Common diseases and affections of laboratroy rabbits, quick review guide

Dr.Pavulraj S, M.V.Sc., Veterinary Pathology, Research Fellow, NRCE, India
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I. Pasteurellosis
A. Etiology: Pasteurella multocida is a small, Gram-negative, nonspore-forming bipolar
rod.
B. Transmission: Transmission occurs by direct contact, aerosol, venereal, and
hematogenous routes. Incidence of infection and disease is high (probably > 90%).
Many rabbits are asymptomatic carriers. The incidence of bacterial carriage is no
different in antibiotic-treated rabbits.
C. Disease Forms: Upper respiratory disease ("snuffles"), pneumonia, otitis media,
pyometra, orchitis, subcutaneous abscesses, conjunctivitis and septicemia are
manifestations of P. multocida infection.
1. Snuffles - This is the most common manifestation of pasteurellosis. Clinical signs
characteristically include serous to mucopurulent nasal exudate with sneezing and
coughing. Exudate may be seen on the medial aspect of the forepaws. Signs may
subside temporarily only to recur throughout life. Lesions include reddened mucosa in
acute infections, thickened mucosa in chronic infections, and exudate in nasal cavity and
paranasal sinuses. Antibiotic therapy (see Table 1) usually causes abatement of clinical
signs. The prognosis for disease improvement or remission is good, however there is a
good chance of recurrence.
2. Enzootic Pneumonia - Affected rabbits frequently die acutely with no signs
(especially young rabbits); anorexia and depression may be observed. Acute pneumonia
lesions include red-grey foci of consolidation of the cranioventral lung lobes with or
without hemorrhage. Chronic pneumonia is characterized by generalized consolidation,
encapsulated abscesses, fibrinopurulent or mucopurulent pleuritis and pyothorax. If the
pneumonia is recognized early, aggressive antibiotic therapy may be of some value. The

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prognosis for all cases of pneumonia is poor.
3. Otitis Media - Usually there are no clinical signs. Torticollis will occur if the
function of the internal ear is compromised, either by direct bacterial invasion or by the
damaging effects of the bacterial toxins. Nervous signs and incoordination are observed
if the bacteria extends to the meninges. Creamy, white exudate in middle ear is found
either uni- or bilaterally. When treated with antibiotics at the first indication of a head
tilt, rabbits with otitis media may improve or stabilize. In rabbits with severe torticollis,
NSAID or corticosteroid therapy may be indicated. Bulla osteotomies and lavage of the
tympanic bullae has proven to be a fruitless approach to treatment. The torticollis may
progress in spite of antibiotic therapy, so the prognosis is
guarded.
4. Genital Infections - Venereal or hematogenous transmission may occur. Affected
rabbits may have a vaginal discharge which may be serous to mucopurulent and/or a
history of infertility. The uterus can be palpably enlarged with pyometra. Acute
infection of the uterus is characterized by slightly dilated horns filled with grey exudate.
In chronic infections the uterine horns are greatly dilated with purulent exudate, and are
fragile. In affected bucks, one or both testicles may be enlarged, tender, firm and may
contain abscesses. The health of affected rabbits can be salvaged by surgical removal of

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diseased tissues coupled with antibiotic therapy. The prognosis for recovery after surgery
is good.
5. Abscesses - Contaminated wounds and septicemia are common routes for abscess
development in a variety of locations, but especially in the subcutis. The presence of
subcutaneous swellings which are filled with creamy exudate and may have draining
fistulous tracts is typical of Pasteurella abscesses. Treatments include sedation of the
rabbit prior to lancing and flushing superficial abscesses t.i.d. with Betadine or
chlorhexidine. Systemic antibiotic therapy should be provided for 1 week. If the
infections persist, surgical resection may be required.
6. Conjunctivitis - Signs include epiphora with blephorospasm, eyelids closed by
excessive mucopurulent exudate and facial staining. Reddened conjuctiva with serous to
mucopurulent adherent exudate are found. Often there is inflammation and eventual
stenosis of the nasolacrimal duct, resulting in chronic epiphora and hair loss. The use of
antibiotic ophthalmic ointments will improve most cases. Occasionally, the nasolacrimal
duct may need to be flushed to remove inspissated purulent
material.
7. Septicemia - Septicemic rabbits usually die acutely; however, one may see
pneumonia or infertility prior to death. Diffuse congestion and petechiation of thoracic
and abdominal viscera as well as abscesses in viscera (kidneys, liver, lungs) may be seen
on necropsy.
D. Predisposing Factors: Onset of clinical disease is often associated with some
underlying stressor, such as a marked change in environmental temperature or humidity,
poor ventilation, poor sanitation, and overcrowding. Physiologic conditions that also
predispose to disease is age (very young or very old), pregnancy, nutritional state, and
genetics. Some rabbit stocks are genetically hardier, and can carry Pasteurella throughout
life without developing clinical disease.

