Hemolymphatic System, Pt. 2 Flashcards by Renee DeAngelis

What 3 conditions are associated with neonatal isoerythrocytosis? What does this result in?

foals inherit RBC type (Ag) from sire
Aa- or Qa- mares become sensitized to Ag and produce antibodies due to exposure from previous pregnancies, blood transfusions, or transplacental contamination
colostrum with antigens are ingested and absorbed by the foal

destruction of foal RBCs by maternal Ab

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In what horses is there a higher incidence of neonatal isoerythrocytosis? What blood groups are strongly antigenic?

10% in mules (1% in TB, 2% in STB)

Aa
Qa
donkey factor
occasionally Ua, Pa, Qc, and Db

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What can possibly prevent neonatal isoerythrocytosis?

Ca —> antibody-mediated immunosuppression

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When does neonatal isoerythrocytosis occur? What clinical signs are seen?

foal is born healthy but develops signs 24-36 hours (or several days if mild)

progressive lethargy and weakness
pale to yellow MM
tachycardia, tachypnea
discolored urine
seizure, death

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What 2 laboratory results are seen in foals with neonatal isoerythrocytosis?

hemolytic anemia: decreased PCV, RBC, and Hb
increased bilirubin, hemoglobinemia, hemoglobinuria

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How can immune reactions be confirmed in cases of neonatal isoerythrocytosis?

INDIRECT COOMBS: test mare serum or colostrum for antibodies
DIRECT COOMBS: presence of antibodies attached to foal RBC

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What test is done on foals to confirm neonatal erythrocytosis?

jaundice foal agglutination test —> foal RBC exposed to mare colostrum or serum, detecting agglutination and NOT hemolysis

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What treatment is recommended in foals within or after 24 hours of developing neonatal isoerythrocytosis?

< 24 hours = withhold milk (muzzle, strip mare) and offer alternative sources

> 24 hours = decrease stress, give fluids and antibodies, and offer a blood transfusion of washed mare RBCs or compatible donors

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What 4 complications are associated with neonatal isoerythrocytosis treatment with blood transfusions?

hyperbilirubinemia - kernicterus (exchange transfusions)
iron toxicity
sepsis
liver failure

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In what 3 ways can neonatal isoerythrocytosis be prevented in the mare?

identify risk —> Aa, Qa, previous NI foal

screen serum 2 weeks before the due date and repeat every 2 weeks
check colostrum for reactivity
Domperidone before foaling

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In what 2 ways can neonatal isoerythrocytosis be prevented in the foal?

provide alternative sources of colostrum

withhold milk with a muzzle or strip the mare
provide frozen colostrum for NI- mare or milk from goats, NI- mare, or Mares Match

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How is the jaundiced foal agglutination test performed?

collect colostrum from mare
collect EDTA tube from foal before nursing
set up 6 tubes and add 1 mL of saline and perform serial dilutions
add 1 drop of foal blood to each tubes and mix
centrifuge tubes for 2-3 mins
invert each tube and pour liquid out to observe clumping
if positive at 1:8 dilution, don’t let foal nurse

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Neonatal isoerythrocytosis:

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What are the main colostrum and foal causes of failure of passive transfer of maternal antibodies? What risk is associated?

COLOSTRUM - none produced, poor quality or quantity

FOAL - cannot get up, suckle, or absorb

sepsis!

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How is failure of passive transfer diagnosed?

SNAP foal IgG test using foal’s blood

< 400 mg/dL IgG = complete failure (spot lighter than both references
400-800 mg/gL IgG = partial failure (intermediate spot color)
> 800 mg/dL IgG = proper nursing (spot darker than both references)

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How is failure of passive transfer prevented?

early recognition is key - often too late by time of diagnosis

educate owner/manager: monitor foal, assist with colostrum administration, clean environment
evaluate pre-suckle colostrum, should be sticky, yellow, and thick and > 1.060 SG

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At less than 12 hours post-partum, what treatment is recommended for foals with failure of passive transfer?

1-2 L of good-quality equine colostrum from a bank of healthy, blood typed, and vaccinated mares (200-250 mL can be collected)

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At over 12 hours post-partum, what treatment is recommended for foals with failure of passive transfer?

at this point colostrum cannot be absorbed, commercial plasma that is from vaccinated mares with known IgG concentrations and negative for Aa and Qa alloantigens

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What should be done if there is no blood typing available for foals treated with plasma in failure of passive transfer?

can use plasma from untransfused geldings that are fully vaccinated and negative for Aa and Qa

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What adverse reactions are associated with plasma transfusions in foals with failure of passive transfer?

muscle fasciculations
increased HR, RR, and T
distress
abdominal pain
pale MM
collapse

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What is the most common hematopoietic neoplasm in the horse? What are 5 forms?

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lymphoma/lymphosarcoma —> > 4-10 yrs

cutaneous
alimentary
mediastinal
multi-centric or generalized
leukemia (rare)

What are the most common clinical signs of lymphoma?

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non-specific signs depend on body system affected, extent, and duration (often diagnosed when advanced)

weight loss, anorexia
depression
edema
recurrent fever
lymphadenopathy

What is multicentric lymphoma? What changes clinical signs?

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most common and widespread lymphoma associated with lymph nodes and multiple organs

correspond to organs involved

In what horses is alimentary lymphoma most common? What organ is most affected? What clinical signs are associated?

