Generalised muscle weakness in rabbits has numerous causes, many of which are extremely rare or have never been conclusively diagnosed in rabbits, but are important to discuss. By its definition, muscular dystrophy is defined as a degeneration of muscular tissue sometimes caused by faulty nutrition. This has been seen to occur in rabbits as well as other mammals.
Muscular dystrophy is a broad term that is used to describe a group of inherited diseases that are categorised by a progressive weakness and degeneration of the skeletal muscles (paresis). As the disease progresses and the muscle fibres weaken, fibrous and fatty tissues replace them. The disease is caused by a gene mutation that is transmitted genetically from parents to off-spring.
The main cause of muscular dystrophy in rabbits is a serious lack of, or no vitamin E in the diet, leading to a deficiency. Clinical symptoms include mortality of neonates during the first 3-10 weeks of age, weakness, coma and eventually death.
Currently there is no cure for muscular dystrophy, nor is there any way of slowing the progression of the disease. Medical management may include supportive treatment, pain management, a good diet and respiratory support. Steroids may be of some benefit, but the potential side-effects need to be taken into consideration.
Floppy rabbit syndrome
Floppy rabbit syndrome (FRS) has been well documented in rabbits but its exact cause has never been truly identified. Rabbits affected with FRS lose all the strength in their limbs, but remain bright and able to eat and drink as long as food is put within reach. Lead poisoning, hypokalaemia (potassium deficiency) and plant toxins have all been cited as potential causes, although no diagnosis based on investigative evidence, has ever been documented.
Often after 2-3 days, with supportive treatment, rabbits seem to spontaneously self-cure of FRS; however some may relapse some weeks, months or years later.
Myasthenia gravis (MG) is an extremely rare autoimmune disease that causes muscle weakness and excessive muscle fatigue. This varies in severity affecting voluntary muscles in the legs, neck, eyes, respiration, etc. Smooth muscles and that of the heart (cardiac muscles) remain unaffected.
Treatment normally consists of anti-cholinesterase medication (pyridostigmine), which prevents the breakdown of acetylcholine and improves the chemical signal at the neuromuscular junction.
Immunosuppression in the form of steroids can also be used to suppress the immune system, however, steroids can have side-effects, so should be used with caution. Due to the side-effects, often additional drugs are used, such as azathioprine or ciclosporin. These also suppress the immune system and allow a lower dose of steroids to be given.
MG is often diagnosed by clinical symptoms and a response to treatment, but can be diagnosed with the TensilonR test, whereby an injection of edrophonium is given, which results in rapid, but short-lived improvement in the symptoms.
Prognosis is guarded to poor, since the condition cannot be cured and the risk of inhalation pneumonia from choking on food is high. Rabbits diagnosed with MG are normally euthanased.
Any length of time without constant throughput of food within the gastrointestinal tract can begin a sequence of events that can prove to be rapidly fatal to the rabbit.
Rabbits who go any length of time without food become hypoglycaemic (low blood glucose), which stimulates the mobilisation of fatty acids from the fat reserves. These are transported to the rabbit’s liver, which are intended to be used as an energy source. The fat accumulates in the hepatocytes (liver cells), leading to liver failure and death, sometimes within a few hours. Symptoms of hepatic lipidosis can include muscle weakness.
Pregnancy toxaemia is a disease that may affect rabbits during late gestation and is characterised by abnormally low levels of sugar and high levels of ketones in the blood.
Predisposing factors are generally obesity and anorexia. The main clinical signs are generalised weakness and incoordination. The rabbit is generally very quiet and unwilling to move. In severe cases, if not treated as an emergency, it can lead to death.
Treatment consists of administration of glucose solution, fluid therapy and assisted feeding.
Encephalitozoon cuniculi (E. cuniculi)
E. cuniculi has been documented as occurring in up to 50% of rabbits; many of whom carry the parasite asymptomatically and remain healthy throughout life and never suffer from any of the symptoms related to the parasite.
However, symptoms can include paresis, including paralysis of the limbs. Other symptoms may include head tilt, urinary incontinence, rolling, nystagmus (rapid flicking of the eyes), uveitis, fitting or even sudden death.
Treatment is aimed at reducing the inflammation within the brain and kidneys, which the parasite has caused and returning the parasite back to its ‘dormant’ stage. This is usually achieved with medication such as fenbendazole for at least 28 consecutive days. Sometimes a longer or repeated course is required. Supportive treatment is aimed at maintaining gastrointestinal function, pain relief and the mental and physical wellbeing of the rabbit, until the rabbit is capable of supporting itself.
Despite intensive treatment, sometimes some rabbits do not respond to treatment and require euthanasia to spare them suffering any further.
Feeding a good diet that is contains adequate amounts of vitamin E is essential; all good quality rabbit foods will contain sufficient amounts of vitamin E.
Rabbits can be blood tested to see if they are positive for E. cuniculi. However, a positive result does not indicate an active infection. It only indicates that the rabbit has, at some point in their life, been exposed to the parasite. A negative result is evidence that the rabbit is clear of E. cuniculi.
Ensure that if your rabbit stops eating, you contact your vet as soon as possible. Hepatic lipidosis and pregnancy toxaemia can begin after only a few hours of anorexia. Obesity should also be addressed and treated.