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Small animal > Respiratory disease > Flashcards

Respiratory disease Flashcards

1
Q

Causes of kennel cough - primary

A

CPiv - Canine parainfluenza virus
CRCoV - Canine respiratory corona virus
CAV-2 - Canine adenovirus type II
Bordetella bronchiseptica - zoonotic - shed 12 weeks post infection

Cause of disease - disrupts mucucilliary escalator - invasion of secondary bacteria

Ususual - Canine distemper – shed in all bodily fluids, purulent ocular/nasal discharge, haemorrhagic vomiting and diarrhoea, hyperkeratosis, neurological signs

Transmission - aerosol and some direct spread - not hugely environmentally hardy

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2
Q

Clinical presentation of Kennel cough

Diagnosis

Treatment

Prevention

A

Hacking cough +/- productive
Submandibular lymphadenopathy
Ocular/nasal discharge
Lethargy +/-
Pyrexia +/-
Need close contact for transmission
Bind to cilia and prevent mucocilliary escalatory from functioning

Diagnosis only important where it will change management - antibiotics, vaccine etc
- Serology, PCR, conjunctival swab for distemper

Treatment
Avoid choke chains, clean eyes, nose, NSAIDs if pyrexic
Butorphanol, codeine (anti tussive)

Antibiotics - not always necessary (bordetella - gram negative cover), secondary bacterial often gram negative - tetracyclines, potentiated sulphonamides, potentiated amoxicillin

Environmental hygiene, dog dog contact, fomites, ventillation, vaccination

Vaccination - parainfluenza - live SC or intranasal with bordetella, distemper live SC
- Intranasal - immunocompromised - LIVE

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3
Q

Describe how to manage a dog or cat which presents with respiratory distress

A

Place animals in oxygen rich environment.
Rest quietly.
Cool if hot.
Could sedate with acepromazine if animal is not hypovolaemic (phenothiazines vasodilate so exacerbate hypovolaemia).
Lower dose with brachycephalics.
Use with opioid (neuroleptanalgesia).
If triggers excessive panting use sedative such as diazepam.

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4
Q

What elements of the physical examination allow you to localise the disease to particular part of the respiratory tract?

A

Stethoscope – listen. Visual. Audio (stertor or stridor)

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5
Q

Cat flu - pathogens

A

Feline herpesvirus
Feline calicivirus
Chlamydia felis (Chlamydophila)
Bordetella bronchiseptica
Mycoplasma felis
- Others
NOT INFLUENZA

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6
Q

Clinical signs - cat flu

A

Can see very mild to severe nasal discharge.
Ocular discharge can just be unilateral
Mouth ulcers – could be something else like corrosive on fur

Flu syndrome
If predominantly FHV or Chlamydia – close contact or poor hygiene
FCV – fomite spread
Stress control important for all

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7
Q

Feline herpes virus - cat flu
Key information

A

Flu signs
Damage to nasal bones – little cat flu kittens becoming chronic snufflers
Ocular ulcers
Herpatic dermatitis – skin ulcers – steroids will make it worse

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8
Q

Feline herpes virus/viral rhinotracheitis - cat flu

Transmission

A

Herpes is for life
Shedding may occur without disease
Prevalence reports variable

DNA virus (FHV-1)
Enveloped
Stress-related recrudescence

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9
Q

Chronic rhinitis - cats - snuffles

A

Can be a sequel to ‘cat flu’
Can be very frustrating to manage!
Rule out non viral causes
Antibiotic therapy? (may need to be prolonged)
Aerosol therapy
Decongestants
Antivirals? - L-lysine, interferon omega, famcyclovir

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10
Q

Feline calicivirus - cat flu

A

Flu signs
tongue ulcers
Floppy kittens – can affect joints in kittens – synovitis
Fast-evolving virus
Very hardy
Shed by >80% of cats in multi-cat environments
Can be shed without disease

Spontaneous outbreaks of severe disease
Adult, healthy vaccinated cats
50% mortality
Fomite spread

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11
Q

FCGS - feline chronic gingival stomatitis - cat flu

A

Associated with FCV
Causation not established
Very frustrating to treat!
Dental, anti-bacterials
Full mouth extraction
Corticosteroids
Interferon

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12
Q

Chlamydia (chylamydophila) felis - cat flu

A

Intracellular bacterium-like organism
Close contact for transmission
Can initially appear unilateral
Antibiotics!!!
Doxycycline (NB oesophageal stricture)
10mg/kg SID for 4 weeks
Treat all in-contacts

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13
Q

Cat flu diagnosis

Control

Prevention

Vaccination

A

When it will change management - Individual vs population
Oral or ocular swabs
Viral transport medium
Virus isolation (FCV/FHV)
Polymerase Chain Reaction (FHV/C felis) – qPCR the best

Supportive treatment
Systemic treatment
Specific

Nutritional support – Nasogastric tubes, oesophageal tube
Prevention – hygiene, barriers, ventilation
Control – Cat-cat transmission
- Stress
Disinfectants
- FHV very labile
- FCV more resistant – quarternary ammonium compounds not effective
Know your disinfectants

“Core”
- Feline panleukopaenia virus (Feline Parvo Virus, FPV, Feline Infectious Enteritis)
- Feline Herpes Virus
- Feline Calicivirus
“Non-core”
- Chlamydia / Chlamydophila felis
- Bordetella bronchiseptica
- Feline Leukaemia Virus
- Rabies Virus

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14
Q

Stertor - localisation

A

Soft tissue vibration

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15
Q

Stridor localisation

A

Hard wheezing - tracheal constriction?

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16
Q

How do we approach animal with respiratory tract disease?

