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Lymphoreticular and Haemopoietic > Equine Neonatal Diseases > Flashcards

Equine Neonatal Diseases Flashcards

1
Q

List some equine neonatal diseases…

A 
Failure of passive transfer
Perinatal asphyxia syndrome
Sepsis
Neonatal isoerythrolysis
Uroperitoneum 
Infectious and non-infectious D+
Colic
Respiratory diseases (neonatal respiratory distress syndrome, infectious pneumonia, persistent foetal circulation)
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2
Q

When do foals produce functional lymphocytes?

A

Function T lymphocytes - 100 days gestation

Function B lymphocytes - 200 days gestation

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3
Q

Are foal capable of a complete immunological response?

A

Yes - they have developed innate and adaptive components

BUT they don’t have any antibodies from their mother (no transfer via placenta)

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4
Q

How do foals get their antibodies?

A

Almost entirely on absorption of preformed antibodies from colostrum

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5
Q

Describe equine colostrum…

A

Produced in the last 2 weeks of gestation
Soluble components
Cellular components (lympho, macro, neutro, epithelial)

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6
Q

What are the soluble components of equine colostrum?

A 
IgG, IgM, IgA
Hormones
Growth factors
Cytokines
Lactoferrin
CD14
Enzmyes
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7
Q

What does the presence of maternal antibodies suppress the production on in foals?

A

Foals own Ig’s

Vaccination should be carried out after maternal Igs have declined.

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8
Q

What volume of colostrum should foals ingest in the first 3 hours of life?

A

1-2 litres of colostrum

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9
Q

When is Ig measurable in the serum of foals?

A

4-6 hours

Peaks at 18-24hrs

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10
Q

Describe the foal’s immune system in terms of colostrum intake…

A

Specialised enterocytes allow absorption of Ig via pinocytosis 12-24hrs

Maximal efficacy of absorption after birth

Half life maternal antibodies = 20-30d

Foal’s own Igs production reaches adult levels at 5-10 months

Very susceptible to disease 1-2months

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11
Q

Why is failure of passive transfer a problem in foals?

A

Predisposes to infectious disease

Especially bacteraemia, sepsis, septic arthritis, diarrhoea, pneumonia, meningitis

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12
Q

What are the maternal factors associated with failure of passive transfer in foals?

A

Lack of colostrum (premature lactation)

Poor colostrum quality (low conc of IgG (specific gravity <1.060 or <3000mg/dL = 30g/L)

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13
Q

What are the factors associated with the foal resulting in failure of passive transfer?

A

Lack of colostrum intake by the foal

  • Inability to nurse (sepsis, perinatal asphyxia, ortho)
  • Foal rejected by mare

Lack of colostrum absorption

  • Colostrum ingested too late
  • Gastrointestinal disease (hypoxic damage)
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14
Q

What values are associated with complete FPT, partial FTP and successful transfer in foals?

A

Complete FTP
< 4.0g/L

Partial FTP
4.0 - 8.0 g/L

Successful tranfer
> 8.0 g/L

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15
Q

How can FTP be diagnosed in foals?

A

History

  • Problems standing or never stood
  • Not nursing until 8-12 hours of age
  • Rejected by mare

Colostrum examination
SG <1.060

IgG concentration in blood
- SNAP test (ELISA)

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16
Q

How can you treat FPT with a nasogastric tube in the foal?

A

Foal <12 hours old and no systemic signs
1.0-20L of equine colostrum (SG >1.060)
200-400ml at the time
Use nasogastric tube, not syringe or bottle => risk of aspiration

17
Q

How can you treat FPT with plasma in the foal?

A

IV Plasma (1-2L)

  • Foal >8hours
  • Foal showing systemic signs
  • No high quality colostrum

Plasma administration

  • Use plasma giving set and monitor carefully for signs of plasma reaction
  • Administer 1 drop per sec (3ml/min)
  • Check heart rate, respiratory rate, and temperature every 5 minutes
  • No reaction after 15 minutes: administer quickly
18
Q

How should you manage a plasma reaction in foals?

A

Stop transfusion
Give flunixin meglumine +/- IV fluids
Wait 1-2 hours, restart infusion slowly
If reaction persists use different plasma batch or donor

19
Q

What is neonatal isoerythrolysis?

A

Immune-mediated haemolytic anaemia of newborn foals

20
Q

What causes neonatal isoerythrolysis?

A

Caused by incompatibility between mare and foal’s blood group

  • Mare produced antibodies against foals RBC antigens
  • Antibodies are secreted into the colostrum and absorbed by the foal
  • Antibodies adhere to and destroy foal’s RBCS
21
Q

What are the prerequisites for neonatal isoerytholysis?

A

Two stage process featuring 2 pregnancies.

Number One

Foal 1 inherits RBC antigens antigens (Aa, Qa) from Sire.
Mare is Aa and Qa negative

⇓

Mare exposed to foal’s RBC (transplacental haemorrhage, parturition..)

⇓

Mare produces antibodies against Aa or Qa

Number Two

Foal 2 inherits RBC antigens (Aa, Qa) from Sire.
Mare has built up antibodies against Aa and Qa

⇓

Foal ingests antibodies with colostrum: absorbed into circulation

⇓

Antibodies coat RBC ⇒ intra- and extra- vascular haemolysis

22
Q

When do clinical signs of neonatal isoerythrolysis develop?

A

At 1 - 12 days (usually under 3)

23
Q

What does the onset and severity of neonatal isoerythrolysis depend on?

A

Amount of ABs ingested
Affinity of antibodies for antigen on RBC
Type of alloantibody: Aa > Qa

24
Q

What are the types of haemolysis associated with neonatal isoerythrolysis?

A

Intra and extravascular

25
Q

What are the clinical findings of neonatal isoerythrolysis?

A 
Normal at birth
Weakness, depression, not nursing
Increased HR
Increased RR
\+/- fever
Icterus
Neurological signs
Potential sepsis
26
Q

What are the laboratory findings associated with neonatal isoerythrolysis?

A 
Anaemia
Haemoglobinuria
Haemoglobinaemia
Increased bilirubin
Metabolic acidosis
Prerenal or renal azotaemia
Toxic hepatopathy
Ig <4.0 g/L
27
Q

How is neonatal isoerythrolysis diagnosed?

A

History and clinical findings
Haemolytic cross match:
- Identifies haemolysis of foal’s RBCs by mare’s serum
- Required addition of external (rabbit) complement
- Can evaluate for signs of agglutination if no complement available, although a negative result does not rule out.

28
Q

How is neonatal isoerythrolysis treated?

A

Prevent further colostrum intake

  • Muzzle foal or separate
  • Prove alternative source of nutrition
  • Provide alternative source of passive immunity

Supportive care:

  • Foals may suffer from other disease
  • May require IV fluids if severe haemogolbinuria

Blood transfusion

  • Washed RBC from mare (NOT mare’s plasma)
  • Blood donor negative for Aa and Qa
  • Cross match
29
Q

How can neonatal isoerythrolysis prevented?

A

Mare with history

  • Determine blood group of sire
  • Test serum alloantibodies
  • Prevent any colostrum intake if same sire or other incompatible sire used
30
Q

Described severe combined immunodeficiency (SCID)

A

Autosomal recessive genetic disease of Arabian foals
Enzymatic defect: no mature function T or B cells
Recurrent infections after passive immunity decreases
Associated with infection with uncommon pathogens (adenovirus), pneumonia, diarrhoea
Fatal at approximately 5 months of age
Dam and sire are carrier of gene, genetic testing available

Lymphoreticular and Haemopoietic (14 decks)

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