موسوعة شاملة مصورة في أمراض الأرانب, خمس حلقات " سلسلة متتابعه "

PROFESSOR RABBIT




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



I. Pasteurellosis

A. Etiology: Pasteurella multocida is a small, Gram-negative, nonspore-forming bipolar rod.

B. Transmission: Transmission occurs by direct contact, aerosol, venereal, and hematogenous routes.

Incidence of infection and disease is high (probably > 90%). Many rabbits are asymptomatic carriers.

The incidence of bacterial carriage is no different in antibiotic-treated rabbits.

C. Disease Forms:
Upper respiratory disease ("snuffles"), pneumonia, otitis media,
pyometra, orchitis, subcutaneous abscesses, conjunctivitis and
septicemia are manifestations of P. multocida infection

.
Snuffles - 1






This is the most common manifestation of pasteurellosis.



Clinical signs characteristically include serous to mucopurulent nasal exudate with sneezing and coughing.

Exudate may be seen on the medial aspect of the forepaws.

Signs may subside temporarily only to recur throughout life.

Lesions
include reddened mucosa in acute infections, thickened mucosa in
chronic infections, and exudate in nasal cavity and paranasal sinuses.



Antibiotic therapy (see Table 1) usually causes abatement of clinical signs.

The prognosis for disease improvement or remission is good, however there is a good chance of recurrence.



2. Enzootic Pneumonia -






This is what these lungs could look like on an autopsy

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.


3. Otitis Media -







Usually there are no clinical signs. Torticollis will occur if the function of the internal ear is compromised,

either by direct bacterial invasion or by the damaging effects of the bacterial toxins.

Nervous signs and incoordination are observed if the bacteria extends to the meninges.

Creamy, white exudate in middle ear is found either uni- or bilaterally.

When treated with antibiotics at the first indication of a head tilt, rabbits with otitis media may improve or stabilize.

In rabbits with severe torticollis, NSAID or corticosteroid therapy may be indicated.


Bulla osteotomies and lavage of the tympanic bullae has proven to be a fruitless approach to treatment.

The torticollis may progress in spite of antibiotic therapy, so the prognosis is guarded.

4. Genital Infections -

The arrows point to the typical appearance of a uterus infected with Pasteurella


In
affected bucks, one or both testicles may be enlarged, tender, firm and

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.


Signs include epiphora with blephorospasm, eyelids closed by excessive mucopurulent exudate and facial staining.

Reddened conjuctiva with serous to mucopurulent adherent exudate are found.

The
use of antibiotic ophthalmic ointments will improve most cases.
Occasionally, the nasolacrimal duct may need to be flushed to remove
inspissated purulent material.


7. Septicemia -

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.

E. Diagnosis:
Tentative diagnosis of pasteurellosis is based on clinical signs and
gross necropsy findings of a mucopurulent exudate associated with
inflamed body parts such as the respiratory tract, subcutis, middle
ears, and reproductive tract.

A presumptive diagnosis may be reached by making a smear or scraping from the affected area and staining with a gram stain.

With
torticollis, radiographs of the tympanic bulla may disclose the
presence of exudate or bony reaction (increased density in the bulla).

Definitive diagnosis requires isolation of the bacteria by culturing the affected site(s).


F. Treatment:
Most Pasteurella isolates are sensitive to penicillin. Only
sulfaquinoxaline and tetracycline have known withdrawal times and can
be used for rabbits raised for slaughter.

Short term use of
certain oral antibiotics, such as ampicillin or amoxicillin, or
prolonged systemic antibiotic therapy with any drug may upset the cecal


If anorexia or diarrhea occurs during therapy, stop treatment immediately.

Dietary
supplementation with high fiber foods, such as alfalfa cubes or high
fiber pelleted diets, or with yogurt containing live Lactobacillus
cultures may reduce intestinal upsets.

TABLE 1: Antibiotics Commonly Dispensed for Rabbits

Enrofloxicin 2.5 to 5 mg/kg b.i.d. for 5 to 7 days (oral and injectable)

Procaine penicillin 40 to 60,000 IU/kg body weight IM s.i.d. for 3 to 10 days

Sulfaquinoxaline 0.256 gm/50 gm feed for 30 days or 226 gm/ton of feed

Tetracycline 300 mg/liter of water for 7 days, or 5 mg/kg q.i.d. for 7 days


G. Control: The best control for pasteurellosis is good husbandry techniques and culling of rabbits with clinical disease.

Since
most all rabbits carry Pasteurella multocida in the nasal cavity,
management measures are aimed at controlling the clinical disease
expression.

The rabbitry must have good ventilation, low
ammonia levels, and low humidity to decrease incidence of this disease.
In a breeding colony situation, all infected rabbits with clinical
disease should be culled for many reasons.

(In spite of antibiotic therapy, the chance of disease recurrence is high.

Rabbits with clinical signs shed large numbers of organisms into the environment.

