Manifestations And Management Of Disease In Foals p243-278

Question 1

What is a bolus rate of fluids for a foal? What’s a maximum rate of bolus fluids?

Answer 1

20 mL/kg over 15-20 minutes, with this repeated up to 3 times for a total of 80 mL/kg

Question 2

What rates should plasma and hetastarch be administered to foals?

Answer 2

Plasma at 10 mL/kg/hr

Hetastarch 3 ml/kg given at a rate of 10 ml/kg/hr

Question 3

If hypotension persists, despite fluid resuscitation, what can be used to increase a foals MAP? What should the MAP be over?

What are the general MOAs of the drugs used?

(4)

Answer 3

The MAP of a foal should be over 60 mm Hg.

Dobutamine, has beta activity - increases the cardiac output, by improving stroke volume
Often administered as a CRI 2-20 ug/kg/min

Vasopressor such as norepinephrine, this acts at alpha1 and alpha2 receptors to mediate vasoconstriction, along with beta1-adrenergic receptors causing positive inotropic and cardiotropic effects.
Given by CRI at 0.05-5 ug/kg/min

Dopamine has combined alpha and beta adrenergic effects, and mediates vasodilation, in renal cerebral and splanchic vascular beds.
Given at 1-5 ug/kg/min, and higher infusion rates 10-25 ug/kg/min

Vasopressin acts at V1a receptors in peripheral circulation, causing vasoconstriction and at V2 receptors in the kidney to facilitate water reposition.
Dosed at 0.25-1 mU/kg/min

Question 4

Define SIRS and what it results in.

Define infection, bacteremia, viremia, fugemia, severe sepsis, septic shock, MODS

Answer 4

Systemic inflammatory response syndrome - that results in at least TWO of the following

• fever
• tachycardia
• tachypnea/hyperventilation
• leukocytosis/leukopenia/bands

Infection - invasion of normally sterile tissues by microorganisms
Bacteremia - presence of viable bacteria in the bloodstream
Viremia - presence of viable virus particles in the blood
Fungemia - presence of viable fungal elements
Severe sepsis - when sepsis is assoc with organ dysfunction, hypoperfusion or hypotension
Septic shock - sepsis-induced hypotension despite fluid adequate fluid therapy
MODS - multiple organ dysfunction syndrome - alteration of organ function and homeostasis cannot be maintained

Question 5

T/F The absorption of Ig is Fc-receptor mediated in the foal

T/F The foal can selectively absorb IgG and IgM over IgA

Answer 5

F The absorption of Ig is Fc-receptor mediated in the foal, unlike other species
T The foal can selectively absorb IgG and IgM over IgA

Question 6

The most common findings in acute sepsis in the foal:

Answer 6

Luekopenia characterized by neutropenia, with L shift and toxicity (Dohle bodies, toxic granulation and vacuolization)

Question 7

A classification of septic arthritis and osteomyelitis in foals has been established based on radiographic and pathological findings. What are these types and how are they defined?

(4)

Answer 7

“S” type - bacterial infection of the synovial membrane of one or more joints, without radiographic changes; joint effusion present, seen in first 2 weeks of life; carpus, stifle, hock

“E” type - epiphyseal, with infection of the joint and osteomyelitis of the adjoining subchondral bone; 3-4 weeks of age; femoral condyles, distal radius, distal tibia, or patella

“P” type - physeal-type involving the physis on the metaphyseal side of the growth plate; 1-12 weeks of age; distal tibia or radius, or distal meta-carpi/tarsi

“T” type - tarsal type involving cuboidal bones of tarsus and carpus

Question 8

List some causes of seizures in the neonatal foal

Answer 8

Neonatal encephalopathy, bacterial meningitis, viral encephalitis, benign juvenile epilepsy, lavender foal syndrome, kernicterus, hepatic failure, head trauma, hypoglycemia, electrolyte disturbances, ivermectin/Moxidectin

Question 9

Neuronal cell death leads to the clinical manifestations of of hypoxia-ischemic syndrome or perinatal-asphyxia syndrome. How is neuronal cell death caused?

