Download - Nutrional disorders
2012 Webinar Series 2/16/2012
Nutritional disorders 1
SUSAN SCHOENIAN (Shāy‐nē‐ŭn)Sheep & Goat SpecialistWestern Maryland Research & Education [email protected] ‐ www.sheepandgoat.com
DISEASES A‐Z Other namesCause(s)
1) Acidosis2) Bloat3) Copper toxicity4) Enterotoxemia5) Milk fever6) Poisonings
P li h l l i
Cause(s)Risk factorsClinical signsTreatment(s)Prevention
7) Polioencephalomalacia8) Pregnancy toxemia9) Scours (diarrhea)10) Urinary calculi11) White muscle disease
2012 Webinar Series 2/16/2012
Nutritional disorders 2
Tx ‐ treatmentVx – requires veterinarianRx – requires prescriptionOTC ‐ over the counterIM – intramuscular injectiont a uscu a ject oSQ – subcutaneous injectionIV – intravenously injection
CAUSE
Large quantities of gas are produced in the rumen resulting in:
∆ Volatile fatty acids (VFAs)Lactic acidRumen pH
Pressure and inability to l l d t d th
RISK FACTORS
Sudden intake of readily di tibl b h d t expel gas can lead to death. digestible carbohydrates: grain, pellets, or by‐products, due to:1. Inadequate adjustment period2. Accidental access3. Variation in intake
Lack of roughage in diet
2012 Webinar Series 2/16/2012
Nutritional disorders 3
CLINICAL SIGNSCLINICAL SIGNS
Reduced appetiteDepressionAbdominal painBloatRumen contractionsSlow down ceaseDi hDiarrheaMild profuseRecumbencyDeath
Death can be rapid! Acidosis may also cause laminitis, a painful inflammation of the hoof.
TREATMENT
Neutralize the acidDiet adjustment: remove grain and feed good quality hay.
Oral drenches▪ Sodium bicarbonate
▪ Vegetable oil
PREVENTION
Gradual introduction of grain, pellets, or by‐products to diet.
▪ Mineral oil
▪ Antacids
Other Tx’s▪ Anti‐inflammatory drugs [Rx]▪ Antibiotics▪ Fluid therapy
Do not crack or grind feeds.Adequate roughage intake.Feed additives (rumen modifiers)
▪ Ionophores (Bovatec®, Rumensin®)▪ Buffers (e.g. baking soda)▪ Yeast
2012 Webinar Series 2/16/2012
Nutritional disorders 4
CAUSE RISK FACTORS
Excess gas in the rumen.Failure to expel gas (belch)
CO2 and CH4
Two kinds of bloat1. Frothy or foamy
Pasture bloat Legume pastures, > 50%alfalfa, red/white clover, lespedeza, birdsfoot trefoil
Small grain pastures.Lush, wet pastures
1. Frothy or foamy (pasture)
2. Free gas (feedlot)
Succulent pasture
Feedlot bloatExcessive consumption of grain
CLINICAL SIGNS
Distended abdomen, mostly on left side.
PainDepressionRestlessnessDiarrheaDifficulty breathingRespiratory failureStaggeringRecumbencyDeath
2012 Webinar Series 2/16/2012
Nutritional disorders 5
TREATMENT PREVENTION
Mild cases1. Encourage belching
Massage stomach, walk
2. Drench with vegetable oil, baking soda, corn oil, antacid, or commercial anti‐bloat medicine [OTC].
3. Pass stomach tube to
Restrict pasture intakeFill animals with dry hay before turning onto lush or legume pastures.Gradual changes to dietFeed additives3. Pass stomach tube to
relieve pressure of gas.
Life or death4. Rumenotomy ‐ puncture
a hole in the rumen with a 16 g needle [Vx ]
▪ Anti‐bloat preparations▪ Ionophores (Bovatec®,
Rumensin®)
CAUSE
Chronic vs. acute
Liver capacity for copper has been exceeded .
Hemolytic crisis (RBC destruction) ‐triggered by stress
Feothers
gg y
The level of Cu that is toxic varies with the levels of Mo and S that are in the diet. Other minerals also affect copper absorption (e.g. Fe).
Cu
S
Mo
2012 Webinar Series 2/16/2012
Nutritional disorders 6
RISK FACTORS OtherSoil chemistryAnimal differences
Goats more tolerant than sheep.Medium wool, Down/British breeds, and dairy sheep most susceptible .Young animals absorb Cu more efficiently than older animals.
Excess copper in dietFeeding minerals or feeds that are
Soil chemistryCopper sulfate foot bathsAnthelmintics with copperCopper plumbing
formulated for other livestock.Errors in feed formulation.Adding copper to feed or mineral.
