LAM 3 Midterm 1 Flashcards
What feedlot changes lead to lameness?
high energy diet + substrate changes - lameness
Where does 90% of dairy cow lameness occur?
rear limb lateral claw
What is the most common lesion associated with sheep lameness?
interdigital space lesions
How will cattle stand if they have lameness in their lateral digit?
base wide stance
How will cattle stand when they have medial claw lameness?
base narrow or limbs are crossed
What are the 3 synovial structures in the ruminant foot
Distan Inter tarsal Joint
Navicular Bursa
Flexor tendon sheath
What is graveling?
deep foot infection has to migrate to release the pressure at which tends to occur at the soft tissue planes
What is the role of the Periolic coria?
it is a moisture barrier to underlying coria
What spirochete is responsible for 50-70% of bovine lameness in the U.S?
Treponema
they live deep in the epidermis and create inflammation
What is considered the dirtiest foot zone + why
zone 0 because spray cleaners don’t reach between the claws
What are clinical signs of mild irritation of the interdigital skin (zone 0)?
small, red ulcers
mild swelling + pain
undermine heel: seperate perioplic corium from the underlying horn of the bulb
What do the cs related to mild irritation of the interdigital skin lead to?
overgrowth of the heel resulting in increased heel weight-bearing + concussive injury = rusterholz ulcer
What is the proper term that is commonly referred to as “foot rot”?
interdigital dermatitis
What bacteria are commonly involved in interdigital dermatitis?
Fuscobacterium +/- dichelobacter or porphoromonas
Define the pathology found in interdigital dermatitis
skin break caused by deep necrosis
What is super foot rot?
necrotizing, penicillin resistant necrobacillosis of the foot
What is the name of the disease condition associate with 80% of all lameness in sheep?
interdigital dermatitis (foot rot)
What are some cs + findings of interdigital dermatitis in sheep?
often malodorous
walk on their carpi (if forelimb disease)
Fuscobacterium + Dichelobacter
What are the 3 phases of digital dermatitis
heel ulcers
strawberry foot rot
hairy heel warts or “mortellaro”
Describe the “heel ulcer” phase of digital dermatitis
circumscribed erosion/ulcer on border of plantar commissure, or at skin horn jxn, near the declaws (zone 10) or interdigital space
Describe the strawberry foot rot phase of digital dermatitis
ulcer fills in with granulation tissue
Describe the hairy heel wart phase of digital dermatitis
papillomatous growth
As chronicity increases, granulation tissue toughens up + frong like growths can occur
What microbe is responsible for causing digital dermatitis
Tremonema spp.
spirochete in the skin leads to irritation then erythema and inflammation + skin breaks resulting in ulcers
What happens when tremonema enters a herd?
epizootics of foot problems and after the adult cows develop partial immunity + mild lesions but if new heifers are introduced they still get severe disease
Describe the progression of Contagious ovine digital dermatitis when it spreads through a herd
it starts at the coronary band and leads to underrunning and sloughing of hooves
Treponema related, spreads via new additions to flocks
What is interdigital hyperplasia + what are the lay terms for it
chronic irritation leads to hyperplastic tissue growth which may become ulcerated
usually secondary to another lesion
lay terms: fibroma or corn
What is interdigital hyperplasia an indicator of?
that there was a breakdown of the cruciate ligaments that are responsible for keeping the digits together
Describe the general treatment plan for soft tissue lesions
- clean foot w/ disinfectant scrubs
- Debride/resect necrotic or proliferative tissue
(be conservative around dorsal commissure) - Sterilize open wounds:
-foot baths, topical disinfectants, +/- topical antibiotics (extralabel use)
4.) Deep infections- systemic anbx
5.) consider bandages/ wires
6.) corrective trimming of contributory hoof lesions
7.) decreased the 4 M’s
What topical anbx would you consider for treponema?
tetracycline
linomycin
spectinomycin
If a patient has a deep infection caused by a soft tissue lesion, what drugs would you consider?
penicillins or sulfas for most
if “super foot rot” oxytetracycline
consider tilmicosin for digital dermatitis
What preventative measures can be taken to prevent ST lesions
adequate draining or lime absorbants
manure scrapings
straw bedding
even atraumatic surfaces
limit puddles +snoes
decrease udder hosing
foot baths regularly
regularly trim hooves
What are the 3 main areas that excessive horn growth tends to occur?
