Diagnosing and treating neurologic diseases in rabbits (Proceedings)


Diagnosing and treating neurologic diseases in rabbits (Proceedings)

Apr 01, 2010

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.