Neuropathology Study Questions Flashcards
What is the function of oligodendrocytes?
Astrocytes?
Microglia?
Gitter cells?
Oligodendrocytes: form the myelin that wraps around axons in CNS.
Astrocytes: star shaped cells that form the blood-brain barrier; interstitial cells of the brain; possibly signal the endothelial cells to make tight junctions for blood-brain barrier
Microglia: phagocytic cells with small nuclei and little cytoplasm. Fixed macrophages of CNS.
Gitter cells: microglia ingesting myelin debris with foamy cytoplasm
What is central chromatolysis?
Degenerative change → first step to neuronal necrosis
Swelling of the cell, nucleus gets pushed off to the side, dispersal of Nissl substance
What is neuronophagia?
Microglia gather around a necrotic neuron and phagocytose it to remove the debris
Seen with viral infections
What are histologic characteristics of axonal degeneration?
Wallerian degeneration: focal damage to a myelinated axon resulting in degeneration of the axon segment distal to the site of damage
Axon degenerates (spheroid) → gitter cells remove axon and myelin debris → empty dilated axon sheath
What is a spheroid?
Focal axonal swellings filled with degenerate organelles
What kind of necrosis is typically seen in the CNS, and what are the characteristics of this type of necrosis?
Neuronal necrosis
“Red is dead,” shrunken, angular, pink cytoplasm indicates a dead neuron
Liquefactive necrosis
Can also have a pyknotic nucleus
What is astrocytosis?
Increase in size and number of astrocytes in response to injury; repair
Swell & divide as cell processes proliferate
What are gemistocytic astrocytes?
Plump, reactive astrocytes with eosinophilic cytoplasm; almost look like a dead neuron
Seen w/ significant damage
What is the appearance of Alzheimer’s type II astrocytes, and what disease process are these cells typically seen in?
Enlarged, vesicular nuclei that tend to cluster around the neurons
Seen w/ hepatic encephalopathy
What is hydrocephalus?
What are the different types of hydrocephalus?
In which breeds of dog is hydrocephalus most common?
Excess fluid in the brain
3 types:
Internal – fluid in ventricles
External – fluid in arachnoid space (rare)
Communicating – fluid in ventricles & arachnoid space (rare)
Most common in brachycephalic dogs and toy breeds
Define microencephaly
Abnormally small brain
Usually the cerebrum is the most affected part; can have smaller cranial cavity
Seen w/ BVD in cattle, classical swine fever in pigs
Define hydranencephaly
Cerebral hemispheres are almost gone or completely gone, leaving fluid-filled sacs formed by the meninges filled with CSF
Associated w/ viral infections → during development, they cause subventricular necrosis
Define proencephaly
Cystic cavitation of the brain, usually involving cerebral white matter
Less severe end of the spectrum as hydranencephaly & is caused by the same things
Define lissencephaly
Brain lacks normal gyri and sulci
Lhasa Apso’s = poster child
Can be normal in some species of mammals, but not normal in any of our domestic mammals (everything that is not a mammal is normally lissencephalic)
Define anencephaly
Absence of the brain = RARE
Define prosencephalic hypoplasia (cerebral aplasia)
Absence of the cerebral hemispheres with preservation of at least some portion of the brainstem
Define canium bifidum/spina bifidum
Defect through which the brain/spinal cord & meninges can protrude
Almost always on dorsal midline
Define meningocele
Herniation of meninges
Define meningoencephalocele
Herniation of meninges & brain/spinal cord
What is the most common brain malformation seen with BVD infection?
Microencephaly
Cerebellar hypoplasia during days 100-170 of gestation
What is the underlying cause of storage diseases?
What happens to cells which accumulate substrate in lysosomal storage diseases?
How are these conditions inherited, and when do they typically present with neurologic signs?
How are storage diseases named (in general, you do not need to know specific names)?
Underlying cause: defective catabolism from a defect in lysosomal enzymes
Cells that accumulate substances don’t die, they just become distended with vacuoles with excess stored material
Autosomal recessive conditions & present with neuro signs early in life → progressive and fatal
Naming: according to the substrate that has defective degradation
Which cells in the CNS are most sensitive to ischemia?
Neurons & oligodendroglia: cerebral cortical neurons, hippocampal neurons, Purkinje cells
Can also affect nuclei if severe/prolonged
Grey matter more sensitive than white matter
What are the causes of polioencephalomalacia?
Where are the lesions located?
Causes: often unknown but can be due to a thiamine (B1) deficiency, defect in thiamine metabolism, or high sulfur intake b/c that cleaves thiamine & makes unusable; occ seen w/ water deprivation
Lesions: necrosis of the grey matter of the brain, laminar cortical necrosis.
What is the cause of leukoencephalomalacia?
Where are the lesions located?
Cause: moldy corn consumption for >1 month → fumonisin toxin is produced by Fusarium verticillioides & Fusarium proliferatum
Lesions: necrosis of the cerebral white matter +/- hemorrhage
What are the lesions of indirect salt poisoning?
What is the cause of indirect salt poisoning?
