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Flashcards in Equine Neonatal Dz Deck (54):

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


Causes of haematuria?

- trauma
- pyelonephritis
- cystitis/urothithiasis
- urethral rent (male)
- neplasia
- coagulopathy/DIC


Causes of chronic regenerative blood loss?

> GI
- parasitism
- neoplasia
- coagulopathy
- ulceration
- granulomatous enteritis
> haemolysis
- infectious (EIA, piroplasmosis)
- toxic (redd maple leaf tox USA)
- iatrogenic


Causes of NON-regenerative chronic blood loss?

> Fe deficiency
- chronic haemorrhage
- nutritional deficiency (rare)
- chronic dz
> BM failure
- myelopthisis
- myeloproliferative dz
- toxins (phenylbutazone, chloramphenicol)
- idiopathic pancytopaenia
> misc
- rhEPO (less common now)
- chronic hepatic/renal dz


Tx anaemia?

> stabilisation (anaemia itself may not need to be treated)
- guided by cliical and lab findings (HR, RR, lactate, PvO2) NOT PCV
- control blood loss if source found
- IVFT if severe blood loss


Presenting complaint and clinical signs of haemabdomen?

> colic
- abdo pain
- hypovolaemia (^HR, slwo capillary and jugular refill time, ^ lactate)
- Dx: ultrasonongraphy


Px of haemabdomen?

depdns on underlying cause, survival ~ 50%


What is periparturient haemorrhage and when is it commonly seen?

- haemorrhge from uterine vessels after more commonly than before parturition
- important cause pp colic and death
- delivery often uneventful!!
> mares may be prone to repeated bleeds in future pregnancy


What 2 forms of pp haemorrhage may occour?

- into broad ligament
- into abdomen (can be rapidly fatal)


Tx pp haemorrhage?

CV stabilisation


2 forms of IMHA?

> 1*
- uncommon: ABs directed against patients RBC ag
> 2*
- Ab formation precipitated by 1* dz, rug administration, neoplasia, immune mediated dz



> coombs test can be attempted
- presence of anti-RBC Ab directly (surface of RBC) or indierctly (serum)
- false +/- possible
> flow cytometry to demonstrate Abs on RBC


Tx haemolytic anaemia?

- tx 1* dz process
- stop lal meds
- transfusion IF signs of inadequate oxygen delivery
- immunosuppressioin (steroids, azathioprine and cyclophosphamide (latter 2 rarely in horse)


What is EIA?

- equine infectious anaemia
- lentivirus
- transmitted via insects, blood contaminated equipment
- not present UK, risk from imports
- persistnet infection - infected horse remains lifelong carrrier


3 syndromes of EIA? What is the associated anaemia associated with?

- acute, chronic and inapparent
- anaemia caused by intra and extravascular haemolysis, BM suppression -> thrombocytopenia also common



Coggins test (AGID) or ELISA


Px/management of EIA cases?

- euthanasia/lifelng quarantine if horse + as danger to other horses


What is seen with haemolytic anaemia d/t oxidatic injury to RBC? WHen may this also be seen?

> Heinz Body Formation
- oxidative damage to Hbg precipitates on RBC membrane
- RBC less deformable and rapidly cleared from circulation
> D/t
- drugs (phenothiazine, methylene blue)
- plants (onions, Brassica spp. red maple)


Pathogenesis of red maple leaf toxicity (not UK)

- wilted leaves
- methaemoglobin results from oxidative change of Hbg Fe to a non usable state for O2 transport


Causes of anaemia d/t inadequate erythropoesis?

> most common d/t chronic dz
- chronic inflam or infection/ neoplasia
- sequestration of iron
- shortened RBC lifespan
- defective erythropoeitin response
> Iron deficiency
- can develop with chronic blood loss
- tx Fe supplmentation
> OTher
- neoplastic process
- +- chronic renal failure
- after adminsitration og hrEPO (cross reacts against endogenous EPO)
- idiopathic


Type of anaemia caused by chronic dz?

- mild - mod
- normocytic, normochromic
- non-regnerative
- not associated with clinical signs (will not present for this)


Tx anaemia d/t chronic dz?

- tx 1* disease not anaemia itself


Why is anaemia important?

- 98% O2 transported by hbg
- CaO2 determined by Hbg
> CaO2 = (1.34xHbxSaO2) + (0.003xPaO2)


What is CaO2 and what should this be in a normal horse? How does this differ in the anaemic and hypoxaemic horse?

> oxygen content of blood
- CaO2 = 1.34ml/g*15g/dl*0.99+0.003*100mmHg
= ~21ml/dl
> Anaemic PCV 10%
- CaO2 = 1.34*[[3.3g/dl]]*0.99+0.003*100mmHg
= 4.7ml/dl (79% decrease)
> hypoxaemic
- CaO2 = 1.34*15*[[0.8]]+0.003*[[45mmHg]]
= 16.2ml/dl (20% decrease)


What is the foals immune system like when born? @ what sage of gestation do T and B lymphocytes develop?

- competent but naive and born agammaglobunlinaemic
( able of mounting an immune response but hasnt been challenged and no trasnfer of Ig d/t epitheliochorial placenta) Ab protective levels reached @ 2 weeks and presenceo f maternal Abs suppresses foals own Ig production (so wait to vax until after maternal Ab waned)
- T lymphocytes funcional @ 100d gestation
- B lymphocytes functional @ 200d gestation
- complement ~10% adult activity
- phagocytosis and killing some organsims low in newborns