Initial signs often non-specific eg dullness and fever.

Tachypnoea (ie >35/min - normal rate immediately postpartum is 60-80/min, declining to 30/min by 1h) is more common than coughing and nasal discharge.

Normal foal’s breath sounds are more audible than adult’s, but are poorly correlated with lung pathology because significant consolidation and/or interstitial disease may occur without abnormal sounds. 

Bronchoscopy,

trans-tracheal aspirate culture,

ultrasonography and radiography are useful.

Haematology and clinical chemistry are less sensitive and specific. Treat with antibiotics, ideally based on culture and sensitivity. 

Suitable empirical bactericidal broad-spectrum antibiotics include penicillin/gentamicin, ceftiofur or cefquinome. Supplement IgG if there is concurrent FPT.

Intensive nursing, oxygen (by mask or trans-nasal tube), IV fluids and frequent turning of recumbent foals are essential. Prognosis dependent on speed of treatment, type of bacteria, severity of lung damage and presence of sepsis in other structures (eg joints). 

hile EHV-1 usually causes outbreaks of abortion in last trimester, occasionally it leads to birth of extremely weak foals which die despite attempted treatment.

Confirm by PCR or detection of pathognomonic histological inclusion bodies in foal’s liver, lungs and thymus (submit fresh foal carcase, placenta and mares blood). Most stud mares are vaccinated against EHV 1 & 4, but protection is incomplete. 

Many foals (20-40%) develop rib fractures as a result of thoracic compression during forceful expulsion.

Most are asymptomatic, or cause only local injury (pain, swelling, haemorrhage). Potentially fatal sequelae include haemothorax, pneumothorax, and laceration of lung, pericardium, myocardium and diaphragm. 

Careful thoracic palpation (handle foals carefully) and ultrasonography are useful.

Neonatal fractured rib sydrome treatment 

The affected segment can be stabilised with adhesive bandage, and foal confined to a stable for a few weeks. Surgical stabilisation is required for flail chest. 

In utero stress may cause foals to defecate and gasp, leading to prepartum aspiration of meconium. This causes obstruction and chemical injury of airways.

Affected foals have meconium staining on coat and a brown coloured, bilateral nasal discharge at birth.

Treatment involves nursing and broad spectrum antibiotics. Aspiration of meconium from airways can be attempted. 

Inadequate lung maturation may lead to increasingly severe expiratory effort and lung dysfunction.

Provide surfactant (expensive), respiratory support, antibiotics.

Prognosis poor <300 days gestation. 

Differential diagnosis of respiratory disease in growing foals 

Rhodococcus equine pneumonia

Streptococcus equi var zooepidemicus infection 

Rhodococcus equine pneumonia

Occurs primarily on intensive rearing farms in warm, dry climates (ie not Scotland!). Foals probably infected as neonates, by inhalation or ingestion of environmental (particularly soil) bacteria, but do not develop clinical signs until 2-6 months old.

Bacteria reside intracellularly, particularly in phagocytes, leading to multifocal pulmonary abscessation. 

Signs include ill thrift, debility, progressive dyspnoea and less commonly coughing and nasal discharge. Systemic spread may cause abscessation in other structures including mediastinal and mesenteric lymph nodes, joints, physes and GIT (-> diarrhoea). Immune-mediated polysynovitis may occur.  

Thoracic radiography, ultrasonography and tracheal aspirate culture aid diagnosis. Hyperfibrinogenaemia, neutrophilia and thrombocytopaenia are common but not specific.

Several serological tests are available but are not 100% accurate. All in-contact foals should be screened, since they are likely to be infected and because early detection and treatment improves the outcome. 

Rhodococcus equine pneumonia treatment 

Prolonged (several weeks) treatment with rifampin and erythromycin, clarithromycin or azithromycin is required. Hyperimmune serum is available in some countries.

Prophylaxis can include (a) improved management – reduce stocking density, collect faeces from paddocks, rotate paddocks, move water and feed areas around paddocks to prevent development of dusty areas, (b) administration of appropriate prophylactic antibiotics to neonates, or (c) administration of specific hyperimmune serum. Vaccines are under development. 

Streptococcus equi var zooepidemicus infection

Common recurrent problem in groups of growing foals. Nuisance rather than concern. Cough, nasal discharge, slight submandibular lymph node enlargement, intermittent mild and pyrexia, but animals are not ‘sick’.

