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ACVP Phase II Exam - Anatomic Pathology > Nervous System > Flashcards

Nervous System Flashcards

1
Q

Alzheimer Type II cells are found in hepatic encephalopathy and represent a reactive type of what kind of glial cell? Where are they normally located and what can be helpful in identifying them?

A

astrocyte; gray matter; they usually occur in pairs (cuddling cells) or clusters

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2
Q

Rosenthal fibers represent what?

A

GFAP aggregates of astrocyte processes and cell bodies. They are complexed with ubiquitin and heat shock proteins. Found in Alexander’s disease AKA axonal dystrophy, a genetic disease of astrocytes that occurs rarely in humans, dogs and sheep

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3
Q

Which mouse phenotype is considered the model for neural tube defects?

A

curly tail mouse

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4
Q

Cerebral aplasia results from:

A

failure of closure of the rostral portion of the neural tube, which allows the skin to not form and exposes rudimentary neural brain cells to the amniotic fluid leading to degeneration.

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5
Q

Meningocele is reported in Burmese cats as a result of treatment during pregnancy with:

A

griseofulvin, hydroxyurea, diphenylhydantoin

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6
Q

Feline panleukopenia virus, BVDV and border disease virus all cause cerebellar hypoplasia through the selective necrosis of what layer of the cerebellum?

A

external granular cell layer

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7
Q

Perosomus elumbus is:

A

agenesis of the lumbar, sacral and coccygeal spinal cord segments; occurs in calves and lambs

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8
Q

Myelodysplasia is best detected histologically by the presence of:

A

aberrant central canals (up to 6)

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9
Q

The classic teratogenic lesion of Akabane virus infection in calves is:

A

arthrogryposis and hydranencephaly

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10
Q

Examples of teratogenic Orthobunyaviruses are? Which one is endemic to North America?

A

Akabane virus, Schmallenberg virus, Cache Valley virus. Cache Valley virus is endemic to NA.

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11
Q

The teratogenic effects of BVD occur during what gestational age?

A

100-170 days

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12
Q

What is the most common teratogenic defect of BVD?

A

Cerebellar hypoplasia

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13
Q

Infection with BVD after 170 days of gestation is most likely to result in what?

A

no teratogenic/abortive effects, potential for growth retardation and atrophy of thymic and lymphoid tissues

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14
Q

Fetal death and abortion are most likely to occur in cases of Border Disease Virus infection in sheep during what gestational age?

A

Days 16-80

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15
Q

The fetal histologic lesion of Border Disease virus infection in sheep infected after 90 days of gestation is?

A

nodular periarteritis of small to medium arterioles, mostly within the meninges and CNS

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16
Q

An early infection fetal histologic lesion in Border Disease Virus is?

A

hypomyelinogenesis

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17
Q

Gross features of Border Disease virus infected lambs include:

A

long hairy birth coats and gross tremors (hairy shaker)

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18
Q

Cavitating cerebral defects and cerebellar dysplasia in Border Disease Virus infection arise from:

A. infection of oligodendroglia

B. infection of astroglia

C. vasculitis

D. infection of glial progenitor cells

A

C. BDV does not infect CNS cells themselves, and the cavitating lesions are most likely secondary to vasculitis

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19
Q

Growth arrest lines are a feature of in utero infection with what family of viruses?

A

pestiviruses, specifically BVD and BVDV

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20
Q

Mucosal disease in BVDV infection in cattle is the result of what two possible situations?

A

Infection of a previously infected calf by a different strain of BVDV (superinfection) or homologous virus mutation in animals that are persistently infected

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21
Q

Teratogenic effects of Border Disease Virus in goat are (more common/less common) than in sheep.

A

They don’t occur at all. Just fetal death/mummies/abortion.

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22
Q

Congenital tremors in piglets can be the result of in utero infection with what organism?

A

Classical Swine Fever

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23
Q

Inclusion bodies of Feline Panleukopenia virus are found in what cell type in the cerebellum?

A

external granular cell layer

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24
Q

GM1 Gangliosidosis is a deficiency of what enzyme? What category of lyosomal storage disease is is?

A

beta-galactosidase; sphingolipidoses

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25
Q

GM2 gangliosidosis accumulates because of a deficiency of what enzyme?

A

hexosaminidase or of activatory protein

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26
Q

Neurons with foamy, faintly eosinophilic cytoplasm is typical of what kind of lyosomsal storage disease?

A

sphingolipidosis (gangliosidoses)

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27
Q

This lysosomal storage disorder, known in people as Tay-Sachs disease, is most likely what based on the EM image?

A

GM2 gangliosidosis

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28
Q

The dual deficiency of beta1-galactosidase and alpha-neuraminidase found in this form of G1 gangliosidosis is present in what species and breed?

A

Suffolk sheep

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29
Q

A mutation in what gene in cats is responsible for sphingomyelinosis

A

NPC2 - this disease has the human analog of Niemann-Pick Disease

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30
Q

Defective degradation of the carbohydrate component of N-linked glycoproteins describes what group of lysosomal storage diseases? What three forms occur in these diseases? How are these diseases detected clinically?

A

Glycoproteinoses: Alpha-mannosidosis, Beta-mannosidosis, Alpha-L-fucosidosis. Detected in the urine.

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31
Q

Alpha-mannosidosis is best characterized in what breeds of what species?

A

Angus, Murray Grey and Galloway breeds of cattle; also cats

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32
Q

Beta-mannosidosis is best characterized in what species and breed?

A

Nubian goats; also Salers cattle

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33
Q

Alpha-L-fucosidosis is best characterized in what breed and species?

