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RESPIRATORY SYSTEM
UPPER RESPIRATORY TRACT
LOWER RESPIRATORY TRACT
Congenital Anomalies
CLEFT PALATE
Abnormal connection between the nasal cavity
and the mouth.
It is otherwise called Palatoschisis.
Fairly common defect seen in newborn animals –
calf, lamb
Affected animals do not survive long.
Sequelae – Death of new born by starvation or
aspiration pneumonia.
EPISTAXIS (Syn. Nose bleeding)
Occurrence - Infrequent in animals, seen in Horse, Dog
Aetiology i. Physical - Trauma - Violent exercise
induces pulmonary hemorrhage in horses
ii. Infectious diseases like Anthrax, Glanders, purpura,
IBR, MCF
iii. Parasites-Eimeria canis in dogs; Oestrous ovis in
sheep.
iv. Erosion of vessels by pathological processes in
nasal cavity
v. Idiopathic – familial in certain race horses
vi. Hemangioma - neoplasm
vii. Poisoning by nitrates, bracken fern, sweet clover
and mercurials.
Clinical signs - Bleeding may be unilateral or bilateral
RHINITIS - Inflammation of mucous membrane
of nasal cavity/nose.
• Classification : 1. Primary or Secondary.
A. Primay rhinitis - occurs independently.
B. Secondary rhinitis - manifestation of some of
acute and chronic infectious diseases.
2. Based on the nature of exudate:
i. Serous ii. Catarrhal iii. Purulent iv. Fibrinous
• 3. Based on the age of lesion:
i. Acute ii. Subacute iii. Chronic rhinitis
• 4. Based on severity of insult:
i. Mild ii. Moderate and iii. Severe rhinitis
• 5. Based on aetiological agent: i. Bacterial
ii. Viral iii. Mycotic and iv. Toxic rhinitis
• Predisposing Factors
• i. Environmental changes ii. Stress
iii. Immunosuppression
iv. Prolonged antibacterial therapy.
Etiology: i. Physical causes
a. Irritants – Dust, pollen
b. Foreign bodies- wheat/rice chaff, insects, flies
c. Injuries – horn, kicking
ii. Chemical -Irritating gases i.e. Formalin and
Ammonia gas arising from litter, smoke.
iii. Bacterial Causes
Bordetella bronchiseptica, Actinobacillus lignieresi,
Actinomyces bovis, Mycobacterium tuberculosis,
Fusobacterium necrophorum,
Pasteurella multocida, Pseudomonas mallei,
Staphylococci, Streptococcus equi,
Hemophilus paragallinarum (Infectious coryza),
Mycoplasma galliseptium,
Pseudomonas aeruginosa,
iv. Viruses - Common cold virus, Infectious
bovine rhinotracheitis, Bovine malignant
catarrhal fever, Rinderpest, Canine distemper,
Equine rhinopneumonitis, Equine influenza,
Swine influenza, Infectious laryngotracheitis and
Fowl pox.
v. Fungus - Aspergillus fumigatus, Cryptococcus
neoformans, Rhinosporidium seeberi
vi. Parasites - Oestrus ovis larvae - Sheep ,
Linguatula serrata - dog
Route of infection - through inspired air.
Sequelae - Rhinitis might extend to cause
bronchitis and pneumonia
Classification of rhinitis
Rhinitis is classified as acute and chronic rhinitis.
ACUTE RHINITIS - Acute inflammation of the
nasal mucosa
Causes – 1. Physical causes - Irritants – Dust,
pollen, Foreign bodies – chaff, insects, flies
ii. Chemical irritants iii. Infectious agents
Gross lesions - Mucous membrane appear
Congested, swollen, may be Dry /moist covered
with Exudate which may be serous / mucous /
mucopurulent /suppurative/ fibrinous in nature.
Histopathology - Lumen contains inflammatory
exudate with leucocytes. Mucosal epithelium
shows hydropic degeneration; Lamina propria is
hyperaemic and infiltration with inflammatory
leucocytes-Neutrophil, Lymphocyte & macrophages
CHRONIC RHINITIS:
is usually a sequel of acute rhinitis
Species affected - Jersey breed of cattle.
Clinical signs - Nasal discharge - Mucous or muco-
purulent, may be Nasal pruritis.
Gross pathology – rough, mucosal surface with tiny
nodules.
Histopathology – Mucosa - Many closely packed tiny
polyps covered by squamous epithelium projecting into
the lumen. Lamina propria: contains oedema, engorged
capillaries, fibroblasts, eosinophils, mast cells and
plasma cells. May be ulceration of mucosa which is
thickened and congested.
.
SINUSES
SINUSITIS – It is inflammation of sinus.
Seen in birds in respiratory infections.
Aetiology - Bacteria- Hemophilus/Avibacterium
paragallinarum in chicken - Infectious coryza
Route of entry – i. Inspired air.
ii. Through wound produced by dehorning
Gross pathology - The head will be swollen, eyelids
may be closed, subcutis contains edematous fluid
and sinus contains mucus or cheesy material.
Sequelae - Spread to eustachian tubes in human
being interfere with hearing.
