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airway defence mechanisms
concerned primary with defending against inhaled particles
filters particles from inhaled air
prevents particles containing and damaging epithelial surfaces
removal of particles
airborne particles
inert matter
water droplets
infectious agents
allergens
airway defence mechanisms
aerodynamic filtration
mucociliary esculator
antibacterial agents
IgA
protective reflexes
leucocytes
aerodynamic filtration
coiled turbinates leads to airflow turbelence causing particles >10um to impact onto airway mucosa
bronchi filter out most particles > 3um
particles ~ 1-5um are deposited in bronchioles and alveoli
mucociliary esculator
most upper airways lined by mucus carpet and swept by cilia
mucus
traps and transports particles from lower airways to pharynx
physical barrier
prevents dehydration
dilutes soluble gases
contains antibacterials
= lysozyme - bacteriolytic protein that hydrolyses peptidoglycan wall
= Fe-binding protein synthesised by neutrophils and ep cells, retarding bacterial and fungal growth

factors affecting mucociliary carpet
change in viscosity of mucus
temp, dehydration
inflammation
injury to epithelium
trauma, infection
chronic irritation may = cell type change
protective reflexes
cough/sneeze
alveolar defences
macrophages
alveolar
interstitial
intravascular
role
phagocytose particles and agents
recruit neutrophils
coordinate inflammation
ascend mucociliary escalator
diseases of upper airways
developmental abnormalities
circulatory disturbances
inflammatory conditions
neoplasia
development abnormalities
cleft palate
failed closure of palatine shelves = aspiration of food
brachycephalic airway syndrome
combination of anatomical problems =
stenotic nares
everted laryngeal saccules
elongated soft pallate = airway obstruction, cyanosis and syncope
circulatory disturbances
epistaxis - bleeding from nose
sources
upper airways
lower respiratory tract
causes of haemorrhage in upper airways
inflammation
infection
trauma
neoplasia
clotting defects
VWD or thrombocytopenia
5 typical sings of inflammation
redness - due to blood vessel dilation and congestion/ hyperaemia/ haemorrhage
swelling - due to infiltration by cells and fluid leakage
heat - due to increased blood supply
pain - due to compression of tissue pressure sensors
loss of function - variable depending on site
acute inflammation - general principles
similar response throughout airways
vasodynamic changes - redness, swelling, exudate
increased secretions - serous, mucus
inflammation classified by type of exudate
serous
clear watery discharge
easily missed
mild - increased production from mucoserous glands
mucosal hyperaemia and oedema
catarrhal
viscous, mucoid
increased mucoserous secretions
minor numbers of inflammed cells
fibrinous
thick, fibrinous and haemorrhagic discharge
increased vascular permeability ± necrosis
purulent
thick, white, green, brown
many inflammatory cells esp neutrophils and cell debris
chronic inflammation = pathological changes
mucosal hyperplasia
goblet cell hyperplasia
seromucous gland hyperplasia
chronic inflammatory cells
macrophages, lymphocytes, plasma cells
fibroplasia
epithelial metaplasia

2o to chronic irritation eg bronchitis, get respiratory epithelial metaplasia ie. ciliated columnar → stratified squamous ep
polyps secondary to chronic inflammation
nasal/ nasopharyngeal polyps
horses and cats
cat - arise in auditory tube or tympanic bulla
may extend into pharynx or along external ear canal
resp noise/ dysphoea

nasopharyngeal polyp - cat
causes of upper airway inflammation
irritants/ allergens
pollen
dust
fomites
foreign bodies
parasites
infectious agents - viral, bacterial, fungal
some viral agents assoc with inflammation of URT
Feline herpesvirus 1 Flu →
Feline calicivirus Flu
Equine herpesvirus 1 + 4
Equine influenza virus
Canine distemper virus
Canine adenovirus 2 KC with BB
Canine parainfluenza virus KC with BB
Bovine herpesvirus 1 (Infectious Bovine Rhinotracheitis)
infectious bovine rhinotracheitis
due to bovine herpesvirus 1
aerosol infection
mixed, stressed and overcrowded
in severe cases = necrosis and fibrinous inflammation of mucosa

IBR - spread of virus throughout upper respiratory tract
neutralising antibodies and cell-mediated immunity responses - over 1-2 weeks
resolution of viral infection and elimination of bacteria
healing

strangles
Streptococcus equi
Colonises nasopharyngeal mucosa
initial serous nasal discharge becomes purulent typical of S. equi infection
lympahatic spread to lymphnodes
absesses within (parotid) LNs can rupture and drain to surface
guttural pouch empyema
sequel to strangles
abscessated retropharyngeal LNs ruptures into guttural pouch creating a pus filled cavity
can be caused by other bacteria
e.g rhodococcus equi

fungal infections - aspergillus fumigatis
dogs, horses, birds
often predisposing immunosuppression
fibrinonecrtotic/ granulomatous inflammation and bone lysis due to cytolytic enzymes from fungus

guttural pouch mycosis
Aspergillus fumigatis
Infection causes severe infm + necrosis
Often unilateral
complications =
damage to cranial nerves = paralysis of facial muscles, tongue, pharynx, larynx
erosion of blood vessels - haemorrhage may be fatal
nasal carcinoma
Ph: Epithelial cells, mostly glands, of the nasal mucosa
Pr: Long-skulled dolichocephalic dog breeds
Sp: Dog, >80% malignant tumours.
Dist: Nasal cavity > sinuses
Gr: Proliferative, destructive masses, white + friable