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Nasal cavity and
sinuses
Mucinous
degeneration
Observed in cases of catarrhal inflammations.
Amyloidosis
Deposition of amyloid in relation to blood
vessels of nasal mucous membrane and submucous
could
be observed in horse. It can be diffuse or in nodules which may
ulcerate. The amyloid deposition may be
accompanied with a granulomatous cellular
reaction.
Disturbance of circulation
Active hyperaemia:
is
observed as a part of inflammatory signs.
Passive hyperaemia:
accompanies general passive congestion.
Hemorrhage:
Petechial
hemorrhages
are observed in
different infections disease.
Epistaxis
or the flow of blood from the naris
(nosebleed. may be traumatic or spontaneous as in cases of chronic
inf1ammations, presence of
ulcers, in some septicemic diseases and
intoxications or in some blood diseases thrombocytopenia.
Epistaxis is common in race horse.
Inflammation
(Rhinitis)
Definition
It is the inflammation of the nasal mucous membrane which may be due to
physical, chemical,
allergic or infectious agent.
Causes and occurrence
According
to the cause rhinitis may be
1. Primary when develops independently as a primary lesion and in this
case the cause may be:
a.
Non infectious as physical or chemical agents e.g. irritating dust
smokes or gases or mechanically acting parasites as oestrus
ovis.
b. Infections such as local acting organisms as
Fusiform
necrophorum,
Streptococci, Staphylococci, Brucella
and
bronchiseptica
2. Secondary when it develops as a part in pathological picture o f a
specific infectious disease. e.g. Malignant
catarrhal fever,
infectious bovine rhinotracheitis and cattle
plague in cattle, equine influenza (Rhinopeumonitis.,
strangles, glanders in equines, distemper in
dog, coryza, fowl pox, infectious
larengiotracheitis,
Newcastle
disease in poultry.
Forms of rhinitis according to its course:
Rhinitis may be acute or chronic. According to
anatomical type of inflammation, it
may be catarrhal, mucopurulent, purulent,
fibrinous (Fig.
1)
 , peudomembrainous or
granulomatous. In severe inflammations and in some specific
disease and infections granulomas, necrosis
sets up and ulcerative rhinitis develops.
Fig. 1:
Nasal cavity showing acute fibrinous rhinitis.
General morphological feature:
1.
Acute rhinitis usually begins as serous inflammation characterized by
hyperemia, edematous
swelling of nasal mucous membrane and a perfuse
serous nasal discharge (usually accompanied with serous
conjunctivitiss..
2.
Soon it is changed to catarrhal and the discharge becomes very rich in
mucus
(Fig.
2).
In this stage there will be an increased
leucocytic infiltration of the mucosa
propria together with sings of mucoid
degeneration
such
as excess of mucus production and desquamation of epithelial cells.
Fig. 2: Sheep showing unilateral
mucopurulent nasal discharge.
3.
In more advanced cases (subacute.
infiltrative and disquamative processes
become greatly increased while the exudative
and other vascular changes become less acute and the discharge is
transformed to mucopurulent. In this stage
the mucous membrane becomes thickened and may show erosions or even
ulcers. In some areas epithelial hyperplasia may be evident.
4.
According to the causal agent a purulent process may develop. The nasal
discharge becomes frankly purulent and collections of creamy yellow pus
are found on the nasal mucosa. In this case,
ulceration frequently happens (e.g.
strangles of horse).
5.
In some specific infections (fowl pox and malignant, catarrhal fever in
cattle. fibrinous or diphtheritic rhinitis
develops.
6.
Chronic rhinitis is the form commonly observed in specific
granulomatous affections (e.g. tuberculosis
in cattle, glanders in horse,
actinomycotic affections,
histiopiasmosis and other
mycotic affections). It may also develop from
acute form (catarrhal and suppurative).
Granulomatous
rhinitis is characterized by the development of the specific
granulomatous or nodular lesions of the
disease. Chronic rhinitis may lead to polypous
thickening of the mucosa,
which may be large enough to be pedunculated
and composed of a core of edematous
strorma resembling myxomatous
tissue and a covering epithelium,
which
is hyperplastic (Rhinitis
hypertrophicans., or it may lead to fibrosis
of the lamina propria with atrophy of the
glands and focal squamous
metaplasia of nasal epithelium (Rhinitis
atrophicans).
Rhinitis hyperatrophicans and
atrophicans are more commonly observed in
pig.
Sequelac
of rhinitis
1.
Development of chronic hypertrophic or
atrophic changes.
2.
Perforation of septum nasi as in
glanders.
3.
Extension of inflammatory process to other parts of respiratory
system e.g. larynx, trachea, bronchi or even to lung parenchyma.
4.
Extension of the inflammatory process to the sinuses.
Sinusitis
Definition
Inflammation of the sinuses, nasal frontal and maxillary.
Causes and occurrence
1. Usually as an extension from a nearby inflammatory process
particularly of the
nasal
mucous membrane.
It may be secondary to alveolar periostitis
as in horse or a
complication
of dehorning wood as in cattle.
2. Sinusitis is also observed in some specific diseases as, in some
chronic respiratory diseases of poultry, malignant catarrhal fever in
cattle and in cases of infestation with oestrus
ovis in sheep.
3. Specific granulomas may develops in the
sinuses such as tuberculosis,
glanders and
actinomycosis
Forms and general morphological features
1. Resemble those of rhinitis but usually tend to be chronic due to the
accumulation of the inflammatory exudate as
the result of closure of draining orifices.
2. The accumulated inflammatory exudate may
be seromucoid in
nature
(hydrop’s or mucocele
of the sinus. or purulent in character (empyema
of the sinus).
3. In advanced cases, there will be ulceration sometimes with
perforation, hyperplastic or atrophic
changes.
Bad sequelae
Extension of inflammation to the brain with fatal termination.
Parasitic infestation of nasal cavity and sinuses
The most important is the oestrus ovis of
sheep (Fig.
3)
which is the main cause of a chronic mucopurulent
or purulent rhinitis and sinusitis particularly of the frontal sinus.
Fig. 3:
Nasal sinus showing parasitic infestation (Oestrus
ovis).
Tumors
of nasal cavity and sinuses
Aren’t common. Fibroma and
myxoma in cattle,
osteoma in cattle and horse, chondroma,
liporna, different sarcomas and carcinomas.
The most important is the infectious adenopapilloma
of sheep.
Laryngeal paralysis (Laryngeal hemiplagia.
It is the usual cause of roaring in horse it is mostly left sided due to
paralysis of the left recurrent laryngeal nerve,
which leads to atrophy of some laryngeal muscles.
The cause isn’t clear, but the extension of an inflammatory process (e.g.
strangles) may produce the case. In some cases, a pressure exerted on
the nerve at
the part of its passage between the trachea and the aorta may be the
cause.
