Ecvp Bone, Joint, Muscle, Tendon, Eye, Ear 2007-2009

Front 1

Connexin 43 and 46 in normal and neoplastic canine bone tissue.
1. Main Cx and expression of both in normal tissue?
2. Expression in neoplastic tissue?
3. IHC neoplastic bone cells?

Back 1

1. Cx43 is main, in intercellular membranes. Cx46 in the trans-Golgi region.
2. Cx43: intercellular membrane and aberrant intracytoplasmic, similar levels to normal. Within tumors, positive correlation between Cx43 expression and collagen deposition.
Cx46: lower levels in neoplasia and retainment in perinuclear region.
3. vimentin +, cytokeratin -, osteocalcin and osteonectin +.

Hint 1

Vet pathol 46, 846-859 (2009)

Front 2

Hepatic growth factor and proto-oncogenic receptor c-Met in canine osteosarcoma.
1. Coexpression present?
2. c-Met correlated with HGF mRNA expression, survival time, disease-free interval, metastasis via the lymphogenic route?
3. IHC staining pattern c-Met?

Back 2

1. Yes.
2. Positively correlated with HGF expression, and with metastatis via lymphogenic route.
3. cytoplasmic staining pattern.

Hint 2

Vet pathol 46, 869-877 (2009)

Front 3

Inherited rickets in Corriedale sheep in New Zealand.
1. Mode of inheritance?
2. Clinical signs?
3. Gross?
4. Histo?

Back 3

1. Autosomal recessive.
2. Similar to rickets in other species. Decreased growth rate, thoracic lordosis, angular limb deformities.
3. Segmental thickening of physes, growth arrest lines, collapse of subchondral bone of the humeral head, thickened cortices and enthesophytes around distal limb joints.
4. Persistence of hypertrophic chondrocytes at site of endochondral ossification, inappropriate and excessive osteoclastic resorption, microfractures and wide unmineralized osteoid seams lining trabeculae and filling secondary osteons.

Hint 3

CP 141, 147-155 (2009)

Front 4

Canine X-linked muscular dystrophy in Grand Basset Griffon Vendeen Dogs.
1. Protein affected?
2. Histo?

Back 4

1. Sarcolemmal protein dystrophin is absent.
2. hyaline hypereosinophilic myofibres, hypertrophy and atrophy, calcification, necrosis, and mild proliferation of endomyseal connective tissue, as well as small basophilic fibres with internalized nuclei in rows (regeneration).

Hint 4

CP 137, 349-352 (2007)

Front 5

Pathologic findings in equine muscle, excluding polysaccharide storage.
1. What are the 9 lesions found and in which percentage of animals?
2. Causes of myonecrosis in this study (7)?
3. Histo chronic myopathic change?

Back 5

1. Muscle lesions in 65% of necropsied animals.
Chronic myopathic change > generalized muscle atrophy > myonecrosis > intramyofiber protozoa > denervation atrophy > neoplasia > focal lymphocytic infiltrates > injection site reaction > degeneration such as ring fibers, fat infiltration, fiber splitting.
2. endotoxic injury > unknown cause > bone fracture > bacterial infections > muscle rupture > selenium deficiency > exertional rhabdomyolysis
3. Excessive fiber variation and internal nuclei, ass. with neuromuscular and non-neuromuscular disorders, mainly older horses.

Hint 5

JVDI 20, 572-579 (2008)

Front 6

Equine polysaccharide storage myopathy, in Cob Normand Draft Horses.
1. Diagnosis?
2. % horses affected and grouping?
3. EM?

Back 6

1. Intracytoplasmic presence of amylase resistant material in skeletal muscle.
2. 38% of the 53 horses sampled, group 1 with low % of fibers with aggregates, clustered, without myopathic change. Group 2 high % of fibers containing aggregates scattered, with chronic myopathic changes.
3. Granular material amoung arrays of filamentous material, subsarcolemmal or central.

Hint 6

Vet pathol 45, 154-158 (2008)

Front 7

Usnic acid and Xanthopharmelia chlorochroa (lichen) toxicity in sheep.
1. Histo of usnic acid lesions?
2. Clinical signs?
3. Clinical signs with pure X. chlorochroa diet?
4. Connection usnic acid and X. chlorochroa?