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E. Diagnosis: Tentative diagnosis of pasteurellosis is based on clinical signs and gross
necropsy findings of a mucopurulent exudate associated with inflamed body parts such as
the respiratory tract, subcutis, middle ears, and reproductive tract. A presumptive
diagnosis may be reached by making a smear or scraping from the affected area and
staining with a gram stain. With torticollis, radiographs of the tympanic bulla may
disclose the presence of exudate or bony reaction (increased density in the bulla).
Definitive diagnosis requires isolation of the bacteria by culturing the affected site(s).
F. Treatment: Most Pasteurella isolates are sensitive to penicillin. Only sulfaquinoxaline
and tetracycline have known withdrawal times and can be used for rabbits raised for
slaughter. Short term use of certain oral antibiotics, such as ampicillin or amoxicillin, or
prolonged systemic antibiotic therapy with any drug may upset the cecal bacterial flora.
If anorexia or diarrhea occurs during therapy, stop treatment immediately. Dietary
supplementation with high fiber foods, such as alfalfa cubes or high fiber pelleted diets,
or with yogurt containing live Lactobacillus cultures may reduce intestinal upsets.
TABLE 1: Antibiotics Commonly Dispensed for Rabbits
Enrofloxicin 2.5 to 5 mg/kg b.i.d. for 5 to 7 days (oral and
injectable)
Procaine penicillin 40 to 60,000 IU/kg body weight IM s.i.d. for 3 to 10
days
Sulfaquinoxaline 0.256 gm/50 gm feed for 30 days or 226 gm/ton of
feed
Tetracycline 300 mg/liter of water for 7 days, or 5 mg/kg q.i.d. for 7
days
G. Control: The best control for pasteurellosis is good husbandry techniques and culling
of rabbits with clinical disease. Since most all rabbits carry Pasteurella multocida in the
nasal cavity, management measures are aimed at controlling the clinical disease
expression. The rabbitry must have good ventilation, low ammonia levels, and low
humidity to decrease incidence of this disease. In a breeding colony situation, all infected
rabbits with clinical disease should be culled for many reasons. (In spite of antibiotic
therapy, the chance of disease recurrence is high. Rabbits with clinical signs shed large
numbers of organisms into the environment. The best way to improve the genetic
hardiness is to remove breeders with clinical disease.) Clean automatic waterers and
cages in which diseased rabbits were housed and then spray with 1% bleach solution to
kill residual bacteria. (Bleach will eventually damage galvanized caging, so alternative
disinfectants can be used.) All new arrivals should be quarantined prior to introduction
into the rabbitry. If possible, weanling rabbits should be raised separately from the
breeding colony.
II. Bordetellosis

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A. Etiology: Bordetella bronchiseptica is a small gram-negative, alpha-hemolytic,
nonfermenting rod. Incidence of infection is high with a low incidence of disease.
B. Transmission: Routes of transmission include aerosol and direct contact. Many rabbits
are asymptomatic carriers, and may harbor both Bordetella and Pasteurella.
C. Clinical Signs: Signs are similar to snuffles and include upper respiratory infection
with serous to mucopurulent nasal exudate and sneezing. Pneumonia uncommonly
develops.
D. Gross Pathology: The characteristic lesion is erythematous nasal mucosa with
adherent exudate.
E. Diagnosis: Definitive diagnosis is made by culture of the organism. Smear and gram
stain of nasal exudate may be helpful.
F. Treatment: Enrofloxian (2.5 to 5.0 mg/kg bid for 5 to 7 days), oxytetracycline (0.1
mg/ml drinking water) or Tylosin (2 to 4 mg/kg IM b.i.d., then s.i.d. for 3 to 5 days) are
effective in reducing clinical signs. As with pasteurellosis, antibiotic therapy may have
to be repeated when rhinitis recurs, which may happen. Antibiotic therapy does not
eliminate the carrier state.
G. Control: Isolation and treatment of sick animals, decreasing stressful conditions, and
preparation of and vaccination with an autogenous bacterin are all adequate control
measures. The bacterin may not eliminate the carrier state, but may help prevent
expression of clinical disease.
BACTERIAL DIARRHEAL DISEASES
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.
III. Colibacillosis
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

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(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

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bismol may be protective. Chlorpromazine (1 to 10 mg/kg IM) may help decrease fluid
loss from the the secretory diarrhea.
IV. Tyzzer's Disease
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.

