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Rabbit Diseases

I. Pasteurellosis
II. Bordetellosis
III. Colibacillosis
IV. Tyzzer's Disease
V. Staphylococcus Infections
VI. Venereal Spirochetosis (Rabbit Syphilis, Vent
Disease, Cuniculosis)
VII. Proliferative Ileotyphlitis
VIII. Salmonellosis
IX. Tularemia
A. Etiology: Pasteurella multocida is a
small, Gram-negative, non spore-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.
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 (Table) usually
causes abatement of clinical signs.
The prognosis for disease improvement
or remission is good, however there is a
good chance of recurrence.
Nasal secretions
Nasal secretions
Nasal secretions

is so
that the
fur is
mucopurulent nasal discharge
Difficulties in Respiration
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 prognosis for all cases of pneumonia is
Pulmonary Edema

Contaminated Lungs by Pasteurella

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,
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
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
The uterus can be palpably enlarged with
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 diseased
tissues coupled with antibiotic therapy.
The prognosis for recovery after surgery
is good.

The healthy pink

uterine horns are easily
seen (white arrow).
Uterine infection

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
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.
This problem is so prevalent, and the symptoms
so characteristic, that Pasteurella is part of the
tentative diagnosis anytime a rabbit shows the
above symptoms.
During the physical exam a fever might be
present along with an increase in the sounds
heard in the lungs with the stethoscope.
Cultures can be performed to confirm that
Pasteurella Multocida is indeed present.
Rabbits with a negative culture result could still
be harboring Pasteurella. Blood samples are
commonly used along with x-rays. X-rays might
show changes in the chest or infection in the
middle ear.
This is what these lungs could look
like on an autopsy.
All the white spots correspond to the
white spots on the radiograph above.
Diagnosis Lung
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,
alfalfa or high fiber pelleted diets, or with yogurt
containing live Lactobacillus cultures may reduce
intestinal upsets.
Antibiotics Commonly Dispensed for Rabbits

Enrofloxicin 2.5 to 5 mg/kg b.i.d. for 5 to 7 days

(oral and injectable)
Procaine 40 to 60,000 IU/kg body weight IM
penicillin 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
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
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.
Abscesses are treated surgically.
Rabbits have a very thick and tenacious
discharge when they form an abscess, and
require more care than the abscesses of
most other animals.
Surgical removal can be difficult, especially
in the chronic cases, because the abscessed
area can become extensive in nature.
Multiple surgeries might be needed, and
wound care at home is necessary.
This is a severe abscess on the back of a
rabbit that has been anesthetized and is
undergoing surgery to correct its
The wound has just been opened by the
scalpel blade at the top left of the screen
The wound is filled with pus (the
correct word is purulent) that must be
completely removed.
Any infection that is not removed will
cause the abscess to return.
It is very thick and does not lend itself
to easy removal.
The underlying tissue that has been
exposed to this infection has to be
removed also.
It is diseased and will be a source of
further infection if it is not completely
This is the final appearance of the wound
after all the purulent material and
diseased tissue has been removed after 30
minutes of surgery.
The rubber tube (arrows) running from
top to bottom is called a penrose drain
Its function is to allow further drainage
of the infection.
The tube will be removed in 5 days, the
sutures will be removed in 10 days.
Some pasteurella abscesses are chronic in
nature, and contain more dead tissue
than purulent material.
The following pictures show a case of a
rabbit referred to us that had been
treated with routine drainage and
antibiotics for several weeks.
The purulent material on the inside was
diminished, but the tissue that remained
was either dead or dying and had to be
surgically removed.
This is the face of the rabbit that is
laying on its left side.
Its mouth is towards the right, the
white arrow points to its right eye.
The abscess is the large circular area
below and to the left of the eye.
The diseased tissue (black arrow) is
gently dissected away from the
healthy tissue.
The healthy jaw muscle (white
arrow) is apparent .
A large incision had to be made to
remove all of this diseased tissue.
It extends from the base of the ear all the
way under the chin.
These sutures will be removed in 10-14
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
The best way to improve the genetic
hardiness is to remove breeders with
clinical disease prior to introduction into
the rabbitry.
If possible, weanling rabbits should be
raised separately from the breeding
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
II. Bordetellosis
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.
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.
C. Clinical Signs:
Signs are similar to snuffles and include upper
respiratory infection with serous to
mucopurulent nasal exudate and
sneezing. Pneumonia uncommonly develops.
F. Treatment:
Enrofloxian (2.5 to 5.0 mg/kg bid for 5 to 7
Oxytetracycline (0.1 mg/ml drinking water)
Tylosin (2 to 4 mg/kg IM b.i.d., then s.i.d. for
3 to 5 days) are effective in reducing clinical
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.
The initial approach to treating diarrhea in
a rabbit is similar to that used for companion
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
Escherichia coli is a gram-negative,
lactose-fermenting, indole positive rod.
Rabbits are known to be affected by non-
toxin producing, enteropathogenic E. coli
EPEC adhere to the intestinal mucosa
through a 2-step process.
First, a bacterial pilus first allows
attachment of the bacterial cell to the
A secretory diarrhea is induced by an
unknown mechanism.
Receptors for EPEC attachment to the
epithelial cells are not present in newborn
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
Edema or hemorrhage can be seen in the
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
The salicylates in Pepto bismol may be
Chlorpromazine (1 to 10 mg/kg IM) may
help decrease fluid loss from the the
secretory diarrhea.
IV. Tyzzer's Disease
Clostridium piliforme, an obligate intracellular
bacterium, is a Gram-negative, pleomorphic,
filamentous organism that can produce spores.
B. Transmission:
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
Tyzzers A
E. Diagnosis:
Histopathological examination of liver or cecum
stained with silver will be diagnostic if
intracellular bacterial rods are observed.
PCR of feces, intestinal tissue or liver can be
used to document the presence of the
bacterium. An ELISA is useful to detect
antibody in recovered or asymptomatically
infected rabbits.
F. Treatment:
No therapy has been uniformly successful.
Supportive therapy may help when the enteric
disease is mild and the rabbit is still eating.
G. Control:
Prevent overcrowding and use good sanitation
techniques. Stresses such as weaning and high
environmental temperature may precipitate an
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 82oC water for no
less than 15 minutes.
V. Staphylococcus Infections

