Misc muscle Flashcards
What are examples of random specific causes of hard tissue swellings in ruminants?
chronic flourosis
CAE
Nutritional osteodystorophy (def in Cu, Ca & Phosph)
Lumpy Jaw (actinomycosis)
Examples of bilateral pelvic limb paresis
congenital
EPM
trauma
thrombosis
infection
Examples of tetraparesis
botulism
polyneuropathies
polymyopathies
Examples of metabolic causes of paresis/weakness in horses?
hypothyroidism
hyperthermia
hepatic lipidosis
Vit A def
Exampels of plant poisons that cause paresis/weakness in horses?
starthistle poisoning
oleander
moldy corn poisoning
white snake root
locoweek
larkspur
delphinium
onion
moldy sweet clover
What are anomalous/congenital causes of paresis/weakness in ruminants?
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
What are infectious/inflammatory causes of paresis/weakness in ruminants?
BSE
tick paralysis
botulism
rabies
pneuomnia
spinal abscess
Parelaphostrongylus tenuis
What are exampels of muscle spasms/myoclonus in horses?
myotonia congenita
HYPP
Insulinoma
Tetanus, rabies, equine influenza, tick-borne encephalitis, meningitis
Toxic: strychnine, organochlories, chlorinated hydrocarbons
Define physitis (epiphysitis)
disturbance in enochodnral ossification at physis
What are causes of physitis in horses?
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
At what age is physitis typically seen (age and location)?
3 to 6 moths: distal metacarpal/metatarsal
8-24 months: distal radius
Define osteochndrosis
failure of defect in endochondral ossification–> cartilage flaps, fragments, subchondral bone cysts
What is the most common inheritable skeletal disorder in sheep?
ovine hereditary chondrodysplasia (spider lamb syndrome)
What clinical signs are seen with ovine hereditary chondrodysplasia (spider lamb syndrome)?
–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
What species of sheep is ovine hereditary chondrodysplasia (spider lamb syndrome) seen in?
suffolk/hampshire lambs
DDX for ovine hereditary chondrodysplasia (spider lamb syndrome)
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
Hematogenous spread of septic arthritis is most common in?
foals (young)
extension of periarticular wound as a cause of septic arthritis is most common in?
adults
What are risk factors for the development of septic arthritis in calves?
FPT
septicemia
feeding mastitis milk (mycoplasma)
What are the most common bacterial isolates in septic arthritis in foals?
actinobacillus equuli
Salmonella
E coli
other enterobacteriaceae
What are the most common bacterial isolates in septic arthritis in older foals?
streptococcus
rhodococcus
What are the most common bacterial isolates in septic arthritis in adult horses?
enterobacteriaceae
streptococci
staphylococci
What are the most common bacterial isolates in septic arthritis in calves?
streptococcus
mycoplasma bovis
What are the most common bacterial isolates in septic arthritis in cattle
mycoplasma bovigenitalium
mycoplasma mycoides
brucella
t pyognes
In cattle what nutritional compounds are implicated in physisits?
Copper deficiency– interactions molybdenum, zinc and sulfates
Copper deficiency causes physitis through what pathophysiologic mechanism?
Cu required for crosslinking of collagen– when deficient cartilage matrix weakens, microfractures occur
If mares milk is low in copper (naturally), where do foals get their appropriate cu nutrition?
foals rely on hepatic Cu stores gained in last trimester of gestation
What are the treatment recommendations for foals with physitis?
1 nutrition- proper mineral balance & reduction of energy
2. exercise restriction: stall rest
angular limb deformities occur due to?
- laxity of periarticular supporting structures
- incomplete ossification
3 asynchronous physeal growth
incomplete ossification is common in what cuboidal bones?
Carpus: ulnar, third & fourth
Tarsus: central and third
When does normal ossification of cuboidal bones occur?
in the 3rd trimester
What endocrinopathy is thought to contribute to angular limb deformities?
hypothyroidism (rare)
— maternal influences– excessive/inadequate dietary iodine intake
– unknown cause in NW US
List pathophysiologic mechanisms behind angular limb deformities
- incomplete ossification
- asynchornous growth (d/t trauma or severe lamness)
- osteochondrosis/abnorm growth cartilage
- hypothyroidism (rare)
What dietary imbalances are seen in calves raised in confinement that predispose to angular limb deformities?
