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Laboratory Animal Medicine Blue Book, 3rd Ed. (2015) > Chapter 10. Biology and Diseases of Rabbits > Flashcards

Chapter 10. Biology and Diseases of Rabbits Flashcards

1
Q

Development of first inbred rabbit colony?

A

1931 - Phipps Institute for the Study, Treatment, and Prevention of Tuberculosis at the University of Pennsylvania
-Used to study natural resistance to infection with TB

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2
Q

Other early inbred rabbit colonies

A
  • University of Illinois College of Medicine Center for Genetics
  • Laboratories of the International Health Division of The Rockefeller Foundation
  • University of Utrecht - Netherlands
  • Jackson Laboratories
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3
Q

Rabbit taxonomy

A 
Class Mammalia
Order Lagomorpha
Family Leporidae (rabbits & hares)
Subfamily Leporinae
8 genera: Brachylagus, Bunolagus, Nesolagus, Oryctolagus, Pentalagus, Poelagus, Romerolagus, Sylvilagus (cottontail rabbits)
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4
Q

European rabbit

A

Oryctolagus cuniculi - the only domesticated rabbit; the only species from which unique breeds have been derived

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5
Q

Genus for true hares?

A

Lepus - 22 species of true hares, jackrabbits

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6
Q

Current number of rabbit breeds?

A

127

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7
Q

Uses in research for rabbits

A
  • Immunology research
  • Production of polyclonal antibodies
  • Lymphoid system has 2 gut associated lymphoid tissues (GALT) with specialized functions in maturation of IgM+ B cells - vermiform appendix at distal end of cecum & sacculus rotundus at ileocecal junction
  • Profile of cytokines in rabbits appears similar to other mammals
  • Cardiovascular research - cholesterol-induced atherosclerosis
  • Genetically modified rabbits: long QT interval, atherosclerosis, expression of human recombinant proteins in rabbit milk, enhanced green fluorescent protein (EGFP) model
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8
Q

Antibody production in different species

A
  • Mice & humans - primary antibody repertoire created by rearrangement of a large number of immunoglobulin gene segments = a portion of the immunoglobulin gene is replaced with a gene sequence from a nonfunctional pseudogene
  • Chicken, sheep, cattle, rabbit - limited number of gene sequences & utilize somatic gene conversion/somatic hypermutation = single nucleotide changes in immunoglobulin genes
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9
Q

Antibody production in rabbits

A
  • Immunoglobulin gene diversification occurs initially in the fetus & the neonate in bone marrow
  • At 4-8 wks of age, immature IgM+ B cells further diversify in the GALT (vermiform appendix, sacculus rotundus, Peyer’s patches)
  • Certain spp of intestinal bacteria (Bacteroides fragilis, Bacillus subtilis) are required for appendix follicle development & antibody diversification
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10
Q

5 classes of immunoglobulins expressed by most mammals

A

IgM, IgD, IgG, IgA, IgE

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11
Q

4 classes of immunoglobulins expressed by rabbits

A

IgM, IgG, IgA, IgE

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12
Q

Cholesterol metabolism rabbit models

A
  • Watanabe heritable hyperlipidemic (WHHL): marked deficiency of low-density lipoprotein (LDL) receptors in liver & other tissues; selective breeding will increase incidence of coronary artery atherosclerosis w/out increasing aortic atherosclerosis
  • St. Thomas Hospital strain: normal functioning LDL receptor but still maintains a hypercholesterolemic state
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13
Q

Transgenic rabbits expressing human recombinant protein in milk

A

-Expression of humans proteins in milk have resulted in antigen production for rotavirus vaccine creation, human factor VIII that could be used to treat hemophilia, and human growth hormone that could supplement a deficiency in that hormone

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14
Q

LQTS transgenic rabbits

A

Models of prolonged QT interval

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15
Q

Rabbit dental formula

A

I 2/1, C 0/0, PM 3/3, M 2-3/3 = 26 or 28 teeth

  • Absence of 2nd incisors in some colonies as a dominant trait
  • Teeth erupt continuously throughout life
  • Molars do not have roots & are characterized by deep enamel folds
  • Masticate with a side to side & front to back chewing motion
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16
Q

Peg teeth

A

Small pair of incisors directly caudal to the primary maxillary incisors
-Used to bite and shear food

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17
Q

Salivary glands in rabbit

A

4 pairs: parotid, submaxillary, sublingual, zygomatic

  • Parotid is largest - lies laterally just below base of ear
  • Zygomatic does not have counterpart in humans
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18
Q

Rabbit esophagus

A
  • 3 layers of striated muscle that extend down to cardia of stomach
  • Different than humans and other species with separate portions of striated and smooth muscle
  • No mucous glands in rabbit esophagus
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19
Q

Stomach in rabbits

A
  • Holds 15% of GI volume
  • Never fully empty in healthy rabbit
  • Contents include large amount of hair from grooming
  • Divided into cardia, fundus, pylorus
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20
Q

Liver in rabbits

A
  • 4 lobes
  • Gallbladder on the right
  • Common bile duct empties into the duodenum posterior to the pylorus
  • Rabbits produce relatively large amounts of bile compared with other species
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21
Q

Pancreas in rabbits

A
  • Diffuse in mesentery of small intestine

- Enters the duodenum 30-40 mm distal to common bile duct

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22
Q

Small intestine in rabbits

A
  • Short relative to other species - ~12% of total GI length
  • GI tract relatively impermeable to large molecules = kits receive most of their passive immunity via the yolk sac prior to birth
  • Peyer’s patches in ileum, particularly near cecal junction; sacculus rotundus also near here
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23
Q

Large intestine in rabbits

A
  • Cecum, ascending colon, transverse colon, descending colon
  • Ileocecal valve regulates flow of chyme into cecum & retards reverse flow to ileum
  • Cecum very large with capacity 10x that of stomach
  • Colon divided into proximal and distal portions by the fusus coli
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24
Q

Fusus coli

A

Junction between proximal & distal colon

Regulates elimination of hard vs. soft feces

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25
Q

Cecotrophs in rabbits

A

1/3 of fecal output

  • Generally produced at night in domestic rabbits; in wild rabbits produced during day when in burrows
  • High moisture content, rich in nirtrogen-containing compounds, B Vits niacin, riboflavin, pantothenate & cyanocobalamin
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26
Q

Nose of rabbits

A
  • Well-developed sense of small
  • Nostrils well equipped with touch cells
  • Nasal breathing characterized by nasal twitching; 20-120 times/min
  • Speculated that inspiration occurs as nostrils move up to direct air flow over turbinate bones where olfactory cells most concentrate
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27
Q

Respiration in rabbits

A
  • Rely mostly on activity of diaphragm (thoracic wall muscles contribute little)
  • Artificial respiration in rabbits easily performed by alternating the head of the rabbit up & down, 30-45 times/min, while holding animals; compression of chest is INeffective means of artificial respiration
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28
Q

Respiratory tract in rabbits

A
  • Pharynx long and narrow
  • Tongue relatively large
  • Lungs have 6 lobes: both sides have cranial, middle, caudal & R caudal further subdivided into lateral and medial
  • Flow volume in L lung higher than R d/t lower resistance of the proximal airways
  • In rabbits, lung volume increases with age (in contrast to humans & dogs where it decreases)
  • BALT present at distinct tissue
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29
Q

Tricuspid valve in rabbits

A

Has only 2 cusps (instead of 3 like in many mammals)

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30
Q

Cardiac function in rabbits

A
  • Small group of pacemaker cells generate impulses to SA node, a feature that facilitates precise determinarion of the location of the pacemaker
  • SA & AV nodes are slender and elongated
  • AV node separated from annulus fibrosis by layer of fat
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31
Q

Cardiovascular system in rabbits

A
  • Aortic nerve responds to baroreceptors only; runs alongside but separate from vagosympathetic trunk - can readily be implanted with electrodes
  • Blood supply to brain is mainly the internal carotid artery; a little from vetebral arteries
  • Aorta has rhythmic contractions that arise for neurogenic stimulation in a pattern related to the pulse wave
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32
Q

Kidneys in rabbits

A
  • Unipapillate - increases ease of cannulization
  • Right kidney more cranial than left
  • Glomeruli increase in number after birth (all glomeruli present at birth in humans)
  • Ectopic glomeruli normal in rabbit
  • Blood vessels in medulla remain open during many conditions where there is cortex vasoconstriction = medulla may be perfused while cortex is ischemic
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33
Q

Urine in rabbits

A
  • Typically cloudy d/t high concentration of ammonium magnesium phosphate & calcium carbonate monohydrate precipitates
  • Normal color may be yellow or reddish or brown (related to eating green feeds or cereal grain)
  • Healthy young rabbits have albuminuria
  • Normal pH: ~8.2
  • Normal adult produces 50-75 mL/kg/day; does produce more than bucks
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34
Q

Reproductive tract in rabbits

A
  • Urethral opening rounded in bucks, slit-like in does
  • Testes can pass between scrotum and abdominal cavity; need to close superficial inguinal ring following orchidectomy
  • Does have two uterine horns connected to vagina by separate cervices (bicornuate uterus)
  • A common tube - the urogenital sinus or vestibulum - is present were the urethra enters the vagina
  • Inguinal pouches located lateral to genitalia in both sexes - scent glands
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35
Q

Placentation in rabbits

A

Hemochorial

-Maternal blood flows into sinus-like spaces where the transfer of nutrients to the fetal circulation occurs

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36
Q

Neonatal rabbit metabolism

A
  • Amount of body fat comparable to human infant (16% of body weight)
  • Essentially an ectotherm until 7 days old; glucose reserves depleted within ~6 hr after birth - the fasting neonatal rabbit becomes hypoglycemic and ketotic quickly
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37
Q

Normal body temperature of rabbits

A

-NZW rabbit: 38.5-39.5 C

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38
Q

Thermoregulatory function of ears

A
  • Large surface area and highly vascular with extensive arteriovenous anastomotic system
  • Countercurrent heat-exchange system to help adjust body temp
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39
Q

