small ruminants dairy

4 ways to dx pregnancy

1. what to look for? is this a sure mehtod?

2. two aspects

3. 2 times you can eval

4. one specific type

1. behavior

   1. no return to estrus (not definitive)

2. Physical appearance

   1. size + udder development

3. Transabdominal Ultrasound

   1. >35d - fluid-filled pockets

   2. >45d - placentomes

      1. ± count embryo

4. Blood tests

   1. ex. BioPRYN for pregnancy specific protein B (glycoprotein)

BioPRYN test

1. what does it test for

2. how?

3. when is it effective + with what accuracy?

4. false positive rate?

   1. why?

5. fees for this test

BioPRYN test'

1. pregnancy!

2. tests for glycoprotein (Pregnancy Specific Protein B) which is produced by placenta

3. >= 30 days w/ 99% accuracy

4. 5%

   1. mostly early embryonic death

5. lab fee = $6.50 + blood tube, needle, + shipping costs

BCS for sheep

1. two areas examined

2. scale

BCS for sheep

1. Transverse spinous processes + dorsal spinous processes

2. 1-5 (1 super low, 5 overweight)

1. how to prevent NEB 6 weeks pre-lambing/kidding

1. feed hay + grain w/ rising plane of nutrition - want BCS of 3.5

3 steps taken @ 4 weeks pre-lambing/kidding

1. how does the second one benefit lambs/kids?

1. crutch - shear wool from around vulva/udder

2. vx against Clostridium perfringens,

   Clostridium tetani, +/- Rabies.

   1. boosts abx in colostrum

3. observe frequently + move those w/ larger udders or softening vulvas into ind. jugs

1. how is normal glucose homeostasis maintained in small ruminants

2. two ways TGs turned into acetyl CoA

1. maintained by microbial fermentation of carbs

2. TGs > glyceral > glucose > pyruvate > acetyl CoA OR TGs > NEFAs > acetyl CoA

last 4-6 weeks of pregnancy

1. 2 increases factors

2. 2 decreases factors

3. what are they at the risk for?

   1. mentally think of this process

Parturation

1. change in energy demands

   1. what for?

2. what is decreased

3. what is there more of

what do maternal tissues use for energy metabolism? fetuses?

last 4-6 weeks of pregnancy

1. increased energy demand for fetal growth + lipolysis

2. decreased rumen capacity + feed intake (due to stress/poor weather/hypocalcemia/dz/poor feed quality)

3. NEB!!!

Parturation

1. increased energy demands

   1. for lactation!

2. feed intake lowers

3. more lipolysis

mom uses lipids for energy metabolism + saves glucose for fetal demands

1. how does ketosis occur

2. possible symptoms of a sick ewe

1. ewes don’t eat > fat breakdown continues to happen > Ketone bodies (acetone, acetoacetate, + B-hydroxybutyrate) overwhelms use by other tissues > KBs accumulate in bloodstream > spill into urine + milk > suppress appetite > leads to metabolic acidosis AKA KETOSIS

2. anorexia, weakness, depressed, neuroligc signs like blindness/tremors/ataxia/teeth grinding, recumbency, and death

1. what happens to NEFAs when ketone bodies accumulate?

2. what happens once everything accumulates once again?

1. NEFAs are continued to be broken down, making them be turned into more ketones OR they are esterified back into TGs

   1. these TGs may be stored as fat or exported as very low density lipoproteins (VLDLs)

2. if body sick of VLDLs, they reform TGs and energy transport decreases

3. livers export of fat is compromised and begins to store fat (TGs) turning into fatty liver

1. casual term for liver accumulating fat

2. medical term

   1. appearance of healthy liver vs unhealthy liver

3. most common + possibly lethal liver dz in cats

   1. process of the dz in cats

1. fatty liver

2. hepatic lipidosis

   1. healthy = dark red/purple

   2. fatty liver = yelllow

3. fatty liver!

   1. stop eating - allows fat to accumulate - esp in high BCS

   2. usual excess lipolysis = TG accumulation = fatty liver in cats

1. two things you can test for to see if an animal is in NEB

   1. 4 things youd see

2. 6 tx for NEB

1. urine sample + blood test

   1. ketones in urine

   2. hypoglycemic, increased NEFAs, + increased b-hydroxy ketone body-bw

2. 6 tx

   1. oral propylene glycol + probios

   2. B vitamins

   3. IV dextrose (± Ca)

   4. correct dehydration + acidosis

   5. pump/drench w/ alfalfa meal or transfaunate

   6. induce parturition/C-section

1. when are cows at risk for NEB vs small ruminants

cows = —> 6 weeks post calving (bc milk production)

sm. rums = 4-6 weeks PRE birth because of multiples

1. 3 stages of lambing

   1. lengths

1. preparation

   1. 1-6 hours

2. fetus delivery

   1. 30 mins-2 hours

3. placenta delivery

   1. 1-12 hours

8 steps to take after delivery of lambs/kids

1. make sure babies breathing

2. dip umbilicus

3. strip ewe’s teats

4. make sure babies stand + nurse w/in 1 hr

   1. get colostrum! tube if neccesary

5. monitor that the mom passes placenta by 12 hours

6. keep babies warm

7. provide fresh water + hay for moms

8. keep good records

6 steps of processing for lambs

1. ear tag

2. weigh

3. tail dock

4. paint brand

5. ± vitamin e + selenium

6. ± castrate

1. how should food be offered to lambs starting at 7 days of age

   1. desired % protein

   2. what can be provided for immunity

   3. important ratio!