Answer 9

ACUTE PHASE: Reduced oxygen delivery —> depletion of ATP and failure of cell membrane ion pumps —> membrane depolarization —> accumulation of sodium into cell —> passive diffusion of water —> swelling and lysis

+ accumulation of glutamate (excitatory neurotransmitter) from increased release from neurons —> interaction with AMPA receptors —> amplification of sodium into the cell —> diffusion of water —> swelling and lysis

SECONDARY PHASE: specific glutamate receptors are activated (NMDA) by the excess glutamate present —> calcium receptors cause influx of Ca2+ —> cascade of events
activation of enzymes
enhanced glutamate release
uncoupling of oxidative phosphorylation 
generation of oxygen-free radicals 
—> cell death and apoptosis

Question 10

What are some common treatment options for seizures in foals?

Answer 10

Diazepam
Phenobarbital
Midazolam

Question 11

How does magnesium supplementation aid in treatment of seizures?

Answer 11

This is used to block the release of glutamate and antagonize the influx of calcium at the NMDA-activated channels

Question 12

Arabian foals of Egyptian bloodlines can have two causes of seizures. What are they?

Answer 12

Benign juvenile epilepsy - age of onset is 2d-6 mths. Cessation of seizures stops by 12 mths of age

Lavender foal syndrome - dilute coat color, unable to ever achieve sternal recumbency; death or euthanasia by 72 hours

Question 13

How does an ivermectin overdose cause seizures?

Answer 13

Opening of gamma-aminobutyric acid (GABA)-gated chloride channels, with resultant membrane hyperpolarization and blockade of neuronal impulses

Question 14

What is a recommended treatment for ivermectin and moxidectin overdose, respectively?

Answer 14

Ivermectin - IV lipid emulsions, 20% soybean oil in water, 1.5 mL/kg IV bolus, followed by 0.25 mL/kg/min for 30 minutes

Moxidectin - benzodiazepine receptor agonist, sarmazenil 0.04 mg/kg IV q2h

Question 15

What is kernicterus and how does it affect foals?

Answer 15

Kernicterus is a neurologic complication of neonatal isoerythrolysis. AKA bilirubin encephalopathy or nuclear jaundice, from deposition of unconjugated bilirubin in the brain, particularly the basal nuclei

Question 16

How high would a foal’s bilirubin rise, to be 17x more likely to develop signs of kernicterus?

Answer 16

If a foal’s serum bilirubin concentration is over 27.0 mg/dL

Question 17

Anemia of chronic disease can occur in foals. What other clinicopathologic abnormalities can be found that contribute to the anemia?

Answer 17

Altered iron metabolism, bone marrow depression, reduced production or action of erythropoietin. Increased levels of hepcidin, released in response to inflammation, decreases iron absorption and iron recycling.

Question 18

What does a twilight foal describe?

Answer 18

A foal with accelerated, but incomplete, maturation of the HPA axis at the time of birth.

Question 19

What should the average weight of the foal be, in relation to the the mare?

Answer 19

The foal should be an average 10% of the body weight of the mare

Question 20

A pregnant mare grazing on a fescue pasture will ingest what, with what consequences?

Answer 20

Fescue is typically infected with Neotyphodium coenophialum. Prolongation of gestation, perinatal mortality and agalactia

The toxin interferes with fetal corticotropin-releasing hormone and delay in maturation of the HPA axis

Foals are also born with a reduced tri-iodothyronine levels

Question 21

Congenital hypothyroidism has been reported in foals. What are some clinical signs of this syndrome?

Answer 21

Prolonged gestation, dysmaturity, flexural deformities, delayed ossification, mandibular prognathism

Question 22

What protects the foal from getting too much cortisol in utero?

Answer 22

The type 2 isoform of 11beta-hydroxysteroid dehydrogenase turns active cortisol into inactive cortisone. Other enzymes such as 3beta-HSD, P450scc, p450C17 are inhibited or deficient during this time as well.

Question 23

Prior to parturition, the fetus will have a change in adrenal activity with an increase in cortisol levels. What does this rise in fetal cortisol stimulate in regards to the placenta and thyroid, so that lung maturation occurs properly.

Answer 23

The rise in fetal cortisol stimulates the conversion of pregnenlone to estrogen; stimulates the placenta to increase prostaglandin H synthase 2, leading to secretion of PGE2; stimulates placental 11beta-HSD-1 to convert cortisone to cortisol.

