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ORDER: Lagomorpha
FAMILY: Laporidae
GENUS: Oryctolagus
SPECIES: cuniculus
OTHER GENERA: Lepus (hares) and Sylvilagus (cotton-tails)
ORIGIN: Western Europe and North-West Africa
Large breeds (5 kg and over), e.g., Flemish Giant and Checkered Giant.
Medium breeds (2- 5 kg), e.g., New Zealand White and Californian.
Small breeds (under 2 kg), e.g., Dutch and Polish breeds.
Short tail, hindlimbs longer than forelimbs, coprophagus, rarely bite, but will scratch with hindlegs if not properly restrained, mature bucks housed together will bite at the testes, induced ovulators, vegetarian, light skeleton prone to fractures, turbid alkaline urine. Ears are highly vascularized and serve in heat regulation and in sound gathering.
Female - 4-12 months; Male - 5-12 months
6 months (6-10 lbs)
Any time of the year
Polyestrus
Induced ovulator (has 1-2 day loss of receptivity every 4-17 days)
Accepts male anytime except with loss of receptivity
28-36 days (average 31)
4-10 (average 7-8)
4-5 litters per year
Induced by copulation; occurs 10-13 hours post coitus
Immediately after birth (usually not rebred at this time
Common; lasts 15-17 daysCHROMOSOME NUMBER: Diploid, 44
30-100 grams
4-8 weeks
2/5 kg (depends on breed)
1/3 years
1/3 years
5-15 years (depends on breed)
1 buck for 10 does (females brought to male's cage)
101.1o F (39.5o C)
38-60 breaths/minute
187-240/minute (varies with age, sex, size)MAMMAE: 3-5 pairs
Minimum: Up to 2 kg: 1.5 feet22-4 kg: 3.0 feet2
Over 4 kg: 4.0 feet2
Height: 14 inches
Temperature: 65-75o FHumidity: 50-60%
Light: 14 hours per day
Commercial rabbit diet fed ad libitum unless obese. High fiber (25%) diet helps in weight loss (not fed to pregnant or lactating does). Consider limited feeding to control obesity.
5 grams per 100 grams body weight per day.
5-10 ml per 100 grams body weight per day.
Marginal ear veins, central artery of the ear, heart, saphenous vein, jugular vein
Innovar-VetR (IM): 0.22 mg/kg (give atropine, 0.04 mg/kg, prior to this)Ketamine (IM): 25-100 mg/kg (give 39 minutes prior to Pentobarbital, 45 mg/kg)
Rompun (IM): 9 mg/kg given 10 minutes prior to Ketamine (IM, 40-50 mg/kg).
Inhalation: Methoxyflurane and Halothane
I 2/1 C 0/0 PM 3/2 M 3/3
Bioassay, diagnostic tests, infectious disease research, genetic studies, immunology, physiology, nutritional research, embryology, reproductive studies, eye research, physiological studies.
Grasp the rabbit over the shoulders with one hand while the other hand is used to support the rear legs and body. DO NOT PICK UP RABBIT BY THE EARS. Can be placed in a somnolent state which resembles hypnosis by a manipulative and vocal procedure. Done by rhythmically stroking the abdomen and speaking in a low soothing monotone.
5.5.2.1 Pasteurella multocida:
Causes upper respiratory disease, conjunctivitis, otitis media, cutaneous abscesses, genital infections, septicemia.
Francisella tularensis:
Tularemia - fatal septicemia characterized by white foci on liver, spleen and lymph nodes.
Bacillus piliformis:
Tyzzer's disease
Treponema cuniculi:
Rabbit syphilis - venereal disease causing superficial dermatitis on the genitalia, perineal areas, nose, eyelids and lips.
Fscherichia coli:
"Colibacillosis" diarrhea in young rabbits.
Fusobacterium necrophoruum:
"Necrobacillosis," or Schmorl's Disease - necrosis, ulceration and abscessation of skin and subcutaneous tissues.
Staphylococcus aureus:
Skin abscesses, sneezing, mucopurulent nasal discharge.
Salmonella enteritidis var. typhimurium
VIRAL DISEASES:
Myxomatosis:
Pox Virus - fatal disease transmitted through arthropod vector.
Shope fibroma:
Pox Virus - mosquitoes serve as mechanical vectors - tumors found in subcutaneous tissues.
Rabbit pox: 2 forms; peracute form without lesions and milder acute form with pox lesions.
Oral papillomatosis:
Papovavirus - papillomas occur on mucus membranes, especially on underside of tongue.
Herpesvirus cuniculi:
Causes no known diseases.
5.5.3.1.1 Eimeria stiedae:
Hepatic coccidiosis - signs related to hepatic dysfunction.
Eimeria magna:
Affects jejunum and ileum - most injurious causing necrosis and blood loss.
Eimeria irresidua:
Affects lower duodenum and ileum.
Eimeria perforans:
Least pathogenic - affects small intestine.
Eimeria media:
Small and large intestine affected.
Toxoplasma gondii
5.5.3.1.2 Encephalitozoon cuniculi:
Predilection for kidney and brain - chronic renal infection is randomly scattered pits on cortical surface of kidney.
Sarcocystis cuniculi:
Cysts in skeletal and cardiac muscle.
Arthropods:
Mites:
Psoroptes cuniculi:
Ear mite - crusty material accumulates in external ear.
Cheyletiella parasitivorax;
Rabbit fur mite
Listrophorus gibbus:
Rabbit fur mite
Sarcoptes scabei
Notoedres cuniculi
Louse:
Haemodipsus ventricosis:
Blood sucking - pruritis, anemia
Flea:
Ctenocephalide cuniculi:
Blood sucking - vector of myxomatosis.