toe, abaxial wall, heel
What sequelae can occur when excessive toe growth is present
straining of the flexor tendons
movement of weight to the heel, splayed toes
What sequelae can occur when there is excessive growth at the abaxial wall ?
can strain the cruciate ligament and splays the claws
What sequelae can occur when there is excessive growth at the heel?
weight is moved to the heel which increases risk of concussive injury
a wide heel traps material in ID space
What can be seen when there is laminitis of the coria that makes up the wall? (coronary coria)
the wall will develop horizontal cracks aka “hardship grooves”
exacerbated by long toes
lever action can put pressure on coria
you can determine how long ago the insult occurred based on how far down the hoof wall it is
Describe the lesion that develops secondary to interrupted growth at the sole or heel
“Double Sole” : Anerobic pocket for bacteria that develops when the horn stops growing then restarts growing
What does white line seperation secondary to interrupted growth allow for?
abscess development
What does interrupted growth at the heel cause?
seperation from the skin known as an “underrun heel” that allows bacterial invasion
What changes does laminitis aka pododermatitis aseptica et diffusa cause to the horn when abnormal horn growth has occurred?
Horn becomes soft, bloody and mealy
it allows for bacterial invasion
no longer protects the soft tissue
When is the most common time we see hardship grooves in cattle?
1-3 months post partum
What are some genetically induced horn lesions in ruminants
screw claw
poor hoof confirmation or quality
What is laminitis induced compartment syndrome
edema + hemorrhage between hoof + bone
T or false: Horn lesions may promote ST lesions lesions and ST lesions may affect the adjacent corium
True! Bad horn lesions can do this
What do most horn problems result from?
abnormal production
this is secondary to diseases of of the corium/ laminae = laminitis
Problems of the ____ are most viable but problems on the ___ are most important
Wall; sole
Where do abscesses like to commonly occur in beef cows?
along the white line
near the toe (zone 1)
Where do abscesses like to occur in dairy cows?
along the white line
the lateral wall near the caudal sole
Why is ventral drainage of abscesses so important?
no ventral drainage means that infections will travel dorsad and reach vital structures
What is the pathogenesis that leads to a rusterholz ulcer?
weak or absent horn (laminitis) + concussive force (overgrowth) lead to injury + increased udder weight
severe injury will destroy the underlying corium and lead to proliferation of granulation tissue
Where do small ruminants tend to get horn overgrowth
abaxial wall grows long + curls under in small ruminants
Where do cows tend to have horn overgrowth?
the heel, abaxial wall and the toe
When performing corrective shoeing, what are important steps to ensure the foot is being reshaped to correctly bear weight?
we want a flat sole to spread weight evenly
remove extra toe, abaxial wall and heel
ensure there is good balance
avoid damaging the periople
dig out onfected tracks + cracks
remove double soles
trim back granulation tissue
place block on the sound claw if the other claw is very sore
check for infection of deeper structures
What can producers do to help prevent hoof lesions?
keep cows healthy - slow adaption to enviornments + diets, good hygiene, good bedding + stalls
exercise without too much standing around
softer substrates
regular hoof trims (2x a yr), foot baths, genetics
T or F donkies + horses have the same pain thresh hold
False, a dull donkey = a thrashing horse! Donkies are extremely stoic.
What causes wind-up pain in horses?
severe colitis, laminitis
What are some examples of patients that aren’t good NSAID candadites
pregnant, hypovolemic, hx of kidney disease,
What NSAIDs impact both the COX-1 and COX-2 pathways?
ketoprofen, meloxicam. flunixin meglumate (banamine), phenybutasone (bute),
What NSAID only targets the COX-2 pathway?
Firoxib
What are we taking away from the patient when we block productive prostaglandin synthesis?
pregnancy maintenance, liver, kidney, GI mucosa, blood clotting
What are indications of NSAIDs ?
pain, inflammation, pyrexia, anti-endotoxemia
Contraindications for NSAID administration
received a full dose less than 12 hours ago
renal compromise (elevated creatinine)
hepatic impairement
NSAID toxicity: right dorsal colitis
gastric ulcers
pregnancy/lactating
neonates
clotting disorder, thrombocytopenia
What q’s about NSAID use must I always ask?
how much is given, how frequently and the last dose given
What is the onset of flunixin meglumine?
