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Disorders of Muscle > Misc muscle > Flashcards

Misc muscle Flashcards

1
Q

What are examples of random specific causes of hard tissue swellings in ruminants?

A

chronic flourosis
CAE
Nutritional osteodystorophy (def in Cu, Ca & Phosph)
Lumpy Jaw (actinomycosis)

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2
Q

Examples of bilateral pelvic limb paresis

A

congenital
EPM
trauma
thrombosis
infection

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3
Q

Examples of tetraparesis

A

botulism
polyneuropathies
polymyopathies

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4
Q

Examples of metabolic causes of paresis/weakness in horses?

A

hypothyroidism
hyperthermia
hepatic lipidosis
Vit A def

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5
Q

Exampels of plant poisons that cause paresis/weakness in horses?

A

starthistle poisoning
oleander
moldy corn poisoning
white snake root
locoweek
larkspur
delphinium
onion
moldy sweet clover

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6
Q

What are anomalous/congenital causes of paresis/weakness in ruminants?

A

progressive degenerative myeloencephalopathy of Brown Swiss cattle
PRgoressive ataxia of charolais cattle
Inherited progressive spinaly myelinopathy of murray grey cattle
inherited myophosporylase deficiecny in charolais cattle

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7
Q

What are infectious/inflammatory causes of paresis/weakness in ruminants?

A

BSE
tick paralysis
botulism
rabies
pneuomnia
spinal abscess
Parelaphostrongylus tenuis

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8
Q

What are exampels of muscle spasms/myoclonus in horses?

A

myotonia congenita
HYPP
Insulinoma
Tetanus, rabies, equine influenza, tick-borne encephalitis, meningitis
Toxic: strychnine, organochlories, chlorinated hydrocarbons

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9
Q

Define physitis (epiphysitis)

A

disturbance in enochodnral ossification at physis

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10
Q

What are causes of physitis in horses?

A

genetic component
overweight foals
groth spurts inf oals
high CHO intake
improper mineral balance (Cu, Zinc)
high or low Ca intake
excessive exercise (hard grown)
single transphyseal screw for ALDs

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11
Q

At what age is physitis typically seen (age and location)?

A

3 to 6 moths: distal metacarpal/metatarsal

8-24 months: distal radius

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12
Q

Define osteochndrosis

A

failure of defect in endochondral ossification–> cartilage flaps, fragments, subchondral bone cysts

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13
Q

What is the most common inheritable skeletal disorder in sheep?

A

ovine hereditary chondrodysplasia (spider lamb syndrome)

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14
Q

What clinical signs are seen with ovine hereditary chondrodysplasia (spider lamb syndrome)?

A

–deformities affecting the appendicular and axial bones– elongated extremities (valgus)
kyphoscoliosis abnormal rib and sternum concavities
roman nose
facial deformities
lack of body fat
scarcity of muscling

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15
Q

What species of sheep is ovine hereditary chondrodysplasia (spider lamb syndrome) seen in?

A

suffolk/hampshire lambs

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16
Q

DDX for ovine hereditary chondrodysplasia (spider lamb syndrome)

A

bluteongue &akabane virus–hydranencephaly & arthrogyposis

border disease – nervous sys, skin, fleece, skeleton

cache valley virus
benizidazoles
locoweeds (deformities in utero)
Vit. D deficiency
phosphorous
Zinc
Manganese deficiency

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17
Q

Hematogenous spread of septic arthritis is most common in?

A

foals (young)

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18
Q

extension of periarticular wound as a cause of septic arthritis is most common in?

A

adults

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19
Q

What are risk factors for the development of septic arthritis in calves?

A

FPT
septicemia
feeding mastitis milk (mycoplasma)

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20
Q

What are the most common bacterial isolates in septic arthritis in foals?

A

actinobacillus equuli
Salmonella
E coli
other enterobacteriaceae

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21
Q

What are the most common bacterial isolates in septic arthritis in older foals?

A

streptococcus
rhodococcus

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22
Q

What are the most common bacterial isolates in septic arthritis in adult horses?

A

enterobacteriaceae
streptococci
staphylococci

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23
Q

What are the most common bacterial isolates in septic arthritis in calves?

A

streptococcus
mycoplasma bovis

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24
Q

What are the most common bacterial isolates in septic arthritis in cattle

A

mycoplasma bovigenitalium
mycoplasma mycoides
brucella
t pyognes

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25
Q

In cattle what nutritional compounds are implicated in physisits?