Fly:
Cuterebra:
Causes "rabbit warbles" - large lumpy areas with perforated breathing holes on skin.
Nematoda:
Passulurus ambiguous:
Rabbit pinworm
Obelscoides cuniculi:
Stomach worm - causes ulceration of stomach wall.
Trichostrongylus calcaratus:
affects small intestine.
Trichuris leporis:
Whipworm
Capillaria hepatica
5.5.3.3.1 Taenia (Cysticercus) pisiformis:
Larval form of dog tapeworm
5.5.3.3.2 Multiceps (Coenurus) serialis:
Larval form of dog tapeworm
5.5.3.3.3 Taenia (Cysticercus) fasciolaris:
Larval form of cat tapeworm
5.5.3.3.4 Cittotaenia ctenodes:
Diarrhea and emaciation with heavy infection
Most common is uterine adenocarcinoma in aged females.
5.5.6.1 Hydrocephalus
5.5.6.2 Buphthalmia
5.5.6.3 Aortic arteriosclerosis
5.5.6.4 Scoliosis
5.5.6.5 Splay let
Pelger abnormality:
(Due to semidominant gene. Homozygous dominants have skeletal deformity and die in utero)
5.5.7.1 Mucoid enteropathy:
Clear mucous diarrhea.
5.5.7.2 Mycoses: richophyton mentagrophytes
Lesions begin on head and ears and spread to paws
5.5.7.3 Mastitis
5.5.7.4 Sore Hocks: Ulcerative pododermatitis
Results from brushing or chafing planter aspect of metatarsus on hard floors.
5.5.7.5 Traumatic vertebral luxation:
From improper handling
5.5.7.6 Hutch burn and wet dewlap:
Cutaneous surface is wet in the presence of microorganisms causing superficial dermatitis.
5.5.7.7 Overheating (Heat Stroke)
5.5.7.8 Hairball (Trichobezoars)
Vitamin E deficiency: Infertility, neonatal mortality, keratitis and muscular dystrophy
Vitamin D excess:
Increased bone resorption and intestinal absorption of calcium resulting in arteriosclerosis.
Copper deficiency:
Fur chewing, coat color changes, anemia
Nitrates:
Causes abortion
Malocclusion:
Mandibular prognathism
Fiber deficiency:
Less than 6% fiber in diet causes diarrhea
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Pasteurella multocida - small, gm (-), nonspore-forming bipolar rod, non-motile and capsulated.
Direct contact; aerosol and venereal transmission can also occur.
Upper respiratory disease ("snuffles") conjunctivitis, otitis media, enzootic pneumonia, pyometra, orchitis, subcutaneous abcesses and septicemia.
l. Snuffles
a. Clinical Signs:
Serous to mucopurulent nasal exudate with sneezing and coughing. May subside temporarily only to reoccur throughout life.
b. Gross Pathology:
Reddened mucosa in acute infections; thickened muscosa in chronic infections; exudate in nasal cavity and paranasal sinuses.
c. Diagnosis:
Stain smear of nasal exudate; culture; clinical signs.
d. Treatment:
Difficult
1) Systemic antibiotics:
- a) 40,000 IU penicillin IM s.i.d for 3-5 days
- b) 0.256 gm sulfaquinoxaline/500 gm feed for 30 days.
- c) 5 mg furazolidone/l00 gm feed for 30 days.
- d) May cause remission of clinical signs but hard to eliminate carrier state.
2) Aerosal Therapy: spray into nares t.i.d. for 5 days.
- a) Acetylcysteine (mucomist) 20%
- b) Neomycin sulfate solution, 6 mg/ml.
- c) Phenylephrine HCl solution 0.5%.
e. Control:
Reduce environmental stress; isolate young from clinically ill and cull chronically infected does; quarantine new arrivals; improve husbandry; acquire Pasteuralla-free stock.
2. Enzootic Pneumonia
a. Clinical Signs:
Usually acute death with no signs (esp. young rabbits); anorexia and depression.
b. Gross Pathology:
Acute pneumonia - red-grey foci of consolidation with or without hemorrhage; chronic pneumonia - generalized consolidation, encapsulated abscesses, fibrino-or mucopurulent pleutritis; usually accompanies signs of septicemia.
c. Diagnosis:
Usually made post mortem; culture to identify etiological agent.
d. Treatment:
Same systemic antibiotics as for snuffles.
3. Otitis Media
a. Clinical Signs:
Usually none; torticollis or "wryneck" or head tilt if internal ear is invaded; may see nervous signs and incoordination if extends to meninges.
b. Gross Pathology:
Creamy white exudate in middle ear; can be uni- or bilateral.
c. Diagnosis:
Radiograph tympanic bulla; if tympanic membrane has ruptured, stain exudate smear and culture. Post mortem. Otoscopic examination of tympanic membrane.
d. Treatment:
Suggested therapy - tympanocentesis with Betadine solution flush t.i.d. along with systemic penicillin; bulla osteotomy has been attempted.
e. Control:
Same as for Snuffles.
4. Genital Infections
Pyometra in female; orchitis or balanopasthitis in male.
a. Transmission:
Venereal, hematogenous.
b. Clinical Signs:
May or may not see vaginal discharge which may be serous-mucopurulent: infertility; one or both testicles-enlarged and firm; uterus palpably enlarged with pyometra.
c. Gross Pathology:
1) Uterus
- a) acute infection characterized by slightly dilated horns filled with grey exudate.
- b) Chronic infection - greatly dilated and filled with purulent exudate.
