Respiratory System Pathology 1

Question 1

Main pathological processes and conditions affecting the respiratory system.

Answer 1

Inflammation.
Neoplasia.
Circulatory disorders.
Congenital and developmental disease.
Degenerative condition.

Question 2

Alveolar wall.

Answer 2

Pneumocyte type I = epithelial cells lining most of the alveoli. Thin and flat. Allow air to pass across and can secrete small amount of fluid. End-stage cell - cannot replicate if they die.
Pneumocyte type II = cuboidal cells. Fewer if these. Secrete surfactant. Can proliferate, spread out and replace type I pneumocytes.
Endothelial cells line blood vessels and are in close contact w/ the pneumocytes, sharing the common basement membrane.
Very thin and delicate.

Question 3

How do agents of disease gain entry to the respiratory system?

Answer 3

Inhalation.
Haematogenous.
Direct extension from surrounding tissues.

Question 4

Respiratory system defence mechanisms (airways).

Answer 4

• Aerodynamic filtration - turbinate bones in nasal cavity.
• Muco-ciliary escalator.
• Lymphoid tissue (bronchus associated lymphoid tissue) – IgA.
• Protective reflexes – cough, sneeze, bronchoconstriction.
• Antioxidants.
• Normal bacterial flora – URT.

Question 5

Mucociliary escalator.

Answer 5

Most respiratory tract lined w/ v delicate pseudostratified epithelium w/ lots of cilia on the top (~100-200/cell). They waft at ~100bpm.
Goblet cells produce mucus.
Mucus layer progressively moves from lower RT to pharynx or from nasal cavity to pharynx and swallow or cough out most of the material.
Mucus layer can also dissolve gases and trap particulate matter w/in it.

Question 6

Respiratory system defence mechanisms (alveoli).

Answer 6

Macrophages.
- w/in alveoli, alveolar wall, some spp. have macrophages w/in the lungs
Antioxidants/antibacterial substances secreted in the fluid lining the alveoli.
Protective reflexes - bronchoconstriction.
IgG.

Question 7

Factors affecting the respiratory defences.

Answer 7

Impairment of immune responses/cell function.
Impaired mucociliary clearance.

Question 8

1. Factors that impair the immune responses/cell function.
2. Impairment of mucociliary clearance?

Answer 8

1. Infectious agents – esp. viruses.
   –> suppress macrophage function.
   Toxic gases (e.g. ammonia).
   Stress e.g. transport, weather, stocking.
   Hypoxia e.g. due to cardiac disease.
2. Cellular injury and loss of function.
   Chronic inflammation&raquo_space; metaplastic change e.g. loss of cilia, goblet cells.

Question 9

Viral-bacterial synergism.

Answer 9

Viral infection first which suppressing the immune system and defence mechanisms, leading to secondary bacterial infection.

Question 10

Term for inflammation of…
1. Nasal mucosa.
2. Paranasal sinuses.
3. Pharynx.
4. Larynx.
5. Trachea.

Answer 10

1. Rhinitis.
2. Sinusitis.
3. Pharyngitis.
4. Laryngitis.
5. Tracheitis.

Question 11

Term for inflammation of…
1. Bronchi.
2. Bronchioles.
3. Lung parenchyma,
4. Pleura.

Answer 11

1. Bronchitis.
2. Bronchiolitis.
3. Pneumonia.
4. Pleuritis (pleurisy).

Question 12

Potential causes of airway system inflammation.

Answer 12

Infectious agents e.g. virus, bacteria, fungi, parasites.
Physical injury e.g. FB e.g. grass awn.
Secondary to neoplasia e.g. nasal adenocarcinoma.
Extension from local disease e.g. tooth abscess, neoplasia.
Allergic diseases e.g. recurrent airway obstruction/equine asthma, asthma in cats.

Question 13

Injury of the airway.

Answer 13

Injury&raquo_space; epithelial cell degeneration&raquo_space; epithelial cell necrosis, death&raquo_space; detachment of these, sloughing off&raquo_space; ulceration

Question 14

Process of acute inflammatory response of airway following injury.

Answer 14

Increased secretions from goblet cells and seromucous glands.
Inflammatory response in submucosa (driven by vasodilation of blood vessels, allowing fluid escape) (redness and swelling).
Oedema and plasma proteins come out of blood vessels.
Inflammatory cells come out of the vessels e.g. leucocytes. (exudate).

