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 180oF 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 104oF 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.


22 | P a g e

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 41oC, 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

http://www.radil.missouri.edu/info/dora/RABBPAGE/rabbit.htm



24 | P a g e

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-102

oF), 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

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


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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.


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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.

Science

Common diseases and affections of laboratroy rabbits, quick review guide