This document summarizes various pathologies that can affect the respiratory system. It begins by discussing various diseases that can cause inflammation in different parts of the respiratory tract, such as epistaxis (nose bleeding), rhinitis (inflammation of the nasal mucosa), sinusitis (inflammation of the sinuses), laryngitis (inflammation of the larynx), and tracheitis (inflammation of the trachea). It then discusses pathologies that can affect the lungs, such as different types of pneumonia (suppurative bronchopneumonia, fibrinous bronchopneumonia, interstitial pneumonia, and embolic pneumonia), pulmonary edema, atelectasis, and pulmonary emphysema. It provides descriptions

1. Pathology of Respiratory System
Oxygen is a vital requirement of animals.
An animal may survive for days
without water
or for weeks without food,
but life without oxygen is measured in
minutes.
Presented by
Dr. Mansoor Tariq
Assistant Professor
Department of Veterinary Pathology

3. TRANSITIONAL
REGION
 Respiratory
bronchioles
 Best developed in
carnivores &
primates
 First level at
which gas
exchange occurs
 Primarily air
passage ways
GAS EXCHANGE
Alveolar ducts
Alveolar sacs
Alveoli

4. 1) Pathology of the nasal cavity
1) Epistaxis
2) Rhinitis
3) Sinusitis
2) Laryngitis
3) Tracheitis
4) Bronchi
5) Bronchioles
6) Lungs (Pneumonia)
Pathology of Respiratory System

5. EPISTAXIS is bleeding from nasal passage
due to trauma, neoplasm and ulcerative lesions as a
result of infections.
Hemoptysis blood comes from mouth, saliva or sputum.
hemorrhage from the nose, usually due to rupture of small vessels
Minor bleeding may be caused by a blow on the nose,
irritation from foreign bodies.
Exercise induced pulmonary hemorrhage in horses.

6. RHINITIS (inflammation of the nasal mucosa)
may be caused by infections or allergies.
& Acute infectious rhinitis is most often caused by viruses and is a
typical manifestation of the
common cold.
Acute rhinitis is present in
certain infectious diseases
such as strangles, influenza
and glanders of horses,
and
distemper in dog.

12. SINUSITIS is the inflammation of sinuses
Frontal sinusitis is usually
associated with dehorning,
and maxillary sinusitis with
infected teeth.

13. e.g.
Frontal sinusitis in dehorned cattle.
The larvae of botfly Oestrus ovis
enters in nasal passage and migrate
upto frontal sinuses and turbinate
bones and cause mucopurulent
inflammation.
Similarly leeches (Dinobdella ferox) is
known to cause nasal cavity
inflammation in domestic animals and
suck blood.

15. LARYNGITIS inflammatory condition of larynx
Necrotic laryngitis ("calf diphtheria") is common in feedlots.
predominantly in calves, usually >3 months old. (calf diphtheria)
Diphtheria means leather, due to the type of exudate that forms.
In truth. the pus that forms in affected cattle is more like curds.

17. TRACHEITIS is the inflammation of trachea.
• In canines, it is tracheobronchitis and caused by adenovirus,
influenza
virus and herpes virus.
• while in poultry it is manifested by laryngo-tracheitis is caused by
herpes virus.
OTHER DISEASE INVOLVED LARYNX AND TRACHEA
• Calf Diphtheria fusiformis necrophorus
• Infectious bovine rhinotracheitis (IBR) caused by a bovine
herpesvirus.
• Feline viral rhinotracheitis caused by feline herpesvirus

18. Avian infectious laryngo-tracheitis (ILT)
In poultry, hemorrhage in trachea and caseous plug in trachea towards
larynx causing obstruction.

20. Inflammation of the bronchi (bronchitis) and bronchioles (bronchiolitis)
The larger bronchi,
well supplied mucous-secreting
and ciliated cells .
The lumen is large enough to
remain healthy even in the
presence of abundant exudate
and such exudate can be
expelled by an effective
cough reflex.
Bronchioles walls are thin and the
Small lumens are easily blocked by
exudate which may be too
far away for the cough reflex to be effective.