A

dog; English Springer Spaniel

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34
Q

Defective catabolism of glycosaminoglycans best describes what lysosomal storage disorder?

A. Alpha-mannosidosis

B. Sphingomyelonosis

C. GM1-gangliosidosis

D. Mucopolysaccharidosis

A

GAG’s are mucopolysaccharides!!

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35
Q

Mucopolysaccharidosis Type I is a defiency of what enzyme?

A

alpha-L-iduronidase

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36
Q

The presence of zebra bodies on EM is characteristic of what group of lysosomal storage disorders?

A

mucopolysaccharidoses BUT THE MATERIAL IS SPHINGOLIPIDS AND SECONDARY TO THE MUCOPOLYSACCHARIDE DISEASE

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37
Q

Type II glyogen storage disease, otherwise known as Pompe disease, is a deficiency of what enzyme

A

alpha-1,4-glucosidase.

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38
Q

Curvilinear bodies within Pukinje cells on EM is characteristic of what lysosomal storage disease?

A

Neuronal ceroid-lipofuscinosis

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39
Q

Vitamin A deficiency causes increased intracranial pressure by what mechanism?

A

Increased production of CSF by choroid plexus and decreased absorption by arachnoid villi; reversible

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40
Q

Feline ischemic encephalopathy is secondary to migration of what organism?

A

Cuterebra

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41
Q

What is the neurologic histologic lesion associated with hepatosis dietetica in swine?

A

hyaline necrosis of meningeal vessels

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42
Q

Cerebrospinal angiopathy in pigs is secondary to what disease?

A

Edema disease causing alimentary enterotoxemia from E. coli

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43
Q

Steroid-responsive meningo-arteritis in the dog is the new name for what disease? What is the major target organ and lesion?

A

Beagle pain syndrome; spinal artery periarteritis

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44
Q

Polioencephalomalacia can be caused by all of the following except:

A. lead poisoning in cattle

B. salt poisoning in swine

C. cyanide toxicity in any species

D. excess production of thiaminase in the rumen

E. yellow star thistle (Centaurea solsitialis) poisoning in horses

A

E. yellow star thistle poisponing in horses causes nigropallidal encephalomalacia

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45
Q

The laminar cortical necrosis in PEM is related to the field of supply of what artery?

A

middle cerebral artery

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46
Q

Sulfur causes PEM by what mechanism?

A

Cleaving thiamine into its constituents, rending it inactive

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47
Q

Chastek paralysis is due to:

A. excess thiamin in the diet

B. decreased dietary thiamine

C. excess sulfur in the diet

D. thiamine converting enzyme present in fish

A

D. Chastek paralysis is found in carnivores like foxes and mink, and is due to a thiamine-splitting enzyme present in fish

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48
Q

The lesions of Chastek paralysis mimic that found in PEM, except that the most profound lesions are located in these two places in the brain:

A

periventricular areas and caudal colliculi

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49
Q

Lead chiefly exerts clinical signs of toxicity in this tissue:

A. kidney

B. liver

C. GIT

D. nervous tissue

A

D. brain. Lead chiefly causes neurologic signs in all species, but does not accumulate in the nervous tissue. The kidney does develop acid-fast lead inclusions in the nucleus of tubular epithelial cells, but no evidence of renal toxicity occurs.

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50
Q

Cerebellar cortical degeneration affecting the Purkinje cells with retrograde degeneration of granular cells is present in what species?

A

dogs

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51
Q

Compressive optic neuropathy of piglets and calves is related to deficiency of what vitamin? What is the pathogenesis? What is the histo lesion?

A

Vitamin A deficiency; stenosis of the optic foramina; Wallerian degeneration of the optic nerves and tracts

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52
Q

The histologic lesion of Equine degenerative myelopathy is:

A

ongoing Wallerian degeneration and post-Wallerian astrogliosis in all funiculi throughout the spinal cord, most severe in the thoracic cord

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53
Q

Equine degenerative myeloencephalopathy involves:

A. ascending tracts only

B. descending tracts only

C. ascending and descending tracts

A

C. ascending (dorsolateral and spinocerebellar) and descending (ventromedial and motor) tracts

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54
Q

Where is Clarke’s column located in the spinal cord?

A

dorsolateral and immediately adjacent to the central canal of the cord between the first thoracic and mid-lumbar segments. It is the nucleus of the dorsal spinocerebellar tract, and where lesions of EDM are most pronounced.

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55
Q

What is the common characteristic of axonal dystrophies in various species?

A

massive numbers of axonal spheroids

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56
Q

Organophosphate toxicity is based on their ability to:

A

inactivate esterases, including acetylcholinesterase (not as important for vet path) and neuronal esterases that are irreversible.

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57
Q

The histologic lesions associated with organophosphate toxicity include

A

degenerative changes in the distal axons, loss of myelin, axon swelling and lysis, microcavitation and neuronal chromatolysis in the brain and spinal cord

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58
Q

What is a common clinical sign associated with organophosphate toxicity and why does it occur?

A

aphonia; results from involvement of the recurrent laryngeal nerve as it undergoes axonal degeneration

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59
Q

Coyotillo poisoning occurs as a result of the toxin __________ and mosly affects this species ________ leading to a central/peripheral axonopathy with secondary CNS changes.

A

tullidinol; goats; peripheral

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60
Q

The gross lesions of arsenic poisoning include:

A

NONE!!

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61
Q

Arsenic causes toxicity through its inactivation of:

A. thiamin

B. sulfhydryl

C. thiocyanate

D. glycine

A

B. sulfhydryl groups are inactivated by arsenic causing general depressions of metabolic activity

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62
Q
A
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63
Q

The loss of white matter in this image is most likely the result of:

A

copper deficiency. This is swayback, a congenital form.

