Inflammation and the lung Flashcards
Inflammation terminology
in general: add suffix “itis” to start of anatomical name
e.g. tonsilitis, pharyngitis
sometimes greek or latin is used i.e. stomatitis and gastritis
Why are lungs vulnerable to airborne infection?
huge area of alveoli
large volume of air entering the lungs continuously
high concentration of noxious elements in the air
Why are lungs vulnerable to problems via hematogenous spread?
lungs vulnerable to blood-borne microbes/toxins/emboli
Entire output of RV enters the lungs; roughly 9% of total blood volume is in the lungs
largest capillary bed in the body= pulmonary capillary bed
1ml of blood occuppies 16km of capillary bed
Important lung features
bronchi: supported by cartilage, efficient mucociliary defenses
bronchioles: transition zone from airway/conducting–>gas exchange; diminished mucociliary defenses; no supporting cartilage; clara cells are metabolically active (i.e. producing reacitve metabolites); alveolar macs and n’phils accumulate–> can release damaging oxidative free radicals.
Important feature of alveoli
delicate, thin-walled
vascular endothelium, basal lamina (alveolar interstitium), thin type I pneumocytes, granular tpye II pneumocytes which produce surfactant
NB: type II can act to repair damage to type I by flattening out.
Normal UPPER respiratory flora
most proximal region of conducting system ONLY (nasal cavity, pharynx, larynx)
Manheimia hemolytica in cattle; pasturella multocida in cats, cattle and pigs; bordetella bronchiseptica in dogs and pigs
Bronchopneumonia
affects cranial aspect of lungs d/t inhaled organisms
common in domestic species
initiates in bronchi and extends into surrounding parenchyma and can involve all airways (including alveoli)
interstitial pneumonia
see rib imprints
increased cellularity, big firm lungs which don’t deflate
inflammation of the pulmonary interstitium (other than the airways); usually involves alveolar epithelium
Granulomatous pneumonia
TB!
parasitic pneumonia: parasites trigger eosinophils which trigger macrophages
embolic pneumonia
collateral circulation, vast blood supply–> hematagenous spread of organisms/debris
pneumonitis: pneumonia with a lot of fibrous material
Causes of bronchopneumonia
bacteria
mycoplasma and viruses- with secondary bacteria
aspirate food or gastric contents
Pathogenesis of bronchopneumonia
inhaled agents–> injury and subsequent inflammation at the bronchoalveolar junction–>acute inflammatory response–> exudation of fluid and plasma proteins into bronchioles and alveoli–> recruitment of alveolar macs and emigration of neutrophils in blood vessels.
nb: can get diphtheritic membrane
Nb: cranioventral aspect of lung commonly affected.
Suppurative bronchopneumonia
exudate: purulent or mucopurulent
distribution: can be patchy, confluent areas or whole lobes
causes: pasturella multocida, brodetella bronchispetica, arcanobacterium pyogenes (truperella pyogenes), strep spp., E. coli
Bland aspiration–> not toxic, but something that shouldn’t be in lungs
Parainfluenza 3, respiratory syncitial virus and distemper.
Fibrinous bronchopneumonia
exudate: fibrin, oedema, n’phils, necrosis
Distribution: spreads rapidly within and between lobules- often affects large confluent areas/whole lobes
Causes: manheimia hemolytica, actinobacillus pleuropneumonia
Irritant aspiration
mycoplasma mycoides
Histopath: necrosis of alveolar walls; dense fibrinous edema fluid
Fibrinous adhesions seen on lung surface.
Acute fibrinous bronchopneumonia in calves
manheimia hemolytica–> colonizes lower respiratory tract
-produces leukotoxin which damages white cells–> lyses alveolar macrophages and neutrphils
lysosomal contents are released–> once outwith cells, tissue necrosis
-tissue necrosis and fibrinous bronchopneumonia
extensive deposition of fibrin in interlobular and interlobar septa
suppurative or fibrinous is determined by severeity of injury: can co-exist
Possible sequelae to acute bronchopneumonia
resolution
chronic pneumonia–> BALT hyperplasia, bronchiolar goblet cell metaplasia (increased secretion), fibrosis
Abscess formation
pleursy/pleuritis
death
Cuffing pneumonia
mycoplasmal bronchopneumonia
hyperplasia of balt–> squishes bronchiole
enzootic pneumonia
collapse and consolidation: collapse of alveoli due to peribronchial cuffing; consolidation due to movement of cells and fluid into alveoli.
Chronic suppurative bronchopneumonia
mucus in airways
mucopurulent: normal lung collapsed, a few areas of overinflation
verminous (parasitic) pneumonia due to dictyocaulus filaria
interstitial: larval migration
bronchitis: intrabronchial adults
granulomatous: aberrant parasites, dead larvae or eggs
LNs with be green with parasitic infection due to presence of eosinophils
areas of collapse and overinflation
Muelleris capillaris
non-immune–> doesn’t cause clinical disease
younger sheep get dramatic puffy coalescing lesions
in older animals, lead shot lesions–> IR walls off organisms with eosinophils–> granulomatous inflammation walls of degenerative larvae.
Angiostrongylus vasorum
in dogs and foxes
molluscs are IMH
parasites of pulmonary arteries and right ventricle
adults–> chronic arteritis
larvae–> alveolar injury, thickened alveolar walls +/- granulomas
Blastomycosis
granulomatous pneumonia
large numbers of small granulomas throughout lungs, many macrophages filled with small punctiform intracytoplasmic dark oval yeast bodies- big, gritty, swollen looking.
Embolic pneumonia
Ruminitis (devitalization of mucosa, bacterial rumenitis, bacteria seed portal circulation)–> hepatic abscesses–> blood through caudal vena cava to lungs–> embolic pneumonia–> caudal vena cava syndrome–> rupture of pulmonary arteries, hemolysis, death.