Circulatory disturbances
•
Active hyperemia is observed in acute
inflammation.
•Passive
hyperemia accompanies general passive
congestion.
•Peticheal
hemorrhages and
echymoses can be observe in acute infectious diseases such as
infectious bovine rhinotracheitis (I.B.R).,
infectious laryngiotracheitis of poultry,
Hemorrhagic septicemia in cattle and hog
cholera in which haemorrhages in larynx is
pathognomonic.
•
Edema
of laryhgeal mucosa and
epiglotis is observed frequently in hemorrhagic
septicemia of cattle. In case of
edema of the lung,
the trachea is usually full with a frothy fluid.
Inflammation
Laryngitis and tracheitis
Causes and occurrence
1. Usually observed as a part of inflammatory diseases of either upper
or lower parts of the respiratory system,
laryngitis and to a lesser extent tracheitis
is expected to accompany rhinitis. Tracheitis
and to a lesser extent laryngitis is expected to accompany acute
pneumonias.
2. Constantly observed in diseases characterized by affection of upper
respiratory tract such as I.B.R.,
malignant catarrhal fever (M.C.F). severe cases of cattle plague
respiratory form of distemper,
coryza contageosa
of poultry,
Fowl
pox, infectious
laryngiotracheitis of poultry, Newcastle disease and chronic respiratory
affections of poultry.
3. Granulomatous lesions in larynx and
trachea may develop in cases of tuberculosis,
glanders, actinomycosis and
mycotic diseases as
aspergillosis in poultry.
4. Necrotic laryngitis may occur as a part of oral
necrobacillosis (calve and pig diphtheria. or may develop
independently as a primary lesion.
5. Corynebacterium
pyogenes is responsible for sporadic cases of laryngeal abscesses
in cattle and sheep.
Forms of inflammation and general morphological features:
The same forms observed in rhinitis can be found in laryngitis and
tracheitis depending on the causal organism
and secondary infections. Most important forms are.
Catarrhal tracheitis or
laryngitis are associated with several viral, bacterial and parasitic
diseases (Figs 4 & 5).
Fig. 4:
Larynx showing catarrhal inflammation characterized by increase number
of goblet cells and few inflammatory cells. (H&E).
Fig. 5: Trachea
showing catarrhal inflammation represented
by massive inflammatory cells infiltration and increase number of goblet
cells. H&E.
The fibrinonecrotic or diphtheritic
laryngitis found in calves and pig diphtheria and in diphtheritic form
of fowl pox and characterised by the presence of diphtheritic membrane
and ILT (Fig.
6 ).
•Necrotic
or ulcerative laryngitis observed in severe forms of cattle plague and
infectious laryngotracheitis in birds (Fig.
7).
•Fibrinonecrotic
and sometimes suppurative laryngiotracheitis
which may develop in complicated forms of M.C.F. and
I.B.R .
•Hemorrhagic
laryngitis in some cases of hemorrhagic septicemia
of cattle and ILT (Fig.
8).
Fig. 6:
Trachea of chicken showing fibrino necrotic
inflammation characterize by complete necrosis of epithelial lining,
congested blood vessels besides presence of fibrin and necrotic material
in its lumen. H&E.
Fig. 7:
Ulcerative laryngitis characterized by necrosis of the epithelial lining
and exposed of lamina propria with congested
blood vessels and inflammatory cells. H&E.
Fig. 8:
Trachea of chicken infected with ILT showing hemorrhagic
tracheitis.
Tuberculous
lesion in larynx and trachea may be of the diffuse infiltrative nodular
form (fungosa
tuberculosa., polypoid form, or
ulcerative form. Tuberculous laryngitis and
tracheitis is commonly observed in cattle in
chronic tuberculosis (period of post infection. and the infection
usually extends intra
canalecular lesion of glanders may be
of the exudative, ulcerative, or productive
form.
Parasitic infestation
Syngamus
trachea affects trachea of poultry. The worms are attached to the mucous
membrane and may cause a productive form of inflammation with wart like
outgrowths.
Bronchitis
Definition
Bronchitis is the
inflammation
of bronchi which tends to spread around the bronchi as a
peribronchitis and frequently to the
alveolar parenchyma producing bronchopneumonia.
Causes & occurrence
1. A virus as in infections viral bronchitis. The virus usually produce
slight inflammatory process and severe inflammatory changes are usually
due to secondary bacterial infections.
2. Observed in infectious diseases characterized by respiratory
affection and in, this case bronchitis accompanies pneumonia.
3. Parasitic infection as in case of severe infection with
Dictyocaulus
viviparus in cattle and filaria
in sheep and goat (Lung worm. (Figure
9).
4. Feeding dusty hay may be the cause of bronchitis.
5. Granulomatous lesions in the wall of
bronchi are observed in tuberculosis and
actinomycosis infection.
5. Mycotic bronchitis as in case of
adiaspiromycosis in sheep (Fig. 10).
Fig. 9: Trachea
showing larvae of nematodes in its lumen
with necrotic debris. H&E
Fig. 10: Trachea showing
adiaspiromycosis in its lumen. H&E
Forms of bronchitis
Generally resemble forms of inflammation of upper respiratory tract.
According to the course there are acute and chronic. According to
anatomical types of inflammation there are catarrhal
mucopurulent, purulent and fibrinous or
pseudomembrainous.
General morphological features
Acute bronchitis is characterized by:
1.
Accumulation of inflammatory exudate in the
lumens of the affected bronchi. The exudate
may be more mucoid or more
purulent, it reveals inflammatory cells and
desquamated epithelial cells. The exudate
may be fibrinous in character as in some complicated cases of M.C.F. and
cattle plague (Figs
11
& 12).
Fig. 11: Bronchitis
showing accumulation of inflammatory exudates in its lumen. H&E.
Fig. 12: Bronchitis
characterized by accumulation of exudates mainly neutrophils in its
lumen. H&E.
2. Inflammatory edema and swelling of
bronchial mucosa which reveals some leucocytic
infiltration. The epithelial
lining reveals features of mucoid
degeneration, acute
necrotic changes and desquamation.
3. Thickening of peribronchial tissue due to
an inflammatory reaction (peribronchitis.
(Fig.
13).
4. Inflammatory process may extend to alveolar tissue giving features
of bronchopneumonia
(Figs
14
&15).
Fig. 13: Thickening of
bronchial wall by edema an inflammatory reaction. H&E.
Fig. 14: Lung showing
gross picture of diffuse bronchopneumonia.
Fig. 15: Lung showing
microscopic picture of bronchopneumonia characterized by bronchitis
besides extend of the inflammation into alveolar
tissue. H&E.
Chronic bronchitis is characterise by
1. The exudate found in the lumen becomes
mostly composed of tenacious mucus which may form a
pluge causing obstruction of the lumen. The bronchial mucosa is
markedly thicked due to excess of cellular
infiltration mainly of monocytes and
lymphocytes and a moderate proliferation of the loss
submucosal connective tissue (Figs.