2 hours
What type of pain is flunixin meglumine best for?
visceral, laminitis pain and ocular pain
Why is IM injection of flunixin meglumine always contraindicated in equids?
IM injection leads to clostridial myonecrosis and death
T or F phenylbutazone is easily reversible from COX
False! It irreversibly binds to COX and is slowly eliminated so overdosing disproportionately increases plasma concentration therefore there is a greater toxicity risk
What is the dosage of phenylbutazone if it is being chronically used?
EOD
How is phenylbutazone metabolized?
hepatic metabolism
T or F phenylbutazone use can cause T4 suppression
True!
Y or N, can pregnant or lactating animals receive phenylbutazone?
NO
T or F: Flunixin meglumine has a anti-endotoxic effect
True!
What type of pain is Firocoxib best for?
musculoskeletal pain
many OA horses take it daily
Describe the elimination of Firocoxib
slow; 2 days
T or F: Firocoxib is metabolized through the kidneys
False! Hepatic clearance
What are the adverse effects that can occur with NSAID use?
clostridial infection if flunixin meglumine is given IM
nephrotoxicity: renal papillary necrosis
Right dorsal colitis (TS +/or albumin will decrease; diarrhea, gastric ulcers, impaired clotting, teratogenic
What are medical options for pyrexia control in an adult horse?
Dipyrone
Acetominophen
T or F: acetominophen + flunixin meglumine can’t be given together because they are both NSAIDS
False! acetominophen is a weak prostaglandin inhibitor and isn’t considered a “true” NSAID so you can give them both together!
What drug is a central target for pyrexia?
Dipyrone
causes smooth muscle relaxation, some analgesia
do NOT give to patients with coagulopathies
What is the MOA of lidocaine?
sodium channel blocker at neuron synapses
When is lidocaine administration indicated
As an anti-arrhythmic (v tach or digoxin)
For use as as propulsive motility promotor of GIT (for ileus, enteritis, refluxing), as an analgesic
What adverse reactions can be seen in horses with lidocaine sensitivity or accidently received a bolus?
seizures, muscle fasiculations, excitability
Why should we be cautious when giving horses lidocaine with a highly protein bound drug?
lidocaine is moderately protein bound in plasma so there is more free drug in the plasma putting the animal at a greater toxicity risk
Why should we be cautious when using an alpha 2 while sedating a patient?
it reduces GI motility
avoid use in animals with arrhythmia’s, neonates,
It alters blood glucose
If a pyrexic horse is given an alpha 2 as part of a sedation protocol and develops tachypnia then what does that tell us ?
the patient has a true fever
What impact does torb administration have on future morphine, pethidine or fentanyl given up to 8 hours after?
torb is a partial k an u agonsit and antagonist
because it is a partial antagonist it will reduce the efficacy of the drugs it proceeds
If a client wants to stop giving their patient steroids, what do you tell them?
NEVER stop a course of steroids abruptly! Taper steroids off according to clinical improvement, then reduce by 20% of your dose every few days
When can procaine pen g cause fatal reactions?
If it if accidently given IV! MUST be given IM route
Why is it important to give penicillin (usually K pen) slowly?
it stimulates GI motility which looses manure and can cause patient to expel loose manure and be crampy + colicky
What is the MOA of Penicillin?
beta-lactam
bactericidal, time-dependent, inhibits cell wall synthesis, hydrophilic
when is penicillin (usually K pen) indicated?
gram positive organisms, some anerobes (clostridium), has poor gram negative coverage
it is commonly a part of broad spectrum therapy
What is the MOA of gentamicin
Aminoglycoside that is synergistic with beta lactams
inhibits protein synthesis, bactericidal, hydrophilic, concentration dependent
Indications for gentamicin use
gram negatives
What do foals often receive instead of gentamicin + why?
Foals get amikacin because it is less nephrotoxic, higher dose for foals
Contrainidications of gentamicin use
concentrates in renal tubular cells (nephrotoxic potental)
not for dehydrated, azotemic, renal-compromised patients
MOA of oxytetracycline
Tetracycline, broad spectrum, inhibits protein synthesis
Bacteriostatic, time-dependent, lipophilic
Good for intracellular pathogens and penetrating tissues
Does not cover enterococcus (not good for foal sepsis)
When is oxytetracycline indicated?
Neorickettsia risticci aka Potomac Horse Fever
Tick-borne disease (anaplasma)
At supratherapeutic doses, for foal flexural limb deformities
What are contraindications of oxytetracycline use
Nephrotoxic (see gentamicin warning)
Why should I avoid rapid oxytetracycline administration?
they will collapse
Given slowly IV, diluted in isotonic fluids because binds calcium
If a patient was receiving IV oxytetracycline in hospital, what drugs will we consider sending them home on?
go home on oral doxycyline or minocycline
MOA of potentiated sulfonamides (TMS), Equisul
Broad spectrum (gram negative and positive, protozoa), nucleotide synthesis inhibition at two points (trimethoprim and sulfadiazine or sulfamethoxazole)
Bactericidal, time-dependent
What drug should be avoided for pseudomonas or bacterioides?
potentiated sulfonamides (TMS) , Equisul
What are indications for potentiated sulfonamides (TMS), Equisul
Good first-line, used frequently for wounds
Strangles
Equine protozoal meningoencephalitis (EPM)
Mild pneumonia
NOT for sepsis
What are contraindications of potentiated sulfonamides (TMS), Equisul
Poorly active in abscesses, purulent material
Must give 2 hours apart from antacids (sucralfate)
May cause diarrhea → stop if noticed
What is the difference berween TMS and Equisul?
Equisul” has a longer half-life than TMS, and improved oral bioavailability
TMS tablets are very inexpensive
MOA of ceftiofur
Bacerticidal, time-dependent, broad spectrum, gram negative
Poor intracellular penetration, but distributes widely extracellularly
Ceftiofur = 3rd generation.
What are the contraindications of ceftiofur use
Protected: 3rd generation
Intracellular pathogens
Should reserve this drug for good stewardship
Indications of ceftiofur use
If nephrotoxicity prohibits aminoglycoside use
Per culture and sensitivity!
WHat is considered a complete course of use of: penicillin, oxytetracycline, potentiated sulphonamides
IV K Penicillin and gentamicin should be at least 3, ideally 5 days
Oxytetracycline: can start with IV and end with oral doxycycline or minocycline
Potentiated sulphonamides: 5-10 days, or more
How should i assess my patient while on antibiotic therapy
Evidence of continued clinical signs? (Fever, dumpiness, respiratory signs, purulent wounds)
Recheck labwork: abdominocentesis, complete cell count, inflammatory markers, BAL/TBA
Is the threat gone? Abscess presence, corneal ulcer, exudative surgical site
Not responding to therapy? Culture and sensitivity…
MOA of omeprazole
proton pump inhibitor
Indications of omeprazole
gastric ulcers, 28 days, full dose
What is the preventative dose of omeprazole
1/4 a full dose
T or F omeprazole must be given after a meal.
False, it needs to be given on an empty stomach
MOA of sucralfate
anti-acid, binds to exposed mucosa, stimulates mucus & bicarb production.
When must you give sucralfate + why?
must be given 1-2 hours apart from other medications because it interacts
Indications for sucralfate use
gastric ulcers, esophageal obstruction (choke), colitis, foals
Withhold for 6 hours before endoscopy
Describe the vax protocol for EEE/WEE for a broodmare with unknown vax hx or is previously unvaxxed
2 dose series:
receive second dose 4 weeks post first vax and then revax 4-6 weeks pre-partum
Vax protocol for WEE/EEE for an adult horse whose never been vaxxed for it or has unknown vax hx
2 dose series
receive second dose 4-6 weeks after first dose
Vax protocol for a horse over 1 yr that has prev vx hx of WEE/EEE
annual revac prior to onset of vector season
In what horses should you consider a 6 month revax interval for WEE/EEE
horses less than 5 yrs of age
horses residing in endemic regions with extended vector seasons
What is the vax protocol for a foal from a mare whose never been vaxxed against WEE/EEE or a foal whose mare has been prev vaxxed against it?