The best way to improve the genetic hardiness is to remove breeders with clinical disease.)


Clean
automatic waterers and cages in which diseased rabbits were housed and
then spray with 1% bleach solution to kill residual bacteria.

(Bleach will eventually damage galvanized caging, so alternative disinfectants can be used.)

All new arrivals should be quarantined prior to introduction into the rabbitry.


If possible, weanling rabbits should be raised separately from the breeding colony.

II. Bordetellosis

A. Etiology: Bordetella bronchiseptica is a small gram-negative, alpha-hemolytic, nonfermenting rod.

Incidence of infection is high with a low incidence of disease.


B. Transmission: Routes of transmission include aerosol and direct contact.

Many rabbits are asymptomatic carriers, and may harbor both Bordetella and Pasteurella.


C. Clinical Signs: Signs are similar to snuffles and include upper respiratory infection with serous to mucopurulent nasal exudate and sneezing.

Pneumonia uncommonly develops.


D. Gross Pathology: The characteristic lesion is erythematous nasal mucosa with adherent exudate.


E. Diagnosis: Definitive diagnosis is made by culture of the organism.

Smear and gram stain of nasal exudate may be helpful.


F. Treatment: Enrofloxian (2.5 to 5.0 mg/kg bid for 5 to 7 days),

oxytetracycline (0.1 mg/ml drinking water)

or Tylosin (2 to 4 mg/kg IM b.i.d., then s.i.d. for 3 to 5 days)

are effective in reducing clinical signs.

As with pasteurellosis, antibiotic therapy may have to be repeated when rhinitis recurs, which may happen.

Antibiotic therapy does not eliminate the carrier state.


G. Control:
Isolation and treatment of sick animals, decreasing stressful
conditions, and preparation of and vaccination with an autogenous
bacterin are all adequate control measures.

The bacterin may not eliminate the carrier state, but may help prevent expression of clinical disease.



BACTERIAL DIARRHEAL DISEASES


The
initial approach to treating diarrhea in a rabbit is similar to that
used for companion animals, and is similar for all infectious
etiologies.

Obtaining a thorough history is imperative.
Questions to ask include recent changes in the rabbits' environment,
husbandry, diet, including supplemental foods, antibiotics or home
remedies. Even the addition of a new pet, especially a carnivore, can
serve as a sufficient stressor.

A diagnostic workup should include a complete physical exam

including
abdominal palpation, fecal flotation for coccidia, and fecal cultures.
Ancillary tests may include blood work, and abdominal radiographs
(plain and contrast studies) if warranted.

Supportive therapy
should be directed at correcting and maintaining hydration (via
parenteral and oral fluid therapy) and stimulating the appetite in an
attempt to restore normal gut flora using live yogurt cultures and
fiber-containing treats.

Antibiotics should be judiciously used as they may further upset the gut flora.



III. Colibacillosis


A. Etiology:
Escherichia coli is a gram-negative, lactose-fermenting, indole
positive rod. Rabbits are known to be affected by non-toxin producing,
enteropathogenic E. coli (EPEC). EPEC adhere to the intestinal mucosa
through a 2-step process.

First, a bacterial pilus first allows attachment of the bacterial cell to the enterocyte.

Second, a more intimate attachment through the eae pathogenicity island disrupts the cytoskeleton and destroys microvilli.

A secretory diarrhea is induced by an unknown mechanism.

Receptors
for EPEC attachment to the epithelial cells are not present in newborn
rabbits. They first appear at 21 days and reach normal adult levels by
35 days.

The stress of weaning and loss of passively acquired maternal antibody contribute to susceptibility at this time.

B. Clinical Signs: Rabbits have diarrhea, fever, anorexia, and may consume more water than usual.





C. Pathology: Fecal-stained perineal fur and fluid-filled intestinal contents with serosal vascular injection are seen.

Mild or subclinical disease is common.

Reluctance to breed and decreased reproductive efficiency may occur.


D. Diagnosis:
Serological tests to identify antibody in actively or recently infected
rabbits include the hemagglutination test, Rapid Plasma Reagin (RPR),
or fluorescent treponema antigen preparation. (FTA).

T. paraluis cuniculi may be found in histosections with silver stain or with darkfield microscopy of fresh specimens.


E. Treatment: A regimen of procaine penicillin, 40,000 IU IM s.i.d. for 3 to 5 days is curative.

Once the spirochete is eliminated, serum antibody drops gradually to undetectable levels.

F. Control: If spirochetosis is a herd problem, treat the entire herd.

Do not breed infected animals.

If
animals are for meat production, do not treat weanlings or fryers;
treat only breeding stock. Maintain a closed breeding colony or
quarantine and medicate new arrivals.

Recovered animals can be used as breeding stock without danger of transmitting infection.

VII. Proliferative Ileotyphlitis


Chronic
diarrhea with wasting and a proliferative enteritis in rabbits have
been associated with infection with a Lawsonia-like organism.