High dietary Fe
low dietary Vit D
What are radiographic signs of asynchronous growth?
wedging of epiphysis
widening of physis
sclerosis adjacent to the physis
What are 2 mechanisms for sx correction of angular limb deformities?
- growth retardation: bridge physis with metallic implants
- alter physeal growth: periosteal transection & elevation (stripping)
What is the mode of inheritance of spider lamb syndrome?
autosomal recessive
The genetic abnormalities in spide lamb syndrome results in what abnormal protein function?
ovine fibroblast growth factor receptor 3
What is the causative organism of contagious agalactiae in kids and goats?
mycoplasma p spp–
M mycoides subsp capri (most common in US)
M agalactiae in mediterranean countires
Where can kids/goats be samples for diagnosis of contagious agalactiae for asymptomatic carrier animals?
ear
**M mycoides subsp capri
What are DDX for agalactia/mastitis in goats?
environmental coliforms
S auerus
fungal organisms
caprine arthritis encephalitis virus
**Mycoplasma mycoides subsp capri– can colonize reprot ract– abortions/DEC repro performance
What are C/S seen in goat kids with contagious agalactiae?
**M mycoides subsp capri
initial signs: fever, lethargy, anorexia, weakness
Following bacteremia: polyarthritis– carpal & tarsal joints most common that are warm/swollen; keratoconjuncitivitis and pneumonia
how are kids infected with M mycoides subsp capri?
infected milk/colostrum from doe
or supplemented bovine milk with M. bovis
How is M mycoides subsp capri transmitted?
oral & nasal secretions
contaminated milk equipment
How is M mycoides subsp capri introduced into a herd?
through an asymptomatic carrier
Treatment options for M mycoides subsp capri?
tetracyclines
flouroquinolones
macrolides
florfenicol
antimicrobials that disrupt the cell wall synthesis are ineffective
What are forms of disease caused by caprine arthritis encephalitis virus (CAEV)?
- leukocenphalomyelitis
- interstitial pneumonia
- chronic mastitis
- debilitating polysnovitis arthritis
Leukoencephalomalacia caused by caprine arthritis encephalitis virus (CAEV) is observed primarily in what age kids?
2 to 6 months of age
caprine arthritis encephalitis virus (CAEV) clinical signs (leukoencephalomalacia)?
ascending paresis leading to paralysis beginning in rear limbs
**severe manifestation– progression of paresis to paralysis to urinary retention & bloat
What are DDX for the leukoencaphlomalacia form of caprine arthritis encephalitis virus (CAEV)?
meningitis
meningeal worm
trauma
Polysynovitis-arthritis caused by caprine arthritis encephalitis virus (CAEV) typically manifests in what age groups?
mature goats most commonly
**reported in goats as young as 6 months
**carpus most commonly affected but can be any joints
caprine arthritis encephalitis virus (CAEV) polysynovitis-arthritis pain is due to?
joint enlargement– d/t hyperplasia of synovial tissues
What is differentiating in joint fluid in septic arthritis in comparison to caprine arthritis encephalitis virus (CAEV) polysynovitis?
CAEV: primarily mononuclear cells
**differes from bact synovitis– predom neuts
A positive caprine arthritis encephalitis virus (CAEV) AGID/ELISA is synonymous with
lifelong viral infection
What are preventative measures that can be performed to prevent the spread of caprine arthritis encephalitis virus (CAEV)?
-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
What are the 2 major factors that lead to the development of osteoarthritis?
- mechanical load
- tissue turnover or metabolism
what are radiographic changes of OA?
-loss of joint space
-subchondral bone sclerosis
-subchondral cystic lesions
-periarticular osteophytes
-periosteal new bone formation @ sites of joint capsules & ligamentus attachments (enthesophytes)
What is the most common congenital abnormalities in cattle?
arthrogyrposis
What are causes of arthrogyrposis (in general)?
