Equine Neonatal Conditions and Care Flashcards
1
Q
what is the adaptive period
A
The perinatal period
the changes that a newborn foal is subjected to during the adaptation from intrauterine to freeliving environment
ability to adapt is crucial for survival in the wild
2
Q
T/F: foals are just small adult horses
A
False
3
Q
the prenatal period
A
gestation lenght where you are predicting the timing of foaling
and risk category of the foal
4
Q
What is the gestational length of the horse
A
Mean: 340 days (many use 335 = 11 months) use shorter length so you are reading
significant variation
-breed, season
-more consistent between pregnancies
5
Q
What is the best method in predicting specific gestation length in mares
A
what her gestational length last year was
really matters because normal foals at shorter of longer gestation
or dysmature at “normal” gestation lenght
6
Q
Why is predicting a mare’s gestation important
A
unpredictable result when foaling is induced or when performing a c-section
7
Q
Why is it important to predict the day of foaling
A
1) Increased vigilance
2) Be prepared
3) Recognize problems early
4) Intervene early
8
Q
What is the most specific measure of predicting the day of foaling
A
milk calcium levels will increase 1-2 days before foaling
Mares with Ca concentration >200ppm have a 54% probability of foaling within 24 hours and 84% probability of foaling within 48 hours and 97% probability of foaling within 72 hours
9
Q
What are general measures of predicting the day of foaling
A
Conformational changes: 1 week to 1 month
Teats fill (2d to 1 week)
Teat waxing (1d to 4d)
Increased calcium in milk (1d to 2d) * most specific
10
Q
Gestational lengths shorter than _____ days in horses are considered premature
A
320 days
seasonal and breed factors impact gestational length
11
Q
Males foaling during _____ days tend to have shortened gestation while mare foaling during ____ tend to have prolonged gestation
A
Long day: short gestation
Short days: long gestation
12
Q
How do you determine calcium concentration in mammary secretions to determine foaling time
A
There are horse specific tests but a cheaper way is water hardness test stripes
13
Q
What are the mare factors when determining the risk category of a foal
A
1) Mare with poor general health
2) Mare with poor confirmation (dystocia, ascending uterine infection)
3) mare with advanced age
4) Mare with prolonged transport prior to parturition (lower calcium concentrations and dystocia)
14
Q
What are parturition factors when determining the risk category of a foal
A
1) Dystocia
2) Premature placental separation
3) Prolonged gestation (hypoxia, dystocia, placenta insufficency, no parturition trigger from foal)
15
Q
What are the management factors when determining the risk category of a foal
A
1) Adverse environmental conditions
2) Poor hygiene
3) Inexperienced foaling attendant
16
Q
What are the foal factors when determining the risk category of a foal
A
Any abnormality noted in the foal increases risk category
17
Q
What does the normal foal heart sound like after parturition
A
1) 60-140 bpm (age dependent)- will later decrease
2) Up to 4 heart sounds
3) Murmurs heard for up to 72 hours (ductus arteriosis persists for several days after parturition) - pansystolic and pandystolic (continuous murmur)
18
Q
What 2 things might pre-mature lactation in a mare tell you that is concerning
A
1) warning sign that there might not be colostrum ready for the foal when they are birthed
be prepared to treat failure of passive transfer
2) Placentitis
19
Q
Why are you able to hear all 4 sounds in the foal
A
you are also able to do this in an adult but the chest wall is a lot thinner so you can hear all 4 sounds
20
Q
The _________ closes typically at birth of a foal but the ________ remains intact for a couple days after parturition and creates a murmur
A
foramen ovale = closed at birth
ductus arteriosus = remains open for a couple days
21
Q
You will hear a murmur in foals for up to
A
72 hours (3 days) after birth
you need to see if there is a decrease in intensity after 3 days but after 3 days there is still same intensity then it is concerning
22
Q