The
bacterium can be demonstrated within ileal or cecal enterocytes by use
of silver chemical stains or amplified by a Lawsonia-specific PCR
assay..

There is little known about the disease pathogenesis,
but the etiologic agent (and the resultant disease) is similar to that
of proliferative enteritis of swine.

Concurrent diseases or
stressors seem to be associated with development of the proliferative
enteric lesion with intracellular bacteria.

Oral administration of kaolin may be helpful when this infection is suspected.



VIII. Salmonellosis


A. Etiology: Salmonella enterica serovars are Gram-negative aerobic, nonlactose fermenting, H2S producing rods.


B. Transmission:
Salmonellae are transmitted by ingestion through direct contact with
contaminated feces, food or fomites. Incidence of infection is rare.


C. Clinical Signs: Acute disease is characterized by anorexia, fever, dehydration, diarrhea (hemorrhagic), death, and abortions.

Rabbits that recover from acute disease are asymptomatic shedders.


D. Pathology:
Lesions are consistent with those of septicemia and include congestion
and hemorrhage of the viscera associated with septicemia, ulcerative
colitis, and focal necrosis of liver.


E. Diagnosis:
Definitive diagnosis is made by isolation of the bacteria through
culture of blood, spleen, mesenteric lymph nodes and feces on selective
media (brilliant green, selenite, citrate, or tetrathionate).


F. Treatment: Since antibiotic therapy does not eliminate bacterial carriage, it is advisable to eliminate the colony and restock.


G. Control:
Good management practices will prevent infection. Disinfection,
replacement with clean stock and prevention of wild bird or rodent
contamination of bedding, water, or food should prevent future or
continued problems.


Public Health Significance: Man can contract Salmonella from infected rabbits.



IX. Tularemia


A. Etiology: Francisella tularensis is a Gram-negative, pleomorphic rod.

B. Transmission:
Blood sucking arthropods (squirrel flea, deerfly, mosquitoes, lice, and
woodticks) may serve as mechanical or biological vectors.

Transmission may occur by direct contact, ingestion, or aerosol (rare). The incidence of infection in domestic rabbits is rare.


C. Clinical Signs: Depression, anorexia, ataxia, and death are the nonspecific signs associated with this disease.


D. Gross Pathology:
Widespread visceral congestion, splenomegaly, consolidated and
congested lungs, and multiple pinpoint white foci on the liver and
spleen are characteristic lesions.

E. Diagnosis: Necropsy findings, and bacterial isolation are recommended diagnostic measures.


F. Treatment: There is no treatment.


G. Control: Elimination or control of vectors and wild mammal populations will prevent exposure.

Public Health Significance: Man is susceptible to infection.

Transmission
can occur by ingestion of contaminated water, penetration of unbroken
skin or contamination of cutaneous wounds, tick bites, or by
aerosolization of the organism in dust, feces, or when skinning wild
rabbits.

Human tularemia is manifest by cutaneous lesions, septicemia, and/or meningitis

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

A. Hepatic Coccidia




1. Etiology: Eimeria stiedae

2. Transmission:
Ingestion of sporulated oocysts (unsporulated in freshly voided feces)
is the mode of transmission. The incidence of infection is moderate to
high.

3. Pathogenesis:
Eimeria stiedae excysts in the duodenum, travels to the liver via the
bloodstream or lymphatics, and invades epithelial cells of bile ducts
to begin schizogeny.

4. Clinical Signs:
Signs predominate in young rabbits and may include anorexia,
debilitation, and pendulous abdomen with hepatomegaly noted on
abdominal palpation. Mortality is low except in young rabbits.

5. Pathology:
An enlarged liver with multifocal, flat, yellow-white lesions
containing yellow exudate and occasionally a distended gallbladder that
contains bile may be seen at necropsy

6. The pathognomonic microscopic lesion
is marked periportal fibrosis surrounding enlarged bile ducts lined
with hyperplastic bile duct epithelium that harbors inflammatory cell
infiltrates, and E. stiedae macrogametes, microgametocytes and oocysts.


7. Diagnosis: An antemortem diagnosis can be made by examination of feces by direct smear, flotation or concentration/flotation methods.

It
can be difficult to identify E. steidae oocysts in fecal specimens
since they may not be readily shed in the bile. On necropsy, the
recognition of the flat liver lesions and identification of oocysts in
the bile provide diagnostic information.

The histological
appearance of liver with identification of intraepithelial coccidial
organisms will allow diagnosis from tissue biopsies.

8. Treatment:
Drugs approved as coccidiostats for rabbits used for meat in US include
sulfamerazine (0.02% in water), sulfaquinoxaline (0.05% in water or
0.03% in feed), sulfamethoxine (75 mg/kg BW in feed), and lasalocid
(68-113 gms per ton of feed).