21. BRONCHITIS is the inflammation of bronchi, characterized by
catarrhal, suppurative, fibrinous or haemorrhagic exudate.
Normal Bronchial wall Inflamed Bronchial wall
Tracheobronchitis is an acute or chronic inflammation of the trachea and
bronchial airways; it may also extend into the lungs.

22. Chronic bronchitis
in cattle and sheep is
parasitic infection.
e.g
Dictyocaulus filaria in sheep/goat
Dictyocaulus vivparus in ox.

24. smooth muscle in the
wall degenerates,
mucosa becomes
thinner and the
walls are destroyed
and
replaced by fibrous
connective tissue

25. The surface area of
the lungs is roughly
the same size as
a tennis court.
The capillaries in
the lungs would
extend 1,600 km
if you placed
end to end
Everyday we lose half a liter of water through breathing.

27. Lungs of horse, sheep, ox, and pig. L, left; R, right; A, cranial (apical);
C, middle (cardiac); D, caudal (diaphragmatic); I, accessory (intermediate).

29. ATELECTASIS (Collapse)
Atelectasis is the failure of alveoli to open or the alveoli are
collapsed and thus do not have air. may affect a part of lobe or
two or all of one lung.
➢ Common cause of atelectasis is a blockage of one of the tubes
(bronchi) that branch off from the trachea (windpipe) and lead
to the lung tissue.
➢ The blockage may be caused by something inside the bronchus,
such as a plug of mucus, a tumor, or an inhaled foreign object.
➢ When a bronchus or a smaller airway (bronchiole) becomes
blocked, the air in the alveoli beyond the blockage is absorbed
into the bloodstream, causing the alveoli to shrink and collapse.

30. blockage of bronchi

31. Types of Atelectasis

32. PULMONARY EMPHYSEMA
Emphysema is the increase in amount of air in lungs characterized
by over dilation of the alveoli. It may be acute or chronic and focal or
generalized.
Pathogenesis is not fully understood but there is 2 possibilities
1. May be degradation and weakening of the interstitium by
proteolytic enzymes, e.g. elastase, released by inflammatory
cells.
2. More common, the condition develops secondary to either
chronic bronchitis and bronchiolitis, which cause obstruction
of airways on expiration but still allow air to enter alveoli.

36. PULMONARY EMPHYSEMA
Two major forms of pulmonary emphysema occur in the lungs
1. Alveolar (vascular) emphysema
2. Interstitial (interlobular) emphysema
There are several conditions in which enlargement of airspaces is not
accompanied by destruction; is called overinflation.

37. 1. Alveolar (Vascular) emphysema
In alveolar emphysema the alveoli are distended by excessive
amounts of air pressure and often times rupture.
Alveolar membrane disturb

38. 2. Interstitial (interlobular) emphysema
In interstitial emphysema the excessive air accumulates in the sub-
pleural, interstitial, and interlobular regions of the lungs.
when air enter in the supporting connective tissue of the lungs,
(Mediastial, Subcutaneous tissues, sub pleural, interstitial spaces).
May occur with a sudden
increase in intra alveolar
pressure cause a tear in
alveolar spaces,
break the alveolar sac
and air come out in the
tissue space of the lung
(i.e. interlobular or
pleural space).

39. Atelectasis

41. PULMONARY EDEMA
is accumulation of serous fluid in alveoli of lungs.
➢ Characterized by accumulation of fluid in interstitium and alveoli.
➢ Failure of the left heart especially results in pulmonary edema - the
pulmonary veins have seriously increased hydrostatic pressure.
Normally lung produces
fluid (transudate) that is rapidly
removed by the lymphatic system.
when fluid production exceeds
lymphatic system unable to
remove cause the
pulmonary edema.

