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

Lecture 3: Neuropathology- Inflammatory and Infectious Flashcards

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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
What are the gross lesions associated with thromboembolic meningoencephalitis caused by H. Somni
Multifocal random, embolic hemorrhagic infarcts in brain +/- spinal cord
26
What could have caused this in cattle
H. Somni
27
What are the histological findings with H. Somni TEME
Necrotizing vascular is and thrombosis Vessels in meninges contain septic fibrin thrombi
28
What do you see and what could have caused this
Vessel with septic fibrin thrombi, vascular necrosis and vascular is Cause: H. Somni leading to TEME
29
How do viruses injury the brain
1. Direct ability to kill CNS cells (cytotoxicity) 2. Induce immune response and inflammation
30
What are some common histological features of viral encephalitides
1. Inflammation- lymphocytes, plasma cells, macrophages 2. Viral inclusions 3. Neuronal necrosis- dead, red neurons 4. Increase number of glial cells
31
What would cause these histological features: bacteria, virus, or fungi
virus
32
What wrong here and what would cause this, bacteria, virus or fungi
Neuronal necrosis- dead, red neurons Cause: viral
33
What domestic species are most commonly affected by rabies
Cats, cattle and dogs
34
What are important wildlife reservoirs for rabies
Raccoons, skunk, foxes, bats
35
What is the incubation period for rabies
30-60 days
36
What is pathogensis for rabies
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
Once symptomatic rabies is fatal in ___days
7-10
38
What is the furious type of rabies
Encephalitic form- infection in limbic system
39
What is the paralytic form of rabies
Dumb form- early muscle weakness, with progression to coma and death
40
What microscopic lesions are associated with rabies
1. Polioencephalomyelitis and craniospinal ganglionitis 2. Inclusion bodies- Negri bodies
41
Lesions for rabies are located in ___
Brainstem
42
In ruminants where are negri bodies found
Cerebellar Purkinje cells
43
In carnivores where are negri bodies found
Hippocampal neurons
44
In horses where are negri bodies found
Brainstem and cervical spinal cord
45
Based on the location of this negri body, what species is likely affected
In Purkinje cells- cattle
46
How do you diagnose rabies
1. Requires head and brain removal 2. Fluorescent antibody testing
47
What is the disease course for canine distemper
Acutely fatal or chronic and relapsing
48
How is canine distemper virus transmitted
Respiratory
49
What are the microscopic findings with canine distemper virus
1. Necrotizing meningioencephalitis 2. Large areas of demyelination 3. Intranuclear/ intracytoplasmic inclusion bodies
50
Dog presents with respiratory signs that progressed and were eventually fatal. Brain histology shows this. What do you see and what is likely cause
Left: demyelination Right; intranuclear inclusions Cause: canine distemper virus
51
What is the pathogenesis for FIP (especially related to brain)
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
What is the unique microscopic lesion for FIP
Pyogranulomatous vasculitis
53
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
Dry form
54
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
Wet form
55
What form of FIP typically affects CNS
Dry form
56
Describe what you are seeing and potential cause
brain: proteinacious exudate in lateral ventricles Histo: pyogranulomatous inflammation in ependymal cells surrounding cerebral vasculature Cause: FIP
57
The ___subfamily of herpes have predilection for infection of nervous system resulting in ___
Alpha, resulting in necrosis- neuronal, glial and endothelial, hemorrhage
58
What virus can cause myeloencephalitis in horses
Equine herpes virus 1
59
Who is affected by EHV-1
Adult horses
60
What is a typical history of EHV-1
Respiratory disease and late term abortion
61
How do horses with EHV-1 present
Ataxic, weakness, dog sitting, recumbent, paralysis
62
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
EHV-1
63
What is the gross appearance of EHV-1
Hemorrhage and malacia in the spinal cord—> brain
64
What is the microscopic appearance of EHV-1
CNS vasculitis and thrombosis
65
How do you dx EHV-1
PCR from blood, nasal swabs or fresh spinal cord
66
Horse spinal cord- what are you two top differentials
1. EHV-1 2. Equine protozoan myeloencephalitis
67
What is the definitive host for toxoplasma gondii
Cats
68
What is the definitive host for neospora spp
Canids
69
What is definitive host for S. Neurona
Opossums
70
What two parasitic infections can cause equine Protozoa myeloencephalitis
1. Sarcocystis neurona 2. Neospora Hughesi (less common)
71
Where does equine protocols myeloencephalitis affect
Spinal cord—> brain stem—> rest of brain
72
What is the most common species affected with cryptococcus
Cats
73
What is the primary site of infection for cryptococcus
Nasal cavity
74
What is the microscopic appearance for cryptococcus
Pyogranulomatous inflammation with intralesional yeast
75
What caused these brain lesions and histo presentation
cryptococcus
76
What is a prion
Proteinacious infectious particle
77
What causes transmissible spongiform encephalopathies
Prions
78
What do prions cause in sheep, cattle, and deer
Sheep: scrapie Cows: bovine spongiform encephalopathy Deer: chronic wasting disease
79
What is pathogensis for transmissible spongiform encephalopathy
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
What are the microscopic findings for transmissible spongiform encephalopathies
Spongiform (vacuolation)/ degeneration of neurons and grey matter neuropil
81
Histo from necropsy of sheep brain, what could have caused this
Transmissible spongiform encephalopathy- scrapie
82
What do most diagnostic labs require for diagnosis transmissible spongiform encephalopathy
OBEX fixed in formalin and fresh
83
Besides OBEX what else can be submitted for transmissible spongiform diagnosis
Retropharyngeal LN or tonsils

Pathology I (23 decks)

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