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Pathology I > Lecture 3: Neuropathology- Inflammatory and Infectious > Flashcards

Lecture 3: Neuropathology- Inflammatory and Infectious Flashcards

1
Q

What is myelitis

A

Inflammation of spinal cord

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2
Q

What is meningoencephalomyelitis

A

Inflammation of meninges, cerebrum and spinal cord

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3
Q

What is polioencephalitis

A

Inflammation affecting the gray matter

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4
Q

What is leukoencephalitis

A

Inflammation affecting the white matter

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5
Q

What is ganglionitis

A

Inflammation of ganglia

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6
Q

What would cause suppurative inflammation

A

Bacteria

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7
Q

What would cause non-suppurative, mixture of lymphocytes, plasma cells and macrophage inflammation

A

Virus or immune mediated

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8
Q

Dog euthanized for extreme mentation changes, hypersalivation and neurological symptoms. Suspected rabies histo of brain showed the following. What does histo show

A

Intracytoplasmic inclusions- negri bodies

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9
Q

What could cause granulomtous or pyogranulomatous inflammation

A
  1. Certain bacteria- mycobacterium
  2. Fungal organisms
  3. Certain virus- FIP
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10
Q

What would cause eosinophilic inflammation

A

Parasites

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11
Q

What is the most common route of neurological infection

A

Hematogenous

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12
Q

How do infections travel up nerves to CNS and what are some examples

A

Travel retrograde up peripheral nerves to brain
1. Herpesviruses
2. Lyssavirus (rabies)
3. L. Monocytogenes

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13
Q

What are the 3 “gatekeepers” to CNS infection

A
  1. Subarchanoid barrier
  2. Blood brain barrier
  3. CSF barriers
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14
Q

What forms the subarachnoid barrier

A

Skull and meninges

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15
Q

What forms the blood brain barrier

A

Intercellular junctions between endothelial cells of blood vessels and astrocytes

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16
Q

What forms CSF barrier

A

Epithelial cells of choroid plexus and endothelial cells of vessels

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17
Q

How does the olfactory portal serve as passageway to brain

A

Olfactory system bypasses physical and cellular barriers through the cribiform plate where olfactory nerves travel to olfactory bulb in brain

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18
Q

L. Monocytogenes causes a bacterial infection of CNS in who

A

Ruminants, typically small ruminants

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19
Q

What is the pathogens is of L. Monocytogenes

A
  1. Previous oral trauma
  2. Ingestion of food/silage that is contaminated with L. Monocytogenes
  3. Bacteria gain access to peripheral nerves via wound in oral cavity and extend to brainstem/cerebellum
  4. Causing a neuritis/ suppurative meningoencephalitis
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20
Q

Where are the lesions located in brain for L. Monocytogenes

A

Brainstem

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21
Q

What is likely cause of this lesion and histo. What does histo show

A

L. Monocytogenes
Histo shows small clusters of neutrophils (microabscesses) that disrupt neuroparenchyma

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22
Q

How do ruminants present with L. Monocytogenes

A

Fever, depression, ataxia, head pressing
Aka circling disease

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23
Q

What cranial nerves are affected with L. Monocytogenes and what symptoms are seen

A

CN V, VII, and VII
Symptoms: unilateral facial paresis/ paralysis, head tilt, ear droop, loss of sensation, depression, recumbency

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24
Q

What causes thromboembolic meningoencephalitis

A

Histophilus somni

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25
Q

What are the gross lesions associated with thromboembolic meningoencephalitis caused by H. Somni

A

Multifocal random, embolic hemorrhagic infarcts in brain +/- spinal cord

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26
Q

What could have caused this in cattle

A

H. Somni

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27
Q

What are the histological findings with H. Somni TEME

A

Necrotizing vascular is and thrombosis

Vessels in meninges contain septic fibrin thrombi

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28
Q

What do you see and what could have caused this

A

Vessel with septic fibrin thrombi, vascular necrosis and vascular is

Cause: H. Somni leading to TEME

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29
Q

How do viruses injury the brain

A
  1. Direct ability to kill CNS cells (cytotoxicity)
  2. Induce immune response and inflammation
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30
Q

What are some common histological features of viral encephalitides

A
  1. Inflammation- lymphocytes, plasma cells, macrophages
  2. Viral inclusions
  3. Neuronal necrosis- dead, red neurons
  4. Increase number of glial cells
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31
Q

What would cause these histological features: bacteria, virus, or fungi

A

virus

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32
Q

What wrong here and what would cause this, bacteria, virus or fungi

A

Neuronal necrosis- dead, red neurons
Cause: viral

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33
Q

What domestic species are most commonly affected by rabies

A

Cats, cattle and dogs

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34
Q

What are important wildlife reservoirs for rabies

A

Raccoons, skunk, foxes, bats

35
Q

What is the incubation period for rabies

A

30-60 days

36
Q

What is pathogensis for rabies

A
  1. Virus enters muscles tissue via bite wound- saliva
  2. Enters PNS via NMJ
  3. Travels from PNS to spinal cord and brain
  4. Virus Undergoes extensive replication leading to neuronal dysfunction
  5. Virus replicates in salivary glands and is excreted in saliva
  6. Enters peripheral nerves of the skin and Purkinje cells
  7. Spreads from brain to infect many tissues and organs
37
Q

