Epidemiology/Diagnostics
There are approximately 50 million cases of Taenia solium infection worldwide. This number is most likely an underestimate as many cases of T. solium are asymptomatic. Highest prevalence is found in areas where pork is undercooked or general environmental conditions are unsanitary. These areas of highest prevalence are Latin America, Southeast Asia, Africa, and Eastern Europe. Areas inhabited primarily by Jews or Muslims who do not eat pork have the lowest prevalence around the world, illustrating the necessity of the pig as an intermediate host to perpetuate the T. solium life cycle. In America- New York, southern California, and parts of Texas are all considered limited endemic areas. These areas have unusually high prevalences of T. solium due to their large immigrant population (especially immigrants from Mexico where T. solium prevalence is extremely high). It is also important to note that certain types of cysticercosis only have prevalence in certain areas. For example, Latin America has an overall high prevalence of cysticercosis, but subcutaneous cysticercosis is very rare. However in India subcutaneous cysticercosis has a relatively high prevalence (sometimes as high as 10%) even though overall cysticercosis prevalence in India is lower than that of Latin America. In addition, as one can see from the map below, there are still large portions of Africa, Asia, and the Middle East where no epidemiological information is available, so there is still much work to be done in charting T. solium's presence globally.
http://www.astrium.com/images_articles/cysticercose.gif
T. solium epidemiology can be established through morphologic observation, mitochondrial DNA analysis, or with serologic tests such as the enzyme-linked immunosorbent assay (ELISA, see pic below) which uses glycoproteins taken from the fluid of T. solium cysticerci and purified by isoelectric focusing. For example, a relatively recent study in Irian Jaya Indonesia using all three of these epidemiological techniques found that an astounding 47.9% of randomly sampled people older than 18 years of age were infected with T. solium. More details on this study can be found at http://www.cdc.gov/ncidod/EID/vol9no7/02-0709.htm
http://www.biocontrol.ucr.edu/photos/WFT/elisa.jpg
Another epidemiological diagnostic method that can use either serum or CSF is the Enzyme-linked immunoelectrotransferblot assay (EITB see pic below) or immunoblot which is considered the most specific test available for the diagnosis of neurocysticercosis. In this test cysticercosis-specific antibodies react with one of 7 diagnostic glycoproteins (whose positions are marked on the strips based on their relative mobilities in SDS-PAGE) derived from T. solium cysts. Sera from patients who do not have cysticercosis will not react with any of the 7 glycoproteins.
http://www.dpd.cdc.gov/DPDx/HTML/ImageLibrary/Cysticercosis_il.htm
In general, cysticercosis
diagnosis is divided into two groups- cysticercosis outside the CNS or cysticercosis
within the CNS:
Cysticercosis outside the CNS
Ocular cysticercosis causes problems with vision and is thus most often diagnosed when the patient undergoes an opthamalogical evaluation.
Subcutaneous cysticercosis is first suspected when nodules first appear under the skin (see pic on symptoms page) and that diagnostic suspicion is confirmed with surgical excision of one of the nodules followed by microscopic or histopatological confirmation.
Muscular cysticercosis often presents with muscular pain and/or muscular hypertrophy. Live or calcified lesions show up in image studies, and calcified lesions also show up in x-rays (see pic below)
http://www.gideononline.net/web/epidemiology/index.php
While cysticercosis in other organs is possible (see pic of liver below), it is rarely diagnosed on its own as it is often asymptomatic.
http://www.fao.org/ag/againfo/subjects/en/health/diseases-cards/cards/cysticercosis.html
Cysticercosis within the CNS
Neurocysticercosis (NCC) is extremely difficult to diagnose due to the plethora of possible symptoms it produces. In fact, NCC has so many associated symptoms that it is often called "The Great Imitator" of other diseases. Due to this multitude of potential symptoms there is no universal protocol for diagnosis. However it is standard procedure to use a combination of several studies to confirm and reconfirm the presence of NCC. In addition, diagnosis is complicated even further by the fact that non-endemic areas who rarely see patients presenting with NCC run the risk of under-diagnosing the disease, while endemic areas run the opposite risk of over-diagnosing the disease. For this reason, it is crucial to ascertain a patient's medical history to reveal travel to or residence in endemic areas, past or present taenosis, and/or late-onset epilepsy.
NCC diagnosis usually begins with clinical suspicion when patients present with hydrocephalus, headache, meningitis, cranial nerve palsies, epilepsy, neurological deficits, dementia and/or stroke-like symptoms.
Such clinical suspicion is then confirmed with imaging studies. X-rays can reveal dead and calcified lesions, but CT scans and MRI's (see pic below) are necessary to detect the presence of still living lesions. When only calcified lesions are present it is very difficult to make a definitive diagnosis.
http://www.medstudents.com.br/image/neuro/cystic/cystic1.jpg
If imaging studies cannot make a definitive diagnosis, immunological/serological studies such as the ELISA or EITB (described and pictured above) can be used. However, it should be noted that such studies may only reveal the presence of a past infection and not necessarily an active NCC. In addition, the sensitivity and specificity of either of these studies has yet to be perfected.