Diagnosing and treating neurologic diseases in rabbits (Proceedings)


Neurological diseases are relatively common in companion rabbits, and are being identified more frequently because of a greater interest by owners to provide better health care to their pets, better trained veterinarians, improved diagnostic aids, and because many rabbits are living longer.

Neurological diseases are relatively common in companion rabbits, and are being identified more frequently because of a greater interest by owners to provide better health care to their pets, better trained veterinarians, improved diagnostic aids, and because many rabbits are living longer. Also, more is known about causes and treatment of neurologic diseases in rabbits in recent years,1-8 increasing our confidence in diagnosis and possible treatment. Detailed references on the neuroanatomy and neurological examination of the domestic rabbit are available.9,10

Head tilt

Neurologic conditions in rabbits, such as head tilt and posterior paresis and paralysis, can be caused by a number of factors, although most of the presentations are a result of infection or trauma. For example, head tilt in dwarf breeds is most frequently caused by Encephalitozoon cuniculi, whereas in standard breeds it is more likely caused by Pasteurella multocida. Fortunately, the diagnostic procedures used in rabbits presented with neurological signs are similar to the neurological work-up in other companion animals. An understanding of the nervous system is, of course, necessary for the diagnosis, management, and treatment of neurological problems.

Torticollis (head-tilt or "wry neck") is usually caused by the extension of Pasteurella multocida infection from the nasal cavity to the middle or inner ear via the eustachian tube, or it may arise centrally, in the medulla or cerebellum. Other rule-outs to consider include encephalitozoonosis, and, less commonly, otitis externa, cranial trauma, listeriosis, ascarid migration, or extension of ear mite infection. Rabbits with suppurative otitis media caused by P. multocida often show no clinical evidence of infection. The otitis may extend into the inner ear, resulting in head tilt or torticollis. If unilateral, the rabbit's head will tilt down on the affected side. Occasionally, nystagmus may be present. Affected middle ears are characterized by tympanic bullae filled with thick, yellow pus. Rupture of the tympanic membrane is possible.

Radiographic examination of the skull may show soft tissue density in the bullae, indicating pus-filled bullae. The head tilt in these rabbits has been reported to be irreversible, but its worsening can be prevented with appropriate antibiotic therapy. Other clinicians report a lower incidence of residual head tilt following successful therapy. Prognosis is favorable if a positive response is exhibited within the first week after therapy, and therapy is continued for 1 week after the resolution of clinical signs. Chloramphenicol, enrofloxacin, and trimethoprim-sulfa combinations have been reported to be successful antibiotic choices. Treatment of otitis media and externa should be long term (i.e., 4 weeks or longer), and generally consists of chloramphenicol (50 mg/kg SC, PO q12h) or enrofloxacin (5-10 mg/kg PO q12h). If the tympanic membrane is ruptured, topical 0.5% enrofloxacin/1.0% silver sulfadiazine otic solution (Baytril Otic, Bayer Corporation, Shawnee Mission, KS) or topical 0.3% gentamicin can be administered. Another treatment option when tympanic bullae are involved is tympanic bulla osteotomy (although complications, including facial nerve palsy, fistula formation, vestibular disease, and hypoglossal nerve dysfunction, have been associated with this surgery).

Encephalitozoon cuniculi, an obligate, intracellular, microsporidian parasite, is often associated with neurologic disease in pet rabbits. Although many rabbits infected with E. cuniculi are asymptomatic, signs of neurologic disease caused by E. cuniculi include behavioral changes, head tilt, nystagmus, ataxia, rolling, or seizures and often follow a stressful event in the rabbits life. Other neurologic signs may include urinary incontinence, stiff rear gait, and posterior paresis. Transmission is generally by ingestion or by oral inoculation of infective spores shed in the urine, although transplacental transmission may also occur. Currently, presumptive diagnosis of encephalitozoonosis is made on the basis of neurologic disease together with demonstration of high levels of serum antibodies or demonstration of spores in affected tissues. Enzyme-linked immunosorbent assays (ELISA's), indirect immunofluorescence assays, and carbon immunoassays are all suitable for detecting antibodies. However, a positive titer with detection of antibodies does not differentiate between rabbits with an active infection, a latent infection, or rabbits that developed an antibody response and are no longer infected, and, therefore, positive results indicate exposure to the organism but do not confirm E. cuniculi as a cause of disease. Follow-up samples may clarify equivocal results where early-stage infection antibody levels will be considerably higher in the 3-4 week follow-up sample. A commonly used source of encephalitozoonosis testing for the practitioner is Sound Diagnostics, Seattle, WA. Definitive diagnosis of encephalitozoonosis requires histopathologic identification of the organism.

