Pediatric Echinococcosis 

  • Author: Robert W Tolan Jr, MD; Chief Editor: Russell W Steele, MD   more...
 
Updated: Jan 10, 2012
 

Background

Echinococcosis is the general term for 3 diseases caused by the larval stage of Echinococcus tapeworms, the smallest tapeworms in the Taeniidae family. Echinococcus granulosus causes cystic echinococcosis. This species occurs worldwide, typically in rural areas of Africa, the Middle East, southern Europe, Russia, China, Australia, and South America (especially Argentina and Uruguay). Echinococcus multilocularis causes alveolar hydatid echinococcosis and occurs only in the northern hemisphere. Echinococcus vogeli causes polycystic echinococcosis and occurs in Central and South America.

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Pathophysiology

The tapeworm's life cycle (see image below) involves a definitive host, usually a dog (although foxes and coyotes have also been implicated), and intermediate hosts such as sheep, goats, and swine. The 3-mm to 6-mm adult tapeworm is found in the definitive host's intestines. Eggs are excreted via the feces into the environment. Dogs typically become infected by eating the remains of infected sheep and other livestock.

Diagram of the Echinococcus life cycle, provided bDiagram of the Echinococcus life cycle, provided by the Centers for Disease Control and Prevention.

Humans are accidental hosts and are not typically involved in the life cycle of the organism. Humans usually become infected through exposure to canine feces. Humans become infected by eating food contaminated with tapeworm eggs, which hatch in human small intestine under the influence of gastric and intestinal secretions. Larvae hatched from these eggs can penetrate the small intestine and become widely distributed in the human body. These larvae develop into a hydatid cyst. In alveolar echinococcosis, the liver is almost exclusively involved.[1] In cystic echinococcosis, the liver is involved in two thirds of cases; in the remaining cases, other sites of involvement, in descending order of frequency, are the lung, spleen, skin, muscle, kidney, retroperitoneum, bone, heart, and brain.

Hydatid cysts may contain many protoscolices, each with the ability to develop into an adult tapeworm in a definitive host. The definitive host usually becomes infected by ingesting the protoscolices in hydatid cysts from the intermediate host; adult tapeworms only develop in the intestines of the definitive host.

Human disease is usually caused by the mass effect of slow-growing hydatid cysts, although bacterial superinfection or allergic symptoms from cyst rupture has also been reported. Because of the hydatid cyst's unhurried growth, infected humans may remain asymptomatic for 20 years.

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Epidemiology

Frequency

United States

Echinococcosis is rare. Indigenous cases have been reported in Minnesota and among Native Americans in western Alaska. Imported cases are uncommon.

International

Human infection rates are generally highest in areas with poor sanitation practices for sheep-raising, particularly in areas with dogs. Dogs in these areas may become infected by eating the entrails of infected butchered sheep or other herded animals. Humans then become infected when they ingest Echinococcus eggs from dog feces. Human infection rates are also high in areas where intestines are part of the diet.

Echinococcosis has been reported in Manitoba and Saskatchewan[2] , Canada. Outside North America, incidence rates vary considerably, from less than 1 case per 100,000 people in many parts of the world, to 13 cases per 100,000 people in Greece, 143 cases per 100,000 people in Argentina, 197 cases per 100,000 people in the Xinjiang province of China, and 220 cases per 100,000 people in Kenya's Turkana district.

The Turkana district's particularly high incidence rate is attributed to 2 cultural practices. Some tribes eat canine intestine that has been roasted on a stick over a campfire; disease transmission likely occurs when infected intestine is not thoroughly cooked. Some tribes also do not bury their dead; carnivores may become the direct intermediate host after eating corpses.

A new species, E canadensis G7, appears to be common in Austria.[3]

Mortality/Morbidity

Most human infection is probably asymptomatic. Death may occur from hydatid rupture, which may lead to anaphylactic shock, or from the extreme progression of cysts in vital organs.

Sex

Males and females are equally affected, according to a Bavarian survey.[4]

Age

A European study reported most patients infected by E granulosus were aged 21-50 years. Patients infected by E multilocularis were typically older; most were aged 31-80 years.

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Contributor Information and Disclosures
Author

Robert W Tolan Jr, MD  Chief, Division of Allergy, Immunology and Infectious Diseases, The Children's Hospital at Saint Peter's University Hospital; Clinical Associate Professor of Pediatrics, Drexel University College of Medicine

Robert W Tolan Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Pediatric Infectious Diseases Society, Phi Beta Kappa, and Physicians for Social Responsibility

Disclosure: Novartis Honoraria Speaking and teaching

Specialty Editor Board

Michael D Nissen, MBBS, FRACP, FRCPA  Associate Professor in Biomolecular, Biomedical Science & Health, Griffith University; Director of Infectious Diseases and Unit Head of Queensland Paediatric Infectious Laboratory, Sir Albert Sakzewski Viral Research Centre, Royal Children's Hospital

Michael D Nissen, MBBS, FRACP, FRCPA is a member of the following medical societies: American Academy of Pediatrics, American Society for Microbiology, Pediatric Infectious Diseases Society, Royal Australasian College of Physicians, and Royal College of Pathologists of Australasia

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Martin Weisse, MD  Program Director, Associate Professor, Department of Pediatrics, West Virginia University

Martin Weisse, MD is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Pediatric Infectious Diseases Society

Disclosure: Nothing to disclose.

Daniel Rauch, MD, FAAP  Director, Pediatric Hospitalist Program, Associate Professor, Department of Pediatrics, New York University School of Medicine

Daniel Rauch, MD, FAAP is a member of the following medical societies: Ambulatory Pediatric Association, American Academy of Pediatrics, and Society of Hospital Medicine

Disclosure: Baxter Honoraria Consulting

Chief Editor

Russell W Steele, MD  Head, Division of Pediatric Infectious Diseases, Ochsner Children's Health Center; Clinical Professor, Department of Pediatrics, Tulane University School of Medicine

Russell W Steele, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American Pediatric Society, American Society for Microbiology, Infectious Diseases Society of America, Louisiana State Medical Society, Pediatric Infectious Diseases Society, Society for Pediatric Research, and Southern Medical Association

Disclosure: Nothing to disclose.

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Diagram of the Echinococcus life cycle, provided by the Centers for Disease Control and Prevention.
 
 
 
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