8.2.2: Equine infectious respiratory disease Flashcards

1
Q

What type of virus is Equine Influenza A and how is it transmitted?

A
  • Negative sense ssRNA virus with segmented genome
  • Transmission is via aerosol and fomites -> highly infectious including 1 mile downwind
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2
Q

Pathogenesis of Equine Influenza A

A
  • Infectious of respiratory epithelial cells of the upper respiratory tract
  • Destroys cilia
  • Virus is shed from nasopharynx
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3
Q

Clinical signs of Equine Influenza A infection

A
  • Fever
  • Cough
  • Nasal discharge: initially serous (viral), may become mucopurulent with secondary bacterial infection
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4
Q

Treatment of Equine Influenza A virus

A
  • Nursing care
  • NSAIDs
  • Antibiotics for secondary infection
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5
Q

Prevention of Equine Influenza A virus

A
  • Vaccines available
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6
Q

Diagnosis of Equine Influenza A virus

A

Nasal swab - hit the back of the nose with a flexible swab
* Virus is only there for a short period of time -> swab in-contact animals
* Detection of viral antigen (ELISA)
* Detection of RNA (RT-PCR)

Serum samples
* Detection of antibodies (serology)
* ELISA
* Haemagglutination inhibition (HI) - 4 fold increase in titre indicates seroconversion

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7
Q

What type of virus is Equine herpesvirus 1 and 4 and how is it transmitted?

A
  • Linear, double-stranded DNA genome
  • Transmitted via aerosol, contact with infected fomites, reactivation from latency
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8
Q

Pathogenesis of Equine herpesvirus 1 and 4

A
  • Infection of respiratory epithelial cells
  • Shed from nasopharynx
  • Multiple cell types affected inc WBCs (cell-associated viraemia) -> this leads to dissemination to sites of secondary replication. Can cause neuro disease in spinal cord or abortion in pregnant uterus.
  • Causes inflammation and thrombi in endothelial cells
  • Latency is established and there is reactivation during times of stress e.g. pregnancy
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9
Q

Clinical signs of Equine herpesvirus 1 and 4

A
  • Commonly: fever
  • Occasional mild cough, slight nasal discharge (less likely to cause cough and secondary bacterial infection that equine influenza)
  • Poor performance (age/ immunity dependent)
  • Occasionally: abortion/ sick neonatal foal
  • Occasionally: neurological disease (equine herpesvirus myeloencephalopathy, EHM)
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10
Q

Treatment of Equine herpesvirus 1 and 4

A
  • Rest in athletic animals
  • EHM: nursing care and NSAIDs
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11
Q

Prevention of Equine herpesvirus 1 and 4

A
  • Vaccines available
  • Hard to vaccinate against because of its ability to be latent
  • Need to develop a cell-mediated response to identify and kill off infected cells where it is hiding as well as just produce antibodies when it invades
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12
Q

Diagnosis of Equine herpesvirus 1 and 4

A
  • Nasal swab / placenta / foetus -> PCR for viral DNA
  • Blood samples: virus isolation in tissue culture (anti-coagulated blood; acute) or detection of antibodies by complement fixation test (serum)
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13
Q

What type of virus is Equine viral arteritis (EVA) and how is it transmitted?

A
  • Positive-sense ssRNA virus
  • Transmission is via respiratory, venereal and congenital routes, or by indirect means (fomites)
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14
Q

Pathogenesis of EVA

A
  • Invades upper and lower respiratory tract
  • Infected monocytes and T lymphocytes transport EVA to the regional LNs e.g. bronchial LNs
  • Here it undergoes a further cycle of replication before being released into the blood-stream (=cell-associated viraemia)
  • 10-70% of stallions may become persistentl infected; carrier stallions may shed the virus into their semen
  • Can cause abortion in mares (this may be due to high fever)
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15
Q

Clinical signs

A
  • Often asymptomatic
  • Fever
  • Nasal discharge
  • Loss of appetite
  • Respiratory distress
  • Skin rash
  • Muscle soreness
  • Conjunctivitis (common)
  • Depression
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16
Q

Is EVA circulating in the UK?

A
  • No but we do see occasional cases
  • ⚠️EVA is notifiable⚠️
  • It is notifiable in all stallions, and in mares that have been mated or inseminated within 14 days
17
Q

Diagnosis of EVA

A
  • Virus detection in body secretions, whole blood, tissues -> by virus isolation, RT-PCR, and in situ hybridisation
  • Identification of viral antigen in tissues
  • ELISA for viral-specific antibodies on serology; routine pre-breeding/ pre-sales
18
Q

Treatment and prevention of EVA

A
  • General supportive care during the acute phase of infection
  • No treatment to eliminate persistent infection in stallions
  • Inactivated virus is available but not widely used
  • Routinely test for this virus before breeding because we don’t want it circulating
19
Q

Life cycle of which parasite?

A

Dictyocaulus arnfieldi
= equine lungworm

20
Q

How do horses become infected with lungworm

A
  • Ingestion of Dictyocaulus arnfieldi larvae L3 from faeces/ pasture
  • Donkeys are the main source of pasture contamination - tend to be the main source of lungworm
  • Pilobolus fungi is involved in dissemination
21
Q

Clinical signs of lungworm infection

A
  • Mucopurulent discharge
  • Moderate to severe coughing (worse with exercise)
22
Q

Diagnosis of lungworm

A
  • L1 in faeces (infrequent and few)
  • Tracheal wash for eggs, larvae, WBCs
  • Consider: previous failure of antibiotic therapy, season, history
23
Q

Pathogenesis of lungworm

A
  • There is mucopurulent exudate and hyperplastic epithelium
  • There is lymphocytic infiltrate in the lamina propria (-> alveolitis, bronchiolitis, bronchitis)
  • Raised areas of over-inflated pulmonary tissue
24
Q

Treatment of lungworm

A
  • Anthelmintics: moxidectin, ivermectin
  • Bring indoors to treat
25
Q
A

Lungworm larvae

26
Q

What is a good protocol to follow for control of respiratory disease outbreaks?

A