II. Coccidiosis
III. Colibacillosis
IV. Enterotoxemia
V. Hairballs (Trichobezoar)
VI. Malocclusion
VII. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis
VIII. Passalurus ambiguus
IX. Proliferative Ileotyphlitis
X. Salmonellosis
XI. Tyzzer's Disease
The initial approach to treating diarrhea in a rabbit is similar to that used for companion animals, and is similar for all infectious etiologies. Obtaining a thorough history is imperative. Questions to ask include recent changes in the rabbits' environment, husbandry, diet, including supplemental foods, antibiotics or home remedies. Even the addition of a new pet, especially a carnivore, can serve as a sufficient stressor. A diagnostic workup should include a complete physical exam including abdominal palpation, fecal flotation for coccidia, and fecal cultures. Ancillary tests may include blood work, and abdominal radiographs (plain and contrast studies) if warranted. Supportive therapy should be directed at correcting and maintaining hydration (via parenteral and oral fluid therapy) and stimulating the appetite in an attempt to restore normal gut flora using live yogurt cultures and fiber-containing treats. Antibiotics should be judiciously used as they may further upset the gut flora.
Wild rabbits are definitive and intermediate hosts for a number of tapeworms. The life cycles of these parasites practically precludes infection of domestic or laboratory rabbits. Taenia pisiformis infections are very common in wild rabbits and are found occasionally in domestic rabbits. The stage found in rabbits is a cysticercus. Most cysticerci are found in the liver or attached to the mesentery and cause little damage. A second taenid found in rabbits is T. serialis. The stage of the cestode seen in rabbits is a coenurus which occurs in connective tissue of muscle. Infection in wild rabbits is less common than T. pisiformis and is extremely rare in domestic rabbits. The dog is the definitive host of both cestodes.
A. Hepatic Coccidia
1. Etiology: Eimeria stiedae
2. Transmission: Ingestion of sporulated oocysts (unsporulated in freshly voided feces) is the mode of transmission. The incidence of infection is moderate to high.
3. Pathogenesis: Eimeria stiedae excysts in the duodenum, travels to the liver via the bloodstream or lymphatics, and invades epithelial cells of bile ducts to begin schizogeny.
4. Clinical Signs: Signs predominate in young rabbits and may include anorexia, debilitation, and pendulous abdomen with hepatomegaly noted on abdominal palpation. Mortality is low except in young rabbits.
5. Pathology: An enlarged liver with multifocal, flat,
yellow-white lesions containing yellow exudate and occasionally a distended
gallbladder that contains bile may be seen at necropsy (A.). The pathognomonic
microscopic lesion is marked periportal fibrosis surrounding enlarged bile
ducts lined with hyperplastic bile duct epithelium that harbors inflammatory
cell infiltrates, and E. stiedae macrogametes, microgametocytes
and oocysts.
7. Diagnosis: An antemortem diagnosis can be made by examination
of feces by direct smear, flotation or concentration/flotation methods.
It can be difficult to identify E. steidae oocysts in fecal specimens
since they may not be readily shed in the bile. On necropsy, the
recognition of the flat liver lesions and identification of oocysts in
the bile provide diagnostic information. The histological appearance of
liver with identification of intraepithelial coccidial organisms will allow
diagnosis from tissue biopsies.
8. Treatment: Drugs approved as coccidiostats for rabbits used for meat in US include sulfamerazine (0.02% in water), sulfaquinoxaline (0.05% in water or 0.03% in feed), sulfamethoxine (75 mg/kg BW in feed), and lasalocid (68-113 gms per ton of feed). Hepatic coccidia are difficult to eliminate with anticoccidial therapy, and lasalocid has been the most successful of the listed drugs in treating hepatic coccidiosis.
9. Control: Rabbits should be housed on wire-meshed floors. Bottoms of cages are to be brushed daily to remove adherent feces, and cleaned and disinfected regularly (1% chlorox). Weanlings should be raised separate from adults. Feeding fresh greens or hay will prevent use of forage that may be contaminated with droppings from wild rabbits.
B. Intestinal Coccidia
1. Etiology: Eimeria magna, Eimeria irresidua, Eimeria perforans, and Eimeria media are frequently observed pathogenic species. All species infect the intestinal tract and replicate in the absorptive epithelium of the mucosa.