Administer penicillin and turn out to pasture, or ignore. May wax and wane over several weeks. 

Identification of aetiology of outbreaks is often not possible on clinical grounds alone because of common presenting signs, including pyrexia, dullness, anorexia, coughing, mucoid to mucopurulent to purulent nasal discharge, and bilateral enlargement of submandibular lymph nodes.

However, influenza is likely cause if outbreak spreads very quickly and strangles is likely cause when horses have marked submandibular lymph node abscessation.

see Horserace Betting Levy Board Codes of Practice for equine infectious diseases (www.hblb.org.uk) and Prevention lecture for state of art information. Antiviral drugs are rarely used. Rest is important. Maintain horses in clean air environment (well ventilated stable, shaving bedding and fed haylage from ground to encourage gravitational drainage of secretions). Antibiotics often administered if horse remains febrile for >4-5 days, respiratory secretions become purulent or if marked respiratory signs occur, particularly in young or very old horses. Clenbuterol may aid mucociliary clearance. 

very high infectivity because (a) a few viral particles can cause infection and (b) aerosol dissemination rapidly spreads infection through a premise. Since late 1970s, influenza vaccination has been compulsory for UK racehorses, and virtually all competitive horses are vaccinated (see prevention lecture). 

EHV-1 and EHV-4 

EHV-4 is probably commonest equine respiratory infection. EHV-1 occasionally causes respiratory disease, but more commonly causes outbreaks of abortion and encephalomyelopathy. All horses acquire EHV early in life, and probably all become asymptomatic carriers of latent virus, which may recrudesce following stress and/or intercurrent disease. Immunity to natural infection is short lived and horses may be repeatedly infected, especially following mixing of horses at sales or races.

EHV-4 is particularly problematic in young horses in training. EHV causes prolonged immunosuppression. EHV vaccines are not very effective but may afford some protection in younger racehorses. 

infections occur in conjunction with other infectious agents, but generally do not cause significant disease. In contrast to influenza and EHV, rhinovirus largely affects the URT.

Equine viral arteritis (EVA) 

Small percentage of UK horses (largely non TB population) are seropositive, but clinical disease has not been recorded in UK.

Clinical signs are variable, including aforementioned general signs of respiratory disease, and severe conjunctivitis (leading to its common name, pink eye), profound depression and periorbital oedema (almost pathognomonic) due to vasculitis. Venereal spread. Effective vaccine available. Details of statutory control of EVA given in reproduction lectures. 

Other causes of infectious respiratory disease; 

Bacteria including Mycoplasma felis and equirhinis (difficult to culture), B. bronchiseptica, S. pneumonia, Actinobacillus and Pasteurella spp. occasionally cause outbreaks of respiratory disease, especially in young horses in training. Likely that other, as yet unidentified viruses and bacteria are also involved. 

Strangles 

(Streptococcus equi var equi); Spreads rapidly via direct contact and via fomites. Bacteria remain viable in environment for weeks-months. 

igns of ‘classical strangles’ include pyrexia, bilateral purulent nasal discharge, dysphagia and marked swelling of submandibular and occasionally other head lymph nodes (sub-parotid and retropharyngeal). ‘Atypical strangles‘ cases have no lymph node abscessation, and may be misclassified as viral respiratory disease unless culture/PCR is done.  

Diagnosis confirmed by culture or PCR of bacteria in nasal, nasopharyngeal or guttural pouch swabs/washes or detection of serum antibodies using ELISA. Biochemical identification required to differentiate bacteria from Streptococcus zooepidimicus var zooepidemicus, a common commensal of nasopharynx. 

Penicillin treatment early in disease course may stop clinical progression, but unclear if horses develop immunity, so must be done in conjunction with effective isolation. Do not administer antibiotics to horses with lymph node abscesses. Nursing care important (as described for viral cases). 

Bastard strangles is rare complication whereby abscessation occurs in other tissues including mediastinal and mesenteric lymph nodes and physes. Affected horses present with fever, malaise, weight loss and signs related to local abscessation.

Poor prognosis.

Purpura haemorrhagica is an immune (type 3) mediated vasculitis occurring 1-3 months after strangles infection. Signs include generalised oedema, petechiation, pyrexia, commonly resulting in multi-organ failure. High (~50%) mortality. Treat with immunosuppressive dose of dexamethasone, penicillin and supportive care.

