Exam 3 Flashcards

Question

Bovine Malignant Catarrhal Fever Not an Alpha virus Mucous and vasculitis (catarrhal) Is it present worldwide? Highly fatal, sporadic What is the primary target tissue? What are the two associated types? Which is the most transmitted vector? Gross lesions WM most often involved Histologic characteristics C/S

Answer 1

-Gammaherpesvirus -Cattle, other ruminants, present worldwide. -Vasculature, lymphoid organs, epithelium (respiratory and GI), others 1. Sheep-associated form Ovine herpesvirus-2 2. Wildebeest-derived form Ovine herpesvirus-2. Africa herpesvirus-1 from wildebeest -Sheep: most transmitted vector -**T-lymphocytes trafficking** endothelial cells -Gross lesions: nonsuppurative meningoencephalomyelitis, necrotizing vasculitis. -Histo: brain, spinal cord, WM most often involved -C/S: trembling, shivering, ataxia, nystagmus (involuntary rapid movement of the eye) **Corneal Edema**

Answer 2

-Canine Distemper -Bronchointerstitial pneumonia -Pantropic (affecting several tissues): Lung, GI, Urinary tract, skin, CNS (including optic nerve). -CNS demyelination without much inflammation -Affects the optic nerve -White matter vacuolation (intramyelinin edema) -All CNS susceptible but OLIGODENDROCYTES infection is usually defective (incomplete) -INIB are present in astrocytes, distinct acidophilic also seen in the cytoplasm of epithelial cells throughout the body. **Eosinophilic inclusions**

Answer 3

-Immunosuppression: secondary bacterial infections (conjunctivitis, rhinitis, bronchopneumonia) -Neurologic signs: myoclonus, tremor, circling, hyperesthesia, paralysis, blindness -Histo: demyelination, nonsuppurative encephalitis, leptomeningitis, preivascular cuffing, microgliosis, astrogliosis, neuronal degeneration, INIB, ICIB (neurons, astrocytes = target cells), cerebral cortex, thalamus, brainstem

Answer 4

-Long-term persistent infection of CNS with a defective form of CDV (in experimental infections) -Lesions: primarily cerebral hemispheres, brainstem -Old-dog encephalitis mature dogs affected -C/S: depression, circling, head pressing, visual deficits, seizures, muscle fasciculations

Answer 5

-Two coronaviruses: antigenically/morphologically indistinguishable -Avirulent (FECV): enteric, ingestion, infects replicates in enterocytes -Virulent (FIPV): mutated coronavirus -Ferrets, domestic cats, wild felids. -Saliva, feces, direct contact (bites, wounds), in utero, replicates in macrophages, liver, serosal surfaces, uvea, meninges, ependyma, spinal cord. -FIP all ages, between 3 months and 3 years most critical, death. -Clinical signs by involvement of blood vessels. Seizures, behavioral changes, ataxia, paralysis. -Pyogranulomatous inflammation distorts and obscures blood vessels in cerebral vasculature of circle of Willis. -Exudate accumulation of serous fluid and fibrin mixed with neutrophils and histiocytes to pyogranulomatous, commonly

Answer 6

-Depends on the type/degree of immunity. -Strong cell-mediated immunity: virus containment, resistance -Wet effusion form (humoral not protective) Th1 response 1. Ag/Ab complement complexes: type III hypersensitivity - effusion, inflammation of small blood vessels 2. Antibody dependent enhancement: Ag/Ab complement complex infected macrophages - cytokines - increased vascular permeability, edema. -Effusive form (wet) -Dry (non-effusive form) partial cell-mediated immunity Type IV hypersensitivity. -Dry form lesions: leptomeningitis, chorioependymitis, encephalomeyelitis, opththalmitis. CNS non-suppurative pyogranumolatous vasculitis. Perivascular WM: especially 4th ventricle, uvea, retina, optic nerve sheath.

Answer 7

-Rhabdoviruses -Replication at inoculation site (skeletal muscles) -Retrogade movement along axons to spinal cord and brain. 12-100 mm per day, gives some time before reaching brain -Intracytoplasmic inclusion bodies called **Negri bodies** Necropsy -Additional protection -Collection of CNS tissues: hippocampus, cerebellum, medulla and optional spinal cord. -Remainder of brain fixed in 10% neutral buffered formalin for histopath (10:1 ratio)

Answer 8

-Coccidiodes immitis -Blastomyces dermatiditis -Histoplasma capsulatum -Cryptococcus neoformans (has particular affinity for CNS) -Does not include Aspergillus unless German shepherd -Lesions: Granulomatous to pyogranulomatous inflammation. Neutrophils, macrophages (epithelioid type), Multinucleated giant cells also. Nodular granulomas -Cryptococcus neoformans

Answer 9

Coccidiodes immitis Largest of the systemic fungi 10 times size of neutrophils, can use that as reference for size

Answer 10

Histoplasma capsulatum -Can be confused with Sporothrix, but that one has cigar shape.

Answer 11

-Cats, dogs, horses -Replicare via narrow based budding -15-25 um and spherical to crescent shaped. -15-20 um thick mucicarmine staining capsule

Answer 12

Blastomyces dermatiditis

Answer 13

Not systemic Zygomycetes group **Targets blood vessels, Hyphae form, ex: guttural pouch mycoses*** -Absidia corymbifera -Mucor spp. -Rhizomucor pusillus -Rhizopus arrhizus Aspergillus spp. -Hyphae that are septae with parallel walls at an angle of less than 90 degrees Angioinvasive: vascular thrombosis and infarcts in CNS

Answer 14

1. Tissue cysts phases. Affinity for brain (cerebellum in dogs). Multifocal necrotizing lesions with glial nodules, mixed inflammatory infiltrate, also abortions **White and grey matter of spinal cord but also pons and medulla** 2. Horses, resembles Sarcocystis neurona causing EPM. Lesion is meningoencephalomyelitis 3. Intraintestinal life cycle and extraintestinal. Encephalomyelitis

Answer 15

-Etioloic agent: Sarcocystis neurona -DH: opossum -IH: avian -Gross: brainstem, spinal cord (cervical, lumbar intumesces). Necrosis, random hemorrhages of white/grey matter. -S. neurona: crescent-round, well-defined nucleus, schizonts with merozoites in aggregates or rosettes -Young adult horses -C/S: depression, behavioral changes, seizures, gait abnormalities, ataxia, unilateral facial nerve paralysis, head tilt, tongue paralysis, urinary incontinence, dysphagia, atrophy of masseter and or temporal muscles, atrophy of quadriceps and or gluteals.

Answer 16

Sarcocystis neurona Equine Protozoal Encephalomyelitis

Answer 17

-Feline Ischemic Encephalopathy -Cuterebra fly larvae migrates from nasal cavity to brain. -Middle cerebral artery preferred and affected -Any age -Unilateral, WM and GM of cerebrum -Necrosis, hemorrhages: CNS leptomeninges -Histo: vasculitis, thrombosis, ischemia, infarction, cerebral cortical atrophy. -C/S: summer months, unilateral, depression, mild ataxia, seizures, behavioral changes, blindness. **Cerebral hemisphere undergoes necrosis, followed by cyst formation and collapse after phagocytic removal of the necrotic debris** **Hydrocephalus ex vacuo**

Answer 18

-Hyperammonemmia: acute/chronic liver failure, hepatic atrophy (vascular shunts) -Ammonia formed in the GI by bacterial degradation of amines, amino acids, purines, urea from proteins in diet. -Liver detoxifies it to less toxic urea normally, then excreted in urine. -Amonia butyrate in urine

Answer 19

-Astrocytes primary lesion (Alzeimer's type II astrocytes) -Similar renal encephalopathy, renal injury leads to inadequate clearance. -Dogs, ruminants, horses

