-
Most important btw nutrition, parasites, and vacc?
nutrition
-
how much roughage does a horse need to eat
- 3% of body wt
- not as much if high quality
- higher in Ca than P
-
how much concentrate does a horse need to eat
- 0.5-1% of body wt
- cereal grains higher in P than Ca
-
how much fat does a horse need to eat
- 6-8%
- energy
- race, endurance, cutting, and reining horse need high end
-
Ca:p in equine diet
want Ca slightly higher than P
-
equine stomach parasites
- bots
- all ages
- seasonal
- tx ivermectin
-
equine SI parasites
- ascarids
- young
- in stables
- tx ivermectin
-
equine end of SI parasites
- tapeworm (A. perfoliata)
- all ages
-
equine LI parasites
- strongyles
- seasonal
- tx ivermectin
-
equine end of LI parasites
- pinworms
- in stables
- tx ivermectin
-
tx parasites in equine
- ivermectin- bots, ascarids, strongyles, pinworms
- moxydectin (Quest)- do not use in thin horse or minis- kills persistant strongyles
-
anaplasma in young
asymptomatic to mild
-
anaplasma in adults
- severity inc with inc in age
- 4 stages- incubation, acute dz, convalescent stage, carrier stage
-
stage I anaplasmosis
- incubation
- 21-45d
- asymptomatic
-
stage II anaplasmosis
- acute dz
- >1% RBCs affected
- fever for a few days
- anorexia
- acute death
- lethargy
- tachycardia
- NO HEMOGLOBINURIA bc this is an extravascular hemolytic event
-
stage III anaplasmosis
- convalescent stage
- 3-4 wks
- wt loss
- icterus
- ill thrift
-
stage IV anaplasmosis
- carrier stage
- for life
- asymptomatic
-
time of year for anaplasmosis
late summer/early fall bc flies
-
pathology of anaplasmosis
- dec PCV
- see organisms on blood smear (may not see in carrier)
- serology to detect carriers
- hyperbilirubinemia
- hyperbilirubinuria
- thin blood
- pale mm
- splenomegaly
- NO HEMOGLOBINURIA
-
transmission of anaplasma
- Dermacentor tick
- iatragenic
- blood feeding flies
-
tx anaplasmosis
tetracyclines
-
prevention of anaplasmosis
- chlortetracycline containing feed- this is not a tx dose, only prevents clinical signs
- control vectors
-
5 forms lymphosarcoma
- cutaneous
- juvenile
- thymic
- hemal LN enlargement
- enzootic
-
form of lymphosarcoma associated with a virus
only the enzootic form is associated with the bovine leukemia virus
-
lymphosarcoma basics
- virus infects lymphocytes
- transmission of lymphs from one animal to another via blood, milk, and colostrum
- 0.48 heritability
-
significance of infection with bovine leukemia virus
- 70% infected will not display any clinical signs
- 25% infected will not have signs but will develop a persistent lymphocytosis
- 5% of 25% will develop solid tumors
- 2-5% will develop lymphosarcoma
-
transmission of lymphosacrcoma
- #1 tattooing, dehorning, castrating, contaminated needles
- #2 rectal palpation
- #3 colostrum
-
diagnosis of BLV
- gp-51 antigen
- organs affected- right atrium (distended jugular vein and tachypnea), abomasum (distended abdomen and melena), LN, uterus
- CBC norml unless lymphocytosis
-
prevention of BLV
- disinfect instruments
- change needles
- use clean rectal palpation gloves
- separate seroneg and seropos cows
- do not feed bulk milk and colostrum to calves
-
control of BLV
- test and slaughter
- test and segregation
- test and implementation of corrective management
-
bovine parturient paresis
- milk fever
- flaccid paralysis near parturition due to hypocalcemia cause by rapid onset of lactation
-
Ca:P
- 50% Ca ionized
- 1:1 or 2:1
- grains- P
- legumes- Ca
