L7&8: Coughing in horses 1 and 2

What are some infectious causes of URT that causing coughing in the adult horse

• Equine influenza

• Equine herpes virus 1&4

• Equine viral arteritis

• Equine rhinitis virus

• Streptococcus equi equi

What are some infectious causes of LRT that cause coughing in adult horses

• Equine influenza

• Equine Herpes virus 1&4

• Equine Viral Arteritis

• Equine Rhinitis Virus

• Streptococcus equi equi

• Streptococcus zooepidemicus

• Streptococcus pneumoniae

• Pasteurella/actinobacillus

What are the clinical signs of upper respiratory tract disease

• Fever

• Nasal discharge

• Coughing

• Enlarged submandibular lymph nodes

What are the clinical signs of lower airway disease

• ± fever

• ± nasal discharge

• Coughing

• Mucoid tracheal secretion

• Poor performance

• May be sub-clinical

Give an overview of equine influenza virus

• Most commonly affects 2 and 3 yo racehorses

• (H7N7) and H3N8

• Reservoir between epizootics unknown

• World-wide occurrence

• Antigenic drift, not shift

• Most common cause of URTI

• Spread by aerosol and direct contact

• Vaccinated animals susceptible to infection within 2 - 3 months

• Partial immunity may suppress clinical signs but allow virus shedding

What is the pathogenesis of equine influenza

• Inhalation

• Incubation 1-3 days

• Infects epithelial cells of upper and lower airways

• Loss of ciliated epithelium, compromise of the mucocilliary mechanism

• Leading to URT ± LRT signs

• May be associated with secondary bacterial infection

• No viraemia

How do you diagnose equine influenza

Serology

• Paired samples, 14 days apart

Nasopharyngeal swab

• Virus isolation (weeks)

• PCR

  • Free via HBLB

How do you treat equine influenza

• Isolate

• Symptomatic and supportive

• Limit stress

• Maintain hydration

• NSAIDS to limit pyrexia and improve appetite

• REST

• ? specific anti-viral therapy

  • Acyclovir

  • Interferon

• Monitor for secondary infection

How do you vaccinate for equine influenza

• Present-day threat from H3N8 Equi-2 Florida strains, which are divided into clades 1 and 2

• Vaccines effective vs H7N7 and some H3N8 strains

• H3N8 strains 10-20 years out of date; H7N7 not isolated since 1970s

• 2003 advised vaccines changed to include Florida clade 1 strain

• 2010 increased recognition of Florida clade 2, advised to include as well

• 2014 and 2019 recommendations unchanged

• Significant effect of adjuvant, cross protection

• Start course >6mo due to maternal Ab

What are the jockey club rules for equine influenza

• Changed 1st Jan 2022

• 1st equine influenza vaccination

• 2nd vaccination after 21 to 60 days from 1st vaccination

• 3rd vaccination after 120 to 180 days from 2nd vaccination

• Thereafter q 6 months

Give an overview of equine herpes virus 1 &4

• Endemic in UK and worldwide

• 75% of horses have latent infection acting as a reservoir for on-going infections

• “Stress” may activate latent infection

  • transport, other illness, influenza, vaccination

What is the epidemiology of EHV 1&4

• site of latency

  • Bronchial LN

  • Submandibular LN

  • Trigeminal ganglia

• EHV2 may be involved in reactivation

• First exposure as foals and weanlings

  • source of infection lactating mares

  • Foal to foal spread

• Immunity short lived (3-5 months)

• Reinfected during breeding or racing careers

  • Respiratory secretions, foetus/placenta, fomites

• Re exposure usually causes mild or inapparent infection

• Except in broodmare; Abortion last trimester or neonatal disease

• Also get neurological disease (strain variation)

What is the pathogenesis for EHV 1

• Inhalation of virus

• Incubation 3-7 days

• Replicates in URT epithelium→URT signs

• Then disseminates to LRT → LRT signs

• Transported to other organs in T lymphocytes

• Viraemic for up to 3 weeks

• Vasculitis – neurological disease, abortion, chorioretinopathy

• May be accompanied by secondary bacterial infection

• May be subclinical

What is the pathogenesis for EHV 4

• Inhalation of virus

• Incubation 3-7 days

• Replicates in URT epithelium URT signs

• Then disseminates to LRT LRT signs

How do you diagnose EHV 1 and 4

clinical signs

Virus isolation

• Blood- 30mls heparinised

• Nasopharyngeal swab +PCR

Serology

• Paired samples

How do you treat EHV 1 and 4

• Isolate

• Symptomatic and supportive

• Limit stress

• Maintain hydration

• NSAID to limit pyrexia and improve appetite

• REST

• Specific anti-viral therapy

  • Acyclovir

  • Interferon

• Monitor for secondary infection

How do you vaccinate for EHV 1&4

• Can vaccinate from 4 month

• Natural immunity short-lived therefore unlikely to improve on that with vaccination

