Respiratory Flashcards
What can be achieved by endoscopy in a respiratory case
In horse can visualise nasal passages, guttaral pouch, nasopharynx, soft palate, larynx and trachea. In SA only see trachea, mainstem bronhci and large division of main bronchi. Can also: > tracheal wash > guided bronchoalveolar lavage > cytology brushes > Biopsy discrete lesions > retrieval of foreign bodies
What are the methods of diagnosis of bacterial respiratory problems in horse
> Nasopharyngeal swab - specific organisms not normal to the commensal of pharynx e.g strep equi equi
> Guttural pouch lavage - lavage and reaspirate
> Endoscopically guided tracheal aspirate - Visualise thorasic inlet where fluid fluid accumulates and insert 30 mls of saline. Representative of the whole lung however contaminated by pharyngeal flora.
> Trans-Tracheal aspirate - incision site at lower third of trachea, catheter advanced between cartilaginous rings. This eliminates pharyngeal contamination, also useful in young foals that cant handle large endoscope. However if horse coughs then catheter contaminated and can cause subcutanoes emphysema
> Broncho-alveolar lavage - Tube advanced until wont advance anymore and balloon inflated. 100-200ml of saline used.
Whats the role of anticholinergic and B2 agonists
bronchodilators
What does an opoid receptor agonist achieve
prevents cough
How do you distinguish between upper and lower airway cough
Upper - Harsh, loud and non productive cough ( larynx upwards)
Lower - Soft, muted productive cough
what are differentials for inspiratory and expiratory distress
Inspiratory:
> Extra-thoracic non fixed airway obstruction - Laryngeal hemiplasia ( Lack of innervation causes atrophy of the dorsal cricoarytenoid muscle (left) causing the arytenoid cartilage to flap into larynx) or soft palate disorders
> Restrictive diseases - Limit lung expansion e.g p[leural effusion
Expiratory distress:
> Intra-thoracic airway obstruction - Severe equine asthma or tracheal collapse
Inspiratory and expiratory = Intraluminal mass/foreign body
What are the differentials for orthopnea (difficults breathing while recumbant)
> Pleural effusion
Diaphragmatic hernia
Congestive heart failure
What does nasal discharge indicate
> Can be serous, mucoid, purulent or haemorrhagic
Unilateral discharge tends to originate rostral to the caudal end of the nasal septum
Bilateral tends to be from caudal structures
Foul odour indicates anaerobic infection, necrotizing condition or connection to oral cavity (rotten tooth)
What are differentials for stridor
Stridor is intense respirtory sounds heard without a stethoscope.
> Fixed/dynamic obstruction - Laryngeal paralysis, stenotic/paralysed nerves, nasal masses or soft palate elongation
What is primary and secondary atelectasis
Primary - Failure of lung to expand at birth
Secondary - Aquired atelectasis. Collapse of all/part of the lung was previously ventilated. Occurs due to compression (air, mass or fluid) or obstruction
What are the 3 types of emphysema
Emphysema = Excessive air in the lungs
- Alveolar - Permanent abnormal enlargement of air spaces distal to the terminal bronchioles, due to obstruction of alveolar wall by neutrophilic enzymes (elastase)
- Interstitial - Air forced into septal lymphatic due to forced expiration.
- Compensatory - Emphysema adjacent to area of consolidation
Name 3 types of circulatory disorders
- Hyperaemia - increased inflow of oxygenated blood, normal venous return
- Congestion - Normal inflow, Decreased outflow leading to an increase in deoxygenated blood.
- Oedema - Pulmonary oedema is flooding of alveoli , mixes with surfactant causing foam which compromises ventilation. Can be caused by:
> Cardiogenic - pressure overload due to LHS heart failure
> Neurogenic - Sympathetic stimulation in acute brain damage resulting in increased pulmonary capillary hydrostatic pressure
> Excessive fluid therapy - Damage to endothelium or epithelium, can be due to toxic substance e.g smoke
Describe bronchopneumonia
Caused by a bacterial infection causing lesions in the cranio-ventral regions of the lung due to increased deposition of infectious agen under gravity, then spreads lobule to lobule. 3 possible outcomes:
- Resolution - Resolves in 7d, back to normal in 3w
- Deteriation - Abscess formation (due to pyogenic bacteria), Pleuritis ( in severe fibrinous pneumonia) or death due to hypoxaemia
- Persistence - Fibrosis and bronchiectasis ( permanent dilation of bronchi due to irreversible damage to walls)
Describe broncho-interstitial pneumonia
Caused by inhaled mycoplasmas and some viruses. Inflammation of bronchioles. Interstitial lymphocytic proliferation results in complete lymphoid follicles around airways
Describe interstitial pneumonia
Secondary to haematogenous. Inflammation centred on interstitial septa rather than airways. Diffuse distribution. Can be caused by distemper virus.