A

Copper deficiency– interactions molybdenum, zinc and sulfates

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26
Q

Copper deficiency causes physitis through what pathophysiologic mechanism?

A

Cu required for crosslinking of collagen– when deficient cartilage matrix weakens, microfractures occur

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27
Q

If mares milk is low in copper (naturally), where do foals get their appropriate cu nutrition?

A

foals rely on hepatic Cu stores gained in last trimester of gestation

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28
Q

What are the treatment recommendations for foals with physitis?

A

1 nutrition- proper mineral balance & reduction of energy
2. exercise restriction: stall rest

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29
Q

angular limb deformities occur due to?

A
  1. laxity of periarticular supporting structures
  2. incomplete ossification
    3 asynchronous physeal growth
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30
Q

incomplete ossification is common in what cuboidal bones?

A

Carpus: ulnar, third & fourth
Tarsus: central and third

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31
Q

When does normal ossification of cuboidal bones occur?

A

in the 3rd trimester

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32
Q

What endocrinopathy is thought to contribute to angular limb deformities?

A

hypothyroidism (rare)
— maternal influences– excessive/inadequate dietary iodine intake
– unknown cause in NW US

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33
Q

List pathophysiologic mechanisms behind angular limb deformities

A
  1. incomplete ossification
  2. asynchornous growth (d/t trauma or severe lamness)
  3. osteochondrosis/abnorm growth cartilage
  4. hypothyroidism (rare)
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34
Q

What dietary imbalances are seen in calves raised in confinement that predispose to angular limb deformities?

A

High dietary Fe
low dietary Vit D

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35
Q

What are radiographic signs of asynchronous growth?

A

wedging of epiphysis
widening of physis
sclerosis adjacent to the physis

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36
Q

What are 2 mechanisms for sx correction of angular limb deformities?

A
  1. growth retardation: bridge physis with metallic implants
  2. alter physeal growth: periosteal transection & elevation (stripping)
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37
Q

What is the mode of inheritance of spider lamb syndrome?

A

autosomal recessive

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38
Q

The genetic abnormalities in spide lamb syndrome results in what abnormal protein function?

A

ovine fibroblast growth factor receptor 3

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39
Q

What is the causative organism of contagious agalactiae in kids and goats?

A

mycoplasma p spp–
M mycoides subsp capri (most common in US)
M agalactiae in mediterranean countires

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40
Q

Where can kids/goats be samples for diagnosis of contagious agalactiae for asymptomatic carrier animals?

A

ear

**M mycoides subsp capri

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41
Q

What are DDX for agalactia/mastitis in goats?

A

environmental coliforms
S auerus
fungal organisms
caprine arthritis encephalitis virus

**Mycoplasma mycoides subsp capri– can colonize reprot ract– abortions/DEC repro performance

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42
Q

What are C/S seen in goat kids with contagious agalactiae?
**M mycoides subsp capri

A

initial signs: fever, lethargy, anorexia, weakness

Following bacteremia: polyarthritis– carpal & tarsal joints most common that are warm/swollen; keratoconjuncitivitis and pneumonia

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43
Q

how are kids infected with M mycoides subsp capri?

A

infected milk/colostrum from doe

or supplemented bovine milk with M. bovis

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44
Q

How is M mycoides subsp capri transmitted?

A

oral & nasal secretions
contaminated milk equipment

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45
Q

How is M mycoides subsp capri introduced into a herd?

A

through an asymptomatic carrier

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46
Q

Treatment options for M mycoides subsp capri?

A

tetracyclines
flouroquinolones
macrolides
florfenicol
antimicrobials that disrupt the cell wall synthesis are ineffective

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47
Q

What are forms of disease caused by caprine arthritis encephalitis virus (CAEV)?

A
  1. leukocenphalomyelitis
  2. interstitial pneumonia
  3. chronic mastitis
  4. debilitating polysnovitis arthritis
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48
Q

Leukoencephalomalacia caused by caprine arthritis encephalitis virus (CAEV) is observed primarily in what age kids?

A

2 to 6 months of age

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49
Q

caprine arthritis encephalitis virus (CAEV) clinical signs (leukoencephalomalacia)?

A

ascending paresis leading to paralysis beginning in rear limbs

**severe manifestation– progression of paresis to paralysis to urinary retention & bloat

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50
Q

What are DDX for the leukoencaphlomalacia form of caprine arthritis encephalitis virus (CAEV)?

