Purpose <p>This study aimed to investigate whether <i>Onchocerca ochengi</i> infection directly causes epilepsy. Although <i>O. ochengi</i>—a cattle parasite phylogenetically related to <i>O. volvulus</i>—shares biological similarities with its human counterpart, it has not been epidemiologically linked to epilepsy in bovines, unlike <i>O. volvulus</i>, which has been associated with onchocerciasis-associated epilepsy in humans. No prior experimental studies have established a causal relationship between onchocerciasis and epilepsy.</p> Methods <p>Gerbils were surgically implanted with <i>O. ochengi</i> worm masses (test group) or underwent sham operations (control group) to assess the infection’s effects. Survival rates were monitored post-implantation, and behavioral assessments were conducted on days 15–19 using the elevated plus maze, open-field, object recognition, and hanging wire tests. On day 21, the gerbils were sacrificed, and their body and organ weights were recorded, along with an analysis of worm mass survival.</p> Results <p>Implantation of 15 worm masses resulted in 100% mortality in the test group. When 10 worm masses were implanted, 53.3% of gerbils died, while all control gerbils survived. By day 21, an average of 1.4 out of 10 implanted worm masses remained viable, with a viability score of 93.3%. Test gerbils exhibited significant reductions in overall body weight and increased spleen weight compared to controls. However, behavioral tests revealed no significant differences between the two groups.</p> Conclusion <p>While <i>O. ochengi</i> worm masses caused notable physical effects, including increased mortality and altered body and organ weights, no conclusive evidence was found linking the infection to behavioral changes indicative of epilepsy. Further research is necessary to explore the potential association between onchocerciasis and epilepsy development.</p>

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Physiological and Behavioral Effects of Onchocerca ochengi Infection in Gerbils: Implications for Onchocerciasis-Associated Epilepsy Research

  • Rene Bilingwe Ayiseh,
  • Fobang Ulrick Anangafack,
  • Judith Christine Etaka,
  • Gamua Stanley Dobgima,
  • Chrysantus Njobinkir Bimela,
  • Stephen Mbigha Ghogomu,
  • Fidelis Cho-Ngwa

摘要

Purpose

This study aimed to investigate whether Onchocerca ochengi infection directly causes epilepsy. Although O. ochengi—a cattle parasite phylogenetically related to O. volvulus—shares biological similarities with its human counterpart, it has not been epidemiologically linked to epilepsy in bovines, unlike O. volvulus, which has been associated with onchocerciasis-associated epilepsy in humans. No prior experimental studies have established a causal relationship between onchocerciasis and epilepsy.

Methods

Gerbils were surgically implanted with O. ochengi worm masses (test group) or underwent sham operations (control group) to assess the infection’s effects. Survival rates were monitored post-implantation, and behavioral assessments were conducted on days 15–19 using the elevated plus maze, open-field, object recognition, and hanging wire tests. On day 21, the gerbils were sacrificed, and their body and organ weights were recorded, along with an analysis of worm mass survival.

Results

Implantation of 15 worm masses resulted in 100% mortality in the test group. When 10 worm masses were implanted, 53.3% of gerbils died, while all control gerbils survived. By day 21, an average of 1.4 out of 10 implanted worm masses remained viable, with a viability score of 93.3%. Test gerbils exhibited significant reductions in overall body weight and increased spleen weight compared to controls. However, behavioral tests revealed no significant differences between the two groups.

Conclusion

While O. ochengi worm masses caused notable physical effects, including increased mortality and altered body and organ weights, no conclusive evidence was found linking the infection to behavioral changes indicative of epilepsy. Further research is necessary to explore the potential association between onchocerciasis and epilepsy development.