What is ‘fog’ fever
Also known as acute bovine pulmonary oedema and emphysema. cattle moved to fast growing lush pasture , causing the ingestion of tryptophan. metabolised to 3-methyl indole which is toxic to type 1 pneumocytes causing pulmonary oedema and emphysema
Whats the cause of undifferentiated bacterial pneumonia in foals and yearlings, clinical signs, diagnosis and treatment
Caused by:
> Strep.zooepidemicus (most common)
> actinobacillus
> s.aureus
Clinical signs:
> cough
> mild pyrexia
> auscuitable changes
Diagnosis: Mucopurelent exudate in trachea on endoscopy. Tracheal aspirate yields increased neutrophils (degenerate) & bacteria
Treatment: Antibiotics that are effective against strept zooepidemicus. can do culture sensitivity test, dust free environment.
What Infectious agents cause URT and LRT issues in foals and yearlings
URT
> EHV 1 & 4
> Equine influenza
> Strept. equi equi
LRT > EHV 1 & 4 > equine influenza > rhodoccus equi > strept. equi equi
Describe the main differences between upper and lower airway disease in horses
Upper airway disease:
> most common in young horses 2-3 years ( immunologicaly naive)
> clinical signs include fever, nasal discharge, coughing and enlarged submandibular lymph nodes.
Lower airway disease:
> Common in race horses
> bacterial cause more often
> CS: coughing, poor performance, mucoid tracheal secretions and + or - nasal discharge and fever
Whats the result of equine herpes virus 1 & 4
75% of horses thought to have latent infection ( sites of latency include bronchial LN, submandibular LN and trigeminal nerve. EHV -4 mainly respiratory
> First exposed as foals by lactating mare
> Immunity only last 3-5 months, hence a vaccine is useless
> Infection during final trimester of pregnancy causes placental vasculitis (EHV-1)
> Replicate in URT (causing URT signs)and disseminate to LRT
Describe the result of equine influenza and how its diagnosed
> Most common cause of URT infection.
Immunity short lived, vaccine can supress clinical signs but still shedding
Short incubation (1-3 days) then spread to URT, causing loss of ciliated cells predisposing to secondary bacterial infection e.g strep zooepidemicus
Diagnosis
> tracheal aspirate yields increased mucous and degenrate neutrophils.
> Neutrophilia indicates secondary bacterial infection
> Lymphocytosis indicates viral infection
> Nasopharyngeal swab (PCR) or paired serology (10d apart)
Treatment - Nsaids, hydration, isolate, limit stress, symptomatic
Describe mild equine asthma
Also known as inflammatory airway disease.
> Common in young race horses
> Characterized by excess mucous in airways and possible cough/reduced performance.
> NO increased RR at rest
> Causes include dusts, ammonia and LPS (bacterial infections)
> Diagnosed by increased mucous production and on BAL increased mucous + neutrophils/mast cells or eosinophils
Treatment
> Reduce airway inflammation
> Bonchodilators (clenbutarol)
> Reduce dust
Describe severe equine asthma
Also known as Recurrent airway obstruction (RAO)
Due to hypersensititvty of inhaled substances
> Naturally occuring Lower airway disease characterized by periods of reversible airway obstruction
> Neutrophil accumulation, mucous production and bronchospasms.
> Lifelong condition usually effecting over 7 years old
> Results in respiratory distress and increased respiratory effort (double expiratory effort)
Diagnosis by BAL, want to rule out bacterial pneumonia as this is major ddx, increased cellularity, especially non degenerate neutrophils
What is strangles, what are the 3 possible clinical presentations
Caused by Streptococcus equi equi. If born from an immune mare will be resistant for 3 months. Mostly effects 1-5 year olds. Transmitted by direct contact of nasal secretions/LN discharge or on fomites (1-3 days). Horses can be asymptomatic chronic carriers (in guttural pouch) for 5-6 months). 3 clinical presentations:
- Classic acute - Causes fever, depression, innapetence, lymphadenopathy, abscessation of mandibular, parotid and retropharyngeal LN (rupture in 7-10d), mucoid to purulent nasal discharge and abscess can compress larynx causing dyspnoea.