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.
Abscesses may occur subcutaneously or in the
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
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
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
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
Limit feed to the doe just prior to kindling to
prevent excessive milk production and
Cull all affected does.
VII. Salmonellosis
Salmonella enterica serovars are Gram-negative
aerobic, nonlactose fermenting, H2S producing
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.
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
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
Disinfection, replacement with clean stock
and prevention of wild bird or rodent
contamination of bedding, water, or food
should prevent future or continued
Public Health Significance:
Man can contract Salmonella from
infected rabbits.
Rabbit Syphilis, Vent disease
Etiology: Treponema paraluis-cuniculi
Treponematosis is also known as rabbit syphilis,
vent disease, or venereal spirochetosis.
The disease is contracted venereally or by young
rabbits in contact with an infected dam.
The disease is characterized by dry, crusty
exudate overlying ulcers in the skin and mucous
membranes. Lesions commonly occur on the
vulva (shown here), prepuce, and anus.
Rabbit Syphilis, Vent disease
Diagnosis is confirmed by Darkfield examination
of scrapings from the lesions for the presence of
the spirochete Treponema paraluis-cuniculi
Treatment Treponematosis can be treated
successfully with three injections of Benzathine
penicillin with procaine penicillin G, 84,000
IU/kg given IM at 7-day intervals.
All animals from an infected colony must be
treated to eradicate the disease
There are NO public health hazards associated
with the disease.
Rabbit Syphilis, Vent disease
II. Encephalitozoonosis
III. Passalurus ambiguus
IV. Baylisascaris procyonis
V. Cestodes
VI. Mites
VII. Fleas and Lice
VIII. Cuterebra Infestation
I. Coccidiosis Hepatic coccidia

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
3. Pathogenesis: Eimeria stiedae exists 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,
Hepatic coccidia

debilitation, and pendulous abdomen with hepatomegaly

noted on abdominal palpation. Mortality is low except in
young rabbits.

