Equine Infectious Respiratory Diseases

Question 1

1. Clinical signs of equine infectious respiratory diseases dept. on?
2. Typical clinical signs of equine infectious respiratory diseases.

Answer 1

1. Virulence of infecting organism and susceptibility of the host.
2. Nasal discharge.
   Cough.
   Pyrexia.
   Lymphadenopathy.
   Tachypnoea.
   Inappetence.
   Depression.
   In athletic horses: fatigue, exercise intolerance, poor performance, prolonged recovery.

Question 2

Differentiating between infectious and non-infectious respiratory disease.

Answer 2

Similar clinical signs - nasal discharge, cough, tachypnoea, exercise intolerance.
But infectious disease may also have:
- pyrexia (should be considered as poss. infectious respiratory disease alone).
- high white blood cells/fibrinogen.
- lymphadenopathy.
- multiple horses affected.

Question 3

Necessity of Dx of infectious respiratory disease in horses.

Answer 3

Some diseases managed based on CE and Hx w/o ID of precise cause.
Tx often the same for uncomplicated respiratory disease.
BUT, important to establish risk to other horses on yard - influences whether ID of pathogen appropriate.
Essential to ID pathogen in outbreaks and respiratory disease associated w/ abortion.

Question 4

Dx test for infectious respiratory diseases.

Answer 4

Ab titres.
Paired samples (clotted blood or serum) taken 10-21d apart preferable to confirm rising Ab titre (long wait).
Cross-reactivity w/ vac-derived Ab’s may obscure interpretation of results.
May be of questionable use in establishing Dx in early stages of an ongoing disease outbreak.

Question 5

Obtaining a diagnostic sample.

Answer 5

Nasal swab.
Nasopharyngeal swab.
- pass long nasopharyngeal swabs via ventral meatus into nasopharynx and stim horse to swallow.
– release of any discharge from guttural pouches onto swab.
Guttural pouch lavage.

Question 6

Virus isolation from samples.

Answer 6

Inoculation of sample in tissue culture and identification of any resultant viral growth - from nasal or nasopharyngeal swab (in viral transport medium), tracheal wash (in phosphate buffered saline), or whole blood (lithium heparin tubes).
- Not always most sensitive and requires minimum 2-5d for results.

Question 7

Virus detection from samples taken.

Answer 7

Immunoassay (ELISA, IF) detects viral protein.
PCR detects viral nucleic acid.
Usually from nasopharyngeal swab (in viral transport medium.
Do not differentiate between live and dead organisms.
Sensitive and quick.
Results may be w/in 48h.

Question 8

Detection of antibodies.

Answer 8

Paired sample (clotted blood or serum).
Take samples 10-21d apart to detect rising Ab titre.
Now one for Strangles.

Question 9

Timings of samples for PCRs and ELISAs?

Answer 9

First day of clinical signs - virus shedding begins here.
S. equi 24-48h after onset of fever so do not sample too early.

Question 10

1. Is equine influenza notifiable?
2. Contagiousness of equine influenza?
3. Which subtype of equine influenza is circulating?
4. Equine influenza incubation period?
5. Equine influenza transmission.

Answer 10

1. Not notifiable to DEFRA but is notifiable to the BHA under their Rules of Racing when in horses on licensed racehorse premises - potential to interrupt the racing calendar.
2. Highly.
3. H3N8.
4. ~1-3d.
5. Inhalation - aerosol over 50 yards, common air spaces in American barn type stables – all horses in barn cold become infected.

Question 11

Equine influenza clinical signs.

Answer 11

URT and LRT.
Damages respiratory epithelium.
Persistent cough (more than other respiratory diseases).
Pyrexia and dry cough common, followed by nasal discharge.
Submandibular lymphadenopathy.
Inappetence.
Depression.
Signs usually subside w/in a few days unless secondary infection.
Signs more severe in unvaccinated horses than in vaccinated horses.

Question 12

Dx of equine influenza.

Answer 12

Clinical signs.
Virus detection (PCR on nasopharyngeal swab).
Serology - acute sample and again 10-14d later. 4-fold increase in Ab titre. Vac can interfere w/ interpretation.

Question 13

1. Best time to swab for virus detection.
2. Best time to blood sample for serology for Ab titres.

Answer 13

1. Active virus shedding.
   During clinical signs.
2. 1st sample during clinical signs.
   2nd sample 10-14d later.

Question 14

1. Tx for equine influenza?
2. Prevention of equine influenza?

Answer 14

1. Rest, clean air, NSAIDs.
   - 1 week rest for every day of pyrexia.
   – allows healing of epithelium, as airway inflammation/coughing prolonged if return to exercise too early.
   ABX only required if secondary bacterial infection.
2. Biosecurity.
   Vaccination - tightly controlled in UK.

Question 15

Controlling equine influenza.