Hepatic coccidia are difficult
to eliminate with anticoccidial therapy, and lasalocid has been the
most successful of the listed drugs in treating hepatic coccidiosis.

9. Control:
Rabbits should be housed on wire-meshed floors. Bottoms of cages are to
be brushed daily to remove adherent feces, and cleaned and disinfected
regularly (1% chlorox). Weanlings should be raised separate from
adults. Feeding fresh greens or hay will prevent use of forage that may
be contaminated with droppings from wild rabbits.

B. Intestinal Coccidia




1. Etiology:
Eimeria magna, Eimeria irresidua, Eimeria perforans, and Eimeria media
are frequently observed pathogenic species. All species infect the
intestinal tract and replicate in the absorptive epithelium of the
mucosa.

2. Transmission: Transmission occurs by ingestion of sporulated oocysts. Incidence of infection is high.

3. Clinical Signs:
Signs vary and are most severe in young rabbits. Poor weight gain,
diarrhea ranging from mucoid to watery to hemorrhagic, polydipsia and
sometimes acute death are seen. Older rabbits may shed coccidial
oocysts without expression of clinical disease.

4. Gross Pathology:
Fluid intestinal contents are often observed in heavily parasitized
rabbits. One may see multiple white patches or ulcers on mucosal
surface of the small or large intestine.

5. Diagnosis: Antemortem diagnosis can be made by examination of feces by direct smear, flotation or concentration/flotation methods.

A
postmortem diagnosis can be made on examination of mucosal scrapings
and by observation of coccidial organisms on histological sections of
intestine.

6. Treatment:
As mentioned in the above section, drugs approved as coccidiostats for
rabbits used for meat in US include sulfamerazine (0.02% in water),
sulfaquinoxaline (0.05% in water or 0.03% in feed), sulfamethoxine (75
mg/kg BW in feed), and lasalocid (68-113 gms per ton of feed) have been
provided in schedules of 3-weeks-on / 3-weeks-off periods.

7. Control:
Rabbits should be housed on wire-meshed floors. Bottoms of cages are to
be brushed daily to remove adherent feces, and cleaned and disinfected
regularly (1% chlorox).

Weanlings should be raised separately from adults.

Feeding fresh greens or hay will prevent use of forage that may be contaminated with droppings from wild rabbits.



II. Encephalitozoonosis

A. Etiology:
Encephalitozoon cuniculi (once called Nosema cuniculi) is a
microsporidian parasite, 2.5 x 1.5 micrometers (oval) with thick wall.

B. Transmission: E. cuniculi is shed in the urine and has been experimentally transmitted by direct contact (ingestion, aerosol).

C. Clinical Signs:
Usually there are no clinical signs (latent infection); however, in
heavy infections there may be torticollis, convulsions, tremors,
posterior paresis, and edema.

D. Pathology: In acute cases the kidneys are swollen.
Chronic lesions are more commonly seen and include multifocal, pinpoint, white, pitted areas on the surface of the kidneys.
Histological
examination of kidneys and brain will reveal a granulomatous
interstitial reaction with fibrosis in the kidney and focal granulomas
in the brain (white arrow) with perivascular plasma cell cuffs and
nonsuppurative meningitis.

The organism may be found in renal tubular epithelial cells or in microglia in the brain.

Encephalitozoon
stains poorly with hematoxylin and eosin stains, but is Gram-positive
(black arrow) and refractile when viewed with polarized light.

E. Diagnosis:
Diagnosis is provided by histopathologic demonstration of organisms and
serologic detection of antibody via ELISA and indirect fluorescent
antibody tests.

Most research animal diagnostic laboratories offer an ELISA or FA test.

F. Treatment and Control: No treatment is effective.

Control
is difficult in colonies, especially breeding colonies. Housing rabbits
on wire and placing the cages away from contact with walls and in
single rows (no stacking) may prevent cage-to-cage urine contamination.


Rabbits will seroconvert 30 days prior to shedding sporocysts
in urine, so a strict program of culling seropositive rabbits can be
instituted based on results of serologic screening every 2 weeks.

Public Health Significance: Encephalitozoon cuniculi has been diagnosed in immunosuppressed humans.

The direct association between rabbit ownership and infection has not been documented.



III. Passalurus ambiguus

The rabbit pinworm does not cause clinical disease in infected rabbits.

The rabbit pinworm has a direct life cycle and adult pinworms reside in the cecum and large intestine.

The males are 4.1 mm long, 300 mm in diameter with a single curved spicule.

The females 6.6 mm long with long tail posterior to vulva (see photo).



The eggs are flattened on one side.

Treatment with
piperazine adipate (0.5 gm/kg to 0.75 gm/kg s.i.d. for 2 days in food
or water) is effective. Ivermectin at 0.2 mg/kg is most likely
effective.

Control of infection is aimed at preventing ingestion of contaminated feces.



