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- A Proposal for Classification of Neurocysticercosis
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Cysticercosis
Classification and external resources

Magnetic resonance image of a patient with neurocysticercosis demonstrating multiple cysticerci within the brain.
ICD-10 B69.
ICD-9 123.1
DiseasesDB 3341
MedlinePlus 000627
eMedicine emerg/119 med/494 ped/537
MeSH D003551

Cysticercosis, or neurocysticercosis, is the most common parasitic infestation of the central nervous system worldwide.[1] Humans develop cysticercosis when they ingest eggs or larvae of the tapeworm Taenia solium. The eggs and larvae are usually found in fecally-contaminated water or food and in undercooked pork. Autoinfection as a result of the entry of eggs into stomach due to retroperistalsis or as a result of accidental ingestion of eggs from the host's own feces due to contaminated hands is also possible.[2]

Contents

[edit] Agent

The cause of human cysticercosis is the larval form of Taenia solium (pork tapeworm). T. solium is a platyhelminth of the cestoidean class, the cyclophyllidea order and the taeniidae family. The common larval stage of T. solium was also known as Cysticercus cellulosae.

[edit] History of Discovery

The earliest reference to tapeworms were found in the works of ancient Egyptians that date back to almost 2000 BC. [3] The description of measled pork in the History of Animals written by Aristotle (384–322 BC) showed that the infection of pork with tapeworm was known to ancient Greeks at that time.[3] It was also known to early Muslim physicians and was one of the reasons for pork being forbidden by Islamic dietary laws.[4] 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. [5]

Cysticercosis was described by Johannes Udalric Rumler in 1555; however, the connection between tapeworms and cysticercosis had not been recognized at that time. [6] Around 1850, Kuchenmeister fed pig meat containing cysticerci of T. solium to humans awaiting execution in a prison, and after they had been executed, he recovered the developing and adult tapeworms in their intestines. [3][6] By the middle of the 19th century, it was established that cysticercosis was caused by the ingestion of the eggs of T. solium. [7]

[edit] Transmission

Pigs and humans are T. solium reservoirs.

Humans can be infected by ingesting the eggs or larvae from eating undercooked pork that contains viable cysticercosis larvae or from fecally contaminated food or water. [8] The adult tapeworm develops in humans after the ingestion of infected meat; however cysticercosis occurs after the ingestion of eggs, either from external sources or from their own feces.[8] Pigs get infected with cysticerci when they ingest human feces.

The incubation period ranges from months to over ten years. [9]

[edit] Morphology

T. solium worms may reach a length of several meters [8]. The scolex has four suckers, and a double crown of prominent hooks, which attach to the intestinal mucosa. [8] T. solium eggs are spherical and 30 to 40 μm in diameter. [9] The cysticercus larva completes development in about 2 months. It is semitransparent, opalescent white, and elongate oval in shape and may reach a length of 0.6 to 1.8 cm. [8]

[edit] Life cycle

Life cycle.gif

The life cycle involves humans as a definite host and pigs as an intermediate host. Pigs ingest contaminated food or water that contains eggs or proglottids from human’s feces. The ova develop into cysticercus in pig muscles. Human becomes infected when they ingest raw or undercooked “measly pork” that contains viable cysticercus. Upon reaching the small intestine, the scolex attaches to the intestinal wall and a proglottid chain grows. T. solium releases three to six proglottids/day, bearing 30,000 to 70,000 eggs (ova) per proglottid into the intestine. Nearly 250,000 ova are passed daily into the human feces and to the environment, and the cycle continues.[9] Infections with cysticercus occur after humans consume the ova from exogenous sources or through self-infection via the fecal-oral route. Humans, in this case, are intermediate hosts. Ova are digested in the stomach and release oncospheres which penetrate the intestinal wall and reach the bloodstream. [10] These oncospheres develop into cysticerci in any organ but are common in brain, subcutaneous tissue, or eyes.

[edit] Clinical Presentations in humans

Cysticercosis in muscles
Cysticerci can develop in any voluntary muscle in humans. [8] Invasion of muscle by cysticerci can cause myositis, with fever, eosinophilia, and muscular pseudohypertrophy, which initiate with muscle swelling and later progress to atrophy and fibrosis. [8] In most cases, it is asymptomatic since the cysticerci die and become calcified.

