Equine Viral Respiratory Disease Flashcards

1
Q

Dominic is kept at a livery yard of 25 horses used for general riding and low level competitions

No other horses are showing similar signs, nor are there any new horses on the yard

The horses share communal grazing with mares and geldings separated in adjacent fields - with a common water trough within the fence, so that they come into close contact

Dominic was depressed for the last two days and yesterday was reluctant to exercise

However there was no discharge until today

Prior to that he appeared normal and competed successfully 5 days ago at a local show-jumping competition

What are the differentials? (5)

A
  • Influenza virus
  • Herpesvirus-1 /-4
  • Streptococcus equi (strangles)
  • Rhodococcus equi
  • Dictyocaulus arnfieldi (lung worm)
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2
Q

Streptococcus equi (Strangles):

  1. Transmission?
  2. Clinical signs? (3)
  3. Diagnostic tests? (3)
  4. Test for carrier status?
A
  1. Transmission: Requires close contact; shared tack; shared water troughs
  2. Clinical signs: Fever; profuse mucopurulent nasal discharge (ND); abscessed lymph nodes of the head and neck (‘strangles’)
  3. Diagnostic tests: (1) Culture of bacteria from pus emitting from enlarged lymph nodes, ND, NP swabs or guttoral pouch wash; (2) qPCR; (3) ELISA for serum antibodies
  4. Testing for carrier status: guttural pouch wash at least three weeks post-resolution of clinical signs
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3
Q

Streptococcus equi (Strangles):

  1. Treatment?
  2. Prevention?
A
  1. Treatment: nursing care and anti-inflammatory medication. Could use antibacterials but controversial sometimes and depends how far along it is?!
  2. Prevention: (1) Management practices important;(2) Vaccine available (submucosal)
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4
Q

What is seen?

A

inspissated pus that has formed a chondroid in the guttural pouch of an infected horse. Viewed by endoscope.

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5
Q

What are the risk factors for strangles? (6)

A
  • Contact with other horses / health status
  • New arrivals, don’t always know their history!
  • May have previously had strangles / carrier status (10%)
  • Health plans: quarantine and/or testing

–Quarantine important!

•Water troughs: separate vs communal

–Do these need protecting, do they need just one each, who do they share with? Etc.

•Personnel traffic between horses

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6
Q

What is the transmission and pathogenesis for influenza virus?

A

•Transmission: by aerosol (also fomites)

–highly infectious, downwind 1 mile!

•Infection of respiratory epithelial cells (URT)

–nasopharyngeal virus shedding

–destroys cilia

•Prone to secondary bacterial infection after influenza

–Bottom pics shows what influenza does

  • Virus usually limited to URT
  • Young / unvaccinated animals susceptible
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7
Q

What are the clincal signs of influenza virus? (3)

A

•Fever, cough and nasal discharge (serous, may become mucopurulent – secondary bacterial infection)

–Cough is harsh and dry – supposedly distinctive, actually quite a lot are vaccinated and the first thing that gets suppressed is the clinical signs – horse might not look ill, but may be shedding the virus

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8
Q

How do you treat influenza virus? (2)

A

•Nursing care and anti-inflammatory medication (might want to give antibiotics for secondary infection)

–If fever goes down and then a bit spike and then mucopurulent discharge etc., might be 2ndry bacterial infection

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9
Q

Why is there a risk for variation wiht inluenza virus?

A

Negative-sense ssRNA virus with segmented genome

Means for variation in this virus is that it is easy to change its appearance – accumulates mutations and appear differently each year, which is why human vaccines are updated every year, it is lower in horse influenza but still happens and as it is segmented, if 2 strains infect the same cell, they can be swapped and a totally new subtype can be made – doesn’t happen often though. Just the one subtypes circulating in horses at the moment

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10
Q

How do you diagnose influenza? (2)

A

•Nasal swab, really far up the nose!

–Detection of viral antigen (ELISA)

–Detection of virus genetic material = RNA (RT-PCR)

–Virus isolation (usually in eggs)

  • Can take a while to do this
  • Serum samples (acute & convalescent)

–Use for the detection of antibodies (serology), typically done by:

•ELISA or

•Haemagglutination inhibition (HI)
4-fold increase in titre technique

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11
Q

What is the pathogenesis for EHV 1 and 4?

A
  • Can occur quite similar to influenza, but this is a virus that can go latent
  • Transmission: inhalation of aerosol / contact with infected fomites / reactivation from latency
  • Infection of:
    • respiratory epithelial cells (NASOPHARYNGEAL VIRUS SHEDDING)
    • multiple cell types including white blood cells (DISSEMINATION)
    • endothelial cells (INFLAMMATION & THROMBI)
  • Cell associated viraemia
    • Can end up in different places of the body, not restricted to the respiratory tract like influenza. If it finds way to pregnant uterus – can cause abortion, and if finds way to spinal cord, can cause neuro disease
  • Dissemination to sites of secondary replication
    • pregnant uterus (ABORTION - rare)
    • spinal cord (NEUROLOGICAL DISEASE - rare)
  • Latency established (CAN HAVE REACTIVATION DURING STRESS)
    • E.G. PREGANNCY – CAN BE DEVASTATING IN PREGNANT MARES
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12
Q

Why doesnt EHV 1 and 4 change very much?

