Equine Viral Respiratory Disease Flashcards
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)
- Influenza virus
- Herpesvirus-1 /-4
- Streptococcus equi (strangles)
- Rhodococcus equi
- Dictyocaulus arnfieldi (lung worm)
Streptococcus equi (Strangles):
- Transmission?
- Clinical signs? (3)
- Diagnostic tests? (3)
- Test for carrier status?
- Transmission: Requires close contact; shared tack; shared water troughs
- Clinical signs: Fever; profuse mucopurulent nasal discharge (ND); abscessed lymph nodes of the head and neck (‘strangles’)
- 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
- Testing for carrier status: guttural pouch wash at least three weeks post-resolution of clinical signs
Streptococcus equi (Strangles):
- Treatment?
- Prevention?
- Treatment: nursing care and anti-inflammatory medication. Could use antibacterials but controversial sometimes and depends how far along it is?!
- Prevention: (1) Management practices important;(2) Vaccine available (submucosal)
What is seen?
inspissated pus that has formed a chondroid in the guttural pouch of an infected horse. Viewed by endoscope.
What are the risk factors for strangles? (6)
- 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
What is the transmission and pathogenesis for influenza virus?
•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
What are the clincal signs of influenza virus? (3)
•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
How do you treat influenza virus? (2)
•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
Why is there a risk for variation wiht inluenza virus?
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
How do you diagnose influenza? (2)
•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
What is the pathogenesis for EHV 1 and 4?
- 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
Why doesnt EHV 1 and 4 change very much?
Its double stranded DNA
What are the common clinicl signs of EHV 1 and 4? (3)
Clinical signs (common)
Fever, occasional mild cough and slight nasal discharge (less obvious), poor performance (age / immunity dependent)
What are the occasional clinicl signs of EHV 1 and 4? (2)
Abortion / sick neonatal foal, neurological disease (equine herpesvirus myeloencephalopathy EHM)
What is the treatment for EHV 1 and 4? (2)
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
How do you diagnose EHV 1 and 4? (2)
•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