Equine Neonatal Dz Flashcards
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
CD14 - 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
8g/l
How can FPT be dx ?
- Total protein (Igs are protein)
- Snap test (ELISA) blood
- Colostrum SG
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
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?
Mules
- 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
- EIPH
- 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 - DIC > haemolysis - infectious (EIA, piroplasmosis) - IMHA - 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
Dx IMHA?
> 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
Dx EIA?
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/g15g/dl0.99+0.003100mmHg
= ~21ml/dl
Anaemic PCV 10%
- CaO2 = 1.34[[3.3g/dl]]0.99+0.003100mmHg
= 4.7ml/dl (79% decrease)
hypoxaemic
- CaO2 = 1.3415[[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
