[2] Cysticercosis is usually acquired by eating food or drinking water contaminated by tapeworms' eggs from human feces.

[2][8] Taeniasis, in the strict sense, is a different disease and is due to eating cysts in poorly cooked pork.

[2] Infection can be effectively prevented by personal hygiene and sanitation:[1] this includes cooking pork well, proper toilets and sanitary practices, and improved access to clean water.

[13] Cysts located within the ventricles of the brain can block the outflow of cerebrospinal fluid and present with symptoms of increased intracranial pressure.

[8] Only a small minority of patients with cysticercosis will harbor a tapeworm, rendering stool studies ineffective for diagnosis.

[21] In cases of human cysticercosis, diagnosis is a sensitive problem and requires biopsy of the infected tissue or sophisticated instruments.

[22] Taenia solium eggs and proglottids found in feces, ELISA, or polyacrylamide gel electrophoresis diagnose only taeniasis and not cysticercosis.

Radiological tests, such as X-ray, CT scans which demonstrate "ring-enhancing brain lesions", and MRIs, can also be used to detect diseases.

X-rays are used to identify calcified larvae in the subcutaneous and muscle tissues, and CT scans and MRIs are used to find lesions in the brain.

[23][24] Antibodies to cysticerci can be demonstrated in serum by enzyme linked immunoelectrotransfer blot (EITB) assay and in CSF by ELISA.

In the CDC's immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of Taenia solium.

[33][34][35] For example, The intervention strategies to eradicate cysticercosis include surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans.

[32] In reality, control of T. solium by a single intervention, for instance, by treating only the human population will not work because the existing infected pigs can still carry on the cycle.

Research studies have been focusing on vaccines against cestode parasites since many immune cell types are found to be capable of destroying cysticercus.

[43] Many vaccine candidates are extracted from antigens of different cestodes such as Taenia solium, T. crassiceps, T. saginata, T. ovis and target oncospheres and/or cysticerci.

In 1983, Molinari et al. reported the first vaccine candidate against porcine cysticercosis using antigen from cysticercus cellulosae drawn out from naturally infected animals.

[44] Recently, vaccines extracted from genetically engineered 45W-4B antigens have been successfully tested to pigs in an experimental condition.

[43] Even though vaccines have been successfully generated, the feasibility of their production and usage in rural free-ranging pigs remains a challenge.

S3Pvac consists of three protective peptides: KETc12, KETc1, and GK1, whose sequences belong to native antigens that are present in the different developmental stages of T. solium and other cestode parasites.

However, in areas where food is scarce, cyst-infected meat might be considered as wasted since pork can provide high-quality protein.

[52] Asymptomatic cysts, such as those discovered incidentally on neuroimaging done for another reason, may never lead to symptomatic disease and in many cases do not require therapy.

[53][54] Neurocysticercosis may present as hydrocephalus and acute onset seizures, thus the immediate therapy is emergent reduction of intracranial pressure and anticonvulsant medications.

The decision to treat with antiparasitic therapy is complex and based on the stage and number of cysts present, their location, and the person's specific symptoms.

[23] Antiparasitic treatment should be given in combination with corticosteroids and anticonvulsants to reduce inflammation surrounding the cysts and lower the risk of seizures.

Therefore, high prevalences are reported in Mexico, Latin America, West Africa, Russia, India, Pakistan, North-East China, and Southeast Asia.

[23][64] However, reviews of the epidemiological in Western and Eastern Europe shows there are still considerable gaps in our understanding of the disease also in these regions.

[65][66] In Latin America, an estimated 75 million persons live in endemic areas and 400,000 people have symptomatic disease.

[70] Prevalence rates in the United States have shown immigrants from Mexico, Central and South America, and Southeast Asia account for most of the domestic cases of cysticercosis.

[71] In 1990 and 1991, four unrelated members of an Orthodox Jewish community in New York City developed recurrent seizures and brain lesions, which were found to have been caused by T. solium.

[79] Recent examination of evolutionary histories of hosts and parasites and DNA evidence show that over 10,000 years ago, ancestors of modern humans in Africa became exposed to tapeworm when they scavenged for food or preyed on antelopes and bovids, and later passed the infection on to domestic animals, such as pigs.