Answer 20

-Polioencephalomalacia -Cattle > sheep > goats -Bracken fern -Polio = gray matter necrosis -Pathogenesis: decreased in ruminal thiamine, inactive thiamine analogues OR overgrowth of thiaminase producing microbes -Causes: carb rich diet in cattle, little roughage > acidosis > rumen microflora changes. - Young ruminants have not fully populated thimaine-producing microbes in rumen yet. Microbes synthesize thiamine. -Gross lesions: if present are limited to cerebral cortex -Swollen (cerebral edema) +/- brain displacement, herniation. -Autofluorescence under UV light 365 -nm, autofluorescent bands of necrotic cerebral cortex. **Difficult to pick up lesions, look for interface between gray matter and white matter. ** **Bilateral symmetric laminar pattern of apple-green autofluorescence (from mitochondrial derivatives) involving full thickness of cortex indicates GM necrosis** -C/S: small ruminants depression, stupor, ataxia, head presssing, cortical blindness, opisthotonos, convulsions, recumbency, paddling, death. -Histo: acute stage = zone of edema and acute neuronal necrosis affecting lamina of cerebral cortex. Chronic stage = areas of microcavitation in deep cortical laminae next to subcortical white matter are poorly stained compared to those in normal cortex. **Laminar cortical necrosis, edema, astrocyte swelling, bilateral symmetric focal lesions in carnivores: thalamus, midbrain or colliculi**

Answer 21

-Dogs, cats, mink, fox. -Gross: necrosis, bilateral symmetric focal lesions, **thalamus, midbrain or colliculi** -Histo: neuronal vacuolation, degenerations, necrosis, hemorrhage, astrogliosis, gitter cells. -C/S: vomiting, wide-based stance, ataxia, spastic paresis, circling, seizures, recumbency, opisthotonus, coma, or death.

Answer 22

1. Swayback congenital form: affects lambs newborn (ewes with inadequate dietary Cu). Lambs born dead, weak or unable to stand -Lesions: cerebrum, brainstem 2. Enzootic ataxia: onset is delayed for up to 6 months after birth. -Lesions: postnatal onset, brainstem, spinal cord. -Gross: 50% of affected lambs have bilateral cerebrocortical rarefration in white matter -Histo: asatrogliosis associated degeneration of white matter, neuronal necrosis.

Answer 23

-Equine motor neuron disease -Dietary factors, long-term (>1 year) of Vit E deficient feeds, other andtioxidant deficiencies -Cell bodies, axons of lower motor neurons (ventral horn cells, cranial nerves) -Histo: cell bodies are lost, replaced by astrogliosis, LMN axons, WALLERIAN DEGENERATION. Abundant lipofuscin in neurons, endothelial cells. -Lesion: atrophy of type 1 myofibers secondary to loss of type 1 lower motor neurons -C/S: progressive degeneration, loss of lower motor neurons, muscle atrophy, weight loss, difficulty standing, muscle fasciculation. **Progressive disease, chronic damage may be too far**

Answer 24

- Selenium Toxicity -Unknown, possible niacin deficiency -Bilateral (symmetric) softening, ventral spinal gray matter -Histo: neural, glial necrosis and loss, microcavitation, astrogliosis, gitter cells WALLERIAN DEGENERATION (injury to axonal body) -C/S: alert, sternal recumbency, quadraplegia with flaccid paralysis of rear limbs. Cutaneous rough hair coats, partial alopecia, separation/sloughing hoofs.

Answer 25

Selenium toxicosis

Answer 26

Equine lower montor neuron disease

Answer 27

-Water deprivation syndrome, or salt poisoning -Pigs, poultry, occasionally ruminants -Overconsumption of sodium chloride complicated by limited drinking water = severe dehydration or water restriction of sufficient duration -Hyperosmolarity (hypernatremia from excessive Na+ or severe dehydration) followed by rehydration and a "rapid" hypernatremic to normonatremic or hyponatremic shift -When given free access to fresh water, acute hypernatremic to hyponatremic shift occurs within minutes the brain offsets osmotis imbalance by eliminating Na+, K+, Cl- ions by actively transporting ions into vasculature, early response cannot offset osmotic stress caused by increased organic osmolytes in brain - water enters the brain - brain swelling ***Drink slowly!!*** Gross: cerebral, leptomeningeal congestion, edema Histo: cerebrocortical laminar neuronal necrosis (PEM) Pigs perivascular eosinophils with laminar cortical necrosis is indicative of salt toxicosis

Answer 28

Salt toxicosis primarily in pigs

Answer 29

-OP esters, pesticides, fungicides, herbicides, or rodenticides, inhibiting cholinesterase -Ach accumulates at synaptic or myoneuronal junctions = persistent depolarization -Acute OP toxicosis = SLUD excessive Salivation, Lacrimation, Urination, Defecation. -Parasympathetic: bradycardia, pupillary constriction. Skeletal muscle fsciculations, weakness, paralysis (death by respiratory failure) -C/S: restlessness, generalized seizures (dogs, cats, uncommon in cattle) -Gross: nervous system absent, nonspecific in other tissues

Answer 30

-Cresyl (triorthocresyl phosphate) in hydraulic fluids, lubricants, flame retardants -Chronic toxicosis: most common cause of chemical induced distal axonopathy in Vet Med -Chronic/delayed toxicosis: unrelated to cholinesterase inhibition as seen in acute OP toxicosis -Axonal injury occurs approximately 10-14 days post exposure -OPs delayed neurotoxicity inhibit activity of enzyme neuropathy target esterase (function of enzyme not fully understood) C/S: delayed 1-2 wks post exposure, sensory/motor neuropathy and spinal cord (proprioceptive deficits) -Young animals: less seriously affected -Adults recover slow and incomplete

Answer 31

Group 2 organophosphates toxicosis due to chronicity

Answer 32

-Ingestion or cutaneous inorganic or organic arsenicals -Yes, multisystemic nervous system -Inorganic compounds: Herbicides and pesticides. C/S: enteric disease with hepatic, renal manifestations, neurologic signs -Organic arsenicals: feed additives in pig, poultry industries as growth promoters and control enteric diseases. >>> potential for neurotoxicity -No gross lesions -Histo: cranial, peripheral nerves, spinal cord, axonal degeneration, fragmentation of myelin sheaths -Distal segments of long ascending fibers can be preferentially injured -Inhibit sulfhydryl enzyme systems, disrupt cellular metabolism (exact mechanism of organic unknown) -Pigs: blindness, tracts, incoordination, paresis, paralysis related to spinal cord and peripheral nerve lesions.

Answer 33

-No gross/histo lesions, if parachute -Acute, subacute, chronic -Cattle -Barn paint (lead), farm buildings, car batteries. -CNS, PNS< liver, kidney, GI, bone marrow, blood vessels, cerebral endothelial cells. -Direct toxin to neurons, astrocytes, cerebral endothelial cells -Gross: contents of rumen. CNS lesions usually absent, can resemble PEM of cattle. -Lesions of lead encephalopathy in ruminants must be differentiated from other causes of PEM -Lesions in dogs with MORE Vascular damage -Cows: down, dead, diarrhea, teeth grinding (bruxism), circling, head pressing, incoordination, blindness.