16
&17).
In small bronchi and bronchiols the
proliferating connective tissue may produce
projections in the lumens causing their narrowing or even obliteration (Bronchiolitis
obliterance. this is more observed in cattle
and horse.
The epithelial lining may be attenuated and
hyperchromatic
or
it may show regenerative hyperplasia. In some
cases of chronic bronchitis squamous
metaplasia of the bronchial epithelium may
be observed (Fig.
18).
Fig. 16: Chronic
bronchitis showing epithelial necrosis and metaplasia besides thickening
of bronchial wall by fibrous tissue and chronic inflammatory cells. H&E.
Fig. 17: Chronic
catarrhal bronchitis characterized by chronic inflammatory cell and
metaplasia of epithelial lining. H&E.
Fig. 18: Chronic
bronchitis showing squamous metaplasia,
damage bronchial wall and accumulation of inflammatory exudates in
lumen. H&E.
3. The peribronchial tissue shows connective
tissue proliferation and an increase in collagen fibres together with
hyperplasia of peribronchial lymphoid
collections.
4. In some areas there will be dilatation of some alveoli and alveolar
ducts (alveolar emphysema. in other areas collapse of alveoli can be
observed (obstructive atelectasis..
Sequelae
1. Bronchial stenosis.
2 .
Bronchiectasis.
3. Atelectasis.
4. Emphysema.
Bronchial stenosis
Causes
1. Changes in wall of bronchi as in cases of chronic bronchitis
particularly when small bronchiols are
included.
2. Pressure from outside e.g. tuberculous
lymph node
or a tumor.
3. Spasomodic contraction of bronchial
muscles as in case of allergic reaction and anaphylactic shock.
Sequelae: depend on degree
Signs and duration
1. Complete closure produce
atelectasis or collapse of corresponding
pulmonary alveoli (obstructive atelectasis..
2. Partial closure produce alveolar
emphysema.
Bronchiectasis
Definition
It
is the dilatation of bronchi due to loss of elasticity and failure to
contract as the result of
certain
degree of chronic inflammatory fibrosis in and around the wall of the
bronchi (Figure
19..
It is usually an indication of previous inflammation.
Fig. 19: Lung
showing gross picture of
bronchoectasia.
Pathogenesis
1. Chronic inflammation which causes complete charge in bronchial wall
as fibrosis and disappearance of elastic and muscular fibres (Figure
20).
2. A mechanical factor as accumulation of bronchial
exudate causing expansion of the
lumen
or fibrous cicatrization of surrounding
tissue as in case of chronic peribronchitis
or bronchopneneumonia and thus
stretshing the bronchial wall outwards (Fig
21).
Causes and occurrence
Bronchiectasis
develops as
the result of chronic purulent bronchitis
characterized by destructive inflammation of the wall
of the bronchi and accumulation of inflammatory
exudate. Bronchiectasis
can be observed.
Fig. 20: Bronchioetasia associated with
chronic bronchitis with damage of bronchial wall which replaced by
fibrous tissue. H&E.
Fig. 21: Bronchus showing
ectasia with accumulation of
caseated material in its lumen and
destruction of the tracheal wall which replaced by fibrous tissue. H&E.
Causes
a. Chronic bacterial bronchitis i.e. tuberculosis, infection with
Corynebacterium
pyogenes in young cattle E.Coli
and Streptococci in dog.
b. Chronic mycotic bronchitis
c. Parasitic bronchitis in sheep goat arid pig.
Forms of bronchiectasis
There are two anatomical forms of bronchiectasis:
1. Cylindrical or fugiform
bronchiectasis (atrophic):
• It is the most common form particularly in cattle in which it affects
more the epical lobe.
•It
appears grossly as cylindrical dilatation of main bronchi and their
branches which are full with viscid mucus.
•
It is characterized microscopically by monocytic
infiltration of the propria and
disappearance of elastic, muscular and glandular elements. The bronchial
wall may be as a narrow band of connective tissue lined with a thin
unchanged epithelium.
2. Succular
bronchlectasis is less common
Collapse or atelectasis
Congenital atelectasis
Congenital atelectasis is
the incomplete expansion of the lung at the time of birth. The
atelectasis may be diffuse or focal in
distribution. If the animal is dead at birth and no air is brought into
the lung, complete atelectasis of the entire
lung is present. If the
animals is
alive at birth,
and
inhales the alveoli become filled with air
and this distension
persists even if death of the individual occurs. The presence of air in
the lungs or actually the dilatation of the lungs is an indication that
the animal was
alive at birth and had breathed .
The finding of complete atelectasis in a
dead, new-born foal is of significance when one is called upon to
determine whether or not the
focal met the requirements for stallion service-fee exemption.
In many sections of the country
the
mare owner is liable for the service fee if the colt
stand
and nurses. Obviously complete atelectasis
in a
newborn
foal
would be evidence animal didn’t even to say nothing of standing to
nurse.
Focal atelectasis is commonly observed in
very young animals. As the thoracic cavity
enlarges,
greater and greater
expansion of the lungs occurs until finally all of the
atelectic areas become distended with air.
In those areas where a bronchus isn’t patient, air will not have invaded
the alveoli and then a persisting focal area of
atelectasis remains (Fig.
22).
Fig. 22:
Lung showing
gross picture of atelectasis.
Acquired atelectasis
General acquired atelectasis of the lung
doesn’t occur in an animal that has once breathed. The animal would be
dead before all of the air could be removed.
Focal acquired atelectasis is very common
and is caused by pressure exerted upon, portions of the lung which force
air out of the area. This pressure is produced by enlarging tumours,
abscesses, hydrothorax, and hydropericardium.
It is also caused be complete bronchial obstruction when the air in the
alveoli distal to the obstruction is absorbed. This
bronchial obstruction is caused by masses of
exudate or parasites in the bronchi,
or the existence of peribronchial tumours or
abscesses which cause compression of the bronchi.
Subpleural atelectasis is very
commonly observed in the cow and is often confused with haemorrhages or
infarcts. Incision of the area reveals the true nature of the lesion.
Lung
Emphysema
Definition
Pulmonary emphysema is the increase of air content or the over inflation
of lung tissue.
Forms of pulmonary emphysema
Alveolar or vesicular emphysema and affects alveolar ducts and alveoli
which become greatly distended with air it may be:
a. Acute when there is simple over inflation without any structural
alteration or rupture of alveolar walls and the lung returns to normal
after the escape of the increased air.
b.
Chronic when prolonged overinflation has
resulted in pressure atrophy, weakness, loss of elasticity rupture and
sometimes disappearance of alveolar walls. In this case the dilatation
is permanent and the lung doesn’t return to normal.