2. what should be perfomed at 4, 8, + 12 weeks

3. what determines weaning timeline/weight?

1. creep feed (separate area mom can’t get in)

   1. 18-20% protein

   2. coccidiostat

   3. 2:1 Calcium to Phosphorus!

2. vaccinations! especially for clostridium bacteria

3. marketing + breeding strategy (ex. winter vs spring born lambs, + market weights)

1. what is urolithiasis

   1. how does it occur

   2. why is this an issue?

2. 3 causes of urolithiasis

1. there are stones in the urinary tract - highly saturated solution of solutes/minerals

   1. when a stone becomes too large to pass through a portion of the urinary tract

   2. it becomes a blockage! bad!

2. 3 causes

   1. urine is too concentrated (less water consumed, more water loss)

   2. timing of castration

   3. mineral combos

      1. low Ca:P

      2. high concentrate w/ P + low-roughage diet

      3. alkaline urine

1. how does diet influence urolithiasis

   1. 3 examples

1. salts become unbalanched

   1. calcium carbonate uroliths (oxalates bind to Ca = precipitates)

   2. Magnesium ammonium phosphate uroliths (High P in diet, Mg, and NH4+ = stones) often in feedlot animals

   3. urine pH (forage-diet = high pH urine = precipitaiton. low pH increases solubility of salts)

4 treatments for urolithiasis

4 methods of prevention

1. tx

   1. anti-inflammatory + sedation

   2. amputate urethral process

   3. catheterize

   4. surgery

2. prevention

   1. always clean, fresh water ± salt blocks

   2. delay castration to 6 months

   3. acidify urine (ammonium chloride, biochlor)

   4. adjust diet for low P (limit grain, find substitute)

1. what type of agent is coccidia

   1. pathogenicity?

   2. how often is it found in flocks

2. pre-patent period

3. effect of one coccidial oocyst?

4. 5 CS

5. dx

6. typical ages effected?

1. protozoa

   1. species variable

   2. in most flocks - animals develop immunity

2. time of ingestion of oocysts to new oocysts being passed = 10-23 days

3. 1 can cause 50 mil intestinal cells to be ruptured

4. diarrhea (bloody, yellow, strain), loss of appetite, weakness, poor body condition, death

5. fecal float + egg count

   1. tricky because high pathogenicity may be difficult to find but dangerous

6. 3-7 weeks

1. two forms of treatment for coccidia

2. 6 methods of prevention

1. tx

   1. antibiotics

   2. fluid

2. prevention

   1. avoid overcrowding

   2. don’t house inside/in small areas for long periods of time

   3. minimize strss

   4. good sanitation

   5. avoid overgrazing

   6. feed coccidiostat in creep feed

1. characteristics of clostridial bacteria

   1. how do they cause dz

2. 2 strains of Clostridium

1. Obligate anaerobic, Gram (+), spore-forming bacterial rods

   1. release toxins

2. Clostridium perfringens (B-D) + Clostridium tetani

Clostridium tetani

1. generic term

2. source

3. pathogenesis

4. 5 CS

5. 5 Tx

6. prevention

Clostridium tetani

1. tetanus

2. spores in soil/GIT of healthy animals

3. spores inoculate a wound - germinate - produce toxin (tetanospasmin) which diffuses in bloodstream > nerves, interferes w/ signaling for muscle relaxation + causes contracted muscles

4. stiffness, tremors, lockjaw, sawhorse stand, ± death

5. Penicillin (abx), sedatives, muscle relaxants, supportive care, open/clean wound

6. vaccinate!

Clostridium perfringens

1. two general types

2. source

   1. pathogenesis (for each one)

3. CS (5 each)

4. 3 Tx

5. prevention

Clostridium tetani

1. types B + C —> type D

2. spores in soil/GIT of healthy animals

3. pathogenesis

   1. B + C - young ingest spores, germinate in GIT + produce toxins

   2. D = sheep ingest spores in GIT - produce E toxin —> overeating high energy feed promotes bacterial proliferation

4. 5 CS

   1. BC = ulceration, inflammation, GIT hemorrhage —> diarrhea + death

   2. D = necrosis, edema, hemorrhage in brain/kidneys/GIT > diarrhea, death

5. abx (penicillin), toxoid, supportive care

6. vx