• Reduce clinical disease, nasal shedding and days of viremia, not complete protection

• Two types – inactivated, modified live

• Two doses 4-6 weeks apart, booster q 6months

• Pregnancy – 5th, 7th, 9th month gestation inactivated vaccine

How do you prevent EHV 1 &4

• Management changes to limit exposure to pathogens is unrealistic

• HBLB code of practice

• Management of breeding stock

• Hygiene

• Vaccination

Give an overview of 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 foetuses and other products of parturition

  • direct contact in droplets (eg from coughing and snorting) from the respiratory tract

• Reservoir of infections

  • Stallions that are chronic shedders

Describe the epidemiology of equine viral arteritis

• Clinical disease in racing TBs has not yet been reported

• UK outbreaks

  • 2002: confined outbreak in southwest, source not identified

  • 2010: confirmed in 2 separate stallions

  • 2019: Two separate, uncontrolled subclinical outbreaks, involved horses imported from other EU countries

what is the pathogenesis for equine viral arteritis

• Spread: respiratory, breeding, aborted foetus/placenta

• Incubation 3 – 14 days

• Variable pathogenicity of EVA strains

• Replicates in macrophages LNs leucoctyeassociated viremia

• Localises in endothelial cells esp smaller arterioles and epithelium of certain tissues esp the adrenals, seminiferous tubules, thyroid, and liver

• Necrotising arteritis oedema and haemorrhage

• Often no clinical signs

• abortion and still birth

  • 10 –34 days following exposure

  • 3 – 10 months gestation

• Fever, anorexia, oedema (limb, prepuce, scrotum, ventral, periorbital), lacrimation, conjunctivitis, nasal discharge, coughing

How do you diagnose and treat Equine viral arteritis

Diagnosis:

• Blood samples, nasal swabs and semen can be used for isolation of the virus or detection of the viral RNA by PCR

• Serology

Treatment

• Symptomatic

How do you vaccine for equine viral arteritis

Can vaccinate seronegative breeding stallions- pre vaccination blood test

modified live vaccine- Atervac

What is the EBLB code of practice for EVA

• Notifiable

• Stop all breeding

• Isolate and treat clinical disease

• Group away in contacts away from other horses on premises and obtain samples for virus isolation

• Screen all other in premises by serology

• test semen from all stallions

• Clean and disinfect

• Repeat testing until freedom from active infection confirmed

  • Declining antibody, no virus isolated

• Monitor semen +ve stallions for persistence of shedding

Give an overview of equine rhinitis virus

• Role as a pathogen is controversial

• Can be isolated from asymptomatic horses as well as those with signs of respiratory disease in outbreaks

• Can induce experimental infection

• most common in young horses

• 60-80% of horses have antibody tires by 5 years of age

• Subclinical or mild URT and LRT signs

• Diagnosis-virus isolation from NP swab or BALF serology

• Treatment-symptomatic

Give an overview of LRT bacterial infections

• Streptococcus zooepidemicus,Streptococcus, pneumoniae, Pasteurella/actinobacillus most common

• Inhaled and overcome defence mechanisms

• Results in LRT only signs

• May occur secondary to viral infection or noninfectious airway disease

How do you identify LRT bacterial infection

• clinical signs / loss of performance

• endoscopy and LRT samples

  • Mucopus

  • Increased degenerate neutrophils + intracellular bacteria

  • Culture and sensitivity

• Haematology

  • neutropaenia/neutrophillia

  • lymphopaenia/lymphocytosis

  • Hyperfibrinogenaemia/ increased SAA

How do you treat LRT bacterial infection

• Antibiotics

• Rest

• improve environment

  • Dust free management

• anti-pyretics

• Mucolytics

• Bronchodilators

What are some common non infectious causes of coughing in adult horses

• Equine asthma

  • Severe equine asthma

  • Mild to moderate EA

What are some fairly common non infectious causes of coughing in adult horses

• Aspiration pneumonia

• Pleuropneumonia

• Pulmonary abscesses

• Epiglottic entrapment

• URT foreign body

What are some uncommon non infectious causes of coughing in adult horses

• Lungworm

• Tracheal stenosis/collapse

• Inhalation pneumonia

• Interstitial pneumonia

• Neoplasia

• Left heart failure

Give an overview of mild-moderate equine asthma

• Seen in young racehorses

  • Prevalence 20-65%; coincides with entering training; decreases with increasing age