- genetic
- infectious
- toxic
What are congenital causes of arthrogyrposis in ruminants?
Charolais calves & Holstein: forelimb arthrogyrposis, spinal dwarfism, cleft palate
Curly calf syndrome (arthrogyrposis multiplex): autosomal recessive defect, angus cattle, kyphoscoliosis, dec muscling
Congenital arthrogyrposis in horses is seen in what breeds?
norweigan fjords
thoroughbred foals
Congenital arthrogyrposis is seen in what breeds of sheep?
suffolk
coffiedale sheep
What are infectious causes of arthrogyrposis?
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
List toxic causes of arthrogyrposis
alkaloids in pregnant animals (conium, lupinus, nicotiania)
lupine tox– “crooked calf syndrome”
sorghum pastures
vetrum californicum (d29 gestation in sheep)
define ankylosis
abnormal fusion of bones in a joint
What clin path finding is associated with osteomyelitis in foals?
fibrinogen >900 mg/dL
define spondylitis
inflammation of vertebral body
define diskospongylitis
inflamm. lesion including intervertebral disc & its adjacent vertebrae
What is the primary cause in pathogenesis of spondylitis/diskospondylitis?
Foals>adults
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
Adult pathogenesis of spondylitis/diskospondylitis?
direct injury to invertebral disc &/or vertebral end plate
Define spondylosis
ankylosing or degenerative condition of intervetebral joints
Bilateral rear limb lameness & paresis is seen in bulls in the artificial insemination industry due to
calcification fo thoracolumbar vertebrae & ligaments
+/- fusion of lu mbar vertebrae
***posterior spinal paresis syndrome
What are differentials for cattle with hind limb neuro deficits?
lymphosarcoma
encephalopathy
progressive degenerative myeloencaphlopathy
downer cow syndrome
posterior spinal paresis syndrome
What are disease states that are associated with laminitis
-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
What is the obel lameness grades for laminitis
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
What are the experimental models for the induction of laminitis?
-carb overload
-fructan overload
-black walnut extract admin
-hyperinsulinemic
What are radiographic measurements that are indicative of laminitis?
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
In acute fluorosis toxicosis where are levels measurable?
high concentrations in plasma & urine in acute toxicosis
What C/S are seen with acute flouride toxicosis?
restlessness
agalactia
salivation
vomiting/regurge
severe depression
urinary incontinence
diarrhea (GI mucosal necrosis)
clonic convulsions
cardiac failure
What are common sources of excess flouride ?
- water w/ naturally high flouride content
- forages contam with flourides from nearby (upwind industrial plants)
- mineral sources & feed supplements with excess flouride content
- forages contam by soil or water
- volcanic activity– deposit flouride containing ash on soil/plants/water/etc.
Chronic flouride toxicosis commonly manifests as:
-dental fourosis or osteoflourosis– developing teeth ar v sensitive to ingeston of excess flourides
What changes are seen with chronic flouride toxicosis?
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
Hypertrophic osteopathy (Maries Dz) in horses is characterized by:
symmetric proliferation of connective tissue and subperiosteal bone along disphyses & metaphyses of bones of distal extremities
What is the pathogenesis of Hypertrophic osteopathy (Maries Dz)?
Unknown
treatment of Hypertrophic osteopathy (Maries Dz):
– treat underlying disease process
**reports of regression with rest, bute and corticosteroid therapy
What is the cause of fescue foot?
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
Clinical signs of the fescue foot occur within what time frame?
w/in 42 days of exposure to endophyte infected fescue
What are clinical signs of fescue foot?
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
DDX for fescue foot
ergotism-claviceps purpurea
seleium tox
salmonellosis
frost bite
sarcocystis– in cattle assoc with loss of tail
**early stages: traumatic injury, laminitis, foot rot
What are treatment recommendations for fescue foot?
-remove from pasture
-necrosis: occurs– tx unrewarding, euth. recommended
early cases: supportive therapy, soft ground, NSAIDS, +/- systemic/local antibiotics
Which animals are at high risk for the development of interdigital necrobacillosis (foot rot) in cattle?