A

meningitis
meningeal worm
trauma

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51
Q

Polysynovitis-arthritis caused by caprine arthritis encephalitis virus (CAEV) typically manifests in what age groups?

A

mature goats most commonly
**reported in goats as young as 6 months

**carpus most commonly affected but can be any joints

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52
Q

caprine arthritis encephalitis virus (CAEV) polysynovitis-arthritis pain is due to?

A

joint enlargement– d/t hyperplasia of synovial tissues

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53
Q

What is differentiating in joint fluid in septic arthritis in comparison to caprine arthritis encephalitis virus (CAEV) polysynovitis?

A

CAEV: primarily mononuclear cells
**differes from bact synovitis– predom neuts

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54
Q

A positive caprine arthritis encephalitis virus (CAEV) AGID/ELISA is synonymous with

A

lifelong viral infection

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55
Q

What are preventative measures that can be performed to prevent the spread of caprine arthritis encephalitis virus (CAEV)?

A

-milk colostrum mgmt: prevent kids contact with dam, heat tx colostrum, kids fed pasteurized milk till weaning, do not pool colostrum

-test kid serologically @ periodic intervals

-isolate seropos animals

-new herd additions tested prior to adding to herd

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56
Q

What are the 2 major factors that lead to the development of osteoarthritis?

A
  1. mechanical load
  2. tissue turnover or metabolism
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57
Q

what are radiographic changes of OA?

A

-loss of joint space
-subchondral bone sclerosis
-subchondral cystic lesions
-periarticular osteophytes
-periosteal new bone formation @ sites of joint capsules & ligamentus attachments (enthesophytes)

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58
Q

What is the most common congenital abnormalities in cattle?

A

arthrogyrposis

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59
Q

What are causes of arthrogyrposis (in general)?

A
  1. genetic
  2. infectious
  3. toxic
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60
Q

What are congenital causes of arthrogyrposis in ruminants?

A

Charolais calves & Holstein: forelimb arthrogyrposis, spinal dwarfism, cleft palate
Curly calf syndrome (arthrogyrposis multiplex): autosomal recessive defect, angus cattle, kyphoscoliosis, dec muscling

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61
Q

Congenital arthrogyrposis in horses is seen in what breeds?

A

norweigan fjords
thoroughbred foals

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62
Q

Congenital arthrogyrposis is seen in what breeds of sheep?

A

suffolk
coffiedale sheep

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63
Q

What are infectious causes of arthrogyrposis?

A

Bunaviridae faimly of virsues: akabane virus, cache valley virus (US)
**see other congenital abnormalities)

Schmallenburg Virus
**(see other congenital abnormalities)

Blue tongue virus

border disease virus in lambs

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64
Q

List toxic causes of arthrogyrposis

A

alkaloids in pregnant animals (conium, lupinus, nicotiania)
lupine tox– “crooked calf syndrome”
sorghum pastures
vetrum californicum (d29 gestation in sheep)

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65
Q

define ankylosis

A

abnormal fusion of bones in a joint

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66
Q

What clin path finding is associated with osteomyelitis in foals?

A

fibrinogen >900 mg/dL

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67
Q

define spondylitis

A

inflammation of vertebral body

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68
Q

define diskospongylitis

A

inflamm. lesion including intervertebral disc & its adjacent vertebrae

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69
Q

What is the primary cause in pathogenesis of spondylitis/diskospondylitis?

Foals>adults

A

secondary to a pre-existing focus of infection elsewhere in the body
–> tail docking wounds, umbilical infections, pneumonia, lung abscesses

–> septic thrombi to metaphyseal arteries of vertebrae, where bact colonize

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70
Q

Adult pathogenesis of spondylitis/diskospondylitis?

A

direct injury to invertebral disc &/or vertebral end plate

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71
Q

Define spondylosis

A

ankylosing or degenerative condition of intervetebral joints

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72
Q

Bilateral rear limb lameness & paresis is seen in bulls in the artificial insemination industry due to

A

calcification fo thoracolumbar vertebrae & ligaments
+/- fusion of lu mbar vertebrae

***posterior spinal paresis syndrome

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73
Q

What are differentials for cattle with hind limb neuro deficits?