Drinking in rabbits

A
  • Body weight of adult rabbit is 58% water
  • Lose about 340 ml daily
  • Rabbits will drink more water when consuming dry pelleted feed compared to high moisture foodstuffs like fresh greens
  • Rabbits deprived of water will decrease food consumption
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40
Q

Hematology of rabbits

A
  • Males have slightly greater hematocrit & hemoglobin values than females
  • Anisocytosis is normal - variation in RBC diameter
  • Reticulocyte count 2-4% in healthy rabbit
  • Neutrophil has red-staining granules in cytoplasm = ‘pseudoeosinophil’ or ‘heterophil’; smaller than eosinophils & their granules are smaller than eosinophil granules
  • Nucleus of eosinophil may be bilobed or horseshoe-shaped
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41
Q

Serum chemistry in rabbits

A
  • AST is present in liver, heart, skeletal muscle, kidney, & pancreas
  • Blood collection by decapitation, cardiac puncture, aortic incision, use of restrain will elevate AST (similar to CK, which is present in skeletal muscle, brain, heart)
  • Rabbits have 3 isoenzymes of ALP - intestinal form & 2 forms both present in liver and kidney (most mammasls have 2 forms - intestinal & liver/kidney/bone form)
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42
Q

GI transit time in rabbits

A

4-5 hours

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43
Q

Number of mammary glands in rabbits

A

8 or 10

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44
Q

Normal TPR in rabbits

A

Temp: 38.5-39.5 C
Pulse: 200-300 beats/min
Resp: 32-60 breaths/min

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45
Q

Diet in rabbits

A
  • Strictly herbivorous
  • Preferred diet is low in fiber, high in protein & soluble carbohydrate
  • Fiber is especially important in early postweaning period when low fiber intake is assoc w/ an increase in digestive disorders
  • Obesity d/t overfeeding is common; prevent by reducing amount of feed or by providing a low-energy, high-fiber maintenance diet
  • Rabbits fed a high fiber diet produce more cecotropes
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46
Q

Calcium in rabbit diet

A
  • Calcium absorption in the small intestine & serum calcium levels increase in proportion to amount of calcium in diet (different than most other species)
  • Prolonged feeding of high calcium diets (lots of alfalfa) can result in renal disease
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47
Q

Vitamin D in rabbit diet

A

Excess Vit D in diet can result in calcification of soft tissues, including liver, kidney, vasculature, muscles

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48
Q

Vitamin A in rabbit diet

A
  • Diets too high or low in Vit A can result in reproductive dysfuntion and congenital hydrocephalus
  • Exact requirement in rabbits undetermined
  • 6000-10,000 IU/kg is generally adequate
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49
Q

Vitamin E in rabbit diet

A

-Vitamin E deficiency assoc w/ infertility, muscular dystrophy, fetal death, neonatal death, colobomatous microphthalmos in rabbits
-Serum levels <0.5 μg/ml are
indicative of hypovitaminosis E

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50
Q

Water intake in rabbits

A
  • Relative to other species, rabbits have a high water intake
  • ~120 ml/kg/day
  • Water consumption influenced by environmental temp, disease states, feed composition & intake
  • Consumption of diets high in dry matter increases water intake
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51
Q

Rabbit housing

A
  • Mature males will fight if placed together
  • Group-housed females allowed to choose between single or paired housing prefer paired
  • Individually housed rabbits show an increase in abnormal behavior compared to pair-housed rabbits
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52
Q

Defensive behavior in rabbits

A

Thumping on cage floor with rear feet, biting, charging

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53
Q

Sexual maturity in rabbits

A
  • Age of puberty varies with breed
  • 4-5 mths small breed, 4-6 mths medium breed, 5-8 mths large breed
  • Female NZW: 5 mths
  • Male NZW: 6-7 mths
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54
Q

Breeding window for rabbits

A
  • Does: ~1-3 years; some remain productive for 5-6 years
  • In later years litter sizes usually diminish
  • Bucks: 5-6 years
  • Does will often engage in reproductive behavior before being able to ovulate = do not breed until fully grown
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55
Q

Estrous cycle in rabbits

A
  • Do not have a distinct estrous cycle - instead have rhythm with respect to receptivity to buck
  • Receptivity punctuated by periods (1-2 days every 4-17 days) of anestrus
  • Receptivity: vulvar swelling & color change, lordosis, restlessness, rubbing of chin on hutch or cage
  • Induced ovulators - occurs ~10-13 h after copulation
  • Up to 25% of does fail to ovulate after copulation
  • Ovulation can also be induced by LH, HCG, or gonadotropic releasing hormone
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56
Q

Breeding in rabbits

A
  • Bring doe to buck’s cage, since doe can be territorial
  • A period of 15-20 min is usually sufficient to determine compatibility btwn doe and buck
  • A single buck is usually sufficient to service 10-15 does
  • Does may be bred immediately after kindling, but most breeders delay until kits weaned; can foster nurse & rebreed doe immediately (allows for up to 11 litters per year vs 4)
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57
Q

Pregnancy determination in rabbits

A
  • Can be confirmed as early as day 11 by radiographs, day 14 by palpation
  • Conception has inverse relationship with temperature but not light cycle
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58
Q

Gestation in rabbits

A
  • 30-32 days
  • Does beyond 2-3 wk gestation will usually refuse a buck
  • Does begin hair pulling during last 3-4 days of gestation
  • Provide a nesting box with soft bedding material and doe will line with own hair; do not be placed in corner of box where doe urinates
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59
Q

Pseudopregnancy in rabbits

A
  • Common in rabbits
  • Can follow mounting by other does, sterile matings by bucks, administration of LH, presence of buck nearby
  • Ovulation is followed by a persistent CL that lasts 15-17 days - the CL secretes progesterone during this time, causing the uterus and mammae to enlarge
  • Toward the end of pseudopregnancy, many does will also pull hair
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60
Q

Parturition in rabbits

A
  • Kindling
  • Normally occurs during early morning hours and takes ~30-60 min
  • Impending kindling signaled by nest building, decreased food consumption during preceding 2-3 days
  • Both anterior and breech presentations are normal
  • Fetuses retained beyond 35 days usually die & may harm future reproductive ability if not expelled
  • Cannibalism of young by doe may occur d/t environmental stressors or hereditary factors
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61
Q

Litter size in rabbits

A

7-9 kits; up to 10

  • Breed, parity, nutritional status, environmental factors influence litter size
  • Polish rabbits: usually fewer than 4 kits/litter, Dutch or Flemish Giant: 4-5; NZW: 8-10
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62
Q

Lactation in rabbits

A
  • Does usually have 4-5 pairs of nipples; bucks have none
  • Marked mammary gland development occurs in last week of pregnancy
  • Does normally nurse kits once daily for several minutes in early morning or evening
  • Milk yield normally between 160-220 g/day
  • During first week of life, kits consume 15-25 g per day; gradually increases to 30 g/day by 17-25 days old
  • Maximum output at 2 weeks, then declines during 4th week
  • Nursing may last 5-10 weeks
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63
Q

Rabbit milk nutritional profile

A

12.5% protein, 13% fat, 2% lactose, 2.5% minerals

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64
Q

Weaning in rabbits

A
  • Kits begin consuming solid food by 3 wks of age

- Weaning generally occurs by 5-8 weeks of age

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65
Q

Caging dimensions for rabbits

A

AWA & Guide: 3 ft2 of floor space & 16 inch cage height for rabbits weighin 2-4 kg

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66
Q

T/F. Mesh floors with catch pens prevent rabbits from engaging in coprophagy

A

False. Rabbits are usually housed in cages with mesh or slatted floors; mesh floor do NOT prevent coprophagy

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67
Q

Conventional vs enriched caging in rabbits

A
  • Rabbits in conventional cages were more restless, groomed excessively, exhibited more bar-gnawing, and were more timid than those housed in enriched cages
  • Fecal glucocorticoid levels declined when provided wooden structure for resting & gnawing
  • Rabbits provided with toys will spend significantly more time chewing than rabbits without toys
  • Rabbits should not be housed near noisy species like dogs or NHP, nor near noise-generating operations such as cage wash
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68
Q

Guide temp range for rabbits

A

61-72 F

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69
Q

Light cycle for rabbits

A
  • No specific illumination requirements for rabbits
  • Common practice is 12-14 hr of light
  • Breeding colonies: 14-16 hr light
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70
Q

Sanitation in rabbit housing

A
  • Catch pans should be cleaned as often as necessary to prevent formation of ammonia - generally at least weekly
  • Rabbit urine contains large amounts of protein & minerals - forms deposits on cages & catch pans - sock equipment with deposits in acid washs to remove scale before washing
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71
Q

Ventilation in rabbit rooms

A

10-15 air change per hour

-Ammonia production can be a significant problem

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72
Q

Pasteurellosis in rabbits

A
  • Pasteurella multocida: G(-), nonmotile coccobacillus; serogroup A isolates = pneumonic and septicemic pasteurellosis in rabbits
  • Rabbits that appear healthy can have capsular type A
  • Subclinical, or “snuffles” - fever, coughing, dyspnea, rhinitis, sneezing, upper airway stentor, pneumonia, otitis, septicemia, meningitis, abscesses of viscera & SC, death
  • Also pericarditis, pleuritis, sinusitis, dacrycystitis, conjunctivitis, iritis/uveitis, phlegmon, mastitis, endometritis, pyometra, salpingitis, orchitis
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73
Q

Epizootiology of pasteurellosis

A
  • Endemic in rabbits & carried in nasal cavity
  • Transmission by direct contact
  • Coinfx with Bordetella bronchiseptica may be seen in clinically affected rabbits
  • Stress factors associated with: crowded or unsanitary condition, transportation, high ammonia concentrations in air
  • Colonization of immature rabbits - more commonly sinuses then trachea, middle ears, lungs
  • Can transmit to humans = ZOONOTIC
  • Subspp. = P. multocida subsp. multocida (most common), subsp. septica, canis, & 1 unknown subsp.
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74
Q

