ECEIM Respiratory Diseases Flashcards
1
Q
What are the 4 surfactant proteins producted by alveolar type II cells and what are their functions?
A
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.
2
Q
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?
A
- 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.
3
Q
Prolonged expiration with increased expiratory effort would make you suspicious of upper or lower airway obstruction?
A
Lower airway obstruction
4
Q
What are the normal bronchial and vesicular sounds heard on thoracic auscultation and how may this change with airway disease?
A
Normal horse:
- Vesicular sounds may be barely audible or may be “rustling” in nature if patient is obese
- Vesicular sounds area 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 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 celophane crumpling, audible during inspiration)
5
Q
What are the landmarks for thoracocentesis?
A
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.
6
Q
List the 4 thoracic radiographic patterns and their features.
A
- 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.
7
Q
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
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.
8
Q
What are the common differentials for secondary sinusitis?
A
- Dental disease to maxillary cheek teeth (6th)
- Sinus cyst
- Neoplasia
- Progressive ethmoid haematoma
- Trauma
- Mycotic infection
- Sino-nasal polyps
- Nasal epidermal inclusion cysts
9
Q
What are the common bacterial and fungal causes of primary sinusitis?
A
Bacteria: Streptococcus spp, Staphylococcal spp, polymicrobial
Fungal: Coccidioides neoformans and Coccidioides immitis causing granulmoa
10
Q
Where do progressive ethmoid haematomas arise?
A
The submucosa of the ethmoidal labyrinth.
11
Q
What is the recurrence rate after surgical or medical treatment of progressive ethmoid haematomas?
A
Medical: 40% recur
Surgical: 20-50% recur
12
Q
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?
A
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.
13
Q
What is the suspected mechanisms behind development of guttural pouch tympany and which breeds and sex are thought to have a genetic predisposition?
A
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.
14
Q
What are the common sites for mycotic plaques in the guttural pouches and potential different neurologic effects of each?
A
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.
15
Q
What is the most frequently isolated fungal organism from guttural pouch mycosis?
A
Aspergillus fumigatus
16
Q
List clinical signs that may be associated with GP mycosis?
A
- Epistaxis
- Dysphagia +/- aspiration pneumonia
- RLN
- Horner’s syndrome
- Head extension
- Parotid enlargement
- Facial nerve paralysis
- Mycotic encephalitis
- Atlantooccipital joint infections
17
Q
List treatment options for GP mycosis
A
- 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
18
Q
List the function and innervation of muscles controlling the tone of the soft palate and discuss abnormalities that occur with their dysfunction.
A
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
19
Q
What are the reported success rates of various surgical interventions for DDSP?
A
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%
20
Q
Differentiate stertor and stridor and their likely origin in the respiratory tract
A
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.
21
Q
What is the prevalence of RLN in various breeds?
A
TB’s 1.6-8%
Draught breeds 42% (risk increases with increasing height in Belgian and Percherons but not Clydesdale)
22
Q
List the Havemeyer grades for RLN
A
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.
23
Q
What is the neuropathy associated with RLN? And what does it cause?
A
Chronic demyelinating peripheral neuropathy, attributed to its length. Causes progressive atrophy of the left dorsal cricoarytenoid muscle and associated loss of arytenoid cartilage abduction.
24
Q
What is the reported success of the tie back procedure in race horses?
A
48-68%
25
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.
26
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.
27
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.
28
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.
29
What immunity does infection with Strep equi equi afford to subsequent infections?
75% of horses will develop protective immunity against challenge for 5+ yrs. However 25% fail to develop pathogen specific immunity and are hence susceptible to re-infection within months.
30
How long does bacterial shedding continue in cases of Strep equi equi?
4-6 weeks despite resolution of clinical disease relatively more quickly.
31
What is the incubation period from exposure to lymph node abscess formation for S. equi equi?
10-14 days
32
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
-
33
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**
* Note: 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.
34
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.
35
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.
36
Why is 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.
37
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
```
38
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.
39
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.
40
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)
41
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.
42
In addition to the influenza strain, what influences vaccine efficacy?
Presence of antigenic adjuvants which enhance the chances of cross reactivity among strains.
43
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.
44
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
45
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.
46
List clinical signs associated with EHV2
- Pulmonary inflammation
- Keratoconjunctivitis
- Fever
- Pharyngitis
- Inappetence
- Immunosuppression
- Lymphoma
- Lymphadenopathy
47
What is the suggested link between EHV2 and EHV1 or other respiratory pathogens?
EHV2 modulates the immune function hence may increase susceptibility to other pathogens, and may even promote EHV1 recrudescence.
48
What are the clinical signs of equine multinodular pulmonary fibrosis (EMPF)?
- Fever
- Abnormal pulmonary sounds (increased bronchovesicular sounds, tracheal rattle, wheezes)
- Oral cavity ulcerations
- Lymphadenopathy
- Reluctance to ambulate, presumably due to pain
- Keratoconjunctivitis.
49
What are some common differentials to EMPF when assessed radiographically or ultrasonographically?
Metastatic neoplasia
Fungal granulomas
Granular cell tumour
50
What is the main differential for EMPF based on BAL cytology?
RAO - in fact EMPF should be suspected in cases of RAO that don't respond to appropriate therapy and environmental management.
51
What are the characteristics of the two types of EMPF and the histologic findings of these?
Disseminated nodular form: multifocal, coalescing fibrotic nodules are present throughout all lung fields with lesions ranging from 1-5cm.
Discrete nodular form: large discrete nodules are separated by normal-appearing pulmonary parenchyma. These nodules can be up to 8-10cm diameter.
Both types histologically are characterised by marked interstitial fibrosis with type 2 pneumocyte hyperplasia. Alveoli are often filled with neutrophils and fewer alveolar macrophages, multinucleated giant cells and eosinophilic proteinaceous material. There may be intranuclear inclusions consistent with herpes virus in macrophages or epithelial cells.
52
What are the treatment options for EMPF and what are poor prognostic indicators?
Treatment: broad spectrum antibiotics, anti-inflammatories including dex, oxygen therapy if hypoxic and antiviral therapy may be useful (high end dosing of valacyclovir 30-40mg/kg PO TID).
Pulmonary hypertension is a poor prognostic indicator.
53
What is the comparable condition to EMPF in donkeys?
AHV-5 causing pulmonary fibrosis in donkeys.
54
How is the equine arteritis virus maintained in equine populations, specifically in which tissue/glands?
Maintained in carrier stallions, requires testosterone. Specifically within the ampulla and vas deferens
55
What is the incubation period for EVA and how might this vary?
2-14 days; more rapid course of disease with venereal transmission.
56
What is the underlying lesion in cases if EVA?
Vasculitis. Results in oedema secondary to damage to the tunica media of small arteries and venules.
57
What are the two most important implications of infection?
Abortion in pregnant mares
| Induction of carrier state in entire males
58
What are the characteristics of abortion with EVA?
Typically occurs late in the clinical disease or early convalescence and associated with a non-viable autolysed foetus.
Rarely neonates may be infected, demonstrate respiratory difficulty and die.
59
What is the risk of vaccination for EAV?
There are 2 vaccines (modified live and inactivated) - if using the modified live vaccine viral shedding can occur post-vaccination so it is important for horses to be isolated for 21 days post vaccination.
This vaccine is not recommended for pregnant mares for this reason
60
What are the vaccination recommendations for EAV?
- Vaccinate all at risk individuals, in particular colts <280 days of age
- Colts and stallions need to be determined to be serologically negative prior to vaccination, then isolated for a minimum of 21-28 days post-vaccine
- MLV requires 1 dose then annual re-vaccination
- Inactivated vaccine requires 2 doses 3-4 weeks apart with isolation during this period, then semiannual boosters.
61
What are the implications of breeding mares to a carrier stallion?
- Only ever breed seropositive or vaccinated mares to carrier stallions
- They must be isolated for 21 days after breeding as they may become viraemic despite being seropositive and can shed virus however won't develop clinical signs of EAV.
62
List the different picornaviruses and the clinical manifestation.
Equine rhinitis virus A (Aphthovirus)
Equine rhinitis virus B types 1-3 (Erboviruses)
These cause respiratory disease manifest as pyrexia, serous to seromucous nasal discharge, coughing, depression, anorexia, pharyngitis and submandibular lymphadenopathy.
63
What are the four clinical syndromes associated with African Horse Sickness?
Peracute: Pulmonary form, incubation 5 days; mortality rate is 95%. Fever, haemorrhagic pulmonary fluid exudate from pulmonary oedema and hydrothorax.
Acute: Mixed. More common and includes pulmonary and cardiac abnormalities. Incubation is 7 days, mortality 50-95%. Cardiac and pulmonary disease (oedema of the head and neck, cough, respiratory distress and pulmonary oedema).
Subacute: Cardiac. Myocardial dysfunction, fever, oedema, lethargy, oedema of supraorbital fossa. Generally less clinically severe but mortality still >50%
Mild: (Horse sickness fever) Develops in reservoir species (zebra etc) or partially immune horses and is associated with mild fever.
64
What diagnostic methods are available for AHS and what prevention methods?
Diagnosis: serology and virus isolation as well as PCR.
Inactivated vaccine available and used in endemic areas. It contains 5 of the 7 strains of AHSV (AHSV 5 and 9 omitted for safety concerns)
65
Which body fluids are Hendra virus excreted in?
Urine, saliva and respiratory secretions
66
What are the typical and non-specific clinical signs of Hendra virus?
- Respiratory dysfunction: dyspnoea, vasculitis and pulmonary oedema with frothy nasal discharge
- Neurological dysfunction: vasculitis, ataxia, encephalitis, subcutaneous oedema
- Colic: generalised signs of GIT discomfort
Non-specific signs: lethargy, anorexia, fever, tachycardia, oedema. Per-acute death may be noted with no clinical signs identified.
67
What is the typical disease progression of bacterial colonisation of the lower respiratory tract?
Initial colonisation of the primary airways causing bronchitis, which may progress into the surrounding pulmonary parenchyma, and then may progress further into the pleural space.
68
What are some differentials for pleuropneumonia?
- Septic infection
- Trauma (with or without secondary infection)
- Neoplastic causes (Eg lymphoma?)
- Congestive heart failure
- Parasitic disease (Eg hydatid cysts)
69
What clinical findings would suggest a pulmonary infarction?
Marked pulmonary consolidation in combination with serosanguineous pleural fluid and epistaxis
70
What are the main differentials for gas echoes within the pleural space?
- Anaerobic gas-producing bacteria within the fluid
- Rupture of a bronchopleural fistula
- Iatrogenic following thoracocentesis
71
How much pleural fluid accumulation would indicate pleural drainage is necessary?
>3cm
72
What are the main risks with rapid pleural drainage?
- Re-expansion pulmonary oedema
| - Hypotension
73
What is the rationale for performing cytology, culture and sensitivity on both pleural and tracheal aspirate samples?
- The tracheal aspirate is likely the primary site and this may provide superior diagnostic information
- Different bacterial populations, in particular different predominant species may be present in each site
- Polymicrobial infections are common
74
What factors associated with pleuropneumonia indicate a more guarded prognosis?
- Presence of anaerobic infections
- Presence of MDR species such as Klebsiella
- Presence of moderate-marked fibrin deposition in the pleural space
75
How often should airway (incl pleural fluid) sampling be performed during treatment of pleuropneumonia?
Every 10-14 days to identify changes in microbial populations
76
What does coughing or expectoration of pleural or lavage fluid from the nares indicate during thoracic lavage? And what diagnostic test could you do to confirm this?
Presence of a bronchopulmonary fistula
| Instillation of fluorescein dye into the pleural space may help to confirm this - presence at the nares confirms.
77
In cases where thoracotomy is indicated, what is the average time of intervention? And what are the implications if this is done too early?
Approximately 60 days into the disease course.
Early intervention may result in bilateral pneumothorax, haemorrhage and removal of viable lung which can have catastrophic case outcome.
78
How can you determine whether a patient is likely to tolerate thoracotomy/whether the mediastinum is complete?
Leave the thoracic drain open on one side for at least 2 hours and monitor for the development of bilateral pneumothorax, and also ensure that the patient can handle unilateral pneumothorax.
79
What are some clinical signs that suggest a mediastinal abscess?
Standing with forelimbs pointed
Evidence of jugular vein occlusion with prominent pulsations
Marked pectoral oedema
80
What is the reported prognosis for recovery and return to athletic function in horses with pleuropneumonia and what influences this?
Prognosis for recovery ranges from 43-95%
Prognosis with fibrin accumulation was 68% and without was 100% survival in one study.
Likelihood of return to athletic function is around 60%
81
What is the pathogenesis of silicosis?
- Inhalation of the toxic agent results in alveolar damage, cell death and increased permeability at the alveoli.
- Pulmonary congestion, interstitial oedema, erythrocyte extravasation and alveolar oedema occur during the exudative phase
- Alveolar infiltrates with inflammatory leucocytes and fibrin and increased permeability lead to fluid accumulation, impairing gas exchange (resp distress)
- Respiratory distress, injected mucous membranes and impaired pulmonary function results.
In subacute and chronic cases:
- Alveolar regeneration with type II pneumocyte proliferation replaces the damaged type I pneumocytes.
- Fibroplasia leads to cellular proliferation and septal thickening, fibrous development and reduced compliance.
- Horses are in respiratory distress with laboured breathing, dark mucous membranes, poor pulse quality and tachycardia.
82
What is the treatment for silicosis?
Improving oxygenation is the mainstay
Anti-inflammatories including steroids, particularly inhaled corticosteroids.
Bronchodilators may be useful - ideally B2 adrenergic receptor agonists
83
What are the common opportunistic and pathogenic fungi associated with fungal pneumonia?
- Aspergillus is the most common isolate and is opportunistic
Primary pathogens include:
- Blastomyces dermatitidis
- Coccidioides immitis (uncommon in horses but may be seen in regions of sandy alkaline soil and warrants a guarded prognosis)
- Histoplasma capsulatum (horses usually considered resistant to infection but disease has been reported)
- Cryptococcus neoformans
- Candida albicans (may complicate sepsis in neonates)
84
What is a common haematological abnormality in horses and humans with fungal pneumonia?
Neutropenia (may be a risk factor for disease manifestation)
85
What are the clinical signs of equine fungal pneumonia?
- Tachypnoea
- Fever
- Nasal discharge
- Epistaxis
- Nasal plaques or erosions
- Abnormal lung sounds
- Pleural friction rubs
86
How is fungal pneumonia definitively diagnosed?
Culture and histology of pulmonary biopsies.
87
What is the treatment for fungal pneumonia?
Amphotericin B is a polyene antibiotic that combines with ergosterol in the fungal cell wall to enhance membrane permeability. However it is a hazardous drug with adverse events including anorexia, phlebitis, cardiac arrhythmias, nephrotoxicity, hepatic dysfunction and hypersensitivity reactions. However it is considered a reasonable choice and may be successful.
Benzimidazole derivative drugs may be effective against fungal pathogens by inhibiting ergosterol synthesis in the cell membrane. Some success with topical and or systemic use is reported.
Iodide-containing agents have limited evidence to demonstrate efficacy but have apparent efficacy against some granulomatous disease and may have anti-inflammatory properties.
88
What are the typical radiographic findings with parasitic pneumonia?
Bronchointerstitial pattern or granuloma/abscess formation in advanced disease
89
What are the two diagnostic tests for the two common respiratory parasites?
Faecal floatation for D. arnfieldi
| FWEC for P. equorum (although it is larval migration rather than adults for this parasite)
90
What is the treatment for parasitic pneumonia in foals?
Ascarids: Initial low dose fenbendazole (5mg/kg) and if this is tolerated, 5 days of daily 10mg/kg. Pyrantel and ivermectin may be useful depending on resistance patterns in a geographic area. However, pyrantel only kills intestinal parasites not migrating ones. An initial course of fenbendazole followed 14 days later by an avermectin is an appropraite treatment protocol for both intestinal and pneumonic parasites
D. arnfieldi: ivermectin, moxidectin, thiabendazole, levamisole
91
In general, what are the cytokines associated with RAO clinical signs and what treatment is advised?