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64
Q

The spinal cord lesions in delayed swayback include Wallerian degeneration of:

A. dorsolateral tracts

B. ventromedial tracts

C. both dorsolateral and ventromedial tracts

A

C. This is a distal axonopathy and affects both tracts.

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65
Q

Equine grass sickness is otherwise known as :

A

dysautonomia

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66
Q

A histologic lesion in the ganglia associated with equine grass sickness would be:

A

central chromatolysis of the neurons

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67
Q

Clinical signs of dysautonomia include:

A. diarrhea

B. drooling

C. dilated pupils

D. constricted pupils

A

C. dilated pupils are characteristic of autonomic dysfunction along with megaesophagus, dry mucous membranes, constipation, vomiting and prolapsed TEL’s

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68
Q

Sampling for dysautonomia should be done from which tissue?

A. dorsal root ganglia

B. mesenteric ganglia

C. superficial cervical ganglia

A

B. mesenteric or pelvic ganglia are the best sampling choices. A is for sensory or afferent neurons. C is an autonomic ganglia but not the best samping site for lesions.

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69
Q

Equine laryngeal hemiplegia result from denervation atropy of what?

A

the intrinsic muscles of the left side of the larynx from idiopathic degeneration of the left recurrent laryngeal nerve leading to inability to retract the arytenoid cartilage and vocal fold, partial obstruction, and roaring (inspiratory stridor)

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70
Q

What are two differentials for equine laryngeal hemiplagia as a result of left recurrent laryngeal nerve damage?

A

lead and OP poisoning can cause widespread axonopathy and can lead to laryngeal paralysis

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71
Q

The presentation of this horse is most consistent with what condition?

A. Bog spavin

B. Stringhalt

C. Locked stifle

D. Tenosynovitis of the deep digital flexor tendon

A

B. This is stringhalt characterized as extreme exaggerated flexion of the hindlimbs. It is most likely a distal axonopathy but a pathogenesis is unclear. Bog spavin is edema, locked stifle is extreme extension, and tenosynovitis would most likely not cause a horse to want to flex like this.

72
Q

Sweeney is characterized by damage to the :

A. left recurrent laryngeal nerve

B. vagus nerve

C. radial nerve

D. suprascapular nerve

A

D. suprascapular nerve as a result of entrapment of the nreve by a tendinous band leading to degeneration and denervation atrophy of the spinatus muscle

73
Q

Globoid cell leukodystrophy occurs as a result of GALC gene mutation in what breeds of dogs?

A

Cairn and West Highland White Terriers

74
Q

Globoid cell leukodystrophy occurs as a result of?

A

deficiency of lysosomal galactocerebrosidase (so it’s a sphingolipidosis lysosomal strorage disease). Causes inability of oligodendrocytes and Schwann cells to make myelin.

75
Q

The globoid cells in “globoid cell leukodystrophy” are actually?

A

macrophages filled with PAS positive galactocerebroside that form large cuffs around blood vessels in the white matter, meninges, peripheral nerve endoneurium.

76
Q

In addition to the globoid cells in globoid cell leukodystrophy, what other histologic lesion occurs?

A

loss of myelination in both CNS and PNS, axonal loss, astrogliosis

77
Q

What species normally demonstrate lissencephaly?

A. Rodents and rabbits

B. Persian cats

C. Merino sheep

D. Kangaroos

A

A. rodents and rabbits normally demonstrate lissencephaly along with birds, reptiles, amphibians and fish. Only mammals have gyri and sulci.

78
Q

Hepatic encephalopathy causes what lesions in the brain?

A

spongy vaculation of the myelin, Alzheimer Type II astrocytes

79
Q

Hepatic encephalopathy is caused by buildup of what components?

A. ammonia only

B. ammonia, cytokines, and LPS

C. ammonia, endogenous benzodiazepines, cytokines and LPS

A

C. ammonia is not the only cause of hepatic encephalopathy, and the lesions are caused by buildup of all of these plus perturbed monoamine neurotransmission, imbalance between excitatory and inhibitory amino acid neurotransmission and systemic infection.

80
Q

Maple syrup urine diseae of Hereford and Shorthorn cattle is caused by a defiency of what? What does it lead to?

A

BKCD complex (mitochondrial branched-chain alpha-ketoacid dehydrogenase). Leads to buildup of branched-chain amino acids which make the urine smell like maple syrup. Maple trees have branches!!

81
Q

What is the histologic lesion of maple syrup urine disease (branched chain alpha-ketoacid decarboxylase defiency)?

A

severe spongy vacuolation of the myelin

82
Q

The protein-only hypothesis for prion disease states all of the following except:

A. PrPSC is the etiologic agent of all TSEs and other prion diseases

B. the transformation of alpha-helical PrP to its misfolded beta-pleated sheet isoform, PrPSC requires either a genetic predisposition or help of a protein cofactor X to serve as a molecular chaperone

C. PrPSC triggers a robust auto-immune response which causes clinical signs of disease

D. PrPSC triggers the PrP gene to produce more PrPSC (self-replicating protein)

E. PrPSC can be infectious itself and be transmitted to other hosts

A

C. PrPSC does not cause an immune response at all. Also, the auto-immune theory of prion diseases caused by an inappropriate response to certain bacteria has been widely refuted for this reason.

The other four factors are all included in the protein-only hypothesis.

83
Q

Varian Creutzfeld-Jacob disease in humans is associated with what?