Answer 34

-Type A, B, or C in N. America -Horses, different forms of botulism affect foals (Toxicoinfectious, ingestion of spores from contaminated soil) and adult horses (contaminated forage, wounds, hoof abscesses, skin wounds, ulcers). -Most prevalent is Type B Mid Atlantic states to Ky -Type A Western US -Clostridium botulinum, necrotic tissue -Horses: progressive paralysis of muscles (limbs, pharynx, eyelid, tongue, tail) -Replicate, produce EXOTOXIN, blood stream, myoneural junctions, binds receptors (presynaptic terminals of peripheral cholinergic synapses), INHIBIT Ach release, flaccid paralysis, diaphragm paralysis = death. -NO

Answer 35

-Tetanospasmin in anaerobic wounds. -Toxin binds myoneural jucntions and or sensory receptors, retrograde axoplasmic flow, accross synaptic junctions to CNS, toxin transferred across synapses, toxin blocks release of inhibitory neurotransmitters (glycine, GABBA) generalized muscular spasms. -Gram (+) spore forming anaerobe; soil. -Except for anaerobic wound, NO -Horses C/S: colic, muscle stiffness (lips, nostrils, ears, jaw (lockjaw), tail, hyperesthetic, rapidly spastic, tetanic paralytic symdrome.

Answer 36

-Pulpy kidney disease, overeating disease -Type D enterotoxemia: EPSILON TOXIN -Sheep: all ages, except newborns, are susceptible. -Peaks between 3-10 wks of age, and in feeder lambs shortly after arrival at a feedlot. -Gross: absent-bilaterally symmetric foci of malacia, hemorrhagic foci with cavitation -Other tissues: soft pulpy kidneys -Histo: acute cases = edema, endothelial cell swollen, vesicular -Both grey and white matter are affected -Neurons and macroglia **Lambs are typically in good condition and found dead**

Answer 37

Type A: alpha toxin Type B: alpha, Beta, and Epsilon Type C: alpha, Beta, Type D: alpha, Epsilon, Type E: alpha, Eiota **Clostridium likes to cause hemorrhage, +/- gaseous necrosis (black leg) ***

Answer 38

-Some strains of E-coli -Feeder pigs rapidly growing, fed high energy ratio. -4-8 wks of age, younger and older pigs can be affected -Gross: facial edema (gastric submucosa, colonic mesentery, lungs, thoracic effusion, pericardial sac, +/- Congestion, hemorrhage, Pallor, spongiosis of CNS parenchyma. -Characteristic brain: bilateral symmetric foci of necrosis in caudal medulla. -Histo: Endothelial cells become swollen and vesicular, but layer remains intact so thrombosis not a feature. -No, inflammation is not the primary process

Answer 39

-Horses: ingestion of moldy corn contaminated with fungus FUSARIUM MONILIFORM -Acute fatal neuroligic disease -Fumonisin B1 -Vascular damage (necrotic, thrombosis) -Gross lesions: WM of cerebral hemispheres most common. Bilateral but now symmetric (unequal in severity) -Characteristic malacia, liquefaction of affected WM due to breakdown of lipids accompanied by hemorrhage -Hepatotoxicity can be the sole manifestation -C/S: depression, head pressing, aimless wandering, blindness, seizures, rapid progression and death. -Other species: pigs, generally with pulmonary, hepatic and renal manifestations.

Answer 40

Leukoencephalomalacia is also associated with hepatotoxicity, or hepatotoxicity can be sole manifestation

Answer 41

-Centaurea spp. -Morph Dx: Nigropallidal encephalomalacia -Histo: necrosis, loss of neurons is primary lesion. Necrotic axons, glia, blood vessels. -Horses: persistent chewing, difficulty in prehension of feed, drinking water. -Lip/tongue paralysis, reduced jaw tone early in disorder -Death due to emaciation, starvation. -Gitter cells

Answer 42

-Meningeal Melanosis

Answer 43

-Cholesteatomas a.k.a cholesterol granulomas -Form in choroid plexuses of ventricles in horses -Tan to yellow-brown firm masses with smooth often glistening surface +/- mineral -Elicit foreign body granuloma, fatty components to it. -Result from edema and minor, but repeated hemorrhages within choroid plexuses - cholesterol deposits

Answer 44

-Young middle-aged small breeds (poodles, terriers) -Female > male -Gross: gray-white to red, expansive areas within WM of brain, brain stem, irregular, well-defined margins, gelatinous, rubbery or granular consistency -Histo: perivascular cuffing (CD3+ lymphs, perivascular CD163+ macs), PCs neuts, restircted to WM -Chronic: abundant perivascular deposition of reticulin collagen -Underlying mechanism: T-lymphocytes mediated Type IV hypersensitivity but not proven

Answer 45

1. Necrotizing meningoencephalitis (NME) a.k.a Pug dog encephalitis. Almost always in small breed dogs -Gross: bilateral foci of malacia, discolored cerebral hemispheres. -Histo: meningoencephalitis, robust inflammation, nonsuppurative, marked gliosis -Unlike GME (granulomatous meningo-encephalomyelitis) spinal cord involvement is not common 2. Necrotizing leukoencephalitis (NLE): predominantes in white matter -Gross: Prominent bilateral cavitation, necrosis of cerebral white matter -Histo: robust nonsuppurative inflammation, cavitation, edema, gitter cell infiltration

Answer 46

-LSDs: substrates can't be degraded by lysosomes, they accumulate and death of affected cells occurs. Macrophages have the same genetic defect, they die and release substrate in phagocytosed by other macs recruited from blood. -Pressure atrophy on other organelles of the cell -Causes: Reduction of lysosomal enzemy synthesis, synthesis of catalytically inactive proteins, defects in posttranslational processing of enzyme - misdirected to sites (extracellular) other than to lysosomes. -Lack of enzyme activator, substrate activator protein required to assist with the hydrolysis of substrate. Lack of transport protein required for elimination of digested material from lysosomes. -General principle: cell swelling, cytoplasmic vacuolation, many lipids and glycolipids are unique to nervous system, when there is lysosomal defect, neural cells often accumulate substrate Gangliosidoses: is inherited autosomal recessive. -Age of onset varies (different lysosomal enzymes) -If mutant, enzyme is not synthesized at all = early onset -If residual synthesis of deficient enzyme = later onset form Gross lesion -CNS vary among different types of LSDs -Brain atrophy occurs with: **Globoid cell leukodystrophy: because of the loss of myelin. Ceroid-lipofuscinosis. Histo Lesions -Neurons: foamy, finely vacillated or granular cytoplasms. -Specific features of stored material best appreciated by EM (electromicroscope)

Answer 47

-VitE deficiency association -Slowly progressive neurologic diseases Characterized by abnormal sphingolipid (lipopigments) metabolism. Cats, dogs, sheep, cattle. **Lysosomal dysfunction not clearly identified** Gross lesions -Atrophy of cerebral gyro, widening of sulci. -Brain atrophy with carotid-lipofuscinosis (later stages of disease) in cerebral cortex, sometimes cerebellum. Histo -Neuron cytoplasm -Eosihophilic granular material (H&E), decreased # of neurons, prominent reactive astrogliosis microgliosis. -Pic: horse with carotid-lipofuscionosis

Answer 48

LSD: Lysosomal storage disease, Globoid Cell Leukodystrophy **White matter target** -Disruption of normal myelin turnover due to deficient galactosylceramidase activity = accumulation of psychosis - primary demyelination, recruitment of phagocytes (resident microglia, trafficking blood monocytes) = Infiltration of macs, become globoid cell after phagocytosis myelin byproducts. Gross: discoloration of WM, especially cerebral hemispheres, spinal cord. Histo: Loss of myelin, globoid cells containing galactocerebroside, PAS (+) **Peripheral Nerves also affected** **Primary demyelination - axonal degeneration and globoid cells. Dx: biopsy sensory branches of peripheral nerves

Answer 49

HYPOMYELINOGENESIS -Hypomyelination Classical swine fever (hog cholera) PESTIVIRUS -Teratogenic in fetus -Hypomyelinogenesis -Cerebellar hypoplasia -Microencephaly -PI that results in inhibition of cell devision, function of selected tissues proposed Border disease virus (also PESTIVIRUS) -Lambs and goats -Hypomyelinogenesis, primarily affecting WM of cerebrum, cerebellum. Gross -Difficult to distinguish between WM and GM of cerebrum, cerebellum. **PNS is unaffected** -In lambs: early inflammation, porencephaly-hydraencephaly, cerebellar hypoplasia, microencephaly, smaller diameter of spinal cord.

