Upper respiratory tract diseases Flashcards
Respiratory clinical exam to include:
Respiratory rate and effort
Nasal discharge
Lymph nodes
Lung auscultation
What resp disease panels will commercial labs sponsor?
Strep equi subsp equi
Influenza
EHV1 and 4
Most likely causative agents of equine respiratory disease in the UK
Rhinitis virus/adenovirus
Strep equi subsp equi
Equine alphaherpes EHV-1,-4
Equine gammaherpes EHV-2, -5
Equine influenza
EVA?
Equine influenza
Orthomyxovirus, ssRNA
Type A (H3N8)
Inhaled -> URT respiratory epithelium
Highly contagious
Rarely fatal
Most overt illness in unvaccinated horses
If vaccinated - reduction in severity (and shedding) not for prevention of infection
Clinical signs of equine influenza
Pyrexia
Inappetence
Lethargy
Nasal discharge - serous to mucopurulent
Hacking, persistent, dry cough - less likely to be seen in other diseases like strangles
Vaccinated horses often more subtle
Diagnosis of equine influenza
Historical/local disease status
NP swabs whilst sick
Try to use viral transport media - survives longer
Consider in-contacts
Collect paired samples 0 +14 days (looking for a rising titre)
Free testing for disease surveillance
Treatment of equine influenza
Isolate for 14 days
§ Remember airborne and direct contamination
Rest/recovery prolonged (tracheitis can cause residual cough for a while after infection cleared)
NSAIDs
Antibiotics only if opportunistic secondary infection
Streptococcus equi subsp equi
Strangles - global distribution (except Iceland)
G+ cocci
Big concern for owners and the equine industry
Less likely to be aerosolised
Can be fatal - either directly (asphyxia), or costs -> PTS
Certain strains likely more severe?
Perhaps younger more severe signs too?
Pathogenesis of Strep equi subsp equi
Oro-nasal infection
Crypt cells of lingual and palatine tonsillar tissue -> regional LN
At this super early stage, may have false negatives from nasal swabs
3-5 days - lymphoid hyperplasia/abscessation
Loads of neutrophils = pus
Rupture of LN 7 days… > +++ after initial infection
Usually pyrexia precedes the purulent nasal discharge
Shedding 1-2 days after pyrexia
The greater the infective load, the faster and more severe the signs
Common clinical signs of Strep equi subsp equi
Pyrexia
Lethargy and depression - not just from the pyrexia
Mucopurulent nasal discharge - bilateral but could be unilateral
Submand and retropharyngeal lymphadenopthy - cause a physical obstruction making it painful and difficult to eat
Inappetence/dysphagia (secondary to neuropraxia, physical obstruction, pyrexia?)
Less common clinical signs of Strep equi subsp equi
Increased respiratory rate and effort
Pharyngeal swelling
Inspiratory noise - stridor
Mimic of choke (oesophageal obstruction) with bilateral food/water down nose
What is special about strangles?
Evolved as a host-restricted pathogen from Strep equi zooepidemicus
Strep zoo is a regular commensal of the URT
Persistent infection in a small % of infected patients
§ Opportunity for endemicity
Will survive for a while in the environment
Guttural pouches are immune privaleged except for the LNs on the floor
States of persistent infection in strangles
Lymphadenopathy (tunnocks teacake)
Empyaema (Mustard)
Pus persists in guttural pouch (feta)
Chondroids (babybels)
Chronic persistent infection
What happens during persistent/chronic Strep equi subsp equi infection?
Dynamic genome
§ Survival in a low-nutrient state
§ Intermittent shedding
§ Potential infection to other animals
But
§ Does the genomic decay lessen ability to cause disease to the extent that no longer contagious risk?
§ PCR on chondroids is often negative
§ Cannot culture organism from a chondroid
§ You have to remove all the material from the guttural pouch to say that it is free from contagion
Antibody responses can be really variable
How can you test for carriers of Strep equi subsp equi
Blood testing
- ELISA
PCR testing of aspirates from other pouches?
