II. Traumatic Vertebral Fracture (Paralysis of the Hindquarters, Broken Back)
III. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis
IV. Enterotoxemia
V. Heat Prostration
VI. Sore Hocks (Ulcerative Pododermatitis)
VII. Dermatophytosis
VIII. Pregnancy Toxemia
A. Etiology: Hairballs can form in the stomach as the rabbit grooms itself or a cagemate. Insufficient fiber in the diet can also lead to increased hair consumption. Incidence of hairball formation is high although abnormal digestive function pribably rarely occurs unless the hair ball is extensive.
B. Clinical Signs: Generally, hairballs are not a problem
and are found incidentally at necropsy. Occasionally, they will cause
a partial or complete obstruction; these hairballs may be palpable, and
the rabbit will stop eating and lose weight. The rabbit may be bright,
alert and afebrile with a history of anorexia and lack of feces excretion
of several days duration.
C. Diagnosis: Palpation and contrast radiography may be used.
D. Treatment: Treatments are centered on correcting dehydration and re-establishing normal gut function. Rehydrate rabbit and administer enteral protectants. Administration of metaclopromide (0.3 mg/kg SQ every 8 hours) will help stimulate peristalsis, and often will stimulate the rabbit's appetite. Past recommendations of feeding fresh pineapple juice at 10 to 15 ml orally once or twice daily for 5 days may provide an energy source but it is unclear whether the cellulitic activity of the papain eliminates the hairball. Force feeding of pulverized food in water or yogurt may help stimulate the appetite.
E. Prevention: Diets high in plant fiber has dramtically reduced the incidence of the clinical syndrome.
II. Traumatic Vertebral Fracture (Paralysis of the Hindquarters, Broken Back)
A. Etiology: This condition has a sudden onset and coincides with struggling or inadequate support of the hindquarters when handling. Frequently, the incident is not observed (or recognized), and the rabbit is found paralyzed in the cage. The occurrence is frequent.
B. Clinical Signs: Posterior paralysis or paresis, loss
of skin sensation, and loss of motor control of anal sphinctor and urinary
bladder are typical signs. 
C. Pathology: The most common site of fracture is the L7 lumbar vertebral body or its caudal articular processes.
D. Diagnosis: The diagnosis is made with clinical signs, neurological examination and/or radiography.
E. Treatment: If bladder and anal sphinctor control remain intact, and there is still hind limb pain perception, complete recovery may occur within 2 to 4 weeks with cage rest. Surgical correction and fixation of the fracture is not recommended because of the fragility of the bones.
III. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis
A. Etiology: The cause(s) of the ME disease complex is not well defined and the disease is uncommon.. However, multiple factors including diet, intestinal flora and the shift from neonatal to adolescent digestive physiology are thought to contribute to development of the disease. Diets low in fiber (<10%) result in a higher incidence of ME. Escherichia coli, Clostridia sp. (C. welchii type A, C. perfringens) have been associated with ME. Coccidiosis has also been incriminated in potentiating or triggering ME. Search for viral agents has been unsuccessful. Reproduction of the disease by causing cecal impaction with subsequent bacterial toxin production, has been successful.
B. Clinical Signs: There is acute onset of disease in 7 to 10 week old rabbits characterized by anorexia, polydipsia, a subnormal body temperature (99o-102oF), a rough hair coat, mucoid to liquid, tan diarrhea with perineal staining, and abdominal distention with gas and fluid-filled intestines. Affected rabbits may grind their teeth. Death usually occurs in 2 to 4 days. Rabbits usually survive the protracted course of 7 to 14 days.
C. Pathology: Grossly distended fluid and gas-filled stomach,
watery duodenal and jejunal contents, pasty contents in ileum, dry matter
and gas in cecum (often impacted), and gelatinous mucus in colon are frequently
observed.
The characteristic lesion is goblet cell hyperplasia with no inflammatory
response in the small and large intestines; occasionally see goblet cell
hyperplasia of gallbladder, pancreatic and bile duct epithelia, and tracheal
epithelial cells may be noted.
D. Diagnosis: Diagnosis is based on clinical signs, gross lesions, and histopathology.
E. Treatment: Supportive therapy, providing alfalfa for fiber and cholestyramine to absorb toxins has been recommended.
F. Control: Provision of high fiber feeds (18 - 20 % fiber) drastically reduces the incidence of mucoid enteropathy. Rabbits received after shipping should not be fed the first day. A small amount of a high fiber diet may be fed the next day, with a gradual increase to a full ration by day 5.
A. Etiology: Clostridial species, principally C. difficile and C. spiroforme, proliferate and produce toxins to induce this disease. Clostridial exotoxins induce secretory and vascular effects. A history of antibiotic therapy with broad spectrum antibiotics including oral ampicillin, clindamycin or lincomycin, may be associated with this disease. Clostridial enteritis may occur in rabbits that have not been treated with any antibiotics. Diets high in carbohydreates enhance the overgrowth of Clostridium species. Change in gut flora and other stressors leading to anorexia may predispose to disease.
