A highly effective treatment for encephalitozoonosis has not been determined,5 and, in fact, some rabbits improve with no treatment at all. There are many studies of both in vitro and in vivo treatment
of encephalitozoonosis, but one recommended treatment protocol includes dexamethasone (0.1 mg/kg subcutaneously once, then
again 48 and 96 hours later), chloramphenicol (50 mg/kg subcutaneously every 12 hours for seven days), and oxibendazole (30
mg/kg orally every 24 hours for seven to 14 days).5 Dexamethasone is intended to reduce the inflammation associated with E. cuniculi and presumably increase plasma concentrations of albendazole (and possibly other benzimidazoles). Although corticosteroids
should be used with caution in rabbits because they are a corticosteroid-sensitive species,9 a single dose of a short-acting corticosteroid (e.g. 1 to 2 mg/kg dexamethasone) has recently been recommended. If further treatment is required, anti-inflammatory rather than
immunosuppressive doses of dexamethasone are indicated (0.2 mg/kg).6 If the neurologic signs abate, reduce the oxibendazole dose to 15 mg/kg every 24 hours for 30 to 60 days. If clinical signs
recur, these patients should receive indefinite oxibendazole therapy (15 to 30 mg/kg orally every 24 hours).5
Another antiparasitical, albendazole, is also often used to treat encephalitozoonosis. This drug is only parasitostatic, so
rabbits require long-term treatment. A dosage of 25 mg/kg/day given orally for 30 days has been suggested.6 Also, a small study has described the eradication of E. cuniculi organisms in rabbits treated with fenbendazole (20 mg/kg/day orally for 28 days).10
In addition, some clinicians have reported a favorable response with the concurrent use of medication used to treat
motion sickness in people (i.e. meclizine).11
Treatment for encephalitozoonosis is not always successful but has resulted in improvement in some cases; a lack of treatment
generally leads to euthanasia.
VERTEBRAL FRACTURE OR LUXATION
The most common cause of acute-onset posterior paralysis is vertebral fracture or luxation. Fractures are more common than
dislocations, and the most common fracture site is L7 (Figure 2).5 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
and applies leverage to the vertebral column. Struggling rabbits, therefore, may kick and twist to exert abnormal stresses
on these vertebrae, which may lead to fractures or luxations of the vertebral column. Rabbits are predisposed to vertebral
fractures because their skeletal system is only 7% to 8% of their body weight (in contrast to a cat in which it is 13%) and
because they have powerful hindlimbs that can kick violently.12 In addition, pet rabbits generally have minimal opportunity to exercise, which further contributes to poor bone density.
2. A rabbit with posterior paralysis resulting from a traumatically induced fracture at L7.
In addition to paraplegia, neurologic signs of fracture or dislocation may include the loss of skin sensation and motor control
of the urinary bladder and anal sphincter, depending on the amount of spinal cord compromise. Decubitus ulcers often develop,
and the perineum may become stained with feces. The extrusion of intervertebral disk material into the vertebral canal can
also cause spinal cord compression and paresis. Posterior paresis or paralysis and other neurologic and locomotor disorders
can also result from spondylosis, kyphosis, or lordosis of the vertebral column.
The clinical diagnosis of posterior paresis or paralysis due to vertebral column disorders is confirmed radiographically,
including myelography if indicated.13 An absence of deep pain sensation on neurologic evaluation generally indicates a poor prognosis. However, this test is not
always reliable in rabbits because of their 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.