EIPH

Question 1

What is EIPH?

Answer 1

Exercise induced pulmonary haemhorrhage

Question 2

What are the clinical signs of EIPH? (5)

Answer 2

• None!
• Most don’t bleed significantly to the point where they get epistaxis usually! EPIH is the most common cause of epistaxis, but not every horse will bleed enough with EIPH will have epistaxis
• poor performance
• sudden onset exercise limitation
• swallowing after exercise
• Epistaxis

Question 3

How do we diagnose EIPH? (2)

Answer 3

Endoscope

Cytology

Question 4

What is the clinical significance of EIPH?

Answer 4

• a large proportion of horses are positive following racing in endoscopic surveys
• there is no relationship between the presence or absence of EIPH and finishing place
• When they bleed a lot, can result in poor performance, but not every horse with small amount of EIPH will result in poor performance

Question 5

What is the pathogenesis of EIPH? (2 theories)

Answer 5

• UNKNOWN – controversial
• haemorrhage is from pulmonary rather than bronchial vessels
• typically located in the caudodorsal lung lobes
• Capillary stress failure theory
• High pressures in pulmonary vasculature due to CO and capillaries rupture
• Mechanical theory
• As horse gallops, pressure from GI onto diaphragm and caudal lung lobes, result in mechanical failure
• Haemorrhage is always from pulmonary vessels and caudal dorsal vessels where pressures are highest

Question 6

What is the CAPILLARY STRESS FAILURE THEORY?

Answer 6

• Pressures generated within the pulmonary capillaries during exercise exceed their stress failure point
• Pulmonary capillaries are an inevitable anatomical weak point due to normal equine cardiopulmonary physiology:
• THIN WALLED
• normal Thoroughbreds become hypoxic and hypercapnic during exercise, at peak gallop. That may be an important contribution as to why you get vasoconstriction
• Hypoxia induced vasoconstriction, don’t perfuse the part that doesn’t have enough oxygen! Therefore by doing this, increase pressure in lungs

Question 7

Why does EIPH affect the CdD lobes?(3)

Answer 7

• Higher blood flow
• lower intrinsic vascular resistance – but if this is exacerbated by vasoconstriction, may have important part
• Displacement of the diaphragm causes transient falls in alveolar pressure
• Lower alveolar pressure leads to greater transmural pressure
• Wall stress: Transmural pressure x radius/ wall thickness

Question 8

What predisposes a horse to EIPH? (5)

Answer 8

Age

Type of horse

• LOWER AIRWAY DISEASE
• E.g. IAD or RAO – important risk factor
• Need to identify the risk factors and take them away
• UPPER AIRWAY DISEASE
• CARDIAC DISEASE
• Increases pulmonary artery pressure
• Atrial fibrillation
• Mitral valve disease
• Only clinical sign for a cardiac abnormality might be bleeding at exercise

Question 9

How can we diagnose EIPH? (5)

Answer 9

• Clinical evidence of EIPH
• only present in more severe cases
• Bilateral epistaxis, but only present in most severe cases
• Endoscopy
• Can be scoped as screening process
• Bronchoalveolar lavage
• RBCs, haemosiderophages
• Radiography
• Not something used regularly
• Scintigraphy
• currently experimental
• Not something used regularly

Question 10

What can be seen here?

Answer 10

EIPH

RBCs, haemoglobin within foamy macrophages – haemosiderinphages

Question 11

What can be seen here?

Answer 11

EIPH

Lots of blood and coating walls of trachea

Question 12

What is this?

Answer 12

Mild case of EIPH

Question 13

How can we manage EIPH? (3)

Answer 13

• Difficult to manage
• Identify and address any predisposing diseases
• Break haemorrhage-inflammation cycle
• Modify training programme to reduce episodes
• Dust-free environment
• Furosemide
• Not allowed in horse races in UK, shown to protect from developing of EPISTAXIS, not EIPH- so less likely to bleed from their nose if they have this
• Probably works by reduced circulation volume – may reduce circulation BP and it is also it is a weak vasodilatory effect
• ?antibiotics
• Horses that have had a severe bleed will need treatment, blood is also culture media for bacteria also – so antibiotics to prevent pneumonia after severe bleed

Question 14

What drugs can we use for EIPH and what 2 effects does it have?

