Aim: As Echinococcosis stands out worldwide as an important zoonotic cestode infection caused by various Echinococcus species, histopathological features of the disease are worthy of in-depth study. Materials and Methods: Histopathological changes in adjacent parenchymal tissue in patients with cystic echinococcosis (CE) were evaluated. The study included 91 patients 4-80 years of age (mean age: 36.24 years). Results: The histopathological findings of 83 specimens were as follows: fibrosis: 77.11%; mono-nucleated cells: 71.08%; necrosis: 67.47%; eosinophils: 51.80%; giant cells: 31.33%; neutrophils: 8.43%. Fibrosis, eosinophils, neutrophils, and giant cell infiltration were observed significantly more often than mono-nucleated cell infiltration, germinal membranes, and protoscolex existence (P < 0.01). Necrosis was noted adjacent to the acellular laminated layer in host parenchymal tissue. Liver and kidneys were significantly more prone to necrosis than other localizations (P < 0.01). Necrosis was seen significantly more often in patients with higher IHA titration positivity (P < 0.01). Conclusions: As necrosis has not been previously considered in CE, histopathological examination in necrosis-dominant cyst walls should be evaluated for a differential diagnosis. One possible explanation for necrosis as a histopathological finding in CE could be that it occurs as a natural course of its immunopathogenesis.

Aim: As Echinococcosis stands out worldwide as an important zoonotic cestode infection caused by various Echinococcus species, histopathological features of the disease are worthy of in-depth study. Materials and Methods: Histopathological changes in adjacent parenchymal tissue in patients with cystic echinococcosis (CE) were evaluated. The study included 91 patients 4-80 years of age (mean age: 36.24 years). Results: The histopathological findings of 83 specimens were as follows: fibrosis: 77.11%; mono-nucleated cells: 71.08%; necrosis: 67.47%; eosinophils: 51.80%; giant cells: 31.33%; neutrophils: 8.43%. Fibrosis, eosinophils, neutrophils, and giant cell infiltration were observed significantly more often than mono-nucleated cell infiltration, germinal membranes, and protoscolex existence (P < 0.01). Necrosis was noted adjacent to the acellular laminated layer in host parenchymal tissue. Liver and kidneys were significantly more prone to necrosis than other localizations (P < 0.01). Necrosis was seen significantly more often in patients with higher IHA titration positivity (P < 0.01). Conclusions: As necrosis has not been previously considered in CE, histopathological examination in necrosis-dominant cyst walls should be evaluated for a differential diagnosis. One possible explanation for necrosis as a histopathological finding in CE could be that it occurs as a natural course of its immunopathogenesis.