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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 180o
F water for no less than 15 minutes.
V. Staphylococcus Infections
A. Etiology: Staphylococcus aureus is a Gram-positive, hemolytic, coagulase-positive
coccus.
B. Transmission: Aerosol and direct contact (organism present in oral cavity of non-
clinical carriers) are primary routes of infection. Incidence of infection is moderate, but
the incidence of disease is low.
C. Clinical Signs: There is a wide range of clinical disease forms. S. aureus may cause
suppurative infection in any organ or any site. Subcutaneous abscesses, mastitis with
abscess formation, dermatitis, upper respiratory infection with mucopurulent nasal
discharge, and septicemia with depression, anorexia, fever, and death have been
reported. Of these disease syndromes, abscess formation and mastitis are most
commonly reported.
1. Abscesses - Abscesses may occur subcutaneously or in the viscera. At necropsy
thick-walled abscesses filled with purulent exudate are found. Diffuse congestion and
petechiation of viscera may be seen in septicemic animals. Clinicopathologic lesions are
similar to those of pasteurellosis. Presumptive diagnosis may be made by making a
smear and gram stain of the exudate. Culture and antibiotic sensitivities are needed for a
definitive diagnosis and choice of treatment. If the organism is sensitive to penicillin,
40,000 IU/kg procaine penicillin, IM s.i.d., for 3 to 5 days may be effective.
Subcutaneous abscesses should be lanced and flushed with germicidal solution along
with administration of systemic antibiotics. Surgical extirpation may be necessary to
resolve chronic abscesses. To decrease the incidence of abscesses, the cages must be
kept clean, fighting animals separated, and clinically ill rabbits isolated.
2. Mastitis - Mastitis or blue breast disease is commonly found in herds with intensified
production. Infection of gland occurs through trauma to the teat, ascending infection
through the teat canal, or secondary to septicemia. Mastitis occurs just after kindling.
The mammary glands are swollen, usually not discolored, and may develop abscesses.
Frequently there is loss of function of the affected gland and rarely the doe may die.
Bunnies may die because of infected milk or not grow as well because of decreased

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function of the gland. Therapy includes hot packing the affected gland, systemic
antibiotic therapy, and transfer of bunnies to a healthy lactating doe. To prevent mastitis,
keep nest boxes clean and dry. Limit feed to the doe just prior to kindling to prevent
excessive milk production and stagnation. Cull all affected does.
VI. Venereal Spirochetosis (Rabbit Syphilis, Vent Disease, Cuniculosis)
A. Etiology: Treponema paraluis cuniculi is a spiral-shaped bacterium related to the
human syphilis organism, Treponema pallidum.
B. Transmission: Genital transmission is most common.
C. Clinical Signs: Cutaneous Infections - Erythema of mucous membrane of external
genitalia which progresses to focal, raised, crusty ulcerations is the most common sign.
Lesions can occur on the perineal area and face due to auto-inoculation. As ulcerations
heal, a dry scaly condition follows. Spontaneous regression usually occurs in several
weeks. The bacteria causes only superficial, cutaneous pathology. There may be
popliteal and inguinal lymph node enlargement. Mild or subclinical disease is common.
Reluctance to breed and decreased reproductive efficiency may
occur.
D. Diagnosis: Serological tests to identify antibody in actively or recently infected
rabbits include the hemagglutination test, Rapid Plasma Reagin (RPR), or fluorescent
treponema antigen preparation. (FTA). T. paraluis cuniculi may be found in
histosections with silver stain or with darkfield microscopy of fresh specimens.
E. Treatment: A regimen of procaine penicillin, 40,000 IU IM s.i.d. for 3 to 5 days is
curative. Once the spirochete is eliminated, serum antibody drops gradually to
undetectable levels.
F. Control: If spirochetosis is a herd problem, treat the entire herd. Do not breed infected
animals. If animals are for meat production, do not treat weanlings or fryers; treat only
breeding stock. Maintain a closed breeding colony or quarantine and medicate new
arrivals. Recovered animals can be used as breeding stock without danger of transmitting
infection.
VII. Proliferative Ileotyphlitis

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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.
VIII. Salmonellosis
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.
IX. Tularemia
A. Etiology: Francisella tularensis is a Gram-negative, pleomorphic rod.
B. Transmission: Blood sucking arthropods (squirrel flea, deerfly, mosquitoes, lice, and
woodticks) may serve as mechanical or biological vectors. Transmission may occur by
direct contact, ingestion, or aerosol (rare). The incidence of infection in domestic rabbits
is rare.

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C. Clinical Signs: Depression, anorexia, ataxia, and death are the nonspecific signs
associated with this disease.
D. Gross Pathology: Widespread visceral congestion, splenomegaly, consolidated and
congested lungs, and multiple pinpoint white foci on the liver and spleen are
characteristic lesions.
E. Diagnosis: Necropsy findings, and bacterial isolation are recommended diagnostic
measures.
F. Treatment: There is no treatment.
G. Control: Elimination or control of vectors and wild mammal populations will prevent
exposure.
Public Health Significance: Man is susceptible to infection. Transmission can occur by
ingestion of contaminated water, penetration of unbroken skin or contamination of
cutaneous wounds, tick bites, or by aerosolization of the organism in dust, feces, or when
skinning wild rabbits. Human tularemia is manifest by cutaneous lesions, septicemia,
and/or meningitis.
I. Coccidiosis
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.