Guttural pouch empyaema 

RAO or heaves (previously erroneously termed COPD) is the most common cause of chronic coughing in temperate climates. It is an airway inflammatory response to pro- inflammatory agents in inhaled organic dust (including moulds, endotoxin, particulates, ammonia) originating from poorly conserved hay and straw. As a consequence of increased client awareness,

RAO cases are often presented early in the disease course, when they have occasional coughing or mild exercise intolerance, and before they develop overt expiratory dyspnoea.

Consequently fewer cases are now diagnosed confidently from history and clinical findings alone, and there is increased reliance on the use of ancillary diagnostic techniques. Controlled exposure to hay/straw may be done to exacerbate clinical signs and thereby aid diagnosis of mild cases. 

clinical signs reflect airway inflammation and obstruction, especially of bronchioles. There is bronchospasm, thickening of airway walls with oedema and leucocyte infiltration (predominantly neutrophils), mucus plugging and epithelial deciliation.

Coughing is most sensitive indicator of equine pulmonary disease, and most frequent presenting sign (85% incidence) for RAO. Coughing is usually exacerbated by exercise, and poor exercise tolerance is common. Bilateral mucopurulent nasal discharge is present in ~55% cases; the remainder have no nasal discharge because they swallow the increased volumes of mucopus. Overt expiratory dyspnoea leads to tachypnoea (>12/min), expiratory heaving and development of heave line. Severely affected horses have audible wheezes or crackles. 

Endoscopy - increased volumes mucopus in thoracic trachea (grade 1-5). Tracheal aspirates, readily collected endoscopically, have >20% neutrophils. BALF has >5% neutrophils. BAL involves lavage of the distal airways with 250-300ml saline via an endoscope or a proprietary BAL tube under heavy sedation. Radiography and ultrasonography are of limited diagnostic value. Blood gas analysis, pulmonary mechanics testing etc are research rather than clinical tools. 

This is essential and highly effective. All sources of airborne organic dust must be eliminated, ideally by keeping horses permanently at pasture. When this is not possible, shavings or paper bedding must be used and all wet bedding removed daily. Do not use deep litter shavings or paper as they rapidly develop mould and bacterial contamination. Haylage (high dry matter silage), chopped dried alfalfa, silage or complete cubed diets are suitable low dust feedstuffs. Feeding soaked hay is ineffective as the dust challenge is not fully eliminated and, additionally, the nutritive content of the hay is reduced. To provide adequate ventilation, the top door is kept open permanently and a louvered vent (>0.3m2) inserted in the back wall of the stable. Affected horses should be housed as far as possible from potential sources of organic dusts, such as stables containing hay and straw, waste bedding and barns. 

(a) turn out or house in dust free environment (b) bronchodilators – best ‘rescue drug’ is atropine, but adverse effects preclude its repeated use - follow up with

clenbuterol or inhaled salbutamol (c) inhaled beclomethasone or oral prednisolone, (d) maintain hydration to avoid respiratory secretions becoming tenacious 

Summer pasture associated obstructive pulmonary disease (SPAOPD) 

Similar clinicopathological features to RAO, but affects pastured horses with no access to hay/straw. Clinical disease occurs between spring and autumn, with remission during winter. Some (frustrating!) horses have both SPAOPD and RAO. Severe and potentially fatal dyspnoea, rather than coughing and nasal discharge, is usual presenting sign. Crackles and wheezes commonly detected on auscultation. 

Diagnosis usually made on basis of history and clinical findings, although marked neutrophilia of tracheal mucus and BALF may be helpful. Aetiology is unknown, but likely represents a pulmonary hypersensitivity to inhaled pollens or outdoor moulds. Intradermal antigen testing with a wide variety of antigens has failed to identify the cause. 

Management is more problematic than for RAO. Some horses may improve when moved to a different environment. If this is not feasible, horses should be housed in a dust free environment as for RAO. Bronchodilators in combination with oral or inhaled glucocorticoids are usually administered, as bronchodilators alone commonly give only a partial and temporary improvement. 

