Equine Anemia: Piroplasmosis Flashcards

1
Q

what is equine piroplasmosis

A

tick borne hemoprotozoan parasite

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2
Q

how is equine piroplasmosis transmitted from the vector

A

tick salivary glands

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3
Q

what infections can equine piroplasmosis cause

A
  1. Theileria equi
  2. Babesia caballi
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4
Q

how is Theileria equi transmitted

A

intrastadial and transtadial transmission

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5
Q

when do the clinical signs of Theileria equi

A

12-19 d after infection

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6
Q

how is Babesia caballi transmitted

A

intrastadial

transtadial

transovarian

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7
Q

when do the clinical signs of Babesia caballi appear

A

10-30 d after infection

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8
Q

what is the life cycle of piroplasmosis

A
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9
Q

what act as vectors in piroplasmosis

A
  • Dermacentor*
  • Rhipicephalus*
  • Hyalomma*
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10
Q

what is the pathogenesis of piroplasmosis

A
  1. release of merozoits cause hemolysis
  2. decreased survival of non infected red cells
  3. microthrombi and vasculitis
  4. thrombocytopenia
  5. SIRS and progression to multiorgan system dysfunction
  6. transplacental transmission in T. equi
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11
Q

what can cause decreased survival of non infected red cells

A
  1. hemoglobinemia may cause nephrosis
  2. hypoxemia
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12
Q

what is the risk to the UK

A

free movement of horses between UK, France and ROI without border inspection

no specific guidelines on tick treatment

no requirement to test horses moving within EU

tick species capable of transmission present in UK

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13
Q

what are the clinical signs for acute piroplasmosis

A
  1. pyrexia, lethargy and hemolysis (PCV to 10%)
  2. systemic signs depends on level of hemolysis: tachycardia, tachypnea, weakness
  3. petechiations & marked thrombocytopenia
  4. recurrent episodes of anemia
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14
Q

what can occur to the kidneys in piroplasmosis

A

acute renal failure –> tubular nephrosis from hemoglobinuria, hypotension and systemic inflammation

pigmented urine (hemoglobin and bilirubin)

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15
Q

what type if piroplasmosis is severe anemic syndrome more common with

A

T. equi

peracute hemolysis

death

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16
Q

what are the less common clinical signs

A
  1. colic
  2. pneumonia
  3. cardiac dysrhythmias
  4. laminitis
  5. infertility
  6. CNS signs
17
Q

which piroplasmosis causes neonatal infection

A

T. equi

18
Q

what can the neonatal infection cause

A

abortion or neonatal piroplasmosis

severe hemolysis & icterus at birth or progressive signs from 2-3 days

19
Q

what are the clinical signs of neonatal infection

A
  1. icterus, fever and anemia
  2. loss of suck
  3. progressive lethargy, weight loss
  4. development of adult signs
20
Q

what are the differentials for non infectious causes of clinical signs

A
  1. immune mediated hemolytic anemia
  2. IM thrombocytopenia (idiopathic, drug related, neoplastic)
  3. purpura hemorrhagica
  4. maple leaf toxicity
  5. neonatal isoerythrolysis
21
Q

what are the differentials for infectious causes of clinical signs

A
  1. equine infectious anemia
  2. equine viral arteritis
  3. trypanosomosis (surra)
  4. equine ehrlichoisis
  5. african horse sickness virus
22
Q

what are the clinical signs of the chronic disease presention

A

commonest presentation

no clinical signs of disease

pregnancy may result in abortion or neonatal infeciton

acute hemolysis at times of concurrent disease

  1. lethargy, poor performance
  2. decreased appetite, weight loss
  3. mild anemia may present
23
Q

how is piroplasmosis diagnosed

A
  1. complement fixation test
  2. indirect immunofluorscent antibody test
  3. competitive ELISAs for T. equi & B. caballi
  4. nested PCR
24
Q

what is the treatment

A

imidocarb dipropionate

carbamate –> causes reversible cholinesterase inhibition

25
Q

how do administer imidocarb dipropionate

A

admin may cause colic and diarrhea

injection site necrosis –> deep IM

26
Q

what is the treatment protocol for acute piroplasmosis

A

imidocarb 2.4 mg/kg

preceded by glycopyrrolate 0.0025 mg/kg IV or hyoscine 0.14 mg/kg IV

  1. blood transfusion may be required prior to imidocarb
  2. fluid therapy to reverse acidosis and improve perfusion
  3. increased drug toxicity with metabolic compromise
27
Q

is eradication possible

A

more likely with B. caballi

persistence of EMA-1 and EMA-2 specific antibodies

28
Q

what are the import/export risks

A

OIE recommends ELISA and IFAT for pre import investigation of horses from endemic countries

positive horses moving for international competition (tick clearance and designated grazing)

risk to UK more likely due to tripartite agreement

legal and illegal trade

29
Q

what is the current UK protocol

A

limited for piroplasmosis

pre-import testing within EU not required

only performed prior to re-exportation

ticks found on imported horses –> send for tick recording

30
Q

in what ways could the UK control piroplasmosis

A
  1. acaricidal treatment to all horses prior to UK import
  2. vet inspection post import (follow up tick treatment)
  3. consider ELISA or nested PCR as screening tests for horses remaining resident
  4. isolation of seropositive horses
  5. screening of cograzing horses with seropositive confirmed
  6. continuation of tick capture with PCR tests
31
Q

should piroplasmosis be considered as a ddx for horses with hemolysis and pyrexia

A

yes

cytological exam as first screening test