Copper antagonists (Mo, S, Fe)Low levels of molybdenum (Mo)Cu:Mo should be < 10: The Texel is the most susceptible to Cu toxicity,
while sheep with Finn breeding are the least.
CLINICAL SIGNS
Sudden onsetWeaknessTeeth grindingThirst Dark brown or red‐colored urineJaundiceYellowing of membranesAnemiaShallow breathingRecumbencyDeath
Source of images: NADIS UK
2012 Webinar Series 2/16/2012
Nutritional disorders 7
TREATMENT PREVENTION (mostly sheep)
Inactivate copper. Ammonium molybdate
Ammonium sulfate
Curprimine [Rx]
Don’t’ add copper to ration or mineral.Don’t feed minerals or feeds that have been formulated for other species.Don’t deworm with copper sulfate or copper oxide wire.Don’t fertilize pastures or hayfields with swine or poultry manure.Don’t use copper sulfate footbaths.If copper toxicity is suspected, test feeds, forages, and soils for levels of Cu, Mo, and S.
RISK FACTORSCopper concentration in legumes
Copper‐deficient soilsLow copper levels in plantsExcessive consumption of Mo or S in pasture or feed.
DIAGNOSISDIAGNOSIS
Laboratory testsLiverBlood Pasture
2012 Webinar Series 2/16/2012
Nutritional disorders 8
CLINICAL SIGNS
SwaybackAtaxia (lack of muscle coordination)
Rough hair coatDull coatHair loss in goatsSteely or stringy wool (lack of crimp)(lack of crimp)
Loss of pigmentation in black‐wooled sheepPoor performanceReproductive problemsAnemiaDeath
TREATMENT
S l t l Supplemental copper1. Injections 2. Oral drenching
▪ Copper sulfate3) Boluses
▪ Copper oxide wire particles
PREVENTION
Feed properly‐balanced rations: Cu : Mo: SDo not feed minerals formulated for sheep to goats.Fertilize with copperSupplemental copper: same as treatment above
2012 Webinar Series 2/16/2012
Nutritional disorders 9
CAUSE RISK FACTORS
An increase in the bacteria produces an endotoxin that is released into the blood stream and causes an inflammation of the intestine and swelling of the lungs and kidneys.
Vigorous, healthy, rapidly growing lambs and kids (e.g. singles)
Sudden intake of large quantities of grain, pellets, or by‐product feeds.
Accidental accessInadequate adjustment period
Affects mostly lambs and kids shortly after birth, through their feeding period.
Adults are mostly immune
Variation in intake
Lush pasturesLoss of litter mateInadequate roughage intake
CLINICAL SIGNSCLINICAL SIGNS
Sudden death[usually best, fastest growing lambs and kids]
Off feedAcute indigestionLethargicColicColicNervous system signsAbdominal discomfortProfuse diarrhea
2012 Webinar Series 2/16/2012
Nutritional disorders 10
TREATMENT
Individual[usually not successful in severe cases]
C & D anti‐toxinPenicillin [OTC]Additional Tx’s▪ Oral electrolytes▪ Anti‐inflammatory drugs [Rx]▪ Thiamine [Rx]
P bi i▪ Probiotics▪ IV fluids
Outbreak ‐whole herdIncrease forage in dietAdd chlorotetracycline to feedAdminister anti‐toxin
PREVENTIONManagement
Gradual feed changesSteady intake of feed or milkFeed additives (Aureomycin®)Limit access to grain and lush pastureLet creep feed run out
VaccinationE d d l b Ewes and does: annual booster during late pregnancyLambs and kids: vaccinate at approximately 6‐8 and 10‐12 weeks of age.Annual vaccination of all adult animals.Some farms may need to vaccinate more frequently to provide adequate protection.
2012 Webinar Series 2/16/2012
Nutritional disorders 11
CAUSE RISK FACTORS
Low level of blood calcium (Ca)
Insufficient intake or absorption of calcium to meet fetal or lactation demands.
Calcium‐poor diets or diets too high in calcium in late gestation.High producing females.Stress and handling.
Occurs anywhere from six weeks prior to parturition to 10 weeks after parturition.
Non‐dairy (before parturition)Dairy (after parturition)
CLINICAL SIGNS
Fever
Sudden onset of symptomsUncoordinatedNervousHyperactivitySluggishCold earsRear legs splayed outRear legs splayed outRecumbencyComatoseDeath
Clinical signs are similar to pregnancy toxemia; diagnosis is based on the response to treatment (calcium).
2012 Webinar Series 2/16/2012
Nutritional disorders 12
TREATMENT
CalciumOral Calcium gluconateSubcutaneousCalcium gluconateIntravenousCalcium borogluconate
Other Tx’sOther Tx’sB‐complex vitaminsGlucoseDextroseMagnesium
PREVENTION
Proper levels of calcium in late gestation diet and over the long run.