5. Pathology:
An enlarged liver with multifocal, flat, yellow-white lesions
containing yellow exudate and occasionally a distended
gallbladder that contains bile may be seen at necropsy (A.).
The pathognomonic microscopic lesion is marked periportal
fibrosis surrounding enlarged bile ducts lined with
hyperplastic bile duct epithelium that harbors inflammatory
cell infiltrates, and E. stiedae macrogametes,
microgametocytes and oocysts.
Hepatic coccidia
Coccidiosis. Enlarged liver with multi-focal grayish-white
Liver Coccidiosis

coalescing lesions and yellowish liquid pus caused by E.

7. Diagnosis:
Hepatic coccidia Diag.

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
On necropsy, the recognition of the flat liver lesions and
identification of oocysts in the bile provide diagnostic
The histological appearance of liver with identification
of intraepithelial coccidial organisms will allow
diagnosis from tissue biopsies.
Hepatic coccidia treat.

8. Treatment:
Drugs approved as coccidiostats for rabbits used for
meat 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
Hepatic coccidia control

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.
Intestinal Coccidia

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: Coccidia

Signs vary and are most severe in young rabbits.

Poor weight gain, diarrhea ranging from mucoid to
watery to hemorrhagic, polydipsia and sometimes
acute death are seen. Older rabbits may shed coccidial
oocysts without expression of clinical disease.
4. Gross Pathology:
Fluid intestinal contents are often observed in heavily
parasitized rabbits.
One may see multiple white patches or ulcers on
mucosal surface of the small or large intestine.
Intestinal coccidioses
Intestinal coccidioses
Intestinal Coccidia

5. Diagnosis:
Antemortem diagnosis can be made by
examination of feces by direct smear,
flotation or concentration/flotation
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 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.
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
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.
The eggs are flattened on one side.

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.
V. Cestodes
Rabbir play as intermediate host for Tape
worm which infected dog & cat
Infection in rabbits is of greater importance
because the larval stages of the parasite
develop in different organs and the
musculature and often cause decreased
food utilization and wasting of the host. The
carcass or portion of the carcass may also
be unfit for human consumption in severe
cases which further contributes to the
economic loss.
Tape worm larvae in rabbits
Cysticercus pisiformis is the cystic
stage of Taenia pisiformis which occurs in
dogs and rarely in cats The mature larvae
are found in the peritoneal cavity and
frequently in the mesentery of rabbits The
cysts are the size of a pea, hence the name
C. pisiformis. They are filled with clear
fluid in early stages. There is formation of
pus in older lesions
Rabbit Cysticercus

Tapeworm larvae in rabbits. Cysticercus pisiformis in

the mesentery of rabbit.
Cysticercus pisiformis in
Cysticercus pisiformis in
Cysticercus fasciolaris

is the cystic stage of Taenia taeniaeformis,

known as the cat tapeworm. This parasite can be
recognized by the lack of a neck and the bell-
shaped posterior segments. The intermediate
host are the rabbit, rat, mouse and other rodents.
Cysticercus fasciolaris is 2.5 cm long and
develops in the liver
Cysticercus fasciolaris
Cysticercus fasciolaris
Coenurus serialis

is the intermediate stage of Taenia serialis, a tapeworm of the

dog and fox. Coenurus serialis is almost fatal to hares, rabbits
and other related rodents. It is passed into the connective tissue of
the lumbar muscles, hind leg muscles and rarely into the jaw
muscles. Coenurus serialis may also occur accidentally in the
brain and muscle tissue of humans. The mature cyst in rabbits is
ovoid or round, approximately 5 cm in diameter and has scolices
the size of a rice grain. It may have as many as forty scolices.
Sometimes these Coenuri behave like hydatids by budding off
new cysts internally or externally. These internal cysts are
frequently fertile. The external cysts are attached by stalks and
are often sterile. They resemble a bunch of grapes
Coenurus serialis
def. : is an infection caused by the protozoal
parasite, Encephalitozoon cuniculi. Protozoa are
one-cell organisms that infect various cells or
tissues of the body and behave as tiny parasites.
Infection with E. cuniculi generally affects some
combination of the kidneys, brain, heart, and
Encephalitozoonosis is transmitted by
ingestion of the parasite, through contact with
contaminated urine, or passed through the
placenta from the mother to her unborn pups.
There is no breed or sex predilection.
Sings :
1. Stunted growth
2. Kidney failure
3. Neurologic abnormalities such as
aggressiveness, convulsions,
blindness or paralysis
4. Sudden death

Treatment usually consists of supportive

therapy. No specific treatment has been
designed to date that successfully kills this
protozoal organism.
Encephalitozoonosis (nosematosis)
chronic interstitial nephritis
Encephalitozoonosis (nosematosis)
ln brain
VI. Mites
Ear Mite

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.