Answer 50

-Diffuse brain injury (often present in concussion) -acceleration/deceleration forces to many areas of CNS -Diffuse axonal injury: variant of diffuse brain injury. Axons of large myelinated nerve fibers injured by shearing forces. -Concussion, contusion, hemorrhage -Compression, stretching, laceration of neurons/axons.

Answer 51

-Brain of a freely movable head is much more susceptible to injury than one that is fixed in place. Cranium and contents impact each other after non penetrating trauma - space between brain and cranium C/S: -transient unconsciousness and return to normal function to depression, abnormal behaviors -Disorientation, irritability, semiconsciousness with responsiveness only to noxious stimuli. -Unconsciousness with no response to stimulus Spinal cord trauma -Signs vary: paralysis (severance of cord or ruptured disc) paresis, ataxia (less severe injury) Concussion -Difficult to produce severe concussion in animals (margin between force os a stunning blow and one causing fatal injury is very small) -Diffuse -Transient (usually reversible) -Temporary loss of consciousness -No gross lesion -Minimal microscopic lesion -Uncommon in animals -The smaller the brain, the less vulnerable it is to rotational forces and the larger are the forces necessary to cause concussion Spinal concussions -Immediate and temporary loss of function that sometimes follows severe direct blows Contusion -Brain bruising -Associated with rupture of blood vessel and hemorrhage as resulting injury **Focal** -Does not always result in unconsciousness Gross -Superficial area of hemorrhage associated with skull fracture -Large blunt object Types of contusion -Coup contusion -Contrecoup -Coup-contrecoup: conditions include head freely moveable, head accelerated rapidly, because the brain does not fill the cranial vault it may lag behind the movement. As a result the inside of the cranial vault may strike the stationary brain at the point of impact (coup injury) or on the opposite side (countercoup)

Answer 52

**Vasculatis (ex: fungal infections), trauma, contusion, penetrating wounds** -Trauma: most common cause = epidural, subdural, and subarachnoid under the pic matter (subpial). Brain (parenchymal) -Diffuse or focal hematoma -Epidural: between the calvaria and dura matter -Subdural: between dura matter and arachnoid -Leptomeningeal or Subarachnoid: in the subarachnoid space and pit matter -Parenchymal: in the brain tissue

Answer 53

1. Neurapraxia: mild injury; axon is intact; temporary conduction block, total recovery of function is possible 2. Axonotmesis: more severe damage, destroys axon but leaves connective tissue framework intact (results in Wallerian degeneration) 3. Mild neurotmesis: severance of nerve + destruction of supporting framework. Wallerian degeneration distal to injury, potential for regeneration but little chance or normal rein nervation. 4. Severe neurotmesis -Destruction of framework - fibrosis between proximal and distal ends of nerve; gap may be large -Fibrous tissue can obstruct regenerating proximal axon from reaching distal supporting framework of axon -If regenerative response is exuberant but unproductive, a "potentially" palpable bulbous-like growth can form at severed stump of the proximal axon called "neuroma"

Answer 54

**Occur dorsally in dogs** Type I Hansen herniation in IVDD -Chondrodystrophic breeds: Dachschund, Pekingese -Acute: progressive degeneration of discs, TRAUMATIC INJURY -Genetic (chondroid) metaplastic change of nucleus pulposus -Very painful -6 mts of age, progresses rapidly - loss of elasticity of nucleus pulposus disk compresses blood vessels and spinal cord segment = ischemia, neuronal excitotoxicity, necrosis - stress on annulus fibrosis (degeneration changes similar to nucleus pulposus; annulus fibrosis is thinnest, weakest at point of contact with spinal cord) **most severe spinal cord damage (no time for collateral circulation to develop) -Multiple disks can be affected Type II Hansen -Older dogs: 8-10 yr old -Non-chondrodystrophic breeds German Shepherds, Labs, Doberman, Obese dogs -Slower degeneration - gradual loss of elasticity places mechanical stress forces on annulus fibrosus = protrusion/compression of spinal canal **Less painful than type I**

Answer 55

-All species, most common in dogs -Larger breed, chondrodystriphic breeds -Young or old Lesion: herniation of fibrocartilage from intervertebral disk (nucleus pulposus) - fragmentation into vasculature - occlusive emboli -Ventral spinal artery/vein and tributaries commonly affected (due to proximity to extruded disk material) Gross -Acute focal infarct involving cervical or lumbar spinal cord most commonly Histo -Emboli histochemically identical to fibrocartilage of nucleus pulposus of IVDs occlude meningeal or CNS arteries or veins, or both, in affected areas. C/S -Sudden onset of spinal cord deficits, sometimes cerebral involvement

Answer 56

PNS Injury -Recurrent laryngeal nerve paralysis -Atrophy of left dorsal cricoarytenoid muscles, dysfunction of larynx **Cricoarytenoid dorsalis: main abductor of larynx muscle** Gross -Recognizable to being inapparent degeneration Histo -Wallerian degeneration -Primarily a disease of large horse breed 2-7 yrs

Answer 57

Equine Cervical Stenoic Myelopathy (CSM) -Yes, Wallerian degeneration present -Both white and grey matter, or either one affected by necrosis -Young rapidly growing large breed horses and dogs -Multifactorial disease: Oversupplemetation (protein, vitamins, minerals) Gross -Visible on saggital section of spinal cord 1. Cervical static stenosis syndrome **C5-C7** compression, horses 1-4 yrs and compression regardless of head position 2. Cervical vertebral instability (dynamic stenosis) syndrome **C3-C5** Narrowing of spinal canal during flexion of neck. Canine Cervical Stenotic Myelopathy -AKA Wobbler syndrome, vertebral instability, vertebral subluxation -Great Dane, Doberman, Saint bernard, Irish setter, Fox terrier, Basset, Rhodesian, Old English sheep dog. -Signs develop between 8 mt - 1 year -Most often **C5-C7** is affected -Basset hound: C3

Answer 58

1. Rabies: CN V (trigeminal ganglion) 2. Pseudorabies CN V 3. Listeriosis CNV 4. Yellow start thistle/Russian knwpweed poisoning (horses): Globus pallidus and substantial nigra nuclei 5. Equine degenerative encephalomyelopahty: Medulla Oblongata 6. Transmissible spongiform encephalopathies: Medulla oblongata

Answer 59

-All are malignant Three types based on degree of differentiation 1. Diffuse astrocytomas -Most well differentiated astrocytes, loosely organized -Slow growing, less malignant, looks similar to normal tissue; solid or firm; gray-white, poorly demarcated **Pilocytic gemistocytic variants: both recapitulate features of astrocytes** 2. Anaplastic astrocytomas: high cellular pleomorphism and mitoses, necrosis 3. Glioblastoma multiforme -Hemorrhage -Increased pleomorphism, high mitotic rate, necrosis -Characterized by glomeruloid-llike vascular proliferation, serpiginous tracts of necrosis lined by neoplastic cells (pseudopalisading ) -Most poorly differentiated astrocytes -Rapidly growing, more malignant, easier to discern because of necrosis, hemorrhage, cavitation, edema 4. Oligodendrogliomas **Brachycephalics: Bostons, Boxers, dogs 5-11 yrs, cats>>horses, cattle, pigs** Common lesion site: cerebrum (temporal, pyriform lobes, that-hypothalamus, midbrain) Less frequent: cerebellum, spinal cord.