Signalment
History
Observation

A

Signalment – age, breed, sex, neuter status.
- Important for breed related disorders and helping to organise your differentials list
- Age moves differentials up and down the list

Full and thorough clinical history Including
- Diet, drinking, eating, urination, defecation, fluctuations in body weight
- Abnormal clinical signs at home/outside
- Any changes in activity level at home
- Any changes in personality/behaviour
- Changes in voice – laryngeal lesions

Observe the patient closely
- First critical aspect is whether the patient requires emergency admission or appears clinically stable
A significant number of animals with respiratory distress will be presented for acute deterioration
- Condition of patient
- Breathing – rate, pattern, regularity, depth, and apparent effort
- Mucus membrane colour – pale, cyanotic, normal
- Behaviours that are worrying the owner

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17
Q

Cardiorespiratory probelms - Respiratory difficulty – “dyspnoea”
+/- cough
+/- cyanosis
Sneezing/nasal discharge
Cough
Respiratory noise – LOCALISE!!
Collapse, weakness, exercise intolerance – SYSTEM!
Heart murmur +/- other clinical signs
Dysrhythmia +/- other clinical signs

A
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18
Q

Breathing pattern - upper respiratory tract disease

A

– slow respiratory rate and an exaggerated inspiratory effort (longer phase)
- Inspiratory effort increased

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19
Q

Normal breathing pattern

A

Normally inspiratory phase is longer than expiratory, in lower airway disease this is often reversed.
Normal respiratory effort is minimal

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20
Q

Lower respiratory restrictive disease - e.g. IPF, pleural effusion
Breathing pattern

A

fast shallow breaths
- Often both phases of breathing altered
- Interstitial fibrotic lung disease often limited to increased inspiratory effort – due to reduced lung compliance

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21
Q

Pleural disease breathing pattern

A

– loss of pleural adhesion increases required effort to breathe.
- Inspiratory and expiratory effort increased

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22
Q

Define orthopnoea

A
  • Dyspnoea in any position other than standing or erect sitting – usually due to bilateral pulmonary oedema
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23
Q

Trepopnoea

A
  • Dyspnoea in one lateral recumbency but not the other – unilateral lung or pleural disease, or unilateral airway obstruction e.g unilateral pleural effusion
  • Often seen in patients when in hospitalised and in lateral recumbency
  • Can be dramatic deterioration so always be vigilant for this
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24
Q

Thoracic exam in breathlessness

A

Thoracic palpation
- Presence of - apex beat, rhonchi, masses, deformities, pain (e.g. rib fractures)
Thoracic auscultation
- Hindered by purring, panting, growling!
- Use both sides of your stethoscope
Normal sounds
- Inspiratory – soft, low pitched
- Expiratory – none or softer and lower pitched

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25
Q

Abnormal respiratory sounds
Crackles
Wheezies

A

Crackles – ‘sweet wrappers’ (rales) – Dry or moist
- moist – CHF and most prominent on inspiration (right hilar position 1st) – usually some respiratory distress
- Dry – acute or chronic

Wheezes (high pitched) and rhonchi (low pitched)
- narrowing of airway (bronchi/trachea)
- Can be inspiration or expiration but most commonly expiration

Moist crackles – low pitched, fine popping inspiratory sounds
Dry crackles – higher pitched inspiratory sounds
All crackles usually discontinuous
Wheezes and rhonchi – usually secondary to bronchial narrowing.

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26
Q

Percussion with breathlessness - use and indications

A

Determine the density of a part by tapping the surface with a finger
Best for larger dogs and cats
Determine whether the tympanic sounds created by the chest wall are normal, increased or decreased
- e.g pleural effusion – dull below fluid line and normal above it
- There are many different causes of increased and decreased tympanic sounds on percussion
Increased tympanic sounds – pneumothorax, feline asthma, emphysema
Decreased tympanic sounds usually unilateral – diaphagmatic hernia, chest masses, unilateral pleural effusion

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27
Q

Respiratory tract investigation with breathlessness

A

History
Clinical examination
Routine haematology and biochemistry
- Specific blood tests - e.g. serum Pro-BNP concentration
- (Blood gas evaluation)
Diagnostic imaging
- Thoracic radiographs, fluoroscopy, CT, ultrasound, MRI
Tracheal washes/Bronchoscopy/BAL
- Lung FNA/biopsies
NB these are often older dogs with concurrent disease other tests as clinically indicated

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28
Q

What is the air conducting and respiratory portion of airways

A

Air conducting portion:
Epithelial lining + surrounding support tissues (cartilage, smooth muscle, elastic fibres)
Respiratory portion:
Simple squamous epithelia + scant (!) loose connective tissue → For optimal gas (O2/CO2) diffusion

Brush cells have microvilli; are thought to be sensory receptors in association with the trigeminal nerve

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29
Q

What extra layer is in bronchi that is not in trachea?

A

Layer of smooth muscle - muscularis - between mucosa and submucosa

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30
Q

More distally - respiratory epithelium

A

Simple columnar or simple cuboidal - still ciliated
With clara cells - bronchiolar exocrine cells
Without cartilage and glands

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31
Q

Alveolar epithelium cell types

A

Type 1 alveolar cell
(type 1 pneumocyte):
Very thin squamous cell, line 95% of the alveolar surface
- Type 2 alveolar cell
(type 2 pneumocyte):
Cuboidal cell, secretes surfactant, cover ~5% of the alveolar surface
- Brush cell
(rare)

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32
Q

Why do we see respiratory difficulty - 4 areas of possible disease

A

It is associated with disease of 1 of 4 areas:
- URT
- Pleural space
- Lung itself – Alveolar, Interstitial
- Non-CRS conditions - Metabolic/physiologic

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33
Q

URT - breathlessness - characterised by

A
  • Inspiratory difficulty
  • Audible noise
  • Mostly surgical
  • Emergency tracheostomy
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34
Q

Pleural space breathlessness - characterised by

A
  • May have characteristic respiratory pattern
  • Muffled heart and lung sounds?
  • US thorax
  • Remove the fluid
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35
Q

Breathlessness from the lung itself - characterised by

A

Stuff in the alveoli - Think about what you might find in the alveoi – blood, pus, parasites etc
Stuff in the interstitium

If severe these may also cause CYANOSIS
The animals may also COUGH

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36
Q

Non CRS conditions - breathlessness - characterised by

A
  • Often metabolic/physiologic
  • Rapid, shallow breathing
  • Rarely severe difficulty
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37
Q

Physiological/metabolic - breathlessness - characterised by

A

Often mouth breathing, panting, shallow
- Hyperthermia/heat stroke/fever
- Obesity
- Excitement/fear/stress/pain/shock
- Parturition/false pregnancy/eclampsia
- Anaemia/abnormal haemoglobin
- Acidosis
- CNS disease
- Endocrine dz, e.g. HAC & steroid tx, hypert4
- Neuromuscular disease

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38
Q

Pulmonary thromboembolism - characterised by

A
  • Acute onset dyspnoea
  • Few radiographic signs
  • Hypercoagulable states
    Trauma/surgery
    Sepsis/DIC
    HAC/exogenous corticosteroids
    HypoT4
    IMHA
    Glomerulonephropathies
    Pulmonary hypertension
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39
Q

What causes loss of thoracic capacity +/- cyanosis

A
  • Pleural effusion
    - blood, pus, chyle, true/modified transudate
  • Pneumothorax
  • Neoplasia - pleural or mediastinal
  • Ruptured diaphragm
  • Abdominal abnormality - severe ascites/mass
  • Gross cardiomegaly
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40
Q

What is the pleura?