Once symptomatic rabies is fatal in ___days

38
Q

What is the furious type of rabies

A

Encephalitic form- infection in limbic system

39
Q

What is the paralytic form of rabies

A

Dumb form- early muscle weakness, with progression to coma and death

40
Q

What microscopic lesions are associated with rabies

A
  1. Polioencephalomyelitis and craniospinal ganglionitis
  2. Inclusion bodies- Negri bodies
41
Q

Lesions for rabies are located in ___

42
Q

In ruminants where are negri bodies found

A

Cerebellar Purkinje cells

43
Q

In carnivores where are negri bodies found

A

Hippocampal neurons

44
Q

In horses where are negri bodies found

A

Brainstem and cervical spinal cord

45
Q

Based on the location of this negri body, what species is likely affected

A

In Purkinje cells- cattle

46
Q

How do you diagnose rabies

A
  1. Requires head and brain removal
  2. Fluorescent antibody testing
47
Q

What is the disease course for canine distemper

A

Acutely fatal or chronic and relapsing

48
Q

How is canine distemper virus transmitted

A

Respiratory

49
Q

What are the microscopic findings with canine distemper virus

A
  1. Necrotizing meningioencephalitis
  2. Large areas of demyelination
  3. Intranuclear/ intracytoplasmic inclusion bodies
50
Q

Dog presents with respiratory signs that progressed and were eventually fatal. Brain histology shows this. What do you see and what is likely cause

A

Left: demyelination
Right; intranuclear inclusions
Cause: canine distemper virus

51
Q

What is the pathogenesis for FIP (especially related to brain)

A
  1. Ingested FIP
  2. Enters and replicates in enterocytes and Peter’s patches
  3. Replicates and mutates in monocytes a and macrophages
  4. Infected monocytes or macrophages have high affinity for meninges
  5. Pyogranulomatous vasculitis
52
Q

What is the unique microscopic lesion for FIP

A

Pyogranulomatous vasculitis

53
Q

Dry or wet form of FIP:
1. decreased cell mediated response
2. Delayed Type IV hypersensivity- pyogranulomatous inflammation and phlebitis
3. More prolonged clinical course

54
Q

Dry or wet form of FIP
1. Anti-viral antibody produced
2. Accumulation of antigen-antibody complexes- type III hypersensitivity that deposit in blood vessels—> pyogranulomatous inflammation
3. Rapid clinical course

55
Q

What form of FIP typically affects CNS

56
Q

Describe what you are seeing and potential cause

A

brain: proteinacious exudate in lateral ventricles
Histo: pyogranulomatous inflammation in ependymal cells surrounding cerebral vasculature

Cause: FIP

57
Q

The ___subfamily of herpes have predilection for infection of nervous system resulting in ___

A

Alpha, resulting in necrosis- neuronal, glial and endothelial, hemorrhage

58
Q

What virus can cause myeloencephalitis in horses

A

Equine herpes virus 1

59
Q

Who is affected by EHV-1

A

Adult horses

60
Q

What is a typical history of EHV-1

A

Respiratory disease and late term abortion

61
Q

How do horses with EHV-1 present

A

Ataxic, weakness, dog sitting, recumbent, paralysis

62
Q

Called out to farm due to horse unable to use hind limbs. Owner informs you there has been some recent respiratory diseases and late term abortions what is top differential

63
Q

What is the gross appearance of EHV-1

A

Hemorrhage and malacia in the spinal cord—> brain

64
Q

What is the microscopic appearance of EHV-1

A

CNS vasculitis and thrombosis

65
Q

How do you dx EHV-1

A

PCR from blood, nasal swabs or fresh spinal cord

66
Q

Horse spinal cord- what are you two top differentials

A
  1. EHV-1
  2. Equine protozoan myeloencephalitis
67
Q

What is the definitive host for toxoplasma gondii

68
Q

What is the definitive host for neospora spp

69
Q

What is definitive host for S. Neurona

70
Q

What two parasitic infections can cause equine Protozoa myeloencephalitis

A
  1. Sarcocystis neurona
  2. Neospora Hughesi (less common)
71
Q

Where does equine protocols myeloencephalitis affect

A

Spinal cord—> brain stem—> rest of brain

72
Q

What is the most common species affected with cryptococcus

73
Q

What is the primary site of infection for cryptococcus

A

Nasal cavity

74
Q

What is the microscopic appearance for cryptococcus

A

Pyogranulomatous inflammation with intralesional yeast

75
Q

What caused these brain lesions and histo presentation

A

cryptococcus

76
Q

What is a prion

A

Proteinacious infectious particle

77
Q

What causes transmissible spongiform encephalopathies

78
Q

What do prions cause in sheep, cattle, and deer

A

Sheep: scrapie
Cows: bovine spongiform encephalopathy
Deer: chronic wasting disease

79
Q

What is pathogensis for transmissible spongiform encephalopathy

A
  1. External prion protein PrPsc ingested
  2. Converts normal alpha helical structure of host protein to misfolded B pleated sheet with unknown protein co-factors
  3. First found in lymphoid tissue and GI
  4. Travel retrograde up nerves to spinal cord and brain
80
Q

What are the microscopic findings for transmissible spongiform encephalopathies

A

Spongiform (vacuolation)/ degeneration of neurons and grey matter neuropil

81
Q

Histo from necropsy of sheep brain, what could have caused this

A

Transmissible spongiform encephalopathy- scrapie

82
Q

What do most diagnostic labs require for diagnosis transmissible spongiform encephalopathy

A

OBEX fixed in formalin and fresh

83
Q

Besides OBEX what else can be submitted for transmissible spongiform diagnosis

A

Retropharyngeal LN or tonsils

Pathology I (23 decks)

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