2. Transmission: Transmission occurs by ingestion of sporulated oocysts. Incidence of infection is high.
3. Clinical Signs: Signs vary and are most severe in young rabbits. Poor weight gain, diarrhea ranging from mucoid to watery to hemorrhagic, polydipsia and sometimes acute death are seen. Older rabbits may shed coccidial oocysts without expression of clinical disease.
4. Gross Pathology: Fluid intestinal contents are often observed in heavily parasitized rabbits. One may see multiple white patches or ulcers on mucosal surface of the small or large intestine.
5. Diagnosis: Antemortem diagnosis can be made by examination
of feces by direct smear, flotation or concentration/flotation methods.
A postmortem diagnosis can be made on examination of mucosal scrapings
and by observation of coccidial organisms on histological sections of intestine.
D. Treatment: As mentioned in the above section, drugs approved as coccidiostats for rabbits used for meat in US include sulfamerazine (0.02% in water), sulfaquinoxaline (0.05% in water or 0.03% in feed), sulfamethoxine (75 mg/kg BW in feed), and lasalocid (68-113 gms per ton of feed) have been provided in schedules of 3-weeks-on / 3-weeks-off periods.
E. Control: Rabbits should be housed on wire-meshed floors. Bottoms of cages are to be brushed daily to remove adherent feces, and cleaned and disinfected regularly (1% chlorox). Weanlings should be raised separately from adults. Feeding fresh greens or hay will prevent use of forage that may be contaminated with droppings from wild rabbits.
A. Etiology: Escherichia coli is a gram-negative, lactose-fermenting, indole positive rod. Rabbits are known to be affected by non-toxin producing, enteropathogenic E. coli (EPEC). EPEC adhere to the intestinal mucosa through a 2-step process. First, a bacterial pilus first allows attachment of the bacterial cell to the enterocyte. Second, a more intimate attachment through the eae pathogenicity island disrupts the cytoskeleton and destroys microvilli. A secretory diarrhea is induced by an unknown mechanism. Receptors for EPEC attachment to the epithelial cells are not present in newborn rabbits. They first appear at 21 days and reach normal adult levels by 35 days. The stress of weaning and loss of passively acquired maternal antibody contribute to susceptibility at this time.
B. Clinical Signs: Rabbits have diarrhea, fever, anorexia, and may consume more water than usual.
C. Pathology: Fecal-stained perineal fur and fluid-filled
intestinal contents with serosal vascular injection are seen.
. 
Edema and pyogranulomatous cellularity of the lamina propria without
mucosal ulceration are prominent histopathologic findings. Edema or hemorrhage
can be seen in the submucosa. Small bacterial rods (arrow) adhered
to and effacing enterocyte margins are common in the ileum and cecum.
D. Treatment: Fluid therapy and supportive care are indicated.
The salicylates in Pepto bismol may be protective. Chlorpromazine
(1 to 10 mg/kg IM) may help decrease fluid loss from the the secretory
diarrhea.
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.
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.
There are both hereditary and environmental causes of malocclusion.
Hereditary mandibular prognathism is apparent by 3 weeks of life and is
due to an autosomal recessive trait with incomplete penetrance. Malocclusion
of premolars and molars has been reported in older rabbits. As a
rabbit's incisor teeth grow 4" per year, it is necessary to clip them (but
not too close) every 6 to 8 weeks. Dog nail clippers (Rescoe or White
styles), bone or wire cutters and a rotary tool with disc attachment (shown
in photo) may be used to trim teeth. Care should be taken to prevent
shattering the incisors. .
VII. 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.
The rabbit pinworm does not cause clinical disease in infected rabbits.
The rabbit pinworm has a direct life cycle and adult pinworms reside in
the cecum and large intestine. The males are 4.1 mm long, 300 mm
in diameter with a single curved spicule. The females 6.6 mm long
with long tail posterior to vulva (see photo). 
The eggs are flattened on one side. Treatment with
piperazine adipate (0.5 gm/kg to 0.75 gm/kg s.i.d. for 2 days in food or
water) is effective. Ivermectin at 0.2 mg/kg is most likely effective.
Control of infection is aimed at preventing ingestion of contaminated feces.