A

Inner wall of the body cavities lined by single layer of mesothelial cells
Pleura covering the surface of the lung is the visceral (pulmonary) pleura
It is reflected around the root of the lung and becomes continuous with the mediastinal pleura
This in turn is continuous with the diaphragmatic and costal pleura
Mediastinal, diaphragmatic, and costal pleura are the parietal pleura
Contains rich lymphatic system that drains the pleural cavity

The narrow “space” between the parietal and viscera pleura is the pleural cavity
It contains a small amount of serous fluid spread over the surface of the pleura ~ 0.1ml/kg
Establishes adhesion
Smooth movement of lungs when breathing
Sub-atmospheric (negative) pressure

Left and right pleural sac around the lungs
Mediastinum is the space between them
More or less in the midline of the thorax
Mediastinum is continuous in most species
More delicate and discontinuous (?) in horses
Thin in dogs/cats
Contains important structures: blood vessels, nerves, oesophagus, heart, trachea etc

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41
Q

What is pleural space disease?

A

Accumulation of:
- Fluid – pleural effusion
- Air – pneumothorax
- Soft tissue mass e.g. abdominal organs
Severity of disease depends on the quantity of fluid or air, or size of the mass
In addition to direct compression of lungs can also lead to a loss of negative pressure causing the lungs to collapse
Fluid etc restricts the ability of the lungs to inflate so is sometimes called restrictive lung disease

42
Q

Clinical signs of pleural space disease

A

Restrictive” breathing pattern: short, shallow breaths
Tachypnoea
Open mouth breathing
Dyspnoea, Respiratory distress
Orthopnoea - elbow abduction, sternal recumbency
Cyanosis
May be acute or chronic
Observe respiratory pattern
Muffled heart/lung sounds?
Percussion

43
Q

Pleural effusion

A

Accumulation of Fluid: Pleural effusion
Auscultation: muffling of lung and heart sounds especially ventrally when standing
Percussion: increased dullness (fluid “line”)
A number of different fluid types can be present:
- Transudate
- Modified transudate
- Exudate
- Non-septic
- Septic
- Blood
- Chyle

44
Q

Pleural fluid dynamics

A

Fluid produced mainly from parietal pleural vessels by capillary filtration
Fluid reabsorbed mainly by parietal lymphatic vessels
Effusion occurs if there is decreased pleural fluid absorption or increased fluid formation
Remember Starling’s forces - Movement of fluid across capillary walls is essential for maintaining a continuous exchange of oxygen and carbon dioxide between the body’s cells and the blood supply
Pleural fluid can be unilateral but is usually bilateral

Transudate/low protein transudate
- Most common cause of pure transudate is due to decreased oncotic pressure due to hypoalbuminaemia

45
Q

Pleural fluid diseased cause by either what? and causes of this

A

Increased fluid formation or decreased fluid absorption

Increased formation
- leaky capillaries - pleural inflammation
- Increase in intravascular pressure - CHF
- Increase in lung interstitial fluid - CHF
- Decrease in pleural pressure
- Increase in pleural fluid protein - increased oncotic pressure
- Disruption of thoracic duct or blood vessels

Decreased absorption
- Obstruction of draining lymphatics - neoplasia, inflammation
- Increased systemic vascular pressure - Right heart failure
- Reduced vascular oncotic pressure - hypoalbuminaemia

46
Q

Common causes of pleural disease

A
  • Modified transudate/high protein transudate
  • The most common cause is due to increased hydrostatic pressure secondary to right sided heart failure (e.g. pericardial disease, cardiomyopathy, pulmonary hypertension, pulmonic stenosis)
  • Diaphragmatic hernia
  • Lung lobe torsion
  • Neoplasia
47
Q

Exudates causing pleural disease

A

Non-septic effusion
- FIP, neoplasia, chronic chylothorax, chronic lung lobe torsion, fungal infection

Septic effusion (pyothorax)
- Penetrating chest wound, foreign body inhalation (grass seed), ruptured oesophagus, ruptured pulmonary abscess / tumour, haematogenous bacterial spread

Chyle (chylothorax)
- Disruption of the thoracic duct
- Lymphangiectasia, cranial vena cava obstruction, neoplasia, heart disease, fungal infection, lung lobe torsion, diaphragmatic hernia, trauma of the thoracic duct

Blood (haemothorax)
- Trauma, coagulopathy, neoplasia, lung lobe torsion

48
Q

Diagnosis of pleural disease

A

Clinical findings
Diagnostic imaging
Thoracocentesis
Look at fluid

Take care with restraint in dypnoeic animals

49
Q

Treatment of pleural disease - immediate

A

Case triage – severity and act as needed
Initial management
Oxygen supplementation
Emergency thoracic ultrasound to make the diagnosis
In severely dyspnoeic patients DO NOT RADIOGRAPH - these patients can be very unstable and will die if they are stressed!
Immediate thoracocentesis
- Immediate relief from clinical signs
- Diagnostic - Cytology, cell counts, protein content, bacterial culture
- Stabilise the patient prior to further investigations

50
Q

Thoracocentesis for pleural disease

A

Local anaesthetic rarely needed unless large bore catheter
Clip area – if possible use quiet clippers (minimal stress esp. cats)
Quickly surgically prepare skin
Butterfly needle or catheter at ICS 6-8
Ideally localise large pocket of fluid with ultrasound first
Aseptic technique

51
Q

Thoracostomy - chest drain - indications

A

Indications for thoracostomy:
- Animals that will require multiple thoracocentesis over a short period of time
- If large volumes of effusion
- Pneumothorax
- Chest wall injuries
- Flail chest / Flail segment
- Bite wounds
- Most pyothorax cases
- Following chest surgery

52
Q

Treating primary cause of pleural disease - Heart failure, pericardial effusion, pyothorax, chylothorax

A

Heart failure - Treatment of HF

Pericardial effusion - Treat effusion - drainage etc

Pyothorax - Antibiotics, systemic & local (broad spectrum and treat anaerobes)
- Be aware that bacterial cultures will often come back as negative!
- Lavage?
- Long course of treatment, guarded prognosis

Chylothorax - Diet and/or surgery

53
Q

Pneumothorax

A

Pneumothorax – accumulation of air
Rupture of major airways / lung parenchyma
Thoracic trauma (e.g. broken rib lacerates pleura, penetrating wound)
Perforation of the oesophagus
Bullous, necrotising or neoplastic lung disease which leak air into pleural space
Iatrogenic (e.g. prolonged ventilation under GA, bronchoscopy)
Gas producing bacterial infection in pleural space
Restrictive breathing (slow – rapid breaths)
Auscultation reveals dull lung sounds dorsally, increased sounds ventrally (bronchovesicular)
Percussion – increased resonance (like a drum!)

