Equine Hematological and Lymphoreticular Flashcards
In horses, what can have a dramatic effect on the packed cell volume during exercise, excitement, and hemorrhage
splenic contraction
Why do you need to mix a blood sample before measuring PCV in horses
because horse’s RBCs have a rapid sedimentation rate
If horses have regenerative anemia, what dont you see
Reticulocytes
oxidized precipitated hemoglobin in the RBC and indicates oxidative damage to the RBC, which typically results in intravascular or extravascular hemolysis
Heinz bodies
What explains the rapid sedimentation rate of equine RBCs
strong tendency to rouleau formation
-need to mix samples
-need to differentiate from autoagglutination
How do you differentiate rouleau from autoagglutination
dilution of the RBC suspension with isotonic saline
saline disperses rouleau formation but not autoagglutination
What is the normal color of equine plasma/serum
yellow
dont jump to icterus just yet
nuclear remnants
that is normal finding in horses in RBCs
Howell-Jolly bodies
T/F: Heinz bodies are normal findings in horses
False - oxidized hemoglobin
T/FL Howell-Jolly bodies are normal findings in horses
True- a small number is normal
a test that detects immunoglobulin or complement on the surface of circulating RBCs
Coomb’s test
Splenic contraction can increase the horse’s PCV as much as
50%
What is the difference between the direct and indirect coomb’s test
Direct: immunoglobulin or complement on the surface of circulating RBCs
Indirect: detects presence of circulating anti-RBCs antibodies in the serum
abnormality in concentrations of individual serum protein fractions
dysproteinemia
What is used to evaluate and quantitate the individual protein fractions
Serum protein electrophoresis
albumin, and different globulin peaks
Where is bone marrow often collected in horses
sternum
tuber coxae
proximal ribs
sternal aspirates are preferable
reduction of the oxygen-carrying capacity of the blood below reference values
a symptom NOT a disease
anemia
a monoclonal gammapathy in horses is almost a slam dunk for
lymphoma
polyclonal gammopathy is indicative of
inflammatory processes
What are the clinical signs of anemia in horses
1) Tachycardia
2) Tachypnea
3) Reduced exercise tolerance
4) Lethargy
5) Pale mucous membranes (icterus)
the PCV level at which the signs are observed depend on
1) Rate of development
2) Severity of anemia
3) Physical demand
Regenerative anemias, the cause is typically
1) Blood loss
2) Increased RBC destruction
Non-regenerative anemias, the cause is typically
Inadequate RBC production
ex:
-Iron deficiency: chronic hemorrhage or nutritional deficiency
-Bone marrow failure: myelophthisis or radiation,
-Chronic renal disease
-Chronic hepatic disease
What are the mst common causes of consumptive, regenerative thrombocytopenia in horses
1) Endotoxemia (
2) Coagulopathy, DIC
3) Vasculitis
-Strangles
-Pigeon fever
-Equine Viral Arteritis
-Snakebite
-Drugs
4) Immune-mediated
What commonly causes vasculitis in horses
-Strangles
-Purpura hemorrhagica
-Pigeon fever
-Equine Viral Arteritis
-Snakebite
-Drugs
What are the 3 broad causes of thrombocytopenia
1) Decreased production
2) Increased Destruction
3) Increased Consumption
What are the clinical signs of vasculitis in horses
Limb / ventral/ sheath / mammary gland edema
serum oozing and hemorrhage
fever
petechiae
What is the most common known cause of vasculitis in the horse
Purpura hemorrhagica
-aspectic necrotizing vasculitis most likely due to immune complex deposition in blood vessel walls
What causes purpura hemorrhagica in the horse
-aspectic necrotizing vasculitis most likely due to immune complex deposition in blood vessel walls against Strangles (M protein) and Pigeon Fever
What are the clinical signs of purpura hemorrhagica
Edema
Petechial bleeding
Ecchymotic bleeding
What might predispose a horse to purpura hemorrhagica
pre-existing high serum antibodies
prior to vaccination in older horse or one with a known exposure to strangles, might want to run antibody titer levels
What might you wanna do for a old horse or one that has had a previous strangles exposure prior to vaccinating them for strangles
Run antibody titer
if high levels, could cause purpura hemorrhagica
horses with levels > 1:3200 are hyperresponders and considered to be at risk
Equine Viral Arteritis replicates in the
endothelial cells
can persist in the gonads of males for further spread
What are the clinical signs of Equine Viral Arteritis
causes vasculitis
-ventral edema
-lower limb edema
-scrotal and mammary gland edema
-urticaria
-conjunctivitis
-abortion and neonatal foal death
What might cause blood loss anemia in horse
1) External hemorrhage
-Laceration/trauma
-Guttural pouch mycosis
-Post castration
2) Internal hemorrhage
-Uterine artery rupture
-ˇTrauma
-Coagulopathy
3) Visceral hemorrhage
-GI tract
-Urinary tract
-Reproductive tract
Is Equine Viral Arteritis reportable
Yes
How do you treat blood loss anemia
1) Stop bleeding- identify site of blood loss, hemostasis, stabilize clots (aminocaproic acid)
2) Judicious use of IV fluids- correct hypovolemia but not to exacerbate blood loss
3) Blood transfusion if severe blood loss
With acute severe blood loss patient will be hypovolemic but will likely not be anemic
What can be used to stabilize clots to stop bleeding in horses
Aminocaproic acid is a medication that blocks the breakdown of clots (fibrinolysis), thereby allowing clots to form and remain.