Pathogenesis of pasteurellosis

A
  • ptfA gene: endoces a type 4 fimbrial subunit of epithelial cells; may be highly prevalent in isolates from rabbits
  • P. multocida toxin is a major virulence factor in atrophic rhinitis in rabbits - causes constitutive activation of G proteins
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75
Q

Pathology of pasteurellosis

A
  • Acute or chronic suppurative inflamm w/ infiltration of large numbers or neutrophils
  • Nasal passages edematous, inflamed, congested, mucosal ulcerations; turbinate bone atrophy
  • CRANIOVENTRAL pneumonia; lungs have consolidation, atelectasis, abscesses, hemorrhage, necrosis
  • Fibrinopurulent pleuritis and pericarditis - probably d/t elaboration of heat-labile toxin in some strains
  • Acute hepatic necrosis, splenic lymphoid atrophy
  • Otitis media - suppurative exudate w/ goblet cell proliferation and lymphocytice and plasma cell infiltration
  • Enlarged uterus with exudate, focal endometrial ulceration
  • Enlarged testes with abscesses
  • Systemic and visceral abscesses have necrotic center, infiltrate made up of PMN neutrophils, and a fibrous capsule
  • Severe pleuritis with accumulation of fibronpurulent exudate in the thoracic cavity and atrophy of lymphoid organs has been observed with experimental infx
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76
Q

Diagnosis of pasteurellosis

A
  • Swab of nares or nasal cavity, nasal lavage
  • Isolates can be classified into 5 serogroups basd on capsular antigens : A, B, D, E, F & 16 serotypes based on somatic LPS antigens
  • REP-PCR using 16S rRNA & rpoB genes to identify isolates
  • Random amplified polymorphic DNA PCR (RAPD-PCR) to subtype isolates
  • PCR can detect capsul biosynthesis genes cap A, B, D, E, & F and virulence-related genes
  • Serology for antibodies
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77
Q

Differential diagnoses for pasteurellosis

A

-Internal mass: abscess, granuloma, neoplasia, parasitic cysts

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78
Q

Vaccination for pasteurellosis

A
  • Studies of vaccines: immunization with inactivated heat-labile P. multocida toxin or commercial swine P. multocisa bacterin-toxoid conferred protective immunity against heat-labile toxin
  • intranasal vaccine significantly reduced nasal bacterial counts
  • Oral immunization with P. multocida thiocyanate extract (PTE) in mircoparticles significantly reduced CFUs in lungs and nasopharnyx
  • PTE SC vaccination can provide heterologous strain protective immunity
  • A P. multocida bacterin called BunnyVac is currently licensed by the USDA
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79
Q

Control and treatment of pasteurellosis

A
  • Test and cull positive animals
  • Abx tx may suppress virulence gene expression without complete elimination of P. multocida; abx may not treat internal abscesses
  • Enrofloxacin tx, C-section or hysterectomy rederivation
  • Use a supplier that excludes Pasteurella
  • Avoid penicllins - may be ineffective & lead to diarrhea and Clostridium difficile colitis in rabbits; oral flouroquinolones are typically useful
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80
Q

Research complications of pasteurellosis

A
  • Considerable economic losses
  • Can affect multiple types of research d/t multisystemic nature of disease = should be excluded from lab rabbit colonies
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81
Q

Clostridial agents

A

-Phylum Firmicutes
-The genera Tyzzerella, Erysipelatoclostridium, and Peptoclostridium have been proposed for C. piliforme, C. spiroforme, and
C. difficile, respectively

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82
Q

Tyzzer’s disease in rabbits

A
  • Pleomorphic, G(-), spore-forming motile obligate intracellular rod-shaped bacterium
  • Infects mice, NHP, gerbils, rats, rabbits, humans with HIV, etc.
  • Microorganisms identified as C. piliforme form 3 clusters within a single clade; closest related species is C. colinum
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83
Q

Clinical signs of Tyzzer’s disease in rabbits

A
  • Profuse watery to mucoid diarrhea, listlessness, anorexia, dehydration, usually followed by death in 12-72 hr in 3-8 wk old rabbits
  • Dams of affected litters occasionally died within a week after a more protracted diarrheal disease than seen in offspring
  • Outbreaks last 6-8 months
  • May be subclinical and transient in immunocompetent hosts
  • Anorexia and stunting in chronic cases assoc w/ intestinal stenosis
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84
Q

Epizootiology of Tyzzer’s disease

A
  • Vegetative cell is the active stage responsible for disease
  • Transmission: contact with soiled bedding or diseased rabbits
  • Immunosuppressive treatments, stress d/t overcrowding or extreme temps, significant changes in intestinal flora can all play a role in infection
  • C. piliforme may be transported from the intestine to the liver through portal circulation & to the heart through lymphatics
  • Some isolates can induce cytopathic effects on cell cultures, and in vivo, concomitant infx with other enteric pathogens such as E. coli may contribute to the severity of the disease
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85
Q

Pathology of Tyzzer’s disease

A
  • Lesions in distal ileum, cecum, proximal colon, liver, heart
  • Intestinal lesions are common, w/ necrosis of mucosa and edema of submucosa and serosa; “criss-cross” sticks of bacilli in the cytoplasm of epithelial cells on surface of mucosa and base of glands
  • Puncture, white spot of necrosis on liver
  • Large numbers of bacilli are found in the cytoplasm of cells in the zone of transition between the necrotic lesion and healthy parenchyma
  • Myocardial lesions: white streaks along the left interventricular groove & across the left ventricle
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86
Q

Diagnosis of Tyzzer’s disease

A
  • CANNOT be cultured in cell-free media; can use liver extract agar; can be grown in primary monolayer of mouse fibroblasts, rat hepatocytes, and in embryonated eggs
  • Serology, IFA, MFIA
  • PCR
  • Serology positive rabbits may be negative on PCR or histopath; therefore serology only is not sufficient for definitive dx
  • Definitive diagnosis: identification of gross lesions & visualization of intracellular C. piliforme at periphery of necrotic foci
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87
Q

What stains may be used to visualize C. piliforme on histopathology?

A

Giemsa solution (pH 4)
Warthin-Starry silver method
Levaditi silver method
Periodic acid Schiff (PAS)

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88
Q

Differential diagnoses for Tyzzer’s disease in rabbits

A
  • Other diarrheal diseases of rabbits

- Multifocal white areas on the liver could also be Eimeria stiedae (hepatic coccidiosis)

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89
Q

Treatment & Prevention of Tyzzer’s disease

A
  • Avoid introduction of rabbits of unknown C. piliforme status
  • Good husbandry practices
  • Tetracyclines in water and food may lower incidence of diarrhea and death; but no antibiotics has been found to be completely inhibiting
90
Q

What disinfectants are effective against C. piliforme spores?

A

-70-80 C heat
-Peracetic acid (1%) in a wetting agent (sodium alkylarylsulfonate)
-Sodium hypochlorite solution (0.3%) for 5 min
(Ethanol, quaternary ammonium, phenolic compounds do NOT work)

91
Q

Research complications of Tyzzer’s disease

A
  • High morbidity and mortality

- Counding of enteric pathogen studies by C. piliforme-associated intestinal pathology

92
Q

Clostridial enterotoxemia in rabbits

A
  • Enterotoxemia refers to conditions of the bowel caused by toxigenic clostridia
  • Dx should be based on culture of a toxigenic clostridium and demonstration of the toxin from the intestinal contents of the diseased animal
93
Q

Clostridium spiroforme in rabbits

A
  • G(+), spore-bearing, helically coiled, semicircular, anaerobic bacterium that can produce iota toxin = ‘iota enterotoxemia’
  • Clin signs: diarrhea, fecal soiling of the perineum, cyanosis; acute moribund or death
  • Acquired from environment
  • Associated with weaning & abx administration (clindamycin); poor hygiene, stress, and diet can influence
  • May be coninfected with E. coli (EPEC), viruses, parasites
94
Q

Iota toxin of C. spiroforme

A

-Binds the same host cell receptor as the iota toxin of C. perfringens & the binary toxin of C. difficile

95
Q

Pathology of C. spiroforme

A
  • CECAL LESIONS: Enlarged cecum with gas, serosal hemorrhage, liquid contents may be stained with blood
  • May also have lesions in proximal colon & distal ileum
  • Histo: mucosal necrosis, mucosa denuded; cellular debris, RBCs, fibrin in intestinal lumen; PMN infiltrate & edema of lamina propria & submucosa
  • Epithelial degeneration and dilation of renal tubules
96
Q

Diagnosis of C. spiroforme

A
  • Gram stain intestinal content smears
  • Clostridial culture & toxin detection assays
  • High speed centrifugation of intestinal contents
  • PCR for C. spiroforme & iota (binary) toxin
  • Ddx: Other clostridia, E. coli, viruses, parasites
97
Q

Treatment & Prevention of C. spiroforme

A
  • Iota toxin from C. spiroforme is neutralized by serum prepared against iota toxin of C. perfringens type E
  • Prevention (reduce risk factors, use abx judiciously) more impt than tx
  • Cholestyramine can prevent experimental enterotoxemia d/t clindamycin in rabbits
  • Fecal flora transplants suggested for competitive inhibition of toxigenc strains
  • No commercial vaccines; but weanling rabbit vaccination with a toxoid imparted protection to IP challenge
  • Treatment usually abx (C. spiroforme has wide range of resistances) & diet (fresh meadow hay)
98
Q

Research complications of C. spiroforme

A

-Mortality d/t enterotoxemia disrupts studies

99
Q

Clostridium difficile in rabbits

A
  • G(+), spore-forming, anaerobic bacillus assoc w/ diarrhea & colitis in animals and humans
  • Clin signs: anorexia, decreased fecal output, abdominal distension, death (peracute common)
100
Q

Epizootiology of C. difficile in rabbits

A
  • Carrier animals that are asymptomatic
  • Acquired from environment d/t persistance of spores
  • Assoc w/ abx tx; but can also develop spontaneously after stressful events
  • Recently weaned most susceptible
  • Disrupts gut flora leading to clinical signs
101
Q

Why are newborn rabbits resistant to C. difficile disease?