Physical examination
Assessment of respiratory status
Thoracic radiographs – if stable enough
[Routine haematology / biochemistry]
Blood gases and pulse oximetry – helps to assess severity

54
Q

Pathophysiology of pneumothorax

A

Loss of negative pressure in pleural space means that lungs are not effectively “coupled” to rib cage. As rib cage is raised lungs do not inflate
Lungs collapse and tidal volume is very low
Severity depends on degree of pneumothorax and underlying disease

Tension Pneumothorax: special case
- Lesion in lung parenchyma or airway acts as “one way valve”
- Pleural pressure rises causing severe lung compression
- Pressure can exceed central venous pressure, reducing venous return and cardiac output
- Rapidly life threatening

55
Q

Traumatic pneumothorax treatment

A

Oxygen
Drain pneumothorax as necessary, avoid over drainage
Approx. 90% recovery with strict cage rest for up to 2 weeks
Some will require chest drains and Heimlich valve (allows air to exit chest but not enter)
If no improvement then surgical exploration and correction will be required.
If open wounds then sterile dressings and surgery as soon as patient is stable.

56
Q

Spontaneous pneumothorax

A

History
- dyspnoea
- anorexia
- vomiting
- most present with rapid progression of respiratory distress
Most common cause is ruptured pulmonary bulla or sub-pleural bleb
Can occur with chronic asthma in cats
Diagnosis as for traumatic pneumothorax
Medical management to stabilise until diagnostic tests decide whether surgical intervention is required
Lobectomy as necessary
Prognosis is dependent on the underlying cause

57
Q

What is mediastinum

A

The mediastinum is the area in the chest between the lungs that contains the heart, part of the windpipe (the trachea), the oesophagus, and the great vessels

58
Q

Mediastinum disease

A

May be benign or malignant tumours, cystic lesions, enlarged mediastinal lymph nodes or haematomas
Pros and cons of diagnostic imaging as for lung masses though CT very useful if surgical
May be hidden behind pleural effusion – check tracheal position
Diagnosis can be very challenging however important as clear distinction in treatment options for e.g. lymphoma vs sarcoma

59
Q

Mediastinal lymphoma - cause, treatment

A

Commonest in young cats (predisposition for siamese?), also seen in dogs with multicentric or stage 3-5 lymphoma if so is considered a negative prognostic indicator
Tachypnoea, inspiratory hyperpnoea, dull heart sounds, pleural effusion (cytology for dx)
Non compressible anterior mediastinum
- NB practice compressing normals
Check FeLV/ FIV status (~50% positive for FeLV)
DDx thymoma – consult a cytologist!
Treatment: chemo +/- radiotherapy?
Generally remission, cure rare

60
Q

Thymoma - cause, diagnosis, treatment

A

Thymoma and thymic carcinoma are diseases in which malignant (cancer) cells form in the thymus. Thymoma and thymic carcinoma, also called thymic epithelial tumors (TETs), are two types of rare cancers that can form in the cells that cover the outside surface of the thymus.

  • RARE, commonest in older dogs
  • From thymic epithelium, often infiltrated with lymphocytes
    • Ddx thymic lymphoma – good cytologist!
  • Benign or malignant, mets rare from both
  • 60% feline version cystic
  • Present with resp distress +/- cranial caval syndrome +/- myaesthenia gravis
  • Megaoesophagus also common if focal MG or disrupted due to presence of mass
    Thoracic radiographs to confirm a mass
    Cytology +/- tru-cut +/- flow cytometry to get diagnosis
  • Be sure of diagnosis as possible - lymphoma is not a surgical disease
  • Adjunctive imaging eg CT may help
    Surgical resection as treatment of choice – excellent prognosis if fully resectable
    Poor prognosis if old, megaoesophagus, invasive
61
Q

Thyroid masses

A

Heavy ectopic masses sink into the thorax
Dogs rarely hyperthyroid, cats usually are
- Dogs diagnosed on mass signs/incidental
- Cats diagnosed as unresponsive hyperthyroids
Confirmation on scintigraphy if active
Treat with 131I or surgery
If >3cm diameter, RTx may be better as poorer px

62
Q

Pleural tumours - cause, diagnosis, treatment

A

Mesothelioma – RARE
From epithelial lining cells – pleural, abdominal, pericardial
Major link with asbestos inhalation, complex mechanism
Causes large volume effusions and pain ++
Multifocal small masses, hard to image, Ultrasound and CT most useful.
Diagnosis
Diagnosis hard, ddx reactive mesothelial cells
Histo ideal, thorascopy best as non-invasive.
Treatment via intra-cavitary carboplatin/ cisplatin, but painful and poor px
Large volume effusion cause of euthanasia

63
Q

Rib tumours

A

Iceberg tumour
Osteosarcomas and chondrosarcomas, but remember overlying soft tissue tumours too eg infiltrative lipomas
OSAs aggressive in this location (cf other axials)
What is visible on the outside may be only 20-30% of the total
Treatment via rib resection = thoracotomy plus post-op chemo if osteosarcoma
Prognosis depends on diagnosis – chondrosarcoma better than osteosarc

The majority of these masses need good history & physical examination
A large number of factors govern how long dogs and cats survive, many outside your control
Good communication and honesty will be appreciated much more than your skills as a surgeon or medic
Get a good biopsy then discuss it with an oncologist/surgeon before doing anything

64
Q

Pumonary parenchymal disease - clinical signs

Physical exam importance

A

Clinical signs of pulmonary parenchymal disease
- Usually increased inspiratory and expiratory effort
- Some interstitial lung diseases however limit compliance and so inspiratory effort predominates
- Cough may or may not be present – MUST involve airways to initiate a cough
- Can see less frequently hemoptysis, collapse/syncope or cyanosis
- Occasionally minimal signs of respiratory disease are noted with even severe disease – notably cats