A

Its double stranded DNA

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13
Q

What are the common clinicl signs of EHV 1 and 4? (3)

A

Clinical signs (common)

Fever, occasional mild cough and slight nasal discharge (less obvious), poor performance (age / immunity dependent)

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14
Q

What are the occasional clinicl signs of EHV 1 and 4? (2)

A

Abortion / sick neonatal foal, neurological disease (equine herpesvirus myeloencephalopathy EHM)

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15
Q

What is the treatment for EHV 1 and 4? (2)

A

Rest in athletic animals;
EHM: nursing care and anti-inflammatory medication;

If ataxic, might need nursing so not recumbent for too long, might need intensive treatment if it gets the mild encephalopathy

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16
Q

How do you diagnose EHV 1 and 4? (2)

A

•Nasal swab (and placenta / fetus samples)

–To detect viral DNA by PCR

•Blood samples

–Virus isolation in tissue culture (anti-coagulated blood - acute)

–Detection of antibodies (in serum)

  • Complement fixation test
  • If suspicion, take serum and couple of blood samples
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17
Q

What is the pathogenesis of Rhodococcus equi?

A
  • Inhalation of air, faeces, water, soil laden with bacterium
  • ‘Foal pneumonia’
  • Rarely detectable bacteraemia
  • Joints – can get into joints and cause swelling
  • Can get into colon
  • Faecal shedding
  • Zoonotic potential
18
Q

Rhodococcus equi:

A) Common clinical signs? (5)

B) Occasional clincial signs (2)

A

A) Cough, mild ^RR, ^respiratory effort & mild tracheal rattling, pulmonary crackling

Fever (bronchopneumonia) – as goes into the lung more than influenza

B) polysynovitis, diarrhoea

19
Q

How do you treat Rhodococcus equi?

A

antibiotics (macrolide & rifampin),

monitored via ultrasound & CBC

passive transfer of hyperimmune plasma

20
Q

How do you prevent Rhodococcus equi? (6)

A

identify high risk farms, improve pasture management / rotation, lower stocking density and surveillance / early detection

21
Q

Who is the host of Rhodococcus equi?

A

Foals under 6 months

22
Q

How do you diagnose Rhodococcus equi? (4)

A

•Tracheobronchial wash / aspirate

–Bacteriology

–Cytology

–PCR (vapA gene)

•[Blood sample]

–CBC, plasma protein, hyperfibrinogenaemia?, neutrophilic leukocytotis

•[Ultrasonography, low specificity]

–Peripheral pulmonary abscesses & “comet tails”

•[Thoracic radiography, unusual]

–Prominent alveolar pattern

  • CBC, ultrasonography and radiography aren’t diagnostic – mainly to monitor but low specificity
  • Ultrasonogram shows comet tails
23
Q

What is the pathogenesis of Parasitic roundworm Dictyocaulus arnfieldi?

A

Ingestion of L3 larvae from faeces / pasture, invasion of intestinal mucosa, migration to mesenteric LNs, moult

L4 migrate via blood and lymph to lung capillaries > alveoli

Adults hatch, migrate to small bronchi, mucopurulent exudate, hyperplastic epithelium, lymphocytic infiltrate in lamina propria (alveolitis, bronchiolitis, bronchitis). Raised areas of over-inflated pulmonary tissue

Adults lay eggs with L1 larvae which hatch & migrate up trachea

Eggs / L1 coughed up & swallowed, pass through intestine then hatch in faeces

24
Q

Dictyocaulus arnfieldi:

  1. Transmission?
  2. Clinical signs?
  3. Diagnosis?
A
  1. Transmission: Donkeys are main source of pasture contamination. ?Pilobolus fungi involved in dissemination
  2. Clinical signs: moderate–severe coughing (exercise)
  3. Diagnosis: (1) first-stage larvae L1 in faeces (infrequent & few); (2) tracheal wash for eggs, larvae & WBCs; [failure of antibiotic therapy, season, history]. Look for the eggs, larvae in tracheal wash etc.!!
25
Q

Dictyocaulus arnfieldi:

  1. Treatment?
  2. Prevention?
  3. Host? (3)
A
  1. Treatment: antiparasitic drugs (esp. moxidectin and ivermectin) – bring indoors to treat
  2. Prevention: (1) Management e.g. not grazing donkeys with horses, regular treatment with anthelmintics. No vaccine
  3. Host: foals, yearlings, adults
26
Q

What do we need to educate owners about? (4)

A
  • Client / staff training in advance
  • Client awareness of disease risk
  • Discuss vaccination needs
  • Develop outbreak strategy in advance, considering available facilities and risk
27
Q

What do we need to consider about a vaccination plan? (9)

A
  • Pathogen, immunogenic protein(s) and protective immune response required ( if known!)
  • Age of animal
  • Pregnancy status

–Don’t always vaccinate when pregnant!