IV. Baylisascaris procyonis

Infection of rabbits with the raccoon ascarid, Baylisascaris procyonis,

occurs by ingestion of bedding or hay contaminated with raccoon feces. Reports of this nematode as a rabbit pathogen are increasing.

Clinically infected rabbits display torticollis, ataxia, tremors, and falling (loss of balance).

At necropsy,
multiple, white raised nodules in the epicardium, endocardium and
serosal surface of the liver may be seen. Larval granulomas and
multifocal necrosis in the cerebrum and cerebellum, and larval
granulomas and tracks in the viscera are typical histologic lesions.

Cross sections of larvae with cuticular alae are often visualized in brain sections.

Diagnosis is made from clinical signs and the presence of larvae in histosections.

Treatment has not been attempted.

Efforts to prevent infection include use of clean bedding and hay.



V. Cestodes

Wild rabbits are definitive and intermediate hosts for a number of tapeworms.

The life cycles of these parasites practically precludes infection of domestic or laboratory rabbits.

Taenia pisiformis infections are very common in wild rabbits and are found occasionally in domestic rabbits.

The stage found in rabbits is a cysticercus.

Most cysticerci are found in the liver or attached to the mesentery and cause little damage.

A second taenid found in rabbits is T. serialis.

The stage of the cestode seen in rabbits is a coenurus which occurs in connective tissue of muscle.

Infection in wild rabbits is less common than T. pisiformis and is extremely rare in domestic rabbits.

The dog is the definitive host of both cestodes.



VI. Mites


A. Psoroptes cuniculi - ear mite

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

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.

California Strain of Virus:
In the peracute form, rabbits die within a week of exposure showing
slight edema of the eyelids and depression immediately prior to death.

With
the acute form in which rabbits survive for 1 to 2 weeks, symptoms are
edema of the eyelids resulting in a droopy appearance of the eye;



inflammation and edema around the anal, genital, oral, and nasal orifices; skin hemorrhages; and convulsions.

A nodular lesion develops at the site of inoculation with both forms, but it is not a clearly defined tumor.



Standard Laboratory Strain of Virus:
This strain induces a mean survival time of 11 days. Around 3 to 4 days
post inoculation, a primary tumor becomes evident, and generalized
tumors are seen on the 6th or 7th day.



At
this time, a mucopurulent nasal discharge and pronounced edema of the
eyes and base of the ears are seen. By day 10, hard lumps cover much of
the body.

European Strain of Virus: This strain is characterized by rapid proliferation of large lumps by day 7.

The lumps may break open by day 10 and release a serous discharge. Lumps may occur on any area of the body.

There
is also pronounced edema of the face and anal regions, seropurulent
discharge from eyes and nose, and considerable skin congestion.

D. Pathology: The most prominent gross lesions are skin tumors and pronounced cutaneous and subcutaneous edema.

Skin hemorrhages and subserosal petechial and ecchymotic hemorrhages in the stomach and intestines may be observed.

Various degrees of congestion will occur in the visceral organs depending on the severity of the disease.

Skin
tumors result from an initial proliferation of undifferentiated
mesenchymal cells in the dermis which become large stellate cells
termed myxoma cells.

These cells lie in a homogeneous matrix of mucinous material.

Necrosis can be observed in the center of this area.

Epidermal
cells overlying the tumor may appear normal in early stages of the
tumor proliferation, or they may show hyperplasia or degeneration in
later stages. Intracytoplasmic inclusions (arrows) are observed most
commonly in cells of the prickle-cell layer of the epidermis, and in
the stellate myxomatous cells.

F. Diagnosis:
A diagnosis can be made from the clinical and pathological picture,
virus isolation, and PCR amplification of viral sequences from tissue
specimens. Serological tests including fluorescent antibody techniques,
plaque-neutralization, and ELISA have been developed but are not
commercially available.

G. Control:
Control is achieved through vector control and adequate screening of
the rabbitry, by quarantine of new animals, and isolation of all sick
animals.

A common practice, once a death from myxomatosis is
diagnosed, is to cull all rabbits whose body temperature exceeds 104oF
in an attempt to remove animals incubating the virus before shedding
occurs.

A vaccine was developed but has not been used as the vaccine caused clinical myxomatosis in some vaccinated rabbits.



II. Rabbit (Shope) Fibroma Virus

A. Etiology:
Fibroma virus is a member of the leporipoxvirus group and is closely
related to myxoma virus. The virus has widespread incidence in both
domestic and wild rabbit populations.

Few cases of
virus-induced fibromas have been diagnosed in rabbits in Missouri
although the majority of cases are reported from the western and
southwestern United States.

B. Transmission: The natural transmission cycle is not known although arthropod vector transmission is likely.

C. Clinical Signs: Tumors occur on the legs or feet, on the muzzle, and around the eyes.

The tumors are subcutaneous and not attached to underlying tissue.



Metastases from the original tumor do not occur.

The infected adult rabbit remains clinically normal otherwise.