Inflammatory airway disease (IAD) 

Syndrome characterised by coughing, exercise intolerance, increased volumes of neutrophilic mucopus within lower airways, and occasionally nasal discharge. Horses are not depressed, sick or pyrexic and do not have the overt airway obstruction that characterises RAO. In contrast to RAO, which invariably affects older horses (> 5yo), all ages of horse may develop IAD. IAD is commonly identified at the start of training (ie as 2yo flat horses, or as 4-8yo National Hunt horses). Syndrome may self resolve within a couple of weeks, or may persist for months to years, with chronic cases being frustrating to manage. Many affected horses have a history consistent with a preceding, acute onset, infectious respiratory disease.

Aetiology is unclear, but appears multifactorial, including bacteria (S. zooepidemicus, Pasteurella spp., Actinobacillus spp, S. pneumoniae, B. bronchiseptica, Mycoplasmas) and inhaled dust/endotoxin 

Treatment is largely symptomatic; including rest and provision of a dust free environment. While those horses with significant bacterial infections may benefit from antibiosis, antibiotic therapy alone is ineffective in many cases. Antibiotics should ideally be selected based on culture and sensitivity of tracheal aspirates. Oxytetracycline, ceftiofur, cefquinome, enrofloxacin or TMPS are commonly used. Some horses with chronic IAD respond favourably to oral or inhaled glucocorticoids. Oral alpha interferon has been shown to be effective in some studies, but is expensive and not widely used. As IAD does not cause overt airway obstruction, bronchodilators are probably not indicated. 

Lungworm (Dictyocaulus arnfieldi) infestation

Uncommon today because of widespread use of effective anthelmintics. Occurs in summer or autumn, in horses pastured with donkeys, which are natural, and usually asymptomatic, reservoir hosts. Infections in horses are usually non-patent and, consequently, the Baermann faecal flotation technique (used in cattle) is unreliable for diagnosis. Diagnosis confirmed by demonstrating eosinophilia (>3%) in tracheal mucus or BALF, rarely by endoscopic visualisation of larvae within the trachea or in respiratory secretions, or by positive response to anthelmintics. Affected horses, and in contact horses and donkeys, should be given an avermectin or benzimidazole and moved to clean pasture. 

Idiopathic pulmonary eosinophilia 

Most eosinophilic lung diseases which affect horses in UK are unrelated to lungworm. These include eosinophil dominated acute alveolitis, chronic small airway diseases and chronic interstitial diseases. These are of unknown aetiology but often respond favourably to corticosteroids. 

Interstitial (restrictive) lung diseases 

Poorly understood and uncommonly recognised. Characterised by acute or chronic inflammatory alveolitis with injury to type I epithelial cells and endothelial cells. Serum proteins leak into alveoli leading to pulmonary oedema in acute cases (acute respiratory distress syndrome). Inflammatory cells infiltrate alveoli and interstitium. If horses survive this early injurious phase, inflammatory response resolves or interstitial fibrosis and granuloma develop over a period of weeks to years. Cause is not identified in majority of cases. Interstitial disease reduces lung compliance, causing predominantly inspiratory dyspnoea. Crackles, especially end inspiratory, and wheezes are common. Nasal discharge and coughing are uncommon. Radiography reveals interstitial or mixed interstitial/alveolar pattern. Early inflammatory phase must be treated aggressively to prevent development of fibrosis. Putative causal agents should be eliminated. Immunosuppressive dosages of glucocorticoids are usually indicated. Frusemide may reduce pulmonary oedema. Bronchodilators are rarely effective. 

Pulmonary oedema 

Causes include acute URT obstruction, cardiac failure, alveolitis/interstitial lung disease, smoke inhalation, neoplasia, plant and drug toxicity, immune mediated and volume overload (rare in adults). Signs include frothy nasal discharge (often blood tinged), increased inspiratory effort (reduced compliance), and widespread fine crackles on auscultation (some cases have relatively quiet chest despite obvious dyspnoea).

Endoscopy - frothy fluid within airways. Radiography - diffuse interstitial or mixed interstitial/alveolar pattern. Treatment - correct underlying cause where possible (eg for URT obstruction insert tracheostomy tube), frusemide, intranasal oxygen and, where appropriate, antibiotics and corticosteroids. 

Rare. Most cases have lymphosarcoma or metastatic disease, with primary lung neoplasia being rare. Clinical signs are variable and include weight loss, anorexia, pyrexia, dyspnoea, chronic coughing, pleural effusion, ventral oedema and jugular distension. Thoracic radiography, ultrasonography, thoracocentesis, pleuroscopy and cytology of pleural fluid or a tracheobronchial aspirate may aid diagnosis. 

