Taenia solium infection (taeniasis) is an intestinal infection with adult tapeworms that follows ingestion of contaminated pork. Cysticercosis is infection with larvae of T. solium, which develops after ingestion of ova excreted in human feces. Adult worms may cause mild GI symptoms or passage of a motile segment in the stool. Cysticercosis is usually asymptomatic unless larvae invade the CNS, resulting in neurocysticercosis, which can cause seizures and various other neurologic signs. Neurocysticercosis may be recognized on brain imaging studies. Fewer than half of patients with neurocysticercosis have adult T. solium in their intestines and thus eggs or proglottids in their stool. Adult worms can be eradicated with praziquantel. Treatment of symptomatic neurocysticercosis is complicated; it includes corticosteroids, anticonvulsants, and, in some situations, albendazole or praziquantel. Surgery may be required.
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 CNS.
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.
|Humans develop intestinal infection with adult worms after ingestion of contaminated pork or may develop cysticercosis after ingestion of T. solium eggs (making humans intermediate hosts).
1. Humans ingest raw or undercooked pork containing cysticerci (larvae).
2. After ingestion, cysts evaginate, attach to the small intestine by their scolex, and mature into adult worms in about 2 mo.
3. Adult tapeworms produce proglottids, which become gravid; they detach from the tapeworm and migrate to the anus.
4. Detached proglottids, eggs, or both are passed from the definitive host (human) in feces.
5. Pigs or humans become infected by ingesting embryonated eggs or gravid proglottids (eg, in fecally contaminated food). Autoinfection may occur in humans if proglottids pass from the intestine to the stomach via reverse peristalsis.
6. After eggs are ingested, they hatch in the intestine and release oncospheres, which penetrate the intestinal wall.
7. Oncospheres travel through the bloodstream to striated muscles and to the brain, liver, and other organs, where they develop into cysticerci. Cysticercosis can result.
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 spp other than T. solium cause neurocysticercosis.
Humans infected with adult T. solium worms are asymptomatic or have mild GI complaints. They may see proglottids in their stool.
Viable cysticerci (larval form) in most organs cause minimal or no tissue reaction, but death of the cysts in the CNS can 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.
Microscopic examination of stool for ova and proglottids
CT and/or MRI and serologic testing for patients with CNS symptoms
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.
Cysticercosis 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 CDC’s immunoblot assay (using a serum specimen) is highly specific and more sensitive than other enzyme immunoassays (particularly when > 2 CNS lesions are present; sensitivity is lower when only a single cyst is present).
For intestinal infection: Praziquantel or niclosamide (outside the US).
For neurocysticercosis: Corticosteroids, anticonvulsants, and sometimes albendazole or praziquantel and/or surgery
Intestinal infection is treated with praziquantel 5 to 10 mg/kg po as a single dose to eliminate adult worms. Praziquantel should be used with caution in patients who also have neurocysticercosis 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
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
To reduce inflammation associated with degenerating cysticerci documented by MRI
To prevent seizures if present or if risk is high
To relieve increased intracranial pressure if present
Corticosteroids (prednisone 60 mg po once/day or dexamethasone 6 mg po once/day) are used to reduce inflammation and increased intracranial pressure.
Conventional anticonvulsants 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, and size of cysticerci; stage of the disease; and clinical manifestations.
Not all patients respond to treatment, and not all patients must be treated (cysts may already be dead and calcified, or the inflammatory response to treatment may be worse than the disease).
When anthelmintic treatment is used, albendazole 7.5 mg/kg po twice/day for 15 days appears to be more effective than the alternative, praziquantel 16.6 mg/kg po tid for 15 days, but some patients who have not responded to albendazole have responded to praziquantel. Albendazole given for ≥ 30 days has been used to treat extensive disease and cysts in the subarachnoid space (racemose cysticercosis), which are less responsive to anthelmintic drugs. Occasionally, albendazole and praziquantel are used together.
Either prednisone or dexamethasone is given concurrently with the anthelminthic to reduce the inflammation that occurs in response to dying cysts in the brain. Corticosteroids increase the CSF level of the active metabolite of albendazole but decrease the CSF level of praziquantel.
Neither albendazole nor praziquantel should be used in patients with ocular or spinal cord cysticerci.
The presence of intraventricular cysticerci is 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.
Careful handwashing is important, especially for food handlers.
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.