2) Testicle
Enlarged and bulge from cut surface; may have abscesses.
d. Diagnosis:
Post mortem: culture vaginal (uterine) discharge; history of infertility; radiograph.
e. Treatment:
Cull infected bucks; clean environment, etc.
5. Abscesses
a. Transmission:
External contamination; septicemia.
b. Clinical Signs:
Subcutaneous swelling with or without draining fistulous tracts.
c. Gross Pathology:
Encapsulated subcutaneous abscesses filled with creamy exudate.
d. Diagnosis:
Aspirate exudate - stain smear and culture.
e. Treatment:
Sedate rabbit, lance and flush t.i.d. with Betadine or chlorhexidine. Systemic antibiotics for l week.
f. Control:
Same as for snuffles.
6. Conjunctivitis
a. Clinical Signs:
Epiphora with blephorospasm or eyelids glued shut with mucopurulent exudate; facial staining.
b. Gross Pathology:
Reddened conjunctiva with serous to mucopurulent adherent exudate.
c. Diagnosis:
Conjunctival scraping - stain and culture.
d. Treatment:
Can use antibiotic ophthalmic ointment (triple antibiotic- Neomycin, Gramacidin, Polymixin B). Can mix acetylcysteine and aqueous Neosporin ophthalmic solution (half and half) and administer q.i.d. Bacteria may reside in nasolacrimal duct - flush.
e. Control:
Same as for snuffles.
7. Septicemia
a. Clinical Signs:
Usually acute death; may see pneumonia or infertility prior to death.
b. Gross Pathology:
Diffuse congestion and petechia of thoracic and abdominal viscera; may see abscesses of viscera, kidneys, liver and lungs.
c. Diagnosis:
Necropsy signs, culture blood or visceral abscesses.
d. Treatment:
None
e. Control:
Same as for snuffles.
A. Etiology:
Bordetella bronchiseptica - small gm (-), Beta-hemolytic, non-fermenting rod.
B. Transmission:
Aerosol; direct contact; can be carried in respiratory tract.
C. Clinical Signs:
Upper respiratory infection with serous to mucopurulent nasal exudate; sneezing.
D. Gross Pathology:
Erythrematous nasal mucosa with adherent exudate.
E. Diagnosis:
Clinical signs; smear and stain exudate; culture.
F. Treatment:
Oxytetracycline 0.l mg/ml of water or Tylosin 2-4 mg/kg (IM) b.i.d., then s.i.d for 3-5 days.
G. Control:
Isolate sick animals and treat; decrease stressful conditions; autogenous bacterin and vaccinate.
A. Etiology:
Pathogenic Staphylococcus aureus - gm (+), Beta hemolytic, coagulase (+) cocci.
B. Transmission:
Aerosol; direct contact (organism present in oral cavity of non-clinical carriers).
C. Clinical Signs:
Wide range of clinical disease forms; can cause suppurative infection in any organ or any site; commonly see subcutaneous abscesses, dermatitis, upper respiratory infection with mucopurulent nasal discharge, mastitis with abscess formation, and septicemia with depression, anorexia, fever, and death.
D. Gross Pathology:
Thick-walled abscesses filled with purulent exudate subcutaneously or in any organ; diffuse congestion and petechiation of viscera in seticemic animals.
E. Diagnosis:
Smear and stain exudate; culture.
F. Treatment:
The organism is sensitive to Penicillin, 40,000 IU, IM s.i.d. for 3-5 days; for subcutaneous abscesses, lance and flush with germicidal solution along with systemic antibiotics.
G. Control:
Improve husbandry: separate fighting animals; isolate and treat clinically ill animals: can culture caretakers.
A. Etiology:
Francisella tularensis is a gm (-), pleomorphic, non-sporeforming rod.
B. Transmission:
Blood sucking arthropods (squirrel flea, deer fly, mosquitoes, lice, and woodticks), can be mechanical or biological transmission; direct contact; ingestion; aerosol (rare).
C. Clinical Signs:
Depression, anorexia, ataxia, death.
D. Gross Pathology:
Septicemia with widespread visceral congestion; spleen enlarged, lungs consolidated and congested: multiple pinpoint white foci on liver and spleen.
E. Diagnosis:
Necropsy findings; guinea pig inoculations (death in 5-l0 days); serum agglutination tests; bacteria culture and gm stain.
F. Treatment:
None
G. Control:
Vector and wild mammal control.
H. Public Health Significance:
Humans are susceptible to infection. Transmission can occur by ingestion of contaminated water, penetration of unbroken skin or contamination of cutaneous wounds, tick bites or to aerosolization of organisms in dust, feces, or when skinning rabbit. Human tularemia is manifested by cutaneous lesions, septicemia, or meningitis.
A. Etiology:
Treponema cuniculi - a spiral-shaped bacteria related to human syphilis organism Treponema palladium.
B. Transmission:
genital most common; extragenital (skin and mucous membrane infection) also has been reported.
C. Clinical Signs:
Erythema of mucous membranes of external genitalia which progresses to focal, raised, crusty ulcerations; can affect perineal area and face (auto-infection). As ulcerations heal, dry scaley condition follows. Spontaneous regression in several weeks.
D. Gross Pathology:
Bacteria only causes superficial, cutaneous pathology. May see some popliteal and inguinal lymph node enlargement.
E. Diagnosis:
Serology - Wassermann test, rapid plasma region card test (RPR) or fluorescent treponema antigen. (FTA). Read histosections with stained with silver or with dark field microscopy.
F. Treatment:
Penicillin, 40,000 IU/Kg IM s.i.d. for 3-5 days.
G. Control:
Don't breed infected animals; periodic observation of breeding animals; closed bleeding colony; can breed recovered animals without danger of transmitting infection.