A. Consumption of scrapie-contaminated lamb

B. Consumption of CWD-contaminated venison

C. Ritualistic cannibalism

D. Consumption of BSE-contaminated beef

A

D. BSE causes variant CJD in humans. C is the cause of the disease known as kuru in humans.

84
Q

The histologic features of scrapie include all of the following except:

A. spongy vacuolation of the neuropil at the level of the obex within the medulla oblongata

B. spongy vacuolation of the neurons at the level of the obex within the medulla oblongata

C. Non-suppurative meningoencephalitis

D. Astroytosis

A

C. inflammation is not a feature of any of the TSEs. There is spongy vacuolation of both the neuropil and neurons, both best observed at the obex, and astrocytosis is variably present.

85
Q

True-False. Amyloid plaques are a common feature in TSEs.

A

False. They only occur commonly in human TSEs, and very rarely in animal TSEs.

86
Q

EM features of scrapie have this characteristic finding:

A

Scrapie-associated fibrils (SAF), which have PrPSC as their major component.

87
Q

Scrapie is usually passed to sheep from what process? BSE is usually passed by what process?

A

Ewe to lamb; Food-borne (no vertical or lateral transmission)

88
Q

The blood-brain barrier is made up of all the following except;

A. endothelial cells lining the blood capillaries

B. pericytes embedded in the capillary basement membranes

C. oligodendrocyte processes

D. foot processes of astrocytes

A

C. oligodendrocytes are responsible for myelination of axons and are not part of the BBB

89
Q

Listeria monocytogenes breaches the blood brain barrier by inhibition of what protein?

A

the efflux protein P-glycoprotein

90
Q

Innate immune components of the brain include all of the following except:

A. perivascular dendritic cells

B. microglia

C. astrocytes

D. oligodendrocytes

A

D. oligodendrocytes have no role in innate immunity of the brain. The other three have PRR’s to detect pathogens.

91
Q

Neonatal bacterial suppurative meningitis in calves and pigs is usually caused by what two organisms?

A

Streptococcus and E. coli

92
Q

An important virulence factor of Listeria monocytogenes is _____ which allows for the internalization of the bacteria after complexing with E-cadherin to breach adherens junctions in the blood-brain barrier, placental barriers and intestinal lining.

A

internalin

93
Q

This virulence factor of Listeria monocytogenes allows for the lysis of the phagosome and escape into the cytoplasm:

A. internalin

B. lysin

C. cholesterol-binding hemolysin

A

C. cholesterol-binding hemolysin is what allows for the bacteria to escape to the cytoplasm from the phagosome. Lysins are produced by bacteriophages. A. is what allows Listeria to breach the adherens junctions in the BBB.

94
Q

The three clinical presentation of Listeria are:

A. in utero infection with abortion, neonatal septicemia with miliary visceral absesses, encephalitis

B. neonatal septicemia with miliary visceral abscesses, mastitis and encephalitis

C. pneumonia, mastitis and encephalitis

D. in utero infection, mastitis and encephalitis

A

A. Listeria causes abortion, septicemia with abscesses in the viscera and encephalitis. Mastitis has been reported from Listeria, but it is not as common as the other 3 syndromes and is the result of a subclinical infection (therefore a public health issue) rather than a clinical sydrome. Neonatal infection is usually the result of septicemia and can result in abscessation.

95
Q

Listeria invades the oral mucosa and travels to the brain via what nerves?

A

trigeminal nerves (CN 5)

96
Q

The characteristic histologic lesion of Listeria is?

A

microabscesses, mostly in the pons and medulla

97
Q

Listeria is Gram (+/-)?

A

Gram positive

98
Q

Histophilus is Gram (+/-)?

A

Gram -

99
Q

Lipo-oligosaccharide (LOS), immunoglobulin Fc binding protein, inhibition of oxygen radicals and intracellular survival are all virulence factors of:

A. Listeria monocytogenes

B. Histophilus somni

C. Mycobacterium tuberculosis

D. Chlamydia pecorum

A

B. Histophilus somni is the only one of these that is Gram negative, hence the variant of LPS which is LOS.

100
Q

What is the function of LOS in Histophilus somni infection?

A

Triggering caspase-3 mediated apoptosis of endothelial cells leading to vasculitis.

101
Q

The characteristic lesion of Histophilus is?

A

vasculitis with thrombosis d/t endothelial damage in mutiple organs, but especially the brain. Hemorrhage and necrosis throughout the brain.

102
Q

What species of ruminant is resistent to Histophilus infection?

A

goats

103
Q

Which of the following are common associated lesions of Histophilus infection?

A. Retinal hemorrhage

B. Laryngeal ulceration

C. Pneumonia

D. Atlanto-occipital arthritis

E. Erosive polyarthritis

A

E. While arthritis is not uncommon, especially in the atlanto-occipital joint, it is not erosive in nature. It tends to be fibrinosuppurative and hemorrhagic. The other options are all commonly found in H. somni cases.

104
Q

Which rabies virus glycoprotein is responsible for neurotropism?

A

RVG

105
Q

The biotype of rabies virus that is neurotropic, localizes to the salivary glands and produces Negri bodies is which type?

A. Fixed type

B. Street type

A

Street type (the feral type). Fixed type is used as the vaccine strain.