Neurocysticercosis
Neurocysticercosis presents in many forms, depending on the localization of the cysts and disease activity. [8] 60% of the patients with cysticerci are found to have them in the brain. [8] As the stage of cysticerci reflect the signs, symptoms and treatment of neurocysticercosis, it is important to understand the natural history of CNS cysts. [9] In the case of cysticerci in the brain parenchyma, four major stages have been classified: [9] In stage 1, immature cysts appear within 1–4 weeks during which the oncosphere lodges to the brain and finally expands into a cyst. It is mainly asymptomatic, although flu-like illness, rare seizures, rare increased intracranial pressure from massive infestation has been recorded. In stage 2, the cysticerci become mature and viable about 2 months after egg ingestion. The cyst possesses a protoscolex with the cyst bladder and causes no or minimal surrounding inflammation or edema. The cysticerci also down-regulate host cellular immunity. Stage 2 cysts are also asymptomatic, and can persist for more than 10 years.

Stage 3 is typified by colloid or degenerating cysts with thick cystic fluid, thickened capsule, and appear two to 10+ years after the cyst becomes mature. The cyst no longer prevents a host immune response and its antigens leak from the bladder wall. The intense inflammation is provoked around the degenerating cyst. Most patients bearing stage 3 develop clinical signs and symptoms such as seizures, occasional focal neurological signs, headaches, nausea, vomiting, lethargy from increased intracranial pressure and altered mental status. [9] At stage 4, the cyst is calcified. The surrounding inflammation drops since the dead cyst no longer produces foreign antigens. Common clinical features includes persistent non-provoked seizures although most of the patients are asymptomatic. [9]

In meningeal cysticercosis, cysticerci often do not develop into typical cysts, and become racemose, lacking a scolex and becoming lobes in thin-walled bladders. These cysts increase and slowly leak their antigen into the subarachnoid CSF producing meningitis and can further develop into arachnoiditis, which may lead to obstructive hydrocephalus, cranial nerve involvement, intracranial hypertension, arterial thrombosis and stroke. [8][9]

In intraventricular cysticercosis, the cysts occur in the lateral, third or fourth ventricles which may be asymptomatic or if they block the flow of CSF, they may cause increased intracranial pressure. [9]

Ophthalmic Cysticercosis
In some cases, cysticerci may be found in the globe, subconjunctiva, extraocular muscles, and subconjunctiva. Depending on the location, they may cause visual difficulties that fluctuate with eye position, retinal edema, hemorrhage, a decreased vision or even a visual loss. [8][9]

Subcutaneous Cysticercosis
Subcutaneous cysts are in the form of firm, mobile nodules, occurring mainly on the trunk and extremities[11]. Subcutaneous nodules are sometimes painful.

[edit] Diagnosis

The traditional method of demonstrating T. solium eggs in stool samples diagnoses only taeniasis.[10] Though the presence of T. solium eggs or proglottids in the feces does not necessary mean the infection with cysticercus, those patients should be evaluated serologically, since autoinfection via fecal-oral route can potentially result in cysticercosis.

In CDC’s immunoblot assay, cysticercosis-specific antibodies can react with structural glycoprotein antigens from the larval cysts of T. solium.[10] Therefore, the serum samples from patients with other microbial infections do not react with any of the T. solium derived antigens. The positions of the seven diagnostic glycoproteins are marked and selected based on how fast they can move in SDS-PAGE. The test is so far 100% specific and has higher sensitivity than any other immunoassay systems.