43. In heart-related pulmonary edema,
when the heart’s left ventricle is not able to pump out enough of the
blood it receives from the lungs, pressure increases in the left atrium,
and then in the blood vessels of the lungs, causing fluid to be pushed
into the lung’s air sacs.

44. Pulmonary Edema
The lungs appear wet, heavy and fail to collapse when the thorax is opened.

46. PLEURITIS
is the inflammation of pleura characterized by serous, fibrinous or
purulent exudate. It is also known as pleurisy.

47. Pneumothorax
Is the presence of gas or air in the thorax cavity.
• Air can leak in from outside (loss of continuity of body wall) or
from inside (break in visceral pleura).
• Air can really compress the lungs, causing atelectasis.

48. Increased vascular permeability transudation of fluid body tissues
(e.g. brain and lungs) and body cavities (e.g. pericardial and thoracic cavities),
but mechanisms responsible for the transudation are poorly understood.
Hydrothorax
Hydrothorax is the accumulation of abnormal quantities of transudate (serous
fluid) in thoracic cavity.
Causes include congestive heart failure, Hypoproteinemia (liver, renal,
intestinal disease, starvation) and lymphatic obstruction.

49. Hemothorax
is the presence of free blood in thoracic cavity.
• It is caused by severe trauma or penetrating wound into the lungs,
rupture of major blood vessels (aneurism), coagulopathies.
• Lesions: blood in thorax cavity.

50. Pyothorax
is the presence of purulent material filled in thorax cavity.
• Pyothorax usually seen in the dog and cats, result of bacterial
infection due to injury.
• Unilateral pyothorax, where one lung is affected.
• Suppurative exudate present in thorax

51. Chylothorax
▪ is the presence of free lymph (chyle) in the thorax and it is caused
by rupture of a major lymphatic duct of thorax cavity.
▪ Most common causes are thoracic trauma and neoplasia. There is
also an idiopathic form of chylotorax in dogs.
▪ Lesions: Milky fluid in thorax cavity.
For diagnosis,
submit fluid to clinical
pathology –
it should be high in
triglycerides and
lymphocytes.

52. Salamander Lizard PigeonPrimate
Nostrils, mouth, and
throat
Trachea
Lung
Air sac
Vertebrate Lungs

54. PNEUMONIA
"inflammation of the lung caused by bacteria, in which the air sacs (alveoli)
become filled with inflammatory cells and the lungs become solid"
Pneumonia is "a severe form of acute lower respiratory infection that
specifically affects the lungs".
During a Pneumonia infection, the alveoli of one or both lungs fill up with pus
or fluid. This increases the labor of breathing, and thus gaseous exchange
cannot occur as it normally would.
Pneumonia is due to infections caused primarily by
1. bacteria
2. viruses
3. Fungi
4. Parasites
Causes of Pneumonia primarily by bacteria or viruses and less commonly
by fungi and parasites.
Young animals are more susceptible to the pneumonia rather than adult.

55. Stages of Pneumonia
Pneumonia has four stages of inflammatory response,
1. Congestion
2. Red hepatization
3. Grey hepatization
4. Resolution

56. Congestion
• This phase represent the acute inflammatory response to bacterial
infection.
• Occurs in the first 24 to 48 hours
• Capillaries in the surrounding alveolar walls become dilated and
congested
• Cellular exudates containing neutrophils, lymphocytes and fibrin
replaces the alveolar air
• The infections spreads to the hilum and pleura fairly rapidly
• Pleurisy occurs
• Grossly, the lung is heavy, enlarge and hyperemic
r

57. Red Hepatization
• Occurs in the 2-4 days after congestion
• At this point the consistency of the lungs resembles that of the liver
• The lungs become hyperemic
• Alveolar capillaries are engorged with blood which shows the red
appearance of lungs.
• Fibrinous exudates fill the alveoli
• This stage is "characterized by the presence of many erythrocytes,
neutrophils, desquamated epithelial cells, and fibrin within the alveoli"