- inverse relationship btw Ca and P
-
hormaonal control of Ca
- parathytroid hormone- low Ca leads to inc PTH
- vit D- allows Caa to be available
- calcitonin- high Ca inhibits PTH
- young have more Ca and P so no milk fever in first calf heifer
-
ddx for milk fever
- grass tetany
- obtorator nerve damage
- trauma
- lymphoma
- low P/K
- myopathy
-
risk for milk fever
- high Ca diet during dry period bc suppressed PTH
- estrogens have antagonistic activity on PTH
-
occurrence of milk fever
- dairy breeds
- hereditary
- rare in first calf heifers
- 90% occur within 48hrs of calving
- high Ca diet in dry period will predispose
-
clinical signs of milk fever
- prodromal- restlessness
- recumbent- head along side body, elevated HR thats hard to hear
- comatose- lateral recumbancy
-
pathlogy of milk fever
no lesions
-
tx milk fever
- Ca borogluconate slowly
- Ca dextrose
- HR slows, tremors appear, sweat on muzzle, defecation, eructation, get up
-
prevention of milk fever
- good management during dry period
- low Ca
- DCAD makes diet more acidic so absorb more Ca
- inc Ca 48 hrs before calving
- avoid feeding poultry litter to beef cows
-
hypomagnesemia
- grass tetany
- inadequate dietary Mg (usually with low Ca)
- tonic-clonic muscle spasms
- low Mg releases acetylcholine leading to tetany
- high K fertilizer will dec Ca and Mg in forage
-
occurrence of hypomagnesemia
- lactating beef cows
- older have higher risk
- thin cows higher risk
-
clinical signs of hypomagnesemia
- sudden death
- "pasture angels"
- anorexia
- muscle tremors
-
ddx hypomagnesemia
- milk fever (cannot tell apart until later bc flaccid)
- rabies
-
diagnosis of hypomagnesemia
-
tx hypomagnesemia
- SQ Mg sulfate
- CMPK IV
- oral Mg oxide
- feed alfalfa
-
prevention of hypomagnesemia
daily feeding of Mg salts
-
bovine ketosis
- lactating dairy cow
- inadequate carb intake
- ketone bodies
- due to high energy demand of early lactation
- hypoglycemia
-
primary vs secondary ketosis
- 1- lack energy in diet
- 2- anything that knocks off feed (displaced abomasum, metritis, mastitis)
-
clinical signs of ketosis
- loss of appetite
- dec in milk prod
- sweet odor of breath
- look for underlying dz
- wt loss
-
pathology of ketosis
- hypoglycemia
- elevated blood ketones
- ketonuria
- ketones in milk
-
steps of ketosis
- dec intake
- lack OA
- no oxidation of ACoA
- more ketone bodies
- dec intake
- cycle continues
-
fatty acids in ketosis
- proprionate- supports gluconeogenesis
- acetate and butyrate- make ketone bodies
-
necropsy findings after ketosis
yellow, pale, friable liver with fatty changes
-
tx ketosis
- tx underlying dz
- IV 50% glucose
-
prevention of ketosis
- BCS 3.5/5 at calving
- lead feed dairy cows
-
fat cow syndrome
- dairy cattle
- overfeeding during the dry period
- overconditioned at calving
-
pathogenesis of fat cow syndrome
- liver overwhelmed by excessive NEFA's
- stored in hepatocytes instead of released as VLDL's
- liver unable to carry out normal metabolic fxn
- formation of ketone badies
- ketosis
-
clinical signs of fat cow syndrome
- rapid wt loss
- BCS>4 at calving then drop to 2.5
- depressed appetite
-
diagnosis of fat cow syndrome
- hx
- clinical signs of ketosis
-
tx fat cow syndrome
- prognosis is poor
- tx presenting or underlying dz
- IV glucose (same as ketosis)
-
prevention of fat cow syndrome
- maitain proper BCS
- no free choice, high energy feeds during dry period
-
pregnancy toxemia
- sheep and goats