Neuroimaging with CT or MRI is the most useful method to diagnose neurocysticercosis. [9] CT scan shows both calcified and uncalcified cysts, as well as distinguishing active and inactive cysts (2). MRI can detect intraventricular cysts while CT scan cannot. [9]

[edit] Management and Therapy

Treatment must be tailored to the specific needs of the patient and may include medical drugs such as antihelminthic drugs and corticosteroids or surgery.[12]

Surgical treatment includes direct excision of ventricular cysts, shunting procedures, and removal of cysts via endoscopy.[8][9] Albendazole is preferable over praziquantel due to its lower cost and corticosteroids and anticonvulsants do not reduce CSF and brain drug levels. [9] Moreover, the results from meta-analysis study have shown that albendazole is more effective than praziquantel in terms of clinically important outcomes in patients with neurocysticercosis [13]
In the case of brain parenchymal cysticercosis, treatment depends on the stage of cyst development. In immature cyst stage (stage 1), high-dose corticosteroids are administered to reduce the edema but antihelminth drugs have been found to be harmful.[9] Vesicular or viable cysts (stage 2) are often asymptomatic, and usually are not treated with antihelminth drugs, while surgical removal of the cyst, along with albendazole is indicated in the colloid cyst stage (stage 3). No antihelminthic treatment is administered in dead calcified cysts stage (stage 4). [9] In the case of cysts in globe, surgical cyst removal is necessary, while antihelminth drug with steroids alone might be sufficient to treat cysts outside globe.[9] Treatment recommendations for subcutaneous cysticercosis includes surgery, praziquantel and albendazole. [11]

[edit] Public Health and Prevention Strategies

Cysticercosis is considered as “tools-ready disease” according to WHO [14]. International Task Force for Disease Eradication in 1992 reported that cysticercosis is potentially eradicable. [15] It is feasible because there are no animal reservoirs besides humans and pigs. The only source of T. solium infection for pigs is from humans, a definite host. Theoretically, breaking the life cycle seems easy by doing intervention strategies from various stages in the life cycle..[16] For example, (a) Massive chemotherapy treatment of infected humans, improving sanitation, and education humans are major ways to discontinue the cycle at step 1, in which eggs from human feces are transmitted to other humans and/or pigs. (b) Cooking of pork or freezing it and inspecting meat are effective means to cease the life cycle at step 3. (c) The management of pigs by treating them or vaccinating them is another possibility to intervene step 4 of the life cycle.

Intervention by concurrent treatment of humans and pigs

The intervention strategies to eradicate cysticercosis includes surveillance of pigs in foci of transmission and massive chemotherapy treatment of humans. [15] In reality, control of T. solium by a single intervention, for instance, by treating only human population will not work because the existing infected pigs can still carry on the cycle. The proposed strategy for eradication is to do multilateral intervention by treating both human and porcine populations.[17] It is feasible because treatment pigs with oxfendazole have been shown to be effective and once treated, they are protected from further infections for at least 3 months.[18]

Limitations

Even with the concurrent treatment of humans and pigs, complete elimination is hard to achieve. In one study conducted in 12 villages in Peru, both humans and porcine were treated with praziquantel and oxfendazole, with the coverage of more than 75% in humans and 90% in pigs [19] The result shows a decreased in prevalence and incidence in the intervention area; however the effect did not completely eliminate T. solium. The possible reason includes the incomplete coverage and re-infection. [20] Even though T. solium could be eliminated through mass treatment of human and porcine population, it is not sustainable.[17] Moreover, both tapeworm carriers of humans and pigs tend to spread the disease from endemic to non-endemic areas resulting in periodic outbreaks of cysticercosis or outbreaks in new areas. [21][22]
Vaccine against porcine cysticercosis