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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

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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.
II. Encephalitozoonosis
A. Etiology: Encephalitozoon cuniculi (once called Nosema cuniculi) is a
microsporidian parasite, 2.5 x 1.5 micrometers (oval) with thick wall.
B. Transmission: E. cuniculi is shed in the urine and has been experimentally
transmitted by direct contact (ingestion, aerosol).
C. Clinical Signs: Usually there are no clinical signs (latent infection); however, in
heavy infections there may be torticollis, convulsions, tremors, posterior paresis, and
edema.
D. Pathology: In acute cases the kidneys are swollen. Chronic lesions are more
commonly seen and include multifocal, pinpoint, white, pitted areas on the surface of the

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kidneys. Histological examination of kidneys and brain will reveal a granulomatous
interstitial reaction with fibrosis in the kidney and focal granulomas in the brain (white
arrow) with perivascular plasma cell cuffs and nonsuppurative meningitis. The organism
may be found in renal tubular epithelial cells or in microglia in the brain.
Encephalitozoon stains poorly with hematoxylin and eosin stains, but is Gram-positive
(black arrow) and refractile when viewed with polarized light.
E. Diagnosis: Diagnosis is provided by histopathologic demonstration of organisms and
serologic detection of antibody via ELISA and indirect fluorescent antibody tests. Most
research animal diagnostic laboratories offer an ELISA or FA test.
F. Treatment and Control: No treatment is effective. Control is difficult in colonies,
especially breeding colonies. Housing rabbits on wire and placing the cages away from
contact with walls and in single rows (no stacking) may prevent cage-to-cage urine
contamination. Rabbits will seroconvert 30 days prior to shedding sporocysts in urine, so
a strict program of culling seropositive rabbits can be instituted based on results of
serologic screening every 2 weeks.
Public Health Significance: Encephalitozoon cuniculi has been diagnosed in
immunosuppressed humans. The direct association between rabbit ownership and
infection has not been documented.
III. Passalurus ambiguus
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 m in diameter with a single curved spicule.
The females 6.6 mm long with long tail posterior to vulva (see

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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.
IV. Baylisascaris procyonis
Infection of rabbits with the raccoon ascarid, Baylisascaris procyonis, occurs by
ingestion of bedding or hay contaminated with raccoon feces. Reports of this nematode
as a rabbit pathogen are increasing. Clinically infected rabbits display torticollis, ataxia,
tremors, and falling (loss of balance). At necropsy, multiple, white raised nodules in the
epicardium, endocardium and serosal surface of the liver may be seen. Larval
granulomas and multifocal necrosis in the cerebrum and cerebellum, and larval
granulomas and tracks in the viscera are typical histologic lesions. Cross sections of
larvae with cuticular alae are often visualized in brain sections. Diagnosis is made from
clinical signs and the presence of larvae in histosections. Treatment has not been
attempted. Efforts to prevent infection include use of clean bedding and hay.
V. Cestodes
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.
VI. Mites
A. Psoroptes cuniculi - ear mite
1. Etiology: This nonburrowing, obligate mite has a high incidence of occurrence in
meat, laboratory and pet rabbits. The life cycle is completed in around 21 days.

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2. Clinical Signs: Scratching at ears with hind feet and the presence of crusty exudate in
the pinnas with an underlying moist dermatitis are characteristic. The parasites do not
cause otitis media since they do not penetrate the tympanic membrane.
3. Diagnosis: Mites can be observed with an otoscope or on a mineral oil preparation of
the crusty exudate. The mites are oval-shaped with well-developed legs, pointed
pedicles, and bell-shaped suckers on the end of
pedicles.
4. Treatment: Crusts are gently removed from the canal. Mineral oil with or without
acaricide in the ear canal will kill the mites. Ivermectin at doses of 0.2 to 0.4 mg/kg SC
will eliminate most infections with a single treatment. Antibiotic cream can be used if
the ear is infected.
5. Control: Infected animals should be isolated. During treatment, the cage should be
disinfected.
B. Cheyletiella parasitovorax - fur mite
1. Etiology: C. parasitovorax is a small, noninvasive mite, with a low to moderate
incidence of infection.
2. Clinical Signs: Partial alopecia of dorsal trunk or scapular region with a fine, grey
scale on erythematous skin results from infestation. (The mite is often called "walking
dandruff.") There is some pruritis.