- hypoglycemia and hyperketonemia
- inadequate energy (hay) intake during late gestation
-
pathogenesis of preganacy toxemia
- energy deficit due to dec nutritional plane or dec in voluntary food intake
- fetus dec abdominal space leading to dec intake and inadequate glucose production
-
clinical signs of pregnancy toxemia
- ewe leaves flock
- anorexia
- depression
- blindness
- recumbency
- tremors
-
tx of pregnancy toxemia
- prognosis grave if recumbent
- decide if want ewe or lamb
- early stage- feed grain bc high energy
- glucose
- induce parturition: goat-PG, sheep- Dex+PG
-
prevention of preganacy toxemia
- prevent ewe/doe from becoming too fat
- inc plane of nutrition during last 1/3 of gestation
-
protein-energy malnutrition
- occurs in pregnant cows on a marginal diet
- winter
- wt loss, weakness, inability to rise
- diet low in quality and quantity
-
diagnosis of protein-energy malnutrition
- not ketotic
- demonstrating dec caloric intake
-
tx protein-energy malnutrition
often unsuccessful
-
vitamin E/selenium deficiency
- Se- glutathione peroxidase- antioxidant- without then hydrogen peroxide accumulates- counteracts toxicity of metals
- vit E- antioxidant- prevents formation of hydrogen peroxide
-
syndromes created by vit E/Se deficiency
- white muscle dz- death 2d after birth, pale streaks in muscle
- retained placenta
- ill thrift
- immune system deficits
- infertility
- abortions
- mulberry heart dz in pigs
- stiff lamb dz
-
diagnosis of vit E/Se deficiency
- whole blood- Se
- plasma- vit E
-
tx vit E/Se deficiency
- inj Se
- salt mix
- Se supplement to total ration
-
copper deficiency
- young
- unthriftiness
- changes in hair color
- diarrhea
- lameness
-
Cu distribution and absorption
- liver (most), brain, heart, kidney
- absorbed in SI
- as Mo goes up, Cu absorption goes down
- as sulfur goes up, Cu goes down
-
transport and excretion of Cu
- transport via albumin to liver
- excreted in bile
-
functions of Cu
- hematopoiesis
- hair pigmentation
- bone formation
- nervous tissue
- keratinization
-
syndromes related to cu deficiency
- neonatal ataxia- swayback, lambs mostly
- anemia- nonreg
- achromotrichia- loss of black pigment
- impaired keratinization of wool and hooves
- painful jts
- diarrhea- adults
-
diagnosis of Cu deficiency
liver Cu concentrations
-
tx Cu deficiency
- Cu glycinate
- Sheep susceptible to Cu toxicity so be careful
- Cu sulfate in ffed- may be toxic in sheep
-
prevention of Cu deficiency
- salt trace mineral supplement
- Cu oxide needle bolus
- this is for cattle- be careful with sheep
-
copper toxicosis
- sheep most susceptible
- accidental feeding of Cu in horse or pig feed
- hemolytic crisis
- >10ppm Cu n diet
- low Mo, S, Zn
-
pathogenesis of copper toxicosis
- Cu accumulates in liver
- when animal stressed Cu is mobilized
- hemolytic crisis
-
clinical signs of Cu toxicosis
- hemoglobinuria
- anemia
- icterus
-
tx Cu toxicosis
- penicillamine
- ammonium molybdate
-
failure of passive transfer
- insufficienct quantity or quality of colostrum produced or consumed
- failure to absorb colostrum
-
colostrum contents
- hormonal (IgG) and cellular (lymphs)
- graetest IgG at parturition
- loses quality even if not milked out
-
factors that dec colostrum quantity
- parity- heifers have less
- breed- dairy has more but poorer quality
- poor nutrition
-
factors that dec colostrum quality
- breed- dairy has more but pooer quantity
- leakage or preparturient milking
-
factors that dec colostrum intake