Given the fact that pigs are part of a life cycle, vaccination of pigs is another feasible intervention to eliminate cysticercosis. Research studies have been focusing on vaccine against cestode parasites, since many immune cell types are found to be capable of destroying cysticercus.[23] Many vaccine candidates are extracted from antigens of different cestodes such as T. 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. [24] Recently, vaccines extracted from genetically engineered 45W-4B antigens have been successfully tested to pigs in an experimental condition. [25] This type of vaccine can protect against cysticercosis in both Chinese and Mexican type of T. solium. However, it has not been tested in endemic field conditions, which is important because the realistic condition in the field differ greatly from experimental condition, and this can result in a great difference in the chances of infection and immune reaction. [23]
The S3PVAC Vaccine
The vaccine constituted by 3 peptide synthetically produced (S3Pvac) has proven its efficacy in natural conditions of transmission .[26] The S3PVAC vaccine so far, can be considered as the best vaccine candidate to be used in endemic areas such as Mexico (20). 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. [23][27]
Non-infected pigs from rural villages in Mexico were vaccinated with S3Pvac and the vaccine reduced 98% the number of cysticerci and 50% the number of prevalence. [26][28]. The diagnostic method involves necropsy and tongue inspection of pigs. The natural challenge conditions used in the study proved the efficacy of the S3Pvac vaccine in transmission control of T. solium in Mexico. [23] The S3Pvac vaccine is owned by the National Autonomous University of Mexico and the method of high scale production of the vaccine has already been developed. [23] The validation of the vaccine in agreement with the Secretary of Animal Health in Mexico is currently in the process of completion.[29] It is also hoped that the vaccine will be well-accepted by pig owners because they also lose their income if pigs are infected cysticercosis. [29] Vaccination of pigs against cysticercosis, if succeeded, can potentially have a great impact on transmission control since there is no chance of re-infection once pigs receive vaccination.
Limitations of vaccines
Even though vaccines have been successfully generated, the feasibility of its production and usage in rural free ranging pigs still remains a challenge. If a vaccine is to be injected, the burden of work and the cost of vaccine administration to pigs will remain high and unrealistic. [23] The incentives of using vaccines by pig owners will decrease if the vaccine administration to pigs takes time by injecting every single pig in their livestock. An oral vaccine is proposed to be more effective in this case as it can be easily delivered to the pigs with the food, though no one has ever achieved it yet.[23]

Other types of interventions and Limitations
 Cysticercosis can also be prevented by routine inspection of meat and condemnation of measly meat by the local government. [30] However, in areas where food is scarce, cyst-infected meat might be considered as wasted since pork can provide high quality protein. [31] At times, infected pigs are consumed within the locality or sold at low prices to traffickers who take the uninspected pigs at urban areas for sale. [32]
Due to these limitations, cysticercosis has not been eliminated in any endemic areas.

[edit] Epidemiology

The tapeworm that causes cysticercosis is endemic to many parts of the world including China, Southeast Asia, India, sub-Saharan Africa, and Latin America. Some studies suggest that the prevalence of cysticercosis in Mexico is between 3.1 and 3.9 percent. Other studies have found the seroprevalence in areas of Guatemala, Bolivia, and Peru as high as 20 percent in humans, and 37 percent in pigs.[33] In Ethiopia, Kenya and the Democratic Republic of Congo around 10% of the population is infected, in Madagascar 16%. The frequency has decreased in developed countries owing to stricter meat inspection, better hygiene and better sanitary facilities. The distribution of cysticercosis coincides with the distribution of T. solium. [34]

In Latin America, an estimated 75 million persons live in endemic areas and 400,000 people have symptomatic disease.[35] Cysticercosis is also found to be associated with Hispanic ethnicity, immigrant status, and exposure to areas of endemicity.[8] In the US, the disease is found in immigrants from Mexico, Central and South America. Current livestock for pigs in the U.S do not play a role in the transmission of Taenia solium, and thus cysticercosis in the U.S is an imported disease.[16]
In the USA during 1990–2002, 221 cysticercosis deaths were identified. Mortality rates were highest for Latinos and men. The mean age at death was 40.5 years (range 2–88). Most patients, 84.6%, were foreign born, and 62% had emigrated from Mexico. The 33 US-born persons who died of cysticercosis represented 15% of all cysticercosis-related deaths. The cysticercosis mortality rate was highest in California, which accounted for ≈60% of all deaths.[36]

[edit] In popular culture

  • Rebecca Adler, the 1st ever patient in the television show House, suffered from cysticercosis.
  • Archer Montgomery, brother of Addison Forbes Montgomery, suffered from neurocysticercosis in the cross-over of the series Grey's Anatomy (season 5) and Private Practice (season 2). He was cured by the surgical removal of the cysts by his former brother-in-law Derek Shepherd.