A

Possible lack of receptors for the toxins

102
Q

Pathology of C. difficile

A
  • Fluid-filled cecum & colon
  • Lesions in small intestine, most commonly ileum
  • Hemorrhagic typhlitis in hares
  • Severe JEJUNAL LESIONS - mural hemorrhages, mucosal necrosis, submucosal edema
  • Inflammation & neurogenic stimulation
103
Q

Toxins of C. difficile

A
  • Toxin A (enterotoxin) & Toxin B (cytotoxin) act synergistically - allow C. difficile to enter host cells through receptor-mediated endocytosis
  • Disrupt the cytoskeleton by disrupting Rho-subtype intracellular signaling molecules that affect cellular funcion
  • Some strains also produce an actin-specific ADP-ribosyltransferase or binary toxin
104
Q

Diagnosis of C. difficile

A
  • GOLD STANDARD = tissue culture cytotoxin assay for toxin B
  • Isolation & toxin assays; selective agar
  • Enzyme immunoassays; PCR
  • Ddx: Other Clostridia or EHEC for peracute death in rabbits
105
Q

Treatment & Prevention of C. difficile

A
  • Reduce risk factors, prudent abx use
  • Cholestyramine may be used for prevention
  • Fecal flora transplants
106
Q

Research complications of C. difficile

A

-Unlikely d/t sporadic nature of deaths

107
Q

Clostridium perfringens in rabbits

A
  • Type E = alpha & iota toxins
  • Uncommon cause of enterotoxemia in rabbits
  • Because of toxin similarity btwn C. spiroforme & C. perfringens Type E - detection alone will NOT differentiate
  • PCR can be used for typing based on toxin gene
108
Q

Pathotypes of E. coli

A
  • Produce 3 general clinical syndromes: enteric/diarrheal disease, urinary tract infx, sepsis/meningitis
  • 6 pathotypes assoc w/ diarrhea in humans: EPEC, STEC (also known as EHEX or verocytotoxin-producing VTEC), ETEC, enteroaggregative EAEC, enteroinvasive EIEC, and diffusely adherent DAEC
  • 2 emerging pathotypes: adherent invasive (AIEC; assoc w/ Crohn’s disease) & Shiga toxin producing enteroaggregative (STEAEC; assoc w/ hemolytic-uremic syndrome)
109
Q

Which E. coli pathotypes are associated with natural disease in rabbits?

A

EPEC & STEC, as well as necrotxigenic (NTEC)

110
Q

EPEC & STEC (EHEC) Etiology in rabbits

A
  • EPEC carries eae gene: encodes intimin, a protein involved in induction of attaching & effacing lesions in the intestine
  • Serotype O15, aka RDEC-1, is the prototype EPEC strain isolated from rabbits with diarrhea
  • STEC carry stx gene; EHEC are a subset of STEC that carry stx & eae genes
111
Q

EPEC & STEC (EHEC) disease in rabbits

A
  • EHEC O153: diarrhea & sudden death in Dutch Belted rabbits
  • EPEC O145:H2: acute diarrhea following shipment in lab rabbits
  • Lab rabbits can be subclinical reservoir hosts
  • Clin signs: diarrhea, patent or occult blood in feces
  • Transmission: fecal-oral
  • Pathology: paintbrush hemorrhages of cecal serosa; petechial or ecchymotic hemorrhages of proximal colon, edema & thickening of proximal colon
  • Histo: attaching & effacing lesions with pedestal formation for EPEC and EHEC
  • Enterocolitis, nephropathy, thrombotic microangiopathy with EHEC
112
Q

Diagnosis of EPEC & STEC (EHEC) in rabbits

A
  • Culture of feces or intestinal contents on blood agar, MacConkey agar, or EHEC-selective media (Sorbitol MacConkey or Raibow agar) - after isolation, samples can be biotyped using API 20 E strips; serotyping by E. coli Reference Center
  • PCR to detect virulence factors
  • Molecular characterization of STEC strains by STEC center at MSU
  • Ddx: Clostridial diseases, intestinal coccidiosis
113
Q

Treatment & Prevention of EPEC & STEC (EHEC) in rabbits

A
  • Avoid introduction of rabbits with unknown pathogenic E. coli status
  • Screen via culture or PCR
  • E. coli can contaminate leafy greens (EHEC O157 can survive for 60 days on grass hay feed)
  • C-section rederivation, abx tx to eradicate
  • ZOONOTIC
  • Antibiotic tx controversial d/t possibility of induction of Stx-encoding bacteriophages and worsening of clinical condition d/t hemolytic uremic syndrome
  • Fluids as nephroprotective treatment
  • Strains may carry extended-spectrum beta-lactamases making them abx resistant
114
Q

Research complications of EPEC & STEC (EHEC)

A
  • High morbidity and mortality in lab rabbit colonies

- Affect studies involving intestinal physiology

115
Q

Treponematosis in rabbits

A
  • Treponema paraluiscuniculi: noncultivable species that infects rabbits
  • Causes veneral spirochetosis or treponematosis (“rabbit syphilis”, vent disease, cuniculosis)
  • Does NOT infect humans; evolved from T. pallidum-like ancestor and adapted to rabbits during loss of human infectivity
  • Can infx hares = seroconversion but no clinical signs
  • T. paraluiscuniculi & T. paraluisleporis may be subspecies
  • Clin signs: lesions at vulva or prepuce; also anal region, nose, eyelid, lip; experimental infx also scrotum, foot
116
Q

Epizootiology of treponematosis in rabbits

A
  • Suceptibility may vary with rabbit strain
  • Prevalence increases with age - suggest horizontal transmission among adult rabbits
  • Infection also occurs at birth (vertical transmission) and during suckling
  • Horizontal transmission by coitus and skin contact
  • Erythematous macules or papules to erosions, ulcers, crusts
117
Q

T. pallidum repeat (tpr) genes

A
  • Thought to code for potential virulence factors

- TprK is the only Tpr homolog found in T. paraluiscuniculi that induced Ab & T cell responses

118
Q

DIagnosis of treponematosis in rabbits

A
  • Serology - nontreponemal antigen tests & rapid plasma reagin, microhemagglutination, fluoresencent treponemal antibody absorption tests - of these, microhemagglutination is optimal
  • Dark-field microscopy of lesions & silver-staining of tissue sections
  • PCR
  • Ddx: abrasions, mycotic infections, acariasis
119
Q

Treatment & Prevention of treponematosis in rabbits

A
  • No vaccines
  • Hysterectomy can eliminate venereal spirochetosis
  • Benzathine penicillin G-procaine penicillin G x 7 days is effective - lesions heal within 2 wks & plasma reagin titers decline markedly and disappear by 6th weeks after the first tx
120
Q

Research complications of treponematosis in rbbits

A

-Can affect studies of T. pallidum in rabbits - partial immunological cross-protection between T. paraluiscuniculi & T. pallidum

121
Q

Proliferative enteropathy in rabbits

A
  • Lawsonia intracellularis: G(-), curved to spiral, obligate intracellular bacteria
  • Clin signs: intraepithelial ‘vibrio’ with acute typhlitis in rabbits 1-4 wks after weaning; diarrhea, histiocytic enteritis; suckling & weanling rabbits with semifluid and mucinous feces; lethargy, inappetence, dehydration, weight loss, death
122
Q

Epizootiology of proliferative enteropathy in rabbits

A
  • Generally occurs as isolated cases or occasional minor outbreaks (other than in pig, blue fox, hamster)
  • Rabbits can be reservoir host, but L. intracellularis appears to adapt to the specific animal it infect
  • IFN-gamma plays a significant role in limiting intracellular infection & increased cellular proliferation assoc w/ L. intracellularis
123
Q

Lawsonia surface antigen (LsaA)

A

Plays a role in attachment to and entry into intestinal epithelial cells
-BALB/cA mice susceptible to rabbit but not pig isolates, suggesting biological differences between isolates in pigs and rabbits

124
Q

Pathology of proliferative enteropathy in rabbits

A
  • Distension & diffuse mucosal thickening of JEJUNUM & PROXIMAL ILEUM; enlarged cranial mesenteric LNs
  • Mucosal thickening, distention of lamina propria with macrophages, enlargement of LNs with infilitration of macrphages
  • Minute bacilli in apical cytoplasm of mucosal epithelial cells = TOLUIDINE BLUE stain
  • Thickening of cecum and proximal colon; reddened cecum
125
Q

Histopathology of proliferative enteropathy in rabbits

A

Two types

1) Erosive and suppurative cecitis and colitis
2) Proliferative lesions in the cecum, sacculated colon, ileum, distal jejunum
- Some animals have both
- Narrow curved or spiral bacteria in lesions with WARTHIN-STARRY stain

126
Q

Diagnosis of proliferative enteropathy in rabbits

A

-16S rRNA of L. intracellularis isolates highly similar, but there are antigenic differences
-PCR of feces; ELISA using synthetic peptides of PsaA; immunomagnetic separation using anti-LsaA Ab to capture L. intracellularis in fecal samples followed by detection by ATP bioluminescence
-Silver stain like Warthing-Starry on tissue sections
-Indirect immunofluorescene on deparaffinized intestinal sections
-IHC using antiserum against synthetic peptides of LsaA
-Electron microscopy: organisms are 0.23-0.32μm
wide and ≤ 1.7 μm long in the apical cytoplasm of villous and crypt epithelial cells
-Culture from homogenized intestinal tissue in cell lines including IEC-18 (rat small intestinal cells) & McCoy cells (mouse fibroblasts)
-qPCR to assess the growth of L. intracellularis in cultured cells
-Ddx: Other causes of diarrhea; Mycobacterium avium subsp. paratuberculosis can cause thickening of intestinal mucosa - examine intestine sections for acid-fast organisms using ZIEHL-NEELSEN stain

127
Q

Treatment & Prevention of proliferative enteropathy in rabbits

A
  • Vaccines developed for pigs & horses but NOT rabbits
  • Test by PCR before bringing into colony
  • Oral neomycin (50 mg/rabbit) to treat surviving rabbits
128
Q