• Also in older National Hunt, SB racehorses and sports horses

  • No decrease with age

• Characterised by excessive mucus in airways

• May exhibit cough and/or reduced performance

• NO increased respiratory rate/effort at rest

• Signs are chronic (>4 weeks duration)

• Frequently subclinical

What is the pathogenesis of equine asthma

• Definitive pathogenesis unknown

• Implicated causes:

• Inhaled dusts, LPS, ammonia etc

• Bacterial infection – inconclusive evidence

  • Strep zooepidemicus, Strep pneumoniae, Actinobacillus, Mycoplasma

• Viral infection – inconclusive evidence

  • Not associated with EHV or rhinovirus

  • Interferon

• Blood from EIPH

  • Inflammation

  • Secondary infection

How do you diagnose mild-moderate equine asthma

• Endoscopy

  • Increased mucus

• Tracheal aspirate/ BAL

  • Increased mucus + neutrophils or eosinophils/mast cells

  • Culture/ bacteria

How do you treat mild-moderate equine asthma

• Environmental changes to reduce dust

• Antibiotics

• Interferon

• Corticosteroids- systemic or inhaled

• Bronchodilators- systemic or inhaled

• Sodium cromoglycate- mast cell stabiliser; preventative only

• Omega-3 polyunsaturated fatty acid supplementation

Give an overview of severe equine asthma

• naturally occurring lower airway disease characterised by periods of reversible airway obstruction

  • Neutrophil accumulation

  • Mucus production

  • Bronchospasm

• Usually >7 years old

• Lifelong condition

• Genetic component to susceptibility

• Clinical signs may be seasonal

what is the pathogenesis for severe equine asthma

• Spores and 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 and can become hypersensitive

• Respond to non-specific allergens

what are the clinical signs of severe equine asthma

Acute and severe respiratory distress

• Increased respiratory effort

• Double expiratory effort/dyspnoea

Chronic

• Varies in severity from poor performance → overt signs of resp dysfunction with/without coughing and hypertrophy of abdominal muscles

how do you diagnose severe equine asthma

• Determine likelihood of SEA

• History and physical examination

• Assess airway inflammation

  • Trans tracheal wash

  • Bronchoalveolar lavage

• Rule out bacterial pneumonia

• Evaluate response to treatment

How do you assess airway inflammation via endoscopy

• rule out pharyngeal disease

• Airway inflammation: hyperemia, corina blunting

• assess tracheal mucus

• Obtain tracheal aspirate

  • Cytology

  • culture

How can you assess airway inflammation with clinical pathology

Options

• Tracheal aspirate via endoscope

• Transtracheal aspirate

• BAL

Cytology

• Increased cellularity

• predominantly neutrophils

  • non degenerate, no intracellular bacteria

• Increased mucus

• Curshmann’s sprials

How do you treat severe equine asthma

• Environmental management

• Reversal of bronchoconstriction

• Decrease pulmonary inflammation

• Decrease pulmonary mucus accumulation

What are some URTs that cause coughing in foals and weanlings

• EHV 1&4

• Equine influenza

• Streptococcus equi equi

What are some LRTs that cause coughing in foals and weanlings

• EHV 1 &4

• Equine influenza

• Undifferentiated respiratory tract infection

• Rhodococcus equi

• Streptococcus equi equi

• Parascaris equorum

What can cause undifferentiated bacterial pneumonia

• Strep. zooepidemicus most common

Also actinbacillus, klebsiella, staph aureus, bordatella, mycoplasma

What are some clinical signs for undifferentiated bacterial pneumonia

• auscutable changes

• Mild pyrexia

• Cough

How do you diagnose undifferentiated bacterial pneumonia

• History

• Clinical signs

• Further diagnostic tests

  • Mucopurulent exudate in trachea or endoscopy

  • bronchointersitial pattern on radiography

  • BAL/tracheal aspirate neutrophils increased, degenerate, Ic bacteria

How do you treat undifferentiated bacterial pneumonia

• Antibiotics

  • Culture and sensitivity

  • If not, ensure good vs streps

• Rest

• Dust free environment

Give an overview on strangles

• Streptococcus equi subspecies equi

• Gram positive

• Not a normal inhabitant of URT

• Does not require prior viral infection for colonisation

• Highly infectious, particularly weanlings and yearlings

• Equine specific

What is the epidemiology of strangles

• Infection primarily 1-5 yo

• Foals born from immune mares resistant for 3 months

• Morbidity 100%

• Mortality up to 10% without appropriate therapy

• 20% complication rate has been reported

• Immunity not lifelong

  • 75% still immune after 3-4 year

• Transmitted by

  • Direct contact with nasal secretions or LN discharges from infected horses

    • Fomites

    • Environment

    • only survives 1-3 days

  • Asymptomatic chronic carriers

    • GP

    • Up to 56 months

what is the pathogenesis of strangles

• Incubation period 3 – 14 days

• Recover over 2-3 weeks

• Nasal shedding continues for 2-3 weeks after the disease

• Some horses for months or years (up to 10% of horses become carriers)