Pulmonary abscesses and pleuropneumonia 

Rare in Europe cf. USA. Often follows prolonged transport, when pulmonary defences are compromised, or sequel to aspiration of saliva and food (eg choke or EGS). A wide range of aerobic and anaerobic bacteria may be involved - commonly mixed infections. Three stages are recognised in development of pleuropneumonia;

1. Initially bacteria colonise lung causing localised pneumonia and/or pulmonary abscesses. Extension of inflammatory response to adjacent pleura causes sterile inflammatory effusion termed a ‘parapneumonic pleural effusion’. Systemic antibiosis alone may be effective at this stage.

2. Extension of bacterial infection into pleurae induces production of large volumes of infected purulent effusion, which requires drainage. Large amounts of fibrin are formed, lining the pleural surfaces and resulting in locule formation.
3. The organisation phase is characterised by significant fibrin deposition, resulting in a thick ‘pleural peel’, which limits thoracic expansion. 

pulmonary abscesses and pleuropneumonia Clinical signs and diagnosis;  

Affected horses are ‘sick’, with lethargy, anorexia, pyrexia, ventral oedema and varying degrees of respiratory distress. Pleural pain (pleurodynia) causes reluctance to move, base narrow stance, elbow abduction, soft muffled coughing and fast shallow ventilation. These signs may be misinterpreted as signs of colic, laminitis or hypocalcaemia. Malodorous breath suggests anaerobic infection or lung necrosis and is a poor prognostic sign. Auscultation, percussion and ultrasonography will identify pleural effusion. Ultrasonography is essential to assess nature and extent (uni- or bilateral) of fluid, and to select optimal site for thoracocentesis. Thoracocentesis is necessary to confirm

L4EEMD02-03 – Alterations in respiratory function I & II 4th Yr ICC Equine 2015-2016 – Prof Bruce McGorum

diagnosis, to facilitate laboratory characterisation of effusion, and for aerobic and anaerobic bacterial culture and antibiotic sensitivity determinations.

Pulmonary abscesses and pleuropneumonia 

Causes include thoracic neoplasia (most common cause in UK), bacterial pleuropneumonia, penetrating chest wall wounds, concurrent peritonitis, congestive heart failure, hypoproteinaemia, chylothorax and diaphragmatic hernia. Identify effusion by auscultation, percussion and ultrasonography. Pleural fluid analysis can facilitate differentiation of transudate, modified transudate and exudate. Perform cytological examination for neoplastic cells, and aerobic and anaerobic culture and Gram smear for bacteria. Treat underlying cause and perform thoracocentesis. 

Rare. Causes include penetrating chest wall wounds, fractured ribs, spread of subcutaneous emphysema from wounds of axilla and neck, and oesophageal penetration. Diagnose by auscultation, percussion, ultrasonography and radiography. Treat underlying cause and, if dyspnoeic, aspirate air 

Rare congenital or traumatic disorder. Usually asymptomatic. GI signs due to strangulation or incarceration of bowel (dd surgical colic), or respiratory signs due to lung compression. Diagnose based on auscultation, percussion, ultrasonography, radiography. Surgical correction possible. 

Exercise induced pulmonary haemorrhage (EIPH) 

During very fast exercise most horses bleed from dorsocaudal lung, because of very high pulmonary capillary pressures, sub-atmospheric inspiratory pressures and presence of other predisposing URT (eg RLN), LRT (eg IAD) and cardiac (atrial fibrillation) disorders. Most bleeds are asymptomatic, however marked EIPH can cause epistaxis, poor exercise performance, pulling up and very rarely, death. Excessive coughing is not a feature of EIPH. Diagnosis is confirmed by bronchoscopy (~30 min post exercise); fresh blood is visible in trachea and large bronchi for a few days following a bleed, while haemosiderin (brown) tinted secretions are visible for up to 1 week. Hemosiderophages (macrophages containing haemosiderin) can be identified in tracheal aspirates and BALF for many months following a bleed.

Treatment is largely unsatisfactory but includes rest, treatment of underlying cardiac, URT and LRT disorders, NSAIDs to reduce interstitial lung fibrosis, dust free environment, and training at slower speeds. Pre-race administration of frusemide is permitted in some countries (not UK), but is of questionable efficacy. Non-responsive horses should be retired to less demanding disciplines.