According to distribution alveolar emphysema may be:
a.
Focal when affects lobuled or groups of
lobules (Fig.
23).
b. Diffuse or universal when affects the subpleural
and interlobular connective
tissue which show collections
of air bubbles and it is usually universal or diffusely distributed (Fig.
24).
Fig. 23:
Lung showing focal alveolar emphysema. Some alveoli showing emphysema
and other showing collapse. H&E.
Fig. 24:
Lung showing diffuse alveolar
emphysema. H&E
Causes and occurrence
Alveolar emphysema:
1. The main cause of chronic alveolar emphysema in animals is the
constriction or the occlusion of bronchi and
bronchiols observed in cases of
bronchitis and bronchiolitis
obliterance, chronic
bronchopeumonia and lung worms in calves, sheep and pigs. In
these cases the strong inspiratory efforts
will permit the air to pass to the alveoli and the expiratory efforts
will be too weak to force the air out again. In this case the
distribution of emphysema may be diffuse or focal depending on
distribution of bronchiolitis.
2. Increased respiratory efforts as happens in case of chronic cough
will help in the development of alveolar emphysema through weakening the
elastic fibers and causing
balooning and even rupture of alveoli.
3. Weakness of alveolar walls associated with loss of elasticity, which
happens in diffuse pneumonias, predispose for alveolar emphysema.
4. Chronic diffuse alveolar emphysema is observed in heaves of horses
which associates heavy work while the digestive organs are distended
with coarse roughage . Development of such diffuse alveolar emphysema is
usually proceeded by chronic bronchitis
brenchopneumonia or chronic
indurating interstitial pneumonia
(Fig. 25).
5. Acute diffuse alveolar emphysema is observed in anaphylactic shock.
It is due to spasmodic contraction of the smooth muscles of bronchi and
bronchiols causing narrowing of their lumens
a matter which will interfere with expiration and air is accumulated in
the alveoli.
Fig. 25:
Lung showing chronic diffuse alveolar emphysema.
6- Acute focal alveolar emphysema can be observed alternating with area
of pneumonia and atelectasis as compensatory
emphysema.
It usually turns chronic when the primary lesion persists for a long
time.
Interstitial emphysema
1. Results from rupture of alveoli as in chronic alveolar emphysema and
violent coughs which leads to the escape of air in the interstitial
tissue.
2. It may be traumatic from a fractured rib or a penetrating
foreign body.
3. Observed frequently in slaughtered animals particularly cattle.
Morphological features
Alveolar emphysema
1. Grossly, emphysematous lung or areas of lung are voluminous spongy in
consistency, pale in color, dry on cut
surface.
2. Microscopically, alveoli and alveolar ducts are irregularly distended
and their septa are thin bloodless and some are ruptured. In acute
emphysema the spasmodically closed bronchilos
are evident histologically while in chronic
emphysema bronchiotilis with variable degree
of obliteration can be observed.
Interstitial emphysema
Air bubbles are observed in subpleural and
interlobular connective tissue.
Sequelae
Because of emphysema there will be an increase in the resistance against
pulmonary circulation with results in blood stasis in the right side of
the heart. In chronic cases right cardiac hypertrophy and chronic
dilatation happen, with subsequent
tricuspid
insufficiency, hydropericardium and general
venous congestion.
Disturbances of metabolism
Hyaline degeneration
It is observed in
different
lung affections in man and also observed in cattle and dog. It begin
between alveolar epithelium and interalveolar
capillaries, latter the whole alveolar septum is include with the
development of a hyaline membrane lining the alveoli, alveolar duct and
sometimes the bronchiols.
The direct cause is usually hypoxia which ma be
toxic and respiratory acidosis. It is usually evident in interstitial
pneumonia.
Calcification (calcinosis
pulmonalis)
As primary or metastatic is observed in dogs
due to chronic renal insufficiency in case of chronic interstitial
nephritis and in cattle in areas rich in calcium. In this case calcium
deposite
is
found on elastic fibres of alveolar walls.
As dystrophic calcification is observed in cases of tuberculosis and
parasitic lesions.
Melanosis
As congenital in general melanosis in
calves.
Disturbances of circulation
Anemia
or ischemia: of the lung is observed in cases of:
1. General anemia.
2. Slaughtered animals.
3. Emphysema, in this case it may not affect the whole lung but parts of
the lung depending on distribution and extent of emphysema.
Active hyperemia
of the lung is observed in cases of:
1. Early stage of acute inflammation (Fig 26).
Fig. 26:
Lung showing congested interalveolar capillaries. H&E
. Inhalation of irritants.
3. Any acute infectious disease .
4. Low atmospheric pressure at high areas.
The lung is slightly swollen congested and its cut surface releases a
blood stained frothy fluid.
Microscopically, the interalveolar
capillaries are greatly dilated and full with blood,
the alveoli may show some red cells
(Fig. 27)
.
Congestion of the lung is frequently accompanied with some degree of
fluid exudation which later predispose the
lung to infection.
Passive congestion
Passive congestion of the lung is usually the result of interference
with blood outflow or any increase in back pressure in the lung
due to some functional defect in the left heart which makes it unable to
clear the blood coming from the lung. Acute passive congestion is
observed in all animals dying from acute heart failure or cardiac
exhaustion as in some cases of acute intoxication and
septisemic diseases. Pulmonary congestion is
constantly present in diseases characterized by
myocardiac degeneration such as the nutritional muscular
dystrophy (white muscle, disease. or myocarditis such as foot and mouth
disease in calves (myocarditis aphthosa.
chronic passive congestion is a common sequel of a left sided cardiac
lesion such as chronic valviolar
endocarditis which results in stenosis or
insufficiency of mitral valve.
Passive congestion of the lung is usually accompanied with lung oedema
and some structural changes depending on duration of congestion i.e.
brown induration in chronic cases (Figs
28 & 29).
Fig. 27: Lung showing
active hyperemia represented with congested capillaries and inflammatory
cells. H&E.
Fig. 28: Lung showing
passive hyperemia showing congested capillaries with non inflammatory
edema. H&E
Fig. 29: Gross picture of
chronic passive congestion of lung.
Lung edema
Definition
It is the accumulation of fluid in alveolar spaces,
bronchiols, bronchi (alveolar edema.
and interlobular connective tissue (interstitial
edema. which may be inflammatory or non-inflammatory
Causes
1. Inflammatory edema early stage of
pulmonary inflammation and it frequently accompanies active
hyperemia.
2. Non inflammatory edema occurs in cases
which disturb the mechanism that regulate tissue fluid exchange i.e. the relation between hydrostatic pressure in
blood vessels and the difference between blood and tissue fluid
osmotic pressure such as:
•
Decrease
in blood osmotic pressure due to hypoproteinemia
the cause
of
general edema.
This
may result from malnutrition parasitic infestation or renal disorders.
