There is evidence of human cysticercosis in both ancient Egypt and ancient Rome, but it wasn't until the 15th century that cysticerci were identified as parasitic cysts and the first human cases were chronicled.

The suspected infectious agent of Cysticercosis is a parasite.

This type of disease was zoonotic. Zoonotic diseases are infections that are spread between people and animals, caused by viruses, bacteria, parasites and fungi.

Bouts of human cysticercosis in non-endemic regions left us valuable lessons on the mechanisms of disease acquisition and spread. These included a large series of cases in the United Kingdom that occurred after the return of troops stationed in India, the epidemic of cysticercosis-related epilepsy in the Ekari people of Papua New Guinea occurring after the gift of pigs with cysticercosis received from Indonesia, and among members of an Orthodox Jewish community of New York City, related to Latin American Taenia carriers working in their houses.

The timeline of this spread is around the end of the 19th Century and the first two decades of the 20th Century, when isolated case reports mentioned the occurrence of cysticercosis in persons with dementia or epilepsy.

There are no number of cases reported from the Ekari people of Papua in New Guinea or the Orthodox Jewish community of NYC, but as for the troops from the United Kingdom, a total of 450 cases were reported but it was estimated that the incidence of symptomatic cysticercosis ranged from 1.2 to 2 per 1000 men among troops stationed in India from 1921 to 1937.

Virulence is described as the ability of an organism to infect the host and cause a disease.

Cysticercosis contains a number of virulence factors that allow it to survive amidst the host immune response. The oncospheres invade the host and are susceptible to antibody and complement responses, but by the time the host actually mounts an antibody response, the parasite begins to transform to the more resistant larval stage, called metacestode. During this stage, the parasite can evade complement-mediated destruction. This stage also manipulates antibody production in such a way that the host produces antibody that cannot kill the mature metacestode, but instead provides a protein source to the parasite. Lastly, taeniaestatin may interfere with lymphocyte proliferation and macrophage functions; therefore, compromising the cellular immune response. But the location of the cysts determines the severity of this disease. If they are located in the skeletal muscle or subcutaneous tissue, there will often times be no signs of symptoms, or may only experience localized pain. If the cysts are located in the eye, vision might become blurry and disturbed. Cysts in the brain or spinal cord cause the most threatening symptoms including seizures, stroke, and even death.

The virulence of Cysticercosis has not changed over time.

Treatment of cysticercosis depends on the location of the infection in the body, and is individualized for each person. Cysticercosis located outside of the nervous system usually does not require specific treatment. The treatment for cysticercosis located within the nervous system (neurocysticercosis) consists of antiparasitic therapy, corticosteroids, antiepileptic drugs, and/or surgery.

Until 1978, the only treatments available were surgery for cyst excision or ventricular shunts or steroids to decrease inflammation. Praziquantel, first used in porcine cysticercosis, was the first effective specific antiparasitic drug. Later, albendazole added a cheaper and more effective alternative.

Lately, computer-based imaging procedures have enabled visualization of the brain and other intracranial soft structures. Currently used techniques include CT and MRI. CT has been claimed to have sensitivity and specificity of over 95% for the diagnosis of neurocysticercosis. MRI is the most accurate technique to assess the degree of infection, the location, and the evolutionary stage of the parasites.

From 1988 to 1991, governmental bodies such as the Los Angeles Health Department would follow-up and perform testing of household members and other close contacts of reported cases of Cysticercosis in an attempt to find tapeworm carriers. This demonstrated at least one active tapeworm carrier among family contacts of 22% of locally acquired cases, and 5% of imported cases.

There is no information regarding innovative initiatives used in combatting Cysticercosis.

Leadership could have had tapeworm carriers who work as food handlers removed from work until successfully treated or confirmation is obtained that the infection is not Cysticercosis.

Beyond the physical effect, some of the societal and sociological impact of Cysticercosis was leading to economic losses to the small-scale pig farmers in several rural areas. It also resulted in lowering the pig’s prices, high treatment expenses, lower labor productivity, and social discrimination.

After finding out about the potential health risks of Cysticercosis, society improved their hand washing with soap and water after using the toilet and/or changing diapers, as well as before handling food. Their standards of poor environmental sanitation, poor pig management and inadequate meat inspected also increased.

There was a low risk of perception of Cysticercosis infection, but after society started to learn more from the physical effect of the disease and how serious it could be, this changed. Before, many people had heard about the pork tapeworm, and about the signs/symptoms and treatment, but the means of transmission and prevention measures were often unknown. Whilst most people were familiar with epilepsy, no one knew anything about human cysticercosis and the link between cysticercosis and epileptic seizures.