Pharynx and Gutteral pouches
Pharyngitis – is inflammation of pharynx.
Pharynx is vulnerable to diseases of both upper
respiratory tract and upper digestive tract.
Causes - i. Penetrating wounds
ii. Foreign bodies-bones, stick, syringe, wire etc
iii. improper use of drenching or balling guns in
cattle and sheep
iv. Use of collars in dogs and cats cause choking
injuries.
Grossly - Local edema and thickening of wall due
to fatal cellulitis. Foreign body may be present
anywhere in pharynx, depending on its size and
location, may cause dysphagia, regurgitation,
dyspnoea and asphyxiation.
Gutteral pouches
are present in horses, as large ventral
diverticula of Eustachian tubes.
They are exposed to the same pathogens as is
the pharynx.
Because of anatomical closeness of guttural
pouches to internal carotid arteries, cranial
nerves, atlanto-occipital joint and middle
ears, diseases of guttural pouches may
involve these structures and cause a variety
of clinical signs in horses.
Gutteral pouch mycosis
is caused by Aspergillus fumigatus, other
Aspergillus sps.
Infection is unilateral and begin with
inhalation of spores from mouldy hay.
Grossly – Dorsal and lateral surfaces of
guttural pouch are covered with diphtheritic
or fibrino-necrotic exudate.
Microscopic lesions – Severe necrotic inflammation
of mucosa and submucosa and widespread vasculitis.
Fungal hyphae are present in lesions. Predilection of
fungi for vessel walls can cause erosion/rupture of
internal carotid artery (located adjacent to roof of
guttural pouch)→Fatal bleeding into guttural pouches
or in some cases, release of mycotic thrombo-emboli
into carotid circulation resulting into multiple brain
infarcts.
May cause dysphagia due to damage to pharyngeal
branches of Vagus and Glosso-pharyngeal nerves (lie
on ventral aspect of pouches).
Equine laryngeal hemiplegia (roaring) can result from
involvement of laryngeal nerves
Gutteral pouch empyema
occurs as complication of suppurative inflammation
of nasal cavity, most commonly to Streptococcus
equi infection (strangles).
In severe cases, entire guttural pouch can be filled
with purulent exudate.
Clinically, characterized by nasal discharge,
enlarged retropharyngeal lymph nodes, dysphagia
and respiratory distress.
Other clinical effects caused are similar to guttural
pouch mycosis, except that it does not produce
erosion of internal carotid artery.
Neoplasms – these are rare in horses, and are
usually Squamous cell carcinoma
Pathology of Larynx
ROARING/Laryngeal hemiplegia
Roaring is impaired sound due to laryngeal
hemiplegia in horses.
Etiology - Injury and degeneration of the left
recurrent laryngeal nerve or secondary nerve
damage by repeated trauma by pulsation in
the aorta, lead poisoning, pressure on the
nerve by aneurysms, enlarged lymph nodes,
abscesses, tumours, oesophageal diverticula
and other traumatic conditions.
Pathogenesis
Hyaline degeneration and fibrosis of the left
dorsal and lateral cricoarytenoideus muscle,
atrophy and paralysis leads to incomplete
dilatation of larynx. The arytenoids cartilage
cannot open and so will stand in the way of
air passing freely into the wind pipe.
This condition is accentuated when animal is
exercised.
A noise is heard by brushing of air with the
arytenoid cartilage and noise is called roaring
Gross pathology –
Affected cricoarytenoideus muscle is pale
and atrophic.
Histopathology - Left recurrent laryngeal
nerve show Demyelination and Wallerian
degeneration, Atrophic changes of muscle
fibres (neurogenic atrophy).
LARYNGITIS
It is the inflammation of the laryngeal mucosa.
Aetiology :
i. Extension of infection from nasal cavity and pharynx
in infectious diseases - Canine distemper in dog;
Strangles and Glanders in horses; Infectious laryngo-
tracheitis in poultry.
ii. Irritant vapours of chemicals.
iii. Mechanical injury by kicks, bites, grass awns, horn,
Injuries while passing probes or stomach tube.
iv. Excessive barking in dogs.
v. Specific diseases – Calf diphtheria, Tuberculosis,
Glanders and Actinomycosis.
Gross pathology - Mucosa of larynx is swollen,
hemorrhagic and dry at first, later becomes
coated with mucus or muco-purulent discharge.
Histopathology - Mucosa is covered with
exudate, may be mucus, blood or necrotic
material. Lamina propria is infiltrated with
leucocytes like N, M, L.
TRACHEITIS
Tracheitis means inflammation of the trachea.
Causes – a. Bacterial - Escherichia coli and
Mycoplasma gallisepticum.
b. Viruses - Ranikhet disease virus, IBV, ILTV
c. Parasite: Syngamus trachea.
Gross pathology - Tracheal mucosa is congested,
its lumen contains mucus or blood tinged mucus
containing red worms.
Histopathology
The mucosal epithelium is denuded and the
lamina propria is infiltrated with leucocytes.
Sequelae :
In heavy worm infections, asphyxia leads to
death.
ACUTE TRACHEO-BRONCHITIS
Condition usually encountered along with upper
respiratory disease and pneumonia.
Route of infection - i. Nasal cavity
ii. Aspiration into trachea
iii. Extension from pharynx and sinuses
Causes – i. Inhalation of irritants like industrial
fumes, smokes, feed particles and dust.
ii. Faulty drenching of medicaments.
iii. Bacterial – Pasteurellosis.
iv. Viral – Infectious bovine rhinotracheitis,
Ranikhet disease, ILT and IBV of fowls.
v. Parasites - Lung worms.
Gross pathology - Mucosa is covered by exudate
which may be catarrhal, fibrinous or purulent type.
Tracheal mucosa is thick and reddish. In gangrenous
tracheitis, there is extensive necrosis of the mucosa
which becomes sloughed.
Histopathology - Lumen contains mucus, leucocytes,
dead epithelial cells, lung worms and their ova.
Mucosal epithelium shows necrotic changes. Lamina
propria congested and infiltrated with inflammatory
cells of which neutrophils predominate.
Sequelae - Recovery may occur in mild cases.
In severe cases, may result in Bronchiectasis, Chronic
bronchitis, peribronchitis and bronchopneumonia.
Abscess may develop, if infected by pyogenic
organisms.
Pathology of Bronchi/Bronchiole
BRONCHOSTENOSIS/ Bronchiolostenosis
It is Narrowing of the bronchial lumen due to obstruction or
peripheral pressure.
Aetiology – i. Aspiration of foreign bodies
ii. Accumulation of exudate and infiltration in to the wall
causing reduction of diameter of the bronchus
iii. Parasites within the lumen
iv. Pressure from outside the bronchial wall by abscesses,
enlarged lymph nodes, tumors and exudate of pleural cavity.
v. Spasms of the muscles of the bronchi as in allergy.
Sequelae – i. A partial closure of the bronchi or bronchioles
results in ballooning of the alveoli as air that enters during
inspiration is not expelled. Repeated inspiration will
therefore lead to ballooning of the alveoli - Emphysema
ii. Complete obstruction of bronchus results in collapse of
lung - ATELECTASIS
BRONCHIECTASIS
It means dilatation of the bronchus.
Aetiology and pathogenesis –
i. Chronic bronchitis - Due to destruction of the elastic
tissue of the bronchial wall, contractile power of the
bronchus is lost and so the bronchus dilates. At the place
of dilatation, exudate accumulates, thereby further
dilating the bronchus.
ii. In chronic pneumonia, the bronchial wall is weak. The
fibrous tissue on contraction, pulls the bronchial wall
which gets dilated.
iii. In bronchostenosis, air accumulates during inspiration
below the level of obstruction and causes dilatation of the
bronchus. When the bronchi are completely closed
resulting in atelectasis, the negative pressure in the
pleural cavity pulls the bronchial wall and cause
dilatation.
Clinical signs - Persistent cough and Debilitation.
Gross pathology:
i. Cylindrical form of bronchiectasis is more common in
cattle and cause uniform dilatation of the bronchus.
ii. Saccular form is less common in which there is an out
pouching of the bronchial wall due to focal necrosis as
occurs in lung worm infections in cattle and sheep.
Histopathology - Destruction and disappearance of the
elastic tissue, musculature and even the cartilage of
bronchus, Mucosa: disappearance of lining epithelium,
Lamina propria infiltrated with mononuclear cells, Lung:
collapsed and carnified; pleural adhesions may develop.
Sequelae - Prognosis: course is chronic and unfavorable
Complications –
i. Development of abscesses with metastasis
ii. Bronchiolitis with emphysema
iii. Bronchopneumonia
iv. Secondary amyloidosis
BRONCHITIS/Bronchiolitis
It means inflammation of the bronchial mucosa.
Causes - Viral – Canine tracheo-bronchitis and
infectious bronchitis in fowls.
Gross Pathology - Trachea is congested and
contains mucus exudate. Bronchial lumen is
obstructed by yellow plugs of caseous material.
Histopathology - Bronchial mucosa is thickened
due to edema and cellular infiltration. Bronchial
lumen may contain neurophil or heterophil
rich exudate.
CHRONIC BRONCHITIS
Causes -i. Mild, continuous irritant like smoke &dust
ii. Extension of chronic infection of upper
respiratory tract as in chronic sinusitis.
iii. Most common cause in animals is Lung worm
infection, abscess, tuberculosis.
iv. Pathological – bronchiectasis – open tract
v. Chronic venous congestion – as in heart diseases.
Gross pathology – Bronchus may be dilated, lumen
may contain exudate – Mucoid or mucopurulent
mixed with worms, Pale (sometimes congested),
mucosa is thickened.
Histopathology
Lumen contains worms and eggs in case of
parasitic bronchitis. Mucosal glands may be
atrophic; ciliated epithelium replaced by
cuboidal epithelium. Lamina propria is
infliltration by lymphoid cells. Peribronchial
glands are hyperplastic (resemble goblet cells).
Walls: Lymphoid follicles may