- poor calf vigor
- poor udder confirmation
- poor footing
-
factors that dec colostrum absorption
- corticosteroids
- stress- dystocia
- resp acidosis
-
diagnosis of FPT
- performed on serum in first 48 hrs of life
- refractometry (best)- measure TP- <5g/dl is FPT
- single radial immunodiffusion (SRID)- gold standard- expensive and slow
- sodium sulfite precipitation test- serum mix with sodium sulfite and pos test is lack of turbidity
- serum gamma glutamyl transferase (GGT)- inc following colostrum absorption
-
tx FPT
- less than 24hr- colostrum
- otherwise- serum transfusion
- may not need anything
-
rules of thumb for colostrum management
- dairy calves get 3-4 L colostrum ASAP
- do no t pool colostrum
- use first milking colostrum only
- beef calves should nurse within 2hrs
- give 1-2L beef colostrum or 1 gallon dairy colostrum if delivered by fetal extraction or c-section (don't wait to see if will suck)
-
neonatal septicemia
life threathening and often fatal systemic dz caused by presence of bacteria/toxins in bloodstream of calves
-
predisposing factor to neonatal septicemia
- FPT
- exposure to e. coli, a. pyogens, salmonella
-
clinical signs of neonatal septicemia
- fever
- depression
- anorexia
- hypopyon
- seizures
- may have diarrhea in dairy calves
-
tx neonatal septicemia
- Ab- ceftiofur
- NSAIDs
- glucose
-
actinomycosis
- lumpy jaw
- A. bovis
- gram + anaerobe
- normal flora of upper resp tract
- infection secondary to mucosal wound
- painless osteomyelitis of mandible or maxilla
-
clinical signs and dx of actinomycosis
- hard non-movable swelling on mandible or maxilla
- dx based on hx of slow growing mass
- rads
- biopsy
-
tx actinomycosis
- salvage
- NaI 3x 7-10 days apart
- long acting oxytetracycline
- ddx- tooth abscess, healing fx, soft tissue abscess, neoplasia
-
actinobacillosis
- wooden tongue
- A. lignieresii
- gram - aerobic
- normal flora of upper resp tract
- mucosa penetrated for infection
- granulomatous
-
clinical signs of actinobacillosis
- swelling of tongue- hard and painful
- masses in buccal or cervical area
-
dx of actinobacillosis
- palpation of base of tongue
- culture of lesion or exudate
-
tx actinobacillosis
- NaI at 3x 7-20 days apart
- long acting oxytetracycline
- tx works better than actinomycosis
- ddx- actinomycosis, abscess, oral FB, impacted cud
-
caseous lymphadenitis
- Corynebacterium pseudotuberculosis
- survive in soil
- transmit via break in skin
- moves thru LNs
- intracellular
- abscess
- life long infection in small rum
-
clincial signs and dx of CL
- enlarged LNs with pus
- resp signs if internal LNs
- culture of organism
-
tx of CL
- decide on strategy for herd
- lance and live with it- will return
- minimize spread- sx removal, tulathromycin
- eradication- cull
-
bovine virus diarrhea
- 70-90% seropos
- transmit via contact or aerosol
- can become PI
- cytopathic vs non-cytopathic
- most infections are subclinical
-
acute BVD
- NCP
- immunocompetent cattle that are naive
- clinically inapparent to rapidly fatal
- mortality high
-
in utero infection of BVD
- NCP
- early- abortion
- <125d- PI
-
PI cattle with BVD- mucosal dz
- NCP+CP
- blunt buccal papillae
- interdigital lesions
- linear striations in esophagous
- BVD recognized as self since inf in utero
- weak calf born- seroneg
- NCP converts to CP
-
dx of BVD
- PCR
- ELISA
- ICH
- virus isolation
- PI demonstrated by 2 pos tests 3-4wks apart
-
vacc for BVD
- killed- requires 2 primary inj, short lived immunity