Inflammatory cytokines released by activated T lymphocytes increase the pulmonary concentration of IL4 and IL8. IL8 primarily is responsible for the recruitment of neutrophils which maintains a heightened level of immune reactivity in the lungs, contributing to enhanced mucous production, bronchospasm and coughing. Hence corticosteroids act as direct inhibitors of this inflammatory cycle.
92
What is the relative potency of inhaled corticosteroids?
Fluticasone > beclomethasone > flunisolide = triamcinolone.
When compared with dexamethasone if Dex has a standard of 1, fluticasone=18, beclomethasone 13.5, triamcinolone 2 and flunisolide 1.9
93
Why does inhaled fluticasone result in reduced adrenal suppression and systemic side effects?
Low oral bioavailability (<2%) so any swallowed aerosolised drug is barely absorbed
Extensive first pass metabolism (99%)
94
What are the most effective bronchodilators for horses with RAO?
B2 adrenergic agonists (eg albuterol and clenbuterol) and parasympatholytic/anticholinergic agents (eg ipratropium or buscopan.
For rescue treatment short acting B2 adrenergic agonists such as albuterol are ideal, as well as atropine or buscopan.
95
What is the rationale against long term use of bronchodilators alone?
With chronic administration B2 adrenergic agonists produce deterioration in pulmonary function, increased airway responsiveness and more frequent exacerbations of bronchoconstriction.
96
When might mast cell stabilisers be indicated?
Horses with IAD characterised by increased mast cell percentage may benefit from mast cell stabilisers such as sodium cromoglycate which blocks Ca channels resulting in stabilisation rather than degranulation, hence inhibiting release of histamine and tryptase.
97
What is the pathophysiology of EIPH?
Pulmonary capillary stress failure due to high pulmonary capillary pressure and very low inspiratory alveolar pressures that occur during intense exercise. Hence the pulmonary capillary transmural pressure is extreme at times of intense, strenuous exercise leading to tissue failure and haemorrhage. The critical point at which stress failure occurs appears to be when capillary pressure exceeds 75-100mmHg.
98
What is the mechanism behind disease progression with EIPH?
With repeat episodes of EIPH veno-occlusive remodelling of pulmonary veins can occur. This happens in intralobar pulmonary veins with the presence of collagen deposition, smooth muscle hypertrophy and intimal hyperplasia within the pulmonary veins. The end result of veno-occlusive remodelling is increased stiffness with reduced vascular compliance. With increased cardiac output and continue high pressure from the pulmonary arterial vasculature, tissue failure can continue and potentially worsen over time, leadnig to propagation of tissue failure and haemorrhage into the alveolar spaces and surrounding interstitium.
99
How long do RBCs last in the airway and how long do haemosideriphages last post haemorrhage?
RBCs should be cleared within 7-14 days
It takes less than 7 days for haemosiderophages to be stimulated and they typically last for 3 weeks. *Note: haemosiderophages will be present in small numbers in normal horses too, it is their relative abundance that determines EIPH.
100
What recurrence rate is expected with EIPH?
After one episode, a recurrence rate of 13% is reported.
101
What is the common radiographic finding in horses with EIPH?
Typically caudo-dorsal lungs affected with alveolar or mixed interstitial opacities
102
What is the treatment for EIPH and how is this proposed to be effective?
Furosemide 4 hours prior to strenuous exercise (note racing/competition withholds) is thought to reduce pulmonary arterial pressure and left atrial pressures. Reducing pulmonary arterial pressure reduces capillary and transmural pressure during exercise, which reduces the impact on the capillary alveolar interface and associated tissue stress failure and disruption.
103
What is the most frequently reported primary neoplasm of the lung and what are their characteristics?
Granular cell tumour.
Originate from Schwann cells and occur as single or multiple masses adjacent to the bronchi and bronchioles. They are locally invasive with no reports of metastasis. Typically they extend into a large-calibre airway resulting in partial or complete occlusion of the lumen. Bilateral disease is uncommon (<20% of cases). Focal pneumonia may occur in pulmonary parenchyma distal to the tumour due to poor clearance of airway secretions and inhaled particulate matter.
104
What is an example of a paraneoplastic complication of granular cell tumour?
Hypertrophic osteopathy
105
Why is an endoscopic biopsy of granular cell tumours commonly non-diagnostic?
The external surface of the mass is typically composed of normal respiratory epithelium hence the biopsy is often non-diagnostic due to insufficient depth.
106
List common pulmonary tumour types
- Granular cell tumour
- Carcinoma & adenocarcinoma
- Bronchogenic squamous cell carcinoma
- Bronchial myxoma
- Pulmonary chondrosarcoma
- Pulmonary leiomyosarcoma
- Pulmonary blastoma
- Mesothelioma
107
What is the main differentiating factor between leiomyosarcoma and granular cell tumour?
Epistaxis occurs with leiomyosarcoma
108
What are the clinical findings with primary mesothelioma?
Weight loss, respiratory difficulty and large-volume pleural effusion. U/S may show multiple small nodules on a thick serosal surface and pleural biopsy is diagnostic. No treatment is available, prognosis is grave.
109
What are the clinical manifestations of thoracic lymphoma?
May get pleural effusion, pulmonary etelectasis and compromised pulmonary function. Cytology may refveal exfoliated cells. Peripheral lymphadenopathy is uncommon but can occur.
Haematological dyscrasias can include hyperglobulinaemia, hypercalcaemia, anaemia, rarely leucopenia. Pruritus associated with paraneoplastic syndrome. Other organs commonly involved include liver, kidney, spleen and GIT
110
Is B or T cell lymphoma more common?
70% in one report were T cell origin.
111
What are the clinical findings with disseminated haemangiosarcoma?
Tachypnoea, pale/icteric MM, respiratory distress, epistaxis, subcutaneous, cutaneous or intramuscular masses.
Anaemia, thrombocytopenia, neutorphilia
Large volume of haemorrhagic pleural effusion in 20% of cases.
Trauma is commonly a differential due to the haemorrhagic pleural fluid. Biopsy is required for diagnosis.
112
Which cytokines are thought to be responsible for fever as part of the paraneoplastic syndrome?
IL1, IL6 and TNF via increased PGE from the hypothalamic endothelial cells.
113
What are some differentials and mechanisms for paraneoplastic syndrome findings of anaemia, pruritus and hypercalcaemia?
Anaemia: can be of chronic disease, associated with transforming growth factor B, IL11, IL6 and interferon gamma which upregulates hepcidin synthesis which antagonises GIT iron uptake and utilisation. May also be from erythropoietin antagonism from TNF affecting bone marrow production and function
Pruritus: could be associated with nerve entrapment or compression, tumour growth, hepatic involvement leading to bile duct obstruction.
Hypercalcaemia: chronic renal failure, iatrogenic hypervitaminosis D, consumption of wild or day blooming jasmine. Other mechanisms include lytic bone metastases, malignant hyperparathyroidism, ectopic tumour production of parathyroid hormone like hormone, tumour-produced PGE and tumour produced osteoclast activating factor. Hypertrophic osteopathy (Marie's disease) has been reported associated with primary and metastatic pulmonary neoplasia.
114
What are the characteristic features of pleural effusion associated with hydatidosis?
- Large volume effusion
- Low-moderate cellularity with 20-80% neutrophils, protein 5-8g/dL
- Negative bacterial and fungal culture
- May see fluid filled cysts within the pulmonary parenchyma, on the surface of the diaphragm and or within the hepatic parenchyma.
- Metacestodes may be attached to a thickened pleural surface or hypoechoic cysts may be seen floating within the pleural or peritoneal fluid
- Treatment with albendazole 10mg/kg PO SID for 30 days may be effective, as well as pleural drainage and surgical debridement of the pleura and cysts
- Disruption of cysts by centesis or surgery may result in anaphylactic reaction or seeding of daughter metacestodes
