This document discusses hypocalcemia in dairy cattle. It covers the medical and economic impacts of hypocalcemia, physiological effects including impacts on neutrophil function, bone resorption markers, and calcium signaling in immune cells. It discusses some potential causes of hypocalcemia including the Dietary Cation-Anion Difference theory and hypoparathyroidism. The document also covers prevention strategies, treatment options, and areas for future research on understanding and addressing hypocalcemia in dairy cattle.
This PowerPoint presentation was prepared for the 2011 Missouri Livestock Symposium by Susan Schoenian, University of Maryland Extension Sheep & Goat Specialist.
This PowerPoint presentation was prepared for the 2011 Missouri Livestock Symposium by Susan Schoenian, University of Maryland Extension Sheep & Goat Specialist.
Far Off To Fresh Cow- Opportunities to Improve Transition PerformanceDAIReXNET
Dr. mike Overton presented this information for DAIReXENT on Monday, March 18, 2013. For more information, please see our archived webinars page at www.extension.org/pages/15830/archived-dairy-cattle-webinars.
Far Off To Fresh Cow- Opportunities to Improve Transition PerformanceDAIReXNET
Dr. mike Overton presented this information for DAIReXENT on Monday, March 18, 2013. For more information, please see our archived webinars page at www.extension.org/pages/15830/archived-dairy-cattle-webinars.
The Causes and Implications of Subclinical HypocalcemiaDAIReXNET
Dr. Jesse Goff presented this for DAIReXNET on November 11, 2014. The recorded webinar is available at http://www.extension.org/pages/15830/archived-dairy-cattle-webinars
The basis principal to prevent milk fever is to maintain a high plasma Ca level at the time of parturition to overcome the sudden high demand for Ca. For that hormonal therapy and dietary manipulations are successful. Among them, hormonal therapy does not seem to work in the field as it needs an accurate prediction of the date of parturition for the administration of hormones. The dietary manipulation may be the best and easiest way to prevent milk fever in this regard. The supplementation of anionic diet salts brings about a mild acidosis in the body thus increasing the rapid absorption of Ca through intestine and bone resorption.Thus the extracellular level of Ca increases which helps in coping with the demand of Ca particularly in the early lactation. To be more sure of prevention of the disease, anionic salts should be supplemented with high Ca diet so that sufficient amount of Ca is absorbed through intestine. Among the anionic salts, MgSo4 may be used commonly as it is more palatable to the animals and cheap. However, ammonium salts such as NH4Cl and NH4SO4 although effective are less palatable. A useful tool is to measure the urine pH i.e. pH 5.5-6.5 to monitor anion cation balance in diet.
Economic consequences of reproductive performance in dairy cattle Henk Hogeveen
For the Congress of the Livestock Production and Health group of the South African Veterinary Association, I gave a presentation about the economics of reproducttive performance. This presentation has quite some double information with other presentations I gave, based for a large part on the PhD work of Chaidate Inchaisri. However, some new elements (work of Niels Rutten) is included as well.
Contents :
Red blood cells
General features of red blood cells
Red cell indicators
Erythropoietin
Hematopoiesis
Peripheral blood smear
Hemoglobin
General features of red blood cell disorders
Hypochromic microcytic anemia
Iron deficiency anemia
Megaloblastic anemia
Pernicious anemia
Anemia of chronic disease
Sideroblastic anemia
Features of hemolytic anemia
Hereditary spherocytosis
G6PD deficiency
Sickle cell anemia
Thalassemia
Autoimmune hemolytic anemia
Microangiopathic hemolytic anemia
Paroxysmal nocturnal hemoglobinuria
Paroxysmal cold hemoglobinuria
Aplastic anemia
Pancytopenia and fanconi anemia
Myelodysplastic syndrome
Myeloproliferative disorders
Polycythemia
Myelofibrosis
Essential thrombocytosis
White blood cells
General features of white blood cells
Neutrophils
Eosinophils
Monocyte
Lymphocytes
Leukocyte adhesion deficiency
General features of leukemia
Acute lymphoblastic leukemia
Acute myeloblastic leukemia
Chronic lymphocytic leukemia
Chronic myelocytic leukemia
General features of lymphoma
Hodgkin’s lymphoma
Non Hodgkin’s lymphoma
Burkitt’s lymphoma
Hairy cell leukemia
Mantle cell lymphoma
Follicular lymphoma
Post transplant lymphoma
Bleeding and coagulation disorders
General features of bleeding and coagulation disorders
General features of platelets and endothelial cells
Pathways of coagulation
Clotting factors
Thrombomodulin
Hemophilia
Von willebrand disease
Glanzmann thrombaesthenia
Bernard soulier syndrome
Wiskott aldrich syndrome
Thrombocytopenia and purpura
Idiopathic thrombocytopenic purpura
Thrombotic thrombocytopenic purpura
Disseminated intravascular coagulation
Antiphospholipid antibody syndrome
General features of hypercoagulable disorders
Budd chiari syndrome
Hemolytic uremic syndrome
Plasma cell disorders
General features of myeloma
Features of multiple myeloma
Management of multiple myeloma
Drugs acting on blood