IX. Proliferative Ileotyphlitis
Chronic diarrhea with wasting and a proliferative enteritis in rabbits have been associated with infection with a Lawsonia-like organism. The bacterium can be demonstrated within ileal or cecal enterocytes by use of silver chemical stains or amplified by a Lawsonia-specific PCR assay.. There is little known about the disease pathogenesis, but the etiologic agent (and the resultant disease) is similar to that of proliferative enteritis of swine. Concurrent diseases or stressors seem to be associated with development of the proliferative enteric lesion with intracellular bacteria. Oral administration of kaolin may be helpful when this infection is suspected.
A. Etiology: Salmonella enterica serovars are Gram-negative aerobic, nonlactose fermenting, H2S producing rods.
B. Transmission: Salmonellae are transmitted by ingestion through direct contact with contaminated feces, food or fomites. Incidence of infection is rare.
C. Clinical Signs: Acute disease is characterized by anorexia, fever, dehydration, diarrhea (hemorrhagic), death, and abortions. Rabbits that recover from acute disease are asymptomatic shedders.
D. Pathology: Lesions are consistent with those of septicemia and include congestion and hemorrhage of the viscera associated with septicemia, ulcerative colitis, and focal necrosis of liver.
E. Diagnosis: Definitive diagnosis is made by isolation of the bacteria through culture of blood, spleen, mesenteric lymph nodes and feces on selective media (brilliant green, selenite, citrate, or tetrathionate).
F. Treatment: Since antibiotic therapy does not eliminate bacterial carriage, it is advisable to eliminate the colony and restock.
G. Control: Good management practices will prevent infection. Disinfection, replacement with clean stock and prevention of wild bird or rodent contamination of bedding, water, or food should prevent future or continued problems.
Public Health Significance: Man can contract Salmonella from infected rabbits.
A. Etiology: Clostridium piliforme, an obligate intracellular bacterium, is a Gram-negative, pleomorphic, filamentous organism that can produce spores.
B. Transmission: The disease is spread by spore ingestion (fecal-oral). Spores can remain viable at moderate to freezing temperatures for extended periods of time (> 1 year). The disease is perpetuated in breeding colonies by the infection of bunnies born into the colony. The incidence of disease is moderate.
C. Clinical Signs: Usually rabbits are affected shortly after weaning when passive immunity, if present, has waned. Acute, profuse watery to mucoid diarrhea, dehydration and death within 12 to 48 hours after onset of diarrhea are typical. The mortality rate is high. Exposure of naive adult rabbits may cause little to no clinical disease.
D. Pathology: Lesions in weanling rabbits include edema and hemorrhage
of mucosa, submucosa, and musculature of intestinal tract (A.). It is unusual
to see an enlarged liver with multifocal tan to yellow foci of necrosis
or hemorrhage of the myocardium as is described in the literature.
Extensive mucosal necrosis with a granulomatous cellular mucosal infiltrate
may occur in the ileum, cecum, and proximal colon. Visualization of the
bacterium is enhanced with use of silver stains. Argyrophilic intracellular
bacteria in clusters or "pick-up-sticks" or haystack clumps are present
in viable enterocytes in areas of granulomatous enteritis (B.), and if
heaptic necrosis is observed, in hepatocytes adjacent to an area of necrosis.
. 
E. Diagnosis: Histopathological examination of liver or cecum stained with silver will be diagnostic if intracellular bacterial rods are observed. PCR of feces, intestinal tissue or liver can be used to document the presence of the bacterium. An ELISA is useful to detect antibody in recovered or asymptomatically infected rabbits.
F. Treatment: No therapy has been uniformly successful. Supportive therapy may help when the enteric disease is mild and the rabbit is still eating.
G. Control: Prevent overcrowding and use good sanitation techniques.
Stresses such as weaning and high environmental temperature may precipitate
an outbreak. To minimize the stress of weaning, let the bunnies stay
in the original cage and remove the doe. Work to prevent temperature
fluctuations and keep the rabbits well-ventilated in high temperatures
with fans. The spores are resistant to many disinfectants.
A 1% bleach solution will inactivate spores that remain after the fecal
material has been washed off soiled cages. Temperatures of water
used to clean cages may also inactivate spores if the cages and supplies
are allowed to contact 180oF water for no less than 15 minutes.
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