Answer 15

Clinical signs/ risk suspected > all equids swabbed > confirm/rule out EI and clarify those that are actively shedding > biosecurity measures > (stud farms - manage mares w/ foal at foot separately from infected group – avoid foal infection which may be worse) > vaccinated horses additionally vaccinated > freedom from infection when all clinical signs resolved and repeat nasopharyngeal swabbing confirms negative PCR tests i.e. no evidence of further shedding of virus – most horses stop shedding virus w/in ~10d after initial uncomplicated infection.

Question 16

Equine Influenza vac protocol.
Mares?

Answer 16

1st vac.
2nd vac 21-60d later.
3rd vac 120-180d later.
Booster w/in 6m or 12m dept. on governing body (also horse cannot compete if had vac w/in last 7d).

Vaccinate mares in last 6-4w of pregnancy - ensure protective level of Ab’s in colostrum.
– foals to these mares should start vac program at 6m when maternal Ab’s have waned.

Question 17

1. Is EHV notifiable.
2. Main age group of horses affected?
3. Most common EHV strains.

Answer 17

1. No legal notification requirements for EHV in UK but recommended O’s inform their national breeders’ association if EHV abortion or neuro diseases occur.
   Important to alert O’s of horses that might be at risk of infection through contact w/ infected horses or premises because of easy infection spread and poss. severe consequences.
2. Young horses (major acute resp. disease outbreaks) (milder respiratory symptoms in older horses).
3. EHV-1 (neuro and abortion) and EHV-4 (respiratory).

Question 18

1. EHV mode of infection?
2. Incubation?
3. URT or LRT?
4. Why is EHV control so difficult?

Answer 18

1. Inhalation.
2. Variable.
3. URT mostly.
4. Lifelong carriers that periodically reactivate virus and start shedding in stress state so it is persistent and difficult to eradicate.

Question 19

EHV clinical signs.

Answer 19

Mild pyrexia.
Occasional cough.
Nasal discharge.
May have submandibular lymphadenopathy.
Depression.
Inappetence.
EHV1 - neuro signs, abortion.

Question 20

Dx of EHV?

Answer 20

Clinical signs.
Haematology initially shows lymphopenia/neutropenia.
Nasal/nasopharyngeal swab or heparinised blood for virus isolation.
Serology for circulating Ab’s from subclinical infection, latent infection and vac.
Virus detection by PCR on nasal swab or aborted foetus material and from fatal neuro cases.

Question 21

Tx of EHV.

Answer 21

No spec. Tx (no antivirals licenced for use).
Rest (at least 3w or longer).
NSAIDs for pyrexia.
Ab’s if secondary bacterial infection.
Palatable feed to encourage eating.

Question 22

Preventing EHV.

Answer 22

Difficult due to carriers.
Isolation of incoming horses to a yard for 21d.
Vac - not common generally – more routine in studs/racing where young horses more at risk and outbreak has serious implications.
Main benefit of vac = reduced shedding rather than dramatic effect on clinical signs.
Primary course = 2 vacs approx. 1m apart, then 6 monthly boosters to maintain level of protection.
In-foal mares vac at 5,7,9 months of pregnancy.

Question 23

1. Strangles organism.
2. Is Strangles notifiable?
3. Which age of horses experience more severe clinical signs.
4. Incubation period?
5. Spread w/in animal.
6. Persistence?

Answer 23

1. Streptococcus equi equi.
2. No legal requirements in UK.
   Advised to inform national breeders’ associations if infection occurs.
   Rules of Racing - trainers obliged to report likely or confirmed strangles to BHA when occurs among horses in training.
3. Younger.
4. ~7-14d.
5. Nasal or oral infection. Organism multiplies in URT LNs.
   Haematogenous or lymphatic spread can lead to infection in remote LNs and other tissues.
6. Following infection, ~10% of horses are outwardly healthy carriers of the infections.
   Persistence of the organism is in the guttural pouches of carriers.

Question 24

Strangles clinical signs.

Answer 24

Depression.
Inappetence.
Pyrexia.
Purulent nasal discharge (bacterial).
Lymphadenopathy w/ or w/o abscessation.
Painful swallowing w/ head outstretched.
Cough.
Severe lymphadenopathy can lead to dyspnoea or dysphagia.
- submandibular LNs may burst outwards.
- retropharyngeal LNs burst into the guttural pouch.

Question 25

Strangles complications.

Answer 25

GP empyema.
- up to 50% horses w/ retropharyngeal lymphadenitis will develop some degree of empyema.
Usually self-limiting.
Some cases persist for months.
- inspissation > chondroids.

Question 26

Strangles rare complications.

Answer 26

Bastard strangles.
- Lymphatic or haematogenous spread of infection to other LNs / organs (lungs, mesenteric LNs liver, spleen, kidney).

Immune-mediated myopathies - rhabdomyolysis/atrophy.

Purpura haemorrhagica - immune mediated vasculitis.

Question 27

Dx of acute strangles.

Answer 27

Haematology: leucocytosis, neutrophilia, hyperfibrinogenaemia.

