Cysticercosis

While the clinical picture varies from one affected individual to another, the symptoms depend on two main factors: 1) number of cysticerci, and 2) location in the body. While the infection is commonly in the muscle, the disease can also affect heart tissue, eyes or brain. Some cases are asymptomatic or mild in presentation. 

Neurocysticercosis is one of the common manifestations and is classified into 4 types according to the location in the CNS. Many remain asymptomatic although others develop serious clinical sequelae. The patient’s immunologic response also plays a role. The shared features of the 4 forms of neurocysticercosis are headaches, seizures, and hydrocephalus. The resultant pressure secondary to the latter leads to papilledema, visual changes, emesis, nausea, and headache [7]. The 4 types are as follows:

1. Parenchymal neurocysticercosis presents with headaches, seizures, behavioral changes, intellectual challenges, and hydrocephalus [8]. These patients may also exhibit ataxia and hemiparesis.
2. Subarachnoid neurocysticercosis is characterized by meningeal inflammation, headaches, seizures and hydrocephalus.
3. Intraventricular neurocysticercosis can result in obstructive hydrocephalus, headaches, and seizures. A collection of cysts at the base of the brain represents a variant called racemose cysticercosis. It results in life-threatening conditions such as a coma. Other features of this variant include mental function decline, headaches, seizures, and hydrocephalus.
4. Spinal neurocysticercosis is rare. Its findings are meningitis and possible spinal cord compression. Headaches, seizures, and hydrocephalus can all occur.

Severe CNS infections can also develop with initial manifestations such as myalgia, weakness, and fever. These infections may progress to serious complications such as stroke or cysticercal encephalitis.

Ocular cysticercosis, as the name suggests, is caused by cysts in the eyes. The picture consists of pain, visual loss, and retinal detachment. Sometimes, the eye is the only organ involved in cysticercosis.

Cysts under the skin can form without any other presentations.

The workup should cover a thorough history and physical exam, including a focused neurological evaluation. Suspicion for cysticercosis is high for patients living in endemic areas, immigrants of these regions, or those who recently visited risky areas. The following is obtained in the workup. 

Microscopy of stool samples is useful since it identifies eggs and/or proglottids. Typically, eggs are found in 50% or less of stool samples. Hence, 3 stool samples are collected on different days to increase the sensitivity [5].

Neurocysticercosis is typically diagnosed with CT or MRI during workup of neurologic abnormalities [9]. The findings on these imaging modalities include solid nodules, calcified cysts, cysticerci, ring enhancing lesions or hydrocephalus.

The CDC (Centers for Disease Control and Prevention) immunoblot serum assay is very specific and more sensitive than other immunoassys. Sensitivity increases in cases with 3 or more CNS lesions.

When considering the therapeutic options of cysticercosis, the clinical presentation, number of cysticerci, and the affected organs are all important factors. Asymptomatic patients may not need treatment while certain cases may require multiple treatments to eradicate the cysts. Moreover, consultation with neurology and infectious disease specialists is recommended to establish an effective treatment regimen. There are a number of options available. 

Anthelminthics

Albendazole and praziquantel are the main examples [10]. The latter is not used as frequently. While they are effective, each case is assessed individually before treatment. One of the side effects of these drugs includes localized inflammation.

Antiseizure

Medications such as carbamazepine and phenytoin [11] are crucial in individuals manifesting with seizures secondary to neurocysticercosis. Patients at risk for recurrent seizures can be prophylactically treated as well. Neurology consult may be beneficial to clarify the treatment plan.

Corticosteroids 

This class of drugs can be used as adjunct or as substitute to antihelminthic treatments [12]. While corticosteroids reduce inflammation, they do not eliminate active cysts.

Surgical intervention

In cases presenting with hydrocephalus, brain shunting can alleviate the pressure. Other surgical procedures may be needed in cysticercosis affecting the eyes or subcutaneous tissue.

The prognosis depends on the clinical presentation. In patients with parenchymal cysticercosis, a majority shows no symptoms or exhibits self-limited seizures. Furthermore, individuals affected with intracerebral calcifications commonly manifest with recurrent seizures although antiseizure medications are usually effective in these cases.