General features of drugs acting on blood
Heparin
Warfarin
Antiplatelet drugs
Thrombolytics
For more details, visit www.medpgnotes.com
You can send your queries to medpgnotes@gmail.com
Contents :
Sensitive and specific antibodies
Specific calcification
Cast / brace/ splint
Enzymes of mitochondria and cytosol
Human leucocyte antigen
Inhibitors in biochemistry
Types of joints
Longest and shortest acting drugs
Male and female analogue
Male and female preponderance
Mode of inheritance
Named fractures
Important tables in nutrition chapter
Specific names in orthopedics
Rate limiting enzymes
Physiology of receptors
Right and left laterality
Sensitive and resistive to radiation
Sensitive and specific investigation
Condition and specific terms
Names of staging/grading/prognostic system
Surgery names
Tumor marker
Vectors
X ray views
Important lists
Important tables in anesthesiology
Important tables in dermatology
Important tables in embryology
Clarke’s grouping of heart diseases in pregnancy
Forrest classification
Classification of leprosy
For more details, visit www.medpgnotes.com
You can send your queries to medpgnotes@gmail.com
This slide covers everything, from the definition of hypertension, to the risk factors, classification and the management of hypertension. However, details on the decisions to start anti hypertensive therapy are not included.
For various people, losing weight in a healthy way entails different things. That's why we've compiled a list of dishes that are low-carb, low-fat, or low-calorie. Here you'll find recipes to help you reach your weight-loss objectives.
This book presents a set of international recipes for foods that help reduce weight while maintaining physical fitness and agility and do not make those who adhere to a diet and weight reduction system deprived from enjoying the pleasure of eating in addition to ensuring the nutritional components necessary for the body within the framework of healthy and sound food
Contents :
General features of pathology
Features of cell injury
Hypoxia
Ageing
Necrosis
General features of apoptosis
Apoptotic and anti apoptotic protein
Calcification
Atrophy and hypertrophy
Hyperplasia and metaplasia
Stem cells
Fixatives and stains
Pigment
Bactericidal system
Hydrogen peroxidase
Oxidative stress
Free radical
NADPH oxidase
Basement membrane
Inflammation
Inflammatory mediators
Hydrostatic and osmotic pressure
General features of inflammation
Systemic inflammatory response syndrome
Autoantigen and associated diseases
Acute inflammation
Chronic inflammation
Chronic granulomatous disease
Granuloma
Complement system
Opsonization
Phagocytosis
Chediak higashi syndrome
Chemotaxis
Neoplasia
Cell cycle
Causes of neoplasia
Features of neoplasia
Protooncogenes and tumor suppressor genes
Management of neoplasia
General features of tumor markers
CA-125
CEA
AFP
Features of tumors
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You can send your queries to medpgnotes@gmail.com
2. 2
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Table of Contents
TABLE OF CONTENTS ......................................................................................................................................................................2
ABSTRACT .........................................................................................................................................................................................3
INTRODUCTION ...............................................................................................................................................................................4
MEDICAL IMPACTOF HYPOCALCEMIA ................................................................................................................................................4
ECONOMIC IMPACTOF HYPOCALCEMIA..............................................................................................................................................5
PHYSIOLOGICAL EFFECTS OF HYPOCALCEMIA ..........................................................................................................................6
NEUTROPHIL FUNCTION....................................................................................................................................................................7
BONE RESORPTION MARKERS............................................................................................................................................................8
CALCIUMSIGNALING IN IMMUNE CELLS.............................................................................................................................................9
CAUSES OF HYPOCALCEMIA..........................................................................................................................................................9
DCAD THEORY ...............................................................................................................................................................................10
HYPOPARATHYROIDISM...................................................................................................................................................................11