A. Etiology:
Pseudomonas aeruginosa - gm (-) motile, non-fermenting rod that produces bluish-green pigment; utilizes ammonia.
B. Transmission:
Common water and soil contaminant; an opportunistic pathogen.
C. Clinical Signs:
Non-specific moist dermatitis in soiled, moist areas such as dewlap or groin region; can progress to ulcerative dermatitis, hair or exudate may be bluish-green; lethargy, fever, dyspnea, oculonasal discharge, and death.
D. Gross Pathology:
Ulcerative dermatitis and cellulitis. Septicemia- congestion and hemorrhage of viscera with clear, serosanguinous fluid in thoracic cavity. Also pulmonary abscesses.
E. Diagnosis:
Smear and stain exudate; culture.
F. Treatment:
Clean Infected skin with Betadine or chlorhexidine; topical antibiotic therapy with Neosporin (containing Polymyxin B) : treatment of septicemia tough; supportive therapy if debilitated; Neomycin p.o.
G. Control:
Infection usually result of poor sanitation; improve husbandry; can acidify (pH 2.4) or chlorinate (l0-12 ppm) water source to reduce Pseudomonas contamination.
A. Etiology:
Bacillus piliformis - a gm (-), pleomorphic filamentous organism. Forms spore and is mobile with peritrichous flagella, obligate intracellular organism.
B. Transmission:
Ingestion (focal-oral); carrier state in older animals.
C. Clinical Signs:
Primarily affects weanling rabbits. Acute, profuse watery to mucoid diarrhea, dehydration and death.
D. Gross Pathology:
Enlarged liver with multifocal yellow foci of necrosis; edema and hemorrhage of mucosa, submucosa, and musculature of intestinal tract; hemorrhage of myocardium.
E. Diagnosis:
History, necropsy signs, histopathological examination of liver stained with PAS, Wrights, or Giemsa stains. Look for intracellular organism in viable hepatocytes adjacent to an area of necrosis. Can isolate organism by inoculating homogenized liver grow into the yolk sac of chick embryo. Does not grow on artificial media.
F. Treatment:
Tough; therapy for infected animals not practical. Oxytetracycline 0.l gm/ml water for 30 days in herd situations.
G. Control:
Good husbandry and clean stock. In stress situations use prophylactic antibiotic therapy.
A. Etiology:
E. coli - gm (-) lactose-fermenting, indole (+) rods.
B. Transmission:
None; rapid shift of predominant gm (+) gut flora to gm (-) flora.
C. Clinical Signs:
Acute outbreak of diarrhea in l-3month old rabbits; sudden death (looks like Tyzzer'sdisease).
D. Gross Pathology:
Subserosal hemorrhage in cecum and colon with mucinous contents; may see foci of necrosis on liver and myocardium.
E. Diagnosis:
Culture cecum (pure culture E. coli): inject cell free extract into loop of rabbit ileum (enterotoxin); rule out Tyzzer's disease.
F. Treatment:
Results of bacterial sensitivities (oxtetracycline 0.l gm/ml water). Supportive therapy- subcutaneous or IV fluids, gastric incubation.
G. Control:
Decrease stress and prevent rapid environmental fluctuations.
A. Etiology:
Salmonella typhimurium and Salmonella enteritidis - gm (-) aerobic, nonlactose fermenting. hydrogen sulfide producing rods.
B. Transmission:
Ingestion (direct contact).
C. Clinical Signs:
Acute anorexia, fever, dehydration, diarrhea (hemorrhagic), death, abortions.
D. Gross Pathology:
Congestion and hemorrhage of viscera associated with septicemia; ulcerative colitis; focal necrosis of liver.
E. Diagnosis:
Culture blood, spleen or feces on selective media (brilliant green, selenite, citrate, or tetrathionate); serology - rise in titer (+).
F. Treatment:
Questionable - carrier state involved; sulfaquinoxaline (0.256 gm/500 gm feed or water for 2 weeks), penicillin (40,000 IU/kg IM s.i.d. for 3-5 days), Chloramphenical (30 mg/kg IM s.i.d. for 3-5 days) fluid therapy; eliminate colony and restock.
G. Control:
Rigid husbandry practices - disinfection, clean stock and prevention of wild bird or rodent contamination of bedding, water, or food; identify and eliminate carriers (culture serology).
H. Public Health Significance:
Man can contact Salmonella infections from laboratory rodents.
A. Etiology:
Yersinia pseudotuberculosis - G(-) cocco-bacilli.
B. Clinical:
Chronic weight loss with or without diarrhea, palpable abdominal masses.
C. Pathology:
Most consistently, enlargement and caseous necrosis of mesenteric lymph nodes.
D. Diagnosis:
Lesions and culture.
E. Control:
Aggressive sanitation.
F. Public Health Hazard:
Yes.
A. Etiology:
Fusobacterium necrophorum - G (-) anaerobic bacilli.
B. Clinical Signs:
Lesions commonly on face (because of coprophagy) and feet. These are necrotizing, ulcerative and fetid.
C. Pathology:
Primary characteristic is caseous necrosis.
D. Diagnosis:
Lesions and culture.
E. Control:
Improve sanitation and husbandry.
A. Etiology:
Listeria monocytogenes - Gm (+), small, motile aerobic, rod.
B. Clinical Signs:
Death and abortion
C. Pathology:
A septicemic disease, cervical and mesenteric lymphadenitis, multifocal necrotizing suppurative hepatitis, splenitis, adrenal adenitis. Suppurative endometriosis in pregnant does.
D. Diagnosis:
Morphology and culture.
E. Control:
Good husbandry
F. Public Health Hazard:
Yes.
