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Experimental comparison of pathogenic potential of two sibling species A nisakis simplex s.s. and A nisakis pegreffii in W istar rat
Author(s) -
Romero María,
Valero Adela,
NavarroMoll María Concepción,
MartínSánchez Joaquina
Publication year - 2013
Publication title -
tropical medicine and international health
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.056
H-Index - 114
eISSN - 1365-3156
pISSN - 1360-2276
DOI - 10.1111/tmi.12131
Subject(s) - biology , genotype , larva , genetics , zoology , gene , ecology
Abstract Objectives There are little data available on the pathology caused by the sibling species A nisakis simplex s.s. and A nisakis pegreffii . The differences shown in their ability to penetrate the muscle of fish may also be manifested in humans. The purpose of this study is to confirm possible differences in pathogenicity between A . simplex s.s. and A . pegreffii using an experimental model which simulates infection in humans. Methods Female W istar rats were infected with 190 A nisakis type I L 3 larvae from the I berian coastline. After the animal was sacrificed, these L 3 larvae were then recovered and identified via PCR ‐ RFLP of the ITS 1‐5.8 S ‐ ITS 2. A logistic regression analysis was performed searching for association between experimental pathogenic potential and species. Results The distribution of A . simplex s.s. and A . pegreffii between A tlantic and M editerranean waters of the I berian P eninsula showed statistically significant differences ( P < 0.001) which were not observed in the hybrid genotypes ( P > 0.3). 21.6% showed pathogenic potential, interpreted as the capacity of the larvae to cause lesions, stick to the gastrointestinal wall or penetrate it. The species variable showed association with the pathogenic role of the larva ( P = 0.008). Taking A . simplex s.s. as our reference, the OR for A . pegreffii is 0.351 ( P = 0.028). Conclusions Despite this difference, A . pegreffii is also capable of causing anisakiasis, being responsible for 14.3% of the penetrations of the gastric mucosa found in rats, which justifies both species being considered aetiologic agents of this parasitic disorder.