PREVENTION OF HYPOCALCEMIA..............................................................................................................................................12
EFFECTS ON BEHAVIOR....................................................................................................................................................................12
DIETARY POTASSIUM (K) .................................................................................................................................................................13
TREATMENT OF HYPOCALCEMIA ...............................................................................................................................................14
SECONDARY HEALTH EFFECTS ..........................................................................................................................................................15
CONCLUSION ..................................................................................................................................................................................15
FUTURE RESEARCH..........................................................................................................................................................................15
REFERENCES....................................................................................................................................................................................17
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HYPOCALCEMIA IN DAIRY CATTLE
Abstract
Subclinical andclinical hypocalcemiaduringthe transitionperiodindairycattle hasdetrimental effects
on animal health,welfare,andproduction. Anarrayof causesfor decreasedcalciumlevelsinhigh-
productiondairycattle have beendiscoveredoverthe lastfew decades.These causescaninclude the
level of calciuminthe pre-partumdiet,Dietary Cation-AnionDifference (DCAD) dietlevel beingfed,and
tissue sensitivityto parathyroidhormone (PTH) levels.Anotherimportantareaof interestfor
researchershasbeenthe physiological effectsof hypocalcemiaonthe immune cells,neutrophil
function,andbone resorptionmarkers. Alongwithdietarychanges,behaviorhasbeenstudiedasa
possible waytopreventhypocalcemia. Behavioral traitshave beenstudied,butfew correlationshave
beenmade betweenacow’sbehaviorandthe developmentof hypocalcemia,especiallysubclinical
hypocalcemia.Several treatmentoptionsforchronicclinical hypocalcemiahave beenimplementedto
on-farmuse, includingoral calciumsupplementsandintravenousinfusionsof calcium.Overall,there isa
greaterunderstandingof hypocalcemiaindairycattle.However,there isstill future researchthatneeds
to be conductedinorder topreventanddetectmore hypocalcemiacasesindairycattle before ithasa
negative effectonthe productionforthe farmer.
Key words: dairycow,hypocalcemia,neutrophilfunction,bone resorptionmarkers,immunecells,
behavior,parathyroidism
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Introduction
Milkproductionindairycattle has continuedtoincrease steadily overthe pastseveral decades.Since
calciumisthe mainmineral componentof milk,the cow’sneedforreadilyavailable calciumatthe
beginningof herlactationhasalsocontinuedtoincrease.However,if the demandbythe mammary
glandfor calciumisnot met,the cow becomeshypocalcemic. Hypocalcemiaisadisorderthatdevelops
whena cow isunable tomaintainadequate blood-calciumconcentrations. Eachyear,approximately5-
10% of dairycattle developclinicalhypocalcemia,andanadditional 25-50% of dairycattle are affected
by subclinical hypocalcemia.
Anymammal can develophypocalcemiaduringthe transitionperiod.However,dairycattle have been
bredto produce such a large amountof milkthattheyare particularlysusceptible tobecoming
hypocalcemic.Whenthe cow’sbodyhassucha large needforcalcium, anincrease incalcium
mobilizationfromthe bone occurs.The mobilizationof calciumfrombone happensbecause dietary
calciumisnot sufficienttosupportthe demandsof lactation.Hypocalcemiahasbeenlinkedto
significantnegative effectsonmilkyieldandreproduction.Additionally,hypocalcemiacanlead toa
varietyof secondaryhealthproblemsordisorders suchasmetritis, retainedplacenta, mastitis,ora
displacedabomasum.Thisarray of issues,stemmingfromhypocalcemia, cancostdairyproducersover
250 milliondollarseachyearinthe UnitedStatesalone.
MedicalImpact of Hypocalcemia
Hypocalcemiais definedas the deficiencyof calciuminthe bloodstream.Thisdisordercanbe clinical in
whichthe animal isphysicallydisplayingsignssuchasmuscle weaknessandadecrease inbody
temperature, orsubclinical where the animalisnotshowinganyreadilyobservable symptoms. Some of
the initial signsof clinical hypocalcemiacanbe excitability,hypersensitivity,andrestlessness.Once the
calciumconcentrationsgetsolowthat tetanybeginstosetin,the cow may experience tachycardiaor
5. 5
HYPOCALCEMIA IN DAIRY CATTLE
mildhyperthermia.Asthe cow’shealthcontinuestodecline,muscleswill weakentothe point atwhich
the cow will be sternallythenlaterallyrecumbent. The cow will appeartobe tremblingatfirst,butthen
she will become a“downer”cowonce she has reachedthe stage of recombency. Some of the more
severe caseswill exhibitsymptomssuchasconstipation,mildtoseverebloating,weakpulses,poor
pupillarylightresponse,flaccidparalysis,comaorevendeath (Bovine PostparturientParesis).
