Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

S&S - Exam 2 > food animal infections of nervous system > Flashcards

food animal infections of nervous system Flashcards

1
Q

What viruses cause congenital malformation?

A

BVDV, blue tongue, akabane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What VIRUSES cause encephalitis?

A

Rabies
Cattle: bovine herpes virus 5, malignant catarrah fever,
Pigs: pseudorabies
Lentivirsues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

DDx?

A

DDx: Border dz***
v. blue tongue v. akabane v. cache valley

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Border Disease signalement? Pathogenesis? Syndromes (4)?

A

Newborn lambs- congenital infection

Syndromes:
1. early embryonic mortality
2. abortion & still birth (@ any point)
3. early in gestation –> lambs = persistently infection (PI)
4. after 85 days in gestation –> normal w/ antibodies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does the Border Disease virus have tropisms for?

A

Lymphoid tissue, CNS - oligodendrocytes, Hair follicles (hair shaker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Pathologic findings for Border Disease?

A

Infection during fetus CNS development –> neurologic or ocular degen.
- cerebellar hypoplasia
- hydranencephaly (loss of cerebral hemis)
- porencephaly (cysts in cerebral hemis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Border disease clinical signs? (5)

A

tremors (hypomyelinogenesis)
ataxia (cerebral hypoplasia)
hairy birth coat
short, boxy stature
facial bone malformations
ocular abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Who gets infected in MCH? How is it shed?

A

Ovine-herpesvirus type 2
Infection by CARRIER domestic or wild sheep/got hosts –> susceptible hosts (CATTLE, BISON, FARMED DEER

Major shedding events = during lambing/kidding!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What virus do corneal edema (blue eyes) and multi-focal hemorrhage manifest in?

A

MCH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What causes Bovine Spongiform Encephalopathy (Mad Cow Disease)?

A

Abnormal prion protein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hallmark lesion for TSE?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DDx?

A

DDx - rabies v. caprine arthritis encephalitis

Latter = a lentivirus - use serology to determine antibody presence! (lentivirus: infected for life, even if no clinical signs [majority of goats])

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where do lentiviruses replicate?T Type of infections?

A

replicate in macrophages
once infected, px is infected for life

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the main findings on histo for caprine arthritis encephalitis

A

severe arthritis; SC granulomatous inflamm. w/ perivascular cuffs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

DDx?

A

classical swine fever v. Atypical porcine pestivirus v. porcine herpes virus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Key trait about pestiviruses?

A

The persistently infected animal spreads the virus to others

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Clinical signs of atypical porcine pestivirus?

A

congenital tremors in suckling / young pigs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Key pathologic finding of classical swine fever?

A

necrotizing tonsilitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What disease in pigs is known as pseudorabies in other species?

A

Aujeszky’s Disease - a herpes disease (stress-induced)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Aujeszky’s Disease route of infection?

A

aerosol transmission
virus replicates in tonsils / oropharnyx –> spreads to regional LN –> latent in trigem gang –> stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

cardinal signs of food animal spinal cord infection (6)

A
  1. limb weakness / ataxia
  2. muscle atrophy / flaccidity (gray matter)
  3. increased or decreased limb reflexes
  4. loss of sensation
  5. recumbency
  6. ABNORMAL menace! (depressed, obtunded)
22
Q

How are spinal cord infections in food animals diagnosed?

A

CSF analysis

23
Q

3 most common congenital / hereditary spinal cord infections?

A
  1. Spastic paresis (elso heel), straight hock syndrome
  2. Periodic spasticity (stretches)
  3. Bovine progressive degenerative myelopathy (BPDME // Brown Swiss)
24
Q

Spastic paresis signalment and clinical signs

A

young ruminants; stiff, asymmetric gait, bilateral but one limb more stiff/stretched than the other.

25
Q

Periodic spasticity signalment and clinical signs

A

adult cattle; spastic extension, abduction of PLs during onset of walking

26
Q

Bovine progressive degenerative myelopathy signalment and clinical signs

A

Onset of bilateral PL ataxia and dysmetria 5-8 months of age -> deficient proprioceptive responses, ataxia in all 4 limbs, progressive paraparesis. normal spinal reflexes and cranial nerve functions

27
Q

5 most common spinal cord infections?

A
  1. Spinal epidural abscess (empyema)
  2. Tetanus
  3. Small ruminant lentiviruses
  4. Parelaphostrongylus
  5. Botulism
28
Q

Spinal epidural abscess (empyema) signalement, pathogenesis, what it can lead to

A

Young ruminants
Iatrogenic (improperly prepared epidural injections) -> bacteria extends from the septic vertebral jt -> vertebral physis -> causes DISCOSPONDYLITIS -> can lead to fx (affects structure of the bone) or compress spinal cord via pressure

29
Q

What are discospondylitis and osteomyelitis? Pathogenesis?

