Common Diseases of Rabbits, Ferrets and Guinea Pigs Flashcards Preview

Semester II Pathology > Common Diseases of Rabbits, Ferrets and Guinea Pigs > Flashcards

Flashcards in Common Diseases of Rabbits, Ferrets and Guinea Pigs Deck (26):
1

COMMON DISEASES IN THE RABBIT

INFECTIOUS- Myxomatosis virus, Rabbit Viral Haemorrhagic Disease (RVHD), Encephalitozoon cuniculi.
NEOPLASTIC- uterine adenocarcinoma.

Rabbits are farmed in many European countries, so these diseases are important from an economic perspective as well.

2

MYXOMATOSIS

Caused by leporipoxvirus (DNA virus)
-Latent period- subcutaneous myxoid mass forms 3-4 days post inoculation
-6-8 days- mucopurulent conjunctivitis, subcutaneous oedema, MULTIPLE SUBCUTANEOUS MASSES (characteristic).
-Rapid progression.
-Lesions and oedema round the nose and mouth can interfere with breathing and food intake.
-PERACUTE form- sudden death (with reddened conjunctiva- other symptoms don't have time to develop.

3

MYXOMATOSIS- DIAGNOSIS

Lesions in the head and neck area are highly suggestive.
The presence of multiple subcutaneous masses is classic.
Virus isolation can confirm diagnosis.

4

MYXOMATOSIS- SPREAD

The virus is spread via FLEAS, which act as arthropod vectors.
It can also spread via direct/indirect contact between rabbits.

5

MYXOMA CELLS

Presence of these cells histologically is characteristic of myxomatosis.
Appear as spindle to stellate shaped mesenchymal cells in the dermis.
The dermis is massively expanded by the presence of these cells.
Typical poxvirus inclusion bodies can be seen in the cytoplasm of other cells.
They are highly eosinophilic.

6

RABBIT VIRAL HAEMORRHAGIC DISEASE (RVHD)

Calicivirus (lagovirus)- single stranded RNA virus.
-Virus shows tropism for HEPATOCYTES and MACROPHAGES- it replicates in these cells.
-Transmission- direct contact, contaminated fomites.
-VERY CONTAGIOUS
-Animals shed virus in the urine for up to 4 weeks, and in the faeces long term.
-PERACUTE form MOST COMMON.
-In some animals, a subacute disease course occurs.
-If animal survives acute phase, it becomes a shedder of virus (latent- could reinfect)

7

RVHD- DIAGNOSIS

Lesions highly suggestive.
Confirm with virus isolation, immunohistochemistry and/or ELISA.

8

RHVD- TRANSMISSION AND CLINICAL SIGNS

-TRANSMISSION- Direct contact, indirect contact- fomites, cages.
Persists in refrigerated meat for up to 9 months, longer in frozen meat.
-RVHD affects domestic and European rabbits. The European hare is not affected, but is susceptible to another closely related virus- Brown Hare Syndrome. There is NO cross-infection.
-Susceptible rabbits under TWO MONTHS of age do NOT develop disease- possible because the liver is still immature.
-Incubation period- 24-28 hours post-incubation.
-Some animals may be resistant to disease and become shedders of virus for 4 weeks- subacute disease.
-Generally the disease has no clinical signs, as it's onset is so rapid.
-If seen: pyrexia, muscle tremors, excitability can be seen
-Mortality- 50-100% in 24 hours.

9

RVHD- PATHOGENESIS AND LESIONS

-Massive liver necrosis- enlarged, pale, diffuse mottled discolouration on PM.
-> Widespread endothelial damage and/or activation of coagulation cascade.
-> Disseminated Intravascular Coagulation
-> Systemic thrombosis and haemorrhagic diastesis (susceptible to bleeding) in multiple organs.
-Epistaxis or presence of bloody fluid in nasal cavity.
-Haemorrhagic lesions in larynx, trachea, lungs, gut.
-Bloody fluid in peritoneal cavity (serosanguinous exudate)
-Pale spleen and kidneys due to massive blood loss.

10

RVHD- DIAGNOSIS, TREATMENT, PREVENTION

DIAGNOSIS- Characteristic lesions, virus isolation from tissue extracts, immunohistochemistry, ELISA serological test.
TREATMENT- none available. Animals die in peracute or after subacute phase.
PREVENTION- inactivated virus vaccines commercially available in some countries- revaccination every 6 months necessary for sustained protection.

11

ENCEPHALITOZOON CUNICULI

This is an obligate intracellular microsporidian (eukaryotic) parasite that infects rabbits, causing clinical disease.

12

ENCEPHALITOZOON- TRANSMISSION AND CLINICAL SIGNS

Wide host range- rabbits, mice, monkeys, squirrels, cats, dogs, humans (ZOONOTIC)
Spores in infected urine transmitted via oral and respiratory routes.
Spores are shed in urine from 1 month up to 3 months post infection.
CLINICAL SIGNS- torticollis, limb paresis, other neurological manifestations, urinary incontinence (aids spread of spores).
Animals can be infected without showing clinical signs- 25-80% animals. High numbers still have positive serology, so are shedding the organism even with no clinical signs.

13

COMMON FINDINGS IN ENCEPHALITOZOON INFECTION

-Cataracts- seen with chronic granulomatous uveitis.
-Pitted kidneys (PM)- typical gross appearance of chronic infection. Fibrotic, inflamed.
-Vestibular disease due to lesions in CNS.
1. OCULAR DISEASE
2. URINARY TRACT DISEASE
3. NEUROLOGICAL DISEASE.