Patients with intraventricular neurocysticercosis typically present with obstructive hydrocephalus, which is a complication that requires brain shunting. Furthermore, while shunt revisions may be necessary for many patients, corticosteroids and antihelminthic treatment may reduce the need for these subsequent procedures. Of note, in cases with focal neurological damage, the surgical procedure could be challenging.

Subarachnoid neurocysticercosis cases reached a 90% 10-year mortality rate even in patients who underwent brain shunting. However, the use of corticosteroids and antihelminthic drugs has significantly improved the outcome as mortality has become rare.

Infected patients become immune to subsequent infections.

Infections in humans occur through the fecal-oral route. Stool from T solium carriers can contaminate food, water, or soil. When humans consume contaminated food (that contains T solium eggs or gravid proglottids), these eggs undergo a complex lifecycle and develop cysts.  

While evaluating cysticercosis, it is pertinent to discuss it in context of geographical location. 

United States
There are about 1000 new cases of neurocysticercosis yearly in the United States. These are more frequently found in Hispanic immigrants in California, Texas, and Arizona. Immigrants from India, Asia, and Africa have also been reported to have cysticercosis. Furthermore, there are documented cases of this infection in Americans who traveled to these endemic areas.

Of note, all carriers of T solium become infected in endemic areas. Moreover, one study estimated that 62% of patients with cysticercosis emigrated from Mexico [2].

Worldwide
While it is estimated that 50 to 100 million people are affected globally, the number is likely to be higher since this disease is underdiagnosed.

Very importantly, neurocysticercosis is a significant cause of adult onset seizures worldwide. Brain imaging with computed tomograhpy (CT) and magnetic resonance imaging (MRI) are instrumental in diagnosing this form of cysticercosis. Adult onset seizures in endemic regions such as Latin America and India have been found in 2% of the population. Approximately 50% of these cases are due to neurocysticercosis.

Central and South America, India, China, southeast Asia, and sub-Saharan Africa are endemic areas [3].

The seroprevalence in Latin America is approx 5 to 24%. India is likely similar. Additionally, rural South American areas are seroprevalent and range from 10 to 25% [4].

The transmission route is fecal-oral. There are 3 main ways this occurs 1) human to human contact, 2) contaminated food such as pork, or 3) autoinfection [5].

Following ingestion of T solium embryonated eggs or gravid proglottids, these go on to invade the intestinal wall and disseminate to other tissues such as muscle, brain, eyes, heart, etc. Once they reach their destination, the embryos develop into larva which then encyst into cysticerci (liquid filled vesicles) [5] over a duration of 3 weeks to 2 months. When these cysts appear in the host’s organs, they can cause an inflammatory reaction, otherwise known as the cystic phase. Eventually, these cysts degenerate and calcify [6].

Prevention of this parasitic infection can be achieved through education and observance of important recommendations. For example, one must practice good personal hygiene by washing hands thoroughly after using the washroom as well as before and after food preparation. Another preventative measure is washing fruit and vegetables thoroughly. Furthermore, it is necessary to avoid consumption of raw food or undercooked meat. Beef, pork, and fish should be inspected and fully cooked. These are all effective ways to prevent the transmission to humans.

Cysticercosis is a parasitic infection secondary to ingestion of Taenia solium eggs or gravid proglottids. This disease is commonly found in developing regions throughout the world. Furthermore, it is a growing issue in communities in the United States that are largely populated by immigrants from endemic areas. 

Following consumption of contaminated food or water, T solium eggs invade the small intestine and possiby other organs as well. The lifecycle results in the formation of cysts in infected tissues, which may include the brain.

Central nervous system (CNS) involvement is referred to as neurocysticercosis [1] which could result in severe complications and potential mortality if untreated. It accounts for half of the adult onset seizures in endemic regions. Brain imaging has helps with the diagnosis of this condition. This is likely the most common parasitic infection that affects the CNS.

The therapeutic approach depends on the clinical picture and other factors as well. Anticonvulsants, antihelminthics, corticosteroids, and surgical interventions are available. 

The route of transmission is through fecal-oral and thus, there are preventative measures that can reduce infection.