Cause: ingestion of a high (>2%) salt diet in conjunction with restricted water intake for several days
Lesions: cerebral edema, laminar cortical necrosis, non-suppurative & eosinophilic meningoencephalitis (pathognomonic)
What are the ways in which bacterial infections get to the CNS?
They breach the BBB and BCSFB
Most commonly secondary to septicemia in young animals
Can have septic embolism with endocarditis; can have abscesses form from hematogenous spread or direct invasion (cribriform plate from nasal infection or middle ear from otitis interna)
In what species do we most often see listeriosis?
What is the causative agent of listeriosis?
What are the characteristic lesions, and where are the lesions typically located?
What is the pathogenesis of the encephalitis?
Most often seen in ruminants (sheep)
Caused by Listeria monocytogenes
Lesions: most common in the brain stem; no gross lesions; histo can have microabscesses, sometimes within foci of microgliosis
Pathogenesis: bacteria invade oral mucosa then spread up the branches of the trigeminal nerve to the brain; outbreaks assoc w/ heavy feeding of improperly fermented silage
What is the causative agent of thrombotic meningoencephalitis?
Which species does it affect?
What is the pathogenesis of development of CNS lesions, and what are the lesions?
Caused by Histophilus somni
Affects cattle (usually young cattle in feedlots) & sheep
Pathogenesis: animals have septicemia which causes cerebral vasculitis with hemorrhages, necrosis, and thrombosis
Gross lesions: multifocal hemorrhage and necrosis
Histo lesions: vasculitis, thrombosis, &, neutrophilic meningoencephalitis, may form abscesses
What are the general histologic features of viral infections?
Nonsuppurative meningoencephalitis +/- myelitis
Perivascular cuffing
Gliosis
+/- viral inclusions, neuronal degeneration/necrosis
What are the principal reservoirs for rabies in the US?
What tissues is the virus tropic for?
What is the pathogenesis of viral infection from inoculation to spread to the CNS?
What are the lesions?
US Reservoirs: skunks, foxes, raccoons, and bats
Tropism for CNS & salivary glands
Pathogenesis: virus inoculated into the wound (usually from a bite) → replicates in the muscle cells near the site → spreads to sensory paravertebral ganglia & travels along the peripheral nerves into the CNS
Lesions: non-suppurative encephalomyelitis, ganglioneuritis, parotid gland adenitis; inflammation & neuronal degeneration are variable; Negri bodies (eosinophilic cytoplasmic inclusions) in the hippocampus of carnivores or Purkinje cells of herbivores.
What is the cause of pseudorabies?
What species are affected by this disease?
What are the clinical signs?
Caused by Suid Herpesvirus-1
Can affect all common domestic species
CS in species other than pigs: intense pruritus (mad itch), high mortality rate, fever, neuro signs; always fatal
CS in most pigs: mild fever, no pruritus
CS in young pigs: prostration, convulsions, muscle tremors/twitching, may have high mortality rate
CS in sows: abortion, stillbirth, mummified fetuses
What are the clinical signs of caprine arthritis-encephalitis virus?
In what age animals is neurologic disease typically observed with this virus?
What are the lesions of this disease?
CS in kids 2-4m: hind limb ataxia, paresis, paralysis, death
CS in adults: arthritis, mastitis, pneumonia
Neuro signs seen in kids 2-4 months
Lesions: non-suppurative leukoencephalomyelitis, demyelination, perivascular cuffing
What are the clinical signs of maedi-visna virus?
In what age animals is neurologic disease typically observed with this virus?
What are the lesions of this disease?
CS in adults >2y: hind limb ataxia, trembling of lips, progressing to hind limb paralysis; death d/t secondary infection or starvation; pneumonia, mastitis, and arthritis
Neuro signs seen in adults over 2 y/o
Lesions: non-suppurative meningoencephalitis most severely affecting the white matter, demyelination
What species are typically affected by fungal infections with Cryptococcus neoformans?
How do infections get into the brain?
What are the histologic lesions?
Affects cats, dogs, and horses
Starts as a nasal or sinus infection (can be very destructive) & enters brain via cribriform plate; can also have a pulmonary infection that travels hematogenously to the brain
Histo: variable inflammatory response (no inflammation or severe granulomatous lesion); thick, non-staining mucopolysaccharide capsule which creates a soap bubble appearance in tissue sections
What is the cause of equine protozoal myelitis?
Why are organisms not seen in most cases?
Cause: Sarcosystic neurona
Most animals with EPM are treated prior to euthanasia with Marquis (ponazuril)
What is the cause of transmissible spongiform encephalopathies (TSEs)?
How do animals typically acquire TSEs?
What are the lesions of TSEs?
Cause: prions which are abnormal isoforms (PrPsc) of a normal cellular protein called the prion protein (PrPc)
Transmission: horizontally by infected feed material; don’t use brain or spinal cord from other mammals in the feed!
Lesions: intracytoplasmic neuronal vacuolation and astrocytosis; no inflammatory component
What are the histologic lesions of FIP?
Periventriculitis & perivasculitis = around ventricle & vessles
Mixed cell population: neutrophils, macrophages, lymphocytes, & plasma cells
May also see reactive astrocytes