Addition of limestone to the grain diet.Feed better quality hay Feed better quality hay ‐ part legumeOverfeed calcium in grain or forage ration.Avoid stressing females.
2012 Webinar Series 2/16/2012
Nutritional disorders 13
CAUSE RISK FACTORS
Plant poisoningsNitrate poisoningCyanide poisoningUrea poisoningMolds and mycotoxins
DroughtFrostPoorly‐managed pasturesStressed plantsAccess to poisonous plants or those that accumulate toxic substancesAccidental exposureImproper mixing of feedContaminated feed
CLINICAL SIGNS
Vary with toxin and can be non‐specific.
Acute vs. chronicSudden deathExcessive salivation
b d b hLabored breathingGastric distressNeural symptomsPhotosensitivityReproductive problems
2012 Webinar Series 2/16/2012
Nutritional disorders 14
TREATMENT
h d b lVaries with toxin and ability to diagnose cause of symptoms.Some poisonings have no effective treatment. Activated charcoal binds to toxins.Removal of the source of the toxin.
PREVENTION
Good pasture and grazing management.Removal of toxic plants.Test feeds for mycotoxins.
CAUSE RISK FACTORS
Acute or sub‐acuteMetabolic disease with neurological symptoms that are caused by a deficiency of thiamine (vitamin B1).
Disturbance of thiamine metabolism
Sudden changes in dietHigh grain dietsHigh sulfur intakeProlonged treatment with Corid (amprolium).Ingestion of plant thiaminasesIngestion of plant thiaminasesor thiamine analogs
2012 Webinar Series 2/16/2012
Nutritional disorders 15
CLINICAL SIGNS
IsolationDepressionLack of appetiteDiarrheaFeverLack of muscle coordination
Differential diagnosis: listeriosis, tetanus
StaggeringBlindness
Star gazingRecumbencyDeath
TREATMENT
Thiamine ‐ 10 mg/kg BWThiamine HCL 200 mg/mL[Rx] IM or SQ▪ B‐complex vitamins [OTC]
(contains less B1 per ml)
Severe casesSevere casesIV injection of thiamine [Rx]Repeated injections of thiamine, IM or SQ [Rx]Anti‐inflammatory drugs [Rx]Fluid therapy
PREVENTION
Good managementAdequate roughage in dietMonitor sulfur intakeSupplemental thiamine in diet
2012 Webinar Series 2/16/2012
Nutritional disorders 16
CAUSE RISK FACTORS
Low blood sugarEnergy imbalanceBreakdown of energy into toxic ketone bodies which overwhelm liver capacity.
Inadequate intake of energy in late gestation
Poor quality forageLack of energy in dietVariable feed intakeReduced rumen capacityLack of feeder spaceac o eede space
Most common in females carrying multiple births.Fat or very thin femalesLack of exercise [?]
CLINICAL SIGNS
~3‐10 day courseLagging behindAnorexiaDepressionSalivation
l d llSa at oNervousness WobblyRecumbencyDeath
Some people can detect a sweet, acetone smell on the animal’s breathThere will be elevated ketones in urine or blood. Clinical signs are similar to milk fever. Diagnosis is based on response to treatment (glucose).
2012 Webinar Series 2/16/2012
Nutritional disorders 17
TREATMENT
Get rid of the nutritional drain1. Induce labor with steroids [Rx]2. Caesarian section [Vx]
Glucose replacement1. Oral propylene glycol
Alternatives: Karo™ syrup, molasses
SQ l2. SQ glucose3. IV glucose
Other Tx’s1. Calcium2. Lactated ringers3. Sodium bicarbonate
PREVENTION
Sufficient energy in diet of females during late pregnancy
ConcentratesBetter quality forage
Identify females carrying twins and triplets and feed twins and triplets and feed them accordingly.Moderate body condition.Avoid stressEncourage exerciseAdequate feeder space
2012 Webinar Series 2/16/2012
Nutritional disorders 18
CAUSE
Scours are not a disease.
Scours are a symptom.
