FAM 2 Small Ruminant Metabolic DZ
| CU Toxicosis:|
When do problems occur?
Are goats susceptible?
| Sheep: 25ppm|
Problems: sheep fed cattle/horse rations
Goats not as suceptible as sheep.
| What is the simple form of Cu toxicosis?|
Cu accumulates at what rate:
| > Cu:Mo & Su Cu >>>>>> MO|
Cu accumulates at 10:1
|CU toxicosis: __ & ___ bind Cu and ____ liver accumulation.|| Mo & Su|
| Cu toxicosis: |
issues with pastures fertilized with ___ or ___ manure - animals fed ___.
Or Lambs fed ___ milk replacers.
| poultry/swine - CuSo|
Lambs fed calf milk replacers
| Cu Toxicosis|
Graze pasture with high ____ ratio.
Young plants ___ in ____
Subterranean clover is __ in ___
| high Cu:Mo ratio|
young plants - lo in MO
clover high in Cu
| Cu Toxicosis|
Hepatogenous - plant toxins damage ____. eg ___ & ____
|Cu in diet binds ___ & accumulates in ___. There is a ___ relese of Cu into ____ due to ___ or _____ --> leads to acute IV ___ decreased blood ____ and _____.|| binds proteins --> liver|
dec blood gluathione
| Signs of Cu toxicosis:|
|depression, anorexia, weakness, watery dark feces, anemia, hemaglobinuria, methemaglobinemia, icterus, muddy MM|
| Cu toxicosis on necropsy:|
Submit what samples? why?
| yellow, friable liver|
Dark red/blue-black kidney
Submit both - post Cu release, Liver may have normal Cu levels
| Cu toxicosis TX:|
PX: ___ once clinical signs
Work by decrease Cu ___ and increase Cu ____.
| PX: poor once clinical signs|
Ammonium molybdate & Na thiosulfate
or Ammonium tetrathiomolybdate - decreases Cu absorption and increase Cu excretion
| Cu deficiency:|
Due to __ ___ owners or a ___ ____ defecit.
| over cautious|
| Cu deficiency:|
Cu + ____ dec Cu availability
____ pastures b/c fertilizer contains ___ and ____ decreases Cu in forages.
hay vs fresh grass, legumes vs grass which worse for deficiency?
| Mo --> dec Cu|
improved fertilizers - contains Mo, --> dec Cu
Lime --> dec in Cu
Hay > fresh grass, Legumes > grass - relative binder amt - and worse vs best for Cu def.
| Cu Deficiency C/S|
| microcytic anemia|
Dec milk production
Washed out hair color
| Cu deficiency|
Enzootic Neonatal Ataxia
Born to __ deficient dam
Progressive incoordination starting at ___
Due to high __ or ___ levels
Death w/i __ of c/s
| Cu deficient|
diarrhea, unthrifty, lo wt gain, loss of hair color, fractures
Loss of wool crimp, looks stringy, kinky
Usually due to high Mo or Su levels
Death within 3-4d of C/s
| Cu deficiency enzootic ataxia dz|
| usu neonates 2-3mo|
+/- recovery with supplementation
Same C/S as enzootic neonatal
Demyelination of spinal cord and cerebral matter cavitation = big holes
| Cu toxicosis - premortem Dx:|
Liver biospsy - are serum levels always high?
| Serum may be normal before Cu release from liver.|
|Rib to take liver biospy near - and position:|| T9-T10|
Cranial surface T10 b/c never, artery, vein off caudal edge
| Cu deficiency: - enzootic ataxia TX|
Feed adequate:___ by supplementinng with __ ___.
Ratio Cu:Mo ideal:
| adequate Cu intake - trace mineral supplmentation|
5:1-10:1 for adequate absorption.
| Vitamin E/Selenium Deficiency|
Happens in which animals:
Milk replacer with what?
High moisture grains have low levels of what?
| -young/rapidly growing|
-NW US & NE seaboard - Se deficiency, also all over US
-Milk replacer with fish, inseed, corn, or soybean oil - PUFAs --> inc free radicals
Low Vit E
| Vit E/Selenium Deficiency:|
Metabolism of PUFAS results in release of ___ ___.
Plants high in PUFAs ___ ____ ___.
Deficiencies result in ___ of ___ ___.
| free radicals|
Young growing plants
breakdown cell membranes
|2 forms of Vit E/Selenium deficiency|| cardiac|
| vit E/Selenium deficiency|
Causes myocardial ____
seen dead w/i ____
| peracute - acute|
Dead w/i 24hrs
Pulmonary edema - nasal froth
Inc HR w/irregular rhythm
Lesions in heart, diaphragm, intercostals
| Vit E/Selenium|
HR? -due to?
