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Classification of Pneumonias in
Domestic Animals
Alfonso Lpez
Atlantic Veterinary College
2014
CLASSIFICATION OF PNEUMONIAS
Controversial topics in veterinary medicine
E
M
O
N
I
A
G
R
O
S
S
F
Suppurative Bronchopneumonia
Fibrinous Bronchopneumonia
Interstitial Pneumonia
Embolic Pneumonia
T
U
R
E
S
Granulomatous pneumonia
This gross classification allows you to predict the most likely port of entry,
gives you good rule-outs and help you to decide which laboratory tests
should be requested. It increases your chances to arrive at the most likely
etiological diagnosis.
Suppurative Bronchopneumonia
normal
Distribution: Cranioventral
Texture: Firm
Color: Red (acute) to grey (chronic)
Cut surface: purulent exudate in bronchi
Port of entry: Aerogenous
Common etiologies:
Bacteria (low grade pathogenicity)
Mycoplasma
Aspiration of bland material
Bovine lung
Cranioventral consolidation (C) while the caudal lung remains unaffected (N). The texture of
consolidated lung would be firmer than normal. Typically, on cut surface purulent exudate
could be expressed from bronchi (insert.
Cranioventral consolidation (C) while the caudal lung remains unaffected (N). The texture
of consolidated lung would be firmer than normal. Typically, on cut surface purulent exudate
could be expressed from bronchi (arrow).
N
N
C
C
unaffected (N).
Acute
Subcute
Chronic
The main microscopic lesion in suppurative
bronchopneumonia would be neutrophils and
macrophages in bronchoalveolar spaces (see next slide).
Bronchiectasis
Pleural Adhesions
Lung Abscesses
Pleural Adhesions
Ffibrous adhesions (arrows) between
Pulmonary Abscesses
Bronchiectasis
Bronchiectasis is the rupture
and dilation of bronchial wall
due to enzymatic effect of
neutrophils and macrophages.
It is a irreversible lesion no
matter how much antibiotics are
given to the animal
exudate.
Pathogenesis of Bronchiectasis
Normal bronchus with cartilage and bronchial glands (arrows)
Proteolytic enzymes
released by neutrophils
degrade mucosa, glands
submucosa and cartilage.
Degraded cartilage
Distended bronchus
Distended bronchus with exudate
Fibrinous Bronchopneumonia
Fibrinous Bronchopneumonia
Bronchopneumonia
Fibrinous
Distribution: cranioventral
Texture: Hard
Color: Red yellow grey
Fibrin on pleural surface
Port of entry: aerogenous
Most common etiologies:
Highly pathogenic bacteria (exotoxins):
Mannhemia haemolytica, Actinobacillus
pleuropneumoniae;
Harsh aspirated materials
normal
Fibrinous
Bronchopneumonia
Fibrinous
Bronchopneumonia
*
Grounded glass
appearance
Only a small part of the dorso-caudal lung appears normal (asterisk). Note typical
appearance of fibrin. Remember, in severe lung injury, plasma fibrinogen leaks out
of the vessels and clots forming the fibrin in tissue
Fibrinous
Bronchopneumonia
Fibrinous
Bronchopneumonia
*
*
*
Fibrinous pneumonia, particularly Pneumonic
Mannhemiosis (Shipping Fever) and Porcine
Pleuropneumonia also cause coagulative
necrosis (asterisk) and notable dissention of the
interlobular spate
Pleural Adhesions
1
pp
vp
With time and assuming that the animal survives, fibrinous bronchopneumonia
will eventually results in thick fibrous adhesions between visceral and parietal
pleura (arrows).
Lung Sequestrum
Lung sequestrum (sequestra pleural) is large pieces of necrotic separated by connective tissue from the
adjacent viable lung. Sequestrum is a nasty sequel of fibrinous bronchopneumonia.
Interstitial Pneumonia
Interstitial Pneumonia
From all the five gross morphologic types of pneumonia, Interstitial pneumonia is
the most difficult to diagnose grossly. Even microscopically sometime is challenging
Interstitial Pneumonia
Failure of lung
to collapse
Rib
Imprints
Interstitial Pneumonia
Rib
Imprints
Elastic
Texture
Heavy Lungs
Diffuse
Interstitial Pneumonia
On cut
surface
Meaty
appearance
Often
edematous
Normal
Hematogenous
Interstitial
IP
Normal
Thickening of
the alveolar
walls
Common Causes of
Interstitial Pneumonia
Virus
Sepsis
Gases
Allergy
Protozoa
Other
Embolic Pneumonia
Distribution: Multifocal
Texture: Nodular
Port of entry: Hematogenous
Color: red when acute, pale when chronic
Embolic Pneumonia
Most common etiologies:
Vegetative endocarditis (right side of the heart)
Jugular thrombosis
Rupture of hepatic abscesses into the vena cava (cattle
Embolic foreign body (hair, septic emboli, etc).
Embolic lesions are very small and often difficult to see as in the lungs of this foal. Look
closely in the inset and you will notice small dark foci with white center (arrows).
Histopathology
Note numerous foci of inflammation in the lungs. The focal lesion have a
white color because they are chronic and the initial hemorrhage has been
resolved. These focal lesions are evolving towards small abscesses
Note numerous small abscesses resulting form septic embolisms due to vegetative endocarditis
affecting the tricuspid valve (right side) of the heart. Septic emboli are easily trapped in
pulmonary vasculature causing embolic pneumonia and its sequel pulmonary abscesses.
Bronchopneumonia may also have abscesses as sequels, except that in this latter type of
pneumonia the distribution is cranioventral and not random as in embolic pneumonia.
Granulomatous Pneumonia
Granulomatous Pneumonia
Distribution: Multifocal
Texture: Nodular (no pus)
Cut surface: granulomas
Port of entry:
Aerogenous
Hematogenous
Etiology:
Myocbacterium spp
Systemic mycoses
Parasitic ova
Trapped food particles (starch)
Source unknown
Granulomatous Pneumonia
Granulomas
Tuberculosis
Typical Granuloma
Note typical granuloma with
macrophages in the center and an
external band of fibrous connective
tissue (double arrows) infiltrated by
lymphocytes and plasma cells (not
seen at this magnification).
Epithelioid macrophages
Necrotic
Centre
Texture would
be nodular
yeasts
Lungs
FMVZ-UNAM
Kidney
Blastomycosis / Dog
Module 4