Deaths from Cysticercosis - Essay Example

Neurocysticercosis Introduction Cysticercosis is a parasitic infection that is caused by the ingestion of the adult tapeworm's (known as Taenia solium) eggs. The kind of cysticercosis that involves the central nervous system is called neurocysticercosis. It is the most common type of parasite that infects the brain and a leading cause of epilepsy in developing and third world countries. Countries mostly affected are India, Latin America, Africa, and China. (Christopher M. DeGiorgio, 2004) The Infection Process This type of tapeworm is also known as the pork tapeworm as it is found in the pig's tissue. It is of different sizes but is notable due to a scolex, or head, with approximately 25 hooklets, 4 suckers, and a body with 700-1000 proglottids. The pig is an intermediate host, which harbors the larvae after ingesting the ova, while the ultimate hosts are humans. (Dhawan, 2007) Neurocysticercosis is caused by the intake of food contaminated with the waste products of a T. solium tapeworm carrier. The adult T. solium inhabits itself in the small intestine of humans, where it attaches itself to the intestinal wall by its suckers and hooks. A few pregnant proglottids are detached from the distal end of the body of the worm every day and passed with the feces; every proglottid contains thousands of eggs, which are fully embryonated, and resistant to all sorts of harsh environments and infective. (Etiopathogenesis of Neurocysticercosis, 2002) If pig products infected with the larvae are ingested, the intestines are subject to a tapeworm infection; when these eggs are ingested and subjected to gastric acid found inside the human stomach, their protective capsule is dissolved and the eggs turn into larval cysts, called oncospheres. Oncospheres travel through the vascular system to the brain, muscle, eyes, and other organs and body parts. The ingested ova develop into larvae (cysticerci) and lodge in soft tissues, especially skin, muscle, and brain. Cysticerci are fluid-filled oval cysts, approximately 1-2 cm in diameter, with an internal scolex. Once in the brain, the larval cysts (cysticerci) initially generate a minimal immune response and may remain in the brain as functional cysts for years. A live cyst can remain in there undetected for as long as 5 years before dying or causing symptoms in the host and cause minor inflammation in the tissue around it. (Christopher M. DeGiorgio, 2004) Finally, Neurologic symptoms by the cyst arise when it dies and the human mounts an associated inflammatory response. (Dhawan, 2007) The symptoms include: Seizures, which are severe involuntary movements of the body, headaches, states of confusion, lack of attention with people around and other things in the surrounding, difficulty with balance, Hydrocephalus or the swelling of the brain in which the cerebral ventricle dilate and lastly, sudden death as a cause of heavy infections. The Stages There are basically four stages of cysts within the parenchyma of the brain: vesicular, colloidal, nodular/granular, and calcified granulomas. In the first stage, the viable cyst larva is known as a vesicular cyst and has a minimum amount of activity which is because of little or no host immune response. As time passes the cyst degenerates, fluid from the larval cyst leaks into the parenchyma, creating a noticeable immune response. An enhancing cyst, without a proper scolex, is called a colloidal cyst. During the colloidal this phase, the parasite begins to demonstrate degenerative changes, the vesicular fluid takes on a gelatinous colloidal form, and the wall thickens. The CT scan shows an annular enhancement bounded by perilesional edema. Performing an MRI, the capsule displays a higher signal than the surrounding brain. As the cyst deteriorates more, it forms a nodule. In the nodular phase, the vesicle usually decreases in size, and its contents turn semisolid, and are slowly replaced by granulomatous tissue. After the parasite dies, a mineralization process takes place that ends up in a calcified nodule that inhibits permanently in the CNS. Ultimately, the degenerating cyst forms a calcified. The cysts that inhibit themselves in the cisterns or ventricles of the brain may cause hydrocephalus and commonly do not have a scolex. (Christopher M. DeGiorgio, 2004) Populations Affected Originally, neurocysticerosis was only found in developing countries from regions such