-
what is a non-painful fluid accumulation in the carpus/hock often due to short stalls/improper bedding? treatment?
- hygroma
- do NOT stick needle in it- can introduce infection/refills anyway; leave it alone unless severe/causing problems
-
what is cow's stance with coxofemoral luxation?
- may or may not be down;
- if standing, luxated leg held back and hip rotated out
-
When evaluating coxofemoral luxation, what are the 3 landmarks you look at for refence? how lame do you expect this cow to be?
- tuber coxae, tuber sacrale and greater trochanter of femur
- 3 or 4 out of 5 lameness
-
for hip luxation, is prognosis better in adult or young? what are tx options?
- better for young; Ehmer sling and stall confinement
- adults recur often
-
In small ruminant with cervical injury, what are limb reflexes usually like? Is sensation still intact usually?
- hind limb reflexes and sensation intact
- limb tone normal or reduced
-
what are the 3 forms of septic arthritis?
- primary: direct puncture
- secondary: infection extends into joint (foot rot)
- tertiary: septicemia (umbilical infection, etc)
-
What is common bacterial isolate in feedlots with septic arthritis? What about Dairy? What will be isolated in nearly all cases with established abscesses?
- feedlot: histophilus somni (shipping fever/pneumonia)
- dairy:mycoplasma (from mastitis)
- established abscess: archanobacterium pyogenes
-
What is the isolate from septic arthritis in sheep? what are 2 other conditions associated with this?
- Chlamydophila pecorum
- KCS and abortion
-
failure of passive transfer is often involved with septic arthritis. How do you test for this? What values indicate failure?
- check total protein in adequately hydrated pt
- 4.5-5 is not good; less 4.5 is complete failure
-
with joint fluid analysis, what results tell you the joint is infected?
- bacteria present (do culture!)
- nucleated cell count >10,000 w/80% neutrophils
- TP >4mg/dl
- (radiographic changes will NOT be visible for 2-3 weeks!)
-
what is tx for septic arthritis?
- systemic Abs based on culture
- joint lavage (only helps if early)
- NSAIDs
- correct sepsis if present
-
what disease is characterized by poor confirmation/strait hocks and deterioration of joint cartilage? How does this affect breeding?
- degenerative joint disease
- should not allow animal to mount, change to AI methods
-
what deficiency is associated with rickets? who is affected?
- phosphorus +/- vit. D deficiency
- osteodystrophy in young, growing; esp. crias in northern hemisphere
-
what are classical findings for rickets in crias? What about on radiographs?
- decreased rate of gain
- "string of pearls" on costochondral junction
- stiff/lame
- enlarged joints/curved limbs
- rads: wide distal physes; metaphysis may be cupped
-
how do you treat rickets?
- injectable vit D for tx (oral for prevention)
- adequate dietary Ca/P
- can supplement dam so colostrum is high in Vit. D
-
what is arthrogryposis? Beef or dairy? what is the cause?
- congenital disease w/flexural deformities - results in dystocia
- Beef breeds
- from blue tongue virus, lupine alkaloids, genetic in charlois
- humanely euthanize
-
how do you treat contracted tendons?
splinting is often successful
-
What is the common name for ovine hereditary chondrodysplasia? what breed is affected by this autosomal recessive trait?
- Spider Lamb syndrome
- Suffolk sheep
-
what is appearance of sheep with spider lamb syndrome? how is this managed?
- knock kneed w/kyphosis
- cull carrier rams
-
What type of virus is caprine arthritis encephalitis? what cells does it infect? Where do these cells localize to?
- lentivirus/retrovirus
- macrophages
- mammary gland, lungs, CNS, synovium
-
how do goats get CAE?
through dam's colostrum/milk - viremic for life
-
leukoencephalomyelitis is the rare manifestation of CAE. What age are affected goats? what is presentation?
- young 2-6 mos
- rear leg paresis/paralysis
- neuro signs and interstitial pneumonia
-
polysynovitis is the more common form of CAE. what age are affected goats? what is presentation?
- adults; >6mos
- walk on carpal jt (hyperplasia of synovium)
- hard utter but normal (decreased) milk
- wt loss
-
other than neuro and arthritis, what are two other forms of CAE?
- mastitis
- interstitial pneumonia ("wasting away")
-
What does it mean if AGID test for CAE is positive?
exposure but not necessarily infected
-
what is tx for CAE? what is important prevention methods?
- symptomatic only
- cull or segregate infected dams; do not let young ingest colostrum from infected dam/can pasteurize
-
How does half life of CK compare to AST?
- CK rises quickly and drops quickly; T1/2 of 2hours
- AST slower to rise and stays longer; T1/2 of 7-10days
-
AST is not specific for myonecrosis because it comes from what other sources?
- skeletal muscle
- cardiac muscle
- liver
- RBCs
-
what does it mean to have elevated AST with decreasing(from previous sample)/normal CK?
resolving myonecrosis
-
nutritional myodegeneration is due to deficiency of what?
White Muscle Disease = deficiency in *Selenium* (and Vit. E)
-
Selenium is a component of what anti-oxidant?
glutathione peroxidase (can test for this)
-
What are the two major forms of nutritional myodegeneration? which is slow onset vs. acute presentation? which form produces frothy nasal discharge?
- cardiac: acute death w/frothy nasal discharge
- skeletal: slower onset, stiff limbs/muscle pain
-
why is pneumonia a common clinical sign associated with white muscle disease?
young can't suckle due to dysfunction of pharyngeal muscles and tongue-- aspiration pneumonia
-
Is it more important to measure selenium or Vit. E levels if you suspect white muscle disease?
- selenium (and glutathione peroxidase)
- vit. E not consistent
-
is myoglobinuria more likely to be present in younger or more mature animals that present with white muscle disease?
- older
- (babies don't have enough muscle mass to develop myoglobinuria)
-
what is zanker's necrosis?
white lines in heart/skeletal muscle w/white muscle disease
-
How do you treat white muscle disease/nutritional myodegeneration?
- injectable Selenium + fluid diuresis (myoglobinu is renal toxin)
- cardiac form doesn't respond to tx
-
what is causative agent for Black Leg? where does this agent exist?
- clostridium chauvoei (G+ anaerobe)
- found in soil and GI of ruminants
-
what is clinical sign of black leg?
- gangrenous myositis following IM injection, trauma, migration from GI
- crepitus, fever, sudden death
-
what would necropsy of black leg reveal?
- linear hemorrages in affected muscles
- necrosis, inflammation/edema, ephysema
-
how is black leg treated?
- debride/open muscle to stop anaerobic environment
- Penicillin (drug of choice for clostridium)
- supportive care
- (feed lots can't go to slaughter with open wounds, euthanize)
-
Is there a vaccine for black leg?
- yes, a good one/efficacious
- multivalent, requires boosters
-
what is causative agent of malignant edema? how do animals become infected?
- clostridium septicum
- in soil - through open wound
- (especially after dystocia - fecal contamination)
-
what are clinical signs for malignant edema?
- wet, doughy swelling around wound, usually goes down one leg
- fever, anorexic,
- death in 1-2 days
-
what is treatment and prevention for malignant edema?
- same vx as for black leg (multivalent clostridum vx)
- Penicillin + debride + supportive care
|
|