Most cows that sufferfromhypocalcemiawillbe diagnosedbasedontheirsymptomstheyexhibit.Since
the illnessissorapidinnature, a laboratorytestisnot a feasible diagnostictool if the animal isshowing
clinical symptomsalready.However,if acow has subclinical hypocalcemia,diagnosisismuchmore
difficult.Subclinical hypocalcemiccowsare diagnosedafterbloodisdrawnanda laboratorytestreveals
lowserumcalciumlevels (BovinePostparturientParesis).
Economic Impact of Hypocalcemia
It iseasyto understandthe negative effectclinical hypocalcemiccowshave onthe profitabilityof the
farm.First of all,a clinical hypocalcemiccow wouldmostlikelyneedtobe treatedbya veterinarian
usingan intravenousinfusionof calcium.Alongwiththe costof the veterinarytreatment,studieshave
shownclinical hypocalcemiacausesadecrease in milkproduction,aswell asahighersusceptibilityto
othersecondaryhealthconditions,which include:metritis,displacedabomasum, retainedplacenta, and
mastitis.Additionally,withmanyof the secondaryhealthproblems,more expensesfromthe producer
will be involvedforthe treatmentof thatanimal.Clearly,aclinical hypocalcemiccow canbe verycostly
for a producer.
Similartoclinical hypocalcemiccows, studieshave shownthat subclinical hypocalcemiccowshave a
higherinstance of secondaryhealthproblems,decreasedmilkproductionandadecreasedchance of
beingbredback.Since subclinical hypocalcemiaaffectsapproximatelyhalf of the cowsondairyfarmsin
the UnitedStates,mostof themgoundiagnosedanduntreated.Thus,the issuesthatarise and decrease
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productionresultinthe lossof over250 milliondollarseachyearinthe UnitedStatesdue to
hypocalcemia.
Hypocalcemiahasa huge economicimpactonthe dairy industryinthe UnitedStatesandaroundthe
world.Inrecentdecades,the studyof hypocalcemiahascontinuedtogrow inorderto try and
understandthe disorderbettertoreduce the amountof moneylostto thisdisorder.A lotof knowledge
relatingtothe causes,prevention,andtreatmentof hypocalcemiahave beendiscoveredandcontinue
to be discoveredbyscientists.
Physiological Effects of Hypocalcemia
Whena dairy cowexperienceshypocalcemicconditions,theyneedtocompensate forthe decreased
bloodcalciumbecause calciumisa veryimportantpartof regulatingawhole hostof bodilyfunctions,
includingsmoothmuscle contraction,intracellularactivity, andetc.Calciumabsorptionbythe intestine
will typicallyincrease.However,the primarymode forthe bodytorestore homeostaticcalciumlevelsis
throughcalciumresorptionfromthe bone.
The primaryhormone that isresponsible
for the mobilizationof calciumfromthe
bonesat the onsetof lactationin
mammalsisparathyroidhormone
related-protein(PTHrP),whichis
synthesizedwithinthe mammarygland
and isonlydetectable inthe circulatory
systemduringlactationandtimesof
metastaticbone cancers.
7. 7
HYPOCALCEMIA IN DAIRY CATTLE
PTHrP issimilartoparathyroidhormone (PTH) andit hasbeenextensivelystudiedinthe humanand
rodentmodels.However,little researchhasbeendone relatingtoitsfunctionindairycattle.Serotonin,
5-hydroxytryptamine (5-HT) regulatesthe inductionof PTHrP.The molecularmechanismsgoverningthis
actionare still unknown.Manipulationof 5-HTnear the end of a pregnancyperiodmaybe a critical
factor inpreventingthe onsetof hypocalcemiaduringearlylactation.5-HTisa homeostaticregulatorof
the mammary gland.5-HT isproducedina two-steppathwayfromthe aminoacidL-tryptophanusing
the rate-limitingenzyme tryptophanhydroxylase 1(TPH1).AfterL-tryptophanisconvertedinto5-
hydroxy-L-tryptophan,itundergoesdecarboxylationtoform5-HT.