-housed in moist, muddy lots
-pastures with standing water
-areas where sharp gravel, concrete or stubble
What bacteria is most commonly associated with foot rot?
fusopbacterium necrophorum– gran neg anaerobe
Other bacteria: Prevotella melaniogenica, porphyromonas levii, Dichelobacter nodosus
What are differentials for interdigital necrobacillosis (foot rot)?
septic arthritis
sole abscess
tenosynovitis
pedal osteitis
interdigital fibroma
laminitis
trauma
What are virulence factors for F. necrophorum?
- high molecular weight leukotoxin, cytotoxic to ruminant neuts, comb with LPS prevents phagocytosis
- LPS
What type of F. necrophorum is commonly isolated in cases of foot rot?
biotype A– more virulent & freq isolated
biotype B
What allows for bacteria to cause interdigital necrobacillosis (foot rot)?
-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
What are antibiotics labelled for foot rot?
oxytet
florfenicol
cetfiofur
tylosin
sulfadimethoxine
tulathromycin
What are recommendations for control and prevention of interdigital necrobacillosis (foot rot)?
-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
What are the two organisms implicated in infectious foot rot in small ruminants?
- Dichelobacter nodosus (obligated parasite of the foot)
- fusobacterium necrophorum
How to differentiate infectious foot rot in small ruminants from contagious ovine digital dermatitis (CODD)?
-low prevalence in US
-severe lameness
-undermining of hoof wall at coronary band–> avulsion of hoof capsule
causative agent: treponema bacteria
How to confirm foot rot (from contagious ovine digital dermatitis)?
culture: D nodosus– challenging d/t fastidious nature of bact.
real time PCR: poor dx specificity
treatment of infectious foot rot in small ruminants
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
Deep penetrating injuries to sole can potentially communicate with:
-navicular bursa
-digital tendon and sheath
-DDFT
-distal phalanx
What is thrush?
bacterial infection characterized by accumulation of black, malodorous necrotic material originating from frog of hoof
What is the most common bacteria associated with thrush?
fusobacterium necrophorum
What are clinical signs of thrush?
variable lameness
-black malodorous d/c, most often from frog sulci
-pain on palpation/manipulation of frog– caudal heel pain
What is white line disease?
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
What is Quittor?
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
What is fistulous withers?
chronic ifnlammatory condition of supraspinous burse & assoc tissues seen in horses, mules &donkeys
What are the two forms of fistulous withers and what bacterial are involved?
- Idiopathic form (more common)– Brucella abortus; O cervicalis
- Traumatic form- 2ndary infection with environ contam or hematogenous spread to devilatlized tissue (ie. strep equi subsp zoo)
What are findings of culture of fistulus withers for Brucella abortus?
B. abortus is difficult to grow in culture & easily overgrown by other bacteria– negative c ulture is misleading
What is the treatment recommendations for fistulus withers?
**med management not successful alone–> comb of aggressive sx debridement
-antimicrobials
-lavage of draining tracts
-stemtic anti-inflamm
-application of maggots
Silicate associated osteoporosis (bone fragility syndrome) geographic distribution is:
-monterey carmel peninsula california
–sonoma & Napa counties
What are clinical signs of silicate associated osteoporosis (bone fragility syndrome)?
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
treatment of silicate associated osteoporosis (bone fragility syndrome)?
palliative & aimed at dec inflammation & osteoclastic bone resorption
-bisphosphonates, exercise restriction, NSAIDS, moving horses (may not halt prgoression of C/S)
prognosis for silicate associated osteoporosis (bone fragility syndrome)
fair- early stages, risk of dec bone strength
guarded to poor: athletic use not reocmmended, common catastrophic fx occur
humane euth in advanced cases
What is temporohyoid osteoarthropathy?
boney proliferation at junction of stylohyoid bone & petrous temporal bone
What is potentially the progression of THO (temporohyoid osteoarthropathy)?
1 boney inflammation & remodelling
– exteion of otitis media, interna or upper resp tract infection, degnerative joint disease
- boney proliferation of tympanic bulla, prox stylohoid bone, petrous temporal bone
3 boney fracture of stylohyoid & petrous temporal bones
What are neurologic C/S associated with temporohyoid osteoarthropathy?