-supporting muscles may be swollen, painful
-gastroc, semi-membranosis, tendinosis, neck, gluteals
-Inc HR from pain
-May improve with treatment
| Vit E/Selenium Def DX|
Look for Selenium in which samples? How to keep samples?
Vit E - how to evaluate?
| -Serum, Liver, Se dependent glutathione peroxidase.|
Found in RBCs - use whole blood
Keep sample refrigerated b4 testing
Vit E - difficult to eval
|Rule outs for Vit E/Selenium Def|| Clostridial myositis|
Spinal cord trauma
| Vit E/Selenium combination|
Main ingredient - vit E?:
Don't use which forms in sheep?
For Vit E?
| Vit E - preservative only, main ingredient = Selenium|
L-Se - for lambs + piglets
Do not use Mu-Se in sheep, or E-Se --> too high
pregnant - half dose or will abort
Vit E - separate supplment
| Vit E/Selenium Def Prevent:|
Test ___ and provide Se ____
Rate of Se:
Mix what 2 things?
Avoid diets hi in ___
| test forage & provide Se dietary supplements|
Mix f/c fresh legumes & grasses
avoid high grains
| Hypocalcemia - often seen with ____ during ____ of ____|
PRegnant ewes need how much of what 2 things?
Serum Ca at what level says supplement:
| preg tox, last 2 weeks gestation|
8g Ca & 4g P/d
Ca <7mg/dL --> supplement
initially muscles are:
What is the final sign:
| Initially hyperactive: - poor membrane stabilization from lack of calcium|
Then ataxia/flacid paralysis - no Ca at synapses to cause Ach release
Bloat - no ruminal contractions
| Hypocalcemia TX|
How much Ca:
What can prevent?
| 1g Ca/45kg body weight|
Oral, IV, SQ - check product
| PRegnancy toxemia|
During ___ trimester
BCS of animals more prone:
| Preg Tox due to ___ ____ ____|
| negative energy balance|
|During ketosis which 2 substances are used in the TCA and which is low?|| Oxaloacetate|
Porprionate --> low
| What is in excess druing ketosis in the TCA?|
What happens to it?
| oxaloacetate, from fatty acid breakdown|
It backs up to Acetyl - CoA and is turned into 3 ketones
| Pregnancy Toxemia C/S:|
Glucose: only source of energy for (3)
| RBC, fetus, brain|
Bruxism - grind teeth b/c headaches
| Pregnancy Toxemia Dx:|
history, clinical signs
| Preg tox: TX|
Slight - moderately affected
| re-establishing balance|
IV dextrose 5% drip
Propyelne glycol - proprionate source
| Preg tox Severe affected TX|
| focus: pregnancy|
C - section
support ewe enough to allow fetal development until 10d pre-term but often lose ewe & lambs
| Prenancy Toxemia Prevention|
| US 50d - determine multiple feti|
separate these and feed higher energy diet
Shear early to mid gestation to dec heat production
| Goiter - breeds|
___ deficient induced
Ingestion of ___ during gestation
____ compounds (4 examples)
___ deficient diet in dam.
| Polled dorset, boer, and angora|
Brassica - goiterogenic cmpds
Peanuts, soybeans, cherries, kale
Iodine deficient diet in dam
| Goiter - |
____ deficient diet during gestation
High ___ block absorption
____ deficient soil or ____ soil
Iodine or sandy
| Goiter - congenital|
what type of gene:
| Merino sheep, dutch, pygmy, Nubian goats|
Outgrow by 1yo
| Goiter C/S:|
| Neck - enlarged thyroid|
weak, hairless/wool-less neonate
Poor fiber quality
Dry, flaky skin
Subnormal fertility, lo libido, poor semen quality
Dead or weak newborns
Poor growth rate
Low milk production
| Goiter DX|
C/S: of __ ___
HX of 3
Low iodine in (3)
Low thyroxine - but stable?
| CS - enlarged thyroid|
HX: poor growth, wt loss, fleece quality
Low I in serum, plasma, milk
Low thyroxine - but variable, poor reliability
| Goiter TX|
During pregnancy esp ___ ___, give __ ___ ___
Avoid ___ plants
Give __ ___ in ___ getsation
or ___ in milk to newborn
congenital ___ response to tx
| late gestation - trace mineral supplementaiton|
200-300mg KIodide PO late gestation
3-5drops Lugos iodine to newborn
Congenital - poor response