- Atypical - Mild inflammation of the URT causing slight nasal discharge, cough and fever. Dangerous because it present as a typical URT infection and can be treated with antibiotics and clears up. Therefore never diagnosed and horse becomes latenly infection shedding bacteria into environment.
- Complication - Internal abscessation - Intermittent colic, pyrexia, anorexia, depression and weight loss.
Purpura haemorrhagica - Generalised vasculitis caused by type III hypersensitivity. Thrombi of small arteries cause skin and muscle necrosis, ventral limb oedema, and guttural pouch emphysema and chondroids (lumps of pus)
How is strangles diagnosed, treated and how is a outbreak managed
Culture & PCR from LN pus or nasopharyngeal swab. 3x swab a week apart.
Treatment - dependent on stage of disease
> Exposed horse - penicillin until isolated
> Early clinical signs - Penicillin, soft food and pyretics
> LN abscess present - Hot water and swab to encourage abscess to burst + antibiotics.
> Abdominal abscess - Long term antibiotics
> Guttural pouch emphysema - Drainage via pharyngeal opening or surgical drainage+ antibiotics
> Purpura haemorrhagica - Penicillin, prednisolone, fluids and any palliative treatment.
> Carriers - Guttural pouch lavage + topical benzypenicillin gelatin - sticks to wallks killing bacteria, repeated in 2 weeks.
- Conformation of resolution when 3 negative PCR nasopharyngeal swabs 7d apart.
What is Rhodococcus equi, what are the clinical signs, how is it treated and prevented
Seasonal challenge in the late spring/summer as theres an increase in aerosol challenge to susceptible foals. Causes bronchopneumonia with wide spread abscess formation.
clinical signs - Anorexia, depression, fever, dyspnoea, tachypnoea and cough.
Can also present with GI signs, an ulcerative enterocolitis, mesenteric lymphadenitis, abscess formation and 2nd peritonitis.
Treated with clorithromycin and rifampin
> If total added diameter <8cm then 75% resolve with no tx
Prevent with increased ventilation, dusty condition, collect manure, isolate sick foals, rotate pasture and can prophylacticly use hyperimmune plasma
Why is equine rhinitis virus maybe not significant
Can be isolated in asymptomatic horses as well as those with mild URT/LRT signs. Treat symptomatically
Describe the pathogenesis of equine viral arteritis, clinical signs, and diagnosis
Notifiable venereal disease of stallions. Incubation of 3-14 days. Replicates in macrophage then spread to LN's causing a leucocyte associated viraemia. Clinical signs: > Fever > Abortion > anorexia > oedema > Conjunctivitis > coughing and nasal discharge
Diagnosed by blood sample, semen or nasal swabs
Treated symptomatically
What is EIPH
Exercise induced pulmonary haemorrhage.
> haemorrhage originates from pulmonary vessels in the caudodorsal lung lobes. Originates here because there high blood flow and mechanical forces transmitted to lung are greatest here.
> Cardiac output + pulmonary vascular pressure increase 10x during exercise. Failure occurs at 100mmHg but PA pressure reaches 120mmHg during exercise
> Predisposed by age, LRT disease (e.g equine asthma), URT obstruction and cardiac disease
What makes up the kennel cough complex, what are the clinical signs and what is the treatment/prevention
Also known as canine infectious disease (CIRD) complex. Mainly due to canine parainfluenza virus and bordetella bronchiseptica. Also canine adenovirus, coronavirus and mycoplasmas can contribute.
Clinical signs: Cough, retching, nasal/occular discharge and sneezing. usually resolve in 1-3 weeks. A secondary bacterial infection can cause bronchopneumonia and systemic disease. If it doesnt resolve in 2 weeks then tracheal-broncheal wash used, PCR to rule out distemper and culture sensitivity with charcaol.
Treatment: Rest, antibiotics, cough suppresant (opoid agonist), mucolytics and bronchodilators
Prevention via live attenuated vaccine (can cause clinical signs) given intranasaly to induce high IgA = stopping at an early stage.