What helps the foal clear the airways from excess fluid
A
the thoracic compression during the passage of the foal through the birth canal
beware during c-sections
23
Q
What is the normal respiratory rate of a foal
A
At parturition typically around 70bpm but then will drop to around 20-35bpm but will still remain higher than adult rate for several days
24
Q
The foal’s chest wall is very compliant, what must they do during adaptation
A
foals must make active respiratory movements for both inspiration and expiration
dystocia might fracture ribs and make it hard for them to breathe
25
If the foal's lungs are immature then
they will develop acute respiratory distress syndrome (ARDS) and result in significant mortality
fetal lungs develop the capacity for gas exchange relatively late in gestation
26
How do you assess fractured ribs in a foal after birth from dystocia
ultrasound
27
Foals need to pass ___________ very soon after parturition
Meconium
(dark, sticky, patent GI tract)
28
What is meconium
the first defecation of a horse that is pelleted, dark, brown, sticky feces
the passage of meconium indicates that the gut is fully patent and there is no physical or neurological (lethal white syndrome) obstruction
29
What does the passage of meconium indicate
the passage of meconium indicates that the gut is fully patent and there is no physical or neurological (lethal white syndrome) obstruction
also colostrum deprived foals will get meconium obstruction
most foals will pass meconium within the first few hours (often within minutes of the first feed)
30
What does milk feces look like vs meconium
Milk feces: pasty, yellow
Meconium: dark, sticky, pelleted, hard
31
What is the #1 colic in foals less than 48 hours is
meconium impaction
32
What are the urinalysis differences noted in foals
1) Some protein + (up to 72 hours)
2) Lower SG (lower ability to concentrate, first urine, dehydration) - 1.010
33
What might help to mature the lungs in premature fetuses
Glucocorticoids- premature fetuses has been shown to increase their survival and decreased the incidence of ARDS after delivery
34
Normal foals should stand to their feet and move within
1-2 hours after birth and move rapidly by 2-4 hours
35
T/F: menace response in foals are weak at birth and might remain that way for several days to months
True
beware, you do not want to diagnose them of being blind
36
Hypothermia in a foal is indicated when it is below
98F
37
Foals might have higher _____ liver values
GGT
38
What is the immunity status of foals
immunologically naive but immunocompetent
it is functioning but it hasnt come across what it needs to
39
The innate immune system is composed of
1) anatomical (skin, mm)
2) Physiological (acidic pH in stomach, fever)
3) Phagocytic (monocytes, macrophages)
4) Inflammatory barriers (leakage of serum proteins with antibacterial activity into areas of tissue damage and inflammation
40
What is true of the foals innate immune system
Antiviral response: Type I interferons
Cytokines, antiviral proteins
41
What is true of the foal's adaptive immunity
Humoral: little produced, need passive transfer
Cell mediated response: poorly developed, requires maturation
42
How does passive transfer occur
High MW: take up by pinocytosis and go to lymphatics and systemic blood
Low MW: absorbed by duodenal cells into portal blood and systemic
both go to urine (why proteins all enter the urine
43
What is the foal's absorption kinetics of colostrum
the foal is only able to absorb colostrum for some time but then the gut closes at 24-48 hours so after 24 hours, you have a bad window of opportunity
closes because pathogens can enter. it closes faster if there is adequate passive transfer
44
When adequate colostrum ingestion occurs then IgG blood levels reach there peak by ______- hours after birth
18 hours after birth
45
How do you ensure adequate passive transfer
Mare
1) Healthy
2) Good body condition
3) udder/teat health
4) exposure to antigens
5) vaccinations
6) age
Foal
1) healthy
2) ability to stand
3) strong suckle
4) mature GI tract
5) timing
46
What kind of placenta does the horse have
Epitheliochorial- prevents transfer in utero.
