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37 Cards in this Set

  • Front
  • Back
How are colostral antibodies absorbed?
through pinocytosis by specialized endothelial vesicles - these absorb protein non-specifically
Good passive transfer requires adequate (5)..when can they be monitored?
before ingestion:
• ab in dam's colostrum
• ingestion/delivery to calf
after ingestion:
• GI motility
• GI cell function
• pinocytotic vesicles
FPT is not a _
disease! But it can be caused by a disease or lead to disease
Recommended colostral abs, colostral delivery, and serum Ig at 24 hrs for calves
• 40-50 g/L
• 100-150 g (4 L)
• 1600-2000 mg/L (settle for 800)
What happens to colostral Ig over time? (3)
• redistributed to other body fluids (entire ECF)
• degrades (1/2 life of IgG is 2-3 weeks)
• consumed
therefore expect NATURAL drop in serum Ig over first months of life
Why is FPT bad? (4)
energy deficit
fat-soluble vitamin deficit
lack of passive immunity
possible delay in gut closure
MAIN CAUSES OF DEPRESSION AND ANOREXIA IN NEONATES
sepsis/toxemia
hypoxemia
hypothermia
hyperthermia
hypoglycemia
acidosis
uremia
developmental abNs
weak calf/lamb syndrome
T/F - warming and feeding a cold, weak calve will correct its condition
False - this shouldn't be assumed
What three causes of depression and anorexia in neonates are easily diagnosed?
hypothermia
hyperthermia
hypoglycemia
What ruminants are susceptible to hypothermia and hypoglycemia, especially under temperature extremes or with low birth weights?
Lambs (and kids)
Causes of hypoxemia in the neonate (7)
• prematurity/dysmaturity
• infection
• depression (↓ ventilation)
• meconium aspiration
• bullous emphysema
• hernias
• other thoracic fluids or tissue masses
T/F - hypoxemia is underdiagnosed
true - dx is difficult without arterial blood gas analysis and thoracic rads
What may be the leading cause of death in calves <3 days old? Tx?
Hypoxemia
Most sick neonates benefit from oxygen treatment.
Weak calf/lamb syndrome - look for (8)
• maternal nutrition
• birth weight and gestational age
• dystocia
• vit E/selenium
• BVD, other infectious pathogens
• FPT - colostrum management
• hygiene
• mothering
What are the most ocmmon casues of morbidity and mortality in ruminants <2 days old?
infections
How do bacteria commonly gain access to the body (3)
GI tract
respiratory tract
skin breaks
What might happen with infections? (4)
cleared completely
cleared except for focal problems
cleared except for focal problems that reinfect the body
become/remain widespread
Localization of focal infection occurs in ares of poor blood flow like (4)
umbilicus
joints
tissue abscesses
bone (verterbral bodies)
Bacteria cause _, activate _, and release _ that in turn have what 3 effects on tissue?
cause tissue damage, activate inflammatory reactions, release toxins

cause tissue damage, inflammatory reactions, and vasomotor dysfunction
Clinical complaints with sepsis (10)
diarrhea (complicated scours)
pneumonia/resp signs
depression/anorexia
tissue mass
lameness
dehydration
weakness/recumbency
comatose
blindness
seizures/neuro signs
TPR and sepsis
usually normal - don't expect a fever, and don't rule out sepsis if you don't have one; P and R can be high
Cx of sepsis
mild/moderate dehydration
scleral injection
hypopyon
swollen joints
tissue masses
MULTISYSTEMIC signs
Chem/blood gas and sepsis
mild acidosis, uremia, glucose inconsistent, CBC abnormal (leukopenia)
Sepsis and FPT test
often reveals low Ig, cannot determine whether this is due to FPT or other reasons
Special tests and sepsis
blood culture, joint tap and culture, IS or rads for tissue mass, fecal culture
_/_ usually more severe than diarrhea/resp signs/dehydration or clin path would suggest - sepsis
depression/anorexia
Which organisms are primarily responsible for sepsis?
• some aggressive, invasive bacteria: E coli (>50%), Salmonella, Clostridia
• most opportunists: E. coli (>50%), Klebsiella, Pasteurella, Strep/Staph/Acitnomyces
• 10-25% are polymicrobial
Treaments for sepsis (6)
• Abx (ceftiofur; other penicillinase-resistant drugs)
• NSAIDs (banamine, ketoprofen)
• fluids (crystalloids)
• plasma (correct hypogammaglobulinemia
• remove nidus (umbilicus, drain joint, tissue abscess)
• supportive care (warmth, comfort, food)
What abx should not be used in sepsis
fluoroquinolones
aminoglycosides
chloramphenicol
Preventing sepsis (9)
• ensure good, fast passive transfer
• clean birth/neonatal environment: hutches or spread out
• provide colostrum
• pay extra attention to high-risk neonates
• reduce risk of high-risk neonates
• good immunity of dam
• dip umbilicus
• closing gut w poor colostrum is better than delaying feeding
• role of prophy abx, neonatal vaccines, colostral supplements have not been evaluated for sepsis
How do you ensure good, fast passive transfer?
high serum Ig
rapid gut closure, decrease absorption of pathogens
What mode of feeding colostrum is best?
tubing>bottle>suckling
faster, known quality/quantity, decrease exposure due to food-seeking behavior
What are high-risk neonates for sepsis?
dystocia
twin
low birth weight
premature
weak
stressed
this may include abx, fluids, O2, warmth, supplemental energy
How do you ensure good immunity of the dam?
nutrition
vaccination
What two things are more important than dipping an umbilicus to prevent omphalophlebitis?
good passive immunity
clean environment
Focal infection of umbilical structures my lead to
sepsis
chronic inflammatory reactions (poor growth)
extension of infection to other sites (bladder and liver)
Reasons to suspect complicated scours (4)
• failure to respond to treatment
• clinical signs far worse than lab work suggests
• sepsis signs - hypopyon, injected sclera, fever, swollen joints or umbilicus
• previous history on farm