Respiratory System Pathology 2

Question 1

1. What is classification of pneumonia based on?
2. Classifications of pneumonia?

Answer 1

1. Morphological features.
   - Distribution of lesions.
   - Macroscopic features.
   - Microscopic features.
2. Bronchopneumonia.
   Interstitial pneumonia.
   Granulomatous pneumonia.
   Embolic pneumonia.

Question 2

Typical causes of bronchopneumonia.

Answer 2

• Bacteria (incl. Mycoplasma).
• Viral infections (and stress, may predispose to bacterial infection).
• Aspiration of food/GI contents (acidity can cause severe lung inflammation).

Question 3

Bronchopneumonia agent route of entry

Answer 3

Inhalation.
- in inspired air or from flora in nasal passages.

Question 4

1. Typical distribution of bronchopneumonia.

Answer 4

1. Mostly cranial and ventral regions (but can affect any region and may be (patchy).

Question 5

Interlobular septum spp. differences.
- clinical significance.

Answer 5

Most prominent in cattle and pigs and less so in other spp.
- more prominent interlobular septa mean infection spread to adjacent lobules is less likely.

Question 6

Acute bronchopneumonia pathogenesis.

Answer 6

Inhale agent > bronchiolar infection w/ acute inflammation and exudation (fluid, proteins, inflammatory cells) > infection spread and inflammation down to alveoli > accumulation of exudate in alveolar spaces > spread to adjacent alveoli > spread to adjacent lobules across septa or via bronchiolar tree.

Question 7

Bronchopneumonia at microscopic level.

Answer 7

Air-filled alveoli, bronchioles, blue dots representing inflammatory cells in exudate in bronchioles and alveolar spaces, showing extensive spread of bronchopneumonia.

Question 8

Gross lung features of bronchopneumonia.

Answer 8

Affected regions are cranial and ventral.
- dark red-brown or greyish w/ time.
- flabby to firm due to exudate filling airspaces and collapse of alveoli due to airway obstruction.
- May be patchy due to some lobules being affected and others being unaffected (most prominent in pigs and cattle).
- May see suppurative bronchopneumonia w/ mucopurulent exudate exuding from airway on cut lung surface (most common type).
- Severe cases – fibrinous bronchopneumonia w/ fibrin (yellow)expanding interlobular septa –> marbling.
- May be associated w/ concurrent pleuritis > fibrin > fibrous adhesions.

Question 9

Possible event following an acute bronchopneumonia.

Answer 9

Agent removed by defence mechanisms and immune response and inflammation resolves and healing begins.
OR agent persists/defences fail and chronic bronchopneumonia results.

Question 10

Gross lung features of chronic bronchopneumonia.

Answer 10

• Thick white-pink bands of fibrosis surrounding parenchyma.
• Grey-ish areas in parenchyma representing chronic inflammation, fibrosis, alveolar collapse
  Airway obstruction, bronchiectasis (destruction and permanent dilation), abscessation.
  Dry, caseous necrosis e.g. mycoplasma infection.

Question 11

List some potential causes of bronchopneumonia.

Answer 11

Bacteria:
- Pasteurella multocida.
- Mannheimia haemolytica.
- Trueperella pyogenes.
- Bordetella bronchiseptica.
- Streptococcus spp.
- Escherichia coli.
- Histophilus somus.
- Actinobacillus pleuropneumoniae.
Mycoplasma:
… hyopneumoniae.
… bovis.
… dispar.
… ovipneumoniae.
Viruses:
- Parainfluenza-3.
- Bovine respiratory syncytial virus.
- Bovine herpesvirus-1.

Question 12

Enzootic pneumonia in pigs.

Answer 12

Mycoplasma pneumonia caused by infection w/ mycoplasma hyopneumoniae.
Inhalation > colonises lower airway ciliated epithelium > cilia and cell loss, altered mucus composition, reduced neutrophil phagocytic function, immunosuppression, lymphoid hyperplasia, hyperplasia of lymphoid tissue in lung creating a ‘cuff’ around airways > predisposition to secondary bacterial infection > suppurative bronchopneumonia.

Question 13

Interstitial pneumonia.

Answer 13

Inflammation in wall of alveoli following an injury to the lung parenchyma which is directed at one or more components of the alveolar wall - pneumocytes, endothelial cells, basement membrane.
Aetiological agents via airways (inhalation) or bloodstream (haematogenous).

Question 14

Causes of interstitial pneumonia.

Answer 14

Many.
Viruses, migrating parasites, protozoa.
Septicaemia.
Toxins.
Toxic metabolites locally.
Allergens.

Question 15

Interstitial pneumonia distribution.

Answer 15

Diffuse / generalised.

Question 16

Interstitial pneumonia pathogenesis.

Answer 16

Aetiological agent causes widespread injury to the alveolar walls > acute inflammation w/ hyperaemia and exudation of fluid > cellular response w/ immigration of inflammatory cells > alveolar walls fill w/ cells and exudate > cells, fluid and exudate spill over into the alveolar spaces (exudative phase).

Question 17

Exudative phase microscopically.

Answer 17

Multiple alveolar spaces.
Alveolar walls have prominent capillaries, full of RBCs due to vasodilation and hyperaemia - inflammatory response.
Some alveolar spaces contain pinkish material which line alveolar wall - hyaline membrane formation – plama proteins have leaked from inflamed blood vessels and mixed w/ surfactant lipids in alveolar space.

