Skip to main content

Keratitis induced by Allovahlkampfia spelaea in experminental rat model: a trial for treatment with ellagic acid

Research Authors
Enas A. M. Huseein
Fatama E. S. Anwer
Gamal H. Abed
Sary Kh. Abdel-Gahfar
Hossam El-Din M. Omar
Research Abstract

Members of family Acanthamoebidae and
Vahlkampfiidae are amphizoic, occurring as human
parasite causing many diseases. This study was aims
to evaluate the efficacy of ellagic acid (EA) to
ameloriate the histological changes in cornea and
the changes in oxidative stress markers in different
organs of rats infected with Allovahlkampfia
spelaea. Thirty rats were intraocular infected with
trophozites of A. spelaea. Fourteen days later, rats
divided into four groups, treated with chlorhexidine
(CHX), EA, EA plus CHX, and lubricant eye drops
for 14 days, respectively. All eyes were examined
clinically then rats were killed and their corneas,
brain, liver, ling, kidney and spleen were excised
and used for histological and biochemicals
evaluation. Eyes from A. spelaea infected rats
showed corneal ulcer with disruption of corneal
layer, congestion and infilteration of the inflammatory
cell in stromal layer. However, the cornea
of CHX, EA, and the combination of CHX and EA
treated rats showed hyperplasia in the epithelial
layer of cornea, hyperplasia in the epithelial layer of
cornea with stromal vascularization and epithelial
hyperplasia, stromal vascularization with fibroblast
cell activation, respectively. The activity of
acetylchoinestase in the brain and the markers of
oxidative stress in the brain, lung, liver, kidney and
spleen were altered in infected rats with A. spelaea
and restored by treatment with CHX, EA, or the
combination of CHX and EA. In conclusion
infection with A. spelaea induced keratitis and
biochemical changes in organs of rats, these changes
were ameloriated by the treatment with CHX or EA
or the combination of both with the priority of the
later one.

Research Department
Research Journal
European Journal of Biological Research
Research Member
Research Publisher
NULL
Research Rank
1
Research Vol
6 (4)
Research Website
NULL
Research Year
2016
Research Pages
299-309