Fracture or dislocation of lumbar vertebrae with compression or severing of the spinal cord is common in both pet and commercial rabbits. Common signs include posterior paresis or paralysis and urinary and fecal incontinence due to loss of sphincter control. Initial signs of paralysis may resolve within 3–5 days as swelling around the cord diminishes. Supportive therapy includes anti-inflammatory glucocorticoids (eg, dexamethasone) to reduce damage from swelling. Paralysis after 1–2 wk or incontinence indicates a grave prognosis and warrants euthanasia.
Young does may kill and eat their young for a number of reasons, including nervousness, neglect (failure to nurse), and severe cold. Dogs or predators entering a rabbitry often cause nervous does to kill and eat the young. Cannibalism of the dead young occurs as a natural, nest-cleaning instinct. If all management practices are proper and the doe kills 2 litters in a row, she should be culled.
Dental disease may present as excess salivation, teeth grinding, or anorexia. Oral examination and palpation along the ventral surface of the jaw should be a part of routine rabbit physical examinations. Dental abscesses may develop as a consequence of foreign bodies (eg, plant material embedded between the tooth and gum), pulp exposure following tooth trimming, or other diseases. Dental abscesses also may appear as retrobulbar abscesses. Rabbit incisors may wear differently depending on diet, and a pelleted diet may predispose the rabbit to dental disease. Multiple teeth are commonly affected. A thorough oral examination and diagnostic radiographs are indicated. Dental extractions may be accomplished using a fine-tipped dental elevator worked along the root to free the tooth. Incisors are curved and require use of a specialized rabbit incisor luxator or similar curved instrument for removal. Curettage of the alveolus to destroy the apical germinal tissue is required to prevent regrowth of the tooth. Regrowth is unlikely if the pulp remains in the extracted tooth, but followup radiographs in 2–3 mo will confirm successful extraction. After lavage, infected sockets can be filled with doxycycline periceutical gel or antibiotic-impregnated polymethyl methacrylate (PMMA) beads. PMMA beads are not commercially available and must be self manufactured. Gingival tissues should be sutured as needed. Surgical removal of the lateral wall of the alveolus may be needed to remove an abnormal tooth. Defect treatment with calcium hydroxide paste results in tissue necrosis and is contraindicated.
Extraction of cheek teeth involves routine elevation and luxation if the dental anatomy is normal. Extraction of multiple cheek teeth carries a very poor prognosis for recovery, although some pet rabbits do well with very few molars if the diet is suitably modified. Continued monitoring of the occlusal surface and followup adjustment is expected. Pain management and extended duration (4 wk to months) systemic antibiotic therapy based on culture and sensitivity are indicated.
The incisors, premolars, and molars of rabbits grow throughout life. The normal length is maintained by the wearing action of opposing teeth. Malocclusion (mandibular prognathism, brachygnathism) probably is the most common inherited disease in rabbits and leads to overgrowth of incisors with resultant difficulty in eating and drinking. Dental trimming is often done with combined anesthesia of diazepam (7–10 mg/kg, IM) followed in 20 min with ketamine (25 mg/kg, IM). Overgrown teeth can be cut with bone or wire cutters, however a grinding tool or dental burr is safer. When trimming with a dental burr, minimal pressure should be applied to keep the burr cool. The pulp, which looks like a pink tinge in the dentin, should not be exposed. If this occurs, the risk of pulp necrosis is avoided by performing a partial pulpectomy. The tooth should be aseptically prepared and the pulp burred out and filled with calcium hydroxide. Hard fillings are contraindicated in the continuously erupting tooth.
Occasionally, the cheek teeth overgrow and cause severe tongue or buccal lesions. Because malocclusion is generally considered to be inherited, rabbits with this condition should not be bred. However, young rabbits can damage their incisor teeth by pulling on the cage wire, which results in misalignment and possibly malocclusion as the teeth grow. This condition is difficult to differentiate from genetic malocclusion, and these rabbits should also be culled. Genetic malocclusion generally can be detected in rabbits 3–8 wk old.