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
What is stringhalt
condition of horses characterized by excessive and prolonged flexion of one or both hindlimbs during forward or backward movement
What is the difference between classical and pasture associated stringhalt?
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
Clinical signs of stringhalt are typically exacerbated when?
walking horse down slope or after a sudden stop or followign hard exercise
What are differentials for stringhalt?
shivers
scandinavian knuckling dz (acq. equine polyneuropathy)
lathrysm
fibrotic myopathy
upward fixation of patella
What nerves are typically affected in pasture associated stringhalt?
-larger nerves usu affected: tibial, deep & superficial peroneal recurrent laryngeal
**most changes seen in dorsal cricoarytenoid mm
Is treatment necessary in pasture associated stringhalt cases?
Most horses resolve over 6 to 18 months
With exercise testing what is indicative of exertional rhabdomyolysis?
-exercise 15 to 30 minutes
–> exertional rhabdomyolysis causes elevations in CK>5 fold
Electromyography detects?
spontaneous or evoked potentials of neurogenic or myogenic origin using electrodes in the muscle
**useful when latered muscle tone
What are abnormal electromyographic changes?
-fibrillation potentials, (sharp waves spontaneous firing of muscle fibers),
Myotonic discharges (bursts of complex high frequency potentials)
complex repetative discharges (fixed amplitude and frequency)
What does a normal electromyography look like?
normal muscle shows little spontaenous electrical activity unless muscle contracts or horse moves
What electrolyte abnormalities are seen with exhaustion in endurance hroses?
hypochloremic metabolic alkalosis with hypokalemia, hypomagnesemia, and low serum ionized calcium concentration
Synchronous diaphragmatic flutter- the diaphgram contractions in synchroncy with
atrial depolarization
Besides the low serum ionized calcium as a cause of synchronous diaphgramatic flutter, what is another cause?
disuprtion of the membrane potential of the phrenic nerve, which passes directly over the atrium, resulting in nerve discharges
Which species of clostridium is most commonly seen during warmer seasons?
C. chauvoei
Which species of clostridium is older in feedlot cattle?
C. sordelli
What forms of rhabdomyolysis are seen with strep equi?
acute myonecrosis
infarctive purpura hemorrhagica
Virus associated myopathy can be seen with which pathogens?
(myocarditis)
foot and mouth disease
equine influenza
equine infectious anemia
myocarditis or skeletal mm involvement: bovine ephemeral fever, malignant catarrhal fever, bovine viral diarrhea, bluetongue
Sarcocystis cysts are commonly seen in what locations?
heart
esophageal
skeletal mm
What are the definitive hosts of sarcocystis spp?
canidae/dogs
Sarcocystis is difficult to differentiate from what other pathogen?
toxoplasma
What is the treatment for sarcosystis?
pyremethamine, TMS–horses
amprolium or ionophores before second stage of parasitemia– cattle
What is the prevention for nutritional myodegeneration?
selenium supplementation
OR
monitoring selenium levels in high risk areas every 60 to 90 days
Masseter muscle myodegeneration can be seen in
adult horses with selenium deficiency– showing acute bilateral swelling of masseter muscles, trismus, dysphagia and salivation
Vitamin E deficient myopathy resembles what disease? and what is the difference on muscle biopsy?
resembles EMND, but sacrocaudalis muscle lacks evident neurogenic atrophy
**contains moth-eaten staining pattern of mitochondria
What two common toxic plants cause myonecrosis?
cassia spp & tremetone containing plants
The myosin heavy chain mutation (MYH1) is associated with what genetic disease?
immune mediated myositis/nonexertional rhabdomyolysis
Describe systemic calcinosis as a consequence of immune mediated myositis
cytokines activate RANKL, INC bone resorption leading to hyperphosphatemia
–>dystrophic calcification through passive calcium phosphate deposition (resulting in calcification of muscle fibers)
ileocolonic agangliosis (lethal white foal syndrome) genetic mutation
endothelin receptor B gene (EDNRB) lcoation on chromsome 17
ileocolonic agangliosis (lethal white foal syndrome) genetic mutation causes
abnormal dvelopment of enteric ganglia and metalnocytes within neural crest
ileocolonic agangliosis (lethal white foal syndrome) genetic mutation is seen in what breeds?