what are the three clinical presentations for strangles

• Classic acute disease

• Atypical strangles

• Complications

what are the clinical signs for classic acute disease

• Fever, depression, inappetence, lymphadenopathy

• abscessation of mandibular, parotid or retropharyngeal lymph nodes, rupture after 7-10 days

• Dyspnoea and dysphagia if abscesses compress larynx or interfere with cranial nerve to pharynx

• Mucoid to purulent nasal discharge

• Cough

  • URT signs

What are the clinical signs of atypical strangles

• Mild inflammation of URT

• Slight nasal discharge

• Cough

• Fever

• Self limiting lympadenopathy

• Probably dependent on bacterial strain plus immunity and genotype of horse

what is the importance of atypical strangles

atypical disease is dangerous because it does not look like strangles

• looks just like any other respiratory infection

• samples not taken for culture

• control and prevention not implemented

‘atypical’ isolates important in disease spread

• bacteria from atypical cases can cause classical strangles in others

• strangles outbreaks with atypical cases often go unrecognised until classical cases appear later

What are some complications of atypical strangles

Internal abscessation

• Intermittent colic

• PUO

• Anorexia

• Depression

• Weight loss

• Depends on site of abscess

Purpura haemorrhagica

• generalized vasculitis caused by Type III hypersensitivity reaction after 3-4 weeks

• 1-2% of infected horses

• Thrombosis of small arteries can occur

• Skin and muscle necrosis may result

• Ventral and limb oedema and petechial hemorrhages on mucus membranes

• Death due to pneumonia, cardiac arrhythmia, renal failure, GI disorder

guttural pouch empyema and chondroids

• Purulent nasal discharge

• RP swelling

• Dyspnoea/dysphagia

How do you diagnose strangles

• Clinical signs

• Leucocytosis, hyperfibringenaemia/high SAA

• Isolation (culture) or detection (PCR) of S. equi from LN pus, nasopharyngeal swab, GP lavage fluid

• Culture of 3x NP swabs 60% sens, 90% if PCR

• Guttural pouch lavage more sensitive than nasopharynx or nasal discharge swab

How do you treat strangles

Depends on phase of disease

Exposed to strangles

• Treat with penicillin

• isolate

• will not become immune

horses with early clinical signs (rhinitis/ pharyngitis phase)

• Penicillin

• May inhibit natural immunity so may contract the disease again with continued exposure

• General nursing, anti-pyretics, soft food

Horses with lymph node abscesses

• Poulticing and drainage of abscesses

• Antibiotics may prolong resolution of the abscess

• General nursing, anti-pyretics, soft food

Horses with complications

• Abdominal abscesses

  • Diagnosis: U/S or rectal

  • Treatment: Long term antibiotics (penicillin or trimethorpim sulfa/rifampin up to 6 weeks

• Guttural pouch empyema ± chondroids

  • Diagnosis: Endoscopy, radiography

  • Treatment: Drainage via the pharyngeal openings or surgical drainage (if inspissated), antibiotics

• Purpura haemorrhagica

  • Diagnosis skin biopsy

  • Penicillin, dexamethasone, pred, fluids, palliative measures

What are the stages of managements of outbreaks

Red: presumed infected, clinical signs

Amber: Direct or indirect contact with red horse

Green: No contact or clinical signs

What does management red group entail

• Confirm resolution of disease once clinical signs have resolved in each horse

• 3 x negative cultures or PCR of nasopharyngeal swabs, taken 7 days apart as shed intermittently

• Or 1 x negative of GP washing

What does management amber and green group entail

• Take temp daily, if pyrexic move to red group

• Screen using blood test for carriers

  • for IgG vs 2 Strep equi specific Ag (A and B)