Screening
Endoscopy of the guttural pouch
Mild version of strangles
In reality you may see
§ Unexplained pyrexia
§ Mild, cloudy nasal discharge
§ No cough
§ Slightly off colour - could easily be missed
May have been given NSAIDs etc, and not responding
All unexplained pyrexia - consider strangles - check the guttural pouches
Why?
§ Attenuated strain, residual immunity, low infective dose?
§ Could still cause significant disease in others…
Complications of strangles
Can spread via haematogenous or lymphatic system
Aspiration of infective material - rare
Bastard strangles
Purpura haemorrhagica
Myopathies
Bastard stangles
Meningitis
Skin swellings
Large mesenteric abscessation - tiger-striped basketball sized abdominal abscesses (FNA to see if G+ (likely strangles) or mixed population (likely not strangles)
Often inoperable
Most common cause of purpura haemorrhagica
Strep equi infection
Purpura haemorrhagica
Severe vasculitis requiring high doses of steroids
pH also triggered by other bacteria and viruses, and neoplasia
Although derived from the greek for purple - they don’t always have petechiae or echy patches
Should have a massively elevated SEM ELISA titre
Strep equi induced myopathies
Infarctions
Acute severe myonecrosis - similar in people with beta-haem strep
Possibly also chronic immune-mediated myopathy - atrophy
Cross-reactivity with the M protein and myoglobin
Treatment of Strangles
Start with NSAIDs +/- paracetamol
Possibly penicillin
Antimicrobials may reduce overall seroconversion and abscess might flare back up after therapy, but these are not reasons to avoid antibiotics where the animal is struggling with strangles.
When is penicilling indicated in strangles?
Persistently pyrexic
Dull and inappetant/miserable/struggling
Dysphagic or has stridor
Treatment of carrier strangles
Dilution
Flush the guttural pouches with saline or povidine iodine via scope or folaey catheter
Systemic antimicrobials if signs indicate
Can wash/instil penicillin into the guttural pouches
Which oral antibiotic causes colitis?
Penicillin
EHV-1, -4
Alphaherpesviruses
Common respiratory pathogens
○ Approx. 80% infected as youngsters
○ Pyrexia, nasal discharge, cough, lethargy
Appears similar to other respiratory infections
○ May not be noticed by owner/reported as respiratory disease
○ Abortion or EHM might be the first you learn about it!
Pathogenesis of EHV-1,-4
Respiratory epithelial cells -> mono/lymphocytes -> blood vessels/lymph nodes
Cell associated viraemia -> sites of replication (vessel endothelium)
§ Biphasic pyrexia
Latent infections are common
Recrudescence -> infection considered relatively rare
Diagnosis of EHV-1,-4
Nasopharyngeal swabs
§ qPCR (fast)
§ Virus isolation (slow)
□ ‘gold standard’
§ Don’t submit dry
Serology
§ Paired titres - rise in antibody using complement fixation
§ Single high CF sample if unvaccinated useful preliminary test
Vaccination for EHV-1,-4
Should be more routinely vaccinated for, especially around competition?
Shedule 1st vacc from 5mo
§ 2nd vacc 4-6 weeks later
§ Boost every 6 mo
Pregnant mares 5, 7, 9 mo
EHV-2
Gammaherpesvirus
We don’t fully understand significance yet
○ Pharyngitis
○ Keratoconjunctivitis
○ Pyrexia
○ Inappetence
○ Pulmonary inflammation
Synergistic with EHV-5?
Recrudescence of EHV-1?
Equine rhinitis virus
A and B
ERAV and ERBV
Adenovirus (EAdV1)
Severe combined immunodeficiency foals
Also EAdV2 isolated from foals with diarrhoea
Equine viral arteritis
Notifiable
Equine arteritis virus
○ Alphaarteritisvirus, RNA virus
Maintained in carrier stallions
Important cause of abortion
Venereal or aerosol spread
Signs of equine viral arteritis
Pyrexia
Inappetence
Serous nasal discharge
Submandibular lymphadenopathy
Conjunctivitis
Vasculitis -> oedema
§ Often hindlimb/ventral
Abortion
