Histopathologic Evaluation, Ultrastructure, and Molecular Characterization of Acanthocephalan Infections in Freshwater Turtles.

Abstract

Turtle acanthocephalans are a depauperate group of helminths, yet they parasitize a quarter of all turtle species in North America. Despite acanthocephalans being common in turtles, their potential as disease-causing agents remains unknown. In other vertebrate hosts, acanthocephalans are known to cause pathologic changes upon attachment (via with their armed proboscis) to the intestinal wall of the host. Herein, we report new turtle host associations, ultrastructural characterization, and molecular data for turtle acanthocephalans. However, the primary goal of this study was to evaluate whether there is pathology associated with acanthocephalans in turtle hosts. In total, 63 turtles comprising six sampled species were examined for acanthocephalans via surveillance of wild turtles in Oklahoma, USA, between 2010 and 2022. A mean intensity of 395 acanthocephalans per turtle was recovered from 30 (83%) of 36 red-eared sliders (Trachemys scripta elegans), morphologically and molecularly identified as Neoechinorhynchus chrysemydis (n=382), Neoechinorhynchus emydis (n=187), Neoechinorhynchus emyditoides (n=1,803), and Neoechinorhynchus pseudemydis (n=2,901). Only one (11%) of nine snapping turtle (Chelydra serpentina) was infected with acanthocephalans, morphologically and molecularly identified as juveniles of N. chrysemydis (n=1) and Neoechinorhynchus cylindratus (n=12), a fish acanthocephalan. Histopathologic examination revealed changes to the intestinal walls of infected red-eared sliders, including villous atrophy and excessive mucus production. Additionally, the presence of boluses of worms expelled within turtle feces was observed. Noninfected turtles showed no evidence of gross or histopathologic lesions in the intestines. Overall, these findings indicate that acanthocephalans can potentially elicit pathologic changes to turtle hosts, probably as a result of intestinal irritation due to acanthocephalan attachment.