Cataract in
rabbits
Esther van Praag, Ph.D.
Warning: this file contains pictures that may be distressing for
people.
The word cataract comes from the Latin
“cataracta”, or from the Greek katarraktēs, meaning waterfall. It reminds the
progressive increase in opacity of the eye lens, which is sometimes referred
to as “looking though a waterfall”. Consequently, a reduced amount of light
passes through the lens. The ability to focus and eyesight sharpness will
decrease with time. This is accompanied by a loss of sensitivity to contrast.
The ability to see objects in bright
light is reduced and an affected rabbit will start to hop furniture or any object
that is on its path. The changes in the lens are due to the oxygen metabolism
and the recycling of the gluthatione protective
molecule. Since the lens has no direct contact with the blood circulation,
its level of oxygen is the second lowest in the body, after the nervous
system and the adrenal cortex. Oxidative respiration, which is carried out by
the mitochondria organelles within the cells of the lens, is sufficient to
produce the ATP (form of stored energy in organisms) necessary for the proper
functioning of cells. This is accompanied by the formation of free radicals
and other oxidative molecules. These molecules are neutralized by a smaller
protein, gluthatione. While gluthatione
is oxidized, the free radicals are reduced and neutralized. The oxidized gluthatione will move to the surface of the lens, where
it will be reduced by the enzyme gluthatione reductase, with the help of a co-enzyme derived from
vitamin B3. The cycle enables to regenerate the glutatione, so it can be used again. Vitamin C also plays
a protective role and its concentration within the lens is about 40 times
higher than in the blood. Once the vitamin C has entered the lens cells, it
will also start to reduce free radicals and other oxidizing molecules.
Cataracts observed in mammals and human beings
can be classified in three categories:
·
Nuclear cataract: it is characterized by a degeneration of the
proteins in the center of the lens (nucleus) due to age. It is typically
related to increased levels of oxidized (dangerous) gluthatione
in the lens. Possibly the movement of the later is slowed down due to age or
to a disbalance between proteins and lipid
oxidation. The lens becomes white and later brown.
§
Cortical cataract: it is related to the disruption of the lens at
the periphery and spreads towards the center. It is typically related to a
decrease in the level of gluthatione, accompanied
by the excessive destruction of proteins, damage of the fiber plasma membrane
or disruption of the calcium homeostasis (maintained relatively constant
state within the body).
§
Posterior subcapsular
cataract: it is
characterized by the development of clusters of swollen cells in the back of
the lens. Several clusters can develop, independently from each other. This
type of cataract is rare and typically stress induced (e.g. UV) or due to
medication (corticosteroids).
In rabbits, there is a fourth cause for
cataract and lens rupture, related to protozoal parasite Encephalitozoon
cuniculi.
Causes
The appearance of cataract is generally
related to age. Further contributing factors are heredity, nutrition,
medication, exposure to sun light, presence of the protozoal parasite Encephalitozoon cuniculi, head-trauma, or a
diet poor in caretonoids. The incidence and the
causes of cataract in rabbit is not well known. On
the contrary to other animals, cataract development is not related to
diabetes, a metabolic disorder that is very rare seen in rabbit.
Increased oxidative stress, due to the presence of free radicals,
a breakdown of the protective mechanism, or a decreased gluthatione
cycle, lead to an accumulation of hydrogen peroxide in the aqueous humor of
the eye. Although gluthatione will reduce
the peroxide, the energy-producing metabolism will be destroyed on the long
term, enabling the diffusion of sodium into the lens. Osmolality
(natural tendency to maintain water balance) will lead to edema (accumulation
of water) in the lens. The proteins inside the lens oxidize, become opaque
and insoluble (similar process as heat induced denaturation
of ovalbumin and egg white proteins).
The free radicals attack the lipids present
in the membrane, which leads to a shrinkage or swelling of the lens capsule.
These changes of pressure inside the lens break the lens fiber membranes and
the space will be filled with water and waste.
