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Cysticercosis in Emergency Medicine

  • Author: Mityanand Ramnarine, MD, FACEP; Chief Editor: Barry E Brenner, MD, PhD, FACEP  more...
 
Updated: May 09, 2016
 

Background

Cysticercosis is a systemic illness caused by dissemination of the larval form of the pork tapeworm, Taenia solium. Encystment of larvae can occur in almost any tissue. Involvement of the central nervous system (CNS), known as neurocysticercosis (NCC), is the most clinically important manifestation of the disease and may present with dramatic findings. Moreover, neurocysticercosis is the most common helminthic infection of the CNS.[1]  Neurocysticercosis is a major cause of seizure disorder in parts of the developing world, and its incidence is increasing within developed countries.

In impoverished countries and those in which pigs are raised, T solium is a significant etiology of seizures. Although neurocysticercosis is not widespread in the United States, it must be considered during the evaluation of a patient with newly onset seizure. Up to 10% of hospitalized patients in the United States with neurocysticercosis die of this preventable disease.[2]

See the image below.

Nonenhanced (left) and enhanced (right) CT scans o Nonenhanced (left) and enhanced (right) CT scans of the brain in a patient with neurocysticercosis show multiple ring-enhancing lesions with perifocal edema.
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Pathophysiology

Humans are the definitive T solium hosts and can carry an intestinal adult tapeworm (taeniasis), often without symptoms. Intermittent fecal shedding of egg-containing proglottids or free T solium eggs ensues, with the intention that the intermediate host (normally pigs) will ingest the excreted eggs in contaminated food or water. T solium embryos penetrate the GI mucosa of the pig and are hematogenously disseminated to peripheral tissues with resultant formation of larval cysts (cysticerci). When undercooked pork is consumed, an intestinal tapeworm will again be formed, completing the life cycle of the worm.

Human cysticercosis occurs when T solium eggs are ingested via fecal-oral transmission from a tapeworm host. The human then becomes an accidental intermediate host, with development of cysticerci within organs. Cysticerci may be found in almost any tissue. The most frequently reported locations are skin, skeletal muscle, heart, eye, and the central nervous system (CNS). Involvement of the CNS leads to the most important manifestation of the disease, neurocysticercosis (NCC).

Symptomatology of neurocysticercosis (NCC) ranges from completely asymptomatic to severe disease and death. Symptoms largely depend on the presence of pericystic inflammation, the absence of which will usually manifest as asymptomatic disease. Lack of perilesional inflammation is seen with both "active" healthy parasites, which are able to evade host immunity (an adaptive feat that may be abetted by the immune privilege afforded to the CNS), and in "inactive" disease in which the cysticerci have completely involuted. As a corollary, inflammation is restricted to currently live but degenerating cysts whose ability to escape host defenses is faltering. Upon imaging, these inflamed degenerating cysts are typically seen as ring-enhancing lesions, an appearance that may be termed colloidal. Eventually, cysts will involute and either vanish or undergo granulomatous change and exhibit calcific scarring. Cysts in various stages of viability can be seen simultaneously in one host.

In patients with advanced HIV disease and compromised cell-mediated immunity, neurocysticercosis may exist without significant host response and is likely to be asymptomatic. For this reason, in symptomatic patients with CD4 counts under 200 cells/mm3, alternative diagnoses should be considered.[3]

Serious pathologic findings of neurocysticercosis (NCC) can include seizures, encephalopathy, obstructive hydrocephalus, meningoencephalitis, cognitive decline, focal deficits, and vascular accidents. Involvement of brain parenchyma is common and leads to the most frequent presentation of seizure or headache. Clinical expression of NCC depends primarily on the number and location of CNS cysticerci and degree of inflammatory response. As previously mentioned, host immune response and resultant pericystic inflammation are considered largely responsible for parenchymal disease manifestations. However, some evidence indicates that involuted calcific lesions may be epileptogenic as well and thus contribute to significant morbidity.

Extraparenchymal ventricular and subarachnoid cysts also are found. These carry a worse prognosis and often lead to obstructing hydrocephalus requiring surgical intervention. Cysticerci within the basilar cisterns or Sylvian fissures may become quite large. Those within the cisterns may also cause vasculitis and stroke. Spinal NCC is rare.

Ocular cysts are mostly vitreous, but they may be found in subretinal locations. Visualization of cysts via funduscopy may be diagnostic of the disease. Subcutaneous nodules represent cysticerci in the skin. Skeletal muscle encystment usually is asymptomatic but may cause muscular pseudohypertrophy with a heavy parasite burden. Cardiac cysts may lead to conduction system abnormalities.

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Epidemiology

Frequency

United States

Incidence in the United States is increasing due to increased immigration from and travel to endemic areas and improved serologic testing and availability of diagnostic imaging. An estimated 1000 new cases are diagnosed per year in the United States. In southern California, with its large population of immigrants, neurocysticercosis (NCC) may account for at least 10% of seizures seen in some emergency departments and more than 2% of neurological or neurosurgical admissions.[4] The diagnosis of NCC should be considered in any patient from an endemic area presenting with new-onset seizures.

