Equine Temperate Diseases Flashcards

1
Q

is equine viral arteritis notifiable

A

yes

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2
Q

what is equine viral arteritis associated with

A

resp disease

abortion

perinatal mortality

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3
Q

what is equine viral arteritis characterized by

A

panvasculitits

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4
Q

what is the main source of equine viral arteritis

A

semen

resp secretions

fetus/placenta/amniotic fluid

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5
Q

what is the incubation period of equine viral arteritis

A

3-14d

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6
Q

what are the do the severity of clinical signs of EVA depend on

A

EVA isolate

Immune status

Age

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7
Q

what are the principle syndromes of EVA

A

Respiratory disease (‘mild influenza’)

Pyrexia and mild nasal discharge

Conjunctivitis (‘pink eye’), rhinitis

Limb/scrotal/mammary/ventral/peri-orbital edema

Abortion in up to 50% infected mares

Neonatal mortality (respiratory distress)

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8
Q

what are the reservoir for infections in EVA and how

A

carrier stallions

continuous viral replication in epithelium of accessory sex gland

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9
Q

how is EVA transmitted to mares via carrier stallions

A

Natural breeding

AI (virus survives freezing)

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10
Q

does EVA effect fertility of mares and stallions

A

no long term effects

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11
Q

how is EVA diagnosed

A

Clinical signs

History

Seroconversion

Virus isolation/detection

Detection of carrier stallions:

  • Serology
  • Virus detection/isolation
  • Test breeding seronegative mares

Hard evaluation co-ordinated by APHA

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12
Q

how is EVA prevented and controlled

A

Establish disease status of breeding stock

  • Serology of all horses prior to breeding use
  • Virus detection/isolation

Breed to seronegative stallions

Vaccination

  • Stallions and teasers
  • Record in passport

Test prior to import/export

Isolate new arrivals (21 days)

Under EU law importation of shedder stallions or semen is NOT permitted

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13
Q

what is equine infectious anemia (EIA) also known as

A

swamp fever

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14
Q

what is the agent that causes equine infectious anemia

A

lentivirus (Retrovirus)

integrates genetic material into the host genome which allows viral replication and persistence for lfie

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15
Q

how do animals become asymptomatic carriers of EIAV

A

viral replication associated with viral mutations

heterogenous population and antigenic variation

aids immune avoidance and persistence

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16
Q

is EIAV notifiable

A

yes

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17
Q

how is EIAV transmitted

A

Biting flies (mechanical vector)

Iatrogenic

Transplacental

Colostral, venereal

Needles, stomach tubes, etc (veterinarians)

Frozen plasma

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18
Q

when is the highest risk for EIAV

A

when infected blood is from horse/donkey/mule with acute clinical disease

Greatest risk when vector density high

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19
Q

can subclinical EIAV carriers spread it

A

no unlikely

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20
Q

what are the acute clinical signs of EIAV

A

Pyrexia

Petechiation

Limb adema

Inappetance

Hemolysis and severe anemia

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21
Q

what is chronic presentation of EIAV

A

Cyclical lethargy

Weight loss

Anemia

Chronic debilitating disease

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22
Q

what is the incubation period of EIAV

A

1-3 weeks to months (14-42d)

23
Q

are EIAV chronic carriers asymptomatic or symptomatic

A

relatively symptom free

24
Q

how does EIAV cause hemolysis

A

Immune mediated and non-immune mediated

  • Not always present, but seen in debilitated
25
Q

what is the evidence of hemolysis in EIAV

A

icterus and high bilirubin

positive coombs results

26
Q

what is the clinicopathology of EIAV

A

hemolysis

concurrent thrombocytopenia

lymphocytosis, monocytosis

27
Q

how is EIAV diagnosed

A

Serological tests:

  • Most horses seroconvert within 45 days
  • Positive on Coggins test (AGID)
  • Incubation of up to 157d reported in Ireland outbreak

