Quiz 7
hypocalcemia, hypophosphatemia
hypomagnesemia, hypokalemia
ketosis and pregnancy toxemia
clostridial disease
dairy cow lameness
hypocalcemia
“Milk fever,” “Parturient paresis”
cellular pool of extracellular Ca is 10g, colostrum takes 20-50g Ca/day
required for Ach release → muscle contraction
stabilizes neuronal membrane → decrease results in hyper-excitability
homeostasis
PTH
produced in response to hypocalcemia
mobilizes bone Ca
increased renal tubular resabsorption
increased vitamin D production in kidney → stimulates intestinal absorption of Ca
can be altered by external factors
hypomagnesemia → interferes with PTH attachment to tissues
metabolic alkalosis → reduces tissue sensitivity to PTH
older cows → fewer osteobasts and PTH receptors
calcitriol
1,25-(OH)2 D → biologically active vitamin d3
increases calcium absorption across intestines
can be affected by:
metabolic alkalosis → reduces renal sensitivity to PTH
hyperphosphatemia → inhibits enzymatic activity for calcitriol production
Vitamin D deficiency or excess
Jersey breed → has fewer D3 receptors
minerals
factors affecting
estrogen → inhibits bone resorption
calcitonin → opposite effect of PTH (minor effect)
acid-base physiology → acidosis = increased bone calcium release, extra Ca excreted by kidneys
other
feed availability
age → reduced number of active bone cells
breed → Jersey cows have higher calcium in colostrum and fewer intestinal Vit D receptors
stages of hypocalcemia
progressive → stages 1, 2, 3
stage 1
ADR
anorexia
ataxia, restless
tremors
can look like respiratory
stage 2
sternal recumbency
clinical presentation
S-Curve
hypothermia
relaxed sphincters
decreased heart sounds + decreased pulses + tachycardia
hypotension
rumen stasis → bloat
stage 3
lateral recumbency
inability to rise
flaccid muscles
EMERGENCY
treatment
remove calf from cow
soft bedding with good footing
keep sternal
DO NOT MILK
calcium borogluconate 23%
IV
10.7g Ca/500 mL
administer slowly while monitoring pulse/HR
decreased HR or increased pulse intensity = reduced rate of admin
lower bottle = slower rate → hold at point of hsoulder
Serum Ca > 25 mg/dL can stop heart
prevention
DCAD
increased consumption of anions (K+ & Na+)
acidify blood pH, urine (5.5-6.5) → induces metabolic acidosis → increases calcium absorption, Mg absorption, Vit D, PTH
MUST BE CONSISTENTLY FED 10 days before calving
low-Ca diets
prime body for calcium absorption
hypophosphatemia
acute: post-parturient hypophosphatemia → increased RBC fragility, “Downer cow syndrome”
chronic: Rickets/osteomalacia
can occur secondary to hypocalcemia
homeostasis
bone metabolism
minimal
PTH, calcitriol, vit D
dietary absorption
majority
Vit D
plasma concentrations indicative of dietary phos absorption
acute hypophosphatemia
beef cattle on late-season pasture (low on P)
late gestation
postpartum down beef cow prognosis is poor
treatment
monosodium phosphATE drench or IV (CMPK has phosphite)
hypomagnesemia
essential for enzymatic activation, protein synthesis, regulation of membrane channels
most is found in bone and soft tissue
no specific hormonal regulation
“Tetany”
homeostasis
relies on dietary intake!!!
very small storage
no specific hormonal regulation → PTH (increased absorption), aldosterone (increased renal loss), Vit D (decreased serum Mg)
absorbed purely through the rumen, reticulum → no compensation by LI/SI
minimum oral intake necessary for net ab
decreased absorption
deficient magnesium intake
high potassium intake→ electrochemical inhibition of Mg absorption
hyponatremia → aldosterone release → increased salivary K → increased serum K
high crude protein (nitrogen)
increased absorption
fermentable carbohydrates
excretion
kidney
fecal
mammary
functions of Mg
ATP formation/use
activation of cAMP
Ach esterase → deficiency = tetany
CNS/Myoneural junctions
tetany
grass
spring/fall cool season grasses
rapid growth of grass → no Mg
wheat pasture
winter wheat and other cereal crops
lactation
most cases occur in lactating cows
winter
feed during winter harvested during spring/fall
milk
calves on milk after 6 weeks (2-4 mo old calves)
GI tract becomes less efficient in absorption of Mg
transport
on marginal diet when transported
stress → anorexia, lack of feed
diagnosis
low normal to hypocalcemic → less agitated
may be hyperkalemic
treatment
IV solutions of Mg salts (Mg hypophosphite, sulfate, lactate, Ca salts)
hypokalemia
rare in healthy adults with adequate dry matter intake
clinical signs
generalized muscle weakness, fasciculations
depression
ileus
K conc <2.5 mmol/L → need labwork, not just clinical signs
treatment
KCl PO → don’t increase recommended dose → diarrhea, hypersalivaiton, muscle tremors
rarely give IV → only for severe, recumbent, with ruminal atony
hyperkalemia
diarrhea, dehydration, acidemia, metabolic acidosis
decreases renal blood flow → decreased ability to excrete K
common in neonates
rare in adults with obstructive urolithiasis → excess K secreted in saliva
treatment
isotonic saline or sodium bicarb
hypertonic saline or sodium bicarb, calcium, glucose + insulin