the foal may begin devleoping IgM in utero
foal develops some immunoglobulin at birth but it isnt apparent until 10-14 days
therefore most of humoral is from ingestion of colostrum
47
How might you determine the colostral IgG concentration
1) Radial immunodiffusion (RID) - direct
2) Colostrometer via specific gravity - indurect
48
The horse would
Stand by ____- after birth
Nurse by _____ after birth
Mare pass placenta by _____ hours after birth
1 hr: stand
2 hr: nurse
3 hr: placenta
draft foals may take a little too long, might need to let them up
49
How do you assess passive transfer in foals
1) Single radial immunodiffusion (SRID): most accurate, requires time (18h) and laboratory
2) Zinc sulfate turbidimetric assay: accurate, IgG to precipitate in a 20% zinc sulfate solution
3) ELISA based: fast, can be done stall-side
assess to the calibration spots
can really only tell if it is High or Low
50
What is the gold standard for assessing passive transfer
Single Radial Immunodiffusion (SRID) - more sensitive
annoying because it takes 24 hours to get results
51
How do most people assess passive transfer
ELISA based
fast, can be done stall slide
can only tell if high or low, cant quantify numerically
52
What might cause failure of passive transfer
1) premature lactation
2) mare failing to transfer sufficient IgG from colostrum
3) Delayed suckling by foal
4) ingestion of too little colostrum or failure of the foal to absorb IgG from colostrum
53
What level of IgG dictates adequate transfer, vs partial and complete failure
Adequate transfer >800 mg/dl
Complete <400 mg/dL at 24 hours of age
numbers dont matter as much: need to have high levels until the foal's IgG takes over, bridge the gap with colostrum immunity
54
By definition, what is failure of passive transfer in foals
<400 mg/dl IgG at 24 hours of age
55
there is a 3-25% partial or complete failure of passive transfer, why is the incidence of septicemia in foals even lower?
management practices
56
How do you treat foals with failure of passive transfer
1) Colostrum:
-useful up to 24 hours (maybe even longer?)
-local mare preferred (hard to find)
-oral serum product
2) Plasma
-Does not rely on GI absorption/function
-No "local" immunity
-Hyperimmune for certain pathogens
-Hypersensitivity
57
What is a major downside of treating failure of passive transfer with colostrum administration
hard to obtain
need to ensure IgG adequate levels
need to rely on GI absorption/function
58
What is a major downside of treating
1) No local immunity
2) Hypersensitivity - make sure the client knows
59
The foal's umbilical stump should be dry within
1-2 days
dip in dilute chlorhexidine
60
What should you dip the foal's umbilical stump in?
dilute chlorhexidine
never straight iodine
61
What are the risk categories of the foal to have failure of passive transfer
1) Maternal/ prenatal factors
2) Poor general health
3) Poor perineal conformation- ascending placentitis
4) Advanced age - lower foaling rate, scarring of uterus and chronic endometritis
5) Premature lactation - colostrum is produced once and only once, low immunoglobulin within 24 hours of onset of lactation
6) Prolonged transport: hypocalcemia
62
How can you assist in the passage of meconium to avoid impaction in foals
prophylactic enema
63
What should you consider when doing prophylactic enemas in foals
1) only do once by owner, 2) never against resistance
3) be careful using potentially irritating solutions
64
What does meconium straining of the newborn or fetal fluids indicate
fetal distress in utero and if present the foal should immediately be classified as high risk
65
What should you do when evaluating the placenta
early detection of potential problems with mare and foal
observe
-body
-gravid horn
-umbilical cord
-non-gravid horn
-cervical star (chorioallantoic)
-weight (10-11% body weight)
-chorionic surface
-allantoic surface
66
What should you do for the foal within the first day of birth
Check colostrum
Examine placenta
Dip umbilicus
Clinical exam
+/- determine early IgG
67
What should you do for the foal on the second day of birth
Dip umbilicus
Determine IgG
+/- Hematology
+/- Chemistry
68
Weakness and abnormal behavior in a foal might be associated with
1) Endotoxemia
2) Hypoxia
3) Trauma
4) Acid/base abnormalities
5) Hypovolemia
6) Hypoglycemia
6) Birth defects
