Professional Documents
Culture Documents
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DR_ABOHEMEED@YAHOO.COM
BACTERIAL 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
X.lestriosis
Pasteurellosis
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.
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 (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
Nasal
discharge
is so
chronic
that the
fur is
actually
missing.
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
poor.
Pulmonary Edema
Pneumonea
Pneumonia
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
material.
Lacrimation
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.
Diagnosis
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.
D
i
a
g
n
o
s
i
s
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
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.
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
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.
Mastitis
VII. Salmonellosis
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.
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.
Rabbit Syphilis, Vent disease
Treponematosis
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
PARASITIC DISEASES
I-Coccidiosis
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
high.
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
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
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
coccidiosis.
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.
Intestinal
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
Oocysts
Treatment
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.
Control
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.
Pinwor
m
III. Passalurus ambiguus
Pinworm
Treatment
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
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
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
VIRALDISEASES
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:
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
otherwise.
Tumors will typically regress after a period of months.
Spontaneous and experimental infections of neonatal
domestic rabbits, however, has produced cutaneous and
visceral tumors.
Rabbit
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
INHERITEDDISEASES
I. Malocclusion
II. Buphthalmia
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.
Miscellaneous
e
l
l
a
n
e
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s
MISCELLANEOUS DISEASES
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
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
(ME)
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 (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
(ME)
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.
Enterotoxemia
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.
PATHOGENESIS
B. Clinical Signs: Enterotoxemia
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
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,
Sore
hocks
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
Pododermatitis
Predisposing factors for pododermatitis include a rough cage floor
such as woven wire, a heavy, mature animal and, according to
some, overgrown toenails.
Pododermatitis
A smooth, impervious resting board should be provided for the
rabbit. If the animal is overweight, it should be placed on a
restricted diet
Pododermatitis
Dermatop
hytosis
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.
Dermatophytosis
Dermatophytosis
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.
Dermatophytosis
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.
Pregnanc
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:
Treatment
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
Overgrown
Prevention
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
NEOPLASTIC DISEASES
I. Uterine Adenocarcinoma
II. Lymphosarcoma
III. Miscellaneous Neoplastic
Diseases
Neoplastics
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
Causes:
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
Signs
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
Treatment consists of administering
di-alpha tocopherol intramuscularly,
as shown, or orally, 15 mg/kg of body
weight for 7 days.
Vitamin E
VITAMIN A DEFICIENCY
Signs of Vitamin A Deficiency
Signs of Vit A
deficiency
ZOONOTIC DISEASES
I.Dermatophytosis
II. Encephalitozoonosis
III. Salmonellosis
IV. Tularemia
V. listeriosis
Dermatophytosis
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.
Dermatophytosis
Treatment
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.
Control
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.
Salmonellosis
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.
Salmonellosis
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
Hepatic necrosis
V. listeriosis
Etiology
Listeriosis usually results from infection by Listeria
monocytogenes, a Gram positive
rod in the family Listeriaceae
Transmission
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
pneumonia
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
decomposition