Path 2 - Neuro 5

drraythe's version from 2016-03-07 17:50

Inflammation/bacteria/viral/fungal/parasitic CONTINUED

Question Answer
How do cestodes (tapeworms) cz CNS inflammation?It happens during their larval stage: Cysticercus
Name the 3 protozoa which can cz CNS inflammationSarcocystosis (Equine Protozoal Encephalomyelitis [EPM])
Toxoplasmosis does what?Tissue cysts in the CNS & muscle
Sarcocystosis czs what?(Protozoa) Equine Protozoal Encephalomyelitis [EPM]
NEOSPOROSIS (neospora caninum, protozoa) has what effect on horses? Dogs? Cattle?HORSES: Meningoencephalomyelitis
DOGS: Polyradiculoneuritis & polymyositis
CATTLE: Multifocal necrosis (+/-abortion)
Fungi cz what types of lesions in the brain? What are the 3 fungi which would cz CNS inflammation?GRANULOMATOUS!
How does Cryptococcus affect dogs & cats differently?DOGS: Meninges & paranasal sinuses (Granulomatous Menigoencephalitis)
CATS: Nasal cavity & pharynx (Nonsuppurative Meningioencephalitis)
Phaeohyphomycosis → what's unique about this (what is it?) What suborder usually czs the CNS problems & what is the CNS problem specifically?It is a PIGMENTED fungus. Cladophialophora bantiana is the neurotropic one & it czs Pyogranulomatous meningoencephalitis
What’s the most common systemic mycosis to involve brain?Cryptococcus neoformans
****TME - THROMBOTIC MENINGOENCEPHALITIS → CZD BY WHAT? WHAT IS THE MAJOR LESION?Histophilus somni, cz VASCULITIS w/ THROMBOSIS (histo made me want to damage blood vessels)
****Listeriosis has an affinity for WHERE & what is the major lesion?Affinity for BRAINSTEM (medulla+pons), will see a Circumscribed collections of MONONUCLEAR CELLS (one (MONO) swish of Listerine will get the MONO out of your brain stem)
****Viral histological changes → vascular rxn to viral infxn is? Neuronal change? White matter change? Meningeal change? Inclusion body types?Vascular= perivascular cuffing (of MONONUCLEAR cells (Lymphocytes, plasma cells, macrophages))
Neuronal= neuronal degeneration
White matter = DEMYELINATION. Meninges: Lympho (+/-plasma) cytic meningitis
Inclusion bodies: intranuc = canine distemper & Rabies
Cytoplasm = Rabies
****FELINE ISCHEMIC ENCEPHALOPATHY is czd by what? What are the 3 major VASCULAR signs?Cuterebra. Hemorrhage, thrombosis, vasculitis

