Abstract

Cystic echinococcosis is considered as an emerging zoonosis that can develop asymptomatically for years, clinically nonpathognomic. The disease is of public health importance due to often late, difficult diagnostics, uncertain results of treatment, the need to remove hydatid cysts surgically in advanced cases, and poor prognosis in untreated patients. Six Polish female patients with diagnosed cystic echinococcosis (CE) were examined. DNA extracted from the liver and lung samples served for amplification of mitochondrial nad1 gene fragment. Sequence alignments of 5 isolates showed identity with the pig strain, Echinococcus canadensis G7. One case was in 100% identical with Echinococcus ortleppi G5, the cattle strain. These data demonstrate first report of E. ortleppi, regarded as extinct species, causing human cystic echinococcosis in Poland, where the most frequent causative agent of human CE is E. canadensis.

Highlights

  • Cystic echinococcosis (CE) is a globally distributed zoonotic disease caused by Echinococcus granulosus sensu lato which is a member of the Taeniidae family

  • Certain patients with cystic echinococcosis had been under medical supervision for many years and were treated with albendazole

  • DNA extracted from all 6 samples and positive controls were used as the template in separate PCRs to amplify region of the mitochondrial NADH dehydrogenase 1

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Summary

Introduction

Cystic echinococcosis (CE) is a globally distributed zoonotic disease caused by Echinococcus granulosus sensu lato which is a member of the Taeniidae family. When intermediate hosts (sheep, goat, swine, cattle, or accidentally human) ingest eggs, they develop into hydatid cysts in the internal organs. The cysts in humans develop most commonly in the liver, and in lungs, brain, heart, and bones. The disease usually develops asymptomatically for years until growing cysts start to press on the surrounding tissues and give nonspecific symptoms. Treatment of CE is considered difficult, because of the involvement of the vital organs and possibility of dissemination of fluid with protoscoleces during the surgery. Both deficient resection and bladder rupture may contribute to anaphylaxis, recurrence, and multiple secondary CE [1,2,3]

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