Physical exam is important
- Any other signs of systemic disease – Pyrexia, lymphadenopathy, lameness
- Cyanosis
- Crackles – dragging air through fluid – not definitive of alveolar disease but shows you need to image them
- Increased/decreased bronchovesicular sounds
Auscultation can be unremarkable, even with severe lung disease – If not upper, not pleural space – probably lung
Respiratory distress – oxygen therapy indicated

65
Q

Causes of alveolar disease

A

Aspiration pneumonia
Pulmonary oedema (cardio vs non-cardiogenic
Pulmonary haemorrhage
Eosinophilic lung disease
Pulmonary parasites
Pulmonary neoplasia – primary/metastatic – primary arise from airway (cause cough), metastatic arrive and grow in interstitium – interstitial disease
Infectious pneumonias

66
Q

Aspiration pneumonia - cause, clinical signs, diagnosis, treatment, outcome

A

Inhalation of material into the lower airway
- Stomach contents with variable amounts of particulate matter
- Care with nursing recumbent patients

Outcome depends on nature and amount of aspiration
- pH, bacterial contents, volume, particle size
- Chemical aspiration – pneumonitis
- Large volumes of fluid – drowning event
- PEG fluids (bowel prep) – pulls interstitial fluid into lungs

Primary infection due to aspiration is less common – usually occurs as a secondary event due to damage
May NOT be supportive history

Signs – cough, harsh/reduced lung sounds, tachypnoea, pyrexia – check oxygenation -serial evaluation

Radiographs alveolar infiltrate (patchy/focal)
- Most common affected lobes are right middle, right cranial, left cranial
BAL to confirm – very benign procedure, not hugely dangerous as will be absorbed
- Will send off and see bacteria, but organism may not be only one, but often don’t grow anything despite seeing bacteria

Treatment
- Supportive oxygen therapy, antibiotics – care with oxidative damage to already fragile lung
- Treat any underlying cause
- Consider anti-acid medication if frequent occurrence – may increase gastric bacterial load therefore caution
- Metoclopramide to improve motility and increase LOS (lower oesophageal sphincter) tone

67
Q

What lung pattern will you see with aspiration pneumonia?

A

Alveolar - border obliteration, air bronchograms,

68
Q

What will you see on histopathology with aspiration pneumonia?

A

Areas of lung packed with neutrophils, some with alveoli.
Areas full of pus, but airways still spared
Air bronchograms

69
Q

What antiobiotics to use for aspiration pneumonia?

A

Antibiotics
Antibiotic selection should ideally be based on C&S
Require high concentration in the lungs
Need to penetrate, dissolve in blood-bronchus barrier – lipophilic antibiotics penetrate this best
Need to be effective against respiratory pathogens – should be bactericidal
- Range of bacterial with aspiration pneumonia
May need to select combination – complex pneumonia/mixed infection
Ensure adequate treatment period at least 4-6 weeks for severe/chronic infections
Primary infection is uncommon in dogs
Secondary respiratory tract infections common
- In chronic bronchitis – compromised mucocilliary clearance
Good airway penetration
- Drugs reach airway by passive diffusion
- Favourable characteristics – lipophilicity – few drugs reach same conc as plasma
Depends on nature of organism
- Mycoplasma inherently resistant to certain antibiotics as no cell wall – choices include macrolides and fluoroquinolones can consider tetracyclines
No current evidence that inhaled antibiotics have any efficacy so oral always required
- However may have a role to play in Bordetella

Fluoroquinolones are concentrated significantly in canine alveolar macrophages good penetration into airway
Fluoroquinolones good for G-ve aerobes, reasonable efficacy against G+ve aerobes, pseudomonas, MRSA, mycoplasma and mycobacteria

Macrolides are reasonably well concentrated into respiratory tract
- Azithromycin very good distribution into pulmonary tissues
- Metronidazole accumulate well in bronchial secretions
- Drugs with long half life accumulate in secretions – doxycycline
Macrolides good for G+ve aerobes and obligate anaerobes, mycoplasma and bartonella

Lincosamides – accumulate well in phagocytes

Penicillins have relatively poor distribution into bronchial tissue
- Some are better than others e.g. amoxicillin > ampicillin

Cephalosporins – variable penetration depending on generation although better than penicillins
Cephalosporins most effect on G+ve aerobes, some effect on penicillinase-producing staphs, group II injectable have better efficacy for G-ve aerobes

Sulphonamides moderate broad spectrum activity

Tetracyclines – reasonable concentration in secretions relative to plasma
The more severe the infection the more important lipid solubility is
- Require concentration to be ‘cidal at the site of infection - Moot point and not essential if immunocompetent as can be bacteriostatic
In severe infections adjuvant mucolytic therapy would be indicated
- Enables better penetration of drugs into respiratory tract
Steam helps thin out mucus so steam room for dog
Tetracyclines good for G+ve aerobes with effect on atypical bacteria e.g. mycoplasma, chlamydia, borrelia

Aminopenicillins good for Gram +ve aerobes and anaerobes, moderate effect on G-ve anaerobes
- Addition of clavulanate improves activity against lactamase producing bacteria
- Some additional evidence that clavulanic acid has effects other than cell wall inhibition

70
Q

Use of mucolytics in aspiration pneumonia

A

Can be useful to help reduce mucus accumulation in chronic bronchitis and other conditions with compromised muco-ciliary clearance
Bromohexine – increases lysosyme activity and IgA concentration in experimental studies
- Licensed product - Bisolvon

71
Q

Causes of pulmonary oedema

A

Consequence of various conditions
- Increased hydrostatic pressure (within capillaries)
- Reduced oncotic pressure (less protein pulling fluid back in)
- Increased vascular permeability
- Impaired lymphatic drainage
This leads to fluid accumulation in the interstitium (as this is where capillaries are) and subsequently in the alveoli at a rate that exceeds removal
Ventilation perfusion mismatching and hypoxaemia (areas being ventilated but not perfused)

72
Q

Difference between cardiogenic and non-cardiogenic pulmonary oedema

A

Cardiogenic or non-cardiogenic - main difference is type of fluid
Cardiogenic is low protein due to increased hydrostatic pressure without increased vascular permeability – more common
Non-cardiogenic is the result of lung damage which increases vascular permeability, so protein leaks out

73
Q

What will you see on radiograph with pulmonary oedema?

A

Alveolar pattern – air bronchograms and border obliteration
Left atrial enlargement and pulmonary oedema
Pulmonary vein bigger than pulmonary artery

74
Q

What will you see on radiograph with pulmonary oedema?