Tumors will typically regress after a period of months.

Spontaneous and experimental infections of neonatal domestic rabbits, however, has produced cutaneous and visceral tumors.




D. Pathology:
The earliest lesion is slight thickening of the subcutaneous tissue
followed by development of clearly demarcated soft tissue swellings
which are evident on day 6 post inoculation. Tumors increase in size
until day 12. They persist for months before regressing.

The earliest microscopic lesion is an acute inflammatory reaction followed by localized fibroblastic proliferation.

Proliferation
continues until a distinct tumor is formed consisting of spindle-shaped
and polygonal connective tissue cells with abundant cytoplasm.

Intracytoplasmic
inclusions are present in stellate cells, and less commonly or rarely
in the epidermal cells. Degeneration of the epidermis overlying the
tumor may result from pressure ischemia.

This leads to necrosis and sloughing of the epithelium.

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

G. Control: This is not considered to be an important problem in domestic rabbits. In outdoor rabbitries, vector control is advised.

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 (Trichobezoar)



A. Etiology:
Hairballs can form in the stomach as the rabbit grooms itself or a
cagemate. Insufficient fiber in the diet can also lead to increased
hair consumption.

Incidence of hairball formation is high
although abnormal digestive function pribably rarely occurs unless the
hair ball is extensive.

B. Clinical Signs:
Generally, hairballs are not a problem and are found incidentally at
necropsy. Occasionally, they will cause a partial or complete
obstruction; these hairballs may be palpable, and the rabbit will stop
eating and lose weight.

The rabbit may be bright, alert and afebrile with a history of anorexia and lack of feces excretion of several days duration.

C. Diagnosis: Palpation and contrast radiography may be used.

D. Treatment: Treatments are centered on correcting dehydration and re-establishing normal gut function.

Rehydrate rabbit and administer enteral protectants.

Administration
of metaclopromide (0.3 mg/kg SQ every 8 hours) will help stimulate
peristalsis, and often will stimulate the rabbit's appetite.

Past
recommendations of feeding fresh pineapple juice at 10 to 15 ml orally
once or twice daily for 5 days may provide an energy source but it is
unclear whether the cellulitic activity of the papain eliminates the
hairball.

Force feeding of pulverized food in water or yogurt may help stimulate the appetite.


E. Prevention: Diets high in plant fiber has dramtically reduced the incidence of the clinical syndrome.



II. Traumatic Vertebral Fracture (Paralysis of the Hindquarters, Broken Back)



A. Etiology: This condition has a sudden onset and coincides with struggling or inadequate support of the hindquarters when handling.

Frequently, the incident is not observed (or recognized), and the rabbit is found paralyzed in the cage.

The occurrence is frequent.
B. Clinical Signs:
Posterior paralysis or paresis, loss of skin sensation, and loss of
motor control of anal sphinctor and urinary bladder are typical signs.

C. Pathology: The most common site of fracture is the L7 lumbar vertebral body or its caudal articular processes.

D. Diagnosis: The diagnosis is made with clinical signs, neurological examination and/or radiography.

E. Treatment:
If bladder and anal sphinctor control remain intact, and there is still
hind limb pain perception, complete recovery may occur within 2 to 4
weeks with cage rest.

Surgical correction and fixation of the fracture is not recommended because of the fragility of the bones.



III. Mucoid Enteropathy (ME) Complex or Cecal Dysbiosis



A. Etiology: The cause(s) of the ME disease complex is not well defined and the disease is uncommon..

However,
multiple factors including diet, intestinal flora and the shift from
neonatal to adolescent digestive physiology are thought to contribute
to development of the disease.

Diets low in fiber (<10%)
result in a higher incidence of ME. Escherichia coli, Clostridia sp.
(C. welchii type A, C. perfringens) have been associated with ME.

Coccidiosis has also been incriminated in potentiating or triggering ME.

Search for viral agents has been unsuccessful.

Reproduction of the disease by causing cecal impaction with subsequent bacterial toxin production, has been successful.

B. Clinical Signs:
There is acute onset of disease in 7 to 10 week old rabbits
characterized by anorexia, polydipsia, a subnormal body temperature
(99o-102oF), a rough hair coat, mucoid to liquid, tan diarrhea with
perineal staining, and abdominal distention with gas and fluid-filled
intestines.

Affected rabbits may grind their teeth.

Death usually occurs in 2 to 4 days.

Rabbits usually survive the protracted course of 7 to 14 days.

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

The characteristic lesion is goblet cell hyperplasia
with no inflammatory response in the small and large intestines;
occasionally see goblet cell hyperplasia of gallbladder, pancreatic and
bile duct epithelia, and tracheal epithelial cells may be noted.

D. Diagnosis: Diagnosis is based on clinical signs, gross lesions, and histopathology.

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

F. Control:
Provision of high fiber feeds (18 - 20 % fiber) drastically reduces the
incidence of mucoid enteropathy. Rabbits received after shipping should
not be fed the first day.