Preventinghypocalcemiacouldgreatlybenefitthe dairyindustry.Cowsthatremainhealthythroughthe
transitionperiodare more likelytoproduce anadequate amountof milk,aswell asanothercalf,and
bothof these factorsare critical inmaintainingthe economicviabilityof the dairyfarmsandthe
sustainabilityof the humanfoodproductionsystem.
Neutrophil Function
Martinezconducteda studythat waspublishedinthe Journal of DairyScience in2013 aboutthe effects
of the neutrophil functioninhypocalcemicdairycattle.The study,conductedatthe Universityof Florida
DairyUnit in Gainsville, Florida,directlycomparedthe neutrophil functionof normcalcemicandinduced
subclinical hypocalcemiaintennon-pregnant,non-lactatingHolsteincows (Martinez).
Amongthe most importantdatacollected,theydiscoveredthat the neutrophilfunctionwassuppressed
incows withsubclinical hypocalcemia.Cowsthathadinducedsubclinical hypocalcemiahadareduced
percentage of neutrophilswithphagocyticactivity.Additionally,subclinical hypocalcemiccowshada
reductioninthe percentage of neutrophilswithoxidativeburstactivity.Finally,phagocytosisand
oxidative burstdeclinedat72 hoursafterthe beginningof the infusioninsubclinical hypocalcemiccows,
where asthose valuesbothincreasedinnormcalcemiccows (Martinez).
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The main outcome of thisstudyrevealedthe dropincalciuminthe bloodthatoccurs during
hypocalcemianegativelyeffectsthe neutrophilsandmakesthe cow lesslikelytofightagainst
pathogenicbacteria.The depressionof bacterial killingiscausedfromthe neutrophil suppressionof
phagocytosis.Thispointalsosupportsthe factthathypocalcemiccowshave an increasedinstance of
secondaryhealthissues. Extracautionshouldbe takenforthese cowsinorderto preventsecondary
bacterial infections.
Bone Resorption Markers
A studyconductedbyLiesegang,publishedinthe Journal of DairyScience in1998, exploredthe bone
resorptionmarkersinhypocalcemicdairycattle.The study,conductedatthe Universityof Zurichin
Switzerland,investigatedwhetherhydroxyproline,deoxypyridinoline,orthe carboxyterminal
telopeptide of type Icollagencouldbe usedasmarkerstoprovide evidence of bone resorptionduring
hypocalcemiaindairycows (Liesegang).
Amongthe most importantdatathat was collected,cowsshowingsymptomsof hypocalcemiahad
increasedurinaryhydroxyprolineconcentrationsfromparturitiontoday14. Deoxypyridinoline
concentrationsinthe urine were increasedafterparturitionuntil day9and carboxyterminal
telopeptidesof type Icollagenpeakedatday5. However,these valueswere the same betweencows
withhypocalcemicsymptomsandcowswithout (Liesegang).
The main conclusionresearchersmade wasthatassaysfor urinarydeoxypyridinoline andserum
carboxyterminal telopeptideof type Icollagendeterminationsare useful toolstofollow the course of
degradationof bone collagenindairycattle duringhypocalcemia. Furtherresearchcoulddevelopon-
farm teststo determinelevelsof these bone resorptionmarkersinordertodeterminethe severityof a
hypocalcemiccow.
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HYPOCALCEMIA IN DAIRY CATTLE
CalciumSignaling in Immune Cells
A studypublishedinthe Journal of DairyScience in2005 by Kimuraoutlinedthe influencesof
hypocalcemiaonimmune cellsindairycows. The study,conductedatthe National Animal Disease
CenterinAmes,Iowa,testedif the increaseddemandforcalciuminperiparturientcowsadversely
affectsintracellularcalciumstoresof immune cells (Kimura).
Amongthe importantdata theycollected, researcherswere able toconclude thatintracellularcalcium
storesdecreasedinperipheral bloodmononuclearcells(PBMC) before parturitionanddevelopmentof
hypocalcemia. Thisisthe cause of a bluntedintracellularcalciumreleaseresponse toanimmune
activationsignal.The studysuggeststhatsystemiccalciumstressprecedesmeasurable hypocalcemia,
especiallyincowsthatwill developclinical hypocalcemia.PBMCintracellularcalciumstoresare amore
sensitivemeasure of calciumstressesintransitioncows (Kimura).
The conclusionresearchersdevelopedwiththe datafromthisstudyshowsa depletionof intracellular
calciumstoresstarts several dayspriortocalvinginhypocalcemiccows.Furtherresearchshouldbe
done inthisarea to develop asimple testforon-farmuse thatmeasuresPBMC.PBMCis responsible for
the flux of calciumthat wouldordinarilyactivatethe cellsandpreventthe cow fromexperiencing
immunosuppression (Kimura).