• Increase in
hydrostatic
pressure inside lung blood vessels as in case of passive congestion due
to a left sided cardiac defect.
• Pulmonary edema is a part in
characteristic pathological picture of some specific diseases i.e.
South African Horse Sickness.
Interstitial edema is particularly observed
in contagious bovine pleuropneumonia,
pasteurellosis of cattle,
hogcholera and acute
strongyloids of sheep.
Macroscopic appearance
The lung volumenous, heavy firmer in
consistency and deep pink or red in colour. In case of
edema accompanying C.V.C. the lung reveals
induration and a brownish colouration (brown
induration..
A foamy
fluid
is found in trachea bronchi and bronchiols
and it oozes from the cut surface. In case of
interstitial
oedema radiating peribronchial and
interlobular geletatinous infiltration is
found. Pulmonary edema is
sometimes
accompanied with increase in pleural fluid.
Microscopic appearance
The alveoli are filled with a fluid containing a variable amount of
coagulable protein and some desquamated
alveolar cells.
In case
of
inflammatory edema the protein content and
cellular elements are
greater.
In case of chronic
passive
congestion there will
be an increase in the
interalveolar
connective tissue
elements and plenty of
hemosiderin
loaded macrophages (heart failure cells..
Hemorrhages
1. By rhexis or traumatic as in fractured
rib or due to explosions .
2. By diabrosis due to damage or necrosis of
wall of blood vessels as in case of glanders
in horse and tuberculosis in man.
3. By diabedesis as in infectious diseases
i.e. hog cholera, pasterellosis etc.,
deficiencies and some poisoning dicomarol
poisoning.. In case of pulmonary hemorrhage,
blood may be accumulated in pleural cavity (haemothorax.,
reaches bronchi and coughed up (hemopetesis.
or resorbed by the lymph (blood
resorbtion..
Thrombosis
Of
pulmonary vessels of
inflammatory origin is common in severe acute
septicemic diseases as in hog cholera, hemorrhagic septicaemia.
It also happens frequently in bovine pleuropneumoia
and in some forms of pneumonias (Figure
30).
Fig. 30: Lung of cattle
infected with CBPP showing thrombosis of pulmonary blood vessels. H&E
Emboli
Are more frequent in man than in domestic animals. The main source of
emboli to the lung in domestic animals is vegetative endocarditis of the
tricaspid valve
(Fig. 31).
Fig. 31: Lung of mouse infested
with Schistosoma mansoni showing Schistosomula in pulmonary blood
vessels. H&E
Infarction
Hemorrhagic infarction of the lung is rare due to the rich
anastomosis of the pulmonary circulation and
the double blood supply
of the lung, however it can happen in
some cases of heart defects (left side. accompanied with venous
congestion.
Pneumonia
Definition
It is the inflammation of lung tissue due to different
etiological
agents with a variety of anatomical patterns producing consolidation and
decrease in air content of affected parts.
Etiological
agents
May be bacteria (bacterial pneumonia. (Fig 32)
.
virus (viral pneumonia., parasite (i.e. verminous pneumonia. (Figure
33 )
,
Mmycotic (Aspergillosis.
(Figure
34)
or physical and chemical locally acting irritants (i.e. as inspiration
and non infectious pneumonias.,
which reaches the lung tissue through:
1. Upper respiratory tract (aerogen or
bronchogen. and it is the most common mode
of infection, in domestic animals and usually produce primary pneumonia.
2. Blood (hematogen. and gives rise to
secondary pneumonia as specific infectious diseases characterized by
other pathological lesions.
3. Lymph (lymphogen..
4. Or it is found as in normal flora of the respiratory and becomes
pathogenic and invade lung tissue when the resistance of the animal is
lowered or the respiratory parenchyma is debilitated by any stress
factor or predisposing cause.
Predisposing causes are important factors in making the lung
susceptible to infection. They are debilitating
systemic diseases, fatigue, transportation, sudden change in
weather; drafty stables, nutritional
deficiencies or inhaled
dust, smokes and gases. Cardiac weakness usually predispose to lung
affection by causing its congestion and oedema (hypostatic pneumonia..
The etiological agent may be responsible for all
the
pathological changes or it may only initiate a primary
mild
inflammatory process while secondary invaders are the cause of the more
advanced changes observed. This happens particularly in majority of
cases of viral pneumonias in domestic animals.
In some cases of pneumonias, the presence of more than one organism is
important while the presence of each of them alone is unable to produce
the change this is experimentally proved in some
pneumonias of sheep
and
cattle.
Anatomical pattern
and forms of pneumonia
The pattern of
inflammation in pneumonia depends
greatly on the
causative agent
and its virulence as well
as on
secondary bacterial infections and therapy.
According to the nature of inflammation and inflammatory exudates
pneumonia can be classified to:
1. Serous pneumonia (Fig 35).
2. Catarrhal pneumonia.
3. Fibrinous or croupous pneumonia (Fig 36).
4. Suppurative or purulent pneumonia which when results from septic
emboli is known as embolic or metastatic
suppurative pneumonia (Fig 37).
5. Necrotic or gangrenous pneumonia which is particularly observed in
aspiration pneumonia.
According to distribution and anatomical pattern pneumonia can be
classified to:
1. Lobar pneumonia in which
a. The inflammatory process spreads rapidly by all available routs to
affect large areas
is of lobes or whole lobes.
b. Type of inflammation is fibrinous hence it is also known as fibrinous
or croupous pneumonia.
c. Inflammatory reaction tend to highly
acute.
d. In majority of cases the pleura is
involved and in this case it is known as
pleuropneumonia.
Fig. 32: Lung , pneumonia
due to infection with tubercle bacilli (Bacterial
pneumonia). H&E.
Fig. 33: Lung, pneumonia
due to infection with Aspergillus (Mycotic..
H&E).
Fig. 34: Lung, pneumonia
due to infestation with lung worm.
Fig. 35: Serous pneumonia
represented by accumulation of serous pale pink fluid and inflammatory
cells. H&E.
Fig. 36: Lung showing
fibrinous pneumonia showing accumulation of fibrin threads in alveoli
with inflammatory cells and congested of interalveolar capillaries. H&E
Fig. 37: Lungs showing
microscopic picture of suppurative pneumonia characterized by massive
infiltration of pulmonary tissue with neutrophils beside congested blood
vessels. H&E.
2. Lobular pneumonia in which
a.
Inflammatory changes are patchy and affect individual lobules with
rather sharp demerkation.
b. Inflammation is usually an extension from
bronchiolitis and bronchitis hence it is also known as
bronchopeumonia.
c. The type of inflammation is usually catarrhal and hence it is also
known as catarrhal pneumonia.
d. The inflammatory reaction tends to be acute or chronic.
3.
Interstitial pneumonia in
which
a.
