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echinococcus

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echinococcus

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  1. Echinococcus granulosus

  2. CLASSIFICATION Kingdom : Animalia Phylum : Platyhelminthes Class : Cestoda Order : Cyclophyllidea Family : Taenidae Genus : Echinococcus Species : granulosus

  3. INTRODUCTION • Echinococcus granulosus, also called hydatid worm belongs to class Cestoda • It causes cystic echinococcosis in livestock and humans being intermediate hosts and parasitize the small intestines of adult canids • It is a zoonotic disease • Definitive hosts are carnivorous predators like dogs, wolves, foxes and lions. While sheep, goat, cattle, pigs and rodents are intermediate hosts. Birds and arthropods act as mechanical vectors

  4. MORPHOLOGY • The adult tapeworm ranges in length from 2 mm to 7mm and has three proglottids when intact — a immature proglottid, mature proglottid and a gravid proglottid. • It has scolex with four suckers andalso has a rostellum withhooks. • Echinococcus is triploblastic, anus is absent and it has no digestivesystem. • Its body is covered by tegument andthe worm is divided into a scolex, a short neck, and three to six proglottids. Its body shape isribbon-like.

  5. E.granulosus

  6. TRANSMISSION • Adult E. granulosus release eggs within the intestine which will be transported out of the body via feces • When contaminated waste is excreted into the environment, intermediate host has the potential to contract the parasite by grazing in contaminated pasture • It is transmitted from the intermediate host (sheep) to the definitive host (dogs) by frequent feeding of offal. • Consuming offal containing Echinococcus granulosus can lead to infection

  7. LIFE CYCLE • The adult is in the small intestines of the definitive host (dogs) • Gravid proglottids release eggs that are passed in the feces • The intermediate hosts are infected by ingesting eggs, the egg hatches in the small bowel and releases an oncosphere • The oncosphere penetrates the intestinal wall and moves through the circulatory system to various organs • In the organs they develop into cysts and enlarge gradually

  8. The cysts produce protoscolices and daughter cysts • Definitive host eats the infected organs and becomes infected • After ingestion, the protoscolices evaginate, attach to the intestinal mucosa and develop into adult stages • In 32-80 days, cycle starts over

  9. The growth rate of cystsis highly variable and may depend on strain differences and cyst location. Estimates of the average increase of cyst diameter vary (approximately 1.5-2 cm/year).

  10. Gross pathology of hydatid daughter cysts Pathologically hydatid liver cyst has three distinct layers: membrane and Ectocyst - fibrous adventitial layer due to host response Middle layer - laminated membrane of proteinaceous material Endocyst - inner germinal layer from which the scolices may be detached from human lung

  11. Hydatidcysts

  12. A hydatid cyst in the cranium of a child (the ruler at the top measures 6 inches long, and the child's brain is below the hydatid cyst). This infection resulted in the child's death.

  13. PATHOGENESIS • Ingested eggs from animal hatch in thegut and releaseoncospheres • Oncospheres penetrate the intestinal wall, migrate via the circulation, and lodge in the liver or lungs or, less frequently, in the brain, bone, or otherorgans. • In tissue , E. granulosus oncospheres develop into cysts, which grow slowly (usually over many years) into large fluid-filled lesions—hydatidcysts • Large cysts may contain >1 L of highly antigenic hydatid fluid as well as millions of protoscolices • If a cyst in the liver leaks or ruptures, infection can spread to theperitoneum.

  14. SIGNS • Signs depend upon the site ofinfection • Liver cysts cause abdominal pain ofa palpable mass. Jaundice may occur if the bile duct isobstructed. • Rupture into the bile duct, peritoneal cavity, or lung may cause fever, urticaria, or a serious anaphylacticreaction. • Pulmonary cysts can causecough, chest pain, andhaemoptysis. • Brain and spinal cord; causeepilepsy and blindness

  15. DIAGNOSIS • Diagnosis in the definitive host, the dog is difficult by ordinary microscopy as it cannot demarcate between Taenia and Echinococcus eggs • Detection of antigens in feces by ELISA is currently the best available technique Other techniques are; Imaging Serologic testing Examination of cyst fluid

  16. TREATMENT • Surgical Removal of Hydatid Cysts 90% effective but can be risky depending on location, size, and advancement of cyst • It may need chemotherapy to prevent recurrance • Chemotherapy: Albendazole is preferred treatment because it penetrates into hydatid cysts. Dosage: 10mg/kg body weight or 400mg 2x daily for 4 weeks Mebendazole Dosage: 40mg/kg body weight 3x daily for 3- 6 months Dogs are effectively treated with Praziquental • PAIR Treatment Puncture, aspiration, injection, respiration • Inject protoscolicidal substances into the cyst

  17. PREVENTION • In order to prevent transmission to dogs from intermediate hosts, dogs can be given anthelminthicvaccinations • Clean slaughter and high surveillance of potential intermediate host during slaughter is key in preventing the spread this cestode to its definitive host • Proper disposal of carcass and offal after slaughter to prevent dogs access to offal from livestock • Boiling livers and lungs which contain hydatid cysts for 30 minutes has been proposed as a simple, efficient and saving way to kill the infectiouslarvae

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