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3. Diagnosis: Examination of the pelt will reveal small white mites with piercing
chelicerae and large curved palpal hooks, and the eggs are attached to hair shafts.
4. Treatment: Rabbits can be dusted or sprayed with pyrethrin preparations or silica gel
acaricides, with repeat treatments at 10 day intervals. Ivermectin at 0.2 to 0.4 mg/kg SC
should also be effective.
5. Control: Infested rabbits should be isolated during treatments. Cleaning and
spraying the rabbit's environment with insecticidal preparations aids in decontamination
of the fomites.
Public Health Significance: This parasite can cause a transient pruritic rash in
hypersensitized people, especially children.
C. Listrophorus gibbus - fur mite
1. Etiology: L. gibbus is a small, nonburrowing mite present at low to moderate
incidence in domestic rabbits. It is an obligate parasite, completing all stages of the life
cycle on the host.
2. Clinical Signs: This mite is currently considered non-pathogenic and is found
primarily on the back and abdomen.
3. Diagnosis: The hair shafts can be examined under a dissecting microscope or with
hand lens for the characteristic brown mite or its nits.
4. Control: Isolate infected animals. Topical acaricides and ivermectin as described for
cheyletiella are thought to be effective in treatment.

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VII. Fleas and Lice
Rabbits are commonly infested with Ctenocephalides sp., especially C. felis. The
infestation may be asymptomatic, but may induce mild pruritis and alopecia. Rabbits can
be dusted and sprayed with pyrethrin products. Do not use the flea product Frontline in
rabbits since rabbit deaths have been associated with its use. The environment should be
treated to control this parasitism.
Haemodipsus ventricosis (Blood Sucking Louse). The anapleurid louse is rarely found
on domestic rabbits. Weakness, anemia, ruffled fur and pruritis (secondary dermatitis) are
common signs of infection. The pelt can be examined with a dissecting microscope or a
hand lens. Nits, as well as the adult anopleurid louse (head narrower than body), may be
found on the hair. Rabbits should be treated with pyrethrin products, silica gel acaricides
or ivermectin (0.2 to 0.4 mg/kg SubQ) at 10 day intervals for 2 treatments. This louse
spends its entire life cycle on the rabbit with little horizontal transmission. Isolation is an
effective means of control while treating the infected rabbit.
VIII. Cuterebra Infestation
Cuterebrid flies are also known as rodent and rabbit warble flies. Cuterebriasis occurs
most frequently in wild rabbits, but may occur in domestic rabbits housed outdoors.
Incidence peaks in the summer and late fall. Single or multiple large subcutaneous
swellings containing encysted larvae with a fistula in the center are the characteristic
lesions (left photo). When the larval fly is ready to pupate, it leaves the swelling and
drops to the ground (right photo). Secondary bacterial infections may complicate the
disease. These lesions are treated by removing the larva (without crushing it) and
flushing the wound, or by surgical resection of the wound. Prevention of infestation
includes moving the cage indoors, or by surrounding the hutch with screen to prevent fly
exposure.
VIRAL DISEASES
I. Myxoma Virus
A. Etiology: Myxomatosis is caused by any one of several strains of myxoma virus, a
member of the leporipoxvirus group. Virulence of the different strains ranges from a
mortality incidence of 99% in European rabbits to less than 30%. Incidence is high in
endemic areas in the Pacific coastal states.

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B. Transmission: The principal mode of transmission is via arthropod vectors
(mosquitoes, fleas, flies, gnats). Transmission may also occur by contact with infected
material from ocular discharges or oozing skin lesions of infected rabbits, contaminated
spines of thistles, and the claws of predatory birds. Virus-infected skin nodules on wild
rabbits, Syvilagus sp., are reservoirs of the agent.
C. Symptoms: In domestic rabbits, the clinical disease picture is largely predicated by
the strain of virus involved as well as genetic resistance of the breed of rabbit.
California Strain of Virus: In the peracute form, rabbits die within a week of exposure
showing slight edema of the eyelids and depression immediately prior to death. With the
acute form in which rabbits survive for 1 to 2 weeks, symptoms are edema of the eyelids
resulting in a droopy appearance of the eye; inflammation and edema around the anal,
genital, oral, and nasal orifices; skin hemorrhages; and convulsions. A nodular lesion
develops at the site of inoculation with both forms, but it is not a clearly defined tumor.
Standard Laboratory Strain of Virus: This strain induces a mean survival time of 11
days. Around 3 to 4 days post inoculation, a primary tumor becomes evident, and
generalized tumors are seen on the 6th or 7th day. At this time, a mucopurulent nasal
discharge and pronounced edema of the eyes and base of the ears are seen. By day 10,
hard lumps cover much of the body.
European Strain of Virus: This strain is characterized by rapid proliferation of large
lumps by day 7. The lumps may break open by day 10 and release a serous discharge.
Lumps may occur on any area of the body. There is also pronounced edema of the face
and anal regions, seropurulent discharge from eyes and nose, and considerable skin
congestion.
D. Pathology: The most prominent gross lesions are skin tumors and pronounced
cutaneous and subcutaneous edema. Skin hemorrhages and subserosal petechial and
ecchymotic hemorrhages in the stomach and intestines may be observed. Various
degrees of congestion will occur in the visceral organs depending on the severity of the
disease. Skin tumors result from an initial proliferation of undifferentiated mesenchymal
cells in the dermis which become large stellate cells termed myxoma cells. These cells

