Hemolymphatic System, Pt. 2 Flashcards
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
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
What can possibly prevent neonatal isoerythrocytosis?
Ca —> antibody-mediated immunosuppression
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
What 2 laboratory results are seen in foals with neonatal isoerythrocytosis?
- hemolytic anemia: decreased PCV, RBC, and Hb
- increased bilirubin, hemoglobinemia, hemoglobinuria
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
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
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
What 4 complications are associated with neonatal isoerythrocytosis treatment with blood transfusions?
- hyperbilirubinemia - kernicterus (exchange transfusions)
- iron toxicity
- sepsis
- liver failure
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
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
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
Neonatal isoerythrocytosis:
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!
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)
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
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)
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
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
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
What is the most common hematopoietic neoplasm in the horse? What are 5 forms?
lymphoma/lymphosarcoma —> > 4-10 yrs
- cutaneous
- alimentary
- mediastinal
- multi-centric or generalized
- leukemia (rare)
What are the most common clinical signs of lymphoma?
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?
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?
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?
- excision of solitary masses
- radiation
- glucocorticoids*
- 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
- HORSES: nitrate reduction positive
- SMALL RUMINANTS: nitrate reduction negative
(cattle can get both)
What are the 3 most common clinical signs of pigeon fever?
- EXTERNAL ABSCESSATION - pectoral, abdomen, mammary glands, prepuce, limbs, head —> edema, fever
- INTERNAL INFECTION - liver, lungs, kidney, spleen —> abscesses, fever, lethargy, inappetence, colic
- 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?
- anemia of chronic disease
- leukocytosis with neutrophilia
- 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?
- excessive bleeding from mucosa or trauma sites
- bruising, ecchymosis, petechia, hematomas
mucosal surfaces and inner pinnae of ear
What are 2 signs of secondary hemostasis?
- spontaneous bleeding
- 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?
- sepsis (endotoxemia)
- acute GI disease
- renal disease
- neoplasia
- 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)
