Tarc LRS Path and Case Studies Flashcards

1
Q

How is thymoma related to paraneoplastic syndromes?

A

> hypercalcaemia
- thymoma, T cell lymphoma and anal adenocarcinoma secrete PTH related peptide (unregulated) -> binds PTH-R and stimulates Ca release from mineral stores
Myasthenia gravis
- as thymoma is neoplasm of epithelial cells, + and - selection of T cells in thymus is affected -> overproduction of autoreactice T cells producing AutoAb (in this case Ach-R targetted)

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2
Q

What infectious organism is thymic lymphoma commonly associated with? Why?

A

FeLV infects T cellls and thymocytes

- oncogenic retrovirus induces malignant transformation

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3
Q

Give 2 examples of chronic lymphadenitis

A

> granulomatous

  • Johnes, Mycobacterium Avium Paratuberculosis (mesenteric LNs -> D+ and wt loss)
  • TB, M. Bovis (bronchial LNs)
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4
Q

How can mycobacteria be demonstrated in a sample?

A
  • stain for acid fast bacteria
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5
Q

Which species get Caseous Lymphadenitis? Clin signs and causitive agent?

A
  • sheep and goats
  • chronic recurring dz, slowly enlarging LNs are non-painful
  • onion ring ppearance of LNs on PME (also in organs)
  • may be no clin signs or pyrexia/cellulitis/anaemia/anorexia
  • Corynebacterium pseudoTB
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6
Q

How do the common sites of lymphoma and SCC differ?

A
  • lymphoma can afect tonsillar tissue and LNs

- SCC commonly affects tonsils then 2* mets to local LNs

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7
Q

Give 5 main dz of the spleen

A

> nodular hyperplasia
- benign, incidental finding at PM
- difficult to distinguish from neoplasia
hydatid cysts
- echinococccus granulosus, IH sheep goats pigs, DefinitiveH dogs and carnivores
- beware dogs on PETS travel scheme who may have ingested cysts from meat in endemic areas, these will shed eggs
splenic HS
- pdf GSD
- very malignant
splenic lymphoma
- massie diffuse enlargement
- discrete areas of infarct w/haemorrhagic borders
splenic infarcts
- seen in DOGS with acute viral hepatitis d/t adenovirus (CAV 1) prevention by VAX
- seen in PIGS with classical swine fever NOTIFIABLE, CONTACT APHA
(any viruses that affect endothelial cells -> pethichial haemorrhage and infarcts)

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8
Q

How is caseous lymphadenitis spread?

A
  • shearing wounds

- fighting rams

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9
Q

How does corynebacterium hide from the immune system?

A
  • intracellular bacteria

- capsule formation

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10
Q

Is corynebacterium sensitive to abx?

A

yes if they reach it

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11
Q

How can caseous lymphadenitis be prevented?

A

biosecurity
- esp shearing equpment
- quarantine new animals
- vaccines decreaseincidence but do not prevent all
eradication by testing for seropositivity in unvax flocks -> cull

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12
Q

Clinical signs of red water disease? Pahtogen?

A

> Babesia DIvergens (spread by Ixodes Ricinis)

  • clinical signs 2w post infection
  • anaemia d/t division of organisms within RBCs
  • Hbg uria
  • tachycardia
  • abortion
  • very rarely death
  • pyrexia
  • D+ for 36hrs then becoming constipation
  • spread by ticks so only affected by tick ridden areas and if new farm is clean and not infected tick population
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13
Q

Tx babesia divergens?

A
  • mild cases recover alone
  • prophlyactic tx in cattle in risk areas
  • no vax UK
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14
Q

CLinical signs of Leishmania Infantum?

A
  • persistent ulcerated lesions esp nose and head
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15
Q

pathogenesis of leishmania

A
  • multiplies in monocytes/tissue macrophages
  • emerging sporadic dz d/t ^ travel dogs into endemic areas
  • sandflly vector necessary for transmission so risk of spread within UK
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16
Q

CLinical signs EIA

A
  • pale mms
  • tachycardia
  • pyrexia
  • et loss
  • lethargy
  • ventral oedema
  • anaemia and htrombocytopaenia on bloods
17
Q

How is EIA confirmed?

A

Coggins test (agar immunodiffusion)

18
Q

Likely source of infection of EIA?

A

vector borne by blood feeding insects from infected animal