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lie in a homogeneous matrix of mucinous material. Necrosis can be observed in the
center of this area. Epidermal cells overlying the tumor may appear normal in early
stages of the tumor proliferation, or they may show hyperplasia or degeneration in later
stages. Intracytoplasmic inclusions (arrows) are observed most commonly in cells of the
prickle-cell layer of the epidermis, and in the stellate myxomatous cells.
F. Diagnosis: A diagnosis can be made from the clinical and pathological picture, virus
isolation, and PCR amplification of viral sequences from tissue specimens. Serological
tests including fluorescent antibody techniques, plaque-neutralization, and ELISA have
been developed but are not commercially available.
G. Control: Control is achieved through vector control and adequate screening of the
rabbitry, by quarantine of new animals, and isolation of all sick animals. A common
practice, once a death from myxomatosis is diagnosed, is to cull all rabbits whose body
temperature exceeds 104o
F in an attempt to remove animals incubating the virus before
shedding occurs. A vaccine was developed but has not been used as the vaccine caused
clinical myxomatosis in some vaccinated rabbits.
II. Rabbit (Shope) Fibroma Virus
A. Etiology: Fibroma virus is a member of the leporipoxvirus group and is closely
related to myxoma virus. The virus has widespread incidence in both domestic and wild
rabbit populations. Few cases of virus-induced fibromas have been diagnosed in rabbits
in Missouri although the majority of cases are reported from the western and
southwestern United States.
B. Transmission: The natural transmission cycle is not known although arthropod vector
transmission is likely.
C. Clinical Signs: Tumors occur on the legs or feet, on the muzzle, and around the eyes.
The tumors are subcutaneous and not attached to underlying tissue. Metastases from the
original tumor do not occur. The infected adult rabbit remains clinically normal
otherwise. Tumors will typically regress after a period of months. Spontaneous and

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experimental infections of neonatal domestic rabbits, however, has produced cutaneous
and visceral tumors.
D. Pathology: The earliest lesion is slight thickening of the subcutaneous tissue followed
by development of clearly demarcated soft tissue swellings which are evident on day 6
post inoculation. Tumors increase in size until day 12. They persist for months before
regressing. The earliest microscopic lesion is an acute inflammatory reaction followed by
localized fibroblastic proliferation. Proliferation continues until a distinct tumor is
formed consisting of spindle-shaped and polygonal connective tissue cells with abundant
cytoplasm. Intracytoplasmic inclusions are present in stellate cells, and less commonly or
rarely in the epidermal cells. Degeneration of the epidermis overlying the tumor may
result from pressure ischemia. This leads to necrosis and sloughing of the epithelium.
F. Diagnosis: Clinical signs and lesion morphology are primary diagnostic tools.
G. Control: This is not considered to be an important problem in domestic rabbits. In
outdoor rabbitries, vector control is advised.
III. Rabbit (Shope) Papilloma Virus
A. Etiology: A member of the papovavirus group. This disease is seen most frequently
in cottontail rabbits of the Midwest with outbreaks in domestic rabbits. Incidence of
disease is low.
B. Transmission: Arthropod vector transmission of the natural disease has been
demonstrated. The mosquito is thought to be the main vector in transmission from feral
to domestic rabbits.
C. Clinical Signs: Horny warts are found on the eyelids and ears. The growths are well
keratinized, and the upper surface is irregular and split. The growths are easily scratched
or knocked off. These sites later heal without complication.
D. Pathology: The tumor has the typical appearance of a papilloma with elongated rete
pegs of epithelium surrounding central cores of connective tissue. A mild inflammatory
cell infiltrate is normally found in the dermal layers underlying the tumor. Failure of the
lesion to resolve may lead to development of squamous cell carcinoma.