106
Q

The histologic lesions of rabies include all of the following except:

A. non-suppurative encephalomyelitis

B. ganglioneuritis

C. parotid adenitis

D. neuronal necrosis in the medulla

E. intracytoplasmic inclusion bodies in the hippocampus or Purkinje cells

A

D. the medulla is relatively spared in rabies encephalitis

107
Q

Negri bodies are:

A. intracytoplasmic, found in degenerate neurons and ubiquitous in rabies cases

B. intracytoplasmic, found in intact neurons, and found inconsistently in rabies cases

C. intranuclear, found in degenerate neurons, and found inconsistently in rabies cases

D. intranuclear, found in intact neurons, and are ubiquitous in rabies cases

A

B. Negri bodies are intracytoplasmic, found in intact neurons and are found inconsistently in rabies cases.

108
Q

This histologic finding should put rabies at the top of the list of differentials:

A. intracytoplasmic eosinophilic inclusions in neurons

B. perivascular cuffs

C. nonsuppurative encephalomyelitis

D. ganglioneuritis of the paravertebral ganglia

A

D. ganglioneuritis is found in almost all cases of Rabies, but can be found in Teschen disease in pigs

109
Q

The definitive test for rabies is:

A

DFA (direct fluorescent antibody) on fresh or fixed tissue or virus isolation is best, followed by IHC, then ISH, EM and PCR

110
Q

Latent pseudorabiesvirus is found in what three locations reliably?

A

trigeminal ganglia, olfactory bulb and tonsil

111
Q

Pseudorabies is spread between pigs most reliably by:

A

nasal secretions and abraded skin

112
Q

The herpesvirus most known for its lack of host specificity is:

A. Bovine Herpesvirus-1

B. Gallid Herpesvirus-2

C. Equine Herpesvirus-5

D. Suid Herpesvirus-1

A

D. Suidherpes virus-1 (or pseudorabies) infects cattle, sheep, horses, dogs, cats, mice, etc. Humans technically but disease does not progress.

113
Q

Pseudorabies is associated with what clinical sign?

A

intense cutaneous pruritis

114
Q

Tissue from a pig. What is the most likely diagnosis?

A. TGE

B. PCV-2

C. PRV

D. Swine influenza

A

C. Pseudorabies virus causes amphophilic intranuclear inclusion bodies in the neurons. PCV-2 inclusions are INTRACYTOPLASMIC, large, basophilic and smudgy (botryoid) and are found in ENDOTHELIAL CELLS, EPITHELIAL CELLS AND HEMATOPOIETIC CELLS, BUT NOT NEURONS. TGE is caused by a mutated coronavirus, so no inclusions, but it can rarely cause neuronal degeneration. Swine flu does not cause inclusions, but can cause neuronal necrosis.

115
Q

PRV has tropism for what tissues?

A

Epithelium and neurons

116
Q

Porcine hemagglutinating encephalomyelitis virus, porcine epidemic diarrhea virus and TGE are all viruses in what family?

A

Coronaviridae family

117
Q

Porcine hemagglutinating encephalomyelitis virus causes what two syndromes in piglets?

A

neurologic and “vomiting and wasting”. Disease is found almost entirely in piglets. High mortality.

118
Q

Differential diagnoses for high mortality in piglets with neurologic signs include all of the following except:

A. PRV

B. Strep suis septicemia

C. Teschen disease

D. Hemagglutinating encephalomyelitis virus

E. Edema disease

A

E. Edema disease is caused by E. coli, specifically a Shiga-like toxin type IIe [Stx2e]-producing E. coli (EDEC). It is a disease of otherwise healthy weanling/grower pigs, not piglets

119
Q

Nonsuppurative polioencephalomyelitis extending from the olfactory bulb to the lumbar spinal cord is suggestive of infection with what virus?

A

Teschovirus

120
Q

Louping ill in sheep is transmitted by what means?

A

Ixodes ticks (Ixodes ricinus, the castor bean tick). Found in Great Britain.

121
Q

Louping ill in sheep has this histologic lesion:

A

acute polioencephalomyelitis

122
Q

The main amplifying hosts of West Nile Virus are ________ which produce a profound viremia.

A. horses

B. humans

C. wild birds

A

C. wild birds, especially corvids, are the main host and produce viremia. Horses are the most susceptible to disease and only harbor virus in the CNS

123
Q

What is the vector of WNV?

A. Culidoides spp.

B. Culex spp.

A

Culex sp. mosquitoes. Culicoides are MIDGES!!!

124
Q

Hepatitis, myocarditis and non-suppurative encephalitis are all features of infection in (equine/avian) Wests Nile Virus infection.

A

avian; horses only get encephalitis

125
Q

The best diagnostic test for WNV in equine tissues is:

A. Acute and convalescent titers on serum

B. IHC on brain tisssue

C. PCR of whole blood

D. PCR on brain tissue

A

D. PCR of brain tissue is the best diagnostic test for horses. Virus is not found in the blood, rendering PCR on it useless. Serology only detects exposure, and horses can be infected and recover from WNV. IHC can be used but Ag in the brain is sparse and this can make interpretation difficult.

126
Q

Japanese encephalitis virus is maintained in _______ hosts and transmitted by ________ before infecting _______as its primary amplifier.

A. Passerines; Culicoides; horses

B. Ardeid water birds; Culex and Aedes mosquitoes; horses

C. Ardeid water birds; Culicoides; pigs

D. Ardeid water birds; Culex and Aedes mosquitoes; pigs

A

D. The virus is hosted in herons and egrets (Ardeid water birds) and transmitted via Culex, Aedes and Armigeres mosquitoes before infecting pigs as its primary amplifier. PIGS ARE THE AMPLIFIER BUT DON’T GET CLINICAL DISEASE EXCEPT FOR ABORTION, WHERE PIGLETS CAN HAVE NEURO HISTO LESIONS. HORSES ARE SUSCEPTIBLE AND GET CLINICAL ENCEPHALITIS, BUT THERE IS NO VIREMIA!!!