A

lymphosarcoma
encephalopathy
progressive degenerative myeloencaphlopathy
downer cow syndrome
posterior spinal paresis syndrome

74
Q

What are disease states that are associated with laminitis

A

-sepsis & sirs (endotoxemia, -pneumonia, septic metritis)
-EMS & PPID
-mechanical & traumatic overload
-overgrazing pastures or unrestricted access to concentrates–> CARB overload
-contralat. limb excess wt bearing
-exposure to toxin in black walnut shavings
-corticosteroids admin
-cattle– overweight heifers fed excess concentrates & housed on concrete

75
Q

What is the obel lameness grades for laminitis

A

obel
1. least severe: shifting weight with no apparent lameness @ alk but a trot
2. willing to walk with stilted gait & willing to lift foot off ground
3. reluctance to ambulate– resistance to left foot off the ground
4. severe: refuses to move

76
Q

What are the experimental models for the induction of laminitis?

A

-carb overload
-fructan overload
-black walnut extract admin
-hyperinsulinemic

77
Q

What are radiographic measurements that are indicative of laminitis?

A

ratio: dorsal measurement/palmar cortical length of distal phalanx
**>32% w/ displacement of distal phalanx

-palmar/plantar rotation of distal phalanx away from hoof wall
**>5 degrees is indicative of rotation

78
Q

In acute fluorosis toxicosis where are levels measurable?

A

high concentrations in plasma & urine in acute toxicosis

79
Q

What C/S are seen with acute flouride toxicosis?

A

restlessness
agalactia
salivation
vomiting/regurge
severe depression
urinary incontinence
diarrhea (GI mucosal necrosis)
clonic convulsions
cardiac failure

80
Q

What are common sources of excess flouride ?

A
  1. water w/ naturally high flouride content
  2. forages contam with flourides from nearby (upwind industrial plants)
  3. mineral sources & feed supplements with excess flouride content
  4. forages contam by soil or water
  5. volcanic activity– deposit flouride containing ash on soil/plants/water/etc.
81
Q

Chronic flouride toxicosis commonly manifests as:

A

-dental fourosis or osteoflourosis– developing teeth ar v sensitive to ingeston of excess flourides

82
Q

What changes are seen with chronic flouride toxicosis?

A

teeth: chalkiness, mottling (striation or patches in enamel), hypoplasia in enamel, hypocalcification

bones: palpable lesions: medial surface of prox 1/3 metatarsal bones, then mandible, metcarpal bones, ribs

83
Q

Hypertrophic osteopathy (Maries Dz) in horses is characterized by:

A

symmetric proliferation of connective tissue and subperiosteal bone along disphyses & metaphyses of bones of distal extremities

84
Q

What is the pathogenesis of Hypertrophic osteopathy (Maries Dz)?

A

Unknown

85
Q

treatment of Hypertrophic osteopathy (Maries Dz):

A

– treat underlying disease process
**reports of regression with rest, bute and corticosteroid therapy

86
Q

What is the cause of fescue foot?

A

Tall fescue (fetuca arundinacea) grass that is infected with endophyte Neotyphodium (Acremonium) coenphilaum– the fungus that produces ergovaline– ergot alkaloid that has a vasoconstrictive effect on feet/ extremities

87
Q

Clinical signs of the fescue foot occur within what time frame?

A

w/in 42 days of exposure to endophyte infected fescue

88
Q

What are clinical signs of fescue foot?

A

limb lesions: most often hind limb (tips of ears, tail), start as red line @ coronary band with edema, hair easily epilated, gangrenous process, lameness

**lesions occur most commonly in winter/cooler weather & worsens vasoconstriction

89
Q

DDX for fescue foot

A

ergotism-claviceps purpurea
seleium tox
salmonellosis
frost bite
sarcocystis– in cattle assoc with loss of tail

**early stages: traumatic injury, laminitis, foot rot

90
Q

What are treatment recommendations for fescue foot?

A

-remove from pasture
-necrosis: occurs– tx unrewarding, euth. recommended
early cases: supportive therapy, soft ground, NSAIDS, +/- systemic/local antibiotics

91
Q

Which animals are at high risk for the development of interdigital necrobacillosis (foot rot) in cattle?

A

-housed in moist, muddy lots
-pastures with standing water
-areas where sharp gravel, concrete or stubble

92
Q

What bacteria is most commonly associated with foot rot?

A

fusopbacterium necrophorum– gran neg anaerobe

Other bacteria: Prevotella melaniogenica, porphyromonas levii, Dichelobacter nodosus

93
Q

What are differentials for interdigital necrobacillosis (foot rot)?