Nutritional deficiencies

Question Answer
Thiamine (vitamin B1) deficiency → who does this occur in naturally?Natural Dz in cat, fox, mink
What are 2 reasons (not medical) that thiamine would be destroyed & then be unable to be used by the body?(1) Thiaminase in fish splits thiamine
(2) Destruction of Thiamine by cooking foods at ≥212°F
**What CS would you see in a Thiamine (B1) deficiency?Anorexia
Convulsions (responsive to thiamine Tx)
Coma (irreversible)
**What do the brain lesions look like in a Thiamine (B1) deficiency? (In general)Edema
Perivascular dilation
BILATERALLY SYMMETRICAL Necrosis (Periventricular Gray Matter)****!
Which animal does not normally get a thiamine deficiency & if it DOES happen, what is it called (& what are the circumstances)?RUMINANTS usually don't get a thiamine deficiency bc their rumen microbes produce it for them. However, if their microbes are not right, then the deficiency has been termed CCN (Cerebrocortical necrosis) (polioencephalomalacia) in ruminants
How do we know that CCN (cerebrocortical necrosis) in ruminants might be linked w/ thiamine?Clinical response to thiamine injxn (in some cases)
↓ in ruminal thiamine
Overgrowth of thiaminase-producing microbes
Ingestion of thiaminase-containing plants, e.g., bracken fern
Production of inactive thiamine analogs
↓ absorption or ↑ fecal excretion of thiamine
Polioencephalomalacia of sheep & cattle is czd by what?Thiamine deficiency
What does polioencephalomalacia of sheep & cattle look like in the brain? What are the CLINIAL SIGNS?You will see multifocal or diffuse yellow areas of necrosis in the brain. Clinically, you will see:
Explain the pathogenesis of how a thiamine deficiency czs polioencepahlomalacia (starting w/ what it does normally)Thiamine fxns as a coenzyme in CHO (carb) metabolism → so a deficiency czs prominent neuro signs (bc neurons & glial cells depend on carb metabolism)
What are the GROSS LESIONS of polioencephalomalacia of sheep & cattle? (Thiamine deficiency)Confined to the CNS → focal or diffuse necrosis (soft & yellow) of the gray matter (cerebrocortical necrosis), w/ deeper laminae of the cerebral cortex most severely affected. WHITE MATTER IS SPARED!
What are the microscopic lesions of polioencephalomalacia of sheep & cattle?(thiamine deficiency)Neurons are shrunken, acidophilic & surrounded by clear spaces. In chronic cases, healing w/ intense gliosis
Ddx for thiamine deficiency?Lead poisoning (subacute or chronic cases), salt poisoning, cases of anoxia, high dietary sulfur
When might a thiamine deficiency occur in HORSES? (What CS will you see?)Happen if the horse was poisoned by; Bracken fern (Pteridium aquilinum) or Horsetail (Equisetum arvense).... CS seen will be incoordination, recumbency, bradycardia (CNS lesions not fully elucidated)
Copper deficiency affects who usually?Sheep & goats
If the Cu deficiency is present at birth, what is this called & who does it usually happen in? Also, what will the lesions look like/where would they be?"Swayback" in lambs. There will be bilateral cerebrocortical lesions → astrogliosis, degeneration of white matter
**If the signs of Cu deficiency have a delayed onset up to 6mo, what is it called? Who does it usually happen in? What do these lesions look like & where are they?Enzootic ataxia in lambs!& kids. They grey & white matter will both be affected & you will see chromatolysis, neuronal necrosis, degeneration of myelinated axons
Avian encephalomalacia is czd by what?A DEFICIENCY of Vitamin E
Avian encephalomalacia (Vit E deficiency) czs what 3 problems in the body? & what 3 supplements can you give to help each problem (problem specific, no cross-helping)Encephalomalacia (synthetic antioxidants)
Exudative diathesis (inorganic selenium)
Nutritional muscular dystrophy (Cysteine))
What kind of diet would encourage avian encephalomalacia to develop?Occurs w/ diets borderline in vitamin E that also contain polyunsaturated fats (cod-liver oil, soybean oil, etc.) in the process of undergoing oxidative rancidity
What are the CS of avian encephalomalacia?Sudden prostration w/ the legs outstretched, toes flexed, head retracted, uncoordinated gait
What/where are the CNS lesions associated w/ Avian encephalomalacia?Usually in the cerebellum, you will see softening (malacia) & necrotic reddish or brownish areas
(This prolly isnt important, but just to read it once: Exudative diathesis usually happens w/ what dietary problem? nutritional muscular dystrophy's dietary problem?)Exudative Diathesis: Frequent when corn or soybean meal diets are grown on selenium deficient soil
Nutritional Muscular Dystrophy: When the diet is deficient in both vitamin E & sulfur-containing amino acids (e.g., Cysteine)
Vitamin E (tocopherol) deficiency-> this czs what in birds? Horses? How common is this in other species?Encephalomalacia in birds. OBSCURE in other species. Neuraxonal dystrophy/axonal spheroids (maybe axonal dystrophy) in Morgan horses (equine degenerative myeloencephalopathy) →
In general, a deficiency in vitamin A czs what problems several species?Night blindness (retinol is vit A... which is stored in the retinal pigment epithelium & it combines w/ opsin to form Rhodopsin, a visual pigment)
What is the condition in calves czd by a vitamin A (retinol) deficiency? What is the pathogenesis?Optic neuropathy occurs in calves. What happens is that there is constriction of the orbital optic nerve that ↑ the CSF pressure resulting in papilledema (edema of the optic disk)