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.
Ear Mite

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.
Ear Mite
Ear Mite

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
Fur Mite

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.
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.
Fur Mite
4. Treatment: Fur Mite

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
5. Control:
Infested rabbits should be isolated during
treatments. Cleaning and spraying the rabbit's environment
with insecticidal preparations aids in decontamination of the
Public Health Significance:
This parasite can cause a transient pruritic rash in
hypersensitized people, especially children.

C. Listrophorus gibbus - fur mite 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.
Fur Mite

4. Control: Isolate infected animals. Topical acaricides and

ivermectin as described for cheyletiella are thought to be effective in
VII. Fleas and Lice 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
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
Haemodipsus ventricosis (Blood Sucking Louse).
The anapleurid louse is rarely found on domestic
Fleas and Lice

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

Cuterebrid flies known as rabbit warble flies.

Cuterebriasis occurs mostly 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
Cuterebrid flies

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
Cuterebrid flies
Outside housed rabbits
Fly eggs laid in open wound
Underlying causes
Depression, skin eroded/necrotic
Check skin folds, perineum, entry into body cavities
Tx Clipping, cleaning larvae removal (surgery)
Viral diseases
Viral diseases

I. Myxoma Virus
II. Rabbit (Shope) Fibroma Virus
III. Rabbit (Shope) Papilloma Virus
IV. Rabbit Oral Papilloma Virus
V. Viral Hemorrhagic Disease (Viral
Hemorrhagic Fever, Viral
Necrotizing Hepatitis)
I. Myxoma Virus
Myxoma V

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.
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. Myxoma V

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.
Myxoma V
Myxoma V

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
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.
D. Pathology: Myxoma V

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 {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
Myxoma V

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 40oC 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.
Rabbit Fibroma V

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. (USA)
B. Transmission: The natural transmission cycle is
not known although arthropod vector transmission
is likely.
Rabbit Fibroma V

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
Tumors will typically regress after a period of months.
Spontaneous and experimental infections of neonatal
domestic rabbits, however, has produced cutaneous and
visceral tumors.
Fibroma V
Rabbit Fibroma V

E. Diagnosis:
Clinical signs and lesion morphology are
primary diagnostic tools.
F. 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 Rabbit Papilloma

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
Oral Papilloma

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
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.
V. Viral Hemorrhagic Disease
Hemorrhagic Fever, Viral Necrotizing
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.
Rabbit Hemorrhagic Disease
Rabbit, liver. All liver lobes are swollen, pale and have a reticular pattern
Rabbit Hemorrhagic Disease
Rabbit, liver. There is a large area of pallor (necrosis) with a prominent reticular pattern
Rabbit Hemorrhagic Disease
Rabbit, liver. This chronically affected liver contains pale areas of postnecrotic scarring
Rabbit Hemorrhagic Disease
Rabbit, kidney. There are petechiae throughout the cortex and the medulla is severely
Rabbit Hemorrhagic Disease
Rabbit, lungs. The trachea is filled with foam, and the lungs are mottled and noncollapsed
(severe pulmonary edema
Rabbit Hemorrhagic Disease
Rabbit, heart. There are multiple epicardial hemorrhages
Inherited diseases
Inherited diseases


I. Malocclusion

II. Buphthalmia

III. Splay Leg

IV. Hydrocephalus
Malocclusion I. Malocclusion
There are both hereditary and environmental
causes of malocclusion.
Hereditary mandibular prognathism is apparent
by 3 weeks of life and is due to an autosomal
recessive trait with incomplete penetrance.
Malocclusion of premolars and molars has been
reported in older rabbits.
As a rabbit's incisor teeth grow 10 CM per year, it
is necessary to clip them (but not too close)
every 6 to 8 weeks.
Dog nail clippers, bone or wire cutters and a
rotary tool with disc attachment may be used
to trim teeth.
Care should be taken to prevent shattering the
incisors. .
Buphthalmia II. Buphthalmia
It is a congenital glaucoma caused by an autosomal
recessive defect with incomplete penetrance.
There is abnormal production and removal of
aqueous from the anterior chamber.
Clinical signs may occur as early as 2 to 3 weeks of
age, but are more common at 3 to 4 months of age.
Signs include slight cloudiness progressing to
increasing cloudiness of the cornea, a prominent
eyeball, conjunctivitis, keratitis, ulceration, and
rupture of the cornea.
The condition may be unilateral or bilateral.
Splay Leg

III. Splay Leg

Is a familial or polygenic condition with varying

clinical manifestations.
Affected rabbits cannot adduct affected limbs.
The condition may affect one or more limbs.
Starvation due to inability to reach food or water
dishes may occur.
Autosomal recessive with incomplete penetrance.
and some homozygous recessives will even be
phenotypically normal.
Splay Leg
Splay Leg
Splay Leg (R=normal)

IV. Hydrocephalus
The mode of inheritance of this trait is questionable
but has been reported to be autosomal recessive
associated with dwarfing and brachygnathism.
Vitamin A deficiency in pregnant does may cause
hydrocephalic young to be born.
Vitamin A toxicity of gravid does has also been
suspected of causing skeletal abnormalities (limb
deformities, large fontanels) and hydrocephalus in
stillborn term offspring as has been reported in
toxicities in humans.

I. Hairballs (Trichobezoar)
II. Traumatic Vertebral Fracture (Paralysis of
the Hindquarters, Broken Back)
III. Mucoid Enteropathy (ME) Complex or
Cecal Dysbiosis
IV. Enterotoxemia
V. Heat Prostration
VI. Sore Hocks (Ulcerative Pododermatitis)
VII. Dermatophytosis
VIII. Pregnancy Toxemia
I. Hairballs (Gastric Tricho-bezoar)
Hair ball

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.
Destination of stomach due to hair ball
Hair ball
Hair ball
C. Diagnosis: Palpation and contrast radiography.

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.
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.
Hair ball

opened stomach with the hair mat.

Hair ball
II. Traumatic Vertebral Fracture (Paralysis of the
Broken back

Hindquarters, Broken Back)

A. Etiology:
This condition has a sudden onset and coincides with
struggling or inadequate support of the hindquarters
when handling.
Frequently, the incident is not observed (or recognized),
and the rabbit is found paralyzed in the cage. The
occurrence is frequent.
B. Clinical Signs:
Posterior paralysis or paresis, loss of skin sensation,
and loss of motor control of anal sphinctor and urinary
bladder are typical signs.
Broken back
C. Pathology:
Broken back

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.
Clinical sign

Clinical signs
The clinical signs of dislocation or
fracture range from hindlimb weakness
to complete motor paralysis of the hind
quarters, loss of skin sensation, and,
possibly, loss of anal sphincter and
bladder control.
III. Mucoid Enteropathy (ME) Complex or
Mucoid Enteropathy (ME)

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
B. Clinical Signs:
There is acute onset of disease in 7 to 10 week old
rabbits characterized by anorexia, polydipsia, a
subnormal body temperature (37o-39oC), a rough hair
coat, mucoid to liquid, tan diarrhea with perineal
staining, and abdominal distention with gas and fluid-
filled intestines.
Affected rabbits may grind their teeth. Death usually

occurs in 2 to 4 days. Rabbits usually survive the

protracted course of 7 to 14 days
C. Pathology:
Grossly distended fluid and gas-filled stomach, watery
duodenal and jejunal contents, pasty contents in ileum,
dry matter and gas in cecum (often impacted), and
gelatinous mucus in colon are frequently observed.

The characteristic lesion is goblet cell hyperplasia with

no inflammatory response in the small and large
intestines; occasionally see goblet cell hyperplasia of
gallbladder, pancreatic and bile duct epithelia, and
tracheal epithelial cells may be noted.
D. Diagnosis: Clinical signs, gross lesions, and

E. Treatment:
Supportive therapy, providing alfalfa for fiber and
cholestyramine to absorb toxins has been
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 BS
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: Enterotoxemia

Sudden death with no previous signs of illness or watery

diarrhea 2 to 3 days prior to death are the usual
signs. Affects all ages, primarily recently weaned rabbits.
C. Pathology: Prominent gross lesions observed include
in a large, fluid-filled edematous cecum with serosal
congestion and hemorrhage and watery mucoid feces in
the colon (A.). Microscopically, severe lesions include a
necrotic erosive or ulcerative typhlitis with swelling and
loss of enterocytes and pseudomembrane formation (B.).
The mucosa and submucosa are infiltrated with
heterophils and there is submucosal edema and
hemorrhage. Large Gram-positive bacilli with spores can
often be observed on the mucosal surface.

D. Diagnosis: Diagnosis is achieved by the history of

antibiotic treatment or environmental/dietary stressors,
and isolation or PCR amplification of Clostridium species
from cecal contents. An antigen capture ELISA is
available for cytotoxins A and B of C.
difficile. C. spiroforme may be seen as a spiral bacillus
on a direct smear.
E. Treatment: Due to the acute course of the disease,
there is usually no treatment. Supportive fluid therapy,
kaopectate, and yogurt may be helpful.
F. Control: Do not use lincomycin or clindamycin in
rabbits. Eliminate extreme dietary changes and
minimize environmental stressors.
Heat Prostration

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 35 oC 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.
Heat Prostration

Initial stage.

Extreme exhaustion.
VI. Sore Hocks (Ulcerative
Sore hocks

Sore hocks occur because of pressure necrosis of the
skin from bearing a heavy body weight on a hard or
wire surface.
There is genetic predisposition in breeds such as the
Rex which have poorly furred footpads and rounded
metacarpal bones .
Common findings are circumscribed ulcers over the
metatarsus and metacarpus, covered by a scab.
There may be purulent exudate under the scab.
Severely affected rabbits may be anorexic, debilitated,

and die.
Use soft dry bedding, a resting board in wire cages, and
topical zinc and iodine ointments or an antibiotic
ointment if secondarily infected.
Use systemic antibiotics if abscesses are present or if
the rabbit is debilitated.
Cull affected animals and do not use for breeding
stock. Decrease environmental humidity.
Caution: Fecal pellets need to be brushed off the
resting board daily to prevent ingestion of infective
parasite ova/oocysts.
Sore hocks
Foot sores
Predisposing factors for pododermatitis include a rough cage floor
such as woven wire, a heavy, mature animal and, according to
some, overgrown toenails.

A smooth, impervious resting board should be provided for the
rabbit. If the animal is overweight, it should be placed on a
restricted diet


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: 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
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
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.

VIII. Pregnancy Toxemia y


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.
Pregnancy Toxemia

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.
Diet, infection (rare)
Unusual calcium metabolism
Urinary fraction excretion rate
Mammals = 2%, rabbits = 45-60%
Dietary levels urine levels
Clinical signs
Anorexia, weight loss, depression, pain urine staining, anuria, dysuria
Palpation, radiographs, urinalysis
Dietary modification, bladder flushing, cystotomy
Moist dermatitis
resulted from drooling. The gross lesions consist
of inflammation, alopecia, ulceration, and
necrosis of the affected skin.
Chronic wetness associated with dental problems,
leaking watering systems, or continual contact
with urine as result of poor husbandry practices
predispose to the condition
The underlying conditions causing chronic
wetness must be identified and corrected. Then
the animal can be treated by clipping nearby hair
and applying mild antiseptic scrubs and antibiotic
Moist dermatitis
Overgrown teeth
Overgrown Teeth
Overgrown teeth

Rabbit teeth grow continuously throughout their lives.

Normal chewing action wears them down just to the
point that they don't overgrow.
This is one of the reasons it is important to feed your
rabbit a high fiber diet.
A rabbit that has a malocclusion does not have this
normal wearing action and can suffer overgrown teeth.
This problem can be serious enough to inhibit the ability
to eat.
Most rabbits do fine if their teeth are trimmed
Overgrown teeth

On select cases we will remove the problem teeth.

This patient has overgrown lower incisors.
They are definitely inhibiting its ability to chew.
They need periodic trimming every 2-4 weeks to
prevent recurrence.
Overgrown teeth
Overgrown teeth

They are trimmed with a special scissors that will

not crack them.
If needed, they are also filed to remove any sharp
This technique should not be tried by
inexperienced people because teeth are brittle in
nature, and in this case are weaker than normal due
to the abnormality.
They can easily fracture because of these two
In addition, rabbits can fracture their back if not
properly restrained.
Overgrown trim
Overgrown teeth

Even though the upper incisors are

not as long as the lower, they also need
trimming because they are growing into
the lower jaw.
Even though the upper incisors are
not as long as the lower, they also need
trimming because they are growing into
the lower jaw.
Overgrown teeth
Overgrown teeth

Our friend feels much better, and can

now get back to normal rabbit activity.
He needs to return in 2-4 weeks to have
his teeth checked.
Overgrown teeth

This rabbit has an upper right

incisor (arrow) that has been
chronically infected.
We decided to remove the incisors
because trimming the teeth was not
solving the problem.
Overgrown teeth
Removal infected incisor

As you saw from the x-ray pictures the

roots of these incisors are very deep and
they curve significantly.
Great care must be taken during their
removal so they don't crack at the root.
In this picture we are gently breaking
down the attachment of the tooth to the
After Removal

This is the appearance immediately after surgery.

In some rabbits the problem is much more serious than
overgrown and unsightly incisors.
These rabbits have severe problems with their molar
teeth, preventing them from eating properly. If untreated
they can die.
A large part of their problem is a diet that is too low in
This causes improper wearing down of the molars, and
even can lead to elongation of the roots of the incisors.
Rabbits with this problem are not eating well, losing
weight, and are slobbering.
Looking into a rabbits mouth is not the easiest thing in
the world to do.
These roots are normal.
The arrow on the left points to the incisors,
the one below points to the molars.
Can you see the difference in the molars
from the abnormal rabbit above.
Overgrown molar teeth
Overgrown molar teeth

Now that Mike is finally anesthetized

we can gain access to his molar teeth.
The white arrow points to one of them
deep in his oral cavity.
These are the teeth immediately after removal.
Removed teeth

The roots are on the bottom.

A close up of one of them shows the infection around the
Removed infected tooth

root (on the right).

Prevention of

One of the most important things you
can do to keep your rabbit's teeth healthy
is to feed a high fiber diet. This consists of
mostly timothy hay or timothy hay pellets.
Regular exams by one of our doctors
will also catch this problem before teeth
get infected or your rabbit becomes ill.
Rabbit neuter
Rabbit Neuter (castration)
Male rabbits are neutered (castrated) for
a variety of reasons.
It helps minimize fighting behavior,
makes it impossible to impregnate females,
and prevents testicular cancer.
Here is the more traditional ways rabbits
have been neutered.
Also, how we do it with the laser.
Rabbit Neuter

The reason the male rabbit in the

following slide has one testicle
substantially larger than the other is due
to cancer.
Removal of this testicle is needed for
If this buck had been neutered at a
young age this problem would not have
Rabbit Neuter
Rabbit Neuter

The followings are the normal

testicles of a rabbit about to
undergo a neuter.
The hair has been clipped on the
abdomen and the surgical site has
been cleaned.
The arrow points towards the
Rabbit Neuter
Rabbit Neuter

Using laser for neuters.

It has significant advantages
over the scalpel blade.
In this picture just starting the
laser incision.
Rabbit Neuter
Rabbit Neuter

With the laser there is no

bleeding and much less post-
operative pain and swelling.
You can see the testicle
appearing on the left where the
scrotum has been incised by the
After the testicle is gently

pulled out of the scrotum it is

ligated with 2 sutures before it is
cut off.
You can see the first suture at
the bottom (arrow).
Again, note the lack of
Rabbit Neuter

Instead of sutures we seal the

scrotum with a special adhesive.
This minimizes surgical time,
there is no post-operative
discomfort or itchiness from
sutures, and you do not need to
return for suture removal.
Rabbit Neuter

I. Uterine Adenocarcinoma
II. Lymphosarcoma
III. Miscellaneous Neoplastic

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
Uterine Neoplastic

The most common tumor of rabbits is the

uterine adenocarcinoma.
Females 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
The period of altered reproductive
Uterine Neoplastic

function precedes tumor detection by 6 to 10

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.
The incidence of neoplasia is most common in
New Zealand rabbits but has been observed in
other rabbit breeds.
Uterine Neoplastic

Uterine adeno-carcinoma
Is the most common neoplasm of rabbits.
Firm, ovoid, hemorrhagic nodules form along
the mesometrial junction.
They can be seen on either side of the cervix in
this image. They are usually 1-5 cm in
diameter and regularly spaced. The time
course of the disease may be five to twenty
months. Late in the disease, metastasis occurs,
and death results.
Uterine Neoplastic
Nutritional deficiencies
Vitamin E

Vitamin E deficiency
The recommended level of vitamin E is 40
mg of alpha tocopherol per kg of feed.
Deficiencies occur if there is an insufficient
amount of the vitamin in the feed or an
increased requirement for the vitamin.
Increased requirements are associated with
liver disease, such as coccidiosis, or if the
animals are on a diet high in unsaturated
fatty acids.
Vitamin E

The signs of vitamin E deficiency are
muscular stiffness, weak knees, reduced
feed consumption, loss of weight,
neonatal mortality, and infertility.
There will be creatinuria and increased
serum creatine phosphokinase.
Vitamin E

Vitamin E deficiency
The gross lesions of vitamin E deficiency are
muscle atrophy and extreme paleness of the
muscle. The paravertebral muscles,
diaphragm, masseter, and voluntary mucles of
the rear leg are commonly affected.
Histologically, hyaline degeneration of
muscle fibers can be seen, with loss of
striations, clumping of sarcoplasm, atrophy of
muscle fibers,
Vitamin E

Treatment consists of administering
di-alpha tocopherol intramuscularly,
as shown, or orally, 15 mg/kg of body
weight for 7 days.
Vitamin E
Signs of Vitamin A Deficiency
Signs of Vit A

The clinical manifestations of Vitamin A

deficiency include:
droopy ears as seen on this image.
This is due to weakening of cartilage.
Other signs are retarded growth and eye
Eye lesions start as cloudy corneas and
advance to full blown keratitis and blindness.
Droopy ears
Pup with hydrocephalus

Vitamin A deficiency impairs

fertility in both sexes.
Fetuses may be aborted or
reabsorbed, or born with
hydrocephalus, as shown in the
lower pup on this image.
Neurologic deficiency

Rabbit with neurologic

Bone deformities and neurologic
disturbances are seen in advanced
states of Vitamin A deficiency.
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.
Kidney Lymphosarcoma
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.

II. Encephalitozoonosis
III. Salmonellosis
IV. Tularemia
V. listeriosis
I. 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.

F. Control:
Disinfect cage and nest boxes with 10% bleach
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.

III. Salmonellosis
A. Etiology: Salmonella enterica serovars are G -ve
aerobic, nonlactose fermenting, H2S producing rods.
B. Transmission: Ingestion through direct contact with
contaminated feces, food. 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.
IV. Tularemia Tularamia

A. Etiology: Francisella tularensis is a G-ve,

pleomorphic rod.
B. Transmission: Blood sucking arthropods (squirrel flea,
deerfly, mosquitoes, lice) as mechanical or biological
vectors. 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.

Hepatic necrosis
V. listeriosis
Listeriosis usually results from infection by Listeria
monocytogenes, a Gram positive
rod in the family Listeriaceae
The reservoirs of infection are the soil &Infected
animals can shed L. monocytogenes in the feces,
milk and uterine discharges.It is also found in
aborted fetuses and occasionally in the nasal
discharges and urine of symptomatic animals
Clinical Signs
meningitis, meningoencephalitis or, less frequently, septicemia. The
clinical signs of a
central nervous system (CNS) infection may include confusion,
seizures, cranial nerve deficits, ataxia, tremors or myoclonus. Brain
abscesses are also seen. Other conditions that have been reported are
endocarditis, septic arthritis, osteomyelitis and rare cases of
The gross lesions were characteristic of, but not diagnostic for, a
number of disease entities of rabbits. In this rabbit, lesions included
necrosis of the liver, uterus, and adrenal gland
Grossly, the liver had diffusely scattered miliary white foci which,
on cut surface, extended into the parenchyma. The uterus was
darkened with multiple serosal ecchymotic hemorrhages, and
contained placentomes and fetuses in various stages of