american paints
QH
minis
rare thoroughbreds
ileocolonic agangliosis (lethal white foal syndrome) genetic mutation on necropsy
constriction of distal small itnestine, complete abscesnce of intrinsic myenteric plexus o fdistal Si, cecum and colon and severely affected– ileum
ileocolonic agangliosis (lethal white foal syndrome) genetic mutation, what is the cause of the white coat?
d/t absence of mealnocytes from the skin
lavender foal s yndrome is a mutation in what gene?
myosin Va
(MYO5a)
Lavender foal syndrome occurs in what breeds?
eqyptian lineage arabian neonates
Lavender foal syndrome pathophysiology
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
cerebellar abiotrphy is seen in what horse breeds
arabian horses
** also reported in oldenburg, shetland pony, eriskay pony
What is the gene mutation for cerebellar abiotrophy?
TOE1/MUTYH
What is the MUTYH gene responsible for?
expression correspond to differential localization in Purkinje (mitochondrial) and granular neurons (nuclear) of the cerebellum
What it the gene mutation leading to occipitoatlantoaxial malformations?
Hoxd3 (homeobox containing gene)
What are the different reported forms of OAAM (occipitoatlantoaxial malformations)?
- Familial occipitalization of the atlas with atlantooccipital of axis in arabian hroses
- congenital assym OAAM non-arbain breeds
- asymm. atlantooccipital fusion
- duplication of axis and/or atlas
- symmetric ooam in non-Arabian horses
- subluxation of atlanto-occipital joint, fusion of atlas and axis with lateral deviation of atlantoaxial joint and rotation of atlas
Hydrocephalus in fresians is seen in what gene mutation?
B3GALNT2
What clinical signs are seen with equine neuroaxonal dystrophy/equien degnerative myeloncephalopathy (Enad/EDM)?
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
Mode of inheritance of neuroaxonal dystrophy/equine degenerative myeloncephalopathy (Enad/EDM)?
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
What is the difference between eNAD and EDM on spinal cord lesions?
eNAD: lesoins in gray matter only
EDM: lesion in Gray and WHITE matter
**clinically same disease
Juvenile idopathic epilepsy is inherited via
autosomal dominant min arabian foals (egyptian)
Sensory deafness in American Paint horses is caused by what gene mutation?
EDNRB
**suspected, additional research required
What is the phenotype of American Paint horses with sensory deafness?
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
What is the pathophysiology of sensory deafness in american paint horses?
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
Fell immunodeficiency syndrome is due to what gene mutation?
SLCSA3
Fell immunodeficiency syndrome occurs in what breeds?
fell and dale pony breeds
**freq of carriers: fell pony 39%, Dale ponies: 18%
Fell immunodeficiency syndrome clinical presentation
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)
What is seen on BW in Fell immunodeficiency syndrome?
profound non-regen anemia, B cell lymphoms and plasma cell depletion
**bone marrow problem
What is the gene mutation resulting in severe combined immunodeficiency?
DNA-PKc
– dnadependent protein kinase catalytic subunit on chromosome 9
severe combined immunodeficiency is seen in what breed?
arbian foals
**autosomal recessive
severe combined immunodeficiency pathophysiology
–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
severe combined immunodeficiency syndrome bloodwork
foals have severe lymphopenia (<1000cells/uL)
Common variable immunodeficiency syndrome is seen in what aged horses?
ave 10 years, range 2 to 23 years
common variable immunodeficiency pathophysiology
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
What is seasonal pasture and atypical myopathy
highly fatal and acquired lipid storage myopathy
seasonal pasture and atypical myopathy cause
Acer species tree seeds (box elder & ACer negudo and europen sycamore maple acer pseudoplatanus)
seasonal pasture and atypical myopathy toxic metabolite
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)
clinical signs of atypical myopathy
acute onset
muscle weakness
sweating
fasculation
stiffness
recumbency
tachycardia
tachypnea
collapse and death