A

septic arthritis
sole abscess
tenosynovitis
pedal osteitis
interdigital fibroma
laminitis
trauma

94
Q

What are virulence factors for F. necrophorum?

A
  1. high molecular weight leukotoxin, cytotoxic to ruminant neuts, comb with LPS prevents phagocytosis
  2. LPS
95
Q

What type of F. necrophorum is commonly isolated in cases of foot rot?

A

biotype A– more virulent & freq isolated
biotype B

96
Q

What allows for bacteria to cause interdigital necrobacillosis (foot rot)?

A

-maceration/lesion of foot with prolonge exposure to moisture or trauma
- early invadors dec O2 tension = ideal environment for anaerobic bacteria

-**actions of bact proteases & WBC action destory local tissues that allow deeper invasion & necrosis

97
Q

What are antibiotics labelled for foot rot?

A

oxytet
florfenicol
cetfiofur
tylosin
sulfadimethoxine
tulathromycin

98
Q

What are recommendations for control and prevention of interdigital necrobacillosis (foot rot)?

A

-eval environment for potential risk factors
-improve hygeine (ie drainage, manure removal etc.)
-no feed additives approved in US for control foot rot
-commerical vs has ltd efficacy
-minerals to support overall hoof health

99
Q

What are the two organisms implicated in infectious foot rot in small ruminants?

A
  1. Dichelobacter nodosus (obligated parasite of the foot)
  2. fusobacterium necrophorum
100
Q

How to differentiate infectious foot rot in small ruminants from contagious ovine digital dermatitis (CODD)?

A

-low prevalence in US
-severe lameness
-undermining of hoof wall at coronary band–> avulsion of hoof capsule
causative agent: treponema bacteria

101
Q

How to confirm foot rot (from contagious ovine digital dermatitis)?

A

culture: D nodosus– challenging d/t fastidious nature of bact.

real time PCR: poor dx specificity

102
Q

treatment of infectious foot rot in small ruminants

A

foot trimming– prolonged recovery of sheep

-oxytet- not labelled for tx of foot rot in sheep
-gamithromycin
-micotil/tilmicosin– whole flock tx not recommended
-florfenicol– german study saw improvement

103
Q

Deep penetrating injuries to sole can potentially communicate with:

A

-navicular bursa
-digital tendon and sheath
-DDFT
-distal phalanx

104
Q

What is thrush?

A

bacterial infection characterized by accumulation of black, malodorous necrotic material originating from frog of hoof

105
Q

What is the most common bacteria associated with thrush?

A

fusobacterium necrophorum

106
Q

What are clinical signs of thrush?

A

variable lameness
-black malodorous d/c, most often from frog sulci
-pain on palpation/manipulation of frog– caudal heel pain

107
Q

What is white line disease?

A

white line disease is separation of hoof wall from its laminar attachments
– a crack/opening allows invasion of bacteria/fungus into the stratum medium close to laminae– cavities develop between laminae & outer hoof wall

108
Q

What is Quittor?

A

chronic infection of medial or lateral collateral cartilage of distal phalanx in the horse

–characterized by: local inflamm & necrosis of affected cartilage, subsequent formation of draining tracts prox to coronary band, infection usu. caused by wound

109
Q

What is fistulous withers?

A

chronic ifnlammatory condition of supraspinous burse & assoc tissues seen in horses, mules &donkeys

110
Q

What are the two forms of fistulous withers and what bacterial are involved?

A
  1. Idiopathic form (more common)– Brucella abortus; O cervicalis
  2. Traumatic form- 2ndary infection with environ contam or hematogenous spread to devilatlized tissue (ie. strep equi subsp zoo)
111
Q

What are findings of culture of fistulus withers for Brucella abortus?

A

B. abortus is difficult to grow in culture & easily overgrown by other bacteria– negative c ulture is misleading

112
Q

What is the treatment recommendations for fistulus withers?

A

**med management not successful alone–> comb of aggressive sx debridement
-antimicrobials
-lavage of draining tracts
-stemtic anti-inflamm
-application of maggots

113
Q

Silicate associated osteoporosis (bone fragility syndrome) geographic distribution is:

A

-monterey carmel peninsula california
–sonoma & Napa counties

114
Q

What are clinical signs of silicate associated osteoporosis (bone fragility syndrome)?