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E. Diagnosis: Clinical signs and histological examination are the basis for diagnosis.
F. Control: Control of the arthropod vectors will eliminate the introduction and spread of
disease. Tumors that fail to spontaneously resolve in 30 days should be removed
surgically to prevent dedifferentiation into neoplasia.
IV. Rabbit Oral Papilloma Virus
A. Etiology: A member of the papovavirus group, this virus is the only member of the
papovavirus group having the domestic rabbit as its natural host. There is moderate
incidence of disease.
B. Transmission: Spread is by direct contact of oral secretions containing sloughed
epithelial cells from the oral warts. Infection occurs in the abraded epithelium of the
tongue.
C. Clinical Signs: This is a benign disease characterized by numerous whitish growths
on the underside of the tongue, oral cavity epithelium or gingiva. These later become
pedunculated and ultimately ulcerate. The growths regress when the rabbit becomes
immune.
D. Pathology: A typical papilloma with verrucous epidermal hyperplasia with rete peg
formation and hyperkeratosis and dermal fibroplasia has been described. Intraepithelial
viral inclusion bodies are not usually seen on microscopic examination of tumors.
E. Diagnosis: The gross lesions are diagnostic.
F. Control: No control measures to prevent exposure are known. Recovered rabbits are
resistant to reinfection.
V. Viral Hemorrhagic Disease (Viral Hemorrhagic Fever, Viral Necrotizing Hepatitis)
The disease was first reported in China in 1984, and has since been reported in Europe,
parts of Asia, Mexico and the United States.
A. Etiology: A calicivirus has been recovered from infected rabbits. Apparently strains
of virus with varying degrees of virulence have been recovered from rabbits from
different parts of the world.
B. Transmission: The agent can be spread by direct contact, biting arthropods and
fomites, including handling of infected rabbit meat and by-products.
C. Clinical Signs: The incubation period ranges from 1 to 3 days, at which time one of
three forms of the disease may be seen. The peracute disease is manifested by death
without clinical signs. In acute disease, acute onset of anorexia and lethargy occur
followed by labored respiration. Body temperature may be elevated from 40 to 41o
C, but

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rapidly declines prior to death. In subacute disease, clinical disease progresses to include
bloody nasal discharge, opisthotonus and vocalization. Death occurs 2 to 3 hours after
the onset of clinical signs. In colony settings, morbidity may reach 90% with 100%
mortality.
D. Pathology: Tracheal hemorrhages, petechia on the myocardium, kidney, and spleen,
pulmonary edema and congestion, and widespread hepatic necrosis are frequently
observed at necropsy.
E. Diagnosis: The disease is tentatively diagnosed based on the rapidly fatal infection
and gross necropsy findings. VHD-specific PCR is used to confirm the postmortem
diagnosis.
F. Treatment: There is no effective treatment.
G. Control: Once the disease is recognized, elimination of all rabbits in the colony has
been the only effective way of preventing perpetuation of the infection. The disease
should be reported to the state veterinarian and the USDA. Frozen carcasses may be
saved for disease confirmation. Killed virus vaccines provide protection of naive rabbits
exposed to the disease.
Back to Disease Categories
I. Baylisascaris procyonis
Infection of rabbits with the raccoon ascarid, Baylisascaris procyonis, occurs by
ingestion of bedding or hay contaminated with raccoon feces. Reports of this nematode
as a rabbit pathogen are increasing. Clinically infected rabbits display torticollis, ataxia,
tremors, and falling (loss of balance). At necropsy, multiple, white raised nodules in the
epicardium, endocardium and serosal surface of the liver may be seen. Larval
granulomas and multifocal necrosis in the cerebrum and cerebellum, and larval
granulomas and tracks in the viscera are typical histologic lesions. Cross sections of
larvae with cuticular alae are often visualized in brain sections. Diagnosis is made from
clinical signs and the presence of larvae in histosections. Treatment has not been
attempted. Efforts to prevent infection include use of clean bedding and hay.
II. Dermatophytosis

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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.
III. Encephalitozoonosis
A. Etiology: Encephalitozoon cuniculi (once called Nosema cuniculi) is a
microsporidian parasite, 2.5 x 1.5 micrometers (oval) with thick wall.
B. Transmission: E. cuniculi is shed in the urine and has been experimentally
transmitted by direct contact (ingestion, aerosol).

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C. Clinical Signs: Usually there are no clinical signs (latent infection); however, in
heavy infections there may be torticollis, convulsions, tremors, posterior paresis, and
edema.
D. Pathology: In acute cases the kidneys are swollen. Chronic lesions are more
commonly seen and include multifocal, pinpoint, white, pitted areas on the surface of the
kidneys. Histological examination of kidneys and brain will reveal a granulomatous
interstitial reaction with fibrosis in the kidney and focal granulomas in the brain (white
arrow) with perivascular plasma cell cuffs and nonsuppurative meningitis. The organism
may be found in renal tubular epithelial cells or in microglia in the brain.
Encephalitozoon stains poorly with hematoxylin and eosin stains, but is Gram-positive
(black arrow) and refractile when viewed with polarized light.
E. Diagnosis: Diagnosis is provided by histopathologic demonstration of organisms and
serologic detection of antibody via ELISA and indirect fluorescent antibody tests. Most
research animal diagnostic laboratories offer an ELISA or FA test.
F. Treatment and Control: No treatment is effective. Control is difficult in colonies,
especially breeding colonies. Housing rabbits on wire and placing the cages away from
contact with walls and in single rows (no stacking) may prevent cage-to-cage urine
contamination. Rabbits will seroconvert 30 days prior to shedding sporocysts in urine, so
a strict program of culling seropositive rabbits can be instituted based on results of
serologic screening every 2 weeks.
Public Health Significance: Encephalitozoon cuniculi has been diagnosed in
immunosuppressed humans. The direct association between rabbit ownership and
infection has not been documented.
IV. Salmonellosis
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.

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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.
V. Tularemia
A. Etiology: Francisella tularensis is a Gram-negative, pleomorphic rod.
B. Transmission: Blood sucking arthropods (squirrel flea, deerfly, mosquitoes, lice, and
woodticks) may serve as mechanical or biological vectors. Transmission may occur by
direct contact, ingestion, or aerosol (rare). The incidence of infection in domestic rabbits
is rare.
C. Clinical Signs: Depression, anorexia, ataxia, and death are the nonspecific signs
associated with this disease.
D. Gross Pathology: Widespread visceral congestion, splenomegaly, consolidated and
congested lungs, and multiple pinpoint white foci on the liver and spleen are
characteristic lesions.

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E. Diagnosis: Necropsy findings, and bacterial isolation are recommended diagnostic
measures.
F. Treatment: There is no treatment.
G. Control: Elimination or control of vectors and wild mammal populations will prevent
exposure.
Public Health Significance: Man is susceptible to infection. Transmission can occur by
ingestion of contaminated water, penetration of unbroken skin or contamination of
cutaneous wounds, tick bites, or by aerosolization of the organism in dust, feces, or when
skinning wild rabbits. Human tularemia is manifest by cutaneous lesions, septicemia,
and/or meningitis.
The incidence of spontaneously occurring tumors in rabbits is generally low. Only
recently has the pet rabbit population survived long enough to permit data collection on
tumor incidence. As with other species, tumor incidence is influenced by such factors as
age, breed predilection for certain tumors, breed resistance, and sex.
I. Uterine Adenocarcinoma
The most common tumor of rabbits is the uterine adenocarcinoma. Females with this
tumor have a history of reproductive disturbance prior to detection of the tumor. Fertility
is diminished, litter size is reduced, stillbirths are more numerous, and desertion of the
litter by the doe is common. Other symptoms are dystocia, fetal retention in utero,
abdominal pregnancy, and fetal resorption. The period of altered reproductive function
precedes tumor detection by 6 to 10 months. The duration in time between clinical
detection and death (usually post-metastasis) is 12 to 24 months. Uterine nodules can be
palated or observed on radiographs or laparatomy.
Histologically, the events of the tumor progression are characterized by increasing
degrees of epithelial cell dedifferentiation and anaplasia with increase of the vascular,
myxoid stroma. There is loss of cellular elements such as cilia and secretory vesicles.
Areas of necrosis are not uncommon in mature tumors. The incidence of neoplasia is
most common in New Zealand rabbits but has been observed in other rabbit breeds.
Ovariohysterectomy is the preventative measure that not only eliminates the source of the
most common cancer, but also prevents the undesirable behavioral changes that often
accompany sexual maturity in pet does.

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II. Lymphosarcoma
The second most common rabbit neoplasm is the lymphosarcoma. Susceptibility to the
disease is believed due to an autosomal recessive gene expressed in the homozygous
state. It is considered a tumor of juvenile and young adult rabbits. A tetrad of necropsy
lesions considered pathognomonic for lymphosarcoma in the domestic rabbit are 1)
enlarged kidneys, light tan in color with irregular lumpy surface, and thickened cortex but
normal medulla; 2) hepatomegaly with a diffuse pattern of small pale foci; 3)
splenomegaly; and 4) lymphadenopathy, in which all of the lymph nodes in the body may
be involved in the neoplastic process. Histologically, the normal architecture of the
nodes is obliterated by masses of infiltrating neoplastic
lymphoblasts.
III. Miscellaneous Neoplastic Diseases
Other commonly reported tumors of the rabbit are embryonal nephromas, bile duct
adenomas, mammary gland papillomas, mammary adenocarcinomas, and squamous cell
carcinoma. The latter tumor has been mentioned previously in conjunction with Shope
papilloma virus (SPV). One type of squamous cell carcinoma occurs if the SPV produces
a papilloma that lasts over 200 days. At this point, spontaneous change from papilloma
to squamous cell carcinoma occurs. Other tumors also caused by oncogenic viruses
(Shope fibroma virus, oral papilloma virus, and myxoma virus) have already been
discussed. Some other tumors that have been reported infrequently in the rabbit include
tumors of the endocrine glands, melanomas, plasma cell myelomas, thymomas,
osteosarcomas, osteochondromas, renal carcinomas, basal cell adenomas, leiomyomas,
and leiomyosarcomas.
Back to Disease Categories
I. Hairballs (Trichobezoar)

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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.

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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
-102o
F), 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.

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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.
IV. Enterotoxemia
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

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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.
V. Heat Prostration
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
95o
F 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

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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.
VII. Dermatophytosis
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.

34 | P a g e
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.
VIII. Pregnancy Toxemia
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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Common diseases and affections of laboratroy rabbits, quick review guide