3.2 Coughing in Horses 1

URT disease: clinical signs

fever, nasal discharge, coughing, enlarged submandibular lymph nodes

LRT disease: clinical signs

+/- fever, +/- nasal discharge, coughing, mucoid tracheal secretion, poor performance, may be subclinical

URT & LRT: equine influenza virus

2-3 year old racehorses

H3N8 and (H7N7)

reservoir between epizootics unknown

world-wide occurrence

antigenic drift

most common cause of URTI

spread by aerosol & direct contact

vaccinated animals susceptible after 2-3 months

partial immunity may suppress clinical signs but allow virus shedding

equine influenza: pathogenesis

-inhalation
-incubation 1-3 days
-infects epithelial cells of upper & lower airways
-loss of ciliated epithelium, compromise of mucociliary mechanism
-URT +/- LRT signs
-may be associated with secondary bacterial infection
-no viremia

equine influenza: diagnosis

serology
-paired samples, 14 days apart (antibody titer)

nasopharyngeal swab
-virus isolation (weeks)
-PCR (free via HBLB)

equine influenza: treatment

-isolate
-symptomatic & supportive
-limit stress
-hydration
-NSAIDs to limit pyrexia & improve appetite
-rest
-specific anti-viral therapy (acyclovir, interferon)
-monitor for secondary infection

equine influenza: vaccination

-present-day threat from H3N8 equi-2 Florida strains, divided into clades 1 & 2
-vaccines effective against H7N7 & some H3N8 strains (10-20 years out of date)
-2003 advised vaccines changed to include Florida clade 1 strain
-2010 advised to include Florida clade 2 strain
-2014 & 2019 recommendations unchanged
-significant effect of adjuvant, cross protection
-start course >6m due to maternal antibodies

equine influenza vaccination: jockey club rules

1st vaccination

2nd vaccination 21-60 days after 1st vaccination

3rd vaccination 120-280 days after 2nd vaccination

thereafter every 6 months

URT & LRT: equine herpes virus 1 & 4

-endemic in UK & worldwide
-75% of horses have latent infection acting as reservoir
-stress may activate latent infection-> transport, other illness, influenza, vaccinations

EHV 1 & 4: epidemiology

site of latency: bronchial LN, submandibular LN, trigeminal ganglia

EHV2 may be involved in reactivation

first exposure as foals & weanlings: infected from lactating mares, foal to foal spread

immunity short lived (3-5 months)

reinfected during breeding or racing careers: respiratory secretions, fetus/placenta, fomites

reinfection causes mild or inapparent infection, except broodmare (abortion last trimester or neonatal disease)

also get neurologic disease (strain variation)

EHV 1 & 4: pathogenesis

EHV1 & EHV4: inhalation of virus, incubation 3-7 days, replicates in URT epithelium then disseminates to LRT

EHV1: transported to other organs in T lymphocytes, viremic for up to 3 weeks, vasculitis (neurological disease, abortion, chorioretinopathy) may be accompanied by secondary bacterial infection, may be subclinical

EHV 1 & 4: diagnosis & treatment

clinical signs

virus isolation
-blood-> 30 ml heparinized
-nasopharyngeal swab (+PCR)

serology
-paired samples

treatment same as equine influenza

EHV 1 & 4: vaccination

-can vaccinate from 4m
-natural immunity short-lived therefore unlikely to improve with vaccination
-reduce clinical disease, nasal shedding, & days of viremia, not complete protection
-two types-> inactivated, modified live
-two doses 4-6 weeks apart, booster every 6m
-pregnancy-> 5th, 7th, 9th month gestation inactivated vaccination

URT & LRT: equine viral arteritis

RNA arterivirus

notifiable

transmission by venereal infection of mares by stallions during mating, AI with semen from infectious stallions, contact with aborted fetuses & other products of parturition, direct contact in droplets (coughing/snorting)

stallions are chronic shedders

clinical disease in UK racing thoroughbreds not yet been reported

equine viral arteritis: pathogenesis

spread through respiratory, breeding, aborted fetus/placenta

incubation 3-14 days

variable pathogenicity of strains

macrophages-> LN-> leucocyte-associated viremia

localizes in endothelial cells (esp. smaller arterioles & epithelium of adrenals, seminiferous tubules, thyroid, & liver)

necrotizing arteritis-> edema & hemorrhage

equine viral arteritis: clinical signs

often no clinical signs

abortion & still birth (10-34 days following exposure, 3-10 months gestation)

fever, anorexia, edema (limb, prepuce, scrotum, ventral, periorbital), lacrimation, conjunctivitis, nasal discharge, coughing

equine viral arteritis: diagnosis & treatment

diagnosis:
blood samples, nasal swabs & semen can be used for isolation of virus or detection of viral RNA by PCR, serology

treatment:
symptomatic

equine viral arteritis: vaccination

vaccinate seronegative breeding stallions (pre-vaccination blood test)

modified live vaccine-> artevac

equine viral arteritis: HBLB code of practice

notifiable, stop all breeding, isolate & treat clinical cases, group in-contacts away from other horses on premises & obtain samples for virus isolation, screen all other horses in premises by serology, test semen from all stallions, clean & disinfect, repeat testing until freedom from active infection confirmed (declining antibody, no virus isolated), monitor semen positive stallions for persistence of shedding

