Equine neonatal disease

Question 1

Does a neonatal foal have have antigenic memory?

Answer 1

No - has no Abs and has not been exposed to pathogens before

Question 2

Outline Ig incorporation into colostrum

Answer 2

• produced by mare in last few weeks of gestation
• contains mainly IgG, some IgA and IgM but also other cellular and soluble factors
• normal foals suckle within 1-3 hrs after birth and consume approx 1-2 L colostrum
• specialised enterocytes allow absorption of large IgG molecules: max capacity at 6 hrs, decreased to none after 24 h

Question 3

What is FPT?

Answer 3

= failure of passive transfer
- predisposes foal to infxn but not a primary dz itself, especially to bacteremia/ sepsis, septic arthritis, diarrhoea, pneumonia

Question 4

Why can FPT occur?

Answer 4

• lack of colostrum/ poor quality (premature lactation, premature parturition)
• failure of foal to nurse (PAS, orthopaedic problems e.g. tendon contracture, mare temperament)
• failure of absorption - GIT of foal unable to absorb colostrum - hypoxic damage

Question 5

Diagnosis - FPT

Answer 5

• Definitive: measure IgG concentration
• 8g/L is complete transfer of passive immunity
• need to consider management, environment etc

Question 6

Tx - FPT

Answer 6

• if foal 12-18hrs old or suffers from systemic dz - IV plasma. 1L will increase IgG concentration by 2g/L, often 2L necessary. If no systemic dz or no high quality colostrum.
• sick foals can use large quantities of IgG: repeated measuring and potentially repeated transfusions necessary.
• treatment for concurrent disease if present (e.g. AMs)

Question 7

What is NI?

Answer 7

Neonatal Isoerythrolysis

Question 8

Outline NI

Answer 8

• haemolytic dz of foals caused by destruction of foal’s RBC by Abs present in colostrum directed against foal’s RBC antigens
• occurs d/t blood group incompataility of mare and foal (foal has inherited stallion’s RBC antigens)
• usually in multiparous mares that have been sensitised to foal’s RBC Ags during a previous Ag - can occur in maiden mares

Question 9

What is the sequence of events in NI?

Answer 9

• foal inherits RBC Ag from sire that is different to mare
• RBC Ag must be strongly antigenic - Aa, Qa
• mule foals (donkey sire x horse dam): NI common d/t donkey factor (RBC Ag) which is not present on horse RBC
• mare must be exposed to RBC Ag and produce Ab to it (via transplacental haemorrhage, prior blood transfusion, during parturition)
• Abs against foal RBC are contained in mare’s colostrum
• foal ingests colostrum adn absorbs Abs against its own RBC Ags
• Ab-coated RBCs removed from circulation or lysed intravascularly
• mare is usually exposed to RBCs in previous pregnancy and affected foal is born subsequently (usually insufficient time in one pregnancy to produce sufficient Abs to cause NI but possible)

Question 10

CS - NI

Answer 10

• foals are normal at birth
• develop signs within first 4 d of life
• weakness
• lethargy
• increased HR and RR
• icterus
• pale MM
• time of onset and severity depend primarily on amount of Abs ingested and affinity of Abs to RBCs

Question 11

Dx - NI

Answer 11

• CS and hx
• haemolytic cross match: if a mare’s serum agglutinates or lyses foals RBCs (for lysis to occur external complement needs to be added to tubes/ slides)
• thrombocytopaenia may accompany anaemia

Question 12

Tx - NI

Answer 12

• if 24-48 hrs old, prevent further colostrum ingestion, give plasma transfusion to establish passive transfer of immunity
• if > 24 hr supportive care
• blood transfusion: mare’s washed RBCs (NOT plasma) or typed donor
• emergency: oxyhaemoglobin (purified bovine haemoglobin) possiible but v expensive alternative

Question 13

Prevention - NI

Answer 13

MARE WITH HX OF NI FOAL:

• check for alloAbs in late gestation
• prevent foal from nursing in first 24-48 hrs and provide alternative colostrum / nutritional source, discard colostrum

Question 14

WHat is SCID?

