Rumi Neonate

sihirlifil's version from 2018-04-28 17:18

Management stuff

Question Answer
In order to assess a neonate, you have to know...What is normal! Differences between species, breed, sometimes sex
Many DAIRY bull calves suffer from? what happens?Mild fetal hypoxia syndrome. will often lay like a bump on a log for the rest of their lives if the calf raiser didn't go get them up, tube them colostrum, and encourage them to stand (more likely to have a dystocia)
In general, who is the fastest to 'figure it all out?'Small rumis (nursing before cleaned & dried off)
Camelids also quick to get sternal (nursing w/in 1 hour)
Neonatal adaptation: what do you want to assess?Sternal, standing, suckle reflex, nursing, organ function (blood glucose, TPR)
Rough guidelines: when should neos be sternal? suckling? standing? nursing?Sternal: 15 min
Suckle reflex: 60 min
Standing: 60 min (30 for camelids)
Nursing: 120 min
Rough guielines: TPR? BG?T: 101-103*F (1-2* higher than dam at birth)
P: 100-140 BPM
R: 30-60/min
BG: 100-150mg/dL
Who are considered high-risk neonates?Premature
Dystocia (osteomyelitis from chains)
Extreme environmental conditions
Neonate without normal adaptation response
What's the 'high-risk' neonate at a high risk FOR?Poor colostral intake & absorption --> insufficient energy & glc metabolism --> incr risk of dz & death
What's the big deal about colostrum?Neonates can mount an immune response but are immunologically naive & depend on maternally derived immunoglobulin absorbed from colostrum
Why is skeletal damage (e.g. result of calf chain) a risk factor?(Damage from pulling calf chains during dystocia) Osteomyelitism deformity, not easy to get up and nurse
What can we do to reduce the neo's risk?Focus more on the female (prebreeding, gestation, postpartum)
(Variable gestation lengths due to?)(BVDV, Border Disease, toxic plants like lupine)
When does gestation take a greater toll on the mom?When she's still young & growing herself
What does the producer need to do in the first 2 trimesters?Nutrition! trace minerals (preg tox, dystocia due to pelvic fat)
Monitor for disease
Last trimester: what's the big deal?Starting to make colostrum! Need to be healthy to make antibodies
Can't fix things in last month/trimester if screwed up in early preg (nutrition, vaccines, quarantining)
T/F Ingestion of colostrum guarantees successful passive transferFalse. Numerous factors interact (management, environment, hygiene, infection pressure, virulence, antibody specificity)
However, severity of disease will be lessened with adequate colostral protection. Infection pressure is critical
Protective mechanisms of colostrum (3)Lactogenic immunity
Systemic humoral immunity
Enteric immunity
Lactogenic immunity = Binds & neutralizes pathogens in gut
Independent of gut closure
Dependent of Ig concentration
Systemic humoral immunity = Absorbed --> circulation
Enteric immunity = IgG secreted back into gut from ECF (provides ongoing protection in gut after closure & when colostrum starts breaking down ~24 hours after birth)
Requirements for successful passive transfer of maternal antibodiesFormation of colostrum w/ adequate IgG
Ingest adequate mass of Ig
Absorb the Ig in timely manner (gut closure!)
How is colostrum made?Active, selective uptake of immunoglobulins from ECF
4-6 weeks prepartum
Influenced by incr estrogen and decr P4, ceases immediately prepartum
IgG1 > _________% of colostral protein90% (5-10x higher than serum!)
What factors influence colostrum quality?Nutrition
How does nutrition influence colostrum quality?
Prolonged protein malnutrition = low fetal growth & colostrum lvls
Minerals: Se, Cu, Vit E
How does breed influence colostrum?Dairy (more dilute) vs Meat
How does parity influence colostrum quality?New: haven't seen as many pathogents (lower concentration & range of antibodies in colostrum)
Not as attentive to nursing needs
More dystocia = tired mom, weak/hypoxic neonate
How does vaccination influence colostrum quality?Not all-encompassing
Natural exposure vs vax
Booster timing vs production schedule (MLV vax while NOT PREG!)
Prenancy risks
Variable duration (not all last an entire year)
How much colostrum must a neonate ingest?(Dependent of colostral IgG1 concentration ) Strive for 10-15% of body weight (100g of IgG1)
Do we always measure colostrum?No, but if problem go back and start checking
Can measure for different groups of animals & get ballpark
Which factors affect ingestion?Mothering instincts (llamas not great lol)
Management methods
Neonatal instincts
Delayed suckling (weak neonate, exhausted/painful dam)
Physical or physiological impediments