International

Cysticercosis affects an estimated 50 million people worldwide. Endemic areas include Mexico and Latin America, sub-Saharan Africa, India, and East Asia. NCC is a leading cause of adult-onset seizures worldwide.[5, 6, 7]

Mortality/Morbidity

Morbidity may result from seizures, strokes, or hydrocephalus and from effects of long-term treatment with anticonvulsants, steroids, or cerebrospinal fluid shunts.

Mortality from cysticercosis is generally limited to cases complicated by encephalitis, cerebral edema, hydrocephalus, and stroke.[8]

Race

Hispanic and Asian populations are more commonly affected due to immigration patterns from endemic areas. The disease is prevalent in South Asia as well, where patients more commonly present with a solitary cyst.

Age

People of any age may be affected. Children may be more likely to develop an unusual encephalitis-type variant.

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Contributor Information and Disclosures
Author

Mityanand Ramnarine, MD, FACEP Assistant Professor of Emergency Medicine, Program Director, Emergency/Internal Medicine/Critical Care, Hofstra Northwell School of Medicine at Hofstra University; Attending Physician, Department of Emergency Medicine, Long Island Jewish Medical Center

Mityanand Ramnarine, MD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American College of Physicians, American Medical Association

Disclosure: Nothing to disclose.

Coauthor(s)

 

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director for Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, Society for Academic Emergency Medicine, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians

Disclosure: Nothing to disclose.

Additional Contributors

William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center

William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Ryan L Tenzer, MD, FAAEM Clinical Assistant Professor of Emergency Medicine, Pennsylvania State University College of Medicine; Consulting Staff, Department of Emergency Medicine, Lehigh Valley Hospital

Ryan L Tenzer, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Acknowledgements

Howard A Blumstein, MD, FAAEM Assistant Professor of Surgery, Medical Director, Department of Emergency Medicine, Wake Forest University School of Medicine

Howard A Blumstein, MD, FAAEM is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, Emergency Medicine Residents Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

References
  1. Garcia HH, Nash TE, Del Brutto OH. Clinical symptoms, diagnosis, and treatment of neurocysticercosis. Lancet Neurol. 2014 Dec. 13 (12):1202-15. [Medline].

  2. CDC. Available at http://www.cdc.gov/parasites/npi/images/cysticercosis_infographic.jpg.

  3. Prasad S, MacGregor RR, Tebas P. Management of potential neurocysticercosis in patients with HIV infection. Clin Infect Dis. 2006 Feb 15. 42(4):e30-4. [Medline].

  4. Ong S, Talan DA, Moran GJ. Neurocysticercosis in radiographically imaged seizure patients in U.S. emergency departments. Emerg Infect Dis. 2002 Jun. 8(6):608-13. [Medline].

  5. Coral-Almeida M, Gabriël S, Abatih EN, Praet N, Benitez W, Dorny P. Taenia solium Human Cysticercosis: A Systematic Review of Sero-epidemiological Data from Endemic Zones around the World. PLoS Negl Trop Dis. 2015 Jul. 9 (7):e0003919. [Medline].

  6. Wandra T, Swastika K, Dharmawan NS, Purba IE, Sudarmaja IM, Yoshida T, et al. The present situation and towards the prevention and control of neurocysticercosis on the tropical island, Bali, Indonesia. Parasit Vectors. 2015 Mar 7. 8:148. [Medline].

  7. Ito A, Wandra T, Li T, Dekumyoy P, Nkouawa A, Okamoto M, et al. The present situation of human taeniases and cysticercosis in Asia. Recent Pat Antiinfect Drug Discov. 2014. 9 (3):173-85. [Medline].

  8. Jain RS, Handa R, Vyas A, Prakash S, Nagpal K, Bhana I, et al. Cysticercotic encephalitis: a life threatening form of neurocysicercosis. Am J Emerg Med. 2014 Nov. 32 (11):1444.e1-2. [Medline].

  9. Rodriguez S, Dorny P, Tsang VC, Pretell EJ, Brandt J, Lescano AG, et al. Detection of Taenia solium antigens and anti-T. solium antibodies in paired serum and cerebrospinal fluid samples from patients with intraparenchymal or extraparenchymal neurocysticercosis. J Infect Dis. 2009 May 1. 199 (9):1345-52. [Medline].

  10. Gonzales I, Rivera JT, Garcia HH, Cysticercosis Working Group in Peru. Pathogenesis of Taenia solium taeniasis and cysticercosis. Parasite Immunol. 2016 Mar. 38 (3):136-46. [Medline].

  11. Kramer LD, Locke GE, Byrd SE. Cerebral cysticercosis: documentation of natural history with CT. Radiology. 1989 May. 171(2):459-62. [Medline].

  12. Kim SD, Kim JH, Lee CY, Kim HW. Ganglioglioma in brainstem : case report and a review of literatures. J Korean Neurosurg Soc. 2014 Mar. 55 (3):164-6. [Medline].

  13. Das K, Mondal GP, Banerjee M, Mukherjee BB, Singh OP. Role of antiparasitic therapy for seizures and resolution of lesions in neurocysticercosis patients: an 8 year randomised study. J Clin Neurosci. 2007 Dec. 14(12):1172-7. [Medline].