Causes of Hypocalcemia
The physiological effectsof hypocalcemiaare verycomplicated anditisdifficulttostudyjustone part of
the calciumhomeostaticregulatorysystem.Since the entire processissocomplex,the causesof
hypocalcemiaare hardto pinpoint.Historically,highlevelsof dietarycalcium have beenbelievedtobe
the major cause of hypocalcemiaindairycattle.Scientistshave begunexploringotherfactorsthatcould
contribute toa cow’srisk of developinghypocalcemia. A majorareaof nutrition relatedtothe cause of
hypocalcemiaisthe DietaryCation-AnionDifference (DCAD)Theory. Hypoparathyroidism,anothercause
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of hypocalcemia, hasrecentlybeenlinkedtohypocalcemiabecause itaffectsthe body’stissue
sensitivitytoparathyroidhormone.Overall,understandingsome of the majorcausesof thisdisorderis
an importantpart of understandinghypocalcemiaindairycattle.
DCAD Theory
The DietaryCation-AnionDifference Theory(DCAD) hasbecome atopicindairyscience thatis being
studiedmore andmore nowadays.DCADisbasicallyanequationof the cations (potassiumandsodium)
and the anions (chlorine andsulfur) inthe dietof adairycow ina relationshipsuchas ( 𝑁𝑎 + 𝐾) − (𝐶𝑙 +
𝑆). DCAD isresponsibleforinfluencingthe animal’sacid-basehomeostasis,calciumstatusaround
calving,andmineral elementutilization.Previousstudieshave showndecreasingthe DCADimproves
calciumhomeostasisatthe onsetof lactation.Additionally,the riskof developinghypocalcemiais
greatestincowsin a state of metabolicalkalosis,whichisinducedfromfeedingahigh-DCADdiet.
A studyconductedin2005 byLean was publishedinthe Journal of DairyScience,revisitedprevious
workrelatedtothe DCADTheory.The study,conductedat the Bovine ResearchAustralasiainAustralia,
aimedtoexamine whichformof the DCADequationprovidedthe bestestimateof hypocalcemiarisk
and to clarifyrolesof calcium,magnesium, andphosphorusconcentrationsof twopre-partumdietsin
the pathogenesisof hypocalcemia (Lean).
Amongthe most importantdatathe researchersfound,hypocalcemiariskwashighest withpre-partum
dietaryconcentrations of 1.35%calcium.Additionally,increasingpre-partumdietarymagnesium
concentrationshadthe largesteffectondecreasingincidence inhypocalcemia.Finally,increasing
dietaryphosphorusconcentrationspre-partumincreasedthe riskof hypocalcemia (Lean).
The main suggestionresearchersmade toproducerswasthe datastronglysupportsthe needto
evaluate macromineral nutritionapartfromDCAD of the diet. It iscritical for producerstoassessand
control the levelsof dietarymacromineralsincludedinthisstudyof the pre-partumdietinorderto
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HYPOCALCEMIA IN DAIRY CATTLE
preventthe instancesof hypocalcemiainthe herd. The diettakingDCADlevelsintoaccountinthisstudy
isso far the bestmodel currentlyavailable forpredictinghypocalcemia incidence indairycattle (Lean).
Hypoparathyroidism
A studypublishedinthe Journal of DairyScience in2013 conductedby Goff aimedtolookat the effect
of high-DCADdietsfedtopre-partumcowstosee if itreducestissue sensitivitytothe parathyroid
hormone (PTH),inducingapseudohypoparathyroid state thatdiminishescalciumhomeostatic
responses.The study,conductedatthe UnitedStatesDepartmentof Agriculture –Agricultural Research
Service inAmes,Iowa,directlycomparedcowsfedlow-DCADandhigh-DCADdietstoinduce a
compensatedmetabolicalkalosisandacidosisstate,respectively,followedbysyntheticPTHinjections (J.
P. Goff).
Amongthe most importantdatatheycollected,theynoticedcowsfedthe high-DCADdiethadplasma
calciumconcentrationsthatincreasedata much lowerrate.Additionally,the cowsthatwere fedthe
high-DCADdietproducedsignificantlyless1,25-dihydroxyvitaminDinresponse tothe PTH injections
than the cowsthat were fedthe low-
DCAD diet.Finally,the cowsthatwere
fedthe high-DCADdiethad
numericallylowerserum
concentrationsof the bone resorption
markercarboxyterminal telopeptide of
type 1 collagenthanthe cowsfedthe
low-DCADdiet.However,the numbers
were notstatisticallydifferent (J.P.
