Flashcards in Equine Neonatal Dz Deck (54)
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1
When is colostrum produced?
Last 2 weeks pregnancy
- selective secretion of Ig from serum and local production
2
What soluble compounds are in colostrum?
- Ig (mainly IgG and IgGT, some IgM and IgA)
- hormones
- growth factors
- cytokines
- lactoferrin
CD14
- enzyems/lysozymes
3
Cellular compounds colostrum
- lymphocytes
- macrophages
- neutrophils
- epithelial cells
4
Hoe much colostrum should foal drnk?
1-2l in first 3h life
5
How is Ig absorbed?
Pinocytosis by specialised enterocytes 12-24hrs after birth
6
When are Ig levels measured?
- 18-24hrs
(detectable in serum @ 4-6hrs, peak 18-24)
7
How long do passive transfer Abs alst? When do foals Igs levels increase?
~ a month
- foals Ig reaches adult level ~5-10 months
so nadir around ~1month old
8
Reasons for FPT?
> maternal
- lack of colostrum (premature lactation)
-poor uality low conc IgG (SG foal
- contracture of tendons, neonatal asphyxia syndrome, sepsis
- rejected by mare
> lack of absorption
- time frame (ingested too late)
- GIT dz (hypoxic damage)
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Consequence of FPT?
- pdf development infectious dz
- sepsis (arthritis, pneumnoia D+, meningitis)
10
Define complete and partial FPT
8g/l
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How can FPT be dx ?
- Total protein (Igs are protein)
- Snap test (ELISA) blood
- Colostrum SG
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Tx FPT
> Colostrum NGT
- if under 12hrs
- no signs systemic compromise
- 1-2L equine colostrum SG >1.060
- 200-400ml at a time
- NGT (not syringe) dont waste and may assphyxiate
> IV plasma
- 1-2L
- foal >8hrs, 12-18hrs
- signs systemic dz
- if no high quality colostrum available
- commercially available (1L bags, 15-17g/L IgG)
- 1L increases IgG conc by 2-3g/L
> 1L plasma w/ >25g/L IgG ^ IgG conc by 4-8g/L
*NB: if foal sick will use up Abs, repeat*
13
Outline plasma administation
- diazepam sedation
- monitor for signs of plasma reaction (slowly so signs will e noticed early)
- 1 drop,sec (3ml/mmin)
- check HR
14
Tx plasma reactions?
- stop
- 1mg/kg flunixin +- IV fluid
- wait 1-2hrs, restart tansfusion slowly
- try using different batch/donor (shouldnt react to multiple)
15
What is neonatal isoerythrolysis? pathogenesis
- IMHA of newborn foal d/t imcompatible bllood types of mare and foal
- mare put to stallion of different blood group, foal inheits this
- placenta breached at some point, mare makes immune response to foals blood (1st preg)
- 2nd preg colostrum full of Abs against its own blood type
- antibodies coat RBC intra and extra vascaulr haemolysis
16
What are the main blood antigens in the horse?
Aa +/-
Qa +/-
17
Which species is NI very common in?
Mules
- d/t donkey factor!!
18
Clinical signs of NI?
- normal at first, no FPT, clinical signs up to 12d pp! but usually
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Dx NI?
> clin path
- anamia
- haemaglobinuria
- haemoglobinaemia
- ^ unconjugated bilirubin
- metablic acidosis
- pre-renal/renal azotaemia
- toxic hepatopathy / hypoxic hepatocellular necrosis
- possible despite IgG Haemolytic cross mach
- ID haemolysis of foals WBC by mares serum with addition of external (Rabbit!) complement
- evaluate for signs of agglutiation if no compleemnt available but false -ve possible.
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Tx NI?
21
NI prevention?
> mare w/ hx NI
- determine blood group of sire
- test serum for alloAbs
- prevent any colostrum intake if same sire/other incompatible sire if is used
22
What is combined immunodeficiency and which foals does it affect?
- Autosomal recessive genetic dz of Arabian foals
- enzyme defect: Non-functional DNA dependant protein kinase -> no mature functional B or T cells
- recurrent infections once passive immunity waned
- associated w/ infection with uncommon agents eg. adenovirus, pnumonia, D+
23
Px and prevention of combined immunodeficiency?
- fatal @ approx 5 mo
- dam and sire must both be carriers of gene - genetic test available
24
Equine specific facts wrt anaemia?
- can compensate with spleen
- regenerative and non-regenerative can ONLY BE DETERINED ON BM ASPIRATE
- circulating lifesplan erythrocytes long (140-150d)
- hroses repsond slowr and take longer to recover from anaemic insult
- Howell-Jolly bodies normal in equine blood and DO NOT INDICATE RESPONSIVE ANAEMIA
25
CLinical/lab signs of anamia?
> indications of inadequate oxygen delivery to tissues
- plasma lactate ^ d/t anaerobic metabolism
- v PvO2 (venous) d/t ^ O2 extractino from blood
> PE
- pale mm
- ^HR, RR
-weakness/excercise intolerance/collapse
26
Why may PCV, HCT and RBC not be affected in acute blood loss?
- RBC and plasma both lost so proportion remains the same within blood sample
- with chronicity interstitial fluid replaces blood volume and RBC conc decreases
27
Classification of anaemia and possible causes during work up?
> acute
- external bleeding
- internal bleeding (haemabdomen, haemothorax, broad ligament, kidneys, DIC)
> chronic
- regenerative (haemorrhage: GI/renal) (haemolysis: IMHA/infectious/toxic)
- non-regenerative (Fe deficiency, chronic dx, BM suppression)
28
Causes of haemabdomen?
- trauma (ruptureed spleen/liver)
- ruptured mesenteric vessel
- uterina a. rupure
- neoplasia
- coagulopathy/DIC
- abdominal abscess
29
Causes of epistaxis
- trauma
- ethmoid haematoma
- EIPH
- neoplasia
- gutteral pouch mycosis
- pulmonary haemorrhage
- coagulopathy/DIC
- rupture rectus capitis m.
- sinus abscess/infection
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