A small amount of a high fiber diet may be fed the next day, with a gradual increase to a full ration by day 5.

a

IV. Enterotoxemia



A. Etiology:
Clostridial species, principally C. difficile and C. spiroforme,
proliferate and produce toxins to induce this disease. Clostridial
exotoxins induce secretory and vascular effects.

A history of
antibiotic therapy with broad spectrum antibiotics including oral
ampicillin, clindamycin or lincomycin, may be associated with this
disease.

Clostridial enteritis may occur in rabbits that have
not been treated with any antibiotics. Diets high in carbohydreates
enhance the overgrowth of Clostridium species.

Change in gut flora and other stressors leading to anorexia may predispose to disease.

B. Clinical Signs: Sudden death with no previous signs of illness or watery diarrhea 2 to 3 days prior to death are the usual signs.

This disease affects all ages, but primarily targets recently weaned rabbits.


C. Pathology:
Prominent gross lesions observed include in a large, fluid-filled
edematous cecum with serosal congestion and hemorrhage and watery
mucoid feces in the colon (A.).

Microscopically, severe
lesions include a necrotic erosive or ulcerative typhlitis with
swelling and loss of enterocytes and pseudomembrane formation (B.).

The mucosa and submucosa are infiltrated with heterophils and there is submucosal edema and hemorrhage.

Large Gram-positive bacilli with spores can often be observed on the mucosal surface.

D. Diagnosis:
Diagnosis is achieved by the history of antibiotic treatment or
environmental/dietary stressors, and isolation or PCR amplification of
Clostridium species from cecal contents.


An antigen
capture ELISA is available for cytotoxins A and B of C. difficile. C.
spiroforme may be seen as a spiral bacillus on a direct smear.


E. Treatment:
Due to the acute course of the disease, there is usually no treatment.
Supportive fluid therapy, kaopectate, and yogurt may be helpful.

F. Control: Do not use lincomycin or clindamycin in rabbits. Eliminate extreme dietary changes and minimize environmental stressors.



V. Heat Prostration

Rabbits
are very sensitive to heat. Tachypnea, cyanosis, prostration, and
blood-tinged fluid on nose and mouth may be observed with heat
prostration. Temperatures above 95oF can be dangerous.

The rabbit should be immersed in cool water, or covered with alcohol or water soaked cloths.

The rectal temperature should be monitored to ensure reduction of body heat and to prevent induction of hypothermia.

Housing in shaded areas provided with fans or water sprays in hot weather will keep rabbits cool.

Limit feeding of rabbit food will prevent obesity, which may be an additional predisposing factor to overheating.



VI. Sore Hocks (Ulcerative Pododermatitis)




Sore hocks occur because of pressure necrosis of the skin from bearing a heavy body weight on a hard or wire surface.

There is genetic predisposition in breeds such as the Rex which have poorly furred footpads and rounded metacarpal bones .

Common findings are circumscribed ulcers over the metatarsus and metacarpus, covered by a scab.

There may be purulent exudate under the scab.

Severely affected rabbits may be anorexic, debilitated, and die.

Use
soft dry bedding, a resting board in wire cages, and topical zinc and
iodine ointments or an antibiotic ointment if secondarily infected.

Use systemic antibiotics if abscesses are present or if the rabbit is debilitated.

Cull affected animals and do not use for breeding stock.

Decrease environmental humidity.

Caution: Fecal pellets need to be brushed off the resting board daily to prevent ingestion of infective parasite ova/oocysts.




VII. Dermatophytosis




A. Etiology: Trichophyton mentagrophytes is an opportunistic, ubiquitous fungal soil organism.

B. Incidence: There is high incidence of the carrier state, with low incidence of disease.

C. Clinical Signs:
A crusty, pruritic, patchy alopecia on the head which spreads to the
paws and other parts of the body is typical (see photo). Secondary
bacterial infections are common.

D. Diagnosis:
Diagnosis is based on clinical signs, scraping and identification of
spores on hair shaft or mycelia within hair shaft, and culture on
Sabaraud or DTM agars.

E. Treatment:
Topical treatment with a fungicide (Tresiderm, Iodine, Conofite cream)
or griseofulvin (25 mg/kg in aqueous suspension or 0.375 gm powdered
form/lb food for 14 days) has been successful. Topical 10% chlorox
solution is also effective. Griseofulvin therapy should be used with
caution in breeding herds, as the incidence of teratogenesis is
associated with treatment.

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

There
is a possibility of transmission of infection to people handling the
rabbits, so gloves should be worn when treating the rabbits.
Ventilation should be improved to decrease the relative humidity, and
all filters, water pads, curtains/blinds or other materials used to
control the air temperature should be replaced weekly to prevent
collection of fungus spores.