A

Alveolar pattern – air bronchograms and border obliteration
Left atrial enlargement and pulmonary oedema
Pulmonary vein bigger than pulmonary artery

75
Q

Causes of non-cardiogenic pulmonary oedema - why does it happen?

A

Non-cardiogenic
- Increased vascular permeability
- Higher protein fluid in alveoli
Removal of the fluid requires active transport of sodium and chloride from the luminal surface across epithelial cell to the basal surface
This is an active process – if the epithelium is damaged this cannot occur
So the damage to the epithelium leads to fluid accumulation and reduced the ability to remove the fluid which makes non-cardiogenic oedema more refractory to therapy than cardiogenic oedema
Non-cardiogenic causes:
- Importantly hypoalbuminaemia rarely causes pulmonary oedema due to efficient pulmonary lymphatics
- Lymphatic damage is more likely to cause a chylous effusion rather than pulmonary oedema
- Neurogenic form (along with electric shock) – pathophys. unclear but thought to be due to intense pulmonary vasoconstriction and inflammation both increase vascular permeability
- Most common cause is pulmonary epithelial injury
- Choking, near-drowning, electric shock, head trauma, smoke inhalation, systemic inflammation (SIRS)

76
Q

Physical lung injury - blood in lungs -

A

Thoracic trauma
- Pulmonary contusion - ventilation perfusion mismatch
- Chest wall damage and pain
Thoracic radiographs to evaluate all thoracic structures
- Lag phase
Supportive care with supplemental oxygen ASAP
Other treatment as required – e.g. stabilisation of the thoracic wall, analgesia

77
Q

Eosinophilic lung disease - eosinophilic bronchopneumopathy, pulomonary infiltrate with eosinophils, eosinophilic pneumonitis - cause, diagnosis, treatment

A

Typically young adults
Acute or chronic presentation - usually coughing, can also see weight loss
Can see alveolar or interstitial patterns
Can see bronchointerstitial pattern - can be dense infiltrates if alveolar pattern
Circulating eosinophilia in 50% dogs

BAL for diagnosis - look for parasites, neoplasia and fungal disease

Treat - prednisolone - outcome good unless other organs involved - guarded

No border obliteration
Bronchial markings - donuts - white rings, dark centres - thickening of airway walls
Lateral inspiratory

78
Q

A. vasorum - Angiostrongylus vasorum

What is it
Lifecycle
Clinical signs
Diagnosis
Treatment
Prognosis

A

Heartworm - lives in pulmonary arteries, up to 2.5cm long
Dog is definitive host, slug/snail intermediate - eggs in pulmonary capillaries, through alveolar wall, L1 coughed and swallowed, faeces. L1-L3 in snail. L5 in migration to HP vein/liver, to pulmonary artery

Cause Type III hypersensitivity (immune complex deposition)

Breathlessness/cough
Bleeding
Neurological signs
Various respiratory signs - chronic cough, exercise intolerance, syncope, dyspnoea, tachypnoea
Signs often relate to degree of burden
- Productive cough, haemoptysis - larval migration through lungs and airway

Coagulopathies - Clinically - anaemia, subcutaneous haematomas, internal haemorrhages, prolonged bleeding from wounds or after surgery
Thrombocytopenia, prolonged APTT and OSPT, elevated D-dimer (previously measurement of FDPs was used) – via consumptive coagulopathy – chronic DIC

Diagnosis - radiography - alveolar infiltrates
SNAP test
PCR on BAL or pharynx swabs

Imidacloprid, moxidectin - licenced
Milbemycin, praziquantel - licenced

79
Q

Interstitial disease - Interstitial pulmonary fibrosis - IPF
History, clinical signs, diagnosis, treatment

A

Typically WHWT and other terriers
Middle aged to older
History - slow onset, chronic breathlessness, coughing, ex intolerance, cyanosis, syncope
Clinical exam - crackles, prolonged expiratory phase and effort

Diagnosis - clinical signs, radiographs (interstitial pattern, R cardiomegaly, pulmonary hypertension)
CT - ground glass appearance - diffuse increased opacity
Bronchoscopy - BAL samples normal, rule out other inflammatory conditions
Lung biopsy - only definitive diagnosis

Treatment - depends if active inflammation
- Symptomatic - avoid collars, smoke inhalation
Inhaled therapy - bronchodilator- salbutamol
Corticosteroids - prednisolone

Manage pulmonary hypertension - Sildenafil, pimobendan

Guarded prognosis - progressive disease

80
Q

Pulmonary parenchymal disease - metastatic disease

A

May be incidental finding or present with cough/ tachypnoea
May be the first an owner knows about animal having cancer
Commonest = osteosarcoma, haemangiosarcoma, thyroid carcinoma, melanoma of the mucocutaneous junction
– check pre-op!

  • Remember not all tumours met to the chest
    Interesting but no great merit in finding 1◦ if no plans to treat
  • Emphasis on finding mets?

Solitary metastasis removal increasingly common
- Need CT to get best info on how many and where, and slow radiographic doubling time
- Thoracoscopic approaches increasing
- Care on seeding to portal sites

May start getting locally delivered chemo
- Delivery and penetration problems
Median survival time 3 months with no tx
- Unclear survival if early detection on CT

81
Q

Causes of cough - Acute

A

Cough – reflex associated with irritation of cough receptors. Glottis closes, intrathoracic pressure increases to expel.

ACUTE CAUSES
Tracheobronchitis - “kennel cough”
Irritation by smoke/dust/chemicals/medicines!
Airway FB - may have been in there some time.
Pulmonary haemorrhage - often + dyspnoea
Acute pneumonia, e.g. inhalation - often + dyspnoea
Acute oedema - often + dyspnoea - cardiogenic/non/cardiogenic
Airway trauma - choke chains/bites etc.

82
Q

When to use anti-tussives

A

Anti-tussives
Don’t use cough suppressants unless absolutely necessary – as coughing IS protective in most cases
- Value particularly in anatomical airway disease
- Intractable non-productive pathological cough
e.g. neoplasia
Butorphanol/codeine

83
Q

Causes of cough - chronic

A

Chronic cough causes
- Chronic bronchitis/bronchiectasis
- L. heart failure
- Oslerus/Aelurostrongylus infestation
- Tracheal collapse
- Airway F.B.
- Bronchopneumonia
- Pulmonary neoplasia - primary or secondary
- Extra-luminal mass lesions - thyroid, abscess, lymphoma
- Eosinophilic disease – EBP/PIE/allergic airway disease
- (Pulmonary “fibrosis”)
Imaging - Bronchial pattern – CB, EBP
- LH failure
- FB?