goal: restore renal perfusion for excretion
hyperketonemia
ketosis
negative energy balance
increased energy requirements with inadequate DMI
increases risk of other disease → indicative of other concurrent diseases and predisposes to other disease development
lose $$$ from low production + treatment
etiology
too much forage = too much acetic acid = not enough glucose
too little grain = too little proprionic acid = no gluconeogenesis
NEB = fat mobilized from stores as NEFAs → not enough oxaloacetate for gluconeogenesis → ketone genesis
exacerbated by low insulin
disease occurs when created amount exceeds cow’s ability to use
clinical presentations
type 1
inappropriate diet + high production
very soon after parturition (7-30 days) in cattle
occurs before parturition in SR
acetone breath
type 2
obese cow with recent stressor (surgery, movement) → decreased intake
obese → increased fat mobilization
diagnosis
test for Beta-hydroxybutyrate (BHB)
ketones concentrated in urine, then blood, then milk
gold standard: BHB in blood
urine dipstick can be used to screen
treatment
propylene glycol 300n mL SID 3-5 days
toxic to rumen bugs → use with caution
dexamethasone to stimulate gluconeogenesis
B12
50% dextrose → nervous ketosis only
induce parturition if fetus is dead (SR)
prevention
monensin (ionophores)
goal: prevalence <15%
feed replacer or frozen colostrum to doe
reduce stressors
clinical signs
usually develop 1-3 weeks before parturition
worse prognosis with dead fetus(es)
stage 1
restlessness
most signs due to decreased mobility
lower limb swelling/shifting limb lameness
stage 2
anorexic
recumbent but able to stand
stage 3
down
obtunded
fatty liver
overconditioned cows
depression
anorexia → NEB
hypoglycemia
hyperammonemia
altered endocrine profiles
secondary/concurrent with metritis, mastitis, DA, hypocalcemia
etiology
NEB → NEFAs overload liver → triglicerides deposit in liver
diagnosis
indirect: assess severity and duration of NEB
direct/definitive: liver biopsy
BHB meter: suggestive
treatment
propylene glycol
dextrose
transfauntion
insulin
B vitamins
fix underlying problem causing anorexia
clostridial diseases
soil borne
spore forming
GPR
2 categories
clostridial cellulitis
invade and reproduce in tissues
produce toxins
enhance spread of infection
tetanus and botulism
toxemia caused by absorption of toxins
botulinum
contaminated feed
muscle paralysis → decreased ability to release Ach
botulinum neurotoxin type A, B, E
horses most sensitive
poor prog → respiratory paralysis
tetani
tetanospasmin → inhibits the inhibitory neurotransmitters GABA and glycine → increased Acetyl choline secretion and binding to receptor action
horses very sensitive
penetrating wound
protruding third eyelid
clostridial myonecrosis
c. chauvoei, septicum, sordelli, novyi, perfringens, carnis
rapid clinical course, high mortality
Black leg
Chauvoei
ingestion of spore → sits until muscle ischemia
Toxin A
young animals at risk
crepitus and swelling of large muscles
PCR of tissues
Big head
C. novyi, sordelli (most common)
nongaseous non-hemorrhagic, edematous swelling of head
young rams → head butting
black disease
clostridium novyi type B
associated with liver flukes
rupture of capillaries of subcutaneous tissues
enterotoxemias
clostridium perfringens A, B, C, D → type B and C most common in FA
foodborne → normal intestinal flora of animals
necrotizing Beta toxin associated with necrotic enteritis and diarrhea
pulpy kidney
“Over-eating disease”
C Perfingens Type D with Epsilon toxin → sometimes type C with beta toxin
more common during lush forage growth or highly fermentable CHO
clostridium difficle
disruption of normal gut flora → overgrowth of C. diff
diarrhea in calves
hx of abx tx or diet change
Tyzzer’s disease
C. piliforme
acute necrotizing hepattiis, myocarditis, colitis
foals
hypophagia + decrased fecal passsage
Red Water disease, Bacillary hemoglobinuria
CLostridium novyi type D → clostridium haemolyticum
most common where liver flukes are present
dairy lameness
lameness is a sign of pain
locomotion changes
shortened strides
asymmetrical gait
arched back
weight shifting
lameness
usually the outside claw (weight-bearing) of the hind feet
welfare problem
decreased production/reproduction
increased risk of other disease
anatomy
bottom of P3 not flat → common location of lesion
corium is between bone and horn → very vascular
sole is softer than walls
white line + heels are softest of all
claw horn disruption lesions
sole ulcers
white line disease
etiology
hormonal changes around calving → softer horn, relaxes tissues, sinking P3
concrete
decreased blood flow to corium under P3
increased rate of wear
increased risk of solar injury and bruising
increased risk of bacterial invasion
poor cow comfort + thin soles = increased risk
treatment
pare away dead stuff and undermining of sole
create drainage
± block foot → must extend under heel, does not have to extend under toe
NO ABX → NOT INFECTIOUS
trimming goals
more upright angle → put more weight on hard hoof