Research complications of proliferative enteropathy in rabbits

A

Mortality disrupts studies

129
Q

Myxomatosis in rabbits

A
  • Myxoma virus: Family Poxviridae, genus Leporipoxvirus
  • Disease severity varies with virus strain and host breed
  • Rabbits of genus Oryctolagus particularly susceptible - fatal disease with mucinous skin lesions & tumors
  • Edema around mouth, nose, anus, genitals; progressive conjunctivitis with serous and mucopurulent secretions from eyes and nose
  • Bacterial pneumonia develops within 10-14 days
  • Transmission: arthropod vectors and direct contact
130
Q

Epizootiology of myxomatosis in rabbits

A
  • Virus genome encodes for a number of immunomodulatory proteins which greatly affect host immune response: inhibit apoptosis, interfere with leukocyte chemotaxis, suppress leukocyte activation
  • Various Sylvilagus & Lepus species naturally susceptible
131
Q

Pathology of myxomatosis in rabbits

A

‘Myxomas’ - composed of undifferentiated stellate mesenchymal cells embedded in matrix of mucinous material & interspersed with capillaries and inflammatory cells

132
Q

Diagnosis of myxomatosis in rabbits

A
  • PCR or ELISA
  • Definitive diagnosis = culture of virus from tissues
  • Ddx: Genus Sylvilagus develop fibroma-like lesions that may be indistinguishable; Oryctolagus rabbits develop fatal diseaes d/t myxomatosis virus or fibromas d/t rabbit fibroma virus
133
Q

Treatment & Prevention of myxomatosis in rabbits

A
  • Spread by fleas and mosquitos & by direct contact = prevent contact with arthropods & quarantine infected rabbits
  • Vaccines used in Europe
  • A live recombinant vaccine for both myxomatosis and rabbit hemorrhagic disease has been released in the UK
134
Q

Rabbit (Shope) Fibroma Virus

A
  • Genus Leporipoxvirus; antigenically related to myxoma virus
  • Endemic in wild rabbits; less virulent strains cause skin tumors in domestic rabbits
  • Transmission: probably spread by arthropods
  • Fibromas are flat, SC, easily moveable tumors; most often on legs & face
  • Tumors may persist for some time but eventually regress; mets do NOT occur
135
Q

Rabbit Pox

A
  • Genus Orthopoxvirus; taxonomically similar to vaccina virus (outbreaks of fatal disease in lb rabbits)
  • Rare
  • Clin signs: fever, nasal discharge; eye lesions - blpeharitis, conjunctivitis, keratitis, corneal ulceration; do not always have skin lesions - when occur, begin as widespread macular rashes that progress to papules up to 1 cm diameter by 5 days post infection; enlarged LNs; facial edema; lesions in oral and nasal cavity
  • Necropsy: Nodules in liver, gall bladder, spleen, lung, repro organs; widespread necrosis; CYTOPLASMIC INCLUSIONS
  • Transmission: aerosol; difficult to control
  • Model of smallpox in humans
136
Q

Herpesvirus infections in rabbits

A

4 herpesviruses in rabbits and hares

1) Leporid herpesvirus 1 (LHV-1): isolated from cottontails; not pathogenic in domestic rabbits
2) LHV-2 (Herpesvirus cuniculi): isolated from O. cuniculus, subclinical
3) LHV-3 (Herpesvirus sylvilagus): isolated from cottonrails; lymphoproliferative disease with lymphoid infiltration of many organs; does not infect domestic rabbits
4) LHV-4: isolate from domestic rabbits, severe disease - wekaness, anorexia, conjunctivitis, keratitis, periocular swelling, skin ulcers - in preweanlings

137
Q

Taxonomy of rabbit herpesviruses

A

LHV-1, -2, & -3: Subfamily Gammherpesvirinae, Genus Radinovirus
LHV-4: Subfamily Alphaherpesvirinae; Genus Simplexvirus

138
Q

Papillomavirus in rabbits

A
  • Cottontail (Shope) papillomavirus: Kappapapillomavirus
  • Cottontail is natural host; widespread geographically; highest incidence in midwest
  • Clin signs: horny warts on neck, shoulders, abdomen; up to 25% of infected Sylvilagus develop squamous cell carcinomas
  • Natural outbreaks in domestic rabbits: papillomas on eyelids and ears
  • Transmission: arthropod vectors
  • Model of oncogenic virus biology & papillomavirus infection in humans
139
Q

Oral papillomatosis in rabbits

A
  • A Kappapapillomavirus that is related to but distinct from the cottontail rabbit papilloma virus
  • Natural lab rabbits lesions: small, white, discrete growths on ventral surface of tongue; lesions may ulcerate
  • Histo: typical papillomas
  • Most lesions regress spontaneously
140
Q

Rotavirus infections in rabbits

A
  • Family Reoviridae
  • All isolates of rabbit rotavirus classified as group A & serotype 3
  • Clin signs: severity variable; mild transient diarrhea; or anorexia, dehydration, watery to mucoid diarrhea, mortality
  • Other associated factors: maternal antibodies, diet, presence of pathogenic bacteria; older rabbits naturally more resistant to combined infection with rotavirus and E. coli
141
Q

Epizootiology of rotavirus in rabbits

A
  • Infections in domestic rabbits common; many rabbits seropositive & shedding in feces
  • Maternal antibodies decline around time of weaning = weaning age rabbits most susceptible
142
Q

Pathology, diagnosis, treatment of rotavirus in rabbits

A
  • Villous atrophy and loss of epithelial cells in the small intestines; lymphocytic infiltrate present
  • ELISA & multiplex fluorescent immunoassay commercially available; a commercial immunochromatography kit for detecting human rotavirus infection was used successfully for rabbit rotavirus
  • Ddx: C. piliforme, C. spiroforme, C. difficile, E. coli, L, intracellularis, coronavirus, coccidiosis, intestinal parasites
  • Treatment: supportive therapy
  • Research complications: colony mortality
143
Q

Coronavirus infection pleural effusion/cardiomyopathy in rabbits

A
  • Pleural effusion disease/infectious cardiomyopathy was diagnosed in rabbits inoculated with T. pallidum-infected stocks of testicular tissue - the stocks were contaminated with coronavirus that become more virulent with continued passage
  • Unknown if virus originated from humans or rabbits
  • Death d/t congestive heart failure; widespread necrosis of heart muscle
  • Might be a model of virus-induced cardiomyopathy
144
Q

Rabbit enteric coronavirus

A
  • Associated with one naturally occurring outbreak of diarrhea in a breeding colony - severe diarrhea, death within 48 hr
  • Could not experimentally replicate - quite probably other microorganisms & unknown environmental factors played a role
145
Q

Calicivirus in rabbits

A
  • Rabbit hemorrhagic disease (RHD)
  • Genus Lagovirus
  • 3 clinical syndromes: 1) Peracute form = sudden death w/out clin signs; 2) Acute form = anorexia, depression, neuro signs, resp signs, ocular hemorrhage, epistasia; high morbidity and mortality; lymphopenia and abnormal coagulation parameters; 3) Subacute form = similar but considerably milder signs and most rabbits survive
146
Q

Epizootiology of calicivirus in rabbits

A
  • First reported in China in 1984
  • Endemic in Europe, Asia, Australia, New Zealand
  • Transmission: fecal-oral route; fomites & arthropod vectors also suspected
  • Incubation period may be as short as 1-2 days
147
Q

Pathology, Diagnosis, and Treament/Prevention of calicivirus in rabbits

A
  • Periportal hepatic necrosis is the ONLY consistent microscopic lesion; animals die d/t DIC and thrombosis
  • Diagnosis: negative-contrast electron microscopy of liver tissue; specific antibodies can be detected by ELISA or hemagglutination inhibition
  • Ddx: European brown hare virus (related calicivirus in Europe) - necrotic hepatitis, hemorrhages in trachea and lungs, pulmonary edema - monoclonal antibody ELISA available for diagnosis
  • Treatment/Prevention: agent resists drying,can be carried on fomites, may be transmitted via respiratory and intestinal secretions
  • Any infected colonies should be quarantined and depopulated; environment thoroughly disinfected
  • Colony mortality disrupts research
148
Q

Other viruses in rabbits

A
  • Several other viruses have been isolated from rabbit tissues but not shown to produce disease: paramyxoviruses, bunyaviruses
  • Serologic titers to togaviruses and flaviviruses have also been demonstrated in rabbits
149
Q

Hepatic coccidiosis in rabbits

A
  • Eimeria stiedae
  • Clin signs: mild infx often subclinical; most clin signs d/t interruption of hepatic function and blockage of bile ducts; hepatomegaly, icterus, anorexia, diarrhea at terminal stages, decreased growth, weight loss
  • More common in juvenile rabbits; age of host strongly affect parasite development - 2 mth old rabbits produce more oocysts than 4 mth old
150
Q

Epizootiology of hepatic coccidiosis in rabbits

A
  • E. stiedae found worldwide
  • Transmission: fecal-oral; also IV, IP, IM administration of oocytes
  • Precise life cycle undetermined
  • Appears to come through blood or lymph into small intrahepatic ducts; sporozoites have been found in LNs
151
Q

Pathology of E. stiedae in rabbits

A
  • Enlarged, discolored liver with multifocal yellowish white lesions of varying size; exudate in biliary tree & dilatation of bile ducts
  • Papillomatous hyperplasia of bile ducts w/ multiple life-cycle stages in biliary epithelium
152
Q

Diagnosis, Treatment, Prevention of E. stiedae in rabbits

A
  • Infected rabbits may have decreased fibrinogen; increased bilirubin; leukocytosis, anemia
  • Fecal flotation or concentration
  • Oocysts can be detected in galbladder exudate; or in impression smears of liver
  • Ultrasound: dilated vessels and bile ducts, increased echogenicity of liver parenchyma
  • Ddx: Neoplasia, other parasitic hepatitis, hepatitis secondary to bacterial infx
  • Control: control infection until natural immunity develops is one strategy; immunity may be lifelong
  • Prevent: sulfaquinozaline in feed (250ppm); sulfonamides effective against Eimeria spp.
  • Treatment: Toltrazuril (50 ppm in drinking water for one day)
  • Research Complications: liver damage, decreased weight
153
Q