127
Q

The reservoir host for Eastern Equine Encephalitis is:

A. horses

B. rodents

C. mosquitoes

D. birds

A

D. birds are the reservoir host for both Eastern and Western Equine Encephalitis. Rodents are the reservoir for Venezuelan Equine Encephalitis. Mosquitoes are the vector, and horses and humans are the dead end hosts since the viral titer in the blood is too low to continue the cycle of infection from a mosquito bite (except in VEE cases, where it can get high enough).

128
Q

EEE, WEE and VEE all have histologic lesions consisting of:

A

neuronal necrosis and neuronophagia, vasculitis, suppurative and lymphocytic encephalomyeltis. The cerebral cortex is the most affected!!!!!

129
Q

These two species are most susceptible to Borna disease virus:

A

horses and sheep

130
Q

Histologic lesions in the brain in Borna disease virus are related to:

A. direct infection of neurons

B. vasculitis

C. immune-mediated effects

A

C. immune mediated effects are driven by first Th1 then Th2 lymphocytes (acute and chronic stages respectively). While the virus does infect neurons, it has no cytopathic effect from infection. Perivascular cuffs are prominent in Borna disease virus, but vasculitis does not occur.

131
Q

What are the four pathologic syndromes of Small Ruminant Lentivirus infection?

A

mastitis, arthritis, interstitial pneumonia (maedi in sheep, AKA ovine progressive pneumonia), and encephalomyelitis (visna of sheep).

132
Q

At what age do clinical signs of visna appear?

A

> 2 years of age

133
Q

Death from visna is secondary to:

A

starvation due to paralysis

134
Q

Visna is characterized histologically by:

A

patchy demyelinating encephalitis of the white matter

135
Q

Caprine arteritis-encephalitis causes neuro signs in goat kids of what age?

A

2-4 months of age

136
Q

Porcine rubulavirus (also known as blue eye disease) causes what in sows?

A. abortion, corneal opacity and nonsuppurative encephalomyelitis

B. corneal opacity, arthritis and nonsuppurative encephalomyelitis

C. pneumonia, corneal opacity and suppurative encephalomyelitis

D. lymphoid depletion, corneal opacity and nonsuppurative encephalomyelitis

A

A. This disease causes fetal death, mummies and stillbirths as well as corneal opacity (hence the blue eye designation) and nonsuppurative encephalomyelitis.

137
Q

Nipah and Hendra viruses are both in the ___________ family and cause fatal _______ and ____________ in humans and animals.

A

Paramyxoviridae family; encephalitis and pneumonia

138
Q

The natural reservoir of Nipah virus is the :

A. mouse

B. fruit bat

C. pig

D. horse

A

B. fruit bat (flying fox). Pigs are the animals most susceptible to infection, although horses can also be infected. Mice carry Hantavirus.

139
Q

The classic histologic lesion of Nipah virus is:

A

necrotizing vasculitis affecting arterioles, venules and capillaries in the brain, lung, glomeruli and lymphoid organs. The virus infects endothelial cells and breaches the BBB this way.

140
Q

Bovine herpesvirus-5 is the cause of what disease:

A. Malignant catarrhal fever

B. Pseudo lumpy skin disease

C. Aujesky’s disease

D. Infectious bovine rhinotracheitis

E. Bovine necrotizing meningoencephalitis

A

E. Bovine necrotizing encephalitis is caused by BoHV-5. MCF is caused by alcephaline herpes virus 1 or ovine herpes virus 2. Pseudo lympy skin disease or bovine mammilitis is caused by BoHV-2. Aukesky’s disease is pseudorabies of swine (Suid herpes virus 1). IBR is caused by BoHV-1.

141
Q

Symmetric malacia, hemorrhage and necrosis in the gray matter of the rostral cerebrum in a cow coupled with histologic lesions of a necrotizing nonsuppurative meningomyelitis and intranuclear inclusions in neurons that occurs in the absence of respiratory disease is most likely the result of what entity?

A

Bovine Herpesvirus-5

142
Q

Canid herpesvirus 1 causes neurologic disease in puppies in what age group?

A

< 3 weeks of age; result of hypothermia predisposition which allow the virus to produce symptomatic infection

143
Q

Equine herpesviral myeloencephalopathy is caused by:

A. EHV-1 and EHV-4 in roughly equal cases

B. Primarily EHV-3 and occasionally by EHV-1

C. Primarily EHV-1 and occasionally by EHV-4

D. Only EHV-1

A

C. EHV-4 causes incidental disease in horses, and the disease is primarily caused by EHV-1. EHV-3 is equine coital exanthema virus.

144
Q

Neuropathic strains of EHV-1 are the result of:

A. Polymorphisms

B. Deletion mutant

C. Missense mutation

D. Nonsense mutation

A

C. Neuropathic strains are the result of a point mutation giving rise to a different amino acid (aspartic acid) rather than asparagine (i.e. a missense mutation). Deletion mutations cause multiple amino acid changes, and nonsense mutations result in STOP codons.

145
Q

Herpesviral pneumonia in donkeys is caused by:

A. EHV-1

B. EHV-2

C. EHV-8

D. EHV-3

A

C. EHV-8 is Asinine herpes virus and causes interstitial pneumonia in donkeys. EHV-1 causes neurologic disease (EHM) in horses, EHV-2 is ubiquitous among horses and does not cause clinical disease on its own, and EHV-3 is equine coital exanthema virus.

146
Q

EHV-1 has tropism for what all of the following cell types except?

A. endothelial cells

B. epithelial cells

C. neurons

D. T cells

E. B cells

A

E. B cells are not part of the viral life cycle of EHV-1. The virus stimulates a T cell and monocytic viremia and remains latent in T cells and neurons for life. Tropism for endothelial cells explains the lesions of thrombo-occlusive vasculitis and secondary CNS damage as well as abortion which is caused by an immune-mediated, Arthus type reaction. The virus also has tropism for epithelial cells, as it initially replicates in the upper respiratory epithelium.