84
Q

Canine chronic bronchitis

A

Daily coughing for >2months
Characterised by:
- Neutrophilic/eosinophilic infiltration of mucosa and thickening of smooth muscle later, fibrosis and scarring of lamina propria
- Increased goblet and glandular cell size and number
- Oxidative injury and inflammatory products damage cells and lead to mucus hypersecretion
- Loss of ciliated epithelial cells and failure of mucociliary clearance and debris

The combination of these events leads to thickening of bronchial tissue, overproduction of airway mucus and narrowing of the airways (particularly terminal bronchi)
* Leads to clinical signs of wheezing and productive coughing
* Complications are common – dilation of airways, airway collapse due to wall weakness (bronchomalacia)

85
Q

Aitiology of canine chronic bronchitis

A

Maybe seen secondary to underlying conditions
- Tracheal collapse, chronic barking
- FB
- Previous infections or inhalant toxins
- Environmental factors
- Chronic smoke inhalation/noxious gas
- But usually cause unknown
Typically seen in small / toy breeds
- Although can see in any age/breed
- Worse on excitement
- Harsh cough with attempts at production - Usually clear/frothy, yellow suggests infection
- Usually externally well, often obese
- Occasionally pant excessively
- Tracheal pinch positive – palpate trachea to induce cough
Often very little to find on exam

86
Q

Diagnosis of canine chronic bronchitis

A

Typical history, physical findings - Often exaggerated sinus arrhythmia due to high parasympathetic tone
Thoracic Radiographs - Increased bronchial lung pattern
Bronchoscopy and BAL
Bronchial pattern – cranial lobe bronchus – can see airway walls. Should taper down to periphery.
Tram lines and donuts
Dilated airways – bronchiectatic – weak and likely to collape on endoscopy

Bronchoscopy – often inflamed and globs of mucus on walls. Pale and fibrotic

BAL results typically show:
- Increased mucus
- Non-degenerate neutrophils, eosinophils and macrophages
- Cushmann’s spirals (airway mucus casts)
- Presence of bacteria / particulate matter are less common and if present would suggest underlying cause present

87
Q

Management of canine chronic bronchitis

A

Weight control
Harness
Avoid irritants
Steam therapy - shower
Glucocorticoids - oral and inhaled
Bronchodilators - theophylline
Coupage - taps to break up mucus
No antitussives unless absolutely necessary
Antimicrobials on need - bacteria on BAL

Prognosis
Long term management - no cure - dog will always cough
Prevent - secondary pneumonia, bronchiectasis, emphysema

88
Q

Use of inhaled medications - Why
Types
Examples
Advantages, disadvantages

A

Minimal absorption into systemic circulation - less side effects, particularly steroids
faster onset of action, lower dose required
Effective in acute

Expensive
Time consuming
Owner compliance, patient compliance

Beta 2 agonist
- Salbutamol (albuterol in USA)
- Salmeterol – longer acting medication
Corticosteroids
- Fluticasone
- Beclomethasone

Salbutamol - Fast onset of action, lasts >3 hours, cleared renally, reaches lower airways
- Side effects - Tachycardia, arrhythmias, tremours

Fluticasone proprionate - slowly absorbed from lung, long half life, long dwell time in lungs
- Side effects - oral infections - candidiasis, coughing, wheezing

89
Q

Feline bronchial disease - feline asthma, feline allergic airway disease

A
  • General considered to be a type I hypersensitivity condition to inhaled allergens
  • Suspected genetic predisposition
  • Some breeds more commonly affected – Siamese

Underlying factors
- Smoke, feathers, aerosol inhalation, dust, cat litters
- Seasonality often seen and helps with ID of cause

90
Q

Bacterial bronchopneumonia

A

Primary infections in healthy dogs (and cats) RARE
- If present should prompt search for underlying cause
Common pathogens are E Coli, Klebsiella, Pasteurella, staphs (coag +ve), streps, mycoplasma and B bronchiseptica.
Primary infections most common with primary pathogens
- e.g. Bordetella bronchiseptica, Streptococcus equi subspecies zooepidemicus, Mycobacteria

Often mixed infections, obligate anaerobes may account for up to 25% pathogens

  • S equi subsp. Zooepidemicus
    Linked with the outbreak of acute fatal haemorhagic pneumonia in dogs in several countries
    Highly contagious sudden onset
  • Pyrexia, dyspnoea, haemorrhagic nasal discharge and haemoptysis
  • Causes a severe fibrino-suppurative necrotising haemorrhagic pneumonia

Factors predisposing to bronchopneumonia
- Debilitation
- Prolonged recumbency
- Systemic immunosuppression (HAC, chemo, pred’s)
- Immunodeficiency states (weimaraners, CKCS)
- Defective respiratory defenses
- Damaged respiratory epithelium
- Aspiration
- Airway obstruction
- Systemic sepsis
- Bronchiectasis

Clinical signs vary:
- occasionally only minor clinical signs
- signs often relate to extent of pneumonia
- cough, respiratory distress, ex intolerance
- More severe infections may produce hyperthermia
- Anorexia and lethargy are common signs
- Increased or decreased lung sounds may be present, may include crackles
- Respiratory distress and cyanosis may develop in severe cases

Diagnostic approach
- CBC, biochemistry, UA, faecal
Thoracic radiographs
- Alveolar pattern with variable distribution
- Aspiraion – cranial-ventral
Early disease may show only interstitial pattern
Airway sampling is helpful
- TTW/BAL
- Culture and cytology on fluid
- Integration of inflammation and bacterial culture

Treatment
- Antibiotics – broad spectrum?
- Supplemental humidified oxygen
- IVFT
- Anti-inflammatories
- Bronchodilators
- Mucolytics
- Physiotherapy
- Nebulisation
- Surgery

91
Q

Bronchial foreign body

A

Sudden onset coughing and gagging
High frequency in working dogs or those living in rural environments
Often have history of signs after exercising in agricultural fields
Often see good initial response to antibiotics
Halitosis may be present and progressive
May see weight loss if infection associated with FB becomes significant
More substantial respiratory signs may suggest progression to pleural disease – can turn to pyothorax if makes its way out of lungs into pleural space

Thoracic radiographs
- Fully evaluate for signs of pleural involvement
- Determine if there is suggestion of LOCAL lobar involvement or disease seems more diffuse
Bronchoscopy
- BAL and culture for specific antibiotic therapy
- Enables visualisation and retrieval of object
Right bronchus more straight on that left – tends to go to right diaphragmatic lobe

92
Q

Primary pulmonary neoplasia
Secondary

A

Primary pulmonary neoplasia
Primary – cough – tumours arise from airways. Airway lining proliferating all the time

Secondary – breathless – Is an interstitial disease

Primary lung tumours are very rare in comparison to humans (1%)
Dog>cat, weak links with passive smoking
Metastatic disease by far the commonest
Oral melanoma, thyroid Ca, osteosarcoma, haemangiosarcoma and mammary Ca.