Answer 60

Oligodendrogliomas -Tend to extend to meningeal, ventricular surfaces, dissemination via CFS, ventricular system to distant brains sites common -Well demarcated mass, variable size, gray to pink-red and soft to gelatinous with areas of hemorrhage +/- cystic

Answer 61

Choroid Plexus Tumors -Papillomas (benign), carcinomas, epithelial cuboidal cells. -4th ventricle > 3rd, lateral ventricles -Hydrocephalus possible sequelae Gross -Well-defined, expansive, granular to papillary growth within ventricular system, gray-white-red, compresses adjacent tissue.

Answer 62

Meningiomas -Dogs 7-14 yrs, cats >10 yrs -Dog lesion: brain, spinal cord, retrobulbar (optic nerve sheath) -Cat lesion: uniquely occurs in 3rd ventricle, cerebral hemispheres, along cerebra, cerebellum and tentorium, rarely at base of brain **Compress (pressure atrophy) or invade underlying CNS parenchyma** Gross -Dog:solitary, vary insize, well defined, spherical, lobulated, firm, encapsulated, gray-white +/- soft, areas of hemorrhage, necrosis -Cat: mm to 2 cm in diameter **multiple, can be incidental, old-age findings** Histo -Microscopic findings, patterns subtypes as Type 1-4 most common in dog. -Transitional -Meningothelial -Psammomatous -Fibrous -Atypical -Malignant -Almost all meningiomas: features typical of maningothelial or transitional type with psammoma bodies (are concentric lamellated calcified structures) being a common feature.

Answer 63

-Most are metastases from other organs -Dogs > other -solitary expansile red to dark red mass within the cerebral cortex -Dx: primary or metastatic melanoma

Answer 64

-Neurofilaments: structural support -Microtubules: (bidirectional axoplasmic flow of nutrients, trophic factors, maintenance of axon, neuronal integrity) Supporting cells Schwann Cells: -Surround myelinated/nonmyelinated axons; produce myelin sheaths -Guides axon during formation, maintenance of PNS, regeneration role Fibroblast: of endomeurium Satellite cells (schwann-like cells): dorsal root ganglia, supportive, non-myelinating role Enteric division of PNS -Digestive motility, secretion, absorption, blood flow. -Myenteric plexuses (Auerbach's plexuses): between longitudinal and circular muscles -Submucosal plexuses (Meissner's plexuses): innervate esophageal, intestinal smooth muscle. -Injury to theses plexuses can lead to dysautonomias (discussed later).

Answer 65

1. Schwannomas -Derived from Schwann cells -Dogs>cats, horses, cow Gross: nodular thickening along nerve trunks/roots; firm/soft (gelatinous), white/gray Histo: neoplastic Schwann cells with two patterns, known as **Antoni type A and type B** 2. Perineuriomas -Derived from perineurial cells -Behaves as a benign neoplasm -Vary rare variant 3. Neurofibromas -Consist of Schwann cells, perineurial cells, fibroblasts -Not common in domestic animals. **Tumors can occur most commonly in cows and dogs. The term nerve sheath tumor groups all morphologic diagnoses under a common umbrella**

Answer 66

Dysautonomias -Key-Gaskell Syndrome -Unknown cause; hereditary? toxins in cats? Histo: neuronal chromatolysis, pyknosis to loss of neurons, proliferation of satellite cells -Minimal to mild WBC infiltrates -NOT overtly inflammatory C/S -Cats, dogs, varied; GI disturbances, urinary incontinence, mydriasis, unresponsive pupils, bradycardia.

Answer 67

Lethal White Foal Syndrome -Functional blockage of ileum and or colon because of lack of innervation -Disorder involving development of the enteric division of the PNS. -Foals of American paint horses with overo markings -Homozygous dominant mutations in the endothelia-B receptor gene Histo: myenteric and submucosal enteric ganglia are absent, areas affected vary; can extend anywhere between ileum and distal large colon **Affected foals die within days birth: functional blockage... born with white or nearly white skin**

Answer 68

Myasthenia Gravis Causes -Aquired: autoimmune mechanism -Antibodies to acetylcholine receptors (type II hypersensitivity) on postsynaptic muscle membranes - blocks Act binding -Congenital: genetic abnormalities. Genetically determined deficiency in number of acetylcholine receptors. -Concurrently with **Thymic abnormalities** Tymoma, thyme hyperplasia. **Results in flaccid paralysis of skeletal muscle** **No gross or microscopic lesions in PNS or CNS** Findings: skeletal muscle atrophy, megaesophagus

Answer 69

1. Primary lymphoid organs -Where B, T lymphocytes proliferate, differentiate, mature. **Thymus, Bone marrow, Bursa of Fibricius (birds)** 2. Secondary lymphoid organs/tissue **Spleen, Lymph nodes (except reptiles, birds, amphibians,) Lymph nodules

Answer 70

Thymus Formed from third pharyngeal pouch in fetus Bone marrow derived progenitor cells lymphocyte population Domestic animals: **Paired cervical lobes (left and right), intermediate lobe at thoracic inlet, and thoracic lobe (may be bilobed) Thymus Anatomy Connective tissue capsule: septa subdivided into lobules, each lobule has central medulla and surrounding cortex 1. Cortex: epithelial reticulum and lymphocytes -Stellate cells of epithelia reticulum form a supportive network -Lymphoid component: differentiation lymphocytes derived from precursor T lymphocytes in BM 2. Medulla: similar epithelial reticular cells -Hassall's corpuscles: distinctive keratinized epithelial structures -Interdigitating dendritic cells (DCs) in medulla -Far fewer lymphocytes than in cortex 3. Thymic vasculature Response to Injury -Lymphoid atrophy -Neoplasia: lymphoma, thymoma -Hemorrhage -Inflammation: rare, infectious agents (porcine circovirus) General causes of Lymphoid Atrophy in Lymphoid Organs -Lack of antigenic stimulus -Toxins: lead, mercury, mycotoxins, halogenated aromatic hydrocarbons -Chemotherapeutic agents: cyclosporin A, corticosteroids -Ionizing radiation -Viruses: CDV, canine and feline parvovirus, FIV, BVDV, classic swine fever virus, EHV-1 **More common cause of thymus atrophy** -Malnutrition and Cachexia -Aging Portals of entry -Main: hematogenous Defense mechanisms -Innate, adaptive immune responses -Viruses, bacteria arriving in lymph and blood interact with cells of monocyte-macrophage system through phagocytosis and antigen presentation MALT: mucosa associated lymphoid tissue -Hematogenous -Migrating macrophages -Dendritic cells -M cells (Peyer's patches)

Answer 71

-EHV-1 in aborted foals -Classic swine fever -BVDV -Canine distemper -Parvovirus feline and canine -FIV -Not common lesion -Other organs also affected **PCV2, enzootic bovine abortion, salmon poisoning in dogs** -Mycotoxins: fumonisins B1, B2 and aflatoxin **There are not many specific toxins that target the thymus, is rather via immunosuppressive, immunostimulatory, DNA damage** Malnutrition and cachexia (may occur with neoplasia) -Lead to secondary immunosuppression -Thymic function is impaired in young malnourished animals: LYMPHOID ATROPHY (physiological/emotional stress): release of catecholamines, glucocorticoids Aging -All lymphoid organs atrophy with advancing age = immunosuppressed -Thymic reduction in size occurs after sexual maturity (thyme involution)

Answer 72

-Autoimmune lynphoid hyperplasia of thymus from Myasthenia graves -Juvinile animals in association with immunizations: symmetrical thymus size

Answer 73

-Dogs: young animals Causes -Anticougulant rodenticides (warfarin, dicoumarol, brodicoum). **Medulla: main site of hemorrhage** -Dissecting aortic aneurysms -Trauma (HBC) -Idiopathic/spontaneous Pic: acute thymic mediastinal, and pericardial sac hemorrhage

Answer 74

Myasthenia gravis 1. Lymphoid component 2. Epithelial component Neoplasms arise from either component Thymic lymphoma: arises from T lymphocytes in thymus (very rarely B lymphocytes) -Young cats, cattle > dogs Thymomas -Arise from epithelial component -Usually benign -Common in goats -IM diseases: myasthenia graves and IM polymyositis occur with thymomas in dogs > cats.