Intestinal coccidiosis in rabbits

A

-At least 14 different pathogenic spp of intestinal coccidia in rabbits, incl: Eimeria
coecicola, E. elongate, E exigua, E. intestinalis, E. flavescens, E. irresidua, E. magna, E. matsubayashii, E. media,
E. nagnurensis, E. neoleporis, E. piriformis, E. vejdovskyi, and E. perforans
-Clin signs: may be subclinical; severe diarrhea, weight loss, reduction in growth rate, severe dehydration, death
-Postweanling rabbits most susceptible to mortality
-E. perforans - may see fecal occult blood

154
Q

Epizootiology of intestinal coccidiosis in rabbits

A
  • Common in rabbits worldwide
  • Transmission: fecal-oral through ingestion of sporocysts
  • Unsporulated oocysts passed in feces & NOT infective - infective within 3 days after shedding; fecal shed can be enormous - environmental contamination can be a big problem
  • Life cycles of Eimeria spp: schizogony, gametogony, sporogony = 3 life cycle phases
155
Q

Pathology, Diagnosis, Treatment/Prevention of intestinal coccidiosis in rabbits

A
  • Necrotic areas of intestinal wall in small and large intestine = white foci
  • Diagnosis: oocysts on fecal, PCR - differentiates between 11 of the different spp in rabbits
  • Ddx: other causes of diarrhea in rabbits = Tyzzer’s disease, clostridial diseases, colibacillosis, L. intracellularis, enteric coronavirus & rotavirus, protozoons, intestinal parasites
  • Prevention: focus is in preweanling period; oral vaccination consisting of nonpathogenic E. magna = sprayed in next box when rabbits 25 days old; other oral vaccines in development
  • Prevention/control: also can be done with 0.02% sulfamerazine or 0.05% sulfaquinoxaline in drinking water; strict sanitation; elimination of infected animals
  • Treatment: Sulfaquinoxaline in feed (250 ppm)
  • Research Complications: can impact studies of GI tract; impact survival of postweaning rabbits
156
Q

Cryptosporidiosis in rabbits

A
  • Cryptosporidium cuniculus

- Clin signs: can be variable; lethargy, anorexia, diarrhea; small intestinal dilatation without other signs

157
Q

Epizootiology of Cryptosporidium cuniculus in rabbits

A
  • Transmission: ingestion of thick-walled sporulated oocysts
  • Experimentally infected juveniles began shedding oocysts 4-7 days post infection & continued to shed to 14 days post infection without clinical signs
158
Q

Pathology of C. cuniculus in rabbits

A
  • Small intestine: shortened, blunted villi and mild edema of lamina propria
  • Dilation of lacteal in ileum
159
Q

Diagnosis, Treatment, Prevention of C. cuniculus in rabbits

A
  • Diagnosis: POTENTIALLY ZOONOTIC; PCR to differentiate C. cuniculus from C. parvum & C. hominis
  • Ddx: Clostridium piliforme, C. spiroforme, C. difficile, E. coli, L. intracellularis, coronavirus, rotavirus, protozoans, intestinal parasites
  • Treatment: supportive care; minimizing stress can minimize or prevent clinical signs
  • Prevention: husbandry & sanitation practices that prevent exposure
  • Research complications: emerging as a human pathogen, so appropriate precautions for personnel
160
Q

Encephalitozoonosis in rabbits

A
  • Encephalitozoon cuniculi
  • 3 strains: I - rabbit strain, II - mouse strain, III - dog strain
  • Clin signs: weeks to months delayed onset to clinical signs; early infx affects kidney, liver, lung & later infx affects kidney & brain
  • Usually latent, but can see convulsions, tremors, torticollis, paresis, coma, kidney failure, intrauterine infection with phacoclastic uveitis & rupture of lens capsule
161
Q

Epizootiology of Encephalitozoon cuniculi in rabbits

A
  • Transmission: likely horizontal via direct contact or environmental contamination - ingestion of infected urine
  • Also vertical transmission in utero
162
Q

Pathology of Encephalitozoon cuniculi in rabbits

A
  • Kidneys: multiple, white, pinpoint areas or gray indented areas on renal cortex = granulomatous inflammation; interstitial infiltration of lymphocytes and plasma cells and tubular degeneration
  • Granulomatous encephalitis; lesions of spinal cord
  • Organisms may be seen floating free in tubules of kidney
163
Q

Diagnosis, Treatment, Prevention of Encephalitozoon cuniculi in rabbits

A
  • Dx: Histopathology with organism in brain or kidney = GIEMSA, GRAM, OR GOODPASTURE’S CARBOL FUCHSIN stain
  • Serology, ELISA, indirect fluorescence; PCR of intestine, brain, heart, liver, lung, or kidney tissue
  • Ddx: Motor paralysis = splay leg; Neuro signs = bacterial meningitis d/t P. multocida or rabbit hemorrhagic disease
  • Prevention: Latent disease in rabbits so use serology or IFA to identify and remove carriers; disinfect with 2% Lysol, 10% formalin, 70% ethanol, 1% hydrogen peroxide, 1% sodium hydroxide
  • Treatment: Fenbendazole; for phacoclastic uveitis: lens removal
164
Q

Research Complications of Encephalitozoon cuniculi in rabbits

A
  • Granulomatous reactions complicate renal physiology and neuro research
  • Depression of IgG response & increase in IgM response to Brucella abortus antigen has been demonstrated in rabbits infected with Encephalitozoon
  • ZOONOTIC to immunodeficient humans
165
Q

Psoroptes cuniculi

A
  • Nonburrowing mite that causes psoroptic mange (also called ear mange, ear canker, otoacariasis); distributed worldwide
  • Clin signs: lesions on inner surface or external ear, head shaking, pain, self-mutilation; tan crust exudate in ears, underlying skin moist & reddened
166
Q

Epizootiology of Psoroptes cuniculi in rabbits

A
  • All stages of mite (egg, larva, protonymph, adult) occur in the host
  • Early in infestation, mites feed on sloughed skin cells & lipids - as inflamm increases feed on serum, Hgb, RBCs
  • Life cycle is 21 days
  • Mites resistant to drying and temperature; can survive off host for 7-20 days in temp range of 5-30 C and relative humidity 20-75%
167
Q

Pathology of Psoroptes cuniculi in rabbits

A
  • Histo: chronic inflammation, hypertrophy of the Malpghian layer, parakeratosis, epithelial sloughing
  • Hypersensitivity response to mites, mite feces, saliva likely contributes to lesions
168
Q

Diagnosis, Treatment, Prevention of Psoroptes cuniculi in rabbits

A
  • Dx: See with otoscope or on dissecting scope: mites are oval shaped with well-developed legs that project beyond the body
  • Ddx: Sarcoptes scabiei, Cheyletiella parasitovorax
  • Treatment: clean ears to remove exudate; 3% rotenone in mineral oil every 5 days for 30 days; ivermectin at 400-440 ug/kg SC or IM x 1 or 2 doses; adjunct vitamin therapy to minimize oxidative tissue damage; topical selamectin 6 mg/kg singly dose; single injection eprinomectin at 200 or 300 ug/kg
  • Treat entire group of rabbits at same time
  • Heat (40 C) and dessication (<20% humidity) will kill parasites not on host
  • Vaccine targets being investigated for gut surface antigen
  • Research complications: Assoc w/ immune suppression, systemic inflammatory rxn; ear trauma can limit access to auricular artery and vein
169
Q

Cheyletiella spp (C. parasitovorax, C. takahasii, C. ochotonae, C. johnsoni) in rabbits

A
  • Nonburrowing skin mites; distributed worldwide

- Clin signs: most commonly over the scapulae; mild hair loss; gray-white scale on skin; NO PRURITIS

170
Q

Epizootiology of Cheyletiella spp. in rabbits

A
  • All stages (egg, larva, pupa, adult) occur on the host
  • Mite remains in association with keratin layer of skin & feeds on tissue fluid
  • Transmission: direct contact
171
Q

Pathology, Diagnosis, Treatment, Prevention of Cheyletiella spp. in rabbits

A
  • Mild dermatitis, hyperkeratosis, inflammatory cell infiltrate
  • Dx: skin scrape or brushing fur onto slide - clear samples with 5-10% potassium hydroxide to better visualize mites
  • Cheyletiella mites have a large, distinctive curved claw on the palpi
  • Ddx: Other skin (Sarcoptes scabei) or fur (Leporacarus gibbus) mites; dermatophytosis
  • Topical acaracids - ivermectin SC or SC and oral; selamectin topical
  • Eggs in environment can reinfest host, so environmental sanitation important
  • ZOONOTIC - transient dermatitis in humans
172
Q

Sarcoptes scabiei in rabbits

A
  • Burrowing mite & causative agent of sarcoptic mange; worldwide distribution
  • Clin signs: intense pruritis with hair loss and abrasions; serous encrustations on skin & secondary infection with bacterial or Malassezia; anemia, leukopenia
173
Q

Epizootiology of Sarcoptes scabiei in rabbits

A
  • Lesions most common on head
  • All stages occur on the host: females burrow into skin & lay eggs - young larvae can also be found in skin, while older larvae, nymphs & males reside on skin surface; feed on lymph & epithelial cells
174
Q

Pathology, Diagnosis, Treatment, Prevention of Sarcoptes scabiei in rabbits

A
  • Amyloidosis of liver & glomerulus reported with severe infestation; skin is hyperplastic and hyperkeratotic
  • Dx: skin scraping - sample may be cleared with 5-10% potassium hydroxide; body shape is round, legs very short
  • Ddx: Other causes of dermatitis in rabbits: Cheyletiella sp., P. cuniculi, dermatophytosis
  • Tx: ivermectin 100 ug/kg SC; single dose selamectin at 10-12 mg/kg reduced number of mites in Angora rabbits & eliminated infestation at 30 mg/rabbit
  • More ‘natural’ treatments being investigated for Sarcoptes & Psoroptes with good preliminary results for eugenol & Eupatorium spp.
  • ZOONOTIC - self-limiting dermatitis in humans
175
Q