Etiology:
Gm (-) bacilli, Campylobacter-like organism.
Disease same as in hamsters.
Common in wild rabbits.A. Etiology:
Yersinia pestis - gm (-) coccobacilli .
B. Clinical Signs and Pathology:
Septicemic, pneumonic or localized with lymphadenopathy.
C. Diagnosis:
Culture.
D. Public Health Hazard:
Yes.
E. Control:
Avoid vectors.
F. Treatment:
Can be treated with antibiotics
Common in wild rabbits,
A. Etiology:
Brucella sp.,
B. Clinical Signs:
Abortion, septicemia and disseminated abscesses.
C. Diagnosis:
Culture.
D. Public Health Hazard:
Yes.
Enterotoxemia:
A. Etiology:
Clostridium difficile, Clostridium
perfringens. Gm (-) anaerobic bacilli.
B. Clinical Signs:
Diarrhea, death in young, abdomen may be distended due to gas filled gut.
C. Pathology:
Necrotizing enterocolitis with extensive edema and hemorrhage.
D. Diagnosis:
Lesion, culture, toxin demonstration.
E. Control:
Unknown, eliminate colony.
5.5.3.1.1 Coccidiosis
1. Etiology:
Eimeria stiedae, Eimeria magna, Eimeria irresidua, Eimeria performans, Eimeria media. All species except Eimeria stiedae affect the intestinal tract replicating in the absorptive epithelium of the villi. Eimeria stiedae exist in the duodenum, travel to liver via bloodstream (possibly via lymphatics) and invade epithelial cells of bile ducts to begin schizogeny.
2. Transmission:
Ingestion of sporulated oocysts (unsporulated in freshly voided feces)
3. Clinical Signs:
a. Hepatic Form:
Anorexia, debilitation, pendulous abdomen with hepatomegaly noted on abdominal palpation; low mortality except in young rabbits.
b. Intestinal Form:
Signs vary - most severe in young rabbits; poor weight gain, diarrhea ranging from mucoid to watery to hemorrhagic, polydipsia and sometime acute death.
4. Gross Pathology:
a. Hepatic Form:
Enlarged liver with focal yellow-white lesions containing yellow exudate; may see distended gallbladder.
b. Intestinal Form:
May see multiple white patches or ulcers on mucosal surface.
5. Diagnosis:
Fecal examination by direct smear, flotation or concentration methods; histological appearance of liver or intestine with identification of macro- or microgametocytes or oocysts; hyperplasia of bile duct epithelium with inflammatory cell infiltrate characteristic of Eimeria stiedae infection.
6. Treatment:
Sulfamerazine sodium 0.02% in water; Sulfaquinoxaline sodium, 0.05% in water, 0.03% in feed; Sulfamethoxine 75 mg/kg for 7 days.
7. Control:
Clean and disinfect cages regularly (l0% ammonia); house on wire-meshed floors; separate weanlings from adults; avoid feeding greens or hay that may be contaminated with droppings from wild rabbits.
1. Etiology:
Encephalitozoon cuniculi (or Nosema cuniculi) microsporidia; 2.5 x l.5 cm (oval) with thick wall; stain poorly with H&E, use Giemsa, Gram's or Goodposture's carbol fucsin stains (helps to differentiate from Toxoplasma spp.).
2. Transmission:
Natural transmission unknown; experimentally transmitted by direct contact (ingestion, aerosol), possibly by endo- and ectoparasites; suspect vertical transmission also.
3. Clinical Signs:
Usually none (latent infection); may see convulsions, tremors, torticollis, paresis, and edema.
4. Gross Pathology:
Multifocal, pinpoint, white, pitted areas on surface of kidneys; no gross lesions in brain.
5. Diagnosis:
Histological examination of kidneys and brain - granulomatous interstitial reaction with fibrosis in kidney and focal granulomas in brain with perivascular plasma cell cuffs and nonsuppurative meningitis. May see organism within renal tubular epithelial cells or in center of granulomas in the brain. To differentiate from toxoplasmosis, E. cuniculi organisms are gram (+) and stain deep purple with Goodpasture stain. Toxoplasma gondii is gram (-) and doesn't stain with Goodposture's stain.
6. Treatment:
None since antemortem detection impossible.
7. Control:
Difficult.
5.5.3.2.1 Passalurus ambiguous ("Rabbit Pin Worm")
Adults found in cecum and large intestine; most common pinworm in domestic rabbits; males 4.l mm long, 300 um in diameter with a single curved spicule; females 6.6 mm long with long tail posterior to vulva; eggs flattened on one side; direct life cycle.
1. Clinical Signs:
None usually.
2. Treatment:
Piperazine adipate - 0.5 gm/kg s.i.d, 2 days in food or water; ( 0.75 gm/kg s.i.d. for 2 days in young rabbits).
Wild rabbits are frequently definitive and intermediate hosts for a number of tapeworms. The life cycle of these parasites practically precludes infection of domestic or laboratory rabbits. Of the tape worms that are found in rabbits, the most important is Taenia spp. because the dog is the definitive host. Taenia pisiformis infection 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 but cause little damage. A second Taenoid found in rabbits is T. serialis. The stage of this 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.