Rise in plasma cortisol also increases the deiodination of T4 to the active form of T3.

Question 24

How can the HPA axis in foals be prematurely accelerated?

Answer 24

Hypoxemia, exogenous glucocorticoids, poor nutrition, cytokines induced by inflammation increasing prostaglandin synthesis

Question 25

What are some findings that may determine short term prognosis for survival for premature foals?

Answer 25

Normal or elevated neutrophil count, neutrophil:lymphocyte ratio or total WBC count are positive indicators of survival since they reflect maturation of the HPA axis

Question 26

When evaluating a foal’s blood gas, what are the two most common respiratory derangements? How is acute vs chronic hypercapnia distinguished?

Answer 26

Hypoxemia with normocapnia or hypoxemia with hypercapnia

Acute hypercapnia is denoted by a larger drop in pH and can lead to circulatory collapse and comma

Chronic exposure permits adaptations and the change in pH is less dramatic because of enhanced bicarbonate reabsorption in the proximal tubules of the kidney

Question 27

List some common causes of diarrhea in foals.

Answer 27

Clostridium perfringens, Clostridium difficile, Salmonella, R. equi, Rotavirus, corona virus, Strongyloides westeri, nutritional, foal heat diarrhea

Question 28

What are the most common causes of intestinal clostridiosis in the foal?

Answer 28

C. perf biotype C, seen in less than 10 days old, with hemorrhagic diarrhea, colic, cardiovascular collapse, high mortality, alpha and beta toxins with variable amounts of enterotoxin

C. perf biotype A, lower mortality than type C, alpha and enterotoxin, diarrhea may or may not contain blood

C. difficile produces an alpha enterotoxin and a cytotoxin B

Question 29

How does R. equi cause diarrhea?

Answer 29

This uncommon cause of foal diarrhea occurs by necrosis of small intestinal Peyers patches and multi focal thickening of the cecum and large intestines

Question 30

What is the importance of foal feces that tests positive for R. equi or Salmonella?

Answer 30

If salmonella is recovered from feces, this has significance as horses that are shedding are typically clinical. R. equi recovery in feces is common in asymptomatic animals. Up to 100% of foals older than 2 weeks of age may shed large numbers of R. equi.

Question 31

What is the most common cause of infectious diarrhea in foals? How does this pathogen cause diarrhea and are there specific serotypes?

Answer 31

Rotavirus is the most common, with Group A the primary cause and G3 the most common serotype.

This pathogen replicates within the intestine and invades the lining of the proximal SI. Villous death causes loss of absorptive area + decrease in lactase production leads to osmotic load of undigested lactose to the immature hind gut. Crypt cell proliferation causes an increase in intestinal secretion and enterotoxin further contributes to diarrhea

Question 32

What is the enterotoxin and cytotoxin produced by rotavirus?

Answer 32

NSP4 is a nonstructured glycoprotein released from virus-infected enterocytes. It is a non competitive inhibitor of the Na-glucose symporter and enhances intestinal chloride secretion

Question 33

How old are foals typically affected with rotavirus

Answer 33

Most commonly 60 days

Question 34

What are the most common laboratory findings in foals with uroperitoneum?

Answer 34

Hyponatremia, hyperkalemia, hypochloremia, azotemia, metabolic acidosis

Question 35

If fluid is drained from a suspect uroperitoneum, what would the findings be of said fluid?

Answer 35

Low cell count, low specific gravity, at least twice the creatinine concentration of peripheral blood

Question 36

What parasite is associated with intussusceptions?

Answer 36

Anoplocephala perfoliata

Question 37

What are pneumotosis cystoides intestinalis and what disease process in foals are they found?

Answer 37

These are gas filled cysts found in the submucosa and subserosa in necrotizing enterocolitis. Predisposing factors of this disease are hypoxia gut injury, presence of intraluminal bacteria and enteral feeding. The bowel can frequently rupture once these cysts are formed.

Question 38

In which of the following species can deprivation of milk or colostrum extend intestinal permeability to immunoglobulins (sometimes up to 5 days!)

Pigs
Lambs
Foals

Answer 38

In neonatal pigs and lambs, it has been shown that deprivation of macromolecules can extend intestinal permeability.