Pathology of the lungs II

pneumonia
inflammation of the pulmonary gas exchange system
– filling of the alveoli with cellular exudate

Pneumonitis
Inflammation of the lung, usually used to designate inflammation of the alveolar walls (interstitial pneumonia)

Causes of pneumonia
Infectious- viral, bacteria, parasitic, fungal, mycoplasmal
Toxic
Immunologic
Miscellaneous- foreign material, HCl, bacteria in aspiration pneumonia

Pulmonary Inflammation Major Concepts
– infection causes inflammation
– inflammation causes damage
– mucosal injury decreases mucociliary clearance
– damaged phagocytic cells don’t work well
– injury is resolved completely or there may be some fibrosis
– pulmonary fibrosis decreases gas exchange

Alveolar epithelium acute injury
– swelling and sloughing of type I alveolar epithelium
– leakage of fluid, protein, and fibrin into alveolar space
– hyaline membranes may form from mixing of proteinaceous fluid with surfactant

Alveolar epithelium normal injury repair
– clean- up by pulmonary alveolar macrophages
– proliferation of type II epithelial cells to replace type I cells

Alveolar epithelium chronic/persistent injury
– Epithelialization (fetalization) due to prolonged proliferation of type II epithelial cells
– persistent inflammation may lead to fibrosis of alveolar walls

Classification of pneumonias
– by exudate: suppurative, fibrinous, granulomatous
– by location: bronchopneumonia (lobular or lobar), interstitial, bronchointerstitial
– by cause: viral, bacteria, verminous, mycotic, toxic
– by route of infection: bronchogenic (aerogenous, aspiration), hematogenous (embolic)

Lobular vs. Lobar
lobular- individual lobules are affected. Results in a patchy lesions. Most common form of pneumonia in animals.
lobar- inflammation spreads quickly to involve large areas

Interstitial
inflammation of the alveolar walls (viral, toxins, some allergic reactions, most mycoplasmal infections)

Bronchopneumonia
– most common form of pneumonia
– route of exposure: aerogenous
– gross distribution: cranioventral distribution
– cause:
Bacteria
Mycoplasma

Bronchopneumonia pathogenesis
– initial damage and subseqent inflammation is centered on the broncho-alveolar junction
– infiltration by neutrophils and macrophages to phagocytose bacteria

Physiologic significance of bronchopneumonia
Obstructive and restrictive changes to the lung
– airways are obstructed
– infiltration and edema of the alveolar walls and filling of the alveoli makes the lung less pliable (more restrictive)
Increased restriction of the lung may be caused by concurrent pleuritis

Suppurative bronchiopneumonia: lobular
Gross: cranioventral firm, red to grey consolidation, individual lobules are affected
Histopath: early lesions are airway oriented, necrosis of bronchiolar epithelium, abundant purulent or mucopurulent exudate in airways and alveoli

Most common pathogens in lobular suppurative pneumonia
Pasteurella multocida
Bordatella bronchiseptica
Arcanobacterium pyogenes
Streptcoccus spp.
Escherichia coli
Mycoplasma spp.

Fibrinous bronchopneumonia: lobar or pleuropneumonia
– bronchopneumonia with abudant fibrin in alveolar spaces
– more lethal than suppurative pneumonias, due to more severe lung injury

Fibrinous bronchopneumonia lesions
gross: cranioventral distribution, can have random distribution in pgis, entire lobes are infected, hemorrhage/fibrinous pleuritis
Histopath: coagulative necrosis, edema, fibrin and vascular thombrosis, degenerate inflammatory cells

Fibrinous pneumonia common pathogens
– mannheimia hemolytica
– hemophilus somnus
– actinobacillus pleuropneumoniae
– mycoplasma mycoides subsp. mycoids

Pathogenesis of M. hemolytica causing fibrinous pneumonia
– colonization of resp. tract bacterium–> depression of pulmonary defense mechanisms–> logarithmic growth of M. hemolytica with leukotoxin production> damage to neutros, macros, release of endotoxin> leukotoxin and endotoxin-mediated tissue damage in conjunction with damage by toxins from neutros and macros

Possible sequelae of Bronchopneumonia
Good:
– resolution with little to no damage
Bad
– variable fibrosis depending on severity
– chronic bp wtih bronchiectasis and or bronchiolitits obliterans
– abscess formation in cranioventral lobes
– pleural adhesions
– septicemia or death

Pathophysiological significance of interstitial pneumonia
– restrictive disease due to thickening and infiltration of the alveolar walls Walls are more stiff than normal, with reduced compliance
– gas exchange is impaired due to reduced diffusion (increased wall thickness). Results in hypoxia.

Common causes of interstitial pneumonia
– respiratory viruses
– Mycoplasma spp.
– bovine pulmonary edema and emphysema
– acute respiratory distress syndrome (ARDS)
– USUALLY NOT BACTERIA (exception septicemia)

Route of exposure for interstitial pneumonia
– aerogenous or hematogenous exposure

Viral pathogenesis of interstitial pneumonia
– virus replicates in the respiratory airway and alveolar epithelial cells, damaging the cells
– virus induces inflammatory and immune response
– inflammation in parenchyma focused on interalveolar septa (alveolar wall)

Gross lesions of interstitial pneumonia
– diffuse distribution
– lungs fail to collapse and are rubbery
– lungs may have imprints of the ribs on the pleural surfaces

Histopathology of interstitial pneumonia
– injury to type I epithelium or endothelium
– exudative phase: fluid and hyaline membranes in alveoli, inflammatory cells, fibrin, and edema thicken alveolar walls
– proliferative phase: hyperplasia of type II pneumocytes, fibrosis with chronicity

