Dental disease is one of the most common reasons for pet rabbits to need veterinary treatment. The continual eruption and growth of the teeth predispose rabbits to dental problems. Any abnormality in the shape, position, or structure of the teeth interferes with normal wear and can lead to malocclusion and crowns that are no longer functional, and may grow into surrounding soft tissue causing pain and eating or grooming difficulties.
All of the rabbit's teeth, the incisors, premolars, and molars, grow throughout the life of the rabbit. This growth is normally kept in check by the normal wearing action of chewing and grinding of opposing teeth. Problems of overgrown teeth can occur when the teeth are positioned unevenly in the jaw. This is known as malocclusion. In severe cases maxillary
incisors grow in a curve and may eventually pierce the palate. Mandibular incisors
protrude from the mouth. The rabbit may be unable to eat and eventually die of
There are both hereditary and environmental causes of malocclusion. Hereditary mandibular prognathism is apparent by 3 weeks of life and is due to an autosomal recessive trait with incomplete penetrance. Malocclusion of premolars and molars has been reported in older rabbits. As a rabbit's incisor teeth grow 4 inches per year, it is necessary to clip them (but not too close) every 6 to 8 weeks. Although some veterinarians will be willing to regularly trim the teeth, this is stressful for the rabbit. Also, clipping the teeth rather than filing or grinding them down can be dangerous, since micro-fractures of the tooth from clipping can travel below the gumline, inviting bacterial infection that can ultimately be life-threatening.
Dental malocclusion in rabbits is not uncommon, especially in the short-faced
breeds such as Netherland Dwarf which have been produced via generation upon generation of inbreeding.
This disease is congenital glaucoma caused by an autosomal recessive defect with incomplete penetrance. There is abnormal production and removal of aqueous from the anterior chamber. Clinical signs may occur as early as 2 to 3 weeks of age, but are more common at 3 to 4 months of age. Signs include slight cloudiness progressing to increasing cloudiness of the cornea, a prominent eyeball, conjunctivitis, keratitis, ulceration, and rupture of the cornea. The condition may affect one or both eyes. Affected individuals should be removed from the breeding colony. Enlargement of the globe due to increased intraocular pressure as a result of the absence or underdevelopment of the outflow channels with incomplete cleavage of the iridocorneal angles characterizes buphthalmia.
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Animals with this condition keep one or more legs spread and appear unable to adduct the affected limbs. The condition becomes noticeable when the young leave the nest box and may affect one or more limbs. There is no known treatment for this abnormality. Starvation due to inability to reach food or water dishes may occur.
Hydrocephalus can occur due to an inherited defect in drainage of CSF from brainstem, or due to either hypo- or hypervitaminosis A. Clinical signs include circling, convulsions, and collapse. The mode of inheritance of this trait is reported to be autosomal recessive associated with dwarfing. Vitamin A deficiency in pregnant does may cause hydrocephalic young to be born. Vitamin A toxicity of gravid does has also been suspected of causing skeletal abnormalities (limb deformities, large fontanels) and hydrocephalus in stillborn term offspring as has been reported in toxicities in humans.