69
What are the 3 most common causes of weakness or abnormal behavior in a foal
1) Prematurity/dysmaturity
2) Septicemia
3) Neonatal Asphyxia Syndrome
70
Assessing prematurity and dysmaturity in a foal
assessing the level of maturity based on both gestational length and clinical presents
-Significant variation
-Unpredictable results induced birth
-Premature <320 days
-Dysmature at normal length
-Clinically similar
71
Prematurity is assessed by _____ while dysmaturity is assessed by
Prematurity: gestational length
Dysmaturity: condition of the foal- foal born within the normal or even prolonged gestational range but shows the clinical signs normally associated with prematurity
72
Dysmature foals often associated with
placental pathology
73
What are the clinical signs of foals with prematurity/dysmaturity *
1) Weakness- decreased muscle tone
2) Floppy ears (pliant)
3) Dome-shaped forehead
4) Silky hair coat
5) Tendon laxity
6) Incomplete ossification small carpal and/or tarsal bones
7) Immature lungs, ARDS- very low or high resp rates
8) Small body size for age
9) Immature GI tract, postprandial colic
74
Foals that are premature/dysmature have an immature GI tract making them more susceptible to
1) Postprandial colic
2) Failure of passive transfer
75
How do you diagnose foal prematurity/ dysmaturity
Based on physical characteristics +/- history
1) Weakness- decreased muscle tone
2) Floppy ears (pliant)
3) Dome-shaped forehead
4) Silky hair coat
5) Tendon laxity
6) Incomplete ossification small carpal and/or tarsal bones
7) Immature lungs, ARDS- very low or high resp rates
8) Small body size for age
9) Immature GI tract, postprandial colic
Do confirmation by various tests (ACTH stimulation)
76
What test can you do to diagnose foal fetal prematurity / dysmaturity
ACTH stim
77
How do you treat foal fetal prematurity / dysmaturity
1) Nursing care *
2) Nutritional support (milk or parenteral)
3) Antibiotics (anticipate issues)
4) Additional therapy based on clinical signs (oxygen, fluid)
5) Incomplete ossification- wrap limbs to maintain positioning and minimize negative effect on nonossified bones.
78
What is the prognosis of
Decreased lung function = short term prognosis
Ossification = long term prognosis (may warrant euthanasia)
good prognosis if >310 days
79
foal fetal prematurity / dysmaturity has good prognosis if
>310 days of gestation and ossification is close to complete
80
Half of foals that become septic are infected ____
in utero
81
What is the number one killer in horses <7 days of age
septicemia
82
How do foals typically get septicemia
1) In utero (placentitis) 50%
2) Respiratory infection
3) Oral Infection
4) Umbilical infection
83
What bacteria typically cause septicemia in foals
Gram negative
-E. coli
-Actinobacillus
-Salmonella
-Klebsiella
Gram positive
-Streptococcus
-Staphylococcus
-Clostridium (anaerobe)
gram negative are more common
84
What are the clinical signs of septicemia in foals
Often unspecific
1) Nurse less (distention of the mare's udder and dripping of milk)
2) Sleeps more and progressively more depressed
3) Death (multiple system involvement develop- joints, lungs, brains, eyes)
85
In foals, bacteremia can spread to what common sites
Eyes
Joints
Lungs
86
How do you diagnose sepsis in foals
definite: isolation of bacteria from blood
Supporting findings:
hypoglycemia
acidosis
azotemia
neutropenia (left shift)
87
What CBC/CHEM results will you see with sepsis in foals
hypoglycemia
acidosis
azotemia
neutropenia (left shift)
88
What samples should you take for sepsis evaluation in foals
1) Blood cultures
2) Hematology - bacteremia
neutropenia (left shift)
3) Chemistry - azotemia
4) Blood glucose - hypoglycemia
5) Blood gas - acidosis
89
What antibiotic considerations should you have when choosing an antibiotic for treating sepsis in foals
1) Broad spectrum - both gram + and -
2) Bactericidal
3) Penetrate the tissue of concern (e.g CNS)
commonly a penicillin and aminoglycoside combination (caution aminoglycoside nephrotoxictiy)
90
What supportive care should you do for foals with sepsis
1) Colloids
2) Add dextrose
3) Plasma
4) Nutrition - enteral, parenteral (dextrose)
5) Gastroprotectants
6) Pressure support
7) NSAIDs
91
What should you beware of when treating foals with sepsis with penicillin and aminoglycoside
aminoglycoside nephrotoxicity!