Acute Respiratory Distress Syndrome (ARDS)
– acute, severe respiratory distress with pulmonary edema; usually fatal

Conditions associated with ARDS
Generalized systemic disease
– septicemia/endotoxemia, extensive burns, pancreatitis
Injury to the lung
– aspiration of gastric contents
– diffuse pulmonary infections (viral, mycoplasma, Pneumocystis)
Injury to other organs
– multiple trauma

ARDS pathogenesis
– endotoxin causes macrophages to produce cytokines and primes neutrophils in pulmonary capillaries to release enzymes and free radicals
– results in diffuse alveolar and endothelial damage
– results in abundant alveolar edema and fibrin exudation, with the formation of hyaline membranes. Fibroblasts use the membranes as a scaffold for deposition of connective tissue
RESULT: fibrosis

histopathology of chronic interstitial pneumonia
– persistence of type II hyperplasia
– fibrosis and inflammation of alveolar wall

Common causes of chronic interstitial pneumonia
– retroviruses in sheep and goats
– hypersensitivity pneumonitis in cattle and dog

Sequelae of interstitial pneumonia
– resolution
– fibrosis of alveolar walls and progressive restrictive lung disease
– death

Bronchointerstitial pneumonia route of exposure
aerogenous

Bronchointerstitial pneumonia causes
virus or mycoplasma

Bronchointerstitial pneumonia pathogenesis
viral infection and damage to bronchial, bronchiolar, and alveolar epithelium

bronchointerstitial pneumonia gross lesions
rhinitis, tracheitis, bronchitis, and interstitial pneumonia

bronchointerstitial pneumonia histopath
bronchitis and bronchiolitis
– necrosis and neutrophil infiltrates
Alveoli
– type I necrosis and type II proliferation

bronchointerstitial pneumonia common pathogens
– respiratory syncytial virus: cattle and sheep
– canine and equine adenovirus
– canine distemper virus
– porcine and equine influenza virus
– porcine mycoplasmosis

Embolic pneumonia route of exposure
hematogenous

embolic pneu cause
bacterial emboli

embolic pneu pathogenesis
lungs flter septic emboli from circulatio

embolic pneu gross lesions
Abscesses in all areas of the lung
– helps to differentiate embolic pneumonia from abscesses secondary to bronchopneumonia

embolic pneu histopath
– early inflammation is centered on small blood vessels
– with progression, abscesses, or microabscesses form

Embolic pneumonia common pathogens
– fusobacterium necrophorum
– archanobacterium pyogenes
– streptococcus equi
– staphylococcus aureus
– erysipelothrix rhusiopathiae

granulomatous pneu route of exposure
aerogenous or hematogenous

granulomatous pneu cause
fungi, less often bacteria, virus, or foreign material

granulomatous pneu pathogenesis
– causative agents have the ability to avoid or survive phagocytosis and persist in tissue
– type IV delayed type hypersensitivity

gran pneu gross lesions
multiple firm nodules distributed throughout lung

gran pneu histopath
granulomas or granulomatous inflammation

gran pneu common pathogens
– blastomyces dermatiditis
– mycobacterium sp
– feline infectious peritonitis virus
– silicosis

Tuberculosis common features
– organisms survive and replicate within phagocytic cells
– granulomatous pneumonia with granulomas in lungs
– oral or intestinal route of infection

tuberculosis organisms
M. bovis: cattle, sheep, goats, cats
M. avium: sheep, goats, pigs, horses and dogs
M. tuberculosis: Primates, elephants

Aspiration pneumonia route of exposure
airways

Aspiration pneu pathogenesis
inhalation of foreign material, bacteria, stomach acid

Aspiration pneu causes
iatrogenic- anesthesia, medication administration
Dysfunctional pharynx- neurologic dz, anesthesia
Meconium aspiration

Aspiration pneu gross lesions
– cranioventral distribution
– may be unilateral
– hemorrhage and atelectasis

Aspiration pneu histopathology
– severe necrosis
– suppurative exudate
– aspirated material may be seen in airways

Pulmonary Infections Occur when normal Pulmonary Defense Mechanisms Fail: 1. Loss of Cough Reflex = Coma / Anesthesia / Post-Op 2. Injury to Muco-Ciliary Escalator = Smoking / Squamous Metaplasia 3. IgA Deficiency (genetic / immunocompromised) 4. Decreased Macrophage Function …

– occur when there is impairment of the normal Pulmonary Defense Mechanism: 1. absent cough reflex 2. Damaged Mucociliary escalator 3. Deficiency in secretory IgA in bronchial mucus 4.↓phagocytic.bactericidal function of alveolar macrophages 5. Pulmonary congestion & edema 6. Presence …

Pulmonary Infections: when there is an impairment of the normal PULMONARY DEFENSE MECHANISM 1. loss of cough reflex (coma, anesthesia..etc.) 2. injury to mucociliary apparatus (smoking) 3. deficiency of secretory IgA in bronchial mucus 4. decreased phagocytic/bactericidal function of alveolar …

Composition of Alveolar Wall Two components 1. Type 1 epithelium: -covers 95% of surface area, but constitutes 40% of epithelial cells. 2. Type 2 epithelium: -covers 5% of surface area, but constitutes 60% of epithelial cells. Characterization of ARDS Severe …

In bacterial pneumonia, what causes lobules to fill with fluid and thus restrict oxygenation? After entering the lungs, bacterial organisms settle in air sacs and reproduce quickly. This causes the lungs to fill with an array of white blood cells …

anatomic alteration of the lungs 1. Inflammation of alveoli 2. alveolar consolidation 3. atelectasis what happens with inflammation of lung with pneumonia fluid & red blood cells move into alveoli, leukocytes move into engulf & kill invading bacteria, macrophages appear …

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