Diagnostik der zystischen Echinokokkose

Kern, Peter; Reuter, Stefan; Buttenschoen, Klaus; Kratzer, Wolfgang

doi:10.1055/s-2001-9880

Cited by 7 publications

(1 citation statement)

References 8 publications

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“…The diagnosis of CE in individual patients is based on identification of cyst structures by imaging techniques, predominantly ultrasonography, computed tomography, X-ray examinations, and confirmation by detection of specific serum antibodies by immunodiagnostic tests (28,84,90,114,149,192). For clinical practice it should be noted that the enzyme-linked immunosorbent assay (ELISA) using crude hydatid cyst fluid has a high sensitivity (over 95%) but its specificity is often unsatisfactory.…”

Section: Vol 17 2004 Biology and Epidemiology Of Echinococcosis 109mentioning

confidence: 99%

Biological, Epidemiological, and Clinical Aspects of Echinococcosis, a Zoonosis of Increasing Concern

2004

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Echinococcosis in humans is a zoonotic infection caused by larval stages (metacestodes) of cestode species of the genus Echinococcus. Cystic echinococcosis (CE) is caused by Echinococcus granulosus, alveolar echinococcosis (AE) is caused by E. multilocularis, and polycystic forms are caused by either E. vogeli or E. oligarthrus. In untreated cases, AE has a high mortality rate. Although control is essentially feasible, CE remains a considerable health problem in many regions of the northern and southern hemispheres. AE is restricted to the northern hemisphere regions of North America and Eurasia. Recent studies have shown that E. multilocularis, the causative agent of AE, is more widely distributed than previously thought. There are also some hints of an increasing significance of polycystic forms of the disease, which are restricted to Central and South America. Various aspects of human echinococcosis are discussed in this review, including data on the infectivity of genetic variants of E. granulosus to humans, the increasing invasion of cities in Europe and Japan by red foxes, the main definitive hosts of E. multilocularis, and the first demonstration of urban cycles of the parasite. Examples of emergence or reemergence of CE are presented, and the question of potential spreading of E. multilocularis is critically assessed. Furthermore, information is presented on new and improved tools for diagnosing the infection in final hosts (dogs, foxes, and cats) by coproantigen or DNA detection and the application of molecular techniques to epidemiological studies. In the clinical field, the available methods for diagnosing human CE and AE are described and the treatment options are summarized. The development of new chemotherapeutic options for all forms of human echinococcosis remains an urgent requirement. A new option for the control of E. granulosus in the intermediate host population (mainly sheep and cattle) is vaccination. Attempts are made to reduce the prevalence of E. multilocualaris in fox populations by regular baiting with an anthelmintic (praziquantel). Recent data have shown that this control option may be used in restricted areas, for example in cities, with the aim of reducing the infection risk for humans

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Section: Vol 17 2004 Biology and Epidemiology Of Echinococcosis 109mentioning

confidence: 99%

Biological, Epidemiological, and Clinical Aspects of Echinococcosis, a Zoonosis of Increasing Concern

2004

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A Case of Sporadic Echinococcus granulosus Infection Originary from Southern Germany

et al. 2007

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A 67-year-old woman with cystic echinococcosis (CE) is presented. She had complained of upper abdominal discomfort due to large hepatic cysts. These cysts showed no typical infrastructure characteristic for CE and she had never left the rural areas of southern Germany. Most remarkably, this area is highly endemic for alveolar echinococcosis, caused by Echinococcus multilocularis, but only sporadic cases of CE have been described. Due to the discrepancy between positive Echinococcus serology, atypical morphology and residency in an area non-endemic for Echinococcus granulosus, diagnostic puncture was performed with albendazole coverage. Puncture was complicated by anaphylaxis, from which the patient recovered without sequelae. The diagnosis of CE was highly likely due to the combination of positive serology with post puncture anaphylaxis, increasing antibody titers and eosinophilia. Retrospectively, the cysts had initially corresponded to the WHO stage CE 1. The patient was treated with albendazole for 15 weeks. Under treatment, the parasitic membrane detached from the cyst wall, revealing characteristic morphology for CE, now corresponding to the WHO stage CE 3. The patient remained asymptomatic during follow-up visits.

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