- modified live- longer lasting, can cause clinical dz
-
mesquite bean toxicity (prosopis)
- beans abundant and other feedstuff in short supply
- clinical signs months after ingestion
-
clincial signs of mesquite bean toxicity
- profuse salivation, chewing, regurge'tongue protrusion bc loss of jaw muscle tone (CN V)
- wt loss
-
tx mosquite bean toxicity
- slow recovery
- often unsuccessful
- prognosis better in goats
-
5 F's of abdominal distension
-
carbohydrate engorgement
- grain overload
- acute acidosis
- highly fermentable feedstuffs- corn, milo, apples, honey
- when unaccustomed to high carb diet
- dairy have become accustomed
-
pathophysiology of carb engorgement
- strep bovis inc and produce lactic acid
- pH falls- gram neg and protozoa die
- S. bovis inhibited and lactobacilli proliferate
- rumen motility dec
-
clinical signs of carb engorgement
- anorexia
- depression
- ab distension- bloat, splashy rumen
- dehydration
- rumen atony
-
lab findings of carb engorgement
- rumen pH <5.5
- rumen fluid smells sour
- gram stain reveals gram + rods
-
tx carb engorgement
- Mild acidosis:
- oral antacids- Mg hydroxide (alkalinize)
- remove grain, feed hay
- Mod acidosis:
- rumen lavage via stomach tube
- plus above tx
- Severe acidosis:
- rumenotomy
- IV fluids- not lactated
- Penicillin
- transfaunation- rumen contents from one to another
-
chronic acidosis
- feedlot cattle
- anorexia
- bloat
- low milk fat test in dairy
- ration analysis
- tx- buffers- NaHCO3
-
frothy bloat
- legumes- alfalfa
- cannot eructate bc of foam
- not a problem of too much gas or rumen motility
- ab distension in left paralumbar fossa
- resp distress
- tx- poloxalene- antisurfactant
-
free gas bloat
- motility disorder
- show/feedlot cattle
- following pneumonia- young
- ruminitis- older
- ab distension in left parlumbar fossa
- relieved when stomach tube passed
- tx- reduce grain, add NaHCO3, transfaunation
-
abomasal ulcers
- stress induced + high grain
- can be caused by lymphosarcoma
- 4 types
-
type 1 abomasal ulcer
- non-perforating
- few clincial signs
-
type II abomasal ulcer
- bleeding ulcer
- anemai
- weakness
- pale mucous membranes
- melena
- rarely perforate
-
type III abomasal ulcer
- perforating ulcer
- localized peritonitis
- rarely bleed
- adhesions
- fever
-
type IV abomasal ulcer
- perforating ulcer
- diffuse peritonitis
- abdominal ccontamination
- spetic shock in 24hrs
-
abomasal lymphosarcoma
bleeding ulcer (type II) in older cattle
-
dx of abomasal ulcer
- fecal occult blood
- clinical signs and hx
- abdominocentesis
- serology to rule out BLV
- necropsy
-
tx abomasal ulcer
- salvage
- high roughage
- remove stress
- tx concurrent dz
- transfusion
- fluids
-
abomasal ulcer/tympany syndrome in calves
- 1-2mth old calves on heavier milking cows
- perforating with peritonitis
- Clostridium perferingens A&E
- Canadian theory- undifferentiated abomasal upset
- Cu deficiency
- BVDV
- Sarcina
- sudden death
-
traumatic reticuloperitonitis
- hardware dz
- foreign object swallowed and penetrates reticulum
- local peritonitis usually
- penetrate diaphragm, pericardium, liver, spleen
- abscesses and adhesions
-
clinical signs of hardware dz
- acute drop in milk prod and feed intake
- rumen stasis
- abdominal pain
- arched back
- elbows out, reluctant to move
-
lab findings in hardware dz
- hyperfibrinogenemia
- hyperglobulinemia if chronic
-
dx hardware dz
- hx
- signs
- ultrasound
- abdomenocentesis
- rads
-