14

ENCEPHALITOZOON- PATHOGENESIS AND LESIONS

Spores excreted in urine infect susceptible animals via oral/respiratory routes, then infect mononuclear cells.
-> LIVER, KIDNEY, LUNG, BRAIN, EYE
-> Infect endothelial cells
-> Organism multiplies, is released from cells and causes INFLAMMATION
-> INTERSTITIAL GRANULOMATOUS INFLAMMATION, NECROSIS
-> Spores pass in to renal tubules and epithelium
-> Spores excreted in urine
etc.

15

ENCEPHALITOZOON- KIDNEYS

Kidney endothelial cells are infected.
Release of organism causes interstitial granulomatous inflammation and necrosis
-> CHRONIC INTERSTITIAL NEPHRITIS
-> RENAL FAILURE- defective tubular reabsorption/secretion
-> ISOSTHENURIA, URAEMIA, OEDEMA- due to protein loss decreasing oncotic pressure.

16

ENCEPHALITOZOON- HISTOLOGY

ZN stain capillary vessels in brain- shows purple intracellular spores in the endothelial lining of the vessels.
ZN stain brain tissue- shows granulomatous reaction against organisms.
CNS lesions- focally extensive round lesion, necrosed centre with peripheral granulomatous infiltrate.
Inflammatory cell infiltrate in perivascular areas.
CNS lesions account for neurological disease manifestation.

17

UTERINE ADENOCARCINOMA

MOST COMMONLY OCCURRING SPONTANEOUS NEOPLASM in rabbits.
4% does 2-3 years old.
80% does 5-6 years old- older animals are high risk.
Pathogenesis- carcinogenic effects of oestrogens?
(Not proven- experimental models have not replicated disease)
-Usually involves both uterine horns- multicentric enlargements
-Cut surface has firm, cauliflower like surface. Central ulceration- necrosis.
-May see serosal implantation, aggressive liver/lung metastases.

18

DIFFERENTIALS- HAEMATURIA IN THE RABBIT

If the rabbit presents with haematuria (blood in urine)/bloody vaginal discharge, consider the causes- uterine or urinary?
UTERINE- Adenocarcinoma, polyps, endometrial venous anuerysms (episodic bleeding and thrombus formation)
URINARY- cystitis, pyelonephritis, polyps.

19

UTERINE HISTOPATHOLOGY

-Papillary projections of proliferating, well differentiated epithelial cells, forming ducts and acini.
-Elongated nucleus, but fairly well differentiated- low mitotic index. Suggests ADENOMA- benign tumour.

20

IMPORTANT DISEASES IN THE FERRET

-Cardiomyopathy
-Dental disease
-Lymphoma
-Endocrine disease (see endocrine lectures)

21

FERRET CARDIOMYOPATHY

Most common cause of heart failure in ferrets.
Dilatative, hypertrophic, restrictive- most common forms.
Can be seen as early as 1 year, but commonly affects animals 5-7 years old.
Familial (inherited) in some North American ferret lines.
10% of ferrets with hyperadrenocorticism (Cushing's) have concurrent cardiomyopathy- predisposing factor.

22

FERRET CARDIOMYOPATHY- HISTORY AND CLINICAL SIGNS

Progressively worsening dyspnoea, lethargy. Mild abdominal distension.
-> Pleural effusion into thoracic cavity compressing lungs/heart, causing dyspnoea, lethargy.
-> Thickened heart (interventricular septum, walls) multifocal pale discolouration- fibrosis.
-> Histopathology- loss of striation of cardiomyocytes, multifocal cardiomyocyte cytoplasmic vacuolation- swelling, replacement by fibrous tissue- increased collagen and spindle cells.

23

FERRET DENTAL DISEASE

Older ferrets affected.
-Broken teeth- most commonly upper canines. Partial or complete rupture. Complete rupture will expose pulp, resulting in more severe clinical signs.
-Dental calculi- moist/semi-moist diets predispose. Subsequent periodentitis.
-Occasionally see tooth root abscess.

24

FERRET NEOPLASIA

-LYMPHOMA is the most common malignancy. May have retroviral aetiology- not yet isolated.
-Clinical signs are age related- older ferrets will show peripheral lymphadenopathy with subsequent visceral spread, organ failure late in course of disease.
-Young ferrets- less than 2 years old- LARGE LYMPHOBLASTIC LYMPHOMA- early visceral spread, often see enlarged thymus causing dyspnoea.

25

COMMON DISEASES IN THE GUINEA PIG

-Vitamin C deficiency (scurvy)
-Dystocia- early fusion of symphisis pubis- leads to mechanical impairment at parturition.
-Skin disease- ectoparasites (Trixacarus caviae- sarcoptic mange), ringworm (Trychophyton mentagrophytes).

26

GUINEA PIG- VITAMIN C DEFICIENCY

Vitamin C is a cofactor for LYSYL and PROLINE HYDROXYLASES.
Activity of these enzymes is required for proper Type I and IV collagen crosslinking (hydroxylation).
Vitamin C must be present in the diet, as guinea pigs cannot synthesise their own.
Deficiency leads to deficient Type IV collagen -> INCREASED CAPILLARY FRAGILITY -> HAEMORRHAGES.
Periarticular haemorrhages in the stifle joint are characteristic.
Swelling (osteodystrophy) and haemorrhage can be seen in costo-chondral junctions.
Defective production of interstitial osseous matrix.
Cartilage in epiphysis/metaphysis is not efficiently replaced with bone.
-> Marked proliferation of poorly differentiated fusiform mesenchymal cells in the periosteal regions and medullary cavity.