URT & LRT: equine rhinitis virus

roles as pathogen controversial

can be isolated from asymptomatic horses as well

can induce experimental infection

young horses

60-80% have antibody titers by 5 years old

subclinical or mild URT & LRT signs

diagnosis-> virus isolation from NP swab or BALF, serology

treatment-> symptomatic

LRT bacterial infection

streptococcus zooepidemicus, streptococcus pneumoniae, pasteurella/actinobacillus most common, inhaled & overcome defense mechanisms, results in LRT only signs, may occur secondary to viral infection or non-infectious airway disease

LRT bacterial infection: identification

clinical signs/loss of performance

endoscopy & LRT samples (mucous, increased degenerate neutrophils & intracellular bacteria, C&S)

hematology (neutropenia/
neutrophilia, lymphopenia/
lymphocytosis, hyperfibrinogenemia/
increased SAA

LRT bacterial infection: treatment

antibiotics

rest

improve environment- dust free management

anti-pyretics

mucolytics

bronchodilators

non-infectious causes of coughing in adult horses

common: equine asthma (severe vs mild to moderate)

fairly common: aspiration pneumonia, pleuropneumonia, pulmonary abscesses, epiglottic entrapment, URT foreign body

uncommon: lungworm, tracheal stenosis/collapse, inhalation pneumonia, interstitial pneumonia, neoplasia, left heart failure

equine asthma: nomenclature

previously: COPD, "heaves", broken wind

RAO + summer pasture associated obstructive pulmonary disease + IAD

now: equine asthma syndrome, mild to moderate= IAD, severe= RAO or SPAOPD

mild-moderate equine asthma

young racehorses

20-65%, coincides with entering training, decreases with increasing age

also older national hunt, SB racehorses, & sports horses (no decrease with age)

excessive mucous in airways

cough and/or reduced performance

no increased respiratory rate/effort at rest

chronic signs (>4 weeks)

frequently subclinical

mild-moderate equine asthma: pathogenesis

implicated causes: inhaled dusts, LPS, ammonia

bacterial infection (inconclusive evidence)

viral infection (inconclusive evidence)

blood from EIPH (inflammation, secondary infection)

mild-moderate equine asthma: diagnosis & treatment

diagnosis: endoscopy (increased mucous), tracheal aspirate/BAL (increased mucous + neutrophils OR eosinophils/mast cells, culture bacteria?)

treatment: environment changes to reduce dust, antibiotics, interferon, corticosteroids (systemic or inhaled), bronchodilators (systemic or inhaled), sodium cromoglycate (mast cell stabilizer, preventative only), omega-3 polyunsaturated fatty acid supplementation

severe equine asthma

naturally occurring lower airway disease characterized by periods of reversible airway obstruction

neutrophil accumulation, mucous production, & bronchospasm

>7 years old

lifelong condition

genetic component to susceptibility

clinical signs may be seasonal

severe equine asthma: pathogenesis

spores & allergens deposit in bronchioles

immune reactions:
type 1 (mast cell degranulation), type 3 (immune-complex), type 4 (delayed)

bronchoconstriction, mucous production, airway inflammation

tissues are primed

can become hypersensitive

respond to non-specific allergens

severe equine asthma: clinical signs

acute & severe respiratory distress: increased respiratory effort, double expiratory effort/dyspnea

chronic: varies in severity from poor performance to overt signs of respiratory dysfunction with/without coughing & hypertrophy of abdominal muscles

severe equine asthma: diagnosis

determine likelihood of SEA

history & physical exam

assess airway inflammation (transtracheal wash, BAL)

rule out bacterial pneumonia

evaluate response to treatment

assess airway inflammation: endoscopy

-rule out pharyngeal disease
-airway inflammation->
hyperemia, corina blunting
-assess tracheal mucous
-obtain tracheal aspirate
-> cytology, culture

assess airway inflammation: clinical pathology

options: tracheal aspirate via endoscope, transtracheal wash, BAL

cytology: increased cellularity, predominately non-degenerate neutrophils, no intracellular bacteria, increased mucous, Curshmann's spirals

severe equine asthma: treatment

environmental management, reversal of bronchoconstriction, decrease pulmonary inflammation, decrease pulmonary mucous accumulation