Vitamin A deficiency czs what to degenerate, resulting in what? What atrophies in this condition & why?Retinal degeneration>> night blindness (lack of things needed to make sight pigments). Also there is optic nerve atrophy (due to compression by stenotic optic foramina)...this compression is bc vitamin A is reqd for osteogenesis as well as bone resorption, so hypovitaminosis A >> ↑ thickness of cranial bones >> compression
Yellow star thistle (nigropallidal malacia) → this toxin is a problem in who? What kinda lesions (in general) does it cz? (Where?)HORSES, malacic lesions, specifically in the pallidus & substantia
What are the CS of yellow star thistle tox, why does this happen?Bc of the localized destruction of the Globus pallidus (pallidal) & substantia nigra (nigro) areas of the brain, the horses ability to take in & masticate food is impeded. You will see them w/ an open mouth & their tongue hanging out, (excess?) salivation, weight loss, aspiration pneumonia, drowsiness
*What are the GROSS lesions of Yellow Star Thistle tox? microscopic?GROSS: Sharply demarcated foci of yellow discoloration & malacia
Microscopically: Necrosis w/ loss of neurons, axons, glia & blood vessels, influx of macrophages
What is the most important poison in FARM animals?LEAD!
In acute poisoning of lead, where do you find the lead? Chronic?Acute: Absorption & storage in liver, kidneys
Chronic: Deposition in bone
*Acute lead poisoning in CATTLE czs dead in how much time? What are the CS in calves? Adults?Death in 12-24 hours. In CALVES you will see: staggering, muscular tremors, recumbency, convulsions, death ADULTS you will see: Head pressing, blindness, convulsions, death
Lead poisoning in CATTLE → what are the ACUTE poisoning CNS lesions? Subacute or Chronic?ACUTE: Minimal or absent, there might be (+/-) mild to moderate edema
Subacute/Chronic: Laminar cerebral cortical necrosis due to ischemia, anoxia & direct toxic effects on neurons, astrocytes & endothelial cells
Lead poisoning in DOGS → what are the CNS lesions you'll see?You will see edema of the white matter (brain & spinal cord), degeneration in the myelin sheaths (deeper white matter of the cerebrum & cerebellum) & neuronal degeneration & necrosis (subthalamus & head of the caudate nucleus)
Do horses usually get acute or chronic lead poisoning?CHRONIC
Selenium czs neurotoxicity in who? What is the syndrome which is resulting called?Pigs, Acute Paralytic Syndrome (they are "dog sitting")
What are the GROSS lesions of Selenium toxicity? Microscopic?GROSS: Bilateral poliomyelomalacia
Microscopically: Status spongiosus, neuronal chromatolysis (Chromatolysis is the dissolution of the Nissl bodies in the cell body of a neuron), neuronal necrosis, Wallerian degeneration
**Salt (NaCl) toxicosis-aka? Who is most affected by this?Aka Water Deprivation Syndrome, swine & sheep are most frequently affected
What are the CS of NaCl poisoning in swine?Blindness, deafness, head pressing, convulsions, convulsions are characteristic in pattern & regularity
*In salt poisoning of swine, the symptom of convulsions are characteristic in pattern & regularity.... describe theseTremors of the snout
Rapidly extend as colonic spasms of the neck muscles w/ jerky opisthotonus → pig walks backward & sits down
Explain the pathophysiology of salt poisoning in swine (what happens that czs all these problems?)Hypernatremia (hyperosmolarity) → brain “shrinks” bc of osmotic loss of water → influx of Na+, K+, Cl-to equalize the sodium imbalance (early response) → –(delayed response): influx or endogenous production of organic osmolytes (amino acids, polyols,, methylamines) to equalize the osmotic imbalance created by hypernatremia → osmotic stress → osmotic gradient → brain swelling → laminar necrosis
**Salt (NaCl) poisoning in swine → what are the microscopic lesions from this & what is the PATHOGNOMIC LESION?Microscopically you will see eosinophilic meningoencephalitis (eosinophils in the meninges & around blood vessels), encephalomalacia & laminar necrosis. The "pathognomonic" lesion is: eosinophils+laminar necrosis =salt poisoning
**Eosinophils+laminar necrosis =?SALT POISONING
Leukoencephalomalacia in horses is associated w/ what? (Agent, toxin & carrier)Associated w/ MOLDY CORN which is contaminated w/ Fusarium moniliforme, which has fumonisin B1
What are the CS of a horse w/ leukoencepahlomalacia?(Moldy corn/fumonsin B1 toxin)
Impaired vision
Partial or complete pharyngeal paralysis
Head pressing
Aimless wandering
Tendency to circle
Explain the pathogenetic mechanisms behind Leukoencephalomalacia in horsesVascular damage → infarction?
Inhibit the enzyme ceramide synthase interfering w/ the synthesis of sphingolipids, disruption of cell membranes, lipid peroxidation, production of TNF-αby macrophages, inhibition of synthesis of DNA
Leukoencephalomalacia in horses → what are the gross CNS lesions you'll see?Necrosis of the white matter of the cerebral hemispheres (frontal & parietal lobes most commonly). You will also see malacic foci which are soft, pulpy, grayish depressions + hemorrhages
Leukoencephalomalacia in horses → what are the microscopic CNS lesions you'll see?Edema of the white matter, degeneration of the myelin sheath, axons & glia (structure less, acidophilic semifluid masses to which the microglial cells react). perivascular cuffing is not a prominent feature! & poliomyelomalacia (grey matter in SC)
***In RUMIs, "“polioencephalomalacia”or “central cortical necrosis (CNN)" affects WHICH part of the brain & what is the etiology?CEREBRAL CORTEX, BRACKEN FERN & HORSETAIL
***Which part of the horse's brain is damaged from eating corn? (Fumosin B1)WHITE MATTER!! FOCAL NECROSIS of the CEREBRAL HEMISPHERES