Abstract

Background:
Toxocara canis is a zoonotic nematode that mainly infects dogs but can produce visceral, ocular, and neurological toxocariasis in humans. The parasite completes its life cycle within dogs. The molecular processes that enable T. canis to adapt to its host remain largely unknown despite the significance of the parasite to public health.

Aim:
To understand the molecular basis of immune evasion, tissue migration, and survival strategies, researchers analyzed T. canis gene expression during different life stages within canine and human hosts.

Methods:
Third-stage larvae (L3) and adult worms were collected from infected tissues at intervals of 7, 14, 28, and 35 days post-infection using both experimentally infected dogs (definitive hosts) and murine models (human equivalent accidental hosts). RNA was extracted, and quantitative real-time PCR was performed to measure the expression of three key virulence genes: Toxocara excretory-secretory protein 1 (TcES-1), Toxocara cysteine protease-like gene (TcCPL-1), and Toxocara heat shock protein 90 (TcHSP-90) were examined for their roles in worm virulence.

Results:
Human-model larvae showed significantly higher levels of TcES-1 and TcCPL-1 expression than canine larvae, indicating stronger immune modulation and tissue invasion abilities in incidental hosts with statistical significance (p < 0.001). Human-model larvae displayed significantly higher levels of TcHSP-90 expression than both dog-derived larvae and adult worms, indicating stress-response adaptation in non-permissive hosts.

Conclusion:
The findings of this study reveal how T. canis adapts to different hosts at the molecular level and identify new opportunities for the development of diagnostic and therapeutic approaches to manage zoonotic toxocariasis.

Key words: Cysteine protease; Excretory-secretory proteins; Host adaptation; Toxocara canis; Zoonosis.