as Africa, China and Latin America. But since a large population has been migrating to the US, the disease is becoming a growing concern, here as well. It is becoming one of the leading causes of seizures in America. Internationally, Neurocysticercosis is widespread in Latin America, Eastern Europe, Mexico, Asia, Spain and Africa. The estimated serologic frequency in Mexican adults is 3.6%, with positive confirmation by autopsy in 1.9%. It is also estimated that 50 million people worldwide are infected. In the United States, Neurocysticercosis is known to be more commonly found among immigrants from widespread infected areas or nyone in contact with these immigrants. Many statistical surveys indicate an approximate 1000 cases in adults and children per year. A study showed neurocysticercosis as the cause of 2% of the neurologic admissions in southern California. With immigration rates from Mexico and other endemic areas, rising, incidence in the southern United States has been increasing as well. Recent meta-analysis data of the US medical literature shows that 1494 cases have been reported during the years 1980-2004. (Dhawan, 2007) Morbidity/Mortality Statistics As far as morbidity/mortality rates and statistics are concerned, following is data over a thirteen year study period: 221 cysticercosis deaths were identified, representing an annual age-adjusted mortality rate of 0.06 per million population. Most persons who died from cysticercosis, 187 (84.6%), were Latino, 15 (6.8%) were white, 13 (5.9%) were black, 5 (2.3%) were Asian, and 1 (0.5%) was Native American By sex, 137 (62.0%) were male, and 84 (38.0%) were female. Mean age at death was 40.5 years (range 2-88 years). Most persons who died, 187 (84.6%), were foreign born, and 137 (62%) of all persons who died had emigrated from Mexico. Ten (77%) of the black and all 5 of the Asian persons who died were foreign born. According to age, the mean age at death was 40.5 years; > 60% of deaths occurred in persons < 45 years of age. At least 1 cysticercosis death was reported from 20 states; California with57% (126 deaths), and Los Angeles County, California, recorded 32% (70 deaths). (Deaths from Cysticercosis, United States, 2007) Treatment Treatment is of basically three types (Treatments for Neurocysticercosis): Anti-parasitic drugs Anti-inflammatory drugs Surgery No treatment Drugs Albendazole and praziquantel are the main antiparasitic drugs usually used to treat neurocysticercosis. Some suggest that antiparasitic treatment might be counterproductive and exposes the patients to increased risk. Surgery Surgical treatment should be restricted to the removal of the parasite found in the subarachnoid or ventricular area. Surgery should not be done for parenchymal cysts without regard to size, location of the cyst or the stage of evolution, because this form of NC can be controlled only by symptomatic treatment. Also, surgical procedures could cause more brain damage than the parasite itself. Cysts in transition or degenerative states should not be biopsied or removed because the parasite is dead and will disappear or be calcified instinctively. Prevention Prevention can basically be done by trying to avoide the tapeworm and its eggs. Stay away from unhygienic conditions and human/pig fecal matter. Treatment for pigs is also available in order to keep them safe from tapeworms. Avoid reinfection and reingestion of ova from the original source. Vaccine development is also underway, which could benefit the prevention process. Works Cited 1. Treatments for Neurocysticercosis. (n.d.). Retrieved June 8, 2008, from wrongdiagnosis: http://www.wrongdiagnosis.com/n/neurocysticercosis/treatments.htm 2. Carpio, A. (2006, April 17). Neuroimaging in Neurocysticercosis. Retrieved June 8, 2008, from emedicine: http://www.emedicine.com/NEURO/topic654.htm 3. Christopher M. DeGiorgio, M. M. (2004). Neurocysticercosis. Retrieved June 8, 2008, from pubmedcentral: http://www.pubmedcentral.nih.gov/articlerender.fcgiartid=1176337 4. Deaths from Cysticercosis, United States. (2007, February). Retrieved June 8, 2008, from CDC: http://www.cdc.gov/EID/content/13/2/230.htm 5. Dhawan, V. K. (2007, September 12). Neurocysticercosis. Retrieved June 8, 2008, from emdeicine: http://www.emedicine.com/ped/TOPIC1573.HTM 6. Etiopathogenesis of Neurocysticercosis. (2002). Retrieved June 8, 2008, from medscape: http://www.medscape.com/viewarticle/438582_2 Read More