3 dose series:
first dose at 4-6 months of age
second dose 4-6 weeks after the first dose
third dose at 10 to 12 months of age
followed by annual vax
Why is there a 2 dose series recommendation in foals whose mare was vaxxed in the prepartum period but only a one dose series at 4-6 months of age in a foal of unvaxxed or unknown history?
foals from vaxxed mares are recommended a 2 dose interval because we want to address the potential for maternal antibody interference
Tetanus dosage interval in foals of mares who were vaxxed in the pre partum period
3 dose series:
1st dose at 4-6 months of age
2nd dose at 4 to 6 weeks
third dose at 10 to 12 months of age
annual revax
Tetanus dosing interval for foals of unvaxxed mares or lacking vax history
first dose at 3-4 months of age
second dose at 4 to 6 weeks after 1st dose
third dose 10 to 12 months of age
annual revax
Tetanus dosing interval for broodmares prev vaxxed
annual
4-6 weeks pre-partum
If a horse over 1 year has no vax history or unknown hx for tetanus what is their dosing interval
2 dose series
receive second dose 4-6 weeks after first dose
When should you booster tetanus in a horse
at time of penetrating injury or before sx if it has been over 6 months since last vax
If you have a broodmare with unknown or no hx of WNV vax, what is the dosing interval
vax naive mares when open
Is WNV a 2 or 3 dose vax series for adults? What about foals?
two for adults
3 for foals
T or F protective titers are avaialble for EEE/WEE
False
How is EEE/WEE spread?
Mosquitos, less frequently other insects and nasal secretions
horses, especially those in endemic areas (South, coastal)
What regions of the US are at risk for rabies exposure
Endemic in every US state (except Hawaii)
What is the vaccine protocol to ensure protection against rabies?
Inactivated tissue culture-derived products
Single dose with annual revaccination
What is the protective titer for rabies
definitive titer not established but >0.5IU/ml considered robust but will not protect animal from quarantine/euthanasia
How is WNV spread
Avian reservoir host, Mosquitos (infrequently by other bloodsucking insects)
When is the best time to administer the WNV vax
USDA Licensed Vaccines:
(2-inactivated whole, recombinant canarypox, inactivated flavivirus vector
Administer in spring before vector season
T or F both horses and humans are dead end hosts for WNV
True
What regions are at risk for WNV
Continental US, most of Mexico and Canada
Is there a protective titer established for tetanus
titer levels >0.01 IU/ml considered to be protective (Cornell)
What exactly is the tetanus vaccine
Formalin inactivated, adjuvanted toxoid - alone or in combination with others
What risk factors should indicate that a horse should be vaxxed for Rhinopneumitis? (EHV)
horses less than 5 yrs of age
horses on breeding farms or in contact with pregnant mares
horses housed at facilities with freq. equine movement on + off premises
performance or show horses in high risk situations
What risk factors should indicate that a horse should be vaxxed for strangles?
if they live on premises where strangles is a persistent endemic problem
less than 5 years of age
What is the fecal egg count reduction test
used to determine if strongyles and/or ascarids are resistant to a given antihelminthic
Why do we monitor ERPs?
has the most practical implication for measuring possible emergence of resistance for common antihelmintics
What are common equine nematodes?
large strongyles
small strongyles
Pinworms
Ascarids (round) worms
T or F Strongyles have intermediate + Paratenic hosts
False, they have direct life cycles!
Where do cyathostomins (small strongyles) encyst
in the mucosal lining of the large intestine
What age group do ascarids like to infect + what cs does it cause?
foals/ weanlings
weight loss, diarrhea, impaction
T or F: most horses develop strong immunity + eventually cease shedding eggs
true
What is the gold standard for detecting anthelmintic resistance
Fecal egg count reduction test
When are fecal egg count reduction tests
more reliable during grazing season as encysted cyathostomins tend to accumulate during autumn and winter months
Adult female worms shed fewer eggs when it is not grazing season
What parasites can be identified with the Baermann technique
lungworms and immature cyathostomin infections
What are reasons to do a fecal egg count
evaluate efficacy of drugs
evaluate and monitor ERP
Determine shedding status of horse
determine parasite burdens in foals and weanlings as round vs strongyle
What are limitations of Fecal egg count
doesn’t accurately reflect true worm burden
doesn’t detect immature or larval stages of parasites
underestimate tapeworm infections
pinworms (scotch tape test) + gastrophilus don’t shed in feces