Oxyuriasis in rabbits

A
  • Passalurus ambiguus (was called Oxyuris ambigua) - rabbit pinworm
  • Clin signs: usually subclinical; one case report of poor condition & breeding performance
  • Direct life cycle: mature pinworms in lumen of cecum & colon; after ingestion, eggs hatch in small intestine, larvae molt with maturation in cecum
  • Prepatent period: 56-64 days
  • Transmission: ingestion of embryonated eggs - are immediately infective when passed out in feces
  • Minimal to no pathology lesions
  • Dx: eggs in feces, cecum or colon
  • Ddx: only reported pinworm in rabbits
  • Treatment: piperazine citrate at 100 mg/100 ml in drinking water for 1 day; 25 or 50 ppm fenbendazole in food for 5 days; SC 0.4 mg/kg ivermetin
  • Strict husbandry and sanitation practices to prevent introduction & spread
176
Q

Dermatophytosis in rabbits

A
  • Species in rabbits: Trichophyton mentagrophytes & Microsporum canis
  • Caused by a dermatophyte: a keratinophilic and keratinolytic fungus; group of closely related filamentous fungi that are able to invade the stratum corneum of the epidermis & keratinized tissues like skin, nail, hair
  • ZOONOTIC: can infect various species
  • Clin signs: area of circular alopecia w/ erythematous margin & thin desquamation; pruritis generally absent; head and anterior body more frequently involved
  • Rabbits: lesions on ears and face (around eyes and nose) with scaling and crusting
  • Asymptomatic rabbits may act as carriers
177
Q

Epizootiology of dermatophytosis in rabbits

A
  • Young or immunocompromised rabbits more susceptible
  • Disease varies depending on host, fungal species, enzyme production
  • Pathogenesis involves contact, adherence, germination, invasion, and penetration - assoc w/ secretion of enzymes that degrade infected tissue components
  • T. mentagrophytes isolated from rabbits with skin lesions showed higher elastase and gelatinase activity compared to isolates from clinically unaffected rabbits; M. canis from rabbits with lesion had higher lipase activity
178
Q

Diagnosis of dermatophytosis in rabbits

A
  • Wood’s lamp UV light - works for M. canis w/ apple-green fluorescence
  • Direct exam of hairs and scales
  • Deep skin scraping to confirm absence of mites that can be assoc w/ dermatophytosis; use 10% KOH to digest keratin on slide; see clusters or chains of arthroconidia
  • Giemsa stained skin scrapings
  • GOLD STANDARD = fungal culture; samples include hair, scales, crusts, skin scrapes, tissue bipsies
  • Media for fungal culture = Sabouraud dextrose agar (supplemented with cycloheximide and antibiotics) & Dermatophyte Test Media (DTM)
  • Histo: Periodic acid Schiff (PAS) or methylamine silver stain to see arthroconidia or hyphae
  • PCR-RFLP and sequencing of the internal transcribed spacer (ITS) region
  • Ddx: dermatoses caused by bacteria or ectoparasites
179
Q

Treatment, Prevention of dermatophytosis in rabbits

A
  • Self-limiting in immunocompetent animals; but affected rabbits should be culled or separated b/c contagious & zoonotic
  • An animal that contacts an infected animal - wash with antifungal shampoo
  • Prevention: two vaccines incorporating live attenuated cells of T. mentagrophytes (Mentavak - Russia & Trichopelen - Czech Republic); Trichopelen also indicated for treatment
  • Disinfection of environment with 1:10 diluted bleach or 0.2% enilconazole solution
  • Tx: systemic griseofulvin (gold standard), azole derivatives (these systemic tx are teratogenic); topical 0.2% enilconazole, 2% miconazole + 2% chlorhexidine, lime sulfur
  • Continue treatment until after two negative fungal culture results
  • Research complications: confound histo studies involving skin
180
Q

Pneumocystosis in rabbits

A
  • Pneumocystis oryctolagi fungus

- Clin signs: immunocompromized can develop severe interstitial pneumonitis; otherwise subclinical

181
Q

Epizootiology of pneumocystosis in rabbits

A
  • Corticosteroid tx can induce disease in infected rabbits, but spontaneous disease can also occur
  • Transmission: direct contact, aerosolization, transplacental
  • Spontaneous pneumocystosis can occur at weaning, evolves during 7-10 days with lung lesions & blood biochemical changes
  • Organisms attach to Type 1 epithelial alveolar cells & proliferate, filling up pulmonary alveoli cavities leading to respiratory failure; changes in surfactant necessary for proliferation
  • Most rabbits recover within 3-4 weeks
  • Spontaneous resolution may be assoc w/ expression of interferon gamma
182
Q

Pathology of pneumocystosis in rabbits

A
  • Histo: cystic forms of organism in lungs with TOLUDINE BLUE, O (TBO), GMS, PAS stains
  • Interstitial thickening of alveolar septa and increased numbers of Type 2 epithelial alveolar cells
183
Q

Diagnosis of pneumocystosis in rabbits

A
  • Nasal cavity, terminal BAL or lung homogenates used for PCR
  • Lung impression smears, lung-homogenate smears, BAL fluid stained for microscopic detection
  • Useful stains: TBO, Gomori-Grocott’s methamine silver nitrate (GMS), methanol-Giemsa, or Giemsa-like stains
  • Phase-contrast microscopy of Pneumocystis-specific fluoresceint-labled antibodies
  • Ddx: P. multocida
184
Q

Treatment, Prevention of pneumocystosis in rabbits

A
  • Cotrimoxazole treatment and PCR as a screening mechanism has been described
  • Decontamination and air filtration practices important for eradication
  • Research complications: studies with corticosteroid or other immunosuppressant drugs; pulmonary lesions
185
Q

Gastric trichobezoar in rabbits

A
  • Clin signs: often subclinical; if causes blockage may have signs of gastric or intestinal obstruction; death d/t prolonged anorexia and metabolic imbalances
  • The obstruction of the pylorus, and not the volume of the gastric mass, is the critical factor in determining clinical progress of animal
  • Hairballs are often incidental findings on routine necropsy
  • May have gastric rupture d/t obstructive trichobezoar
  • Dx: often difficult b/c signs nonspecific; manual palpation with firm mass in cranial abdomen; gastric rads with contrast; definitive diagnosis = explorative sx
  • Ddx: constipation, intestinal foreign body
  • Tx: often unsuccessful; mineral oil at 10 ml/day; 5-10 ml fresh pineapple juice daily; if medical tx does not correct, gastrotomy
186
Q

Traumatic vertebral fracture in rabbits

A
  • Subluxation or compression fractures of lumbar vertebrae
  • Often secondary to struggling during restraint
  • L7 or its caudal articular processes most common site for fractures
  • Clin signs: posterior paresis/paralysis, loss of sensation in the hindlimbs, urinary and/or fecal incontinence, perineal staining
  • Pathology: spinal cord hemorrhage & necrosis
  • Dx: based on history, clinical signs, palpation and/or radiographs
  • Ddx: spinal cord trauma
  • Treatment: subluxation with spinal edema may resolve over time; supportive care w/ expression of bladder, prevention and tx of decubital ulcers; corticosteroid and diuretic therapy may be effective for subluxation with spinal edema
187
Q

Ulcerative pododermatitis in rabbits

A
  • Most frequently the plantar surface of the metatarsal, and to a lesser extent metacarpal, regions
  • Risk factors: Wire-floor housing, foot stomping, thin plantar fur pads, poor sanitation, increased body condition, high-energy diet
  • Provide solid resting areas to decrease incidence
188
Q

Genetic engineering techniques for rabbits

A
  • Pronuclear injection of single cell embryos, injection of genetically modified embryonic stem cells into blastocysts, sperm-mediated gene transfer, genetically modified somatic cell and nuclear transfer
  • Commercial companies have been formed to provide genetic modification services with emphasis on production of a unique protein in rabbit milk
189
Q

Hydrocephalus in rabbits

A
  • Dilatation of the cerebral venricles, usually accompanied by accumulation of CSF within the dilated spaces
  • In rabbits, may be related to single autosomal recessive gene (hy/hy)
  • May be inherited along with various ocular anomalies as an autosomal gene with incomplete dominance
  • Can also occur related to hypovitaminosis A in pregnant does
190
Q

Buphthalmia (congenital glaucoma, hydrophthalmia) in rabbits

A
  • Inherited autosomal recessive trait; penetrance presumably incomplete since severity & age of onset vary greatly
  • bu/bu; some bu/by individuals do not develop buphthalmia
  • Clin signs: high IOP (in newborns high by 1-3 mths, 24-48 mmHg, can return to normal or subnormal after 6-10 mths); cloudy or bluish cornea, corneal edema, increased corneal vasulature, flattening of cornea; increased corneal diameter as globe enlargers while sclera still immature
  • Widening of the anagle, thickening of Descmet’s membrane, atrophy of ciliary process, excavation of optic disc;
  • Impaired aqueous outflow may be d/t incomplete cleavage of the drainage angle with abnormal insertion of uveal tissue into the cornea
  • Marked reduction in semen concentration, decreased libido & spermatogenesis
191
Q

Epizootiology & Pathology buphthalmus in rabbits

A
  • Common in NZW rabbits
  • By 2 wk of age, congenital glaucoma trabecular network becomes abnormal
  • By 6 wk of age, iris pillars with extensive lateral extensions in the angle recess are observed
192
Q

Diagnosis, Treatment, Prevention buphthalmus in rabbits

A
  • Dx: clinical signs & IOP
  • Tx has not been described
  • Individuals should not be used for breeding
193
Q

Mandibular prognathism (Malocclusion, Walrus Teeth, Buckteeth)`

A
  • Most common inherited disease in domestic rabbits
  • Recessive trait (mp/mp) with incomplete penetrance
  • Clin signs: weight loss, anorexia, malocclusion may be apparent as early as 2-3 wks old
  • Dx: based on clinical signs
  • Ddx: malocclusion d/t fracture
  • Tx: trim teeth every 2-3 weeks with a dental bur (bone cutter may crack teeth!); avoid exposing pulp cavity
  • Do not breed b/c condition hereditary
194
Q