  14. Del Brutto OH, Roos KL, Coffey CS, Garcia HH. Meta-analysis: Cysticidal drugs for neurocysticercosis: albendazole and praziquantel. Ann Intern Med. 2006 Jul 4. 145(1):43-51. [Medline].

  15. Salinas R, Counsell C, Prasad K. Treating neurocysticercosis medically: a systematic review of randomized, controlled trials. Trop Med Int Health. 1999 Nov. 4(11):713-8. [Medline].

  16. Gongora-Rivera F, Soto-Hernandez JL, Gonzalez Esquivel D, Cook HJ, Marquez-Caraveo C, Hernandez Davila R, et al. Albendazole trial at 15 or 30 mg/kg/day for subarachnoid and intraventricular cysticercosis. Neurology. 2006 Feb 14. 66(3):436-8. [Medline].

  17. Botero D, Tanowitz HB, Weiss LM, Wittner M. Taeniasis and cysticercosis. Infect Dis Clin North Am. 1993 Sep. 7(3):683-97. [Medline].

  18. Buitrago M, Edwards B, Rosner F. Neurocysticercosis: Report of fifteen cases. Mt Sinai J Med. 1995 Nov. 62(6):439-44. [Medline].

  19. Carpio A, Kelvin EA, Bagiella E, Leslie D, Leon P, Andrews H. Effects of albendazole treatment on neurocysticercosis: a randomised controlled trial. J Neurol Neurosurg Psychiatry. 2008 Sep. 79(9):1050-5. [Medline].

  20. Del Brutto OH. Cysticercosis and cerebrovascular disease: a review. J Neurol Neurosurg Psychiatry. 1992 Apr. 55(4):252-4. [Medline].

  21. Del Brutto OH, Rajshekhar V, White AC. Proposed diagnostic criteria for neurocysticercosis. Neurology. 2001 Jul 24. 57(2):177-83. [Medline].

  22. Garcia HH, Del Brutto OH. Imaging findings in neurocysticercosis. Acta Trop. 2003 Jun. 87(1):71-8. [Medline].

  23. Garcia HH, Del Brutto OH. Neurocysticercosis: updated concepts about an old disease. Lancet Neurol. 2005 Oct. 4(10):653-61. [Medline].

  24. Garcia HH, Pretell EJ, Gilman RH. A trial of antiparasitic treatment to reduce the rate of seizures due to cerebral cysticercosis. N Engl J Med. 2004 Jan 15. 350(3):249-58. [Medline].

  25. Kalra V, Dua T, Kumar V. Efficacy of albendazole and short-course dexamethasone treatment in children with 1 or 2 ring-enhancing lesions of neurocysticercosis: a randomized controlled trial. J Pediatr. 2003 Jul. 143(1):111-4. [Medline].

  26. Lamont EB, Sayah A. An occult cause of persistent nausea and vomiting. J Emerg Med. 1997 Sep-Oct. 15(5):633-5. [Medline].

  27. Loyo-Varela M. Surgical treatment of cerebral cysticercosis. Eur Neurol. 1997. 37(2):129-30. [Medline].

  28. Mitchell WG. Pediatric neurocysticercosis in North America. Eur Neurol. 1997. 37(2):126-9. [Medline].

  29. Mitchell WG, Crawford TO. Intraparenchymal cerebral cysticercosis in children: diagnosis and treatment. Pediatrics. 1988 Jul. 82(1):76-82. [Medline].

  30. Richards F Jr, Schantz PM. Laboratory diagnosis of cysticercosis. Clin Lab Med. 1991 Dec. 11(4):1011-28. [Medline].

  31. Rosenfeld EA, Byrd SE, Shulman ST. Neurocysticercosis among children in Chicago. Clin Infect Dis. 1996 Aug. 23(2):262-8. [Medline].

  32. Salgado P, Rojas R, Sotelo J. Cysticercosis. Clinical classification based on imaging studies. Arch Intern Med. 1997 Sep 22. 157(17):1991-7. [Medline].

  33. Sciutto E, Chavarria A, Fragoso G, Fleury A, Larralde C. The immune response in Taenia solium cysticercosis: protection and injury. Parasite Immunol. 2007 Dec. 29(12):621-36. [Medline].

  34. White AC Jr. Neurocysticercosis: a major cause of neurological disease worldwide. Clin Infect Dis. 1997 Feb. 24(2):101-13; quiz 114-5. [Medline].

  35. White AC Jr. Neurocysticercosis: updates on epidemiology, pathogenesis, diagnosis, and management. Annu Rev Med. 2000. 51:187-206. [Medline].

 
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Nonenhanced CT scan of the brain demonstrates the multiple calcified lesions of inactive parenchymal neurocysticercosis.
Enhanced CT scan of the brain in a patient with neurocysticercosis demonstrates a live cyst with a minimally enhancing wall and an eccentric hyperattenuating scolex.
Nonenhanced (left) and enhanced (right) CT scans of the brain in a patient with neurocysticercosis show multiple ring-enhancing lesions with perifocal edema.
 
 
 
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