B. Clinical Signs: Sudden death with no previous signs of illness or watery diarrhea 2 to 3 days prior to death are the usual signs. This disease affects all ages, but primarily targets recently weaned rabbits.
C. Pathology: Prominent gross lesions observed include
in a large, fluid-filled edematous cecum with serosal congestion and hemorrhage
and watery mucoid feces in the colon (A.). Microscopically, severe lesions
include a necrotic erosive or ulcerative typhlitis with swelling and loss
of enterocytes and pseudomembrane formation (B.). The mucosa and submucosa
are infiltrated with heterophils and there is submucosal edema and hemorrhage.
Large Gram-positive bacilli with spores can often be observed on the mucosal
surface.
D. Diagnosis: Diagnosis is achieved by the history of antibiotic
treatment or environmental/dietary stressors, and isolation or PCR amplification
of Clostridium species from cecal contents. An antigen capture ELISA
is available for cytotoxins A and B of C. difficile. C.
spiroforme may be seen as a spiral bacillus on a direct smear.
E. Treatment: Due to the acute course of the disease, there is usually no treatment. Supportive fluid therapy, kaopectate, and yogurt may be helpful.
F. Control: Do not use lincomycin or clindamycin in rabbits. Eliminate extreme dietary changes and minimize environmental stressors.
Rabbits are very sensitive to heat. Tachypnea, cyanosis, prostration, and blood-tinged fluid on nose and mouth may be observed with heat prostration. Temperatures above 95oF can be dangerous. The rabbit should be immersed in cool water, or covered with alcohol or water soaked cloths. The rectal temperature should be monitored to ensure reduction of body heat and to prevent induction of hypothermia. Housing in shaded areas provided with fans or water sprays in hot weather will keep rabbits cool. Limit feeding of rabbit food will prevent obesity, which may be an additional predisposing factor to overheating.
VI. Sore Hocks (Ulcerative Pododermatitis)
Sore hocks occur because of pressure necrosis of the skin from
bearing a heavy body weight on a hard or wire surface. There is genetic
predisposition in breeds such as the Rex which have poorly furred footpads
and rounded metacarpal bones . Common findings are circumscribed
ulcers over the metatarsus and metacarpus, covered by a scab. There
may be purulent exudate under the scab. Severely affected rabbits
may be anorexic, debilitated, and die. Use soft dry bedding, a resting
board in wire cages, and topical zinc and iodine ointments or an antibiotic
ointment if secondarily infected. Use systemic antibiotics if abscesses
are present or if the rabbit is debilitated. Cull affected animals
and do not use for breeding stock. Decrease environmental humidity.
Caution: Fecal pellets need to be brushed off the resting board daily
to prevent ingestion of infective parasite ova/oocysts. 
A. Etiology: Trichophyton mentagrophytes is an opportunistic, ubiquitous fungal soil organism.
B. Incidence: There is high incidence of the carrier state, with low incidence of disease.
C. Clinical Signs: A crusty, pruritic, patchy alopecia on
the head which spreads to the paws and other parts of the body is typical
(see photo). Secondary bacterial infections are common. 
D. Diagnosis: Diagnosis is based on clinical signs, scraping and identification of spores on hair shaft or mycelia within hair shaft, and culture on Sabaraud or DTM agars.
E. Treatment: Topical treatment with a fungicide (Tresiderm, Iodine, Conofite cream) or griseofulvin (25 mg/kg in aqueous suspension or 0.375 gm powdered form/lb food for 14 days) has been successful. Topical 10% chlorox solution is also effective. Griseofulvin therapy should be used with caution in breeding herds, as the incidence of teratogenesis is associated with treatment.
F. Control: Disinfect cage and nest boxes with 10% bleach solution. There is a possibility of transmission of infection to people handling the rabbits, so gloves should be worn when treating the rabbits. Ventilation should be improved to decrease the relative humidity, and all filters, water pads, curtains/blinds or other materials used to control the air temperature should be replaced weekly to prevent collection of fungus spores.
Public Health Significance: People handling rabbits with T. mentagrophytes induced lesions have developed dermatophytosis.
A. Etiology: The pathogenesis of pregnancy toxemia is not well known, but may be similar to ketosis in sheep. Predisposing factors include breed, age, sex, obesity, and number of previous litters. There is a high incidence in some rabbitries.
B. Clinical Signs: Signs range from a mild, nearly asymptomatic condition to a severe, rapidly fatal disease. The most common signs are depression, dyspnea, acetic odor to the breath, decreased urine production, abortion, CNS signs, and sudden death just prior to or just after kindling.
C. Pathology: Gross lesions are general obesity, areas of necrosis in the mesenteric fat, and pale yellow liver, heart, and kidneys. Fatty changes are seen microscopically in the liver, heart, and kidneys.
D. Control: Weight gain in breeding and non-pregnant does should be monitored, and controlled by limiting the amount of feed they are allowed to consume.
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