What is the problem in the UK?

Answer 14

• Diuretic effect
• Reduce circulating volume
• Reduce weight
• Vasodilator effect
• In USA, but not UK, horses can race on furosemide

Question 15

What is a nasal strip? What do they do?

Where can and can’t we use them?

Answer 15

•Hold nostrils open and widely used in eventing world, not allowed in racing in the UK at this point – can train with them though

Question 16

What is the prognosis for EIPH?

Answer 16

• GOOD TO FAIR
• if associated with respiratory infection or other predisposing cause can be identified and treated
• or having minimal impact on performance
• POOR
• for idiopathic bleeders with performance limitations

Question 17

What is the impact of EIPH on UK racing? (3)

Answer 17

• No restrictions on ‘bleeders’
• Furosemide is not allowed for racing
• Nothing to make them rest them

Question 18

What is the effect of EIPH on the ROW horse racing? (2)

Answer 18

• 3 Strikes and out
• If epistaxis, not acceptable – they are removed from racing
• Furosemide allowed

Question 19

What diseases are foals susceptible to? (3)

Answer 19

• Infectious causes (bacterial)
• Congenital abnormality
• Sepsis, trauma, other

Question 20

What diseases are weanlings susceptible to?

Answer 20

•Infectious causes (bacterial) & contagious

Question 21

What disease are youn adults susceptibe to?

Answer 21

• Inflammatory airway disease
• Infectious causes (bacterial and viral and mycoplasma)

Question 22

What disease are old horses susceptible to?

Answer 22

•Recurrent airway obstruction

Question 23

IS URT more or less common than LRT?

What type of horse is it more common in?

Answer 23

• Less common than lower airway disease
• Mainly young horses (yearlings and two-year-olds)

Question 24

What viral (3) and bacterial (1) disease is tehre of the URT?

Answer 24

• VIRUSES
• Equine influenza
• Equine Herpes Virus 1&4
• Equine Viral Arteritis** Notifiable Disease
• BACTERIA
• Streptococcus equi equi

Question 25

What viral (4), bacterial (5) and mycoplasma diseases are there of the LRT?

Answer 25

* VIRUSES * Equine influenza * Equine Herpes virus 1&4 * Equine Rhino virus * Equine Viral Arteritis ND * BACTERIA * Streptococcus zooepidemicus * Streptococcus pneumoniae * Pasteurella/actinobacillus * Rhodococcus equi * Streptococcus equi equi * MYCOPLASMA * M. felis

Question 26

What horses are most at risk of bacterial infection? ## Footnote * Strep. pneumoniae * Strep. zooepidemicus is the most common isolated pathogen from equine lung * Pasteurella/Actinobacillus spp.

Answer 26

•Horses entering training yards for the first time (2 and 4 years) are at particular risk

Question 27

M. Felis causes what? How to we identify? How do we treat?

Answer 27

LAD ## Footnote * Culture from tracheal aspirates requires specialised laboratory and strict transport conditions * Sensitive to oxytetracycline

Question 28

What do the 5 different EHV cause?

Answer 28

* EHV1 - respiratory disease, abortion, neonatal, neurological * EHV2 - respiratory disease in foals * EHV3 - penile vesicles * EHV4 - respiratory disease * EHV5 – Equine Pulmonary Nodular Fibrosis

Question 29

What is the epidemiology of EHV 1 and 4?

Answer 29

* EHV1 and EHV4 endemic in UK and worldwide * Incidence: 4.4 cases/100horses/month * 75% of horses have latent infection acting as a reservoir for on-going infections * Become infected when young, then are permanenetly infected for life – stress will reactive and lead to spread throughout herd. * “Stress” may activate latent infection * transport, other illness, influenza, vaccinations

Question 30

What is the pathogenesis of EHV 1 and 4?

