Human cysticercosis is caused by the larvae of T solium (Cysticercus cellulosae).
Life cycle of T solium
The definitive host is human that acquires infection by consuming larval cysts in the uncooked tissues of Pig. Pig is the intermediate host. For T solium humans serve as either intermediate or definitive hosts.
In Swine (intermediate host)
The larval tape worm (oncosphere) penetrate the intestinal wall and enters the blood stream, and eventually enters tissues and encysts.
Tissue cysticerci may remain viable for 2-5 years, and infect humans when undercooked pork is ingested.
In human (intermediate host and definitive host)
Individuals who ingest T. solium eggs develop tissue infection with parasite cysts (cysticercosis), while those who ingest larval cysts acquire 'pork' tape worm, i.e., the adult form of T. solium.
It is acquired with consumption of undercooked pork
- Upon exposure to stomach acid and bile salts in the digestive tract, the larvae excyst and develop into mature tapeworms within the intestinal lumen.
- Adult tapeworms contain two sections: a scolex (or head) used to adhere to the wall of the intestine and a strobila, or tapelike chain of developing segments called proglottides.
- The hermaphroditic proglottides produce large numbers of fertile, infectious parasite eggs that reach the environment either free or enclosed within parasite segments in the host's feces.
Mature tapeworm infection is strictly intra-luminal. Autoinfection can occur.
The incubation period for taeniasis, the time from ingestion of the larvae until segments are passed in the feces, is 2 to 3 months.
T. solium tapeworms are relatively short (3 meters) but may survive for several decades once established in the human jejunum.
- Cysticercosis represents tissue infection with larval cysts of the cestode Taenia solium, in which the patient serves as an intermediate host for the parasite.
The eggs liberate oncospheres in the intestine that migrate to tissues throughout the body, including the central nervous system where cysts form.
For cysticercosis the incubation period is months to years.
Prevalence rates are high in Mexico, Central and South America, Africa, Asia, Spain, and Portugal.
Although most cases of cysticercosis in the United States have been imported from Mexico and Central and South America, cysticercosis in the United States can be acquired from index cases who recently immigrated from an endemic area and still have T solium intestinal stage infection.
Infection often is asymptomatic.
Cysticercosis Manifestations depend on the location and numbers of pork tapeworm cysts and the host response. The brain. eye, muscle and subcutaneous tissue can be involved. Eventually, the cysticerci die and become calcified, usually within 2 years
Cysticerci in brain tend to grow to a larger size than in other tissues.
CT and MR1 are the most effective means of diagnosis for neurocysticercosis.
The travel history. The prevalence of Taenia solium (pork tapeworm) infection is high in Mexico.
The diagnosis is strengthened by serology. Serum and CSF ELISA and immunoblotting assays are available commercially and through the CDC.
Sensitivity of antibody testing is higher (94%) for patients with multiple cysts than a single cyst (28%).
In the presence of a characteristic scan, negative serology does not exclude the diagnosis.
Demonstration of the larva in a biopsy sample confirms the diagnosis.
Infection with the adult worm is made by detection of eggs and proglottides. on stool examination. The eggs are morphologically indistinguishable from those of T. saginata, study of the proglottid or head of the tapeworms is required for species identification.
Drug therapy is the treatment of choice. High doses of praziquantel (50 mg/kg per day for 15-30 days), or albendazole (10-15 mg/kg per day for 8 days) results in drug levels sufficient to kill remaining living cysts.
Cyst death is often accompanied by increased local inflammation at the site of infection, leading to a transient increase in symptoms.
The use of dexamethasone to reduce CNS inflammation is controversial, as it may lower praziquantel levels.
Surgical therapy may be required especially for cysts outside the CNS.
Anti-epileptic medication and shunting for hydrocephalus are also important.