Hair Chewing and Hairballs
Rabbits groom themselves constantly, so the stomach contents often contain hair. This is normally passed through the GI tract and excreted with the fecal pellets. Hair chewing is generally a result of low fiber in the diet and can be corrected by increasing the fiber or feeding hay along with the pellets. Adding magnesium oxide to the diet at 0.25% also may be helpful. In some cases, hair chewing is a result of boredom. Providing environmental enrichment often halts this abnormal behavior.
The hair becomes a problem only if excess amounts are consumed or if it accumulates in the stomach and blocks the pylorus. If this happens, the rabbit becomes anorectic, loses weight, and dies within 3–4 wk. Premortem diagnosis of pyloric obstruction can be difficult, as palpable hairballs can be an incidental finding and radiography is often nondiagnostic.
GI hypomotility or gut stasis is the primary concern when presented with clinical illness associated with a hairball. Hairballs are more likely a result of anorexia, not its cause. Gas accumulation creates visceral distention and pain. Decreased food intake and GI hypomotility result in elevation of cecal pH and alteration of cecal microflora, creating cecal dysbiosis. Alterations in water and electrolyte balance result in ketoacidosis and hepatic lipidosis. Gastric ulceration and gastric rupture may occur.
The goals of treatment are to remove the obstruction, stimulate motility, restore GI microorganism balance, and relieve dehydration and anorexia. Treatment includes motility stimulants such as metoclopromide (0.5 mg/kg, PO or SC, tid-qid), fluid therapy, pain medication, and antiulcer therapy. Reestablishment of GI microflora may be assisted by probiotic treatment or cecotrophs from healthy rabbits.
Several remedies have been proposed to assist in the break up or passage of a hairball. Pineapple juice contains the digestive enzyme bromelain and has been used to treat early cases of trichobezoars; an adult rabbit is given 10 mL of fresh or frozen juice through a stomach tube or intubation needle, sid-bid for 3 days. Both the fluid and the enzyme help to break up the matrix of the hairball. Canned pineapple juice is not as effective because the canning process destroys the enzyme. Papaya contains the enzyme papain, also called papayazyme. Papain enzymes do not break down the hair itself, but may help break down the mucus that holds the hairball together. Human health food or nutrition stores carry bromelain and papayazyme supplements as aids to digestion. Mineral oil and laxatives are not effective in removing the hair mass. Roughage (hay or straw) should be fed during the treatment to help carry the hair fibers through the GI tract and out with the feces. Surgical treatment is certain but risky.
Prevention is the best option. Providing a high fiber diet, avoiding stress and obesity, environmental enrichment, and daily combing to remove loose hair effectively prevents this condition. Clinical research does not support routine doses of mineral oil, wetting agents, or proteolytic enzymes as effective preventives.
Rabbits are sensitive to heat. Hot, humid weather, along with poorly ventilated hutches or transport in poorly ventilated vehicles, may lead to the death of many rabbits, particularly pregnant does. Affected rabbits stretch out and breathe rapidly. Hutches should be constructed so that they can be sprinkled in hot, humid weather. Free access to cool water should be provided. When the environment can be controlled, optimal conditions are a temperature of 50–70°F (15.5–21°C) and a relative humidity of 40–60%, with 10–20 air changes/hr. Wire cages are preferable to solid hutches. Treatment consists of immersing rabbits in cold water during the heat of the day, especially those that will kindle in the next day or two. Breeding bucks may lose a majority of viable sperm and might not breed successfully for several weeks while new sperm production replaces the sperm killed by thermal stress.
Hutch burn is often confused with treponematosis and can be truly differentiated only by the absence of spirochetes on darkfield microscopy and by the lack of antibodies to Treponema cuniculi. It is caused by wet and dirty hutch floors and affects the anus and external genitalia. Also, rabbits that lack adequate sphincter control of the bladder constantly dribble urine and may be affected. The membranes of the anus and genital region become inflamed and chapped. The area soon becomes secondarily infected with opportunistic pathogenic bacteria. Brownish crusts cover the area and a hemorrhagic, purulent exudate may be present. Keeping hutch floors clean and dry and applying nitrofurazone or an antibiotic ointment to the lesions hastens recovery.