Culture/PCR from abscess swab / nasopharyngeal swab (x3) / GP lavage.
- culture rate approx. 50%, PCR far more sensitive.

ELISA - serum - seroconversion 2w after exposure - not ideal in early stages.
- Test positive for approx. 6m post infection.
- Can take blood sample early on then if have difficulties confirming Dx by PCR, can take second blood sample >2w later.

Question 28

Strangles Dx/exclusion of carriers.

Answer 28

Perform approx. 4w after end of clinical signs.
Carrier state may be diagnosed or excluded by:
- 3 sequential NP swabs (5-7d apart) (Culture and PCR).
- 1 GP lavage (culture and PCR).
- Presence of Ab’s on ELISA blood test.
– approx. 90% carriers maintain Ab’s in blood, but not all will so neg results do not guarantee absence of carrier state and positive ELISA does not automatically mean horse is a carrier –> it could have had recent exposure and now have fully resolved.
Best after outbreak to blood sample all horses that did not show clinical signs to exclude them as carriers, then GP lavage for all clinical cases and any who test positive on blood sample.

Question 29

GP washes considerations.

Answer 29

Sample from both L and R.
- only one may be infected – can be pooled for analysis to reduce cost.
–> but this does dilute the overall sample so may miss low positives.
When multiple horses on a yard are being examined and samples taken for testing, useful to record order of sampling and ceasing collection if an overtly affected carrier identified.
- adequate disinfection of equipment, environment and personnel should then be carried out to avoid any risk of onward transmission.

Question 30

Tx of strangles.

Answer 30

Isolate (until confirmed uninfected).
- whole yard closed until all horses confirmed uninfected.
Strict hygiene.
Enhance maturation of abscesses by applying hot packs and flush thoroughly when ruptured.
NSAIDs.
Soft palatable food.
Convalesce 4-6w.
Penicillin in peracute cases but may reduce immune response and increase infection susceptibility.
- can prolong disease.
- may predispose to Bastard strangles - no evidence.
ABX may be indicated:
- critical cases w/ life-threatening airway obstruction.
- cases of purpura haemorrhagica.
- Tx internal/disseminated abscesses in bastard strangles
- Adjunctive Tx for GP empyema.
- Tx of thoroughly investigated chronic carriers.

Question 31

Strangles vac.

Answer 31

2004 - vac launched then withdrawn 3y later.
2022 - new protein strangles vac licensed for UK use.
Immnity fairly short lived but shown to reduce clinical signs and abscesses.

Question 32

Differences between horse biosecurity compared to farming.

Answer 32

More limited with horses.
Variable knowledge and awareness by owners.
Horse seen as individual rather than part of a herd.
Equestrian business requires more movement of animals compared to farming e.g. competing etc.
- some biosecurity principles difficult to implement.

Question 33

What measures could you implement on a yard to prevent intro of infectious disease?

Answer 33

Quarantining of new horses.
Test carrier status of certain diseases before introducing new horses e.g. Strangles.
Monitor for evidence of disease - temps, early intervention and Dx.
Hygiene - handwashing, separate feed and water bowls, equipment etc.
Optimise health and welfare - nutrition, clean fresh water access, clean and dust free stable, minimal stress.
Vac program where appropriate.

Question 34

Measures to implement on a yard when an infectious disease identified.

Answer 34

Control outbreak.
To new premises.
Prevent infection of new arrivals to infected premises.
Within infected premises.
Ensure all horses are free of infection at end of outbreak i.e. no carrier, esp. strep equi.

3 groups:
- Horses w/ signs of infection - barrier iso.
- Horses been in contact - monitor (temps) and barrier iso as appropriate.
- Group of horses w/o signs and not been in contact.
HYGIENE!!!
Keep youngstock away from broodmares.

Question 35

Control of respiratory disease outbreak.

Answer 35

Movement of horses on and off premises stopped.
Separate zones and groups (as prev.)
Handlers of infected horses must have no contact w/ healthy horses.
Fly control.
Dedicated equipment in infected area.
Disinfect stable/equipment and burn bedding.

Controls implemented for 28d after resolution of last case.
Strangles - ensure all horses tested for carrier status before opening yard.

Question 36

Prevention of outbreaks.

Answer 36

Vac.
- Population rather than individual.
- Some unrealistic expectations from O’s.
– 100% effective = complete protection from clinical disease and also complete virological/bacterial protection so don’t shed pathogen and act as contagion to others.
–> no vac can achieve this!
- Herd immunity.
– vac a sufficiently high proportion of population to provide protection for non-vaccinated individuals in that population.
– reduced spread as too few susceptible horses to propagate outbreak.
–> opportunity of virus to infect reduces.

Question 37

1. What % of horse population need to be vaccinated against EI to establish herd immunity?
2. What is the critical vaccination threshold?

Answer 37

1. > 70%.
2. Point where the size of the susceptible population is too small to for efficient virus transmission.