Answer 75

-Soft, pale tan, round, oval, or reniform organs -Stroma capsule, trabeculae, reticulum -Cortex "superficial (outer) cortex: lymphoid follicles, B lymphocytes -Paracortex "Deep" T lymphocytes -Medulla : medullary sinuses and cords -Blood vessels: arteries, arterioles, High endothelial venueles, efferent veins -Lymphatic vessels: afferent/efferent vessels; sinuses (sub scapular, trabecular, medullary) -Monocyte-macrophage system - Sinus histiocytes Response to injury -Based in the systems: 1. Sinus histiocytes of monocyte-macrophage system (antigen presenting cells): first line of defense against infectious and noninfectious agents in incoming lymph -Hyperplasia of macrophages ("sinus histiocytes") notable in medullary sinuses -Leukocytes (monocytes), harbor intracellular pathogens, arrive in blood or lymph - LN - disseminated throughout the body. 2. cortex (lymphoid follicles) antigenic ally stimulated lymph node (follicular hyperplasia): enlarged 3. paracortex: Paracortical atrophy: deficiency in lymphocyte production in BM, reduced differential selection of lymphocyte in thymus, or destruction of lymphocytes in lymph -Paracotical hyperplasia: nodular or diffuse appearance 4. medulla (medullary sinuses and medullary cords): dilation of sinuses, proliferation of histiocytes ("sinus histiocytes") dilation of sinuses due to edema, inflammation, occasional fibrin, in addition to hyperplastic resident sinus histiocytes Patterns -Generalized enlarged LN: lymphadenopathy or lymphadenomegaly (more than one, multiple). systemic infection, inflammatory or neoplastic processes -Single lymph node (or regional chain), area drained by that LN should be checked for lesions. -Large mesenteric LNs: follicular hyperplasia, enlarged

Answer 76

-Afferent lymphatic vessels: lymphatic spread -Blood vessels: hematogenous spread -Organisms to regional LNs through lymphatic vessels - transported to next LNs in chain - lymphatic vessels to cervical or thoracic ducts - disseminated Defense mechanisms -Innate, adaptive immune responses -Structural: thick fibrous capsules Responses to injury 1. Hyperplasia 2. Atrophy 3. Inflammation 4. Neoplasia: primary (lymphoma), metastatic **Macrophages**

Answer 77

Hemal Lymph nodes -Filter blood, remove senescent RBCs (blood supply is small and functional important is not clear) -Mostly found in ruminants, horses, primates, some canids. -Small, dark red to brown nodes

Answer 78

Red -Draining from hemorrhagic or acutely inflamed area -Acute lymphadenitis -Acute septicemias with endotoxin-induced vasculitis or DIC -Postmortem hypostatic congestion Black -Tracheobronchial LN (draining of carbon pigment (pulmonary anthracosis)) -Skin tattoos Brown (black/brown/rust) -Melanin: animals with melanosis, chronic dermatitis, **distinguish from metastatic melanomas** -Parasitic hematin: Fascicola magna (cattle) and Fascicola hepatica (sheep) in liver - hepatic lymph nodes -Hemosiderin: hemorrhagic node or hemosiderin from congested, inflamed, hemorrhagic areas. Iron dextran intramuscular injections in piglets (supplement) Green -Tattoo ink -Ingestion of blue-green algae (mesenteric LN) -Massive eosinophilic inflammation -Mutant Corriedale sheep (genetic defect: deficiency in excretion of bilirubin and phylloerythrin by liver) Miscellaneous -IV injected dyes (methylene blue or trypan blue) -SQ drug injections -Icteric LN

Answer 79

-Congenital disorders: SCID severe combined immunodeficiency -Lack of antigenic stimulation: smaller organs as a result. SPF animals (specific pathogen free animals) Viral infections -EVH-1 -CSF -BVDV -CDV -Fe/K9 parvovirus Cachexia and malnutrition: glucocorticoids -Aging -Radiation Enlarged LNs -Lynphoid hyperplasia (follicular, paracortical) -Hyperplasia of sinuses histiocytes, macrophage-monocyte system **FIV, MCF** -Acute or chronic lymphadenitis -Lymphoma: FeLV, BLV, Marek's -Metastatic neoplasia

Answer 80

-Streptoccocus equi asp. equi -Left and right retropharyngeal lymph nodes Types -Chronic suppurative lymphadenitis: **C. pseudo tuberculosis** (recurrent infection) -Discrete granulomas: Mycobacterium tuberculosis complex, Foreign bodies, fungal infections ( can be disseminated, but individual fungi still invoke MF to coalescing granulomas) -Diffuse granulomatous inflammation: Johne's (mycobacterium paratuberculosis), PCV2 **Pic: Caseous lymphadenitis Corynebacterium seudoparatuberculosis, LNs Sheep**

Answer 81

-Malignancies arise in lymphoid tissue OUTSIDE the BM -Diffuse to nodular enlargement of 1+ LNs. -Cut surface is sift, white, bulging **Effaces corticomedullary architecture** -Lots of necrosis -Lots of loss of architecture Pic: lymphoma cranial mediastinal LNs cat

Answer 82

-Mediastinal or alimentary tract -10 yrs + -Brain, spinal cord, kidney, nasopharynx.

Answer 83

-Highly vacularized -No lymphatics -Nutrient foramen artery, periosteal arteries, anastomose, from sinusoids within medullary cavity of bone -Myelinated and non-myelinated nerve, low numbers of resident macrophages, lymphocytes, and plasma cells. -Macrophages: role in iron storage and erythrocyte maturation Injury and disease -Hematopoietic tissue stem cells system: highly proliferative, undergoes sequential division as they develop and mature after they have stopped dividing -Mature cells have different normal life spans, hours (neutrophils) to days (platelets) to months (erythrocytes) years (some lymphocytes) -Respond rapidly and predictably to various stimuli -Production and turnover of blood cells are balanced (numbers are maintain within normal ranges) **Composition of BM changes with age** RED MARROW: regresses in young animals, replaced with fat (YELLOW MARROW) in older animals. -Bone marrow releases mostly mature cell types: but can release immature cells in response to certain physiological/pathological stimuli

Answer 84

1. Myeloma or multiple myeloma -Arise in bone marrow 2. Extramedullary plasmacytoma (sites other than bone) -Skin of dogs > cats, horses -Pinnae, lips, digits, chin (most common). Also found in oral cavity, intestine > liver, spleen, kidney, lung, brain -Solitary most frequent **Most cutaneous extra medullary plasmacytomas are benign** -complete excision is curative -Oral cavity, colorectal likely to have similarly -May produce monoclonal immunoglobulins MONOCLONAL GAMMOPATHY -Amyloid deposition observed in a proportion of cases YES 3. Both tumors -Characterized perinuclear golgi or "halo" (plasma B cell) -Karyomegaly (large nucleus), binucleation -IHC (MUM1/IRF4 is particularly sensitive and specific for plasma cell neoplasms)

Answer 85

Histiocytic Disorders Categorized as 1. Macrophages 2. Dendritic cells -Largerhans cells (LCs): skin, GI, respiratory, reproductive epithelia mucosa. -Interstitial dendritic cells: perivascular spaces most organs **Histiocytic sarcoma and hemophagocytic histolytic sarcoma dog> cats** Histiocytic disorders: LN involvement in many conditions -Canine cutaneous histiocytoma -Canine LC histiocytosis -Canine cutaneous and systemic histiocytosis -Feline pulmonary LC histiocytosis -Feline progresive histiocytosis -Dendritic cell leukemia (dog) -Canine reactive histiocytoses: not clonal neoplastic proliferations. Immune dysregulation consisting of activated dermal iDCs (and T lymphocytes) a. Cutaneous histiocytoma (CH): skin draining LN b. Systemic histiocytosis (SH): more generalized; skin and other sites (lungs, liver, bone marrow, spleen, LNs, kidneys, and orbital nasal tissues).