  • Takes 2 weeks from exposure to be +ve

• If positive, isolate and test via 1 x GP lavage or 3 x NP swabs

• If positive, treat as per carrier

What do you do with carriers with strangles

• Identification and treatment

• Endoscopic GP lavage

• Retrieve chondroids via GP ± surgery

• Instil topical benzylpenicillin in gelatin

• Repeat GP lavage and PCR after 2 weeks

How do you prevent strangles

• Modified live vaccine was available in UK in 2005

  • Withdrawn due to adverse reactions

• Recombinant protein (Strangvac)

  • Reduce clinical signs and number of URT LN abscesses

• Isolate new horses for 3-4 weeks

  • + Test for carrier status

give an overview on rhodococcus equi

• gram positive, pleomorphic coccobacillus

• widespread in environment

• Survives in GIT of mares

• Survives and multiplies in GIT of foals

• Survives in GIT of earthworms (reservoir)

• survives in soil for at least 12 months in hot dry conditions, therefore more common in USA, Australia, and Ireland than in UK

What is the epidemiology for rhodococcus equi

• Spread via inhalation of soil/faeces, also detected in exhaled air from infected foals

• amplified with high risk management practices

  • concentrated facilities

  • dusty paddocks and stables

  • incomplete manure removal

• Seasonal – late spring/summer

  • High aerosol challenge + high no. of susceptible foals

• Occurs sporadically and endemically

  • In endemic farms, morbidity 15-60%

  • Mortality 1-12%

What is rhodococcus equi pneumonia like

• Affects foals 1-6 months old

• Inhalation of contaminated dust

• Scavenged by alveolar macrophages, but not killed

• Destruction of these macrophages leads to a pyogranulomatous response

• Bronchopneumonia with widespread abscess formation

What are the clinical signs of rhodococcus equi pneumonia

• Anorexia

• Depression

• Fever

• Dyspnoea, tachypnoea

• Cough

• Varies from insidious to extremely acute onset

• Subacute form

  • Rare

  • May be found dead or with acute respiratory distress + pyrexia leading to death in 48 hours

What are the common extrapulmonary clinical signs for rhodococcus equi

• Diarrhoea

• Ulcerative enterotyphlocolitis

• Intra-abdominal abscesses

• Intra-abdominal lymphadenitis

• Immune mediated synovitis

What are the uncommon extrapulmonary clinical signs for rhodococcus equi

• Bacteraemia

• Cellulitis/lymphangitis

• Mengitis

• IMHA

• Intracranial abscesses

• Osteomyelitis

• Peritonitis

• Pleuritis

• Septic arthritis / synovitis

What does rhodococcus equi extrapulmonary signs have alongside them

• Often concurrent

• Can be found alone

• Can have >1 EP disorder concurrently

• Decreases prognosis

How do you diagnose rhodococcus equi

• Fibrinogen

• Neutrophilia

• Tracheal wash

  • Culture

  • gram-stain cytology

  • PCR VapA gene

• Ultrasonography

• Radiography

  • Less sensitive than US

• Serology

  • Not sensitive or specific enough

• Post mortem

How do you treat rhodococcus equi

• Total US abscess diam <8cm and mild clinical signs, 75% recover without treatment

• Do not tx if: no clinical signs, WCC <20x109/L, abscess score <10cm

• Tx if mild signs and abscess score >10cm

• Tx if moderate to severe signs

How do you choose antibiotics in rhodococcus equi

• Clarithromycin or azthromycin with rifampin

• Short and long term outcome better with clarithromycin

• Some clinicians no longer add rifampin, but still recommended to reduce resistance

• Treat until there is radiographic resolution of lesions and CBC and fibrinogen are normal…maybe 4-12 weeks

• Treatment is expensive

• 4% resistance

How do you prevent rhodococcus equi

• Difficult since the organism is shed in faeces

• increase ventilation and decrease dusty conditions

• Avoid dirt paddocks and crowding

• Rotate pastures to minimize grass destruction

• Vacuum or collect manure

• Isolate sick foal

How do you prevent rhodococcus equi

• Prophylaxis with hyperimmune plasma

• Decrease farm incidence by 30-40% in some studies, no effect in others

• Will not prevent disease in every foal

• Optimal timing and dose not clear

• Surveillance mechanisms and environmental changes still necessary

• Prophylactic azithromycin not beneficial

• No effective vaccine

  • Either for mare or foal

• Early diagnosis

• Weekly vet exam: PE, US, WCC

• A WCC >13×10 ^9/L is suspicious and >15 ×10^9/L is v v sus

give an overview of parascaris equorum

• See lecture on respiratory parasites (M Fox)

• Not a major pathogen

• Eggs on ground from previous year’s foal crop

• Can cause transient nasal discharge and cough as larvae migrating through lungs

• Diagnosis = FEC

• Treatment = anthelminthics