Answer 30

* Inhalation / direct contact much more important than aerosol spread * Incubation 3-7 days – SLOW PROGRESSION in yards * Replicates in URT epithelium * Transported to other organs in T lymphocytes, can induce vasculitis (and abortion due to this) * Viraemic for up to 3 weeks * Vasculitis * May be accompanied by secondary bacterial infection

Question 31

What is the pathogenesis of eqine influenza?

Answer 31

* Inhalation * Infects epithelial cells of upper and lower airways: larygnitis, tracheitis, bronchitis, bronchiolitis - Incidence 0.8/100horses/month * No viraemia phase * Attaches to the epithelium via Haemagglutinin spike and gains entry to the cells * Styas within resp tract and therefore diagnosis will require sampling of this tract * Loss of ciliated epithelium, compromise of the mucocillary mechanism * May be associated with secondary bacterial infection * Severity of signs depends on dose of virus

Question 32

What is equine rhinovirus? Where is it most common?

Answer 32

* Picornavirus, types 1 and 2 * Role as a pathogen is controversial * can be isolated from asympomatic horses as well as those with signs of URTI – don’t know the importance of it * Most common in young horses

Question 33

What is the pathogenesis of equine viral arteritis?

Answer 33

* Transmission by respiratory and venereal routes * direct contact with an infected horse and its secretions * Reservoir of infections * Stallions that are chronic shedders and until they are castrated, will continue to spread disease * Prevalence of seroconversion * Thoroughbreds: 0.5 - 6% - severe signs if infected * Standardbreds: 80% - mild signs

Question 34

What does equine viral arteritis cause? (4)

Answer 34

NOTE: NOTIFIABLE * abortion and still birth * peripheral oedema * rhinitis and bronchitis/bronchiolitis * Respiratory signs mild * conjunctivitis and periorbital oedema

Question 35

Why is there variability of pathogenicity of EVA strains?

Answer 35

•Replicates in macrophages and endothelial cells and disseminates via the circulatory system

Question 36

What supportive treatment can we give for respiratory infections? (3)

Answer 36

* Rest * Improve environement - dust free management – to prevent IAD following this * Anti-pyretics

Question 37

How do we manage an EHV 1 outbreak according to the national trainers federation and TB breeders association?

Answer 37

* Impose isolation policy on premises * Serology on all in-contacts * Separate negative and positive horses, re-test two weeks later * Repeat until all horses have two negative samples * NB - these are totally voluntary schemes. Vets important fomite for spread of disease

Question 38

What are the neonate respiratory diseases?

Answer 38

* Neonatal septicaemia (bacterial pneumonia) * Viral pneumonia * Usually secondary and failure of passive transger plays an important part * Respiratory distress syndrome * Meconium aspiration * Aspiration pneumonia * Usually occurs with bottle fed foals, foals should not be bottle fed! * Haemothorax and pneumothorax * Central respiratory depression * Non-respiratory disease

Question 39

What are the risk factors for foal resp disease? (10)

Answer 39

Question 40

What is respiratory distress syndrome and what is it associated with (2)?

Answer 40

* Atelectasis (failure of lungs to expand) due to * inadequate surfactant function * structurally immature lung and muscles of respiration * associated with prematurity and dysmaturity * Maturity of lungs requires formation of surfactant to break down lung surface tenion so airways can be patent

Question 41

What is the pathogenesis of meconium aspiration?

Answer 41

* Stress in utero or during parturition leads to defecation, * meconium enters airways with fetal fluid, * aspirated when foal is born and starts breathing * chemical pneumonia develops – poor prognosis * secondary bacterial pneumonia

Question 42

What are the clinical signs of meconium aspiration? (2)

Answer 42

Respiratory distress Nasal discharge

Question 43

How can we diagnose meconium aspiration? (2)

Answer 43

* meconium staining * Faecal material down nostrils

Question 44

What can cause aspiration pneumonia in foals? (3)

Answer 44

* Dysphagia * neurological - uncommon, transient, manifestation of NMS * Cleft palate * Inappropriate bottle feeding * very common in sick foals with inexperienced nursing staff * Largely due to inappropriate poor management through bottle feeding! DO NOT BOTTLE FEED A SICK FOAL

Question 45

What are the common causes of PNEUMOTHORAX & HAEMOTHORAX in foals? (2)

Answer 45

* trauma at birth * rib fractures are common and affected foals are often asymptotic

Question 46

What is Perinatal Asphyxia Syndrome and when is it apparent?

