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Y3 - CNS Pathology > Nervous system pathology 3 > Flashcards

Nervous system pathology 3 Flashcards

1
Q

Describe the pathology of FIP in the CNS

A

Antibody-antigen immunocomplexes deposit within the vessel wall

  • > Immunemediate aggression
  • > Diffuse pyogranulomatous meningo-chorio-subependimitis
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2
Q

Describe the dry form of FIP

A
  • Dry form is dominated by granulomas – nodular lesions that aren’t rich in fluid
  • First lesion can be seen in the eye which shows CNS involvement
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3
Q

Describe the wet form of FIP

A
  • Wet form is characterised by the over-exudation of fluid

- Abdomen is distended by large volumes of fluid

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4
Q

What are the histological characteristics of FIP

A
  • Prevalence of plasma cells and macrophages

- Vasculitis is the histological hallmark of the disease, with formation of microtrombi

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5
Q

Which other organ is infected by the dry form of FIP?

A

The kidney – white nodules on the surface are obliterating the profile of the vein – they are purposefully located over the vein

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6
Q

How would a slide of the cranial portion of brain appear for FIP?

A
  • ‘Empty’ cavities represent the lateral ventricles. They are much wider and distended than normal
  • The outlining silhouette is a blue line, this is abnormal as the CNS is normally completely pink staining, the blue represents a lot of nuclei (inflammatory cells) which are removing the coverage of the ventricular system
  • Round aggregates are perivascular cuffs which show a paler area (vessel) surrounded by a ‘doughnut’ shape of dotted cells around it = hallmark of inflammation
  • The ependyma is normally columnar epithelium with cilia has gone and is replaced with inflammatory cells
  • The ventricle is filled with a protein rich fluid which is not normally present = outcome of vessel damage
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7
Q

Louping ill is seen in which 3 species?

A

Sheep
Horses
Pigs

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8
Q

How is Louping ill transmitted?

A

By ticks

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9
Q

What is the inflammatory pattern of Louping ill?

A

Non-suppurative polioencephalitis with neuronal necrosis, glial nodules and neuronophagia

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10
Q

For Louping ill, in which cells is the viral antigen seen?

A

Purkinje cells

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11
Q

Which part of the brain is affected by Louping ill?

A

Cerebellum

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12
Q

What are the signs shown by sheep with Louping ill, what is the cause of these signs?

A

Sheep ‘bounce’ because they have no coordination because the virus kills the purkinje cells in the cerebellum where perception is controlled

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13
Q

Which 4 diagnostic factors indicate Louping ill?

A

Sheep
Cerebellum
Lymphocytes
Plasma cells

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14
Q

What are 3 viral causes of viral vasculitis?

A
  • Classical swine fever
  • Hepatitis contagiosa canis (canine adenovirus type 1)
  • Malignant catarrhal fever
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15
Q

Herpetic encephalomyelitis is caused by which virus?

A

Equine herpes virus 1

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16
Q

What is seen grossly in Herpetic encephalomyelitis?

A

Petechial or ecchymotic haemorrhages in white and grey matter of the spine

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17
Q

Describe the inflammatory pattern of herpetic encephalomyelitis

A

Vasculitis with thrombosis, suppurative myelitis and haemorrhages

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18
Q

Compare the lesion distribution of Equine herpes virus and West Nile virus

A
  • Equine herpes virus, because of the disease being primarily a vasculitis, is randomly distributed so is seen in both the grey and white matter
  • In the case of WNV where the main interest of the virus is replicating inside neurones which are located within the grey matter
19
Q

How can bacteria enter the CNS?

A

Through blood, ears, eyes, nose, nerve (trigeminal from a tooth abscess)

20
Q

How is the inflammatory pattern of bacterial infections of the CNS characterised?

A

Dominated by the recruitment of neutrophils (suppuration), tissue lysis and gliotic reaction

21
Q

What are common distributions of bacterial infections in the CNS?

A

Disseminated (e.g. thromboembolism) and focal or multifocal (abscess) distribution patterns are characteristic

22
Q

Which bacteria doesn’t show the typical distribution pattern? How is theirs different?

A

L. monocytogenes,

  • Haematogenous spreading
  • Extension of local inflammations (otitis media, etc..)
23
Q

Which spp are affected by Listeriosis?