A

Early clin features:
-intermitten lamness affecting one or multiple limbs
-exercise intolerance
-generalized stiffness

Late stages:
-severe lameness
-scapular bowing- pain elicited on palpation
-dec range of motion of cervical spine
-generalized wt loss
**pot respiratory dsiease

**potential consequence can be catastorophic fx of affected bone

115
Q

treatment of silicate associated osteoporosis (bone fragility syndrome)?

A

palliative & aimed at dec inflammation & osteoclastic bone resorption
-bisphosphonates, exercise restriction, NSAIDS, moving horses (may not halt prgoression of C/S)

116
Q

prognosis for silicate associated osteoporosis (bone fragility syndrome)

A

fair- early stages, risk of dec bone strength

guarded to poor: athletic use not reocmmended, common catastrophic fx occur

humane euth in advanced cases

117
Q

What is temporohyoid osteoarthropathy?

A

boney proliferation at junction of stylohyoid bone & petrous temporal bone

118
Q

What is potentially the progression of THO (temporohyoid osteoarthropathy)?

A

1 boney inflammation & remodelling
– exteion of otitis media, interna or upper resp tract infection, degnerative joint disease

  1. boney proliferation of tympanic bulla, prox stylohoid bone, petrous temporal bone

3 boney fracture of stylohyoid & petrous temporal bones

119
Q

What are neurologic C/S associated with temporohyoid osteoarthropathy?

A

facial & vestibular signs:
- ear droop, ptosis, muzzle deviation, nystagmus, collapse
**corneal ulceration (CN VII loss parasymp portion dec lacrimation)
-circling, ataxia, occasionally dysphagia

**rare: seizures, sudden death– fx extend into cranial vault

120
Q

What is stringhalt

A

condition of horses characterized by excessive and prolonged flexion of one or both hindlimbs during forward or backward movement

121
Q

What is the difference between classical and pasture associated stringhalt?

A

classical stringhalt involves only on behind limb, most often following injury to one dorsal tarsal/metatarsal region

pasture assoc stringhalt– exposure to plant-derived neurotoxin or neurotoxins

122
Q

Clinical signs of stringhalt are typically exacerbated when?

A

walking horse down slope or after a sudden stop or followign hard exercise

123
Q

What are differentials for stringhalt?

A

shivers
scandinavian knuckling dz (acq. equine polyneuropathy)
lathrysm
fibrotic myopathy
upward fixation of patella

124
Q

What nerves are typically affected in pasture associated stringhalt?

A

-larger nerves usu affected: tibial, deep & superficial peroneal recurrent laryngeal
**most changes seen in dorsal cricoarytenoid mm

125
Q

Is treatment necessary in pasture associated stringhalt cases?

A

Most horses resolve over 6 to 18 months

126
Q

With exercise testing what is indicative of exertional rhabdomyolysis?

A

-exercise 15 to 30 minutes

–> exertional rhabdomyolysis causes elevations in CK>5 fold

127
Q

Electromyography detects?

A

spontaneous or evoked potentials of neurogenic or myogenic origin using electrodes in the muscle
**useful when latered muscle tone

128
Q

What are abnormal electromyographic changes?

A

-fibrillation potentials, (sharp waves spontaneous firing of muscle fibers),
Myotonic discharges (bursts of complex high frequency potentials)
complex repetative discharges (fixed amplitude and frequency)

129
Q

What does a normal electromyography look like?

A

normal muscle shows little spontaenous electrical activity unless muscle contracts or horse moves

130
Q

What electrolyte abnormalities are seen with exhaustion in endurance hroses?

A

hypochloremic metabolic alkalosis with hypokalemia, hypomagnesemia, and low serum ionized calcium concentration

131
Q

Synchronous diaphragmatic flutter- the diaphgram contractions in synchroncy with

A

atrial depolarization

132
Q

Besides the low serum ionized calcium as a cause of synchronous diaphgramatic flutter, what is another cause?

A

disuprtion of the membrane potential of the phrenic nerve, which passes directly over the atrium, resulting in nerve discharges

133
Q

Which species of clostridium is most commonly seen during warmer seasons?

A

C. chauvoei

134
Q

Which species of clostridium is older in feedlot cattle?

A

C. sordelli

135
Q

What forms of rhabdomyolysis are seen with strep equi?