Inflammatory process is restricted to alveolar septa.
b. Inflammatory changes are characterized by cellular infiltrations and
proliferations rather than by excudation
(Lobar and lobular are exudative
pneumonies..
c. Inflammation is largely confined to pulmonary tissue (alveolar walls.
hence it is the only synonym to pneumonitis
(in other forms changes are mostly observed in alveolar lumens..
It is generally accepted that lobar and lobular pneumonias are due to
bacterial infection, while interstitial pneumonia denote a viral
infection.
Pneumonia in domestic animals
Pneumonia in domestic animals has got certain features which have to be
considered before any further study:
1. The distinction between lobar and lobular
pneumoniae which is originally applied to the
exudative inflammation of human lung is
arbitrary in domestic animals.
2. Etiological agents in both forms aren’t
necessary different, the usual organisms which
causes
fibrinous pneumonia in animals (Fig. 39)
(i.e.
Pasteurella.
are frequently encountered in catarrhal bronchopneumonia.
Fig. 38:
Lung showing gross picture of fibrinous pneumonia.
3.
Majority of exudative bacterial pneumonia whether catarrhal or fibrinous
are
aerogenous
and primary bronchogenic and spread to the
parenchyma occurs from bronchiolitis.
4. Both forms catarrhal and fibrinous begin with lobular distribution
which
persists
in less sever cases fibrinous pneumonia while advanced severe catarrhal
bronchopneumonia while advanced severe catarrhal
bronchopeumonia may coalesce to produce a partial or total lobar
distribution.
5.
Typical lobar pneumonia of man due to pneumococci
with the involvement of the whole lobe at the
same time
and stage doesn’t practically exist in domestic animals (pneumococci
produce in calves a form of catarrhal bronchopneumonia..
6.
Non specific pneumonias and pneumonias complicated by secondary
invadors
are more common in domestic animals and the inflammatory process isn’t
necessary to be distinctly
catarrhal or fibrinous, it is more frequently to observe a variety of
inflammatory
reactions overlapping
each other.
According to all mentioned peculiarities pneumonia in
domestic animals can be classified
depending on the most
predominant changes into:
l.
Patchy
fibrinous pneumonia.
2.
Patchy
catarrhal bronchopneumonia.
3. Interstitial pneumonia.
Fibrinous or croupous
pneumonia
Definition
It is a
form of pneumonia in which the inflammatory reaction is fibrinous in
nature, tends to be acute and it spreads rapidly to affect large areas
of lobes or whole lobes.
Causes and occurrence
1. Predisposing causes are important for developing of fibrinous
pneumonia in domestic animals.
2. Direct causes are bacterial infections such as
mycoplasma in endemic contagious
pleuropneumonia of cattle and sheep.
Pasteurella in sporadic fibrinous
pneumonia
of cattle, sheep and swine, and in fowl cholera, Streptococci with or
without E. coli in horse. Fibrinous pneumonia is very rare in dogs.
Pathogenesis
Fibrinous pneumonia in domesticc
animals is inmost of cases aerogenous, the
infection extends, as it happens in catarrhal
bronchpneumonia, from
the bronchiols and the inflammatory reaction
retains
some degree of lobular distribution but it differs by the absence of a
distinct phase of bronchitis. The inflammatory reaction begins in the
respiratory bronchiols and rapidly spreads
by peribronchial
and endobronchial
routes. By the first rout the infection
reaches
the peribronchial
lymphatics
which are well
developed particularly
in cattle and
swine
and are in connection with perivascular
spaces
and sublpeural
lymph vessels
leading to
lymphangiectasis
and
inflammatory thrombosis.
By the second rout the infection extends along the bronchial mucosa to
the related pulmonary alveoli giving the anatomical pattern of lobular
distribution then from one lobule to another by aspiration until big areas or even a whole
lobe is involved
given the anatomical
pattern of lobar distribution.
Different organisms appear to have some preference for one or other rout
Mycoplasma, and
Pasteuralla favour the peribronchial
root
so
fibrinous inflammation of the septa tends to be remarkable feature of
these infections.
Due to the involvement of affected areas an
lobules not at the same time different stages of the reaction are
usually observed in different lobules.
Difference between fibrinous pneumonia in man (lobar pneumonia. and in
animals:
1.
Cause
In man it is a specific microorganism (pneumococoi..
In animals it is a variety of microorginism
majority of them non-specific.
2. Pathogenesis
In man it is believed to depends on an
allergic reaction which involves the whole lobe.
In animals it depends on the spread of the infection by
peribronchial and
endobronchial routs.
3. Anatomical pattern
In man it follows a lobar pattern of distribution. In animals
it follows a patchy distribution with different stages of
inflammatory
reaction in different affected lobules. (Patchy fibrinous pneumonia is
observed in pulmonary form of human pest..
4. Pathological changes
In spite of above mentioned difference the same four stages of fibrinous
pneumonia in man
can
be observed affecting different lobules and areas in patchy fibrinous
pneumonia of animals (Fig 39)
.
Fig. 39: Lung showing
gross picture of fibrinous pneumonia.
Stage of inflammatory oedema (congestion.
Macroscopic appearance
1. The apical and cardiac lobes and the
anteroventral
parts
of the diaphragmatic lobes are mainly affected.
2. Affected lobules or areas are swollen,
dark red
(Fig. 40)
moderately firm in consistency and on cut surface reveals a blood tinged
exudate.
3. The changes may be bilateral (but tend always to be asymmetrical..
Microscopic appearance
1. The interalveolar capillaries are greatly
dilated and full with blood.
2. The alveoli are full with a pink oedema fluid containing some red
cells and alveolar macrophages..
Fig. 40: Lung showing
stage of congestion characterize by dark red in colorcongestion.
. Peribronchial and
perivascular lymphatics are dilated
with
a fluid rich in protein.
Stage of red hepatization
Macroscopic appearance
1. Affected tissues become solidified (hepatized.,
darker, in color enlarged and with a dry
cut surface. Hepatized
parts sinks in water.
2. Septal connective tissue becomes greatly
thickened.
Microscopic appearance
1- The alveolar capillaries are still engorged.
2- A net of fibrin threads begin to develop the meshes of which are
occupied by plenty of cells, but also increased number of leucocytes and
alveolar macrophages (Figs 41& 42).
.
3. Threads of fibrin can be observed passing from alveolus to alveolus
through the pores of khon.
Fig. 41: Alveoli filled
with fibrin threads and inflammatory cells.
H&E.
Fig. 42: Alveoli filled
with fibrin threads and inflammatory cells.
H&E.
4. The amount of fibrin usually less copious in pneumonia of animals
than it is in pneumococcal pneumonic of man.
5. Acute thrombosis of lymyphatics and
veins and engorgement of arteries which may be
thrombosed are frequently observed.