Goff).
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Researchersinthisstudymade one mainsuggestiontodairyproducerstotry anddecrease instancesof
hypocalcemiaintheircattle.Itisimportantthatcowsthat are nearingparturition,especially
multiparouscows,are consuminglow-DCADdiets.Low-DCADdietscanincrease the intestinal
absorptionof calcium, aswell asenhance the release of calciumfrombones.AccordingtoGoff,
“because cowsfedlow-DCADdietsdoexcretemore calciumintheirurine,ithasbeensuggestedthat
renal reabsorptionof thispotentialpool of calcium(5-7g of Ca/d) couldprovide the calciumneededto
preventthe developmentof hypocalcemiaandmilkfever.”
Prevention of Hypocalcemia
Preventingclinical andsubclinical hypocalcemiacasesinadairyherdis the keyto reducingthe
productionlossesfromthe effectedcows. Bypreventingthe hypocalcemicissuesfromoccurring,the
cow’schancesof havingsecondaryhealthissuesare eliminatedaswell.Several wayshypocalcemiais
beingpreventedisthroughthe studyof a cow’sbehavioraroundthe transitionperiodandthroughthe
manipulationof the potassiumlevelsinthe cow’sdiet.
Effectson Behavior
A 2011 study,publishedinthe Journal of DairyScience byJawor,aimedtodescribe the associationsof
subclinical hypocalcemiawithmilkyield,feeding,drinkingandrestingbehaviorduringthe periodaround
calving.Thisinformationcouldhelpproducerspredictwhencowsare beingaffectedbysubclinical
hypocalcemiabasedontheirbehaviors.The study,conductedatthe Universityof BritishColumbia’s
DairyEducationand ResearchCentre,directlycomparedthese behaviorsinHolsteindairycowswhich
had subclinical hypocalcemiawith control cows (Jawor).
Amongthe importantdata theycollected,cowswithsubclinical hypocalcemiaproducedanaverage of
5.7 kg/dmore milkduringweeks2,3, and 4 of lactationcomparedto control cows.Also,hypocalcemic
cowsthat were intheirthirdlactationsustainedgreatermilkyieldsthroughout280 DIM. Additionally,
13. 13
HYPOCALCEMIA IN DAIRY CATTLE
dry matterintake was,onaverage,1.7 kg/dgreaterduringthe weeks -2and -1 and fewervisitstothe
waterand feedbinsoccurredinthe firstfew weeksaftercalvingamongcowswithsubclinical
hypocalcemia.Finally,the cowswithsubclinical hypocalcemiaonaverage stoodfor2.6 h longerduring
the 24-hour periodbefore calvingand2.7 h lessstandingduringd+1 (Jawor).
The researchersmade twomainsuggestionstodairyproducersrelatingtohypocalcemiccows’behavior.
First,dairycattle withsubclinical hypocalcemiaduringthe 24-hperiodpostpartumdidnotexhibitany
majorchangesin productionorbehaviorthatwouldtypicallybe associatedwithpoorhealth.Forthis
reason,cowsneedtobe closelymonitoredduringthistime periodincase symptomsdoappear.
Secondly,the resultsrelatedtothe amountof tripsto the feedandwaterbinspost-partumdisplayed
the importance of ensuringcowshave adequate accesstofeedinganddrinkingareasduringthe period
followingcalving. Thisisnecessaryinorderto allow the cowsto meettheirnutrientrequirements.
Therefore,itisimportanttomanage the pensof freshcowscloselytoensure a low stockingdensity.
DietaryPotassium (K)
A studyconductedbyR. L. Horst in 1997, publishedinthe Journal of DairyScience, lookedatstrategies
for preventinghypocalcemiaindairycattle.The study,conductedatthe National AnimalDiseaseCenter
inAmes,Iowa,studiedwaystominimizethe effectsof dietarypotassiumonhypocalcemiaincidences
(Horst).