147
Q

In the horse, the finding of a nonsuppurative necrotizing vasculitis, thrombosis and hemorrhage within the brain is most consistent with what etiology?

A. WNV

B. EEE/WEE/VEE

C. EHV-3

D. EHV-1

A

D. EHV-1

WNV and EEE/WEE/VEE are primarily lesions of neuronal necrosis and lymphoplasmacytic to neutrophilic (in the case of EEE/WEE/VEE) meningoencephalitis rather than a primarily thrombotic and vasculitic lesion. EHV-3 causes equine coital exanthema.

148
Q

Multifocal canine distemper encephalomyelitis in mature dogs is differentiated from “old dog” encephalitis by the fact that:

A. the cerebral cortex is affected in old dog encephalitis but not in MCDEMD

B. Old dog encephalitis is caused by the distemper vaccine

C. MCDEMD occurs as a result of persistent infection of a non-replicative state of distemper virus

D. There are abundant inclusion bodies in MCDEMD

A

A. The cerebral cortex is consistently affected in old dog encephalitis, but is spared with MCDEMD in which the lesions are mostly in the cerebellum and the spinal cord. Neither is caused by the vaccine, although a syndrome in young dogs post-vaccination called “post-vaccinal” canine distemper encephalitis does occur. ODE occurs as a result of persistent nonreplicative infection, MCDEMD occurs as a result of infection of an older dog (between 4-8 years of age). While ODE itself is incredibly rare, the inclusions are easy to find in ODE, but not MCDEMD.

149
Q

The primary histologic lesion of E. cuniculi is ______ which accounts for lesions being found in multiple organs.

A

segmental vasculitis as a result of parasitism of vascular endothelial cells

150
Q

EPM in horses is caused by all of the following except:

A. Sarcocystis neurona

B. Neospora hughesi

C. Neospora caninum

D. Sarcocystis cruzi

A

D. S. cruzi causes disease in cattle, with the dog as its definitive host

151
Q

The infectious stage of Sarcocystic neurona for the defintivie host is the _________ and the tissue stage is the __________.

A. sporozoite

B. merozoite

C. tachyzoite

D. sporocyst

A

D. sporocysts; B. merozoite (which is found in a schizont)

152
Q

Neospora caninum and Toxoplasma gondii have 3 infectious stages. What are they?

A

tachyzoites, tissue cysts and oocysts

153
Q

A very common, almost pathognomonic lesion in fetuses with Neospora infection is? What are common associated lesions in the fetus?

A

multifocal discrete foci of necrosis in the brain; lymphoplasmacytic to histiocytic hepatitis, myocarditis, placentitis, and myositis.

154
Q

Match the larval stage to the adult tapeworm:

A. Coenurus cerebralis; Taenia solium

B. Coenurus cerebralis; Taenia multiceps

C. Cysticercus bovis; Taenia solium

D. Cysticercus cellulosae; Taenia multiceps

A

B. Coenurus cerebralis is the larval form of Taenia multiceps. The host is the dog/wild carnivores.

Cysticercus bovis —– Taenia saginata——humans

Cysticercus cellulosae——Taenia solium——–humans

155
Q

This parasite is known for causing ischemic necrosis in the brains of white-tailed deer:

A. Parelaphostrongylus tenuis

B. Elaeophora schneideri

C. Baylisascaris procyonis

A

B. E. scheideri causes ischemic necrosis as a result of occlusion of the leptomeningeal arteries. P tenuis is the meningeal worm and is an incidental finding in WTD but may cause disease in other cervids. Baylisascaris causes necrotzing tracts througout the brain from migration, not ischemia.

156
Q

Sporadic bovine encephalomyelitis, which causes vasculitis and polyserositis as its hallmark lesions in young calves, is caused by this organism.

A

Chlamydia pecorum, can also be caused by C. psittaci

157
Q

Sporadic Bovine Encephalomyelitis causes three grossly visible inflammatory lesions:

A. pericarditis, peritonitis, pleuritis

B. pneumonia, hepatitis, meningitis

C. meningitis, pleuritis, pericarditis

D. erosive arthritis, pericarditis, peritonitis

A

A. pericarditis, peritonitis and pleuritis are hallmarks of C. pecorum infection in SBE.

158
Q

Pug dog encephalitis is known as :

A. GME

B. NME

C. NLE

A

B. Necrotizing meningoencephalitis was formerly known as “pug dog” encephalitis, but affects other small breeds. NLE affects white matter more than NME which is confined to the cortex.

159
Q

NME is characterized by (focal/multifocal) necrosis of the (gray/white/gray and white) matter.

A

multifocal distribution, bilateral and asymmetric. It is almost entirely in the gray matter.

160
Q

Which of the these conditions affects the white matter?

A. NME and NLE

B. NME and GME

C. NLE and GME

D. NME and GME

A

C. NLE and GME both affect primarily the white matter.

161
Q

GME lesions consist of what two types of leukocytes?

A

MHC Class II macrophages and CD3+ T cells

162
Q

The main histologic feature of GME is:

A

perivascular cuffs in the white matter consisting mostly of lymphocytes and plasma cells with clumps of macrophages that gradually increase in number during the course of disease.

163
Q

Macrophages in GME frequently develop into what two morphologies:

A

epithelioid cells and syncytia

164
Q

In which disease are mitoses fairly common:

A. NME

B. NLE

C. GME

A

C. GME commonly has at least a few mitotic figures.

165
Q

Polyradiculoneuritis, or coonhound paralysis, has what clinical signs? What are the histologic lesions?