if nephrotoxicity present, might want to stay away
92
a syndrome to describe fewborn foals that exhibit behavioral or neurological abnormalities that are not caused by infectious or toxic agents, metabolic disorders or due to congenital/ developmental abnormalities
Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy / Neonatal Maladjustment Syndrome
93
What are other names for Neonatal Asphyxia Syndrome (NAS)
1) Hypoxic-Ischemic Encephalopathy
2) Neonatal Maladjustment Syndrome
94
Why is it called Neonatal Asphyxia Syndrome
because the majority of neonatal foals that exhibit CNS signs have suffered from lack of cerebral oxygen delivery (either due to ischemia or hypoxemia)
95
Why are the hypotheses behind the etiology of Neonatal Asphyxia Syndrome
1) Anything that interferes with O2 delivery during parturition (placentitis, dystocia, red bag, foal resuscitation)
Hypoxemia and ischemia leading to decreased PaO2, then cell death, swelling, and increased intracranial pressure
2) Abnormal levels of neurosteroids (sedative effect)- stress during normal parturition (e.g passage through birth canal) signals the decrease in neurosteroids
96
Are the clinical signs of Neonatal Asphyxia Syndrome acute or delayed
Delayed
foals appear normal for first few hours up to >2 days
onset and severity of signs depend on the degree and duration of oxygen deprivation (and sequelae)
97
What is the typical history for doals with Neonatal Asphyxia Syndrome
1) Gestational problems (vaginal discharge- placental infection, premature lactation, prolonged or shortened gestational length) in the mare
2) Dystocia and premature placental separation
3) Delivery through emergency c-section
all result in development of hypoxic insult before or shortly after delivery
98
What is the hypothesis of neurosteroids in Neonatal Asphyxia Syndrome
Abnormal levels of neurosteroids (sedative effect)- stress during normal parturition (e.g passage through birth canal) signals the decrease in neurosteroids
but these levels stay high and have a sedative effect to the foal
99
What is the typical onset of Neonatal Asphyxia Syndrome
foals appear normal for first few hours up to >2 days
could be as late as 4-5 days after birth
100
What are the clinical signs of Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy
Inability to find udder
wandering
head-pressing
lip smacking
loss of coordination
seizures
coma
death
101
How do you diagnose Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy
1) Diagnosis of exclusion (history and clinical signs) - eliminate other possible causes of CNS disease in a newborn foal
2) Increased creatinine, CK, AST may be suggestive
102
Increases in ______
_____
_____
might be indicative of
Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy
Increased creatinine
CK
AST
103
How do you treat Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy
Symptomatic
1) Adequate ventilation: Intranasal oxygen, caffeine, mechanical ventilation
2) Maintain perfusion: IV fluids, colloids, pressure agents
3) Maintain adequate glucose levels: IV dextrose admin, PPN/TPN, oral nutrition
4) Controlling seizures: diazepam, midazolam, phenytoin, phenobarbital
5) Reduce cerebral edema and neuroprotection: DMSO, mannitol, hypertonic saline, hypothermia, allopurinol, magnesium, vitamin C, vitamin E, thiamine, melatonin, xenon
6) Madigans foal squeeze procedure for abnormal neurosteorids
104
What is Madigan's foal squeeze procedure for?