Answer 46

* Ischaemia, oedema and reperfusion injury to foal’s brain, kidneys, intestine and other organs due to lack of oxygen * In utero hypoxia * Interruption of oxygen supply during birth * May not be apparent until the foal is 12-24 hours old * Severe cases may have central respiratory depression and might stop breathing completely

Question 47

What events often lead up to Perinatal Asphyxia Syndrome?

Answer 47

* Foals born through dystocia, get brain reperfusion after ischaemic event, results in multi organ failure * Born normal and within 12-24h, become a bit ill and then can become recumbent

Question 48

Why do we need to be careful with cardiac auscultation in foals? (4)

Answer 48

* not a sensitive diagnostic tool * extensive parenchymal disease may be unremarkable * normal foal lungs have harsh bronchovesicular sounds, little skin, don’t sound like normal adult horse lungs so often difficult to differentiate pathology from these * crackles are present in the ventral dependent side if in lateral recumbency

Question 49

What is this?

Answer 49

BACTERIAL & ASPIRATION PNEUMONIA Focal, bronchialveolar ventral and hilar area

Question 50

What is this?

Answer 50

ATLECTASIS Alveolar Premature foal No visible lung tissue, can only see cartilage enclosed main stem bronchioles

Question 51

What is this?

Answer 51

VIRAL PNEUMONIA Diffuse, Interstitial

Question 52

Why do we need to be careful when assessing MM colour?

Answer 52

* Cyanosis: \< PaO2 30 - 40 mmHg * Will only come when arterial oxygen below 40mmHg, wont see it above this

Question 53

What signs should we be looking out for in foal MM?

Answer 53

* Also looking for signs of sepsis: congestion/injection, petechiae * Results in congestive MM * Inappropriate MM vasodilation in a face of an animal that is hypovolaemic Right pic - pinna of ears with petechial haemorrhage

Question 54

Rather than a diagnosis, what is it more important to do in foals? (3)

Answer 54

* Identify sepsis * Determine need for respiratory support * Oxygen insufflation bottom pic * Top pic – sternal on a ventilator to improve lung function * Determine need for general supportive care

Question 55

What bacterial pneumonia is seen in weanlings\> (4)

Answer 55

* Strep. equi equi, * other Streptococcus spp. * Pasteurella / actinobacillus spp. * Rhodococcus equi

Question 56

What parasitic pneumonia is seen in weanlings?

Answer 56

•Parascaris equorum – important cause of mild nasal discharge to weanling – yearling age group, fairly normal sub mandibular LN, discharge whiter than creamy of strangles, not typically pyrexic. Also important cause of GI disease

Question 57

Where might Combined immunodeficiency syndrome be seen in weanlings and what is it?

Answer 57

* Seen in arabs * No B-cells or T-cells * As soon as maternal antibodies go – they get every infection going and often die

Question 58

What is the pathogenesis of Rhodococcus Equi?

Answer 58

* Inhaled pathogen * Ingested from soil (via faeces) * Foals 2-6 months of age * As Maternally derived Antibodies reduces * Intracellular survival * Likes to live within macrophages, so they cannot target it * Granuloma formation and abscess formation (bottom pic) * Respiratory, intestinal, sporadic, bone * Also non-septic synovitis * Farms that have this will usually get it year to year as lives in soil

Question 59

What is the problem with Parascaris Equorum?

Answer 59

* Not a major pathogen * Can cause transient nasal discharge as migrating through lungs

Question 60

What do foals with COMINBINED IMMUNODEFICIENCY SYNDROME present with?

Answer 60

•Affected foals frequently present with respiratory disease at around 2 months of age