tx hardware dz
- rumen magnet
- Ab- penicillin, oxytet, ceftiofur
- rumenotomy
- rib resection and pericardiectomy
-
-
right sided pings
- spiral colon
- rectum
- RDA
- AV
- small intestine
-
displaced abomasum
- dairy cows
- within one mth parturition
- dec milk prod
- high conc diet
-
LDA
- not emergency
- looks like RDA
- ping from 8-9th rib to PLF
-
RDA
- emergency bc can become abomasal volvulus
- looks like LDA
- ping from 8-9th rib to PLF
-
lab findings in displaced abomasum
- hypokalemia
- hypochloridemia
- alkalosis
- ketonuria
- ketonemia
-
-
bar suture to tx displaced abomasum
- only LDA
- dorsal recumbency
- trochar inserted and then toggle pins
- for mariginal cows
-
right paramedian abomasopexy
- LDA or RDA
- dorsal recumbency
- abomasum sutured in place as incision closed
-
right paralumbar omentopexy
- LDA or RDA
- standing procedure
- omentum near pylorus is sutured into incision
-
left paralumbar abomasopexy
- LDA only
- standing
- long tailed sutures placed in abomasum and then through the body wall and tied
-
abomasal volvulus
- drop in appetite and milk prod
- dairy cows
- depression
- dehydration
- palpable per rectum
- ping in right side
- hypochloridemia
- alkalosis
- hypokalemia
- emergency slaughter
- paramedian abomasopexy
- right paralumbar abomasopexy
- omentopexy
- fluid therapy
-
neonatal calf diarrhea
- rotavirus
- coronavirus
- ETEC- <2wk
- Crypto- zoonotic, >2wk
- Salmonella- typhimurium and dublin
-
ETEC
- cause neonatal diarrhea <2wks
- heat stable enterotoxin- ST
- attach to pilus- K99
- secretory diarrhea- no morphologic damage
-
rotavirus and coronavirus
- causes neonatal diarrhea
- R- proximal SI
- C- distal SI
- destroy villus tips and sides
- malabsorption
-
cryptosporidium
- causes neonatal diarrhea
- malabsorption and secretory
- villus blunting
- 10d-3wks
- hypoglycemia
-
salmonella
- cause neonatal diarrhea
- >2wk
- malabsorption and secretory
-
clincial signs of neonatal diarrhea
- profuse watery yellow to whitish diarrhea with no blood or mucus
- except salmonella- bloody foul smelling diarrhea with mucus strands
-
lab findings for neonatal calf diarrhea
- dehydration
- acidosis- lactic acid build up, dec acid excretion, production of VFAs
- hyperkalemia- plasma K rises bc total body K dec due to loss in stool and urine
- hypoglycemia
-
tx neonatal calf diarrhea
- fluids
- Ab if concurrent septicemia/other dz
- neomycin, tetracyclin, ampicillin cause more malabsorption
- ceftiofur (gram neg)
- anticholinergics CI
- keep calves on milk
- do not mix electrolytes and milk
- do no mix milk and biocarbonate
-
Johne's dz
- paratuberculosis
- acid fast rod
- dairy cows
- fecal-oral, colostrum, in utero
- infected early in life but no signs until 2-5yrs
- older cattle need a bigger dose
-
pathogenesis of Johne's dz
- ingestion
- organisms in M cells of gut
- granulomatous enteritis of the ileum
- thickened intestines
- malabsorption, maldigestion, protein losing enteropathy
-
clinical signs of Johne's dz
- chronic diarrhea
- wt loss
- good appetite
-
dx Johne's dz
- ELISA- 99% specific
- culture feces- definitive dx
- PCR- quick
- necropsy
- there is no sure way to prove that a living cow is free of infection
-
tx Johne's dz
- no cure
- feeding monensin is extra label use- still shed organisms
-
prevention of Johne's dz
- prevent contact of susceptible young calves with infected feces
- vacc not legal in Texas bc cross rxn with TB
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