In acute severe blood loss, why is the horse hypovolemic but likely not anemic
splenic contraction
a tissue plasminogen activator (tPA) inhibitor that blocks the breakdown of clots (fibrinolysis)
Aminocaproic acid
T/F: there are no transfusion tirggers established in the horse
True
What might indicate you to give a horse a blood transfusion
1) Clinical: tachypnea, tachycardia, weakness, cool extremities, pale membranes, weak pulses
2) Laboratory data: PCV <12%, 30-40% volume lost,
Hg <8g/dL, uncontrolled bleeding, persistent hypotension
3) Additional diagnostics: central venous pressure
Blood lactate
Blood pH
no transfusion triggers established in the horse - use all of these parameter
What are some considerations when giving a horse a blood transfusion
1) Transfused RBCs: will not result in return of PCV to a normal level, will only be in circulation for a few day
2) Possible long term effects
-Development of alloantibodies (esp brood mare)
-Increases risk for future transfusion reactions when doing 2nd time (do them close together)
-Risk of NI in foals of transfused mares
3) Potential infectious risks
-EIA
-Theilers
-WNV
What are the infectious risks when giving horses blood transfusions
-EIA
-Theilers
-WNV
T/F: heritable coagulopathies in horses are extremely rare
True
What might cause coagulopathies in horses
1) Decreased production of coag factors - liver failure
2) Consumptive coagulopathies with
-Endotoxemia
-Poisoning (coumarin derivatives in rodenticides or sweet clover)
Ingestion of what 2 things can cause coagulopathies in horses
1) Coumarin derivatives in rodenticides
2) Sweet clover
Endotoxemia results in what in horses
consumptive coagulopathies
In horses, how might IMHA occur
1) Neonatal isoerythrolysis
2) Blood transfusions
3) Infectious agents (piroplasma)
4) Drug induced- Penicillin, TMS
5) Lymphoma
In horses, what drugs could potentially cause IMHA
Penicillin
TMS
Hemolytic anemia is mostly due to
increased rate of extravascular destruction
no hemoglobinemia or hemoglobinuria is seen
T/F: in horses, intravascular hemolysis can occur but it is rare
True
What do you not see with extravascular hemolytic anemia
No hemoglobinemia
No hemoglobinuria
What will the plasma serum look like with IV hemolysis
red
What will the plasma serum look like with equine rhabdomyolysis
clear to yellow
myoglobin is very clear
What will the plasma serum look like with equine hematuria
clear to yellow
What does the urine of IV hemolysis in horses look like
red
What does. the urine of IV hemolysis in horses look like
red to brown
What does the urine look like with hematuria
clear to yellow but once you let it sit will see sedimental of RBC
What one the textbook cause of truly intravascular hemolysis in the horse
Red maple leaf toxicity
also >10% DMSO administration
Giving >10% DMSO administration in horses can cause
intravascular hemolysis - associated with hemoglobinemia and uria
What might cause intravascular hemolysis in the horse
1) Red maple leaf toxicosis
2) >10% DMSO administration
3) Hypotonic fluid admin
4) Acute hemolytic transfusion reaction
5) Severe cases of neonatal isoerythrolysis
What anemia does red maple leaf toxicity cause
Heinz-Body Anemia
What causes piroplasmosis
tickborne, iatrogenic
-Babesia caballi
-Theileria equi
Where is piroplasmosis located
Latin America
Carribean
Southern USA (TX, NM, CO, FL)
Southern Europe
Balkan
Middle East
Russia
What are the clinical signs of Piroplasmosis in horses
1) Fever
2) Anemia
looks similar to vasculitis
How do you diagnose Piroplasmosis in horses
1) Cytology (low sensitivity when looking at bloodsmears, might increase with steroids)
2) Competitive ELISA
3) PCR analysis
Is piroplasmosis infection more severe with Babesia caballi or Thelieria equi
Theileria equi
How does piroplasmosis cause erythrocyte lysis in horses
1) Rupture of RBCs during release of parasite (intravascular hemolysis)
2) Removal of infected RBCs from circulation (extravascular hemolysis)
What causes swamp fever
Equine Infectious Anemia virus (retroviridae)
How do you treat Piroplasmosis
1) Imidocarb diproprionate IM
2) Tetracyclines IV
Curative with B. caballi
more dofficult to cure if infected with T. equi
Do palliative care with T. equi
When treating piroplasmosis with Imiocarb diproprionate or tetracyclines , is there a better chance of curing with B. caballi or Theileria equi
Babesi caballi - more easy to cure and less severe form of piroplasmosis
Imiocarb diproprionate should only be administered
IM injections