  • Leisure or athletic competition animal
  • Timing of vaccination in relation to competition
  • Previous vaccination history

–Following correct procedure for primary, secondary and booster vaccines

  • Course of vaccination i.e. timing of primary then intervals between secondary and booster vaccinations
  • Risk of infection (don’t forget tetanus!)
  • Requirements of governing body
28
Q

What vaccines can we give to horses? (3) How do these work?

A

•Equine influenza

–Antibody and cellular immunity

–Live attenuated (USA), live vectored, killed

•Equine herpesvirus

–Stimulate antibody and cellular immunity

  • Want cellular immunity as virus can get into cells and travel around the body etc. so need this immunity importantly too!
  • Strangles

–Cell-free extract

–Mucosal vaccine

•Sensitive area! But get an immune response at mucosal surfaces where it is needed basically

29
Q

Who regulates influenza virus? (3)

A
  • Vaccination mandatory for racehorses in France, Ireland, UK
  • BHA
  • British show jumping
  • FEI
30
Q

Who regulates equine HSV vaccine?

A

•Vaccination mandatory for racehorses in France

–Hasn’t recently been mandatory

Thoroughbred bloodstock industry – who needs protection due to impact on abortion

31
Q

How can we use mangement for virus control? (7)

A

•Maintain horses in small, consistent groups

–Strangles more likely to occur is larger groups!

  • Use separate tack (bridles / head-collars) and equipment (forks, barrows etc)
  • Avoid shared water sources / contact across stable or field boundaries
  • Handle new or young horses last
  • Monitor at risk animals (observation, temperature etc.)
  • Clean boxes, trailers / lorries between each occupant
  • Quarantine horses that come in
32
Q

How do you control an outbreak?

A

Disinfection

Isolation*

Submission (samples for diagnosis)

Hygienic procedures – particularly important for vets!

33
Q

What are the common hurdles to controlling outbreaks? (4)

A
  • Rapid identification of affected horses
  • Delay in diagnostic test results
  • Owner compliance

–Especially at livery yards! Lots of different owners, want to try and control but not everyone does as you say

•Declaration of end of outbreak?

–If you have potential carriers in strangles for etc., can take a while, to decide everything is clear!

34
Q

What needs to be considered for sampling protocols? (3)

A

Type of sample

  • Correct sample & storage (e.g. anti-coagulant; swab transport medium; temperature) – ask lab!

Timing of sampling

Who to sample?

35
Q

What does this show?

A

Graph shows when virus shedding occurs, based on influenza but would be the same for herpes, tells us that shedding coincides with peak clinical signs

  • Horse might be shedding virus at a lower rate by the time the owner calls you out, so might take a blood sample during the acute phase (as nasal swab might not be that useful by this stage) and then take a 2nd sample a few weeks later to look for antibodies. Taking 2 samples if especially important if you have vaccinated horses. If you see 4 fold difference in sample, can be confident that seen an infection of that virus
  • Might catch virus in the contact horses before clinical signs appear
36
Q

What vaccines would you recommend the following groups of horse receive?

–4-year-old Warmblood gelding purchased for eventing (2)

A
  • Influenza and tetanus
  • Tetanus doesn’t need to be given every time, can be combined with influenza vaccine
  • If just purchased – ask for vaccine history and find out how up to date it is
37
Q

What vaccines would you recommend the following groups of horse receive?

–6-month-old Thoroughbred filly intended for racing (2)

A
  • Influenza and tetanus
  • In terms of schedule – if first time of vaccine, might need primary, secondary and then booster at 6 months or at least by the year
  • But can look up on data sheet for the vaccines
38
Q

What vaccines would you recommend the following groups of horse receive?

–12-year-old breeding stallion (4)

A
  • Influenza and tetanus
  • Equine viral veneral transmitted viruses
  • Equine herpes virus as don’t want him passing this to mares
39
Q

What vaccines would you recommend the following groups of horse receive?

–12-year-old Shetland pony (pasture pet) (2)

A
  • Might be sat alone in the field alone?
  • Might not be at much risk, but if other horses coming and going – might want to vaccinate about influenza and tetanus if others coming and going
40
Q

What are the influenza vaccines available? (3)

A

The 3 influenza vaccines available

1st – based on pox virus that replicates in the horse but doesn’t cause any illness. Getting antibodies to HA (haemagglutinins surface protein)

2nd – ISCOM – immune stimulating complex. If you get a bit of redness and swelling at site of vaccine – shows its doing its job really – provoking immune response

3rd – adjuvant is matrix C. killed virus

Strains listed – probably guess that the strain name shows you where its isolated from and the year usually

Which one would you purchase? Proteq flu – has most recent strains in!

Process by which strains are monitories and recommendations made by OIE as to which strains should be used in vaccines and where they predominate.

Equip – very much out of date!!

Proteq – first ones to get updated quickly

Equilis – not quite there yet