Public Health Significance: People handling rabbits with T. mentagrophytes induced lesions have developed dermatophytosis.



VIII. Pregnancy Toxemia



A. Etiology:
The pathogenesis of pregnancy toxemia is not well known, but may be
similar to ketosis in sheep. Predisposing factors include breed, age,
sex, obesity, and number of previous litters.

There is a high incidence in some rabbitries.

B. Clinical Signs: Signs range from a mild, nearly asymptomatic condition to a severe, rapidly fatal disease.

The
most common signs are depression, dyspnea, acetic odor to the breath,
decreased urine production, abortion, CNS signs, and sudden death just
prior to or just after kindling.

C. Pathology: Gross lesions are general obesity, areas of necrosis in the mesenteric fat, and pale yellow liver, heart, and kidneys.

Fatty changes are seen microscopically in the liver, heart, and kidneys.


D. Control:
Weight gain in breeding and non-pregnant does should be monitored, and
controlled by limiting the amount of feed they are allowed to consume.



NEOPLASTIC DISEASES

I. Uterine Adenocarcinoma
II. Lymphosarcoma
III. Miscellaneous Neoplastic Diseases



The incidence of spontaneously occurring tumors in rabbits is generally low.

Only recently has the pet rabbit population survived long enough to permit data collection on tumor incidence.

As
with other species, tumor incidence is influenced by such factors as
age, breed predilection for certain tumors, breed resistance, and sex.



I. Uterine Adenocarcinoma




The most common tumor of rabbits is the uterine adenocarcinoma.

Females with this tumor have a history of reproductive disturbance prior to detection of the tumor.

Fertility
is diminished, litter size is reduced, stillbirths are more numerous,
and desertion of the litter by the doe is common.

Other symptoms are dystocia, fetal retention in utero, abdominal pregnancy, and fetal resorption.

The period of altered reproductive function precedes tumor detection by 6 to 10 months.

The duration in time between clinical detection and death (usually post-metastasis) is 12 to 24 months.

Uterine nodules can be palated or observed on radiographs or laparatomy.
Histologically,
the events of the tumor progression are characterized by increasing
degrees of epithelial cell dedifferentiation and anaplasia with
increase of the vascular, myxoid stroma.

There is loss of cellular elements such as cilia and secretory vesicles.

Areas of necrosis are not uncommon in mature tumors.

The
incidence of neoplasia is most common in New Zealand rabbits but has
been observed in other rabbit breeds. Ovariohysterectomy is the
preventative measure that not only eliminates the source of the most
common cancer, but also prevents the undesirable behavioral changes
that often accompany sexual maturity in pet does.



II. Lymphosarcoma




The second most common rabbit neoplasm is the lymphosarcoma.

Susceptibility to the disease is believed due to an autosomal recessive gene expressed in the homozygous state.

It is considered a tumor of juvenile and young adult rabbits.

A tetrad of necropsy lesions considered pathognomonic for lymphosarcoma in the domestic rabbit are

1) enlarged kidneys, light tan in color with irregular lumpy surface, and thickened cortex but normal medulla;

2) hepatomegaly with a diffuse pattern of small pale foci;

3) splenomegaly; and

4)
lymphadenopathy, in which all of the lymph nodes in the body may be
involved in the neoplastic process. Histologically, the normal
architecture of the nodes is obliterated by masses of infiltrating
neoplastic lymphoblasts.

III. Miscellaneous Neoplastic Diseases


Other
commonly reported tumors of the rabbit are embryonal nephromas, bile
duct adenomas, mammary gland papillomas, mammary adenocarcinomas, and
squamous cell carcinoma.

The latter tumor has been mentioned previously in conjunction with Shope papilloma virus (SPV).

One type of squamous cell carcinoma occurs if the SPV produces a papilloma that lasts over 200 days.

At this point, spontaneous change from papilloma to squamous cell carcinoma occurs.


Other
tumors also caused by oncogenic viruses (Shope fibroma virus, oral
papilloma virus, and myxoma virus) have already been discussed.

Some
other tumors that have been reported infrequently in the rabbit include
tumors of the endocrine glands, melanomas, plasma cell myelomas,
thymomas, osteosarcomas, osteochondromas, renal carcinomas, basal cell
adenomas, leiomyomas, and leiomyosarcomas.



Inherited diseases

I. Malocclusion
II. Buphthalmia
III. Splay Leg
IV. Hydrocephalus



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 4" per year, it is necessary to clip them
(but not too close) every 6 to 8 weeks. Dog nail clippers (Rescoe or
White styles), bone or wire cutters and a rotary tool with disc
attachment (shown in photo) may be used to trim teeth. Care should be
taken to prevent shattering the incisors. .



II. Buphthalmia




This disease is 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. Affected individuals should be removed from the breeding colony.



III. Splay Leg



Splay
leg is a familial or polygenic condition with varying clinical
manifestations. Affected nursing 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.



IV. Hydrocephalus