Epizootiology of mandibular prognathism in rabbits

A
  • Normally, mandibular incisors wear against the maxillary incisors & the maxillary secondary incisors (peg teeth) wear at right angles to the mandibular incisors
  • Incisors wear more quickly at the posterior aspect in rabbits, partly b/c enamel is thinner on that side
  • Mandibular prognathism = maxilla is short relative to mandible of normal length - problem is the maxilla!
195
Q

Normal growth rate of rabbit incisors

A

2-2.4 mm/week

196
Q

Splay leg in rabbits

A
  • 3-4 weeks of age
  • Cannot adduct limbs; have trouble with locomotion
  • Most commonly the right rear leg
  • May be d/t imbalance of development of the neural, muscular, and skeletal systems; possibly some animal compensate with torsion and exorotation of the limb at the hip
  • Usually seen secondary to femoral endotorsion w/ a shallow acetabulum & femoral luxation
  • The semitendinosus muscle of affected animals is abnormal w/ smaller fibers & abnormal mitochondria
  • May be assoc w/ achondroplasia of the hip & shoulder, or recessively inherited anteversion of the femoral head
197
Q

Inherited self-mutilating behavior in rabbits

A
  • Reported as an inherited trait in a Checkered cross rabbit
  • Autrotraumatization of feed & pads
  • Abnormal behavior could be interrupted by administering haloperidol
198
Q

Atropine esterase activity in rabbits

A
  • Presence of serum atropine esterase allows rabbits to inactivate atropine
  • Also allows rabbits to consume diets containing belladonna compounds
  • Enzyme produced by semidominant gene Est-2F: 3 phenotypes recognized depending on number of genes expressed
  • Enzyme first appears in serum at 1 mth of age; enzyme levels greater in females
  • Est-2F gene also linked to genes controlling black pigment in coat
199
Q

Complement 3 deficiency in rabbits

A
  • Found in a strain of rabbits that also had C8 alpha-gamma deficiency
  • Serum C3, hemolytic C3 activity, and total competent hemolytic activity were reduced
  • Transmitted as a simple autosomal co-dominant trait
  • Rabbits with this trait have lower survival at 3 months than normal rabbits
200
Q

Complement 6 deficiency

A
  • Autosomal recessive inheritance
  • Whole blood clotting time prolonged & prothrombin consumption decreased in blood
  • Other blood coag parameters normal
  • Abnormal platelet response is also characteristic
  • C6-deficient rabbits are protected against diet-induced atherosclerosis despite having similar cholesterol and plasma lipoprotein levels; differences in athersclerotic plaque formation compared to normal rabbits
201
Q

Progressive neurologic syndrome in C6-deficient rabbits

A
  • Clin signs: subacute motor neuropathy
  • Pathology: severe axonal degeneration in sciatic nerve involving mainly motor fibers; occasional peripheral axonal enlargement closely assoc w/ axonal degeneration; presence of structured abnormal material in normal-size myelinated fibers of PNS & CNS; widespread dystrophic axons & axonal spheroids in gray matter of CNS
  • Dystrophic axons filled with tubulovesicular material = stalks of parallel membranes and dense bodies similar to what is seen in human neuroaxonal dystrophies (NAD) - may be animal model for this
202
Q

Complement 8 deficiency in rabbits

A
  • Deficiency in alpha-gamma subunit of C8 found in substrain of NZW rabbits
  • Simple autosomal recessive inheritance
  • Clin signs: smaller body size (dwarfism) and weight, smaller thymus, lower survival rates at 3 months of age, fertile but reduced delivery rate of C8D x C8D or C8D x dwarf crosses
  • There is also a discrete recessive dwarf gene (dw-2) NOT linked to C8 deficiency; rabbits double-homozygous for C8D and dw-2 are even smaller
  • Locus loosely linked to C3 hypocomplementemic locus (C3-hypo)
203
Q

Hypercholesterolemia (Kuroawa and Kusanagi Hypercholesterolemic) in rabbits

A
  • Produced by inbreeding mutants
  • Have persistent hypercholesterolemia, triglyceride & phospholipid levels 8-10x greater than normal rabbits, decreased serum HDL
  • Serum lipoprotein electrophoretic patterns characterized by strong broad beta-lipoprotein band & diminshed alpha-protein band
  • High LDL values, low HDL values
  • Single autosomal recessive inheritance
  • Have a 12 base pair deletion in the LDL receptor mRNA
  • Atheromatous lesion in aorta at 2 months of age, drastically increased lesional areas at 8 months of age in aorta, & high incidence of coronary atheromas & xanthomas
204
Q

Hyperlipidemia in rabbits

A
  • Spontaneous phenotype with elevation of serous lipid ingredients - cholesterol & beta-lipoprotein (beta-LP)
  • Atheroscelortic lesions in aorta and renal arteries
  • Nodular xanthomas on front and rear feet
  • Watanabe-heritable hyperlipidemic rabbit (WHHL-rabbit) - spontaneous aortic atherosclerosis by 5 mth of age & xanthoma of digital joints in 60% by 16 mths
205
Q

Most common neoplasia in female rabbits

A
  • Endometrial adenocarcinoma in aged female rabbits
  • 79% of 5 year olds
  • Historically neoplasias not commonly reported in rabbits b/c very uncommon before 2 yrs of age & lab rabbits often not maintained that long
206
Q

Uterine neoplasia in rabbis

A
  • Uterine adenocarcinoma by far most common tumor in rabbits; typically multiple tumors & malignant w/ mets to liver, lung, etc.; inheritance plays a role, parity does not
  • Uterine leiomyomas & leimyosarcomas much less common
  • Few reports of vaginal squamous cell carcinomas, ovarian hemangioma
207
Q

Mammary neoplasia in rabbits

A
  • Mammary adenocarcinomas fairly common in older female rabbits & may occur in animals with uterine adenocarcinoma; malignant & metastasize; tumors are preceded by cystic mastopathy & changes in adrenal and pituitary glands
  • Papillomas have been described
  • Small prolactin-secreting pituitary adenomas in rabbits with mammary dysplasia
208
Q

Testicular tumors in rabbits

A
  • Relatively uncommon
  • Interstitial tumors most common of them
  • Seminomas & teratomas also reported
209
Q

Embryonal nephromas in rabbits

A
  • One of the most common tumors in lab rabbits
  • Found incidentally, occur in younger animals
  • Rarely have clinical signs
210
Q

Bladder & renal neoplasia in rabbits

A

-One report each of renal carcinoma & leiomyoma of urinary bladder

211
Q

Hematopoietic neoplasia in rabbits

A
  • Malignant lymphomas (lymphosarcomas) relatively common; may occur in rabbits less than 2 yr old; see enlarged kidneys, splenomegaly, hepatomegaly, lymphadenopathy; older rabbits may have skin nodules, eye lesions; resemble lymphoblastic subtype in humans & mice; some evidence for retroviral cause
  • True thymomas (containing both lymphoid & epithelial components) & plasma cell myelomas are rare
  • One report of myeloid leukemia
212
Q

Skin and SC neoplasia in rabbits

A
  • Basal cell tumors rare but may be underreported
  • Squamous cell carcinomas uncommon, no apparent predilection for any particular area of body
  • Trichoepithelioma, sebaceous gland carcinoma, malignant melanoma reported
213
Q

Bone, muscle, connective tissue neoplasia in rabbits

A
  • Osteosarcomas extremely rare - most in mandible or maxilla
  • Some reported osteosarcomas had cartilaginous elements
  • One rhabdomyosarcoma reported
  • Few fibrosarcomas & one fibrosarcoma involving the foot reported
214
Q

Miscellanous neoplasia in rabbits

A

-Peritoneal mesothelioma, intracranial teratoma, ependymoma, neurofibrosarcoma, hemangiosarcoma, malignant fibrous histiocytoma, lung tumors

215
Q

Neoplasia models derived from rabbits

A
  • Several tumor models in which cells originally derived from rabbits: vx-2 carcinoma, Brown Pearce carcinoma, Greene melanoma
  • vx-2 carcinoma originated from a squamous cell carcinoma in a rabbit carrying a Shope papilloma
  • Brown Pearce carcinoma arose from a tumor in a rabbit testis
216
Q

Hydrometra in rabbits

A
  • Reported in unmated rabbits
  • Clin signs: abdominal distension, tachpnea; distension of uterine horns with transudative fluid
  • One case assoc w/ uterine torsion; one case reesolved with diuretic therapy only to return later
217
Q

Liver lobe torsion in rabbits

A
  • Most commonly the caudate lobe & an incidental finding
  • Clin signs if clinical: acute onset lethargy, anorexia, abdominal pain, jaundice, pale mucous membranes, hematuria, anemia, elevated alanine aminotransferase
218
Q

Urolithiasis in rabbits

A
  • Normal rabbit urine contains calcium carbonate & triple phosphate crystals
  • A possible cause of hematuria in rabbits d/t secondary urethral obstruction, hemorrhagic cystitis
219
Q

Causes of hematuria in rabbits

A

Uterine adenocarcinoma, uterine polyps, renal infarction, urolithiasis, chronic cystitis, DIC, bladder polyps, pyelonephritis, endometrial venous aneurysm

220
Q

Lumbar hernia in rabbits

A
  • Herniation of kidney along with pernephric fat has been reported
  • Affected rabbit was clinically normal except for SC mass
  • May have occurred d/t trauma?
221
Q

Anomalous nasolacrimal duct apparatus

A
  • Occlusion of the nasolacrimal duct, d/t accumulation of fat droplets, is a potential cause of epiphora in rabbits
  • Obstruction reported to occur at dorsal flexure; unclear if congenital or acquired stenosis
  • Often unilateral
  • Receive abx for treatment
  • Assoc w/ malocclusion, rhinitis, or no underlying cause

Laboratory Animal Medicine Blue Book, 3rd Ed. (2015) (16 decks)

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