Amongthe most importantdatacollected,Horstfounddirectevidence thatcowsfedadietlow in
potassiumandsodiumhave lessmilkfeverthanthose ondietshighinKor Na. Second,overfertilization
of alfalfawithKresultsinplantswithhighconcentrationsof Kthat are detrimental tothe healthof the
periparturientdairycow.Finally,since manydairyproducerspurchase aportionof theirfeedstuffs,soil
K concentrationscontinue tobuildovertime asmostof the K broughtontothe farmin purchasedfeed
remainsonthe farm (Horst).
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Researchersmade one mainsuggestionwiththisstudyrelatingtodietaryK.Itis importanttofeedlow
levelsof dietaryKindairycattle rationsbecause Kplaysa significantrole inpredisposingcowsto
hypocalcemia.The researchersalsoshowedthe importance of the acid-base balanceof the dieton
calciummetabolism.Finally,Horstsuggested,“future researchshouldfocusoneffective methodsfor
managingdietaryK,resultingindecreasedreliance onanionicsalts.”
Treatment of Hypocalcemia
The amount of researchbeingdone related tothe treatmentof clinical andsubclinical hypocalcemiahas
beenslowlydecreasingoverthe yearsbecause of the factthat causesand prevention forhypocalcemia
are becomingthe focus. The specifictype of treatmentforhypocalcemiadependsonthe severityof the
disorder.A standingcowwouldbe treateddifferentlythanacow whichisunable tostandup on her
own(Oetzel).
Cowsthat are experiencingsubclinical hypocalcemiaorare displayingclinical signsof hypocalcemia and
are still able tostandon theirownare in the verymildstagesof the disorder.Atthispoint,cowscan be
treatedwithoral calciumsupplementation.Withinahalf hourafterthe supplementation,the cowis
able to absorban effectiveamountof calciumintoherbloodstream. The calciumconcentrationsinthe
cow’sbloodwill remainelevatedfromthe supplementationfor4-6hours afterward (Oetzel).
In more severe hypocalcemiacases,whenthe cow isunable tostand,a fastertreatmentisrequired.The
mostrapid treatmentfortreatingseverelyhypocalcemiccowsiswithintravenouscalciuminfusions.
Withthistreatment,calciumlevelsinthe bloodare restoredalmostimmediately.The downfalltothis
type of treatmentisthat bloodcalciumconcentrationsare raisedtoextremelyandpotentially
dangerouslevels.Therefore,if acowis experiencingseverehypocalcemia,aveterinarianshouldbe
involvedinthe treatment.
15. 15
HYPOCALCEMIA IN DAIRY CATTLE
SecondaryHealth Effects
A wide arrayof issuescanstemfromsubclinical andclinical hypocalcemiaindairycattle.Firstof all,
studieshave shownmetabolicdisordersimpairimmunefunctionwhichpredisposesthe cow touterine
infectionsandmastitisfollowingparturitionandatthe beginningof theirlactation.Additional
researcherhaslinkedthe instancesof ketosiswithsubclinical hypocalcemia.Finally,retainedplacenta
and endometritishashighersusceptibilityratesincowsthathave had hypocalcemiaatthe beginningof
theirlactation.If a cow developshypocalcemia,aproducershouldtake extracare to insure the riskof
any of the secondaryissuesisreduced.A veterinariancanhelpdetermine the besttreatmentand
aftercare fora hypocalcemiccow (J.P.Goff).
Conclusion
Subclinical andclinical hypocalcemiaare majorhealthproblemsinamajorityof dairycattle and oftengo
untreated.Cowswithsubclinical hypocalcemiatypicallydonotshow signsorsymptomsuntil the
problemissevere.A cow’sbehaviorshouldbe closelymonitoredbefore andafterparturition,and
propermanagementstrategiesshouldbe enforcedondairyfarms.Takingthese simple stepsasa
producercouldendup saving themthousandsof dollarseveryyearfromthe earlydetectionof
hypocalcemiainthe cows. Byfocusingthe effortsonthe preventionof hypocalcemia,throughfocusing
on majorfactors contributingtohypocalcemia,suchaspseudohypoparathyoidism,the instancescanbe
greatlydecreased.Inall,thiswouldbe beneficialtodairycowsand producersworldwide.
Future Research
The study of clinical andsubclinical hypocalcemiahasbeenincreasingoverthe lastfew decades.Thisis
due to the large economicimpactthat the disorderhason dairyindustry.However,studiesare moving
away fromthe treatmentof hypocalcemiaandshiftingtowardfocusingonthe causesandpreventionof
the disorder. A lotof researchshould continued tobe done focusing onthe developmentof on-farm
17. 17
HYPOCALCEMIA IN DAIRY CATTLE
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