Ketosis is a rare disorder that may result in death of does at or 1–2 days before kindling. The disease is more common in first-litter does. Predisposing factors include obesity and lack of exercise. The probable cause is starvation. For some reason not well understood, there is anorexia. Other signs are dullness of eyes, sluggishness, respiratory distress, prostration, and death. The most significant lesions are fatty liver and kidneys. The body mobilizes fat and transports it to the liver to be broken down for energy, thus the fatty liver. Diagnosis depends on clinical signs and necropsy lesions. Injection of fluids that contain glucose may be helpful in correcting the disease. Breeding junior does early, before they become too fat, is also helpful. Hairballs in the stomach are often a factor in ketosis.
Female rabbits have a heavy fold of skin on the ventral aspect of the neck. As the rabbit drinks, this skin may become wet and soggy (“slobbers”), which leads to inflammation. Contributing factors include dental malocclusion, open water crocks, and damp bedding. The hair may slip, and the area may become infected or flyblown. The area often turns green if infected with Pseudomonas sp. Automatic watering systems with drinking valves generally prevent wet dewlaps. If open water receptacles are used, they should have small openings or be elevated. Once the area is infected, the hair should be clipped and antiseptic dusting powder applied. In severe cases, parenteral antibiotics may be necessary.
Corneal ulceration is the most common ophthalmic problem seen in rabbits. Many potential underlying issues should be ruled out, although trauma is the most frequent cause. The cornea should be carefully protected during anesthetic procedures. The lack of tear production associated with keratoconjunctivitis sicca or dry eye may increase the risk of corneal damage. Exophthalmia as result of orbital or dental disease or facial paralysis associated with encephalitocytozoonosis can make blinking difficult and lead to corneal damage. Superficial ulcers can be treated with broad-spectrum ophthalmic antibiotic solutions. Twice-daily topical atropine can be beneficial. Treatment progress should be assessed in 1–2 days. Epithelial lips indicate a nonhealing ulcer. Such ulcers should be debrided after application of a topical anesthetic, followed by the same treatment as for a superficial ulcer. If the ulcer does not respond, surgery and placement of a conjunctival pedicle graft may be required. Differential diagnoses of corneal lesions in the rabbit include corneal occlusion (overgrowth of conjunctival tissue) and limbic or corneal dermoid (skin-like tissue in an abnormal location over the cornea). Hair may protrude from a limbic dermoid. These growths do not appear painful.
Recently, anterior uveitis secondary to Encephalitocytozoon cuniculi has been recognized to present as iridal swelling and white or pink nodules on the iris, which are bacterial iridal or corneal stromal abscesses. Spores replicating in the lens may result in cataract formation and even lens rupture. Diagnosis is confirmed by the presence of organisms on histopathology of excised tissue or DNA probe on removed lens material. Treatment involves lens removal by phacoemulsification or enucleation. Spontaneous lens regeneration may occur. Prosthetic lens insertion is not recommended. The prognosis is guarded without surgery; glaucoma develops in most patients. Topical treatment includes NSAID and mydriatic and antibiotic medications. If there is no ulceration, corticosteroids can be used with caution. After initiating topical medications, progress and intraocular pressure should be checked in 5–7 days. Monitoring should continue every 2–3 wk for the next 2 mo.
Inherited glaucoma is discussed below (see Rabbits: Buphthalmia (Blue Eye, Moon Eye, Infantile Glaucoma)).
This disease does not involve the hock but the plantar surface of the metatarsals and, less commonly, the volar surface of the metacarpal-phalangeal region. The cause is either pressure on the skin from bearing the body weight on wire-floored cages or trauma to the skin from stamping, with secondary infection of the necrotic skin. Several factors, including accumulation of urine-soaked feces, nervousness, posterior paralysis after a spinal cord injury, and the type of wire used, may influence development. Genetics are also involved. Heavy-breed rabbits such as the Rex, Flemish Giant, and Checkered Giant are more susceptible. Affected rabbits sit in a peculiar position with their weight on their front feet; if all 4 feet are affected, they tiptoe when walking. Various debriding agents can be used to clean the lesion, followed by topical antibiotic treatment along with parenteral antibiotics. Radiographs rule out osteomyelitis with severe lesions. The rabbit must be removed from the cage or given a solid floor (board or mat) on which to sit or rest. Because treatment is difficult and time consuming and the condition often recurs, affected commercial animals should be culled. Because big feet and thick footpads are hereditary, selection of breeding stock for these traits has reduced the incidence of pododermatitis.