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older horses

SI > LI

colic
diarrhea
malabsorption

What is the most common neoplasm of the thorax? What clinical signs are associated?

mediastinal lymphoma - respiratory distress - coughing - distended jugular vein - muffled heart sounds - pleural effusion

What form of lymphoma carriers the best prognosis? What clinical signs are associated?

cutaneous - surgical removal easier - multifocal SQ nodules - yellow exudate from nodules - ulcerations

Lymphoma:

What is seen on blood work is horses with lymphoma?

- anemia, erythrocytosis - leukocytosis and altered morphology - hyperfibrinogenemia - hypoalbuminemia - hyperglobulinemia

What 4 treatments are most common for lymphoma?

1. excision of solitary masses 2. radiation 3. glucocorticoids* 4. chemotherapy (expensive!)

What is the main reservoir for Corynebacterium pseudotuberculosis? What causes entry? How is it transmitted?

ground, feces, hay, shavings small scrapes or wound in skin or MM abrasions direct, indirect, insects

What causes Pigeon fever (dryland distemper, pseudotuberculosis)? What are the 2 most common biotypes?

Corynebacterium pseudotuberculosis - G+, pleomorphic, intracellular, facultative anaerobe found worldwide 1. HORSES: nitrate reduction positive 2. SMALL RUMINANTS: nitrate reduction negative (cattle can get both)

What are the 3 most common clinical signs of pigeon fever?

1. EXTERNAL ABSCESSATION - pectoral, abdomen, mammary glands, prepuce, limbs, head ---> edema, fever 2. INTERNAL INFECTION - liver, lungs, kidney, spleen ---> abscesses, fever, lethargy, inappetence, colic 3. ULCERATIVE LYMPHANGITIS - limb swelling, cellulitis, fever, lethargy, draining tracks, sores, severe lameness

What is used to diagnose pigeon fever? In what cases is synergistic hemolysis inhibition (SHI) helpful?

- blood work - ultrasound - culture internal infection and ulcerative lymphangitis

What 3 things are seen in blood work in patients with pigeon fever? How is it cultured?

1. anemia of chronic disease 2. leukocytosis with neutrophilia 3. hyperfibrinogenemia, hyperproteinemia (globulins) blood agar 24-48 hr on samples from abscesses

What serology is used to diagnose pigeon fever?

synergistic hemolysin inhibition - measures IgG against exotoxins, helpful for internal abscesses (NOT external)

How are external abscesses from pigeon fever treated? What is prognosis like?

- drainage allows faster resolution - lavage to prevent environmental contamination excellent

How is internal infection from pigeon fever treated? What is prognosis like?

- antimicrobials: rifampin and ceftiofur, doxycycline, enrofloxacin able to penetrate tissues - guided ultrasound and clinical pathology 30-40% mortalities, can be 100% without medication

How is ulcerative lymphangitis from pigeon fever treated?

- early aggressive antimicrobials: penicillin G or ceftiofur and rifampin - NSAIDs - physical therapy for lameness

How is pigeon fever prevented?

- reduce environmental contamination - fly control (sheets, spray, ointment) - feed-through products with insect growth regulators - manure management and sanitation - PPE, barriers, cleaning, disinfection - wound care and prevention

How should suspected abscesses from pigeon fever be approached?

culture and sensitivity ---> can also be Strangles or MRSA (re-assess practices)

What are 2 signs of primary hemostasis? Where should these be looked for?

1. excessive bleeding from mucosa or trauma sites 2. bruising, ecchymosis, petechia, hematomas mucosal surfaces and inner pinnae of ear

What are 2 signs of secondary hemostasis?

1. spontaneous bleeding 2. shock with severe blood loss (depends on organ system)

Why must primary hemostasis be carefully diagnosed? What is pseudothrombocytopenia?

venipuncture can cause excessive bleeding and must be collected directly into anticoagulant blood collected in EDTA or heparin tubes, which destroys platelets ---> use citrate or look at blood smear

How is primary hemostasis diagnosed on blood work?

- PLT count - PLT function testing ---> temporal bleeding time, flow cytometry - vWF

How is secondary hemostasis diagnosed?

clotting times > 120% above range - PT = extrinsic, common - APTT = intrinsic, common - ACT = intrinsic, common - TCT = fibrinogen to fibrin

What is disseminated intravascular coagulation?

acquired hypercoagulable state (NEVER PRIMARY) resulting from widespread fibrin deposition in microvasculature and activated coagulation or depression of anticoagulation

What are 5 causes of DIC?

1. sepsis (endotoxemia) 2. acute GI disease 3. renal disease 4. neoplasia 5. hemolysis

What clinical signs are seen in DIC?

- petechiae, ecchymosis, prolonged bleeding - thrombosis (thrombophlebitis) - ischemic organ damage - hemorrhage by the time signs are seen, death is close

What is seen on lab results in cases of DIC (FYI)?

PROCOAGULANTS - low platelets, increased clotting times, decreased fibrinogen ANTI-COAGULANTS - decreased antithrombin FIBRINOLYSIS - increased FDP, D-dimer

How is DIC treated?

- treat underlying disease - support: treat shock, decreased perfusion, and acid-base/electrolyte abnormalities - NSAIDs - antimicrobials - fresh platelet-rich plasma - LMWH, aspirin, pentoxifylline

Can thrombocytopenia be due to a laboratory error?

YES ---> make sure citrate tubes are used (NOT EDTA or heparin)

Hemolymphatic System, Pt. 2 Flashcards

(51 cards)