5.5.3.3.1 Taenia (Cysticercus) pisiformis:
Larval form of dog tapeworm
5.5.3.3.2 Multiceps (Coenurus) serialis:
Larval form of dog tapeworm
5.5.3.3.3 Taenia (Cysticercus) fasciolaris:
Larval form of cat tapeworm
5.5.3.3.4 Cittotaenia ctenodes:
Diarrhea and emaciation with heavy infection
5.5.3.5.1 Psoroptes cuniculi ("Ear Mite of rabbits") - Non-burrowing, Obligate mites.
a. Clinical Signs:
Scratching at ears with hind feet; crusty exudate in pinna with moist dermatitis underneath.
b. Diagnosis:
Observe mites with otoscope; mineral oil prep; oval-shape mites with well-developed legs, jointed pedicles and bell-shape suckers on the end of pedicles. Lifeccyle lasts around 21 days.
c. Treatment:
Gently remove crusts and clean pinna; treat with mineral oil with or without acaricida; antibiotic cream if infected.
d. Control:
Isolate animal if more than one in colony; disinfect cage.
5.5.3.5.2 Cheyletiella parasitivorax ("Fur Mite of rabbits")
Small, non-invasive mite.
a. Clinical Signs:
Partial alopecia of scapular region; may see fine, grayscale with ecythematous skin; no pruritis.
b.Diagnosis:
Pelt examination; (265-384 um) small white mite with piercing chelicerae and large curved palpal hooks; eggs attached to fur.
c.Treatment:
Insecticide dusts or selica gel acaricides, repeat at l0 day intervals.
d.Control:
Same as treatment - clinical disease not often evident.
5.5.3.5.3 Listrophorus gibbous ("Fur Mite of rabbits)"
a.Clinical Signs:
Currently considered non-pathogenic; found primarily on the back and abdomen.
b.Diagnosis:
Pelt examination under dissecting microscope. All stages may be encountered as the mite is an obligate parasite and spends its entire life cycle on the hosts.
c.Control:
Isolation of infected animals. Acaricides are thought to the effective in treatment.
5.5.3.6.1Hemodipsus ventricosis ("Blood sucking louse")
a.Clinical Signs:
Weakness, anemia, ruffled fur and pruritis (secondary dermatitis).
b.Diagnosis:
Pelt examination - mite on hair and identification of anoplurid louse (head narrower than body).
c.Treatment:
Insecticide dusts or silica gel acaricides, repeat at l0 day intervals.
d.Control:
Spend entire life cycle on rabbit with little transmission.
5.5.4.1 Myxoma Virus (Leporipoxvirus; Poxviridae)
A.Etiology:
Myxomatosis is caused by any one of several strains of myxoma virus, a member of the poxvirus group. Virulence of the different strains ranges from a mortality incidence of 99% in European rabbits to less than 30%.
B.Transmission:
The principal mode of transmission is via arthropod vectors (mosquitoes, fleas, flies, gnats). Transmission is also thought to occur by contact: with ocular discharge or oozing skin lesions of infected rabbits, contaminated spines of thistles, and the claw of predatory birds.
C.Symptoms in Oryctolagus Species:
The clinical disease picture is largely predicated by the strain of virus involved as well as genetic resistance of the strain of rabbit.
1.California Strain:
In the peracute from, rabbits die within a week of exposure showing a slight edema of the eyelids and cerebral depression immediately prior to death. With the acute form, in which rabbits survive for l-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.
2.Standard Laboratory Strain:
This strain has a mean survival time of 11 days. Three to four 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 l0, hard lumps cover much of the body.
3.European Strain:
This strain is characterized by rapid proliferation of large lumps by day 7. The lumps may break open by day l0 and ooze a serous discharge. Lumps may occur on any area of the body. There is also a very 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 the skin tumor and pronounced cutaneous and subcutaneous edema. Skin hemorrhages and subserosal petechial and ecchymotic hemorrhages may be observed in the stomach and intestines. Various degrees of congestion will occur in the visceral organs depending on the severity of the disease.
E.Microscopic Lesions:
Skin tumors result from an initial proliferation of undifferentiated mesenchymal cells 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. Epithelial 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 are observed most commonly in cells of the prickle-cell layer.
F.Diagnosis:
Made on the clinical-pathological picture, virus isolation, fluorescent antibody techniques, plaque-neutralization, and/or agar gel diffusion.
G.Control:
Control is achieved through vector control and adequate screening, quarantine of new animals, and isolation of all sick animals.
5.5.4.2 Rabbit (Shope) Fibroma Virus (Leporipoxvirus; Poxviridae):
A.Etiology:
Fibroma virus is a member of the poxvirus group closely related to myxoma virus. The virus has an apparent widespread incidence.
B.Transmission:
The natural transmission cycle is not known although arthropod vectors transmission is the most likely method.
C.Clinical Signs:
Tumors occur on the legs or feet, muzzle, and around the eyes. The tumors are subcutaneous and not attached to underlying tissue. Metastasis from the original tumor do not occur. The infected adult rabbit remains clinically normal otherwise. Experimental inoculation of newborn rabbits however, has produced generalized and fatal infections.
D.Pathology:
The earliest lesion is a slight thickening of the subcutaneous tissue followed by the 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.
E.Microscopic Lesions:
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. Inracytoplasmic inclusions are present. Degeneration of the epidermis overlying the tumor may result from pressure ischemia. This leads to necrosis and sloughing of the epithelium.
F.Diagnosis:
Based on clinical signs, virus isolation, and virus neutralization.
G.Control:
Not considered to be an important problem in domestic rabbits. In outdoor rabbitries, some means of vector control is advised.
5.5.4.3 Rabbit (Shope) Papilloma Virus (Papillomavirus; Papovariri-dae):
A.Etiology:
A member of the papovavirus group. This disease is seen most frequently in cottontail rabbits of the Midwest, and natural outbreaks have been reported in domestic rabbits.
B.Transmission:
Arthropod vector transmission in the natural disease has been demonstrated. The mosquito is thought to be the main vector in transmission from feral rabbits to domestic rabbits.