There are many causes:1. Infectious2. Non‐infectious
NON‐INFECTIOUS
P iti
INFECTIOUS
B t i lParasiticWorms barber pole worm
NutritionalDietary changesSimple indigestion or allergyPoor quality feedHigh moisture content of feedToxins in feed
BacterialE. coliSalmonellaClostridial diseasesJohne’s disease
ViralRotavirusCoronavirusManagement
Poor sanitationOvercrowding
StressWeaningWeatherShipping/transportation
Coronavirus
ProtozoanEimeria (coccidia)CryptosporidiaGiardia
2012 Webinar Series 2/16/2012
Nutritional disorders 19
CLINICAL SIGNS
Increased frequency, fluidity, or volume of feces.May have mucous or blood
DehydrationDirty legs and hocksS il d lSoiled woolRough hair coatIll thriftPoor performance
TREATMENT
Depends upon underlying cause (and age of animal)
Non‐infectious▪ Bismuth Subsalicylate [OTC]▪ Kaolin‐Pectin [OTC]▪ ImmodiumAD [OTC]▪ Probiotics [OTC]▪ Fluid therapy
Infectious▪ Antibiotics
▪ Penicillin [OTC]▪ Spectinomycin® [Rx]▪ Corid, sulfa drugs [Rx]
PREVENTION
Gradual changes in dietRoughage (dry) in dietGood sanitationCoccidiostats
2012 Webinar Series 2/16/2012
Nutritional disorders 20
CAUSE RISK FACTORS
Calculi (stones) lodge in the urinary tract of mostly male animals and prevent urination. Stones are usually composed of phosphate salts, but may also be composed of calcium salts.
Primarily wethers (castrates)Early castration
Sometimes intact malesImbalance of Ca and P in diet.Concentrate diets excessive in PHigh grain: low roughage dietsForage diets excessive in CaLack of good quality waterg q y
Ca: PCALCIUM: PHOSPHORUS
CLINICAL SIGNSCLINICAL SIGNS
IsolationDiscomfortRestlessnessAnxietyAbdominal painUrine dribblingUrine dribblingHumped up appearanceDistention of abdomen (edema)Rupture of bladderDeath
2012 Webinar Series 2/16/2012
Nutritional disorders 21
TREATMENT PREVENTION
Very earlyAmmonium chloride drench
Early amputation of urethral
2:1 ratio of Ca to P in the dietFeed alfalfa‐only diet to malesAddition of ammonium chloride to the dietSalt to stimulate water intake
process
LaterUrethrostomyEuthanasia
water intakeAdequate forage in the dietAmple supply of fresh water at all timesAdequate vitamin ADelay castration [?]
CAUSE RISK FACTORS
Degeneration of skeletal and cardiac muscles caused by a deficiency of vitamin E and/or selenium.
Congenital vs. acquiredCardiac vs. skeletal
Dietary deficiency of selenium and/or vitamin E.
Se: selenium‐deficient soils and plantsVitamin E: poor quality hay or lack of access to pasture
Selenium content of forages
2012 Webinar Series 2/16/2012
Nutritional disorders 22
CLINICAL SIGNS
CardiacSimilar to pneumoniaIrregular and elevated heart and respiratory ratesDeath
SkeletalStiffnessWeaknessPainMuscle tremblesArched backHunched appearanceStilted gaitInability to stand
TREATMENT
CardiacIneffective to treat
SkeletalSupplemental selenium and vitamin E (Bo‐Se®)
2012 Webinar Series 2/16/2012
Nutritional disorders 23
PREVENTION
Good nutritionBalanced rationsGood quality foragesAccess to pastureFree choice minerals
Supplemental seleniumSupplemental selenium0.10 to 0.30 ppm Se in total dietDaily intake not to exceed 0 0.7 mg/head/day
Feed and mineral supplementationOral gelInjections
Increased mortalityyIll‐thrift ScouringPoor growth ratesInfertility
Failure of embryo to implantRetained placentasDiminished fiber growthPeriodontal diseaseImpaired immunityChronic health problems
Unfortunately, none of these symptoms are specific to a Se deficiency. Only white muscle
disease offers a definitive diagnosis.
2012 Webinar Series 2/16/2012
Nutritional disorders 24
Labeled dosage (SQ or IM)1 ml/40 lbs for lambs 2 weeks of age and older (1 ml min )older (1 ml min.)2.5 ml/100 lbs. for ewesPregnant ewes Has caused abortions
Not approved for goats or lambs under 2 weeks of age.Seek advice of a small ruminant veterinarian before giving selenium injections to your animals.
Feed supplementation is preferred to giving injections for providing adequate Se to sheep and goats.
Should confirm selenium deficiency by post‐mortem, blood test, or measured response to Se supplementation.
An overdose can be toxic.
Feed balanced rations
Life cycle feeding
Simple rations
Gradual feed changes
Adequate roughage in diet
R l b d di i iRegular body condition scoring
Maintain animals in moderate body condition (2‐4).
Exercise and sunlight.
2012 Webinar Series 2/16/2012
Nutritional disorders 25
This is the final webinar in the 2012 six‐part webinar series on sheep and goat feeding and nutrition.
Thank you for your attention.
Any questions?
Susan [email protected]
www.sheepandgoat.com