Answer 86

Histiocytic sarcomas - Disseminated -Involves distant sites (replaced term malignant histiocytosis) -Arises in almost any tissue (spleen, lung, skin, meninges, LN, BM, synovium) -Secondary liver involvement -Localized histiocytic sarcoma: focal solitary lesion or multiple nodules within a single organ -Dessiminated histiocytoma: involve distant sites **Rapidly aggressive** Gross -uniformely enlarged organs and or multiple coalescing Histo -marked cellular atypical (karyomegalic, multinucleate cells)

Answer 87

Hemophagocytic Histiocytic Sarcoma -Dogs, cats -Neoplasm of macrophages of spleen and BM -Clinically, hemolytic regenerative anemia -Coombs negative -Worst prognosis -Metastasis frequent to liver, +/- emboli in lung -Non-mass forming infiltrate within BM and splenic red pulp, causing diffuse splenomegaly?

Answer 88

-Carcinomas: regional LNs -Other common metastatic neoplasm: mast cell tumor, melanoma -Sarcomas most often metastasize hematogenously. More aggressive sarcomas (osteosarcoma) may spread to regional LN

Answer 89

LEFT cranial region of the abdomen Pancreas on the right -Thick smooth muscle and elastic fiber capsule 1. Red pulp -Monocyte-macrophage system, vascular spaces, hematopoiesis in red pulp. -Filters blood -Removes foreign particles, bacteria, senescent or damaged RBCs, or infected with parasites 2. White pulp -Consists of PALS (peiarteriolar T lymphocytes) each with splenic lymphoid follicle surrounded by a marginal zone -Immunological functions: Activation of macrophages (APCs), proliferation of B lymphocytes, production of antibody, interaction of T lymphocytes and antigens, macrophages in white pulp follicles remove apoptotic B lymphocytes -Marginal zone: interface of white and red pulp. Consists of macs, DCs, T and B gyms. Macrophages of marginal zone bridge the innate and adaptive immune responses. -Germinal zone (B lymphocytes) -Primary follicle -Periarteriolar T lymphocytes (PALSs) **Pink/red: RBC, Purple/blue: Lymphocytes**

Answer 90

-Liver is primary in fetus, spleen makes minor contribution -Shortly before or after birth the bone marrow becomes the primary hematopoietic organ -Under certain condition (severe demand in prolonged anemia): splenic hematopoiesis can be reactivated = EMH extra medullary hematopoiesis -EMH also found in nodular hyperplasia: severe bone marrow failure, myelostimulation, tissue inflammation, injury, repair, abnormal chemokine production. -Dogs, cats: splenic EMH most commonly occurs with degenerative or inflammatory condition (hematomas, thrombosis); may occur without concomitant hematologic disease

Answer 91

1. Asplenia 2. Splenic hypoplasia 3. Congenital and Acquired Accessory Spleens a.k.a splenic choristomas 4. Splenic fissure

Answer 92

1. Congestion due to gastric volvulus and splenic entrapment, splenic volvulus, all compress splenic vein 2. Acute hyperemia (septicemia) ex: anthrax = marked congestion, lymphocytolysis of follicles and PALS. Intravascular free bacilli (impression smears of peripheral blood) not normally necropsy due to aero sporulation spread. 3. Acute hemolytic anemia (autoimmune disorder or chemotropic parasite). Acute babesiosis, hemolytic crises in equine infectious anemia IMHA. 4. Barbiturate euthanasia, anesthesia, sedation **Ooze blood on cut surface**

Answer 93

1. Hematomas -Induced by nodular hyperplasia or hemangiosarcoma, trauma. -Capsule (splenic capsule, visceral peritoneum) over the hematoma can rapture - hemoperitoneum, hypovolemic shock, death. 2. Incomplete contracted areas of spleen -Smooth muscle fails to contract in response to circulatory shock (hypovolemic shock, cariogenic or septic) or sympathetic response, resulting in a lack of splenic evacuation of stored blood. 3. Acute splenic infarcts -Wedge-shaped or triangular lesions at margins of spleen -Dogs: hyper coagulable states (liver, renal disease, cushing's), neoplasia, cardiovascular disease -Cattle: splenic vein thrombi with traumatic reticulates, splenic abscesses, portal vein thrombosis, arterial thrombosis in bovine theileriosis. Vascular endocarditis > multi organ infarcts. -Splenic infarcts are common in pigs with **Classical swine fever** -Acute splenic infarcts > subacute > chronic infarcts gross appearance similar to that of kidney 4. Hemangiosarcomas

Answer 94

-Do not ooze on cut surface -Marked phagocytosis of cells, debris, or foreign material -Proliferation or infiltration of cells: diffuse lymphoid and histiocytic hyperplasia, large disseminated, visible, white, bulging nodules. -Diffuse granulomatous disease -EMH -Neoplasia -Storage diseases or amyloidosis Splenic Nodules with a Firm consistency -Lymphoid nodular hyperplasia -Complex nodular hyperplasia -Primary neoplasms -Secondary metastatic neoplasms -Granulomas: mycobacterium, fungal organisms -Abscesses Pic: meaty spleen and hyperplasia

Answer 95

-Mycobacterium, Brucella, Francisella tularensis -Systemic mycoses: nodular but disseminated: Blastomyces, Dermatitidis, Histoplasma capsulatum. -Protozoal infections that infect macrophages, Leishmania spp. Gross lesion -Multiple sub capsular splenic abscesses ex Rhodococcus equi, spleen horse pic

Answer 96

Arise from -Round cell tumors (LSA, leukemia, visceral mast cell tumor, histiocytic sarcoma). -Stroma cells (fibroblasts, smooth muscle, endothelium) Primary neoplastic disease of the spleen that result in firm nodules -LSA (multiple subtypes) -Histiocytic sarcoma -Leiomyoma, leimyosarcoma -Fibrosarcoma -Myelolipomas, liposarcomas -Myxosarcomas -Unedintified pleomorphic sarcomas -Solid hemangiosarcomas Consistency and cut surface appearance varies -Spindle cell tumor (leiomyosarcoma and fibrosarcomas) will be white and firm -Liposarcomas, myelolipomas are soft and bulging -Myxomatous neoplasms are gelatinous

Answer 97

-Malignant neoplasm of endothelial cells -Common primary tumor of spleen especially is dogs Gross -Single multifocal, coalescing, dark red-purple masses and can not be easily differentiated from a hematoma -Cut surface: bloody with varying amounts of soft red neoplastic tissue; in more solid areas neoplasm can be slightly more firm and white tan. **Metastatic spread occurs early in disease process: in dogs also right atrium of heart, retroperitoneal fat, and skin (dermal and or subcutaneous).** -MUltiorgan hemangiosarcomas: described in horses, cats, and cattle **Often metastasized at time of initial diagnosis, so may be difficult (and futile) to determine the primary site**

Answer 98

-Due to metastasis, often form nodules in spleen, not a uniform splenomegaly -Include: sarcomas, carcinomas, or malignant round cell tumors -Metastatic sarcomas: fibrosarcomas, leiomyosarcomas, chondrosarcomas, osteosarcomas -Mammary, prostatic, pulmonary, anal sac gland, neuroendocrine carcinomas metastasize.

