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risk based “big four“ vaccines
EHV-1/rhinopneumonitis (high-density events)
equine influenza (aerosolized spread)
streptococcus equi/strangles (endemic premises)
clostridium botulinum (endemic soils and specific forages)
Testing for equine herpesvirus
veterinary nasopharyngeal swab and whole blood EDTA for qPCR
shedding begins 1-2 days post fever
don’t rule out if early test is negative
testing for equine influenza
nasal swab for rapid PCR or stall-side antigen test
identifies pathogen rapidly to justify immediate perimeter expansion
testing for botulism
clinical diagnosis is primary
test feed/forage or GI contents, not live horse
don’t wait for lab confirmation to initiate antitoxin/supportive care
testing for strangles
active = aspirate mature node or nasopharyngeal wash for qPCR
clearance = guttural pouch lavage and qPCR
wait 24-48 hrs post-fever to swab
use SeM serology to check for purpura risk vaccinating
Important steps to build defense against outbreaks
risk-based vaccines
early detection and testing
exposure control/biosecurity
What is important in the first 24 hrs of an outbreak
stop movement, separate risk
what do you do hour 0-2 of outbreak?
halt movement
isolate index case immediately
contact attending vet
what do you do hour 2-6 of outbreak?
temperature sweep
take temperatures of every horse on property
categorize into red, amber, and green based on temp and contact history
what do you do hour 6-24 of outbreak?
enforce barriers
establish dedicated personnel, separate equipment and footbaths/PPE for each zone
work clean to dirty
red zone
febrile or showing clinical signs
strict isolation (30ft perimeter)
dedicated staff and equipment
no movement
amber zone
direct/indirect contact with index
currently afebrile
temp check 2x daily
no co-mingling
green zone
no contact with index
afebrile
temp check 2x daily
staff attends this group first
Signs of EHV-1 and influenza outbreaks
clusters of unexplained fever or respiratory signs in a high density/mixing environment
Signs of botulism outbreaks
clusters of weakness, dysphagia, or recumbency, especially linked to shared feed source
Signs of strangles outbreak
new arrivals with fever, or resident horses developing fever followed by lymph node swelling/discharge
respiratory contact
agent = EHV-1, EI, S equi
core action = stop movement and event competition immediately
separation = isolate clinical horses, cohort exposed vs clean animals
hygiene = dedicated staff and equipment for each zone, work from clean to dirty, disinfect fomites
feedborne toxin
agent = clostridium botulinum (preformed toxin)
core actions = stop feeding suspect feed immediately, precent animal access areas
preservation = retain original labels, lot codes, invoices, and unopened packages for authorities
investigation = trace feeding dates by group, look for visual contaminants
vaccine limitations of EHV-1
current EHV-1 vaccines labeled for reduction of respiratory disease and prevention of abortion
no commercial vaccine is labeled to prevent equine herpesvirus myeloencephalopathy
vaccination may mask respiratory signs (nasal discharge), leaving fever as only early indicator of viremia
vaccinated horses can become subclinical (Trojan Horse) shedders, appearing healthy while transmitting high viral loads
clinical red flags and testing for EHV-1
fever (102-106) typically precedes neurologic signs by several days
neurologic progression = ataxia, hind limb weakness, urine dribbling, loss of tail tone
testing = nasal shedding begins 1-2 days after onset of fever
immediate outbreak action of EHV-1
do not attempt to vaccinate your way out of active EHM outbreak
isolate febrile horse immediately
institute twice-daily temperature monitoring for entire herd
establish strict 30ft perimeter isolation zones and halt movement
CES Valencia Spring Tour Outbreak 2021
forced massive reevaluation of equestrian event biosecurity
underscored critical distinction between EHV-1 infection and EHM in dense, stressed sport-horse populations
Botulism type B
spoiled, wet, moldy forage (anaerobic)
endemic in Mid-Atlantic US/KY soils
progressive flaccid paralysis, dysphagia, weak tongue tone, muscle fasciculations
highly effective toxoid available
vaccine recommended for endemic regions
Botulism type C
decomposing animal carcasses baled into forage
global risk
rapid onset identical to type B
high attack rate in exposed herds
zero cross protection with type B vaccine
Botulism type A
endemic to soils west of the Mississippi River
similar neuromuscular blockade and profound weakness
no commercial vaccine
transmission threat of EI
highly contagious orthomyxovirus spreading rapidly via aerosolized droplets and fomites
morbidity approaches 100% in naive herds, heavily targeting unvaccinated horses
vaccine role in EI outbreak
vaccines effectively reduce both clinical severity and virus shedding
slows transmission velocity, protect herd and prevent barn-wide shutdowns, even if individuals get mildly sick
outbreak mitigation tactic EI outbreak
early in outbreak vet administer modified-live intranasal vaccine to unaffected at risk horses
strict isolation of clinical horses and aggressive fomite disinfection must occur simultaneously
strangles vaccine
modified live, can cause reversion to wild type and have side effects