[edit] References

  1. ^ García HH, Evans CA, Nash TE, et al. (October 2002). "Current consensus guidelines for treatment of neurocysticercosis". Clin. Microbiol. Rev. 15 (4): 747–56. doi:10.1128/CMR.15.4.747-756.2002. PMID 12364377. PMC 126865. http://cmr.asm.org/cgi/pmidlookup?view=long&pmid=12364377. 
  2. ^ Southwick, Frederick (2007-12-10). "Chapter 12: Parasitic Infections". Infectious Diseases: A Clinical Short Course, 2nd ed.. McGraw-Hill Medical Publishing Division. pp. 313-314. ISBN 0071477225. http://pharma-books.blogspot.com/2009/01/infectious-disease-clinical-short.html. 
  3. ^ a b c Wadia, NH, Singh, G. “Taenia Solium: A Historical Note” Taenia Solium Cysticercosis: From Basic to Clinical Science CABI Publishing, 2002. 157-168.
  4. ^ Oscar H. del Brutto, Brutto Et Al, Julio Sotelo, Gustavo C. Román (1998), Neurocysticercosis, Taylor and Francis, p. 3, ISBN 9026515138 
  5. ^ http://www.ars.usda.gov/is/AR/archive/may01/worms0501.htm
  6. ^ a b Cox, F.E.G. “History of Human Parasitology” Clinical Microbiology Reviews. October 2002. 15(4) 595-612.
  7. ^ Küchenmeister, F. The Cysticercus cellulosus transformed within the organism of man into Taenia solium. Lancet 1861 i:39.
  8. ^ a b c d e f g h i j k l m Markell EK, John DT, Krotoski WA. Medical Parasitology Eighth Edition. Pennsylvania: Saunders, 1999.
  9. ^ a b c d e f g h i j k l m n o p q Davis, LE. “Neurocysticercosis” Emerging Neurological Infections edited by Power, C and Johnson RT. Taylor & Francis Group, 2005. 261-287.
  10. ^ a b c http://www.cdc.gov/ncidod/dpd/parasites/cysticercosis/factsht_cysticercosis.htm.
  11. ^ a b Wortman PD. “Subcutaneous cysticercosis” J Am Acad Dermatol. 1991 (2 Pt 2): 409-14.
  12. ^ White, Jr., A. Clinton (2009). "New developments in the management of neurocysticercosis". The Journal of Infectious Diseases 199: 1261. doi:10.1086/597758. 
  13. ^ Dimitrios K. Matthaiou, Georgios Panos, Eleni S. Adamidi,Matthew E. Falagas “Albendazole versus Praziquantel in the Treatment of Neurocysticercosis: A Meta-analysis of Comparative Trials” PLoS Negl Trop Dis. 2008 March; 2(3): e194
  14. ^ WHO, “Global Plan to Combat Neglected Tropical Diseases 2008-2015. World Health Organization 2007
  15. ^ a b CDC, International Task Force for Disease Eradication, 1992. MMWR weekly. 1992. 41(37); 691, 697-698. http://www.cdc.gov/mmwr/preview/mmwrhtml/00017648.htm
  16. ^ a b Schantz, P. “Eradication of T. solium Cysticercosis” International Conference on Emerging Infectious Diseases 2002. CDC. ftp://ftp.cdc.gov/pub/infectious_diseases/iceid/2002/pdf/schantz.pdf
  17. ^ a b Gonzalez AE, García HH, Gilman RH, Tsang VCW, Cysticercosis Working Group in Peru. “Control of Taenia solium” Acta Tropica 2003 87(1): 103-109.
  18. ^ Gonzalez, A.E., Gavidia, C., Falcon, N., Bernal, T., Verastegui, M., Garcia, H.H., Gilman, R.H., Tsang, V.C., 2001.“Protection of pigs with cysticercosis from further infections after treatment with oxfendazole.” Am. J. Trop. Med. Hyg.65, 15-18.
  19. ^ Garcia, H.H., 2002. “Effectiveness of an interventional control program for human and porcine Taenia solium cysticercosis in field conditions.” In: International Health. Johns Hopkins University, Baltimore, p. 250.