re-enact the foaling procedure, aims to decrease the neurosteroids amount
might have beneficial effects if minor brain damage
105
the prognosis for survival of premature/dysmature foals is usually dependent on ________ while the prognosis for future use is strongly dependent on _______
Survival: lung maturation
Future use prognosis: cuboidal bone ossification
106
What is a common, often deadly sequelae of primary infections such as enteritis and pneumonia in the foal
sepsis
107
What is the prognosis of Neonatal Asphyxia Syndrome / Hypoxic-Ischemic Encephalopathy
dependent on the severity of the initial insult and the progression of cellular damage. If cerebral damage results in fixed, dilated, and non-responsive pupils then the prognosis is grave
108
What causes icterus
Increased level of bilirubin (indirect, direct, or both)
109
Pre-hepatic causes of icterus in foals
Septicemia
Neonatal isoerythrolysis
Neonatal HGB turnover
others
110
Hepatic causes of icterus in foals
Tyzzer's Disease
Sepsis
In utero EHV-1 infection
others
111
Post-hepatic causes of icterus in foals
1) Bile duct aplasia (congental)
2) Duodenal ulcers (bile duct obstruction)
112
caused by a blood group incompatibility between the foal and the dam
results from absorption of maternal antibodies against fetal erythrocytes (alloantibodies) from the colostrum and subsequent loss of RBCs by both intravascular hemolysis
Neonatal isoerytholysis
113
What are the prerequisites for neonatal isoerythrolysis
1) Foal must express erythrocyte antigen (alloantigen) that the mare does not possess (most blood groups arent antigenic)
2) Mare must become sensitized to the incompatible alloantigens and produce antibodies to it - likely occurs from transplacental hemorrhage during a previous pregnancy
114
foals most typically associate with what times of RBC antigens in neonatal isoerythrolysis
Type Aa
factor Qa
C occasionally (milder disease)
115
What antigen has a milder outcome of neonatal isoerythrolysis than Type A and factor Q
neonatal isoerythrolysis
116
What is the pathogenesis of neonatal isoerythrolysis in horses
after the mare becomes sensitived to her foal's isoerythrolysis, the alloantibodies concentrate in the colostrum.
Foals are protected to these antibodies prior to birth
thus, in foals neonatal isoerythrolysis only develops after ingestion and absorption of colostrum containing alloantibodies specific for the foal's alloantigens
117
Are alloantibodies worse for Aa or Qa?
alloantibodies against Aa are potent hemolysins and are generally associated with more severe clinical disease than antibodies against Qa
118
Why is there a neonatal isoerythrolysis frequency in mules as high as 8-10%
because in donkey sire X horse mare mating ALL are incompatible matings
-donkey factor
119
Dam that is Qa-
Sire is Qa +
Foal will be
Qa+
the foal will have neonatal isoerythrolysis after ingesting colostrum
alloantibodies could have developed during mating
120
Dam is Aa+
Sire is Aa-
the foal will be
Aa+
the foal will not have neonatal isoerythrolysis
121
What are the clinical signs of neonatal isoerythrolysis
born normal then become depressed and weak
secondary signs: tachycardia, tachypnea, dyspnea
pale mucous membranes and then icteric (although not always present)
hemoglobinuria is not common but may be observed in severe cases
122
What are other differential diagnoses for neonatal isoerythrolysis in foals
blood loss anemia due to birth trauma
icterus due to sepsis or liver dysfunction (Tyzzer's)
should all be considered
123
How do you treat neonatal isoerythrolysis in foals
<24 hours of age: withhold dam's milk and strip out mare and feed different source
>24 hours: alloantibody levels are minimal because gut is closed
Supprotive care: Fluids- Hydration to minimize nephrotoxicity
Blood transfusion is warranted if PCV<12%
124
How do you diagnose neonatal isoerythrolysis
tentative: lethargy, anemia, icterus during first 4 days of life
definitive: alloantibodies in the dam's serum or colostrum that are directed against the foal's erythrocytes
125
In neonatal isoerythrolysis, when PCV is ________ then you should consider transfusion to prevent cerebral hypoxia
PCV< 12%
126
Donor RBC vs Recipient serum
Major cross match
127
Recipient RBC / Donor serum
Minor cross match
128
What is the issue with doing a crossmatch prior to blood transfers for neonatal isoerythrolysis
it takes lab and about 1 hour of time
129
How do you choose a blood donor for neonatal isoerythrolysis
1) Cross match
2) Prescreened donor that is negative for Aa, Ca, Qa
if none available use washed RBCs of the foal's dam or a young gelding - removing the plasma and just giving the blood
130
What are typically not good blood donors for neonatal isoerythrolysis
1) Broodmares
2) Horses that had a transfusion