A

acute myonecrosis

infarctive purpura hemorrhagica

136
Q

Virus associated myopathy can be seen with which pathogens?
(myocarditis)

A

foot and mouth disease
equine influenza
equine infectious anemia

myocarditis or skeletal mm involvement: bovine ephemeral fever, malignant catarrhal fever, bovine viral diarrhea, bluetongue

137
Q

Sarcocystis cysts are commonly seen in what locations?

A

heart
esophageal
skeletal mm

138
Q

What are the definitive hosts of sarcocystis spp?

A

canidae/dogs

139
Q

Sarcocystis is difficult to differentiate from what other pathogen?

A

toxoplasma

140
Q

What is the treatment for sarcosystis?

A

pyremethamine, TMS–horses

amprolium or ionophores before second stage of parasitemia– cattle

141
Q

What is the prevention for nutritional myodegeneration?

A

selenium supplementation
OR
monitoring selenium levels in high risk areas every 60 to 90 days

142
Q

Masseter muscle myodegeneration can be seen in

A

adult horses with selenium deficiency– showing acute bilateral swelling of masseter muscles, trismus, dysphagia and salivation

143
Q

Vitamin E deficient myopathy resembles what disease? and what is the difference on muscle biopsy?

A

resembles EMND, but sacrocaudalis muscle lacks evident neurogenic atrophy
**contains moth-eaten staining pattern of mitochondria

144
Q

What two common toxic plants cause myonecrosis?

A

cassia spp & tremetone containing plants

145
Q

The myosin heavy chain mutation (MYH1) is associated with what genetic disease?

A

immune mediated myositis/nonexertional rhabdomyolysis

146
Q

Describe systemic calcinosis as a consequence of immune mediated myositis

A

cytokines activate RANKL, INC bone resorption leading to hyperphosphatemia
–>dystrophic calcification through passive calcium phosphate deposition (resulting in calcification of muscle fibers)

147
Q

ileocolonic agangliosis (lethal white foal syndrome) genetic mutation

A

endothelin receptor B gene (EDNRB) lcoation on chromsome 17

148
Q

ileocolonic agangliosis (lethal white foal syndrome) genetic mutation causes

A

abnormal dvelopment of enteric ganglia and metalnocytes within neural crest

149
Q

ileocolonic agangliosis (lethal white foal syndrome) genetic mutation is seen in what breeds?

A

american paints
QH
minis
rare thoroughbreds

150
Q

ileocolonic agangliosis (lethal white foal syndrome) genetic mutation on necropsy

A

constriction of distal small itnestine, complete abscesnce of intrinsic myenteric plexus o fdistal Si, cecum and colon and severely affected– ileum

151
Q

ileocolonic agangliosis (lethal white foal syndrome) genetic mutation, what is the cause of the white coat?

A

d/t absence of mealnocytes from the skin

152
Q

lavender foal s yndrome is a mutation in what gene?

A

myosin Va
(MYO5a)

153
Q

Lavender foal syndrome occurs in what breeds?

A

eqyptian lineage arabian neonates

154
Q

Lavender foal syndrome pathophysiology

A

Myo5a mutation impairs lading of myosin Va to organelles with appropriate receptors, leads to loss of vesicel traffic (melanosomes & dendritic cargo–> interferes with function of melanocytes and neurons

155
Q

cerebellar abiotrphy is seen in what horse breeds

A

arabian horses
** also reported in oldenburg, shetland pony, eriskay pony

156
Q

What is the gene mutation for cerebellar abiotrophy?

A

TOE1/MUTYH

157
Q

What is the MUTYH gene responsible for?

A

expression correspond to differential localization in Purkinje (mitochondrial) and granular neurons (nuclear) of the cerebellum

158
Q

What it the gene mutation leading to occipitoatlantoaxial malformations?

A

Hoxd3 (homeobox containing gene)

159
Q

What are the different reported forms of OAAM (occipitoatlantoaxial malformations)?

A
  1. Familial occipitalization of the atlas with atlantooccipital of axis in arabian hroses
  2. congenital assym OAAM non-arbain breeds
  3. asymm. atlantooccipital fusion
  4. duplication of axis and/or atlas
  5. symmetric ooam in non-Arabian horses
  6. subluxation of atlanto-occipital joint, fusion of atlas and axis with lateral deviation of atlantoaxial joint and rotation of atlas
160
Q

Hydrocephalus in fresians is seen in what gene mutation?

A

B3GALNT2

161
Q

What clinical signs are seen with equine neuroaxonal dystrophy/equien degnerative myeloncephalopathy (Enad/EDM)?