In the absence of controlled studies it is difficult to assess the efficacy of therapeutic agents against E. cuniculi because latent infections occur and some clinical cases may improve spontaneously without treatment, presumably as a result of the host's immune response. In addition, clinical signs may not be associated with presence of the protozoa itself, but rather with the inflammatory response that persists after the organism has been eliminated. Unfortunately, there is not really an effective treatment for encephalitozoonosis, but some recommend treatment with oxibendazole (30 mg/kg PO q24h x 7-14 days). If the neurologic signs abate, the oxibendazole dose is reduced to 15 mg/kg q24h x 30-60 days. Fenbendazole (20 mg/kg q24h x 5-28 days) has also been recommended. If clinical signs reoccur, these patients are continued indefinitely on oxibendazole (15-30 mg/kg PO q24h). Although some veterinarians have had success with albendazole (30 mg/kg PO q24h for 30 days), this drug is embryotoxic and teratogenic in rabbits and has been associated with anecdotal reports of pancytopenia, fever, and death in rabbits, and evaluation of an intra-treatment CBC is recommended. For severe vestibular signs (rolling, torticollis) or seizures, administer midazolam at 1-2 mg/kg IM. For vestibular signs, administer meclizine (2-12 mg/kg PO q12h) in an attempt to reduce clinical signs, control nausea, and induce mild sedation. Again, treatment is not always successful, but has resulted in improvement in some cases; lack of treatment generally leads to euthanasia.

Encephalitozoon cuniculi has also shown zoonotic potential especially in immunocompromised humans such as transplant recipients or those infected with human immunodeficiency virus (HIV) as well as children, travelers, contact lens wearers, and the elderly.

Posterior paresis/paralysis

Vertebral fracture or luxation

The most common cause of posterior paralysis of acute onset is vertebral fracture or luxation. Fractures are more common than dislocations. The most common fracture site is L7. This injury often results from improper handling but can also occur in caged rabbits that are startled or frightened. Injury occurs when the heavily muscled hindquarters are allowed to twist about the lumbosacral junction, which acts as a fulcrum in the application of leverage to the vertebral column. Struggling rabbits, therefore, may kick and twist to exert abnormal stresses on these vertebrae, which may lead to dislocation of the spine.

In addition to paraplegia, neurologic signs may include the loss of skin sensation and of motor control of the urinary bladder and anal sphincter, depending on the amount of compromise to the spinal cord. Decubital ulcers often develop, and the perineum may become stained with feces. The extrusion of intervertebral disc material into the vertebral canal, particularly in the area of the lumbar spine, can also cause spinal cord compression and paresis.

The clinical diagnosis of posterior paresis/paralysis is confirmed radiographically, including myelography if necessary. An absence of deep pain sensation on neurological evaluation is generally a poor prognosis. However, this test is not always reliable in the rabbit, where signs of pain may be concealed because of a rabbit's ability to hide clinical signs of pain and disease. Likewise, a withdrawal reflex restricted to the hindlimbs might be a purely local reflex and may not confirm a functionally intact spinal cord. If treatment is delayed, rabbits with broken backs can become azotemic or uremic because of the retention of urine in the urinary bladder. Occasionally, mildly affected rabbits respond to conservative medical management if the spinal cord is not transected. Supportive therapy must include manual expression of the bladder. However, euthanasia is more often indicated. Alternatively, some house rabbits have been fitted with a trolley or cart to support the hindquarters. If the owners are attentive enough to prevent problems associated with urinary retention, pressure sores, etc., some of these rabbits may continue to lead a life of reasonable quality.

Spay leg

Splay leg, generally a developmental musculoskeletal condition, is commonly seen in pet rabbits ranging in age from a few days to a few months. These rabbits are unable to adduct from one to all four limbs, and thus they cannot ambulate affectively. Hind limbs are more commonly affected, with femoral neck anteversions, femoral shaft torsion, and subluxations of the coxofemoral joint. This condition is inherited in a simple autosomal recessive pattern. Culling is the most effective long-term management. Occasionally older rabbits are presented with similar clinical signs, which appear to have resulted from a traumatic insult.

Pregnancy toxemia

Pregnancy toxemia can manifest neurologic signs in rabbits. Although primarily a problem of late gestation, toxemia also occurs in postpartum and pseudopregnant does. Neurologic signs may include weakness, depression, incoordination, convulsions, and coma. Death may occur within a few hours after the signs are first noted. Obesity and fasting are predisposing factors. Treatment for the associated ketosis includes IV administration of lactated Ringer's and 5% glucose solutions. Prevent toxemia by avoiding fasting and preventing obesity in pregnant does, and by providing a high-energy diet during late gestation.

Heat stroke

Rabbits are particularly susceptible to heat stroke or heat stress. The patient may be in shock, and seizures are common presenting signs. Neurologic signs may resemble those of pregnancy toxemia, but evidence of ketosis is not present. Signs are accompanied by an elevation in rectal temperature to greater than 40.5C (105F). Treatment includes the slow reduction of the body temperature by spraying it with or immersing it in tepid water, or wrapping the patient in cool wet towels, and the administration of IV fluids (LRS or other crystalloid fluids at 60-90 mg/kg/hr IV, IO over 20-60 minutes, followed by maintenance rate; or crystalloid bolus at 30 ml/kg plus hetastarch at 5 ml/kg initially, followed by crystalloids at a maintenance rate and hetastarch at 20 ml/kg divided over 24 hours). Treatment may also involve the control of seizures (diazepam at 1-2 mg/kg IV to effect), mannitol to reduce cerebral edema, and, if necessary, tracheal intubation and artificial ventilation. Administer sodium bicarbonate (2 mEq/kg IV) if metabolic acidosis is suspected. Rabbits that recover from heat stroke should be monitored closely for several days for metabolic abnormalities or renal failure. Rabbits with heat stroke usually do not respond well, and the prognosis is poor. Pet rabbits housed outdoors during the summer when the ambient temperature can exceed 29C (85F) require shade, good ventilation, and an adequate supply of cool drinking water.

Cerebrospinal nematodiasis

Cerebrospinal nematodiasis (cerebral larval migrans), caused by Baylisascaris procyonis (the common roundworm of raccoons), has been reported in rabbits, and may produce fatal or severe neurological disease. Interestingly, severe encephalophathy can be caused by just a few B. procyonis larvae. Neurologic signs include ataxia, circling, opisthotonos, tremors, and torticollis. These parasites are most commonly acquired by rabbits from hay or bedding that has been contaminated by raccoon feces. Eggs remain infective for at least 1 year. Diagnosis is by postmortem histologic evaluation of the brain. Evidence of larval migration can be found in the cerebrum, cerebellum, midbrain, and medulla and includes multifocal areas of necrosis with aggregations of inflammatory cells (eosinophils, lymphocytes, plasma cells, and macrophages). The Baermann technique can be used to recover larvae from brain tissue. To prevent this disease, guard against fecal contamination of rabbit housing, feed, and bedding by raccoons. Once in the brain, larvae of B. procyonis cause destruction of nervous tissue that is basically nonresponsive to medical therapy. Although euthanasia is generally indicated in affected rabbits, some veterinarians have had success slowing the progression of presumptive cerebrospinal nematodiasis by treating with oxibendazole (60 mg/kg PO q24h indefinitely).

Lead poisoning

Lead poisoning in rabbits may be characterized by subtle neurologic signs, depression, and lethargy; however, anorexia and weight loss are the most common presenting signs. Take abdominal radiographs to search for gastrointestinal metallic densities in rabbits with suspected lead poisoning. Institute appropriate therapy in rabbits with blood lead levels greater than 10 μg/dl if clinical signs of plumbism are present. The treatment of choice for lead poisoning is chelation with Ca-EDTA (calcium versenate) at a dosage of 25 mg/kg SC q6h for 5 days. Two courses of treatment 1 week apart may be required. Rabbits allowed to wander unrestrained in homes and basements are more likely to encounter a source of lead on which to gnaw.


Although the prevalence of rabies in pet rabbits is low (only 30 cases reported in the US between 1971-1997), one should consider rabies in rabbits with a history of: being housed outdoors; contact or bites from wild animals; change in attitude; erratic behavior; disorientation; incoordination, seizures, or paralysis; blindness; or excess salivation or frothing.7 One case of rabies resulted from an encounter with a skunk. Neurologic signs, which developed approximately 1 month after exposure, included blindness and forelimb paralysis. Pet rabbits housed outdoors should be protected from contact with wildlife, especially in areas where rabies is endemic or where a rabies epizootic is underway. Although no vaccine is approved for use in rabbits in the US, some practitioners have vaccinated rabbits according to standard recommendations and state and local requirements for cats and dogs using a killed vaccine.

Other neurological conditions

Seizures in rabbits may be caused by hypoxia secondary to empyema, pneumonia, or metastatic tumor, or may result from the azotemia and electrolyte imbalances associated with renal disease. Bacterial encephalitis, primary caused by P. multocida, can also cause seizures in rabbits. Epilepsy is a rare diagnosis in this species.

Neurologic signs in rabbits have also been associated with trauma, toxoplasmosis, listeriosis, other infectious organisms, etc. Although rare, some neurologic diseases in rabbits also have a nutritional basis.


1. Boydell, P. 2000. Nervous system and disorders. In: Flecknell, P.A., ed. Manual of Rabbit Medicine and Surgery. Gloucester, G.B.: British Small Animal Veterinary Association, pp. 57-61.

2. Carpenter, J.W., ed. 2005. Exotic Animal Formulary. 3rd ed. St. Louis, Elsevier Saunders, pp. 409-444.

3. Carpenter, J.W. 2006. Diagnosing and treating common neurologic diseases in rabbits. Vet. Med. (Nov.):728-736.

4. Deebs, B.J., J.W. Carpenter 2004. Neurologic and musculoskeletal diseases. In: Quesenberry, K.E., J.W. Carpenter, eds. Ferrets, Rabbits, and Rodents: Clinical Medicine and Surgery. 2nd ed. Philadelphia, WB Saunders, pp. 203-210.

5. Harcourt-Brown, F. 2002. Textbook of Rabbit Medicine. Oxford, UK, Butterworth-Heinemann.

6. Harkness, J.E., J.E. Wagner. 1995 The Biology and Medicine of Rabbits and Rodents. 4th ed. Philadelphia, Williams & Wilkins, pp. 305-307.

7. Oglesbee, B. 2006. The 5-Minute Veterinary Consult: Ferret and Rabbit. Ames, IA, Blackwell Publishing, pp. 238-243, 270-274, 288-289, 308-316, 324-325, 339-340, 354-355, 381-383.

8. Percy, D.H., S.W. Barthold. 1993. Rabbits. In: Pathology of Laboratory Rodents and Rabbits. Ames, Iowa State University Press, pp. 179-224.

9.Osofsky, A., R.A. LeCourteur, K.M. Vernau. 2007. Functional neuroanatomy of the domestic rabbit (Oryctolagus cuniculus). Vet. Clin. N. Am.: Exotic Anim. Pract. 10:713-730.

10. Vernau, K.M., A. Osofsky, R.A. LeCourteur. 2007. The neurological examination and lesion localization in the companion rabbit (Oryctolagus cuniculus). Vet. Clin. N. Am.: Exotic Anim. Pract. 10:731-758.

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