Question 15

1. Serous discharges and exudates.
2. Catarrhal discharges and exudates.

Answer 15

1. Excess fluid produced by serous glands.
   Clear, watery fluid.
2. Substantial increase in mucus production from goblet cells/mucus glands.
   Translucent/clear/slightly opaque.
   Mucoid/tacky.

Question 16

1. Purulent discharges and exudates.
2. Fibrinous/fibrinonecrotic discharges and exudates.

Answer 16

1. Typically bacterial infection w/ necrosis and exudate containing many leucocytes, esp. neutrophils.
   Thick and opaque/coloured - white, yellow, green.
2. Typically severe inflammation w/ exudation containing fibrin.
   May be mixed w/ necrotic debris.
   Soft, yellow/tan/grey, fibrin layer on the mucosal surface.

Question 17

Potential outcomes following acute inflammation.

Answer 17

Immune response succeeds&raquo_space; insult ceases&raquo_space; healing and resolution.

Immune response fails&raquo_space; insult persists or is repeated&raquo_space; chronic inflammation.

Question 18

1. Examples of important causes of acute airway inflammation in cattle.
2. In horses.

Answer 18

1. Infectious bovine rhinotracheitis (BHV-1).
   Parainfluenza virus 3.
2. Streptococcus equi spp. equi (strangles) and spp. zooepidemicus.
   Equine herpesvirus (EHV-1, EHV-4).
   Equine influenza.

Question 19

1. In cats.
2. In dogs.

Answer 19

1. “Cat flu” - FHV-1; Feline calicivirus.
2. “Kennel cough” (Canine infectious respiratory disease complex):
   - Bordetella bronchiseptica, various viruses e.g. Canine parainfluenza virus.

Question 20

Process of infection w/ IBR.

Answer 20

Infected animal (can be latently infected and then re-excrete virus in stress etc.)&raquo_space; susceptible population&raquo_space; infection of susceptible animals e.g. by aerosol (cough, sneezing etc.), direct contact w/ nasal secretions, indirect contact e.g. food and water contamination&raquo_space; virus replicates in nasopharynx&raquo_space; lysis of epithelial cells&raquo_space; inflammation&raquo_space; release of virus which can then disseminate wider throughout the respiratory tract (mainly URT).

Question 21

1. Incubation period of IBR.
2. How can pneumonia develop in IBR?

Answer 21

1. 2-6d.
2. Material of affected tissue in URT break off and get aspirate.
   AND/OR virus suppresses macrophages, causing secondary infection and pneumonia in the lungs.

Question 22

Immune response to IBR.

Answer 22

Cell-mediated immune responses (from ~5d), neutralising antibodies at ~10d.
Healing and repair of respiratory mucosa follows over a period of ~2-3w.

Question 23

Process of infection w/ equine strangles.

Answer 23

Infected animal&raquo_space; contact w/ uninfected animal w/ nasal secretions (direct, indirect, snorting, coughing) or discharges e.g. from draining abscesses&raquo_space; bacteria in nasopharynx causing an acute pharyngitis&raquo_space; serous discharge&raquo_space; may become purulent&raquo_space; bacteria invade mucosa, moves through lymphatic system to local LNs&raquo_space; LN abscesses&raquo_space; rupture internally (into RT) or externally&raquo_space; internal rupture may lead to aspiration or guttural pouch empyema.

Question 24

Less common sequalae to Streptococcus equi ssp. equi infection.

Answer 24

• Spread of bacteria to other sites – organs/LNs (bastard strangles).
• Purpura haemorrhages (rare) – immune complex deposition causing vasculitis causing oedema and haemorrhages (can be caused by other infections).

Question 25

Changes seen in chronic inflammation of the respiratory tract.

Answer 25

Increased mucus production (narrowing of airway).
- Goblet cell hyperplasia.
- Goblet cell metaplasia in the bronchioles.
- Seromucous gland hypertrophy and hyperplasia.
Squamous metaplasia - effect of defences.
Mucosal thickening (narrowing of airway).
- Epithelial and glandular hypertrophy.
Submucosa.
- Inflammatory cells.
- Granulation tissue/fibrosis.
Inflammatory polyps anywhere in RT.
Destruction and weakening of bronchi wall - permanent dilation = bronchiectasis (distended bronchi usually filled w/ exudate > obstruction > collapse of dept. lung parenchyma = obstructive atelectasis).
*airway narrowing can be exacerbated by bronchoconstriction.