58. Grey Hepatization
• Occurs in the 4-8 days after Red Hepatization
• This is an avascular stage
• The lung appears "gray-brown to yellow because of fibrinopurulent
exudates, disintegration of red cells, and hemosiderin"
• The pressure of the exudates in the alveoli causes compression of
the capillaries
• "Leukocytes migrate into the congested alveoli"

59. Resolution
• It start with 8th day and completed in next 3 weeks.
• Characterized by the "resorption and restoration of the
pulmonary architecture"
• A large number of macrophages enter the alveolar spaces
• Phagocytosis of the bacteria-laden leucocytes occurs
• "Fibrinous inflammation may extend to and across the pleural
space and it may lead to resolution or to organization and
pleural adhesions“
• Alveolar capillaries are engorged, progressive removal of
cellular exudate, resulting in restoration of normal lung
parenchyma with ventilation.

60. Pathogens Stressors
Viruses Mycoplasma Bacteria
Upper
respiratory disease
Damage
Pneumonia
Physical Environmental
Immune System

61. PNEUMONIA
is an infection that inflames the air sacs in one or both lungs.
The gross appearance of the pneumonia will help you to classify it into
one of the four categories below, which in turn will help you to think
about the etiology, and consequently the treatment and/or prognosis.
1. Suppurative Bronchopnemonia
2. Fibrinous Bronchopneumonia
3. Interstitial pneumonia
4. Embolic pneumonia
5. Granulomatous pneumonia

63. Distribution of lesions in
Pneumonias

64. Suppurative Bronchopneumonia
Bronchopneumonia starts in the airways. It may be an extension
from a bronchitis or it may be a primary inflammation at the
bronchiole-alveolar junction.
• Aerogenous route
• Cranioventral distribution
• (Acute) Red in color to grey (Chronic)
• Purulent exudate in bronchi, and abscesses

65. Suppurative Bronchopneumonia

66. The cranio-ventral areas are dark, consolidated, and on the left there is
even some roughening on the surface that might be fibrin. A bacteria has
come in through the airways and started this disturbance.
Suppurative Bronchopneumonia
a classic picture of
severe bronchopneumonia
in a dog.

67. Pulmonary abscesses and bronchiectasis are two important results of the
suppurative bronchopneumonia.
Note: several large abscesses in the consolidated cranial and intermediate
lobes are seen whereas the Caudal lobes are essential normal
Suppurative Bronchopneumonia

69. Note cranio-
ventral
consolidation
affected.
Affected lung is
covered
with fibrin.
Several injury to
the lung with
leakage of fibrin
into the
airspaces.
Only small
portion of
the lung appears
grossly
normal
(asterisk)
Fibrinous Bronchopneumonia

70. Fibrinous Bronchopneumonia

72. Interstitial Pneumonia

73. These
lungs
came from
a foal
suffering
from
septicemia
Interstitial Pneumonia
Most of the
alveolar
lining cells are
responding to
damage, and
that is a huge
amount of
surface area to be
affected and so
they
are DIFFUSELY
swollen.
Inflammation of alveolar interstitium is commonly caused by injury and
destruction of pneumocytes.
It may be the results of viral infections, deposition of antigen-antibody
complexes, inhalation of toxic gases (nitrogen dioxide, sulfur dioxide).

76. The port of entry in
embolic Pneumonia is
hematogenous.
Commonly, due to
• jugular thrombosis,
• vegetative endocarditis
(right side of heart),
• rupture of hepatic
abscesses into the vena
cava (in bovine)
• Embolic foreign body
(hairs, septic emboli)

79. Granulomatous pneumonia
Chronic, sever, granulomatous Pneumonia
There are some organisms that tend to incite a
predominantly macrophage response and the
lungs have a difficult time overcoming the
organism and so lots of macrophages accumulate
in GRANULOMAS. These pneumonias are
characterized by having focal granulomas
scattered throughout.