Urolithiasis is seen routinely in pet rabbits and occasionally in commercial rabbitries. It is generally suspected when hematuria is seen. (A dipstick can quickly rule out normal pigment causes of red urine.) Uroliths are caused by calcium carbonate and triple phosphate crystals precipitating out of normal urine when the pH increases to 8.5–9.5. Normal rabbit urine has an average pH of 8.2. Several factors have been incriminated in urolithiasis, including nutritional imbalance (especially the calcium:phosphorus ratio), genetic predisposition, infection, inadequate water intake, and metabolic disorders. Treatment involves surgically removing the uroliths, acidifying the urine, and reducing dietary calcium. Because alfalfa is high in calcium and one of the main dietary components of rabbit pellets, removal of the pellets and a switch to grass or timothy hay and rolled oats is beneficial in preventing recurrence.
Hydrocephalus, characterized by an enlarged head, is occasionally seen in neonatal rabbits. The top of the skull appears dome-shaped, and the fontanelle is wider than normal. Most affected rabbits are born dead; occasionally, they live for several weeks but generally exhibit neurologic signs. At necropsy, the brain is enlarged; on cut section, the ventricles are greatly enlarged and filled with CSF. The cause can either be genetic or result from dietary deficiency or excess of vitamin A. In the case of a dietary deficiency or hypervitaminosis, poor reproduction (low fertility, small litter size, abortion, etc) also is seen in the breeding herd. A correct assessment of vitamin A becomes critical in treatment, and both serum and liver should be analyzed. In deficiency, the serum level of vitamin A is below normal (2.6–4.2 IU/mL). In toxicity, the serum level can be normal, but the concentration of vitamin A in the liver is very high (>4,000 IU/g). Treatment of the deficiency involves increasing the carotene content of the diet or adding a vitamin A supplement. Treatment of hypervitaminosis A requires reducing vitamin A in the diet. However, reducing the amount of vitamin A stored in the liver is extremely difficult. If the doe's reproduction has been impaired, replacing the doe is probably more cost-effective than trying to decrease the vitamin A level. Because genetic hydrocephalus appears to be inherited recessively, control requires culling both parents.
Buphthalmia (Blue Eye, Moon Eye, Infantile Glaucoma)
Buphthalmia is an autosomal trait with incomplete penetrance that results in variable clinical severity. Intraocular pressures begin to rise as early as 3 mo. One or both eyes may be affected. Glaucoma can be treated medically (dorzolamide 2%; 1 drop tid) or by surgical enucleation. Affected animals should not breed.
Splay leg is presumed to be an inherited disorder presenting with abduction of one or more legs as early as 3–4 wk of age. The right rear limb is most commonly affected, although the condition may be unilateral or bilateral. Hip dysplasia can occur during postnatal development among rabbits housed on slick nest boxes or flooring.
By far, the most common tumor in rabbits is uterine adenocarcinoma. Susceptibility is related to breed. The disease may present as multiple tumors that often metastasize to the liver, lungs, and other organs; cystic mastitis may develop concurrently. This disease is the primary reason to recommend spaying of nonbreeding female rabbits. Monitoring for metastasis should follow surgical removal of uterine adenocarcinoma. Malignant lymphomas (lymphosarcoma) are relatively common and may occur in rabbits <2 yr old. Typically, lymphosarcoma presents with a tetrad of lesions including enlarged kidneys, splenomegaly, hepatomegaly, and lymphadenopathy. Anecdotally, thymoma or thymic lymphoma is the most common mediastinal mass in rabbits.
Last full review/revision July 2011 by Diane McClure, DVM, PhD, DACLAM