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Flashcards in Equine Neonatal Dz Deck (54)
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When is colostrum produced?

Last 2 weeks pregnancy
- selective secretion of Ig from serum and local production


What soluble compounds are in colostrum?

- Ig (mainly IgG and IgGT, some IgM and IgA)
- hormones
- growth factors
- cytokines
- lactoferrin
- enzyems/lysozymes


Cellular compounds colostrum

- lymphocytes
- macrophages
- neutrophils
- epithelial cells


Hoe much colostrum should foal drnk?

1-2l in first 3h life


How is Ig absorbed?

Pinocytosis by specialised enterocytes 12-24hrs after birth


When are Ig levels measured?

- 18-24hrs
(detectable in serum @ 4-6hrs, peak 18-24)


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


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)


Consequence of FPT?

- pdf development infectious dz
- sepsis (arthritis, pneumnoia D+, meningitis)


Define complete and partial FPT



How can FPT be dx ?

- Total protein (Igs are protein)
- Snap test (ELISA) blood
- Colostrum SG



> 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*


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


Tx plasma reactions?

- stop
- 1mg/kg flunixin +- IV fluid
- wait 1-2hrs, restart tansfusion slowly
- try using different batch/donor (shouldnt react to multiple)


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


What are the main blood antigens in the horse?

Aa +/-
Qa +/-


Which species is NI very common in?

- d/t donkey factor!!


Clinical signs of NI?

- normal at first, no FPT, clinical signs up to 12d pp! but usually


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.


Tx NI?


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


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+


Px and prevention of combined immunodeficiency?

- fatal @ approx 5 mo
- dam and sire must both be carriers of gene - genetic test available


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


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


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


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)


Causes of haemabdomen?

- trauma (ruptureed spleen/liver)
- ruptured mesenteric vessel
- uterina a. rupure
- neoplasia
- coagulopathy/DIC
- abdominal abscess


Causes of epistaxis

- trauma
- ethmoid haematoma
- neoplasia
- gutteral pouch mycosis
- pulmonary haemorrhage
- coagulopathy/DIC
- rupture rectus capitis m.
- sinus abscess/infection


Causes of haemothorax?

- trauma (rib fx esp foals, lacerated heart/large vessel)
- pulmonary haemorhage
- necrotising pneumonia
- ruptured pulmonary vessel/embolism
- ruptured pulmonary abscess
- coagulopathy/DIC
- neoplasia