EIA ELISA more sensitive and rapid to complete

28
Q

what is the infectious agent of african horse sickness

A

orbivirus

9 serotypes

29
Q

is african horse sickness notifiable

A

yes

OIE list A

30
Q

where is african horse sickness endemic

A

sub-saharan africa

31
Q

what is the vector of african horse sickness

A

culicoides

32
Q

what is the pathogenesis of african horse sickness

A

infection –> regional lymph nodes –> primary viremia –> target organs –> secondary viremia

causes microvascular endothelial cell injury

infection and activation of monocyte – macrophages (pulmonary intravascular macrophages)

capillary leakage, edema, hemorrhage, inflammation, DIC

33
Q

what are the clinical signs of african horse sickness in the incubation period

A

5-7d (2-10d)

fever

anorexia

edema

hemorrhage

sudden death

34
Q

what is the mortality of acute ‘dunkop’ pulmonary form of african horse sickness

A

>95%

35
Q

what is the mortality of the subacute ‘dikkop’ cardiac form

A

50%

36
Q

what does the dunkop pulmonary form of african horse sickness cause

A

peracute respiratory distress and death

pulmonary edema

37
Q

what does the cardiac form of african horse sickness (dikkop) cause

A

supraorbital edema and head swelling

38
Q

how is african horse sickness diagnosed

A

clinical signs/PM

virus isolation

serology

real time reverse transcription quantitative PCR (RT-PCR) (whole blood or tissue sample)

39
Q

what is the risk of AHSV to the UK

A

potential culicoides vector in UK and ROI

unlikely to become resident unless climate change

into through international horse movement or wind-borne spread of vector

40
Q

what would be the likely sequelae of a AHSV outbreak in the UK

A

Interaction of AHVLA with local bodies

  • EU notification with trade restrictions

Restricted to insect proof stabling at outbreak site

  • Vector control

Immediate slaughter of infected cases

20km control zone around outbreak

Surrounded by 100km protection zone

Testing programme and vector surveillance

New vaccine development may promote ring vaccination if multiple cases

41
Q

how is AHSV prevented

A

Prevent/minimize exposure to vector, using multiple techniques

Vaccination programme

Risk of reversion to wild type in use of attenuated vaccines, with infection of susceptible individuals; generic recombination

Recombinant modified Vaccinia Ankara virus expressing different viral proteins has been developed; may offer better prospect in non-endemic regions

42
Q

how could AHSV exposure to the vector be prevented/minimized

A

Stabling at peak times of midge activity

Vector proof stabling and traps at entrance to stables

Repellents, midge proof sheets

43
Q

what is the vaccination protocol of AHSV

A

Live attenuated polyvalent vaccine strains depends on multiple doses, such that animals may become immune to all strains only by age of 4 years

Monovalent vaccines used in disease outbreak situations when strain is isolated

44
Q

what is the agent that causes dourine

A

trypanosoma brucei equiperdum

45
Q

is dourine notifiable

A

yes

46
Q

how is dourine transmitted

A

venereal tranissmion

possible biting fly spread

47
Q

how is dourine diagnosed

A

complement fixation test (CFT) and immunofluorescence antibody test (IFAT)

48
Q

what are the clinical signs of dourine

A

swelling of urogenital tract

abortion

infertility

wasting

ataxia

49
Q

how is dourine treated and controlled

A

No effective treatment reported

Culling of infected animals in countries where this is notifiable

Infection makes breeding programmes very difficult in countries where there is no screening

No vaccine available

Cross-reaction of all lab rests between this trypanosome and those spread by tsetse fly and other biting flies

50
Q

what are the clinical signs of equine trypanosomoniasis

A

Weight loss

Inappetence

Pyrexia

Progressive anemia

Variable edema

Metabolic acidosis

Collapse

Peripheral parasitemia

Hindlimb UMN signs first (8/8)

  • Weakness, truncal sway
  • Low head carriage
  • Some with F/L proprioceptive lesions
  • Occasional urogenital swelling
  • Later stages changes in mentation
  • Progressive weakness, collapse
  • Inability to rise
51
Q

what causes the chronic progression of multifocal neurological signs in equine trypanosomoniasis

A

infiltration of blood-brain barrier with all subspecies of T brucei

52
Q

how is equine trypanosomoniasis treated

A

Isometamidium is treatment of choice

Low therapeutic index

Routine health screening for PCV/TSP and parasite burden required throughout the year

Prophylactic intervention

53
Q

how is equine trypanosomosis controlled

A

Minimize exposure to biting flies, including tsetse flies

Local repellents

54
Q

how is the UK equine industry protected from infectious diseases

A

Veterinary vigilance for unusual field clinical cases key

  • Prompt reporting and isolation
  • Dourine, EIA, EVA, WNV, AHSV

Particular care with imported horses, those travelling on 10day health certificate and those moving from within EU

Increased vigilance for incorrect/absent passports

Vaccination could be considered for WNV in at risk horses

Continuous updating and attention to disease outbreak status

Recognition that early detection and testing massively beneficial in reducing spread

Continued monitoring

  • Sentinel birds (WNV)
  • Resident Culicoides species (AHSV)
  • Endemic tick population (Piroplasmosis)