A

Progressive ascending paralysis and muscle atrophy with recovery in most cases; the lesion is Wallerian degeneration of the ventral roots of the spinal cord and peripheral nerves, denervation atrophy of the muscle, and a mononuclear perivascular infiltrate

166
Q

Cauda equina syndroms in horses is primarily characterized by:

A. lymphoplasmacytic meningomyelitis of the sacral and caudal spinal roots

B. granulatomatous inflammation with extensive fibrosis of the sacral and caudal spinal roots

C. multifocal areas of malacia and hemorrhage in the sacral spinal cord with sparing of the roots

D. severe Wallerian degeneration in the sacral spinal cord and minimal fibrosis of the perineural tissues

A

B. granulomatous inflammation with extensive fibrosis of the sacral and caudal spinal root perineural tissue. There is some axonal degeneration and regeneration present. Hemorrhage is also present but malacia is not a feature. While lymphocytes and plasma cells are present in the infiltrate, this is primarily a granulomatous disease.

167
Q

Steroid-responsive meningitis-arteritis (formerly known as Beagle pain syndrome) is characterized histologically with all of the following lesions except:

A. perivascular and transmural arteritis of the brainstem and spinal cord meninges

B. fibrinoid necrosis of small to medium sized arteries

C.Wallerian degeneration of the spinal cord

D. thrombosis

E. myocardial arteritis

A

C. spinal cord changes are few and related only to adjacent meningeal artery inflammation. Wallerian degeneration is not a feature.

168
Q

Post-infectious encephalomyelitis is best characterized by what process:

A. peri-arterial inflammation

B. demyelination

C. granulomas

D. eosinophilic infiltrates

A

B. this is a demyelinating disease that occurs in the context of the post-vaccine period and has a predominantly peri-venous inflammatory pattern composed mostly of lymphocytes/plasma cells and monocytes/macrophages. Granulomas and eosinophils are not present.

169
Q

Features of meningiomas in cats include:

A. more likely to be easily removed during surgery

B. more likely to be solitary than multiple

C. more likely to be a paranasal meningioma

D. more likely to be associated with the lateral ventricles

E. more likely to have more than one histologic pattern

A

a. cat meningiomas are more likely to be easily excised during surgery, even though they often occur in multiples. Paranasal meningiomas are rare and only reported in dogs and horses. Cat meningiomas are more likely to be associated with the tela choroidea of the third ventricle. They are also more likely to have a uniform histologic pattern and are consistent with a canine Grade I meningioma for this reason.

170
Q

Which of the following are considered Grade II meningiomas?

A. papillary and anaplastic

B. chordoid and atypical

C. meningothelial and angiomatous

D. psammomatous and transitional

A

B. Chordoid and atypical are the only Grade II meningiomas. Papillary and anaplastic are the only Grade III meningiomas. All other types are Grade I.

171
Q

IHC for almost all meningiomas should have this expression pattern:

A. vimentin +, GFAP -, Synaptophysin -, CD34 +, E-cadherin +

B. vimentin -, GFAP -, Synaptophsin -, CD34 -, E-cadherin -

C. vimentin +, GFAP -, Synaptophysin -, CD34 -, E-cadherin -

A

A. Meningiomas should be positive for vimentin, and most of them will be positive for CD34 and E-cadherin. They can weakly express cytokeratin, NSE and S100. They should never express GFAP or Synaptophysin.

172
Q

Which marker is over-expressed in all meningiomas?

A. hogwarts

B. frodo

C. merlin

D. medusa

A

C. merlin (protein product of NF2 tumor suppressor gene) is overexpressed in all meningiomas The others are completely made up.

173
Q

Astrocytomas should have this IHC expression pattern:

A. Vimentin +, Nestin +, GFAP +, S100 +

B. Vimentin +, Nestin -, GFAP -, S100 -

C. Vimentin +, Nestin +, GFAP -, S100 -

A

A. Astrocytomas should be positive for vimentin, nestin, GFAP and S100.

174
Q

Glioblastomas frequently have endothelial and adventitial vascular proliferation leading to the production of glomeruloid blood vessels. What factors are over-expressed in glioblastomas that fit with this feature?

A. EGFR, PDGFR-alpa, insulin-like growth factor binding protein 2

B. RANKL and BMP

C. SRY

D. E-cadherin and CD34

A

A. Epidermal growth factor, platelet-derived growth factor receptor-alpha and insulin-like growth factor binding protein 2 are all over-expressed in astrocytomas which explains their production of glomeruloid blood vessels. RANKL and BMP are found in osteoblasts. SRY is the sex determing region of the Y chromosome, and E-caderin and CD34 are cell adhesion markers which are upregulated in meningiomas.

175
Q

This type of brain tumor has a cell membrane that stains and cytoplasm that doesn’t, giving a honeycomb type of effect.

A

Oligodendroglioma

176
Q

This neoplasm is most likely to occur in the lining of the third ventricle and is composed of both pseudorosettes (those surrounding a blood vessel) and true rosettes (those lacking a central lumen).

A. Meningioma

B. Medulloblastoma

C. Choroid plexus papilloma

D. Ependymoma

E. Astrocytoma

A

D. Ependymomas have both pseudorosettes and true rosettes and are more likely to occur in the lining of the third ventricle. While choroid plexus tumors do frequently occur in the lateral, third and fourth ventricles, they have a papillary appearance rather than rosettes and pseudorosettes. Medulloblastomas ONLY OCCUR IN THE CEREBELLUM, OTHERWISE THEY ARE A PNET. Medulloblastomas do have pseudorosettes and rosettes.

177
Q
A

ACVP Phase II Exam - Anatomic Pathology (25 decks)

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