Answer 14

= Severe Combined Immunodeficiecny

• arab foals
• test for SCID gene
• test for non-functional DNA-dep protein kinase as this causes non-functional TC and BCs: fatal by several months of age (once maternal immunity diminishes)

Question 15

Causes - adult equine anaemia

Answer 15

• haemorrhage (internal vs. external)
• IMHA
• oxidative damage to RBCs (Heinz Body anaemia)
• EIA = equine infectious anaemia
• anaemia d/t inadequate erythropoiesis (anaemia of chronic dz and Fe deficiency anaemia)

Question 16

Outline causes of external blood loss in horses

Answer 16

• external wound involving large artery (proximal or distal limb)
• GP mycosis: fungal infection in GP erodes into internal carotid artery with severe epistaxis that is often rapidly fatal. May see CN dysfunction: facial nn paralysis and dysphagia
• post-sx haemorrhage (post-castration)
• blood loss into GIT lumen: parasitism (small strongyles, Strongylus vulgaris), NSAID use, neoplasia, coagulopathy
• haematuria: uncommon cause of anaemia in the horse. can be d/t pyelonephritis, cystitis, urolithiasis, idiopathic renal haematuria, neoplasia, coagulopathy, urethral rent in male horses

Question 17

Types of internal blood loss

Answer 17

• HAEMOPERITONEUM: spleen or liver rupture, mesenteric vessel rupture, uterine artery rupture, neoplasm (HSA), internal bleeding post-castration (rare)
• HAEMOTHORAX (less common than haemoperitoneum): secondayr to trauma, erosion large BV d/t abscess or neoplasm, rupture of aneurysm, rupture of aorta or pulmonary artery (rare), coagulopathy, neoplasia
• BLOOD LOSS VIA UROGENITAL TRACT: uterine artery rupture, usually via middle uterine artery. Can be before or usually after parturition, usually older mares. CS rapid - sweating, colic, tachycardia. Blood can be lost into abdo cavity or retained in broad ligament

Question 18

Describe IMHA in hroses

Answer 18

• PRIMARY: uncommon
• SECONDARY: Abs attach to RBC membranes because of alterations in RBC membrane d/t primary infxn, neoplasm or other I-M dz process
• Ag-Ab complex deposition on RBC surface
• durgs that cause immunoproteins to react indirectly with RBCs (penicillin, bute, TMPS)

Question 19

Tx - IMHA

Answer 19

• discotinue all tx if possible
• tx priamry condition
• blood transfusion if necesssary
• immunosuppression if necessary (corticosteroids are most commonly used: dexamethasone, prednisolone)

Question 20

What is Heinz Body (HB) anaemia?

Answer 20

= HBs are preciptations of oxidatively denatured Hg on RBC membrane
- causes: rarely used drugs (methylene blue, pheothiazine) or plants horses rarely consume enough of (kael, brassicas, onions) EXCEPT red maple leaf as toxin in wilted leaves causes intra- and extravascular haemolysis and methaemoglobinaemia (chocolate-brown MM)

Question 21

Tx - HB anaemia

Answer 21

supportive but high mortality rate

Question 22

What is EIA?

Answer 22

= Equine Infectious Anaemia

• exotic to UK but present in some European countries
• lentivirus
• PI: no tx, horses remain lifelong carriers

Question 23

2 causes of anaemia d/t inadequate erythropoiesis

Answer 23

• anaemia of chronic dz

- Fe deficiency anaemia

Question 24

Outline anaemia of chronic dz

Answer 24

• commonest cause of anaemia in adult horses
• mild-mod non-regen. anaemia
• not severe enough to cause CS
• PATHOGENESIS: Fe sequestration (anti-bacterial mechanism), defective EPO response, decreased RBC lifespan)
• Tx: usually not necessary, tx primary dz

Question 25

Outline Fe deficiency anaemia in horses

Answer 25

• rare
• chronic external blood loss (e.g. chronic parasitism)
• tx with oral Fe supplementation