Answer 99

Amyloid -May occur with primary (AL) or secondary (AA) amyloidosis. -Spleen is firm, rubbery to waxy and light brown to orange -Plasma cells tumors within the spleen may be associated with amyloid (AL) deposits Lysosomal storage disease -Group of inherited defects in metabolism characterized by accumulation of storage material within the cell (lysosomes) -Genetic: lack of enzyme, produce inactive enzyme, last of activator proteins, or defect in posttranslational processing -Acquired: exogenous toxins, plants that inhibit a particular lysosomal enzyme **Swainsonine toxicity in Astragalus Oxytropisplants** -Animals < 1yr old Major materials -Mucopolysaccharides -Sphingolipids -Glycolipids -Glycoproteins, glycogen -Oligosaccharides **Macrophages are commonly affected by storage disease**

Answer 100

Gamma-Gandy bodies: siderocalcific plaques 1. Hemosiderosis = plaques 2. Siderofibrotic Plaques: Most extensive along the splenic margins. Extremely common in aged dogs and may represent sequelae to previous hemorrhages from trauma to spleen

Answer 101

1. Rupture 2. Chronic splenic infarcts 3. Parasitic Cysts

Answer 102

Mucosal Associated Lymphoid Tissue -Site of mucosal immunity -Diffused lymphoid tissues and aggregated lymphoid nodules, subcategorized 1. BALT bronchus associated lymphoid tissue 2. NALT Nasal-larynx and auditory tube .. 3. LALT Larynx ... 4. ATALT auditory tube ... 5. GALT Gut associated lymphoid tissue. Peyer's patches and diffuse lymphoid tissue in the gut wall 6. CALT Conjuctiva ... 7. Other lymphoid nodules (genitourinary tract) Portal of entry for pathogens Hematogenous: most common migrating macrophages, DCs, M cells. -BVDV -Bovine Coronavirus -Rinderpest virus -MCF -FPV -Canine parvo virus =Lymphocyte depletion within MALT -Escherichia coli -Yersinia pestis -Mycobacterium avian sap. paratuberculosis (MAP) -L. monocytogenes -Salmonella spp. -Shingella flexneriulate **Site of replication for viruses (BVDV)**

Answer 103

-Even though some species don't have lymph node they still have lymphoid follicles - nodules Horses SCID -Arabian foals, autosomal recessive primary immunodeficiency disorder. Lack of T & B cells. Genetic mutation in gene encoding DNA-PKcs. Hypoplasia -Normal at birth > diarrhea, pneumonia by 10 days -Common secondary infections: Adenovirus, Cryptosporidium, Pneumocystis cabrini -Die before 5 months of age -Gross: hypoplastic LN and thymus (often grossly undetectable), spleen Strangles -Streptococcus equi ssp. equi -Inhaled/ingested > invade tonsils, enter regional LN > Larged abscesses -Retropharyngeal abscesses lead to compression of pharynx - respiratory stridor, dysphagia -Abscesses rupture to skin surface or spread medially into guttural pouches, from chondroids -Ruptured abscesses spread via blood/lymph to other organs **Bastard strangles** Pupura Hemorrhagica -Type III hypersensitivity reaction -Necrotizing vasculitis in some horses with repeated natural exposure to S. equi ssp. equi or after vaccination in horses that have had strangles. Rhodococcus Equi -Chronic pyogranulomatous bronchopneumonia, lymphadenitis -50% of foals also develop: pyogranulomatous ulcerative enterotyphlocolitis

Answer 104

Johne’s Disease -Domestic, wild ruminants (rarely pigs, horses) -Mycobacterium paratuberculosis Characteristic lesions: Granulomatous enteritis to ieum, cecum, proximal colon; lymphangitis/Lymphadenitis or regional LN Pathogenesis: bacteria are ingested, engulfed by monocyte cells overlying Peyer’s patches - transported to macrophages in lamina propria and submucosa Anthrax -Bacillus anthracis (Gram + bacillus) present in the soil in spores -Cattle, sheep, goats: **Fulminant septicemia** -Spleen markedly enlarged and congested Bovine Viral Diarrhea -BVDV: pestivirus -Preferentially infected macrophages, dendritic cells, lymphocytes -Cattle, sheep, goats -Lymphoid depletion in mesenteric lymph nodes and Peyer’s patches (lymphocytois and depletion) -Histo: marked lymphocytosis, necrosis of germinal centers in Peyers’s patches, thymic atrophy. Splenic Abscesses -Result of bacteremia or direct penetration by a foreign body from reticulum Caseous Lymphadenitis - C. psudotuberculosis (Gram + intracellular bacterium) -Shearing, tagging, tail docking, castration -Sheep, goats -External abscesses most often detected in mandibular and paranoid LN

Answer 105

Porcine Reproductive and Respiratory Syndrome (PRRS) -Arterivirus -Most connected: Streptococcus suis, Salmonella choleraesuis, Bordetella bronchiseptica, Mycoplasma hyopneumoniae. Two overlapping clinical syndromes 1. Reproductive failure 2. Respiratory disease -Bodily fluids - colonizes tonsils or upper respiratory tract (predilection for lymphoid tissue), spleen, thymus, LNs, Peyer's patches - Replication in macrophages of lymphoid tissues, lungs - resulting in reduction in phagocytic and functional capacity of macs - secondary infections Major lesions: interstitial pneumonia, generalized lymphadenopathy (tracheobronchial, mediastinal most commonly affected). Pale tan, occasionally cystic, and firm; some strains of virus also cause nodal hemorrhage. Coinfections complicate the gross and histopathologic changes

Answer 106

Porcine Jowl Abscess -Streptococcus porcinus -Colonizes oral cavity - tonsils - regional LN -Mandibular LN most affected. -Now rare because of improvements in husbandry, feeder design, and hygiene. "Teeth clipping in baby pigs"

Answer 107

Disorder of dogs Severe Combine Immunodeficiency Disease -An x-linked form of SCID in Basset hounds **Reduced numbers of T lymphocytes (which are nonfunctional** -Normal numbers of circulating B lymphocytes that are unable to class switch to IgG or IgA and reduced numbers of T lymphocytes (which are non-functional). -Susceptible to bacterial/viral infections -Rarely survive past 3 to 4 months of age -Lesions: small thymus, tonsils, LN, Peyer's patches (often grossly unidentifiable). -Similar disease in Cardigan Welsh corgi puppies (but autosomal mode of inheritance)

Answer 108

-Protozoa of genus Leishmania -Dogs, other animals -Sand fly 1. cutaneous 2. Visceral: emaciated, general enlargement of abdominal lymph nodes and hepatosplenomegaly -Looks similar to trypanosome -Macrophages target. **Flagellated in blood**

Answer 109

Canine Distemper Virus - Macrophages in tonsil, respiratory tract, disseminates to spleen, LN, BM, MALT, Kuffner cells - necrosis of lymphocytes (especially CD4T) and depression of lymphopoiesis in BM - severe immunosuppression -Secondary infections: Bordetella bronchiseptica, Toxoplasma gondii, Nocardia, Salmonella spp., and generalized demodicosis Canine Parvovirus type 2 (CPV-2) -Highly contagious dogs -Feco-oral or oronasal - tropism for rapidly dividing cells - replication begins in lymphoid tissues of oropharynx, thymus, mesenteric LN - disseminated to SI crypt epithelium -Lymphocytolysis and bone marrow depletion of lymphocyte precursors - immunosuppression -Lymphocytolysis and bone marrow depletions of lymphocyte precursors - immunosuppression -Marked lymphoid atrophy of thymus and follicles of spleen, LN, MALT - (especially Peyer's patches)

Answer 110

Feline Panleukopenia -Parvovirus -Target: rapidly dividing cells in S phase of division: lymphoid tissue, BM, intestinal mucosa. -Feco-oral (nasal) route -Replicates in macrophages in oropharynx