  20. ^ Gilman, R.H., Garcia, H.H., Gonzalez, A.E., Dunleavy, M., Verastegui, M., Peru, T.C.W.G.I., 1999. Short cuts to development: methods to control the transmission of cysticercosis in developing countries. In: Garcı´a, H.H., Martı´nez, M. (Eds.), Taenia solium taeniasis/cysticercosis. Editorial Universo, Lima,313-326.
  21. ^ Margono, S.S., Subahar, R., Hamid, A., Wandra, T., Sudewi, S.S., Sutisna, P., Ito, A., 2001. “Cysticercosis in Indonesia: epidemiological aspects.” Southeast Asian J. Trop. Med.Public Health 32 (Suppl. 2), 79-84.
  22. ^ Wandra, T., Subahar, R., Simanjuntak, G.M., Margono, S.S.,Suroso, T., Okamoto, M., Nakao, M., Sako, Y., Nakaya, K., Schantz, P.M., Ito, A., 2000. Resurgence of cases of epileptic seizures and burns associated with cysticercosis in Assologaima, Jayawijaya, Irian Jaya, Indonesia, 1991-1995. Trans. R. Soc. Trop. Med. Hyg. 94: 46-50.
  23. ^ a b c d e f g Sciutto E, Fragoso G. Aluja, A.S.de, Hernandez M, Rosas G. Larralde, C. 2008 “Vaccines Against Cisticercosis” Current Topics in Medicinal Chemistry. 8: 415-423.
  24. ^ Molinari J. L, Meza R, Suarez B, Palacios S, Tato P, Retana A. 1983 “Taenia solium : immunity in hogs to the Cysticercus.”Exp. Parasitol 55: 340-57.
  25. ^ Luo X, Zheng Y, Hou J, Zhang S, Cai X. 2009 “Protection against Asiatic Taenia solium Induced by a Recombinant 45W-4B Protein Clinical and Vaccine Immunology, 16 (2): 230-232.
  26. ^ a b Huerta M, De Aluja AS, Fragoso G, Toledo A, Villalobos N, Hernandez M, Gevorkian G, Acero G, Diaz A, Alvarez I, Avila R, Beltran C, Garcia G, Martinez J J, Larralde C, Sciutto E. (2001) Synthetic peptide vaccine against Taenia solium pig cysticercosis: successful vaccination in a controlled field trial in rural Mexico. Vaccine 20: 262-6.
  27. ^ http://www-lab.biomedicas.unam.mx/cistimex/s1.html#capitulo6
  28. ^ Sciutto E, Morales J, Martinez JJ, Toledo A, Villalobos MN, Cruz-Revilla C, Meneses G, Hernandez M, Diaz A, Rodarte LF, Acero G, Gevorkian G, Manoutcharian, K, Paniagua J, Fragoso G, Fleury A, Larralde R De, Aluja AS, Larralde C. (2007) “Further evaluation of the synthetic peptide vaccine S3Pvac against Taenia solium cysticercosis in pigs in an endemic town of Mexico.” Parasitology 134: 129-33.
  29. ^ a b E-mail interview with Edda Sciutto. Feb 26 2009.
  30. ^ http://www.cwgesa.org/CWGESA%20Action%20Plan/CWGESA%20Action%20Plan.aspx
  31. ^ CWGESA. 5th General Assembly of the Cysticercosis Working Group in Eastern and Southern Africa. 2007. CIRAD http://pigtrop.cirad.fr/sp/recursos/publications/procedimientos/5th_general_assembly_of_the_cysticercosis_working_group_in_eastern_and_southern_africa
  32. ^ Morales J, Martínez JJ, Garcia-Castella J,Peña N, Maza V, Villalobos N, Aluja AS, Fleury A, Fragoso G, Larralde C, Sciutto E. (2006) “Taenia solium: the complex interactions, of biological, social, geographical and commercial factors, involved in the transmission dynamics of pig cysticercosis in highly endemic areas” Annals of Tropical Medicine and Parasitology, 100(2) 123-135.
  33. ^ http://virtualmentor.ama-assn.org/2008/04/cprl1-0804.html
  34. ^ http://www.who.int/zoonoses/diseases/taeniasis/en/index.html
  35. ^ Bern C, Garcia HH, Evans C, Gonzalez AE, Verastegui M, Tsang VC, Gilman RH. “Magnitude of the disease burden from neurocysticercosis in a developing country.” Clin Infect Dis 1999 Nov 29 (5): 1203-9.
  36. ^ http://www.cdc.gov/EID/content/13/2/230.htm
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