injection site reactions are not uncommon
look for sweating, agitation, colic, and diarrhea
Equine Infectious Anemia is most commonly transmitted by
1) insect vectors
2) re-use of needles
3) test blood/plasma donors for EIA
What is a hotzone for Equine Infectious Anemia
Where the vector is most prevalent- typically south and midwest but ir is located in other states, including CO
Equine Infectious Anemia is a retrovirus meaning that
once a horse has it, they have it for life
need to take regulatory measures
T/F: mosquitos are effective vectors for Equine Infectious Anemia
false- despite the fact that they transmit blood
the biting flies are better vectors
Why are tabanids effective vectors for Equine Infectious Anemia
because their painful bite, frequently inter-rupted, sever small vessels and contaminate mouthparts with blood
incontrast, mosoquitos dont bite for as long on multiple horses
What horses are much more likely to transmit EIAV
Horses with high titered viremia and clinical disease are much more likely to transmit EIAV than are inapparent carriers with very low levels of viremia
What are the clinical signs of acute Equine Infectious Anemia
1) Fever
2) Thrmobocytopenia (immune mediated?)
3) Lethargy
4) Inappetance
5) Anemia
after initial episode, majority of infected horses experience recurrent episodes of acute clinical disease, lasting 3-5 days
What are the clinical signs of chronic Equine Infectious Anemia “swampers”
Anemia
Thrombocytopenia
Weight loss
Dependent edema
Splenomegaly
Lymphadenopathy
Neurological signs
Icterus
How do you diagnose Equine Infectious Anemia
Serological testing- since the virus is not cleared by the host then the serolgical test indicates infections
-Agar gel immunodiffusion (AGID) = Coggins Tests
-ELISA (positives must be confirmed with AGID test)
all look for antibodies
What is the serological test approved by USDA by Equine Infectious Anemia
Agar gel immunodiffusion (AGID) = Coggins Tests
What is the most common reason a vet would draw blood on a horse is to
test for EIA to do a Agar gel immunodiffusion (AGID) = Coggins Tests
Why might you do a Coggins test
many states require negative test result prior to transport into the state
may be required by show or event
may be required i some state if change of ownershup
may be part of pre-purchase or insurance examination
How do you control for Equine Infectious Anemia
1) No vaccine
2) reportable in US
3) Control through detection of carriers
4) Removal from the populations
-euthanasia, slaughter, or quarantine
How do you treat EIA
there is no specific therapy available for EIAV infection
humane euthanasia is the most common
horse can be quarantined for lifelong
In horses, thrombocytopenia is most commonly due to a
regenerative, consumptive process (e.g sepsis, vasculitis, etc)
in horses, hemolytic anemia is most commonly _______and is more often
most commonly immune mediated and more often extravascular
What are the most common causes of nonregenerative anemia in horses
1) Nutritional deficiency (#3)
2) Chronic inflammatory disease (#1) (bastard strangles, pigeon fever, rhodococcus equi)
3) Secondary to organ dysfunction (#2)
4) Bone marrow damage or dysplasia- drugs, cancer, etc (#4)
What chronic inflammatory disease cause nonregenerative anemia in horses
Strangles (Bastard)
Pigeon Fever (C. pseudotuberculosis)
Rhodococcus equi (foals)
etc
What causes pigeon fever in horses
C. pseudotuberculosis
How might chronic inflammatory disease (strangles, pigeon, rhodococcus) cause non-regenerative anemia
1) Impaired flow of iron from storage
2) Decreased erythrocyte life-span
3) Inadequate bone marrow response
-macrophages sequester iron with a purpose
How do we differentiate anemia of chronic inflammation from true iron deficiency anemia?
1) CBC - might see inflammation
2) Protein and Electrophoresis
-see increase globulin (inflammatory)
3) Iron and Storage
decreased serum iron
decreased transferrin saturation
Iron binding capacity
Iron binding capacity will be increased in _________ while decreased in _______
Increased: iron deficiency
Decreased: chronic inflammation
With chronic inflammation, the iron binding capacity is
decreased
With iron deficiency, the iron binding capacity is
increased
What might cause nonregenerative anemia secondary to organ dysfunction in horses
1) Reduction of production or absorption of elements essential for erythropoiesis
2) Decreased clearance of toxins
3) Interference with production or action of erythropoietin
ex: liver or kidney disease