3) Unusual breeds
131
How do you prevent neonatal isoerythrolysis
blood group of a mare can be checked at any time
Ab titer in mares can be checked during late pregnancy
Test is relatively inexpensive and just requires serum from mare to complete the test
muzzle the foal and milk out the mare until antibody in colostrum is depleted, must provide alternate source of colostrum and nutrition
132
What is the prevalence of neonatal isoerythrolysis
typically 1-2% prevalence of NI causing antibodies in mares
typically seen in pluriparturient mares
133
Tyzzer's disease causes
acute hepatitis in 7 to 42 days in foals
no signs of disease (variable: fever, anorexia, icterus, seizures, coma)
often peracute (sudden death)
134
What is the causative agent of Tyzzer's disease
Clostridium pilifrome
-filamentous gram negative pleomorphic rod
135
How do you treat Tyzzer's disease in foals
usually unsuccessful - no reports of successful treatment in foals
136
It is uncommon for Tyzzer's disease to cause non peracute disease (not death) in foals. But if you do, what do you see
Fever
Anorexia
Icterus
Seizures
Coma
clinicopathological: hyperbilirubinemia, hyperfibrinogenemia, hypoglycemia, and metabolic acidosis
137
How do you diagnose Tyzzer's disease
Definitive: made only on portmortem examination
organism is demonstrated on Warthin-Starry stained sections
138
T/F: Tyzzer's disease often cause sudden death in foals with no known signs
True
139
What is the prognosis of Tyzzer's disease in foals
Extremely poor
140
What might cause a newborn foal with a distended and painful abdomen
1) Meconium impaction
2) Uroperitoneum
3) Enteritis
4) GI ulcers
141
What is the key finding of distinguishing neonatal isoerythrolysis from other causes of icterus (ie Tyzzer's) is _______ *
the patient will be anemic
142
Most commonly meconium becomes impacted in the
rectum and small colon
143
What are the clinical signs of meconium impaction
affected foals have abdominal distension with gas which may be percussed
foals will stain frequently to defecate evidenced by a humped back, the rear limbs placed under the body, swishing of the tail and restlessness
144
How do you diagnose meconium impaction
digital examination often reveals a rectum packed with hard fecal material
x-rays or ultrasound may be warranted if located more proximally (large or small colon)
145
How do you treat muconium impaction
enema with mild soap and warm water, commercial enma, a small amount of dioctyl sodium sulfosuccinate
146
Commonly uroperitoneum results from
a tear in the urinary bladder or urachus
usually present at birth, despite looking normal
147
What are the clinical signs of uroperitoneum in foals
1) Stranguria
2) repeated posturing to urinate
3) Depression
4) Cardiac arrhythmias - bradycardia
5) Abdominal distension
presence of urine DOES NOT rule out uroperitoneum
148
T/F: the presence of urine rules out uroperitoneum in foals
False - it could be a small leak
149
How do you diagnose uroperitoneum in foals
1) Clinical signs
2) Hyponatremia
3) Hyperkalemia
4) Hypochloremia
5) Ultrasound
6) Creatinine ratio >2:1
7) ECG changes
150
What Creatinine ration of abdominal fluid : blood makes you confirm uroperitoneum
Fluid : Blood ratio of > 2:1
151
How do you treat uroperitoneum
Usually surgically
stabilize foal: correct electrolyte, fluid and acid / base disturbances (saline, dextorse, sodium bicarbonate) to correct potassium
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What might cause diarrhea in foals
Foal heat
Parasites
Bacteria
Antibioitcs
Nutrition
Viruses
Mechanical obstructions
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What causes intestinal clostridiosis in foals
1) Cl perfringens Type A, C
2) Cl difficile
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What is the clinical presentation of intestinal clostridiosis in foals
Neonatal foal with acute to peracute lethargy, anorexia, colic, diarrhea (with blood)
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Neonatal foal with acute to peracute lethargy, anorexia, colic, diarrhea (with blood) likely is caused by
Intestinal Clostridiosis
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diarrhea that occurs between age 5 and 14 days and diarrhea is usually mild, transient, and requires no treatment
frequently coincides with the mare's post-foaling estrus, hormonal or constitutional changes in milk composition but the cause is unknown
Foal heat diarrhea
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condition where an animal ingests its own feces
Coprophagy
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the most common parasitic infection in young foals
Strongloides westeri
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How is strongloides westeri transmitted to foals?