Median age 11 years
Generally carcinomas, classified by location, often hard to tell exact origin
- Can also see pulmonary lymphoma, pulmonary lymphomatoid granulomatosis, malignant histiocytosis
- Rare to see mesenchymal tumours in the lung
>50% solitary (often right caudal lobe)
Present with non productive cough or exercise intolerance
Hypertrophic osteopathy as rare paraneoplastic disease
Prognosis
Depends on size, location (resectability) and spread – adjunctive chemo little use?
Best case scenario 50% alive at 1 year
Adenocarcinoma > SqCC survival (squamous cell carcinoma)

Direct airway sampling – Through thoracic wall. Do not do if full of air – pneumothorax. Don’t do if bleeding
BAL rarely helpful
Transthoracic FNA
- Ultrasound guidance in patients with discrete lesions
- Can also use fluoroscopic or CT guidance
- Lesions >1cm
Contraindications
- Pulmonary bullae or cysts
- Coagulopathies
- Pulmonary hypertension
- Pre-existing pneumothorax
- Suspected infectious process
Potential complications
- Pneumothorax, empyema, bleeding, implantation, seeding of neoplasia

93
Q

Lower airway disease in cats
Signalment
History
Assess urgency
Physical exam

A

Old and young - infectious
Pneumonia - rare with viral (FCV, FHV)
Lower - tends to be young to middle aged
Older - hyperthyroid, neoplasia, cardiac
Younder - infectious, viral, parasitic, mycoplasma, bacterial, toxoplasma

History
- Low grade chronic
Coughing, wheezing, ex intolerance
Acute - emergency, resp distress, mouth breathing
Episodic - self limiting, resp effect
Any triggers, changes, seasonal, productive cough, weight loss, anorexia, queiter, grooming less

How critical - respiratory reserve - hands off assessment

Assess - respiratory pattern - localise

Laryngeal - laboured inspiration - stridor, increased effort, slow inspiratory phase
Upper - Dysphagia, coughing, gagging, head shaking (nasal)
Lower - laboured expiration, prolonged exp, wheeze, increased resistance - bronchospasm, mucus, thickening

94
Q

Feline asthma

A

Reversible
Inhaled allergen
Airway hyper reactivity
Bronchoconstriction
Eosinophilic airway inflammation?
Signs: episodic respiratory distress and dyspnoea, coughing

95
Q

Chronic bronchitis - feline

A

Response to infection or inhaled irritants
Airway damage
Excess mucus
Neutrophilic airway inflammation?
Signs: coughing is a key feature

Hyper-reactivity of the bronchial smooth muscle
- type I hypersensitivity
- autonomic imbalance
- mucociliary imbalance
Acute bronchoconstriction in response to a trigger factor
Inflammation of bronchial mucosal lining
- histamine and leukotriene release
Airway obstruction occurs due to
- bronchoconstriction
- inflammation
- mucus plugs in narrowed bronchioles
Air trapping  destruction of alveoli
End result is chronic damage
- irreversible situation due to remodelling
- may see spontaneous rib fractures
Extreme acute deterioration
- rare cases develop pneumothorax

96
Q

Feline coughing - ddx

A

Coughing:
- Upper respiratory tract disease
- Inflammatory lower airway disease
- Infectious – bacterial, viral, parasitic
- Foreign body
- Neoplasia
Heart disease rarely causes coughing in cats

97
Q

Feline hyperpnoea/tachypnoea - ddx

A
  • Stress/pain/fear response
    mouth breathing
    8/103 cats improved with sedation only (Sigrist et al 2011)
  • CNS disease
  • Anaemia/hypovolaemia
  • Heatstroke
  • Cardiac disease
  • Respiratory disease – airways, lung parenchyma
  • Pleural space disease
  • Mediastinal disease
  • Ruptured diaphragm
  • PPDH – peritoneo pericardial diaphragmatic hernia
98
Q

Management of suspected airway disease - feline

A

Treatment in a crisis:
Manage inflammation
- dexamethasone iv
Manage bronchospasm
- terbutaline
selective β2 receptor agonist
- smooth muscle relaxant
- bronchodilation
ideally rule out heart disease 1st
inhaled salbutamol
- selective β2 receptor agonist
- can give every 30 mins for 2-4 hrs
- stop if stresses the patient
Oxygenate
Risks: hyper reactive airways prone to bronchospasm during bronchoscopy and BAL procedures…consider pre treating with terbutaline

Treatment longer term:
- reduce allergens? Not always possible
- prednisolone po 2-3 weeks
- consider inhaled fluticasone if improved
studies have confirmed route of delivery works
some oral ingestion/absorption might occur
- if no response to prednisolone
review case
- repeat test for Mycoplasma/or try a treatment trial?
- have we ruled out lungworm?
- consider ciclosporin
Risks: steroids are diabetogenic in cats. If side effects include polydipsia and polyuria treatment must stop!

99
Q

Feline lungworm - presentation, diagnosis, treatment

A

Aelurostrongylus abstrusus
Paratenic hosts required (rodents, birds)
PPP 1-2 months
Most infected cats are asymptomatic
Clinical presentation
- usually young cats
- mild coughing but might  dyspnoea
- radiography: similar to inflammatory airway disease +/- alveolar component if severe
Diagnosis: identify L1 larvae but be aware that false –ves can occur
- consider faecal flotation / Baermanns technique
- airway wash analysis
Treatment trial: fenbendazole

100
Q

Mycoplasma pneumonia cat

A

M felis associated with lower airway disease in cats
- might also cause URT signs
Not all infections are significant
- might be a contributing factor in feline inflammatory airway disease
Clinical signs: fever, cough, tachypnoea, lethargy
Diagnosis: PCR on tracheal wash
Treatment: doxycycline

Small animal (11 decks)

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