Stage of gray
hepatization:
Macroscopic appearance
1. Solidified tissues become ischemic
and greyish in color and it is still dry on
cut surface (Fig. 43).
2. Septal
connective
tissue still greatly thickened.
3. Hepatized parts sinks
in water.
Fig. 43:
Lung showing gross picture of gray hepatization. H&E.
Microscopic appearance
The grey colouration in this stage is produced by:
1.
Ischemia of the interalveolar capillaries
due to the pressure exerted by the accumulated inflammatory
exudate and thrombosis of some of them.
2. Lysis and removal of red cells by
macrophages.
3. Excessive leucocytic infiltration.
Fig. 44:
Lung showing pneumonia characterize by organize fibrin threads and
inflammatory cells filling the alveoli. H&E.
Stage of resolution
1. In this stage there will be lysis of
fibrin and leucocutes and
liquification of
exudate which is partly reabsorbed by
lymphatics or coughed through the bronchial system.
2. The alveolar epithelium regenerate, alveoli become again full with
air and the capillary net return back to its normal condition.
3. Compete resolution of fibrinous pneumonia isn’t common in
animals
due to:
a. The
severe damage of peribronchial,
perivascular and
subpleural lymphatics
which are
important in resorption of
exudate.
b. Frequency of thrombosis, necrosis and suppuration.
4- Organization is much more common involving the
peribronchial, perivascular and
septal tissue and replacing the
exudate in the alveoli.
Fig. 38: Lung showing
congestion.
3. Peribronchial and
perivascular lymphatics are dilated
with
a fluid rich in protein.
Complications of fibrinous pneumonia
1. Fibrinous pleuritis is a common
accompanying change which when heals it results in adhesion.
2. Pericarditis.
3. Extensive suppuration or gangrene.
4. Extensive fibrosis with a permanent dysfunction of a great part of
the pulmonary parenchyma.
5. Toxaemic degeneration of parenchymatous
organs.
Catarrhal bronchopneumonia
Definition
It a form of pneumonia in which the inflammatory reaction is catarrhal
in nature. Usually affects individual lobules with sharp demarcation and
happens always as an extension from bronchiolitis
and bronchitis.
Causes and occurrence
l. It is the usually from of pulmonary inflammation in domestic animals
and is particularly common in young calves, sheep and pigs, also present
in horse and dog.
2. Predisposing cause is important for the development of this type of
pneumonia.
3. The cause is always a bacteria and in majority of cases it arise as a
secondary infection or a complication of a viral diseases i.e.
Brucella bronchoseptica
in canine distemper corynebacterium
equi, although may be primary in foals it is
secondary in equine infectious anemia and
equine rhinopneumonitis and
Hemophilus
suis in swine influenza and hog cholera.
Pneumococci is
a primary cause of bronchopneumonia in calves.
4. Bronchopneumonia is an enzootic disease calves and, sheep and most
cases it is primarily a viral infection complicated with secondary
bacterial invasion.
5. Bronchopneumonia is usually observed in heavy infestation of lung
worm.
6. It is commonly observed in aspiration and hypostatic pneumonia.
Pathogenesis
l. Bronchopneumonia is usually an extension of an upper respiratory
tract infection. It begins as bronchitis and
bronchiolitis then the inflammatory reaction spreads along the
bronchial mucosa to reach the alveoli. Catarrhal ventilation (pors
of khon. may help in spread of infection
between adjacent alveoli.
2. The principal route of spread is endobronchial
by continuous progression of the bronchitis and
bronchiolitis and adjacent lobules are involved by the aspiration
of exudate more deeply into the lung.
3. Extension of inflammatory reaction through the bronchial wall (peribronchial.,
when happens is usually limited to the surrounding alveolar tissue.
Lymphatics as a path way for spread of
infection isn’t important in bronchopneumonia (except in horse..
Macroscopic appearance
1. Changes
are
mainly present in apical, cardiac, intermediate and
anteroventral
portions of diaphragmatic lobe.
2. Characterized by the presence of multiple irregularly distributed
areas of consolidation mostly in the size of lobule (lobular pattern of
distribution. in advanced severe cases the involvement of adjacent
lobules gives rise to bid areas of consolidation (confluent
bronchopneumonia..
3. In the early stage, the lesions are red in
colour. Later they become paler and grey,
they are solid and more prominent than the adjacent healthy tissue.
4. Association with these areas of consolidation are areas of 5-7cm. When
the out surface is squeezed mucopurulent
exudate escapes from the bronchi and bronchiols (Fig. 45).
.Fig. 45:
Gross picture of lung showing catarrhal bronchopneumonia.
Microscopic appearance
1. Bronchiolitis is a basic lesion the
lumens of bronichiols constantly contain a
catarrhal inflammatory exudate with obvious
damage of the epithelial lining and inflammatory reaction in their
mucosa propria (Fig 46).
2. Alveoli show an inflammatory exudate rich
in neutrophils, desquamated alveolar cells and alveolar macrophages (desquamative
catarrhal pneumonia).
3. Giant cells may be found in the alveoli this is particularly when
bronchopneumonia is secondary to viral pneumonia in some cases of
pneumonia associating distemper of dog (giant cell pneumonia..
4. Hyaline membrane may develop, which is a change that can be related
to a primary viral infection.
Fig. 46:
Microscopic picture of catarrhal bronchopneumonia showing bronchitis
represented by inflammation of bronchial wall which extend to alveoli.
H&E.
Sequellae
and complications
1. Complete resolution isn’t common, it
usually tends to be chronic and results
in induration and contraction of lung with
all sequelae of chronic
bronchiolitis and bronchitis as
bronchial obstruction and bronchiectasis,
atelectasis
and emphysema.
2. Suppuration
and
abscess formation.
Interstitial pneumonia
Definition
It is a form of pneumonia characterized by infiltrative and
proliferative cellular reaction in the alveolar septa and for the most
part is caused by a virus. This is the restricted true
interstitial pneumonia in its broad meaning interstitial
pneumonia can be considered to be a productive inflammatory process
affecting any part of the connective tissue stoma of the lung, in this
case it can develop from any chronic affection characterized by
development of excess of connective tissue i.e. chronic fibrous or
catarrhal pneumonia chronic verminous
pneumon-contageous bovine peluropneumonia,
lung tuberculosis, glanders,
pneumococcosis etc. according to
distribution of the change it can be classified into:
1-
Interstitial intralobular pneumonia.
2- Interstitial interlobular pneumonia.
3- Interstitial peribronchial pneumonia.
General features of interstitial pneumonia (viral pneumonia:
1. It is very difficulties find a pure viral pneumonia particularly in
field cases most of them are associated by bacterial infections with
complicates the picture.
2. Only in advanced cases the lung become grossly heave and fleshy in
constancy.