A

Cows, sheep and pigs

24
Q

How does Listeria gain access and spread in the body?

A

Oral cavity -> cranial nerves -> brainstem

  • Retrograde transport along axons and trans-synaptic spreading
  • Bacterium gains access to the body through wounds on the tongue and oral mucosa
25
Q

What are some characteristics of Listeriosis?

A
  • Can be more marked on one side (asymmetrical)
  • Small leukomalacic (softening of white brain tissue) areas (gross)
  • Paralysis of tongue and lips, with drooling
26
Q

What are some histological characteristics of Listeriosis?

A
  • Mid-line shows where the hemispheres are divided
  • One side appears slightly more heavily inflamed
  • Core of suppurative inflammation = micro-abscesses – not visible to the naked eye
  • Dense clusters of neutrophils
  • Perivascular cuffs
27
Q

Describe the inflammatory pattern of mycotic encephalitis

A

Necrotizing and suppurative-granulomatous or granulomatous meningoencephalitis/
myelitis

28
Q

What are the two common hallmarks of Mycotic encephalitis

A

Necrotic vasculitis and thrombosis

29
Q

What characteristic features do fungi show in mycotic encephalitis?

A
  • They love the endothelium
  • When the hyphae grow, they love branching through walls of vessels causing haemorrhage
  • If there is this infection in the guttural pouch then blood can be coughed up due to the fungal erosion of vessel walls
30
Q

How odes mycotic encephalitis appear histologically?

A
  • Focal, multifocal, chronic granulomatous encephalitis with fungal hyphae
  • Lots of macrophages which remove fungal hyphae
31
Q

Give an example of a fungi which may cause Mycotic encephalitis

A

Aspergillus spp

32
Q

Name the cells that have a comma shaped profile and live in the brain to show areas of inflammation

A

Microglia

33
Q

What are microglia?

A

Macrophages that live in the brain, they become visible and migrate to an area of the brain as a very early sign that inflammation is starting

34
Q

What is the cause of Encephalitozoonosis?

A
  • Encephalitozoon cuniculi, family Microsporidia: classified between the fungi and a protozoa
  • Obligate intracellular Gram-positive parasite
35
Q

What is the inflammatory pattern of encephalitozoonosis

A

Disseminated granulomatous encephalitis

36
Q

What are the histological characteristics of Encephlitozoonosis?

A
  • Compact epithelioid macrophages
  • Multifocal to massive dissemination thought the encephalon
  • The hippocampus of the brain where a big granuloma is visible (mainly macrophages with some lymphocytes and plasma cells), perivascular cuffs can also be seen
37
Q

What is the main clinical sign of encephalitozoonosis?

A

Affects rabbits

- continuing to chew with the head twisted on the side

38
Q

Describe the hosts of Toxoplasma gondii

A

Intermediate hosts are all warm-blooded animals, including humans, while definitive hosts are members of the family Felidae (e.g. domestic cat)

39
Q

Describe the pathogenesis of toxoplasmosis

A

Toxoplasmosis can cause chronic inflammation in areas of the body that are not regulated strictly by the immune system by selecting certain organs for migration and by hiding themselves within the cytoplasm of skeletal muscle or neurones

40
Q

Describe the inflammatory pattern of Toxoplasmosis in young and adult animals

A
  • In young animals: non-suppurative (not many neutrophils, more lymphocytes and plasma cells) polioencephalitis with gliosis
  • In adult animals: necrotizing and granulomatous encephalitis
41
Q

Describe the two biological forms of the Toxoplasma gondii parasite

A

Tachyzoites – extracellular, high metabolism

Bradyzoites – slow metabolism, good for the evolution of the parasite as they aren’t targeted by the immune system

42
Q

Describe the features of granulomatous meningoencephalitis

A
  • Dogs, adult (1-3 years old), more females

- Non clarified cause. Postulated anti-GFAP autoantibodies

43
Q

Describe the inflammatory pattern of granulomatous meningoencephalitis

A

Multifocal to coalescing granulomatous meningoencephalitis

44
Q

What is the histological characteristic of granulomatous meningoencephalitis

A

In perivascular cuffs, abundant recruitment of macrophages and lymphocytes (the latter are characteristically “pushed” to one side)

Y3 - CNS Pathology (5 decks)

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