Cysticercosis is a tapeworm infection that occurs when humans eat food contaminated with the parasite. This parasite can be found in raw or uncooked pork or beef. It also can be present in water and soil. This infection can also develop due to contact with contaminated feces. 

This disease is frequently found in India and developing countries in Latin America and Southeast Asia. In America, it is a growing problem in Latin immigrants that now reside in states such as California, Arizona and Texas. These people may be carriers or even be infected themselves. 

The way this infection manifests is by forming cysts in different parts of the body. One of the main organs that can be affected is the brain. Some patients remain without symptoms and others develop neurological issues such as headache, visual impairment, seizures, or even hydrocephalus (increased of fluid and pressure in the brain). 

To establish the diagnosis, the clinician will obtain a detailed history and perform a physical exam. Suspicion is high for people that come from risky areas in the world. Patients with neurological symptoms undergo brain imaging such as CT scan or MRI, which will show evidence of the infection. 

Therapy depends on the signs and symptoms, if present. Patients with seizures are treated with anticonvulsant medications. Also there are antiparasitic medications and corticosteroids available. Patients react well on these treatment regimens. As for patients with hydrocephalus, surgery may be needed to help relieve the pressure.

Prevention of cysticercosis is important. Practicing good hygiene is one of the best ways to prevent this infection. It is highly recommeded that people wash their hands with soap after using the bathroom, changing diapers and before/after preparing food. Moreover, pork, beef, and fish should be well cooked before eating. Anyone traveling to risk regions should be cautious when eating and drinking. Water or other beverages should be consumed from sealed bottles. Food from street vendors or unsaitary restaurants should be avoided. Packaged food is to be preferred.

1. Hawk MW, Shahlaie K, Kim KD, Theis JH. Neurocysticercosis: a review. Surgical Neurology. 2005;63(2):123–32. 
2. Sorvillo FJ, DeGiorgio C, Waterman SH. Deaths from cysticercosis, United States. Emerging Infectious Diseases. 2007; 13(2):230-5.
3. Wu W, Qian X, Huang Y, Hong Q. A review of the control of clonorchiasis sinensis and Taenia solium taeniasis/cysticercosis in China. Parasitology Research. 2012;111(5):1879-1884. 
4. de Bittencourt PR, Adamolekum B, Bharucha N, et al. Epilepsy in the tropics: I. Epidemiology, socioeconomic risk factors, and etiology. Epilepsia. 1996; 37(11):1121-7.
5. Cantey P, Coyle C, Sorvillo F, Wilkins P, Starr M, Nash T. Neglected Parasitic Infections in the United States: Cysticercosis. American Journal of Tropical Medicine and Hygiene. 2014;90(5):805-809. doi:10.4269/ajtmh.13-0724.
6. Del Brutto OH, Sotelo J, Roman GC. Neurocysticercosis: a clinical handbook. Lisse, The Netherlands: Swets and Zeitlinger; 1998.
7. Sawhney I, Singh G, Lekhra O, Mathuriya S, Parihar P, Prabhakar S. Uncommon presentations of neurocysticercosis. Journal of the Neurological Sciences. 1998;154(1):94-100. 
8. Malik A, Shamim M, Ahmad M, Abdali N. Neurocysticercosis presenting as focal hydrocephalus. Case Reports. 2014;2014(jun24 1):bcr2014204269-bcr2014204269. 
9. Garcia HH, Del Brutto OH. Taenia solium cysticercosis. Infectious Disease Clinics of North America. 2000; 14(1):97–119.
10. Baird RA, Wiebe S, Zunt JR, et al. Evidence-based guideline: treatment of parenchymal neurocysticercosis: report of the Guideline Development Subcommittee of the American Academy of Neurology. Neurology. 2013; 80(15):1424-1429.
11. Garcia H, Evans C, Nash T et al. Current Consensus Guidelines for Treatment of Neurocysticercosis. Clinical Microbiology Reviews. 2002;15(4):747-756. 
12. Del Brutto O. Meta-Analysis: Cysticidal Drugs for Neurocysticercosis: Albendazole and Praziquantel. Annals of Internal Medicine. 2006;145(1):43. doi:10.7326/0003-4819-145-1-200607040-00009.