Question 18

Proliferative phase.
Microscopically.

Answer 18

Early healing response.
V thick alveolar wall.
- Still vasodilation and hyperaemia of capillaries w/in alveolar walls.
- Still inflammatory cells.
- Alveolar walls lined by plump, cuboidal cells = type II pneumocytes.
– reserve cells that are normally present w/in alveoli, and they produce surfactant.
– proliferate and differentiate to replace type I pneumocytes that have been injured and/or lost –> differentiate into flattened type I pneumocytes once conditions favourable to complete healing process.
Alveolar spaces contain accumulations of plump cells = alveolar macrophages.
- reacting to lung injury and the presence of material in alveolar spaces.
– phagocytosing and removing exudate and cell debris.
– dealing w/ cause of alveolar injury.

Question 19

Possible events following acute interstitial pneumonia.

Answer 19

Source of injury removed by defences and immune responses and healing and resolution occur.
Source of injury persists or repeats due to failure of immune response and defences and chronic interstitial pneumonia occurs.

Question 20

Chronic interstitial pneumonia microscopically.

Answer 20

Alveolar walls much more thickened.
- Expanded by fibrous tissue.
- Chronic inflammatory cells.
- Persistence of type II pneumocytes.

Question 21

Gross chronic interstitial pneumonia.

Acute.
In cattle?

Answer 21

Can be difficult to detect grossly as diffuse.
Colour ranges from diffusely red (acute) to pale grey or mottled red and grey (chronic).
Lungs may fail to collapse when thorax opened due to wall thickening - rib impressions on lung surface.
Heavier.
Firmer, rubbery or elastic.

Acute - pulmonary oedema – excess fluid in airways or exuding from cut surface if lung.
Cattle - acute interstitial emphysema.
– air escapes alveoli and accumulates w/in interlobular septi.
–> where there is partial obstruction of bronchioles by oedematous fluid/exudate and also due to strenuous respiratory efforts and gasping prior to death.

Question 22

List some potential causes of interstitial pneumonia.

Answer 22

Infections:
- Septicaemia salmonellosis.
- Ascaris suum (pulmonary migration).
- Ovine lentivirus – causes ovine progressive pneumonia (maedi) in sheep (chronic).
Hypersensitivity reactions:
- Farmer’s lung: Type III hypersensitivity reaction to fungal spores (acute or chronic).
Toxins:
- Tryptophan (Fog fever) (acute bovine pulmonary oedema and emphysema).
- Paraquat – selectively taken up by pneumocytes.
Inhaled irritants:
- Smoke.

Question 23

Cattle Fog Fever / Acute Bovine Pulmonary Oedema and Emphysema.

Answer 23

Lush grass grows in autumn after pasture has been cut for silage and hay (foggage).
Grass contains high levels of L-tryptophan.
L-tryptophan converted to 3-methyl indole in rumen once ingested by cows.
3-methyl indole absorbed into bloodstream and carried to the lungs.
Bronchiole epithelial cells (club cells) can convert 3-methyl indole into toxic metabolite - necrosis of bronchiole calls and type I pneumocytes, causing acute interstitial pneumonia.
Variable outcomes - mortality in severe cases.

Question 24

1. Embolic pneumonia cause.
2. Route of embolic pneumonia entry.
3. Distribution of embolic pneumonia.

Answer 24

1. Bacteria (septic emboli).
2. Haematogenous.
3. Random foci.

Question 25

Gross features of embolic pneumonia.

Answer 25

Random distribution.
Multifocal, sometime coalescing.
Round, also irregular, lesions.
Yellow-green lesions.
Some reddened areas of parenchyma surrounding the lesions.

Question 26

What do the yellow-green lesions associated w/ embolic pneumonia represent?

Answer 26

Suppurative foci where bacteria embolised to the lungs and successfully established site of infection.

Question 27

Some potential sources of septic emboli.

Answer 27

Liver abscesses (cattle).
Bacterial endocarditis (R heart).
Umbilical infections.
Chronic skin or hoof infections.
Mastitis.
Endometritis.
IV catheterisation.

Question 28

1. What is granulomatous pneumonia?
2. Granulomatous pneumonia cause.

Answer 28

1. Type of pneumonia in which a granulomatous inflammatory response is occurring.
   Chronic.
   Cellular infiltrate contains many macrophages.
   Macrophages may form aggregates or granulomas.
   Typically present as nodular lesions/masses.
2. Agents that persist in the tissues and are resistant to phagocytosis and the acute inflammatory response.

Question 29

Causes of granulomatous pneumonia.

Answer 29

Bacterial:
- mycobacteria (e.g. TB), actinomyces, rhodococcus.
Parasitic:
- lungworms.
Fungal:
- cryptococcus.
Viral:
- FIP.

Question 30

1. Routes of entry for agents causing granulomatous pneumonia.
2. Granulomatous pneumonia distribution.

Answer 30

1. Inhalation or haematogenous.
2. Variable - focal / often multifocal.

Question 31

1. M. bovis spp. affected.
2. BTB lung gross lesions.

Answer 31

1. Cattle, alpacas, pigs, cats.
2. Nodular to focally extensive.
   Large lesions.
   Mottled, cream, brown, yellow lesions.
   Firm lesions.
   Possibly mineralised lesions.
   Granulomatous inflammation.
   Caseous necrosis.
   Fibrosis of interlobular septa (white-grey).
   Can get numerous small nodular foci w/in lungs - haematogenous spread.