A

symmetric ataxia (more severe in pelvic limbs) varying degree of pelvic limb paresis, hypreflexia of cervicofacial and cutaneous trunci; absent laryngeal adductor reflex; stance abnoraml at rest; icnosistent menace; varyign degrees of obtundation; neuro abnoraml
**stablized by 2 to 3 years and remains stable
– typically Equine NAD & EDM not typically distinguishable

162
Q

Mode of inheritance of neuroaxonal dystrophy/equine degenerative myeloncephalopathy (Enad/EDM)?

A

strong evidence t hat inherited as an autosomal dominant or polygenic trait
** environmental effects– alpha tocopherol, received during early life, play a role in determine overall phenotype

163
Q

What is the difference between eNAD and EDM on spinal cord lesions?

A

eNAD: lesoins in gray matter only

EDM: lesion in Gray and WHITE matter

**clinically same disease

164
Q

Juvenile idopathic epilepsy is inherited via

A

autosomal dominant min arabian foals (egyptian)

165
Q

Sensory deafness in American Paint horses is caused by what gene mutation?

A

EDNRB
**suspected, additional research required

166
Q

What is the phenotype of American Paint horses with sensory deafness?

A

affected horses have extensive white facial markings and one or more blue irises

**assoc coat colors: splashed white overo and frame splashed white over breeds

167
Q

What is the pathophysiology of sensory deafness in american paint horses?

A

small population of melanocytes within the inner ear that are essential for the development of the stria vascularis–> blood vessel rich zone of cochlia that plays a role i n modulating the chemical composition of endolymph an resultant production of an endocochlear potential
**many spp congenital deafness assoc witha abnormal migraiton of these melanocytes from neural crest

168
Q

Fell immunodeficiency syndrome is due to what gene mutation?

A

SLCSA3

169
Q

Fell immunodeficiency syndrome occurs in what breeds?

A

fell and dale pony breeds

**freq of carriers: fell pony 39%, Dale ponies: 18%

170
Q

Fell immunodeficiency syndrome clinical presentation

A

born apparently healthy, then owithin first weeks of life develope C/S of dullness, weight loss and signs of ifnection (necrotizing entercolitis &/or bronchpneumonia, septicemia)

171
Q

What is seen on BW in Fell immunodeficiency syndrome?

A

profound non-regen anemia, B cell lymphoms and plasma cell depletion
**bone marrow problem

172
Q

What is the gene mutation resulting in severe combined immunodeficiency?

A

DNA-PKc
– dnadependent protein kinase catalytic subunit on chromosome 9

173
Q

severe combined immunodeficiency is seen in what breed?

A

arbian foals
**autosomal recessive

174
Q

severe combined immunodeficiency pathophysiology

A

–affects the development of B and T cells in male and female foals
–thymus– infiltrated by adipose tissue
–lymph nodes are hypocellular & lack germinal centers

175
Q

severe combined immunodeficiency syndrome bloodwork

A

foals have severe lymphopenia (<1000cells/uL)

176
Q

Common variable immunodeficiency syndrome is seen in what aged horses?

A

ave 10 years, range 2 to 23 years

177
Q

common variable immunodeficiency pathophysiology

A

B cell depletion caused by impaired B cell differentiation: sex dec in CVID affected horses when compared with healthy horses–> dvelpoment failiure in trnasion between pre-pro B cells and pro-B cells in bone marrow seems progresseive until total B cell depletion in secondary lymph tissues 7 blood

178
Q

What is seasonal pasture and atypical myopathy

A

highly fatal and acquired lipid storage myopathy

179
Q

seasonal pasture and atypical myopathy cause

A

Acer species tree seeds (box elder & ACer negudo and europen sycamore maple acer pseudoplatanus)

180
Q

seasonal pasture and atypical myopathy toxic metabolite

A

hypoglycin A– metabolized in liver to mCPA–> MCPA coA irreversibly binds to multiple acelCoA dhydrogenases (enzymes essential for metabolism of short and medium chain FA and branched chain aa)
–> accumulation of fat esters (damage to muscle cell membranes ) and iability to metabolize fat (energy deficiency)

181
Q

clinical signs of atypical myopathy

A

acute onset
muscle weakness
sweating
fasculation
stiffness
recumbency
tachycardia
tachypnea
collapse and death

Disorders of Muscle (3 decks)

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