3. There is often some exudate in alveolar
spaces but the most characteristic changes are observed in alveolar
walls. The alveolar wall is greatly thickened due to cellular
infiltration particularly of lymphocytes, plasma cells and
histiocytes. In early stages the thickening
is due to inflammatory edema and
neutrophilic infiltration.
4. The alveolar epithelium shows desquamation (desquamative
pneumonia. proliferation with occasional production of giant cells
(giant cell pneumonia. and sometimes metaplastic
changes.
5. Hyaline membranes develop which line the alveolar spaces and alveolar
ducts.
6. Peribronochia1 lymphocytic collections
show obvious hyperplasia.
7. In
majority of cases specific inclusion bodies are present.
8. In
chronic cases there will be increase in
interalveolar connective tissue.
N.B.
Some forms of interstitial pneumonia can
be
observed in some peracute
septicemic
bacterial diseases.
Fig. 47:
Gross picture of interstitial pneumonia.
Some special forms of pneumonia
Suppurative pneumonia
Definition
It is a form of pneumonia characterized by suppurative inflammation with
frequent abscess formation which may be embolic or
metastatic
or bronchogenic as a complication of
purulent bronchopneumonia (Fig 48).
General features
1- In case of embolic or metastatic type,
uniformly symmetrically distributed multiple abscesses of nearly the
same size and age are present.
2. In
bronchogenic type the abscesses are usually
found in relation to affected bronchi.
3. In
both types the abscesses are surrounded with area of pneumonia (Fig
49).
Fig. 48: Gross picture of
suppurative pneumonia.
Fig. 49: Lung showing
microscopic picture of suppurative pneumonia represented by
liquefactive necrosis surrounded by line of
defense. H&E.
Fig. 50: Lung showing
microscopic picture of microscopic picture of suppurative pneumonia
characterized by focal replacement of pulmonary tissue with neutrophils.
H&E.
Gangrenous pneumonia.
Definition
It isn’t an independent type of pneumonia it is usually a complication
of other forms associated with severe necrosis of tissues or it may be
primary observe in cases of aspiration pneumonia or as the result of
a penetrating foreign body from the reticulum of cattle.
General features
1. Grossly areas of catarrhal or fibrinous pneumonia reveal small or big
yellowish green or green black foci which have all features of soft
gangrene as complete loss of structure, softening and having an
offensive odour in advanced cases gangrenous cavity may develop.
2.
Microscopically changes of partly purulent but mostly of severs
necrotizing character are observed with mainly affect bronchi and
surrounding pulmonary tissue.
3. In
aspisation pneumonia foreign particles are
usually present in the lumen of bronchi and
bronchiols.
Tumors
of lung
Metastatic
tumors are frequently observed particularly
in dog (Fig 51).
Primary tumors are less common in domestic
animals than in man. The most common tumors
found in the lung are:
1. Adenoma or adinomatosis of lung (sheep
and cattle. (Fig 52).
2. Alveolar cell adenoma and adenocarcnoma
.
3.
Bronchogenic
adenocrcinoma.
4-Mesothelioma (Fig 53).
Fig. 51: Lung showing metastatic
adenocarcinoma represented by
presence of malignant cells arranged in mass or pseudoalveoli. H&E
Fig. 52:Lung of sheep showing microscopic picture
of pulmonary adenomatosis.
Fig. 53:Microscopic picture of
mesothelioma. H&E
The pleura
Abnormal content of the pleural cavity
Abdominal viscera, may enter the cavity as a
result of congenital or acquired opening in the diaphragm (Diaphragmatic
hernia..
Foreign bodies, such as nails, pieces of wire, and various other sharp
metallic objects, my penetrate from the four stomachs of cattle, penetration is usually
slow
therefore, a local fibrinous pleuritis
develops. Later the body may become encapsulated.
Air (Pneumothorax):
may result from trauma of the thorax (fractured ribs. trauma of lungs
(foreign bodies penetrating from the four stomach.
spontaneous
perforation of the lung (rupture of an abscess in the lungs..
Fluid (Hydrothorax):
Hydrothorax accompanies general edema.
Blood
(Hemothorax.: usually result from the
trauma.
Pus (Pyothorax):
Suppurative
pleuritis
or the rupture pleural cavity.
Circulatory disturbance
Hemorrhages
Petechiae
of the pleura appear in some acute septicemic
diseases (Hog-cholera, Anthrax,
Heamorrhagic septicemia and
purpura hemorrhagica..
Their locaton is in the
subserous tissue. Large collections of blood (Gaemothorax)
are usually due to trauma.
Hydrothorax
It is a collection of clear pale yellow fluid in the pleural cavity in
the absence of inflammatory changes.
The fluid is transudate from the vessels. It
is seen in connection with chronic passive
hyperemia due to chronic heart, lung and kidney disease and in
general oedema developing in cases leading to
hypoprpteinemia.
Pleuritis
Pleuritis
in general is caused by the same traumatic and infections agents as
pneumonia. The infection reach the pleura
either by direct extension from lung or pericardium or by
hematogenous rout as in some of the acute
septicemic diseases. The course of
pleuritis may be acute or chronic.
Serous, serofibrinous
and fibrinous peuritis
These forms of pleuritis occur in
contagious bovine pleuropneumonia, calf
pneumonia, hemorrhagic septicemia and other
pasteurallosis.
Macroscopically
There are varying quantities of serous fluid
containing fibrin flocculi (Fig 54)
. The
fluid may cause compression atelectasis. The
pleura is rough and dry. The appearance of
dryness is due to the presence of fibrin upon the parietal and visceral
pleura.
Microscopically
The
mesothelial
lining
of the
serous membrane
in serous pleuritis
remains intact while in the fibrinous form it is usually
damaged . In all forms the
propria is oedematous and the
subpleural
vessels are dilated. In the fibrinous from the fibrinous
exudate is rich in leucocytes (Figs 55 & 56).
The termination of the serous and fibrinous
forms is either by absorption of the serous exudate
and of the fibrin which is digested by the
leucocytic enzymes followed by regeneration of the serous
membrane, or by organization of the exudate
with the formation of adhesions between the visceral and parietal pleurae
if the exudate is so
extensive
that it cannot be liquified and absorbed.
Fig. 54: Gross picture of fibrinous
pleurisy and pneumonia.
Fig. 55: Microscopic picture of
fibrinous pleurisy characterized by thickening of pleura by fibrinous
exudates. H&E.
Fig. 56: Chronic fibrinous pleurisy
showing thickening of pleura by fibrous connective tissue. H&E.
Suppurative pleuritis
It is
diffuse
form of pleuritis which happens usually
as
an extension from a suppurative pneumonia. A focal form is seen mostly
in pigs in the region of pulmonary abscess caused by
Coryne
pyogenes.
In such cases, small encapsulated abscesses containing pale green pus
appear in the pleura.
Tuberculosis:
Follows that of serous membranes. |
