation, people should be careful to avoid foods that might be contaminated by human feces and avoid raw and inadequately cooked pork.
Ingestion of T. solium cysts may cause intestinal infection; ingestion of eggs may result in tissue cysts (cysticercosis), which are particularly problematic when in the brain.
Patients with neurocysticercosis may have seizures, signs of increased intracranial pressure, altered mental status, focal neurologic signs, or aseptic meningitis.
Diagnose intestinal infection with adult worms by identifying proglottids in stool and microscopic examination of stool samples for ova.
Diagnose neurocysticercosis by neuroimaging and serologic testing.
Give praziquantel for intestinal infection.
Consult an expert for neurocysticercosis; typically corticosteroids are given with antiseizure drugs to patients who have associated seizures or are thought to be at high risk of seizures.
Use of anthelmintics and/or surgery for neurocysticercosis depends on the location, number, and size of cysticerci; stage of the disease; and clinical manifestations.
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