C.Clinical Signs and Gross lesions:
Horny warts are found on the eyelids and ears. The growths are well keratinized and the upper surface are irregular and split. The base portions are softer to the touch. The growths are easily scratched or knocked off, and these sites later heal without complication.
DMicroscopic Lesions:
The tumor has the typical appearance of a papilloma. It consists of elongated rete pegs of epithelium surrounding central cores of connective tissue. There is a sharp delineation where the tumor meets normal epithelium. A mild inflammatory cell infiltrate is normally found in the dermal layers underlying the tumor. The dermis is thickened over the papilloma and is often incompletely keratinized.
E.Diagnosis:
Based on clinical signs and histological examination.
F.Control:
Control of arthroped vectors.
NOTE:This virus is thought to be a precursor to squamous cell carcinoma. This virus is distinct from rabbit oral papilloma virus.
5.5.4.4 Rabbit Oral Papilloma Virus (Papillomavirus; Papovaviridae):
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.
B.Transmission:
Spread is by direct contact of oral secretions containing sloughed epithelial cells from the oral warts. Infection occurs in the abraided epithelium of the tongue.
C.Clinical Signs and Gross Lesions:
A benign disease characterized by numerous whitish growths on the underside of the tongue. These later become pedunculated and ultimately ulcerate. The growths regress when the rabbit becomes sufficiently immune.
D.Microscopic Lesions:
A typical papilloma as described above.
E.Diagnosis:
Based on clinical signs.
F.Control:
None reported. Recovered rabbits are resistant to reinfection.
The incidence of spontaneously occurring tumors in rabbits is generally low. Tumors are rarely reported in wild rabbits because of the decreased life span of the wild rabbit, the infrequent survival of tumor-prone groups, the unavailability of animals for necropsy and the insufficient numbers of domesticated wild rabbits available for long-term studies. More information, however, is available on domestic rabbits, but even so, few domestic rabbits survive 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.
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 symptoms precedes tumors detection by 6-l0 months. The duration in time between clinical detection and death from metastasis is 12-24 months. Histologically, the events of the tumor progression are characterized by increasing degrees of differentiation 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 second most common rabbit neoplasm is the lymphosarcoma. It is considered a tumor of juvenile and young adult rabbits. A tetrad of necropsy lesions have been established that are considered pathognomonic for lymphosarcoma in the domestic rabbit:
Virtually all of the lymph nodes in the body may be involved in the neoplastic process. Histologically, the normal architecture of the nodes are obliterated by masses of infiltrating neoplastic lymphoblasts. Susceptibility to the the disease is believed due to an autosomal recessive gene expressed in the homozygous state.
Other commonly reported tumors of the rabbits are embryonal nephromas, bile duct adenomas, bile duct adenocarcinomas, mammary gland papillomas, mammary adernocarcinomas, and squamous cell carcinomas. 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.
Some other tumors that have been reported only 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.
5.5.6.1 Hydrocephalus:
Questionable mode of inheritance: reported to be autosomal recessive and associated with dwarfing and brachygnathism; vitamin A deficiency in pregnant does leads to hydrocephalic young.
5.5.6.2 Buphthalmia:
(Congenital glaucoma) autosomal recessive with incomplete penetrance; abnormal production and removal of aqueous from anterior chamber. Clinical Signs: May see changes as early as 2-3 weeks of age; slight cloudiness progressing to increasing cloudiness of cornea, prominent eyeball, conjunctivitis, keratitis, ulceration, and rupture of cornea.
5.5.6.3 Splay Leg:
Clinical manifestation of several disease entities including syringomyelia, hypoplasia pelvis femoral luxation, hereditary distal forleg curvature, and achondroplasia of hip and shoulder joints.
5.5.6.4 .Malocclusion:
Hereditary and environmental causes; hereditary mandibular prognathism apparent by 3 weeks of life; autosomal recessive with incomplete penterance; also malocclusion of premolars and molars reported in older rabbits - questionable genetic influence.
5.5.6.5 Short Limbs:
Skeleton malformations have been described in rabbits which were used in teratological studies. (Teratology is that division of embryology and pathology which deals with abnormal development and congenital malformation of fetuses.) However, spontaneous occurrence of malformations are uncommon. Any of the following may occur.
A.Hemimelia:
Developmental anomaly characterized by the absence of all or part of the distal half of the limb or limbs.
B.Dysmelia:
Malformation of a limb as a result of embryonic development.The term also includes excessive development or reduction of deformities.
C.Micromelia:
Abnormally short limb or limbs.
D.Amelia:
Congenital absence of limb or limbs.
E.Phocomelia:
Developmental anomaly characterized by absence of proximal portion of a limb or limbs of foreleg or hindleg.
F.Hypophalangy:
Less than the usual number of phalanges of a finger or toe.
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5.5.7.1 Mucoid Enteropathy (ME):
Classified as enterotoxin induced diarrhea
A.Etiology: ?
E. coli frequently isolated although condition has not been reproduced using E. coli cultures or endotoxins; serotypes of E. coli from rabbits with ME not same as that from rabbits with colibacillosis - histological appearance of also ME differs from that of colibacillosis. Clostridium spp. (C. welchii type A, C. perfringens) may contribute as secondary invader similar to E. coli. Coccidiosis also incriminated in potentiating or triggering ME. Search for viral agents unsuccessful.
B.Clinical Signs:
Acute disease; anorexia, polydipsia, subnormal temperature (99o -l02o C) and rough hair coat; mucous to liquid, tan diarrhea with perineal staining; abdominal distention with gas and fluid-filled intestines; death in 7-8 days, grinding of teeth also common.
