Respiratory Flashcards
What are the 4 surfactant proteins produced by alveolar type II cells and what are their functions?
SP-A: hydrophilic and antimicrobial (from the collectin family) and provide innate defence mechanisms.
SP-B: hydrophobic, provides for low surface tension within the alveoli, preventing lung collapse
SP-C: hydrophobic, provides for low surface tension within the alveoli, preventing lung collapse
SP-D: hydrophilic and antimicrobial (from the collectin family) and provide innate defence mechanisms.
What are the common commensals of the URT and oral cavity in horses and the risk factors associated with their colonisation o the lower respiratory tract?
- Streptococcus spp
- Pasteurella spp
- E. coli
- Actinomyces spp
Oral cavity: - Bacteroides fragilis
- Fusobacterium spp
- Eubacterium spp
- Clostridium spp
- Veillonella spp
- Megasphaera spp
Risk factors for LRT colonisation: transport, stress, oesophageal obstruction, prolonged head elevation, aspiration.
Prolonged expiration with increased expiratory effort would make you suspicious of upper or lower airway obstruction?
Lower airway obstruction
What are the normal bronchial and vesicular sounds heard on thoracic auscultation and how may this change with airway disease?
Normal horse:
- Vesicular sounds may be barely audible or maybe “rustling” in nature if a patient is obese
- Vesicular sounds are heard over the middle and diaphragmatic lung lobes; these are the quietest
- Bronchial sounds are loudest and heard over the trachea and base of the lung
- Sounds heard more easily on the right than on the left
Abnormal horse:
- Bronchial sounds adjacent pathology may give the false idea of well ventilated pulmonary regions
- Breath sounds may be difficult to hear if there is alveolar over-inflation, pneumothorax or pleural effusion.
- Adventitious pulmonary sounds may be superimposed on the normal breath sounds :
* Crackles are short explosive and discontinuous sounds like cellophane crumpling, audible during inspiration.
* Wheezes light-pitched musical vibration of airways walls in inspiratory and expiratory phases.
* Pleuritic friction.
What are the landmarks for thoracocentesis?
Right side: 6-7th ICS 10cm dorsal to the olecranon, dorsal to the costochondral junction
Left side: 7-8th ICS 10cm dorsal to the olecranon, dorsal to the chostochondral junction.
Cranial border of the caudal rib to avoid the neuro-vascular bundle.
List the 4 thoracic radiographic patterns and their features.
- Interstitial: increased background opacity, non-specific and often associated with the early phase of disease. Can be normal in older horses.
- Alveolar: patchy and often with soft tissue dense areas that impair the ability to see the vascular structures and airways. Characteristic feature is air-bronchograms which characterise small airways and seen as a branching leucency with the airway wall not visible but opaque parenchyma due to fluid filling of alveoli. Eg pulmonary oedema, haemorrhage, consolidation, collapse
- Bronchiolar pattern is characterised by thickening of the bronchial structures with increased visibility of the bronchi. Increased opacity of the bronchial walls may be due to peribronchiolar infiltration of intraluminal exudate. This representes chronic disease with mineralised changes within the bronchiolar wall. A peribronchiolar pattern indicates inflammatory disease surrounding the bronchi such as ROA.
- Vascular pattern characterised by increased vascular pattern usually associated with pulmonary overcirculation in association with left-right shunt.
What do the following reflect:
A: Reduced dynamic compliance without a change in pulmonary resistance?
B: Increased pulmonary resistance without a change in dynamic compliance?
A: Pulmonary parenchyma is stiffened by alveolar disease or by obstruction of the peripheral bronchioles.
B: Obstruction exists in the respiratory tract but URT vs LRT is not differentiated.
What are the common differentials for secondary sinusitis?
- Dental disease to maxillary cheek teeth (6th)
- Sinus cyst
- Neoplasia
- Progressive ethmoid haematoma
- Trauma
- Mycotic infection
- Sino-nasal polyps
- Nasal epidermal inclusion cysts
What are the common bacterial and fungal causes of primary sinusitis?
Bacteria: Streptococcus spp, Staphylococcal spp, polymicrobial
Fungal: Coccidioides neoformans and Coccidioides immitis causing granulmoa
Where do progressive ethmoid haematomas arise?
The submucosa of the ethmoidal labyrinth.
What is the recurrence rate after surgical or medical treatment of progressive ethmoid haematomas?
Medical: 40% recur
Surgical: 20-50% recur
What important structures are in the medial versus the lateral compartment of the guttural pouch and how do you differnetiate the compartments in an image?
Medial compartment is 3 x bigger than the lateral
Med: internal carotid, CN IX, XI, XII, pharyngeal branch of CN X (along the floor) and cranial sympathetic ganglia. Rectus capitus ventralis and longus capitus muscles run medially to the pouch.
Lat: external carotid and maxillary artery, branches of CNVII, VIII and mandibular branch of CN V.
What is the suspected mechanisms behind development of guttural pouch tympany and which breeds and sex are thought to have a genetic predisposition?
Thought to be due to a mucosa flap (plica salpingopharyngeus) causing a one-way valve effect that prevents release of air and/or fluid from the affected guttural pouch. Other proposed mechanisms are persistent cough, metabolic dysfunction and upper airway infection (viral or bacterial)
A gender-specific quantitative trait locus has been identified in Arabian and German Warmblood horses, with fillies more affected than colts.
What are the common sites for mycotic plaques in the guttural pouches and potential different neurologic effects of each?
Roof of the medial compartment associated with the internal carotid artery. Neuro signs might include dysphagia, Horner’s. Less common sites are the lateral wall of the lateral compartment associated with the external carotid or external maxillary artery. Neuro signs might include facial nerve paralysis, peripheral vestibular signs.
What is the most frequently isolated fungal organism from guttural pouch mycosis?
Aspergillus fumigatus
List clinical signs that may be associated with GP mycosis?
- Epistaxis
- Dysphagia +/- aspiration pneumonia
- RLN
- Horner’s syndrome
- Head extension
- Parotid enlargement
- Facial nerve paralysis
- Mycotic encephalitis
- Atlantooccipital joint infections
List treatment options for GP mycosis
- Systemic itraconoazole
- Topical clotrimazole
- Laser salpingopharyngotomy
- Surgical vessel occlusion (coil or nitinol plug, balloon) - complications arise with the presence of aberrant vessels; success has been reported up to 84% survival with 71% return to performance
List the function and innervation of muscles controlling the tone of the soft palate and discuss abnormalities that occur with their dysfunction.
Tensor veli palatini: tenses the rostral aspect of the soft palate (mandibular branch of trigeminal nerve). Transection destabilises the rostral aspect of the soft palate causing inspiratory airway obstruction but not DDSP
Levator veli palatini: elevates the palate during swallowing (pharyngeal branch of vagus nerve)
Palatinus: shortens and depresses the palate (pharyngeal branch of the vagus nerve). Dysfunction causes DDSP
Palatopharyngeus: Shortens and depresses the palate (pharyngeal branch of the vagus nerve). Dysfunction causes DDSP
What are the reported success rates of various surgical interventions for DDSP?
Strap muscle resection and Llewellyn procedure success 58-73%
Conservative therapy success up to 61%
Surgical advancement of the larynx (tie forward) success 80-82%
Differentiate stertor and stridor and their likely origin in the respiratory tract
Stertor is a low pitch snoring sound that usually originates in the URT
Stridor is a high pitch sound associated with the LRT with the exception of recurrent laryngeal neuropathy, which causes stridor.
What is the prevalence of RLN in various breeds?
TB’s 1.6-8%
Draught breeds 42% (risk increases with increasing height in Belgian and Percherons but not Clydesdale)
List the Havemeyer grades for RLN
Grade I: all movements are normal, synchronous and symmetrical with full abduction achieved and maintained
Grade II: Arytenoid cartilage movements are asynchronous and/or the larynx is asymmetrical at times but full abduction can be achieved and maintained
Grade IIa: transient asynchrony, flutter or delayed movement seen
Grade IIb: asymmetry of the rima glottis much of the time due to reduced arytenoid and vocal fold mobility but there are occasions, particularly after swallowing or nasal occlusion where full abduction is achieved and maintained
Grade III: arytenoid cartilage movements are asynchronous and/or asymmetric and full abduction cannot be achieved.
Grade IIIa: Asymmetry of the rima glottidis much of the time but on occasions full abduction is achieved but not maintained
Grade IIIb: Obvious abductor deficit and arytenoid asymmetry; full abduction is never achieved
Grade IIIc: marked but not total arytenoid abductor deficit and asymmetry with little arytenoid movement. Full abduction never achieved.
Grade IV: complete immobility of the arytenoid cartilage and vocal fold.
What is the neuropathy associated with RLN? And what does it cause?
Chronic demyelinating peripheral neuropathy, attributed to its length. Causes progressive atrophy of the left dorsal cricoarytenoid muscle and associated loss of arytenoid cartilage abduction.
What is the reported success of the tie back procedure in race horses?
48-68%
What occurs with rostral displacement of the palatopharyngeal arch and what are the treatment options and prognosis?
Forward displacement of the fold of tissue (palatopharyngeal arch) over the apices of the arytenoid cartilage. May be associated with malformation of the laryngeal cartilages and the cricopharyngeal and cricothyroid muscles.
Tx: if severe enough to cause clinical signs of dysphagia, pevent deglutition and coughing, resection of the arch by surgery or laser can be attempted but historically this has not enabled successful athletic performance hence the prognosis is guarded.
What is nasopharyngeal cicatrix and what are the clinical signs?
Condition of upper airway inflammation and subsequent scarring of the pharynx, ostia to the guttural pouches, epiglottis and arytenoid cartilages. Geographically confined to Gulf Coast region of Texas as well as Mississippi, Louisiana and Florida. Clinical signs are airway noise, exercise intolerance and occasionally dysphagia. Nasal discharge may be seen during acute stages. With scarring you can get >50% airway obstruction. Removal from pasture and management on a dry lot is associated with no further disease progression; repeated bouts lead to further fibrous remodelling. Permanent tracheostomy is treatment of choice.
What are potential side effects of coil placement in treatment of guttural pouch mycosis?
Embolism of fungal plaque, air or clot to the cerebrum resulting in seizure and CNS dysfunction
Cerebral hypoxia if the occipital vessel comes off at an atypical location or the incorrect vessel is coiled; may manifest as seizure or other forms of CNS dysfunction
Thromboembolism in the maxillary artery - Tx is to coil the palatine artery to prevent travelling of the emboli.
How do you differentiate a colon of Strep equi equi from Strep equi zoo?
Strep equi is unable to ferment carbohydrate sugars, specifically lactose, sorbitol or trehalose. Some atypical strains may ferment some sugars but never sorbitol.
What immunity does infection with Strep equi equi afford to subsequent infections?
75% of horses will develop protective immunity against challenge for 3 - 5 yrs. However 25% fail to develop pathogen specific immunity and are hence susceptible to re-infection within months.
How long does bacterial shedding continue in cases of Strep equi equi?
4-6 weeks despite resolution of clinical disease relatively more quickly.
What is the incubation period from exposure to lymph node abscess formation for S. equi equi?
10-14 days
What host immune evasion mechanisms does S. equi equi have?
- The sortase-processed M protein confers antiphagocytic property in the form of acid-resistant fibrillar molecules that project from the bacterial surface
- Antiphagocytic activity is associated with the fibrinogen binding capacity of these protein moeities; blockage of the C3b-binding site inhibits the activity of the alternate complement cascade of C3 and C5 convertases
- The hyaluronic acid capsule further enables host evasion and limits host destruction as it mimics the host molecule that is present in mammalian tissues.
- The capsule is anti-phagocytic by virtue of its negative charge and hydrophilicity
- H factor (Se18.9)
- Mac Protein + indeterminate factor
Under which circumstances is antimicrobial treatment of Strep equi equi indicated?
IN horses with early clinical signs (lethargy, fever) in the absence of lymph node abscess formation, treatment with penicillin for 5 days may halt progression. Isolate++ (sufficient bacterial antigen to elicit a protective immune response will likely not have been produced, hence they remain susceptible).
- Don’t give during abscess formation antibiotics are contraindicated as they slow the progression of abscessation.
- Horses that are systemically ill or develop complications (dysphagia, pneumonia etc) should receive ABx.
What is purpura haemorrhagica and what relevance are the IgA titres?
A type III hypersensitivity leading to vasculitis that can occur after exposure to S. equi equi naturally or via vaccination. In this condition there is immune cmplex deposited in the vascular intima that results in marked oedema and necrosis. IgA titres will be markedly elevated against SeM-like proteins and culture supernatant compared with IgA titres in horses with uncomplicated strangles.
What are the main reported complications of Strangles?
- Purpura haemorrhagica
- Bastard strangles
- Endocarditia
- Myocarditis
- Cardiac conduction abnormalities.
- Myositis (infactive purpura haemorrhagica)
These later 4 may be associated with primary colonisation or secondary immune-mediated inflammatory disorders.
Why S. equi equi vaccination not necessarily reliably for provision of immunity?
Vaccination leads to circulating antibodies however these are not necessarily protective because local mucosal immunity plays a significant role in the resistance to infection.
What is the vaccination protocol for strangles?
Submucosal vaccine (Equilis StrepE) (approved in Europe): 2 doses 4 week intervals followed by boosters every 3mo in high risk areas. Intranasal vaccine: 2 doses at 2 week intervals followed by annual booster
What are the two equine influenza type A strains and which one is clinically relevant today?
H7N7 and H3N8.
H3N8 hasn’t been isolated since the 1980’s.
What is the pathogenesis of equine influenza?
Inhaled virus infects respiratory ciliated epithelium leading to loss of mucociliary escalator for pathogen and particle clearance.
Incubation period is 1-3 days
High fever, depression and paroxyssmal coughing is seen
Nasal discharge may initially be serous and change to more mucopurulent with disease progression
Submandibular lymphadenopathy is common.
Myositis, anorexia and persistent cough are common.
What diagnostic methods are available for equine influenza?
- Virus isolation
- Influenza A antigen detection (need baseline and convalescent samples with rising titre)
- Real-time PCR (ideally nasopharyngeal lavage sampling rather than simply nasopharyngeal swab)
Which equine influenza clades should be included in a vaccine schedule?
Clade 1 and Clade 2 ideally; clade 1 involved in most recent UK outbreak.
In addition to the influenza strain, what influences vaccine efficacy?
Presence of antigenic adjuvants which enhance the chances of cross reactivity among strains.
What are the clinical findings with EHV1 and EHV4?
Typically induce pyrexia, serous nasal discharge and occasionally cough. Lymphadenopathy and serous ocular discharge may be seen.
Respiratory disease is usually worse in young horses
EHV4 is more common than EHV1.
In pregnant mares, infection with EHV-1 may result in abortion 2-12weeks later (often with no preceding signs of illness). In rare cases EHV myelitis may develop.
What diagnostic methods are available for EHV and what are the limitations?
- Virus isolation from URT swab/lavage and buffy coat samples is the gold standard. (EDTA blood)
- q-PCR testing (EDTA blood)
- Paired serum collected 12-21 days apart for virus neutralisation and ELISA for serology - main limitation with this is that in cases of mares that abort or with EHV myelitis the initial immunologic response is rapid and has often already occurred when the first sample is obtained so the convalescent sample typically declines rather than inclines. Particulalry in mares that abort as the viraemia was typically some time previous.
- Virus isolation and histology from aborted foetuses/perinatal deaths
Is there benefit to using antivirals and if so which ones and in which cases?
Valacyclovir is the most effective. Probably limited benefit in most cases of EHV however exceptions would include sick neonates and adults with EHM in which it may have some benefit although likely the best use of it would be prophylactically in unaffected horses that are in contact/vicinity of affected horses if there is an outbreak of EHM, for preventing additional cases.