Back 7

1. Severe degenerative appendicular skeletal myopathy: pale swollen myocytes with flocculation and fragmentation, myocytes with granular basophilic cypoplasmic mineralization, macrophages and edema.
2. lethargy, anorexia, abdominal discomfort.
3. red urine (not hemoglobin or myoglobin), probably lichen pigment, incoordination.
4. usnic acid is secondary metabolite of lichen, but dosage must be so high that sheep can't eat enough. Probably more compounds, or seosonal influences e.d.

Hint 7

JVDI 20, 760-765 (2008)
Vet pathol 45, 19-25 (2008)

Front 8

Canine leishmaniosis and ocular disease.
1. % of dogs with ocular lesions?
2. Type of inflammatory infiltrate and % of eyes with parasites found?
3. Structures affected?

Back 8

1. 25%
2. Granulomatous infiltrate, 30%, 26% of dogs had IHC + Leishmania in the globe.
3. conjunctiva and limbus > ciliary body> iris>cornea > sclera and iridocorneal angle> choroid and optic nerve sheath.

Hint 8

CP 138, 32-29 (2008)

Front 9

Canine duplication of Descemet's membrane.
1. Composition of second membrane?
2. layer between the two membranes?
3. Most associated clinical histories?

Back 9

1. basement membrane nature.
2. In 40% of the eyes, a fibrous collagenous matrix component was present between the corneal layer and the anterior chamber layer., which contains vimentin + and alpha-SMA - spindle cells.
3. Chronic glaucoma, previous intraocular surgery, lens luxation, blunt trauma.

Hint 9

Vet pathol 46, 464-473 (2009)

Front 10

Canine oral papillomavirus in eye lesions.
1. Virus?
2. Lesions?
3. Histo?
4. PCR DNA, which genes where found?
5. ISH, staining pattern?

Back 10

1. Lambdapapillomavirus, canine oral papillomavirus, DNA virus.
2. Viral pigmented conjunctival plaque and conjunctival squamous papillomas.
3. Epithelial hyperplasia, acanthosis, and hyperkeratosis with koilocytosis (with basophilic INIB).
4. E6, E7 and L1 gene fragments.
5. Intranuclear in hyperplastic epithelium.

Hint 10

Vet pathol 46, 34-38 (2009)

Front 11

Feline eyelid tumors.
1. Which were found (8)?
2. Relative age MCT and SCC?
3. More in nonpigmented areas (2)?
4. Which did and did not recur after excisions ?
5. Average survival time for SCC?

Back 11

1. Squamous cell carcinoma, mast cell tumor, hemangiosarcoma, adenocarcinoma, peripheral nerve sheath tumor, lymphoma, apocrine hidrocystoma, hemangioma.
2. MCT younger, SCC older (mean 10 years).
3. SCC and HSA.
4. Not: MCT, HSA, HA, AHC
Wel: SCC, ACA, lymphoma, PNST
5. 7,4 months

Hint 11

Vet pathol 46, 916-927 (2009)

Front 12

Equine recurrent uveitis.
1. Associated with Leptospira?

Back 12

1. No, in this study no Leptospira DNA via real-time PCR, or IHC(2 +, nonsignificant).

Hint 12

JVDI 19, 686- 690 (2009)

Front 13

Retinal function in cattle with experimental prion disease (transmissible mink encephalopathy).
1. Functional alterations
2. Disruption of rod bipolar cell synaptic terminals via which IHC?
Activation of Muller glia via which IHC?
3. Immunoreactivity to PrPsc in which layers of the retina?

Back 13

1. Prolonged implicit time of the electroretinogram b-wave.
2. decreased alpha isoform of protein kinase-C and vesicular glutamate transporter 1.
- increased glial fibrillary acidic protein (GFAP) and glutamine synthetase expression.
3. Immunoreactivity to PrPsc in the synaptic layers and the cytoplasm of retinal ganglion cells.

Hint 13

Vet pathol 46, 810-818 (2009)

Front 14

Retinal changes in sheep with scrapie.
1. Histo?
2. Retinal bipolar cells affected: which markers?
3. Muller glia + or -?
4. Retinal ganglion cells via which marker?
5. Which cell type was most specifically affected by PrPsc?

Back 14

1. No lesions.
2. alpha isoform of protein kinase-C and vesicular glutamate transporter 1.
3. +, via glutamine synthetase.
4. microtubule associated protein 2 (MAP2).
5. Rod bipolar cells: rod mediated vision may be impaired.

Hint 14

CP 138, 12-22 (2008)