C.Gross Pathology:
Grossly distended fluid-filled stomach, duodenum and jejunum; pasty contents in ileum and dry matter and gas in cecum (often impacted), gelatinous mucus in colon.
D.istopathology:
Goblet cell hyperplasia with no inflammatory response in small intestine; occasionally see goblet cell hyperplasia of gallbladder, pancreatic and bile ducts and trachea.
E.Diagnosis:
Based upon clinical signs, gross lesions, and histopathology.
F.Treatment:
Disappointing at best; fluid therapy and chloramphenicol succinate (6.6 mg/kg IM) or penicillin (40,000 IU/Kg IM) for 5 to 7 days.
G.Prevention:
Feed antibiotics (tetracyclines, sulfas) for 6 weeks between second and eight weeks of life (herd situation).
A. Etiology:
Attempts to isolate and identify the specific causative agent are not always successful. A pathogenic E. coli has been implicated as well as Clostridium difficile, Clostridium perfringens, and other Clostridium spp. A history of antibiotic therapy with lincomycin and subsequent clostridial isolation may be associated with this disease. The disease is caused by toxin production.
B.Clinical Signs:
Sudden death with no previous signs of illness, watery diarrhea 2-3 days prior to death; affects all ages but primarily neonates.
C.Gross Pathology:
Large, fluid-filled cecum; congestion and hemorrhage of the intestinal serosa ranging from the duodenum to the colon but usually isolated to the cecum and proximal colon; edema of the cecal wall; watery, mucous feces.
D.Histopathology:
Marked necrosis of the surface epithelium may be present as well as an inflammatory cell infiltrate (primarily neutrophils) in the lamina propria and submucosa, and edema of the submucosa. Hemorrhage and congestion may be seen.
E.Diagnosis:
History of lincomycin treatment, isolation of Clostridium spp. from cecal contents intraperitoneal inoculation of cecal filtrates with and without clostridial antitoxin into mice.
F.Treatment:
Usually none; supportive fluid therapy.
G.Control:
Do not use lincomycin in rabbits.
A.Etiology:
Trichophyton mentagrophytes - opportunistic obiquitous soil organism.
B.Clinical Signs:
Patchy alopecia on head that is crusty and pruritic spreads to paws and other parts of the body; secondary bacterial infections common.
C.Diagnosis:
Clinical signs, scraping and indentification of spores on hair shaft or mycelia within hair shaft; culture on Sabaraud or DTM, rule out mites.
D.Treatment:
Topical fungicide (Tresiderm, Iodine, Conofite cream); griseofulvin 25 mg/kg in aqueous suspension of 0.375 gm powdered form/lb food for l4 days.
E.Control:
Public health significance; disinfect cage.
A.Etiology:
Pressure necrosis of skin from bearing of heavy body weight on hard or wire surfaces. Common in large breeds.
B.Clinical Signs:
Circumscribed ulcers of metatarsus and metacarpus covered by a scab; may have purulent exudate under scab; can see anorexia, debilitation and death.
C.Treatment:
Use of soft dry bedding, resting board in wire cages; topical zinc and iodine ointments; antibiotic ointment if secondarily infected; systemic antibiotics if abscesses or debilitation present. infected; systemic antibiotics if abscesses or debilitation present.
A.Etiology:
Chronic saturation of chin, intermandibular space and groin area with water, saliva, or urine, often with secondary bacterial infections; poor husbandry, malocclusion and water from crocks contribute to disorders.
B.Clinical Signs:
Moist dermatitis with serous to mucopurulent exudate; alopecia and ulceration of skin can occur; often systemic illness follows chronic infections.
C.Treatment:
Clip hair of the area and wash with gentle germicidal solution; apply topical antibiotic cream for l0-l4 days; use systemic antibiotics in chronic infections.
D.Control:
Clean, dry bedding or wire floor, water bottle feeding (instead of crocks or pans), clip maloccluded teeth.
A.Clinical Signs:
Rabbits are very sensitive to heat; tachypnea, cyanosis, prostration and blood-tinged fluid on nose and mouth may be observed.
B.Treatment:
Quick cooling - immerse in cool water or cover with alcohol or water spaked cloths.
C.Control:
Provide fans or water sprays (sprinklers) in hot weather.
A.Etiology:
Unknown. Predisposing factors include breed, age, sex, obesity, and number of previous litters. The disease is seldom reported in domestic rabbits.
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, and CNS signs.
C.Pathology:
Signs are obesity, areas of necrosis in the mesenteric fat, and pale liver, heart, and kidneys. Fatty changes are seen microscopically in the liver, heart, and kidneys.
D.Control:
Control weight gain in breeding does.
A.Etiology:
The condition has a sudden onset and usually 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.
B.Clinical Signs:
Posterior paralysis or paresis, loss of skin sensation, loss of motor control of anal sphincter and urinary bladder.
C.Pathology:
The most common site of fracture is the vertebral body or its caudal articular processes.
D.Diagnosis:
Made with clinical signs and/or radiography.
E.Treatment:
If bladder and anal sphincter control remain intact and there is still hind limb pain perception, complete recovery may occur within 2-4 weeks with cage rest.
A.Etiology:
These can form in the stomach as the rabbit grooms itself or a cagemate.
B.Clinical Signs:
Generally, hairballs are not a problem and are found incidentally at necropsy. Occasionally, they will cause a partial or complete obstruction. In this case the hairball may be palpable and the rabbit will stop eating and lose weight.
C.Treatment:
Mineral oil administered via stomach tube or a mild laxative, in advance cases surgery may be indicated. If not treated rabbit will die within l0 to l4 days after first sign of anorexia is noted.
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