transmammary
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What are your top 2 differentials for a foal that presents with hemorrhagic diarrhea
1) Intestinal clostridiosis
2) Salmonella
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With intestinal clostridiosis, what do the potent exotoxins result in
Gi wall necrosis
sepsis
death
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How do you diagnose Intestinal Clostridiosis in foals
1) Clinical signs (think hemorrhagic diarrhea)
2) Demonstration of bacterium
3) Presence of exotoxins *
-Culture (anerobic)
-PCR on toxins
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How do you treat intestinal clostidiosis in foals
1) Antibiotics (Metronidazole)
2) Anti-inflammatory agents
3) Biotype C antitoxin
4) Bio-Sponge to bind clostridial toxins in luimen of tract
5) Supportive care
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What antibiotic is used to treat intestinal clostidiosis in foals
Metronidazole
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How do you prevent intestinal clostidiosis in foals
foal out in pasture
separate cows from horses
wash udder prior to foal nursing
vaccinate mares
reduce grain feeding
administer antitoxin
prophylactic use of antibiotics and Biosponge
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What does Bio-Sponge do
binds clostridial toxins in the lumen of the intestinal tract
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What is the pathogenesis of Rotavirus in foals
1) Destroy epithelial cells at tips of villi in small intestine
2) Decrease absorptive surface area
3) Malabsorptive diarrhea because cells normally produce lactose
4) Secretory diarrhea
maldigestion, malabsorption, and osmotic forces _ secretory viral protein
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What are the clinical signs of Rotavirus in foals
1) Profuse watery diarrhea that can sometimes scald the skin
2) Weight loss
3) Stunted growth
4) Anorexia
foals less than 2 months of age
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How does rotavirus cause diarrhea
1) Maldigestion
2) Malabsorption
3) Osmotic forces and secretory viral protein
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How do you diagnose Rotavirus in foals
Electron microscopy and PCR to rule out other causes
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How do you treat rotavirus in foals
supportive care (lactase?)
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T/F: E coli is pathogenic in foals
False - it has not been found to be
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How do you prevent rotavirus in foals
reduce crowding
vaccination
hygiene
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Is mortality in foals higher with C perfringens type A or type C
Type C
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Gastric ulcers occur in ______% of sick foals <90 days of age
50%
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Where do gastric ulcers typically occur in foals
in the glandular region of the stomach
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What are the clinical signs of gastric ulcers in foals
1-4 months: bruxism, excessive salivation, colic, diarrhea
Neonatal foals: gastric perforation, pyloric obstruction
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What is controversial in the treatment of equine neonates with gastric ulcers
Proton pump inhibitors
1) Stomach acid provides barrier function
2) Gastric acid assists digestion of milk
3) Glandular ulcer formation most likely not a function of increased HCl production
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Why are proton pump inhibitors controversial in the treatment of equine neonates with gastric ulcers
1) Stomach acid provides barrier function
2) Gastric acid assists digestion of milk
3) Glandular ulcer formation most likely not a function of increased HCl production
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How do you treat gastric ulceration in foals
histamine Ha2 receptor antagonists (ranitidine, cimetidine)
mucosal protectants (sucralfate, bismuth) and anticacids
treatment of perforated ulcers is unsuccessful
use of proton pump inhibitors is controversial
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What is the prognosis of gastric ulceration in foals
depends on stage and location
not good if perforated
might affect duodendal scarring and bile duct obstruction
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what species has a high prevalence of neonatal isoerythrolysis
mules
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concurrent finding of icterus and moderate to severe anemia in a neonatal foal is suggestive of
NI
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Prior to surgical intervention, what should be done in foals with uroperitoneum
electrolyte, fluid and acid/base disturbances should be corrected