Diagnosis
A comprehensive
diagnosis enables to diagnose a cataract and monitor its development with
time. Rarely, lens rupture is observed.
Treatment
The treatment of choice for cataract is
surgical removal, using the phacofragmentation of
the lens techniques, without replacement of the lens. Indeed, regeneration of
the lens has been observed in numerous rabbits. If this will not be the case,
the rabbit will nevertheless be able to discern light and differentiate
shapes.
If the cause of cataract relates to the
parasite E. cuniculi, living in the nervous system of rabbits, the
treatment includes the administration of fenbendazole (20 mg/kg, q 24 h., during
a month) during 28 days. Longer treatments must be avoided as onset of
secondary effects such as bone marrow depression has been observed in
rabbits. The use of albendazole should be avoided
in rabbits. It has lead to sudden death in healthy and/or young rabbits,
immediately after administration of the drug (private communication, Prof. P.
Deplazes, DVM, Faculty of Veterinary Medicine,
University of Zurich, Switzerland)
If uveitis is
present and the lens cannot be removed surgically, the use of a topical NSAID
or non-NSAID medication (e.g. prednisolone acetate 1%) is necessary.
Cataract may cause pain. If this is
observed, the use of analgesics is recommended. If treatment does not bring
relief or improvement, eye surgery or enucleation
may help the rabbit.
Acknowledgement
My gratitude goes to Amy Carpenter (USA), to
Susan L. (USA), to Lisa Hutcheon (USA), to Christine Goodhand,
to Melanie Kuenzel and Heather Bechtel (USA), to
Sandy Minshull (Canada) and to Akira Yamanouchi (Veterinary
Exotic Information Network), for the permission to use their pictures
and/or their help. Many thanks also to the rabbits that helped illustrate
this page.
Further
information
Arnesen K, Nordstoga K.
Ocular encephalitozoonosis (nosematosis) in blue
foxes. Polyarteritis nodosa and cataract. Acta Ophthalmol (Copenh). 1977; 55: 641-51.
Ashton N, Cook C, Clegg F. Encephalitozoonosis
(nosematosis) causing bilateral cataract in a
rabbit. Br J Ophthalmol. 1976; 60: 618-31.
Felchle LM, Sigler RL. Phacoemulsification for the
management of Encephalitozoon cuniculi-induced phacoclastic uveitis in a
rabbit. Vet Ophthalmol. 2002;
5: 211-5.
Flecknell P., editor Gloucester, BSAVA Manual of Rabbit
Medicine and Surgery, UK: British Small Animal Veterinary Association2000.
Gelatt KN. Congenital
cataracts in a litter of rabbits.
J Am Vet Med Assoc. 1975; 167:598-9.
Giordano C, Weigt A,
Vercelli A, Rondena M, Grilli
G, Giudice C. Immunohistochemical identification of
Encephalitozoon cuniculi in phacoclastic
uveitis in four rabbits. Vet Ophthalmol.
2005; 8: 271-5.
Gwon
A, Gruber LJ, Mantras C. Restoring lens capsule integrity enhances lens
regeneration in New Zealand albino rabbits and cats. J Cataract Refract Surg.
1993; 19: 735-46.
Gwon
A, Gruber L, Mantras C, Cunanan C. Lens
regeneration in New Zealand albino rabbits after endocapsular
cataract extraction. Invest Ophthalmol Vis Sci. 1993;
34: 2124-9.
Harcourt-Brown F., Textbook of Rabbit
Medicine, Oxford, UK: Butterworth-Heinemann, 2001.
Quesenberry K.E., Carpenter J.W., Quesenberry
P., Ferrets, Rabbits and Rodents: Clinical Medicine and Surgery Includes
Sugar Gliders and Hedgehogs. Elsevier Health, 2004.
11. Weisse I, Niggeschulze A, Stotzer H. Spontaneous congenital cataracts in rats,
mice, and rabbits. Arch Toxicol.
1974; 32:199-207.
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