How can you get colostrum into the neonate?Tube/bottle/syringe feed, put lamb on ewe when recovering from C-section
Cessation of sbsorption of colostral immunoglobulins occurs when?About 24 hours of age
What can significantly decrease IgG absorption?Dystocia, hypothermia
T/F Transfer of IgG1 from gut to ECF is nonselectiveTrue IgG1 = IgG2, IgM, IgA, albumin, cheese burgers, etc...
T/F Transfer if IgG1 from gut to ECF is non-receptor mediatedTrue
T/F Transfer if IgG1 from gut to ECF is non-saturableFalse! Receptors take up a certain amount than dont take any more
Transfer if IgG1 from gut to ECF is affected byAdministration route: Dam > bottle > tube
Dystocia (stressed wont absorb as well)
When do we test for Ab absorption? More interest in herd than individual (esp dairy)
Test after absorption is complete (about 24-36h)
Equine & critical/valuable livestock: often check early since 12h gives an idea
Herd: test percentage or all w/in 7d of life
Measurement of passive transferSerum refractometer (Bo)
SRID (Bo, Cam)
Serum GGT
Zn sulfate (Bo)
Glutaraldehyde coag (Bo)
Serum GGT (Bo)
(No SNAP test for livestock yet)
What is GGT? Why is it in colostrum?Liver/kidney enzyme, produced by mammary glands (only liver enzyme out of whack if you take blood)
FPT testing: Bottom line?Refractometry easiest to perform, has reasonable predictive value in ruminants
Limitations of refractometry? something else to remember?Dehydration, illness (artifactual TP increase)
Acute phase proteins (big buffy coat layer when spun down)
Species variations
BUT...! numerical reference values are guidelines! Other factors also influence the concentration of Ig needed for protection (management, environment, infection pressure, virulence, antibody specificity...)
If you have >80% dairy calves on a farm with TP >5.2g/dL at 48h of age, what can you do with this information?(herd status more important than individual) Only 20% FPT. Use to evaluate disease outbreaks & interventions; indicates success or deficiencies in management
In what situations might you not have colostrum from the dam?Premature
C-section (not enough stim for milk letdown)
Mastitis (not caught when dried off previous year)
If you don't have colostrum from the dam, what other alternatives are there?Plasma transfusion, frozen colostrum
Dz transmission risks in colostrum (6)Salmonella
Johne's (MAP)
Bovine leukemia virus
CAE virus
Mycoplasma bovis
(Other bacteria)
Commercial 'colostrum' products: careful of what?Substitutes vs Replacers READ THE LABEL! Substitutes don't have globulins!
If contain IgG, regulated by USDA
Tx of FPTPlasma or whole blood: 20-40mL/kg IV, IP
Oral colostrum: lactogenic immunity
Supportive care: Abx, NSAIDs, nutrition, environment
**Advantages of giving plasma/whole blood IP?
Larger volumes faster, less risk pulmonary edema

Diseases Intro

Question Answer
One of the most important causes of death & economic loss to livestock industry is...Neonatal diarrhea (infectious enteric dz)
Is neonatal D+ common? Prognosis?Infection is common, disease is not
Prognosis often excellent
Importance of brush border enzymes?Digestion
E.g. Lactase, maltase, peptidases
Normally, what is the electrolyte balance in the enterocytes?Reabsorption >> Secretion
Water & electrolytes secreted by pancreas & duodenum, critical to resorb in jejunum & ileum (otherwise lost in feces)
Mechanisms of diarrheaSecretory
Secretory D+: e.g.? mechanism?ETEC
Pili attach to certain receptors on cell mb of young enterocytes (dz occurs under a week of age, peaks at 3-5d)
Secretory D+: result?Can lose 12-15% BW in a few hours
High HCO3- released by hypersecreting enterocytes --> metabolic acidosis & alkaline feces (D & L lactic acidosis)
Malabsorptive D+: e.g.? mechanism?Rotavirus (mature cells at tips), coronavirus (entire villus except crypts), cryptosporidiosis, MILD coccidiosis (severity varies with organism; INVASIVE!)

Malabsorptive D+: result?Immature cells do not absorb nutrients well, lack digestive enzymes --> blunted villi = decreased surface area for absorption --> nutrients (milk fat, lactose) head to LI
Dense bacterial population of LI ferments nutrients into organic acids which exert osmotic effect: D+ & dehydration, acidemia, acid fecal pH
Inflammatory D+: e.g.? mechanism?Severe coccidiosis, clostridial enteritis, salmonellosis... often normal flora!
"Trigger" causes massive proliferation (heavy milker, massive dose) in ideal location (anaerobic, no protective microflora yet, warm, nutrients, trypsin inhibitors in colostrum)
Toxemia is common: endo & exotoxins
Endemic infectious juvenile D+ aka? Why?Undifferentiated (etiologic dx not essential to successful tx)
Characteristics of endemic infx juvenile D+Common, newborns 2m.o., normally low case fatality rate (<10%) with appropriate tx, no superimposed FPT
Endemic infx juvenile D+ e.g.ETEC
Endemic infx juvenile D+ CS?+/- prodromal colic (mild, transient)
Watery, yellow-green-white D+ (undigested milk, green tinge if starting to eat forage)
Dehydration, CV shock
Weakness (wet lips, milk staining on face = uncoordinated suckle)
Endemic infx juvenile D+: auscultation?
Fluid/gas splashing sounds on ballottement (hypermotile)
Endemic infx juvenile D+: metab derangement?Acidosis
Dehydration --> poor perfusion, L-lactate accumulation --> D,L-lactate absorbed from colon --> bicarb loss in feces
Endemic infx juvenile D: severe metabolic acidosis inducesLethargy
Poor CVS performance (augments shock) (floppy kid syndrome)
What electrolyte abnormality happens with acidosis?Hyperkalemia ...but D+ can lead to hypokalemia! and calf is not eating. So supplement K+ when giving fluids
What else can cause altered mentation & weakness in calves?
Younger ages (<2w), cold ambient temp, superimposed illness
Signs of hypoglycemiaLethargy, ataxia, weakness
Poor suckle
Progressive --> convulsions then death
What is going on here? which body systems involved?
Toxemia/septicemia (scleral injxn)
Confined to GIT UNLESS FPT is present! (multi-organ involvement rare)
Increases susceptibility for translocation of bacteria & toxins from gut into bloodstream
R/O in LA neonatesSepsis (scleral injxn, toxic line, left shift)
Suffocation (esp w/ dystocia)

Recent badges