A

Disco = Inflammation of the intervertebral disc and adjacent vertebral bodies
Osteo = inflammation of the vertebra without concurrent disc infection

Calves with failure of passive transfer (IgG). hematogenous spread.

No tx, poor-to-guarded prognosis

30
Q

Signalment of tetanus-infected animals?

A

Neonates via umbilical cord (1-4 weeks of age), post-partum in adult cattle (1-4 weeks), 1-4 weeks after castration, dehorning

31
Q

What antibiotic class is given for tetanus? Prevetion?

A

Penicillin
Prevention = VACCINATION

32
Q

Signalment of botulism-infected animals? How is it diagnosed?

A

Any age, any species. Dx = flaccid tongue / clinical signs; PCR on GI contents or feed

33
Q

Treatment for botulism?

A

Anti-toxin; remove contaminated feed; Type B vaccine (EQUINES ONLY)

34
Q

Caprine Arthritis Encephalomyelitis (CAE) signalment? Pathogenesis? Prognosis? Prevention?

A

GOATS
1-5 m/o kids** and adults (via colostrum** or close contact)

POOR PROGNOSIS -> death within weeks-to-months

PREVENTION: test biannually or annually and cull positive animals; heat milk or use replacement

35
Q

Examination findings of CAE-positive goat? Dx?

A

BAR, no fever, normal appetite
Neuro: UNILATERAL paraparesis and ataxia -> asymmetric tetraparesis and ataxia
Dx: CSF fluid = hyperproteinemia & monocytosis

36
Q

Ovine Progressive Pneumonia (OPP / Maedi Visna) signalement / clinical signs? Prevention?

A

Sheep, usually older than 2 years. Progressive ataxia, flock mates with respiratory signs, “hard bag” arthritis

37
Q

Hosts of the meningeal worm (parelaphostrongylus tenius)?

A

Natural = white-tailed deer
Intermediate = snails and slugs
Aberrant = camelids & ruminants –> CNS SIGNS***

38
Q

Clinical signs of the meningeal worm? Why is the prognosis guarded?

A

sudden / rapid progression of unilateral or bilateral, asymmetric paraparesis or tetraparesis, ataxia

Guarded prognosis due to damage by the migrating worm!

39
Q

Treatment for meningeal worm?

A

Ivermectin + Fenbendazole; anti-inflammatory; omeprazole or pantoprazole

40
Q

What are 2 of the most common types of nutritional / toxic spinal cord infections in FA?

A

Enzootic ataxia (Swayback) and delayed organophosphate toxicity

41
Q

Pathogenesis of enzootic ataxia and the two forms

A

dietary copper deficiency of mother -> in-utero copper deficiency of kids & lambs; congenital and delayed (2 weeks to 4 months old)

42
Q

Clinical signs of enzootic ataxia?

A

progressive weakness and ataxia (caudal to cranial) -> para-to-tetraparesis; flaccid paralysis

43
Q

Clinical signs of delayed organophosphate toxicity?

A

SLUD - d+, loss of bladder function; DELAYED NEURO SIGNS (8-90 DAYS POST EXPOSURE); weakness

44
Q

Clinical signs of peripheral nerve compression

A

limb weakness, ataxia, muscle atrophy, reduced skin sensation, reduced limb reflexes

45
Q

What nerves are vulnerable to compression / paralysis during calving?

A

Sciatic*, obturator, femoral, peroneal

46
Q

What does this cow exhibit?

A

Knuckling, weakness due to calving paralysis

47
Q

Tx plan for compression neuropathy (calving paralysis)

A
  1. Dexamethasone IV or IM ASAP
  2. Move to comfortable area + supportive care
  3. Turn sides at least 4x/day (avoid secondary ischemic necrosis)
  4. Euthanasia if cow does not remain sternal / lays in lateral recumbency
48
Q

What neoplasia can bovine leukemia virus (BLV) cause? Clinical signs? Tx?

A

Epidural Lymphosarcoma (LSA). Progressive asymmetric ataxia and paraparesis. Tx = EUTHANASIA!

49
Q

What areas of the body do LSA have an affinity for?

A

Right atrium of the heart, the uterus, the spine, the abomasum, the lymph nodes

50
Q

Cardinal signs of neuromuscular disease

A

flaccid tetraparesis, mydriasis, dysphagia, bloat, recumbency

51
Q

Cardinal signs of neurological disease:

A

blindness, seizures, mental depression, dementia

52
Q

How does thiamine (VitB) deficiency manifest in ruminants? Signalment?

A

thiamine deficiency (VitB) -> cerebral edema -> head-pressing, dull, ataxia, opisthotonos, seizures.
SUCKLING CALVES & KIDS; feedlot weanlings

S&S - Exam 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions