pathogenesis of optic neuritis caused by Angiostrongylus cantonensis in BALB/c mice

• Published in: Parasites & vectors 2014-07, Vol.7 (1), p.339-339, Article 339
• Main Authors: Feng, Ying, Zeng, Xin, Li, Wei-Hua, Wang, Wen-Cong, Chen, Wei, Ou-Yang, Li-si, Sun, Xi, Feng, Feng, Wu, Zhong-Dao
• Format: Article
• Language: English
• Subjects: Analysis; Angiostrongylus cantonensis; animal disease models; Animals; BALB/c mice; Care and treatment; complications (disease); Development and progression; dexamethasone; electroretinography; evoked potentials; ganglia; Health aspects; histology; hosts; humans; Infection; inflammation; Meningitis; Mice; Mice, Inbred BALB C; Mollusks; Multiple sclerosis; nerve tissue; Optic neuritis; Optic Neuritis - parasitology; Parastrongylus cantonensis; pathogenesis; patients; pulmonary artery; Random Allocation; rats; retina; sclerosis; Strongylida Infections - parasitology; therapeutics; Travel; vision
• ISSN: 1756-3305; 1756-3305
• DOI: 10.1186/1756-3305-7-339

BACKGROUND: One of the most common causes of meningitis in South East Asia is angiostrongyliasis or infection by the parasitic nematode Angiostrongyliasis cantonensis. Although this nematode usually resides in the pulmonary arteries of rats, its incidental occurence in other hosts such as humans can cause optic neuritis and lead to serious vision sequelae. Nevertheless, there are currently no systematic studies conducted in this area. METHODS: In order to study the pathogenesis of optic neuritis, mice were tried as a new animal model to study and challenge with A. cantonensis on 7d, 14d and 21d, respectively. Electroretinogram (ERG), visual evoked potential (VEP), ophthalmoscopy and histology were examined on day 7d, 14d and 21d and tribendimidine (TBD) was later used to treat optic neuritis on day 14d for a week to evaluate its therapeutic effects. RESULTS: Infection of A. cantonensis caused obvious inflammatory cell infiltration in the retina and optic nerve adventitia in day 14d and 21d followed by optic nerve fiber demyelination and retinal ganglion swelling at day 21d in the challenged mice. Prolonged VEP latency and decreased ERG amplitude were also observed on day 21. After treatment of TBD in the infected mice, retinal and optic nerve inflammation were alleviated, but VEP latency and ERG amplitude did not improve on day 21d and 28d. CONCLUSIONS: The current study provides evidence that A. cantonensis can cause optic neuritis along with optic nerve demyelination and retinal ganglion cell damage in a mouse model. TBD alone treatment can improve the symptoms of optic neuritis, but does not aid in vision recovery, suggesting that both neuroprotective agents and Dexamethasone should be administered, along with treatment for the infection, to protect the optic nerve and ganglion cells. Furthermore, as the symptoms of optic neuritis caused by A. cantonensis in mice are similar to the optic neuritis in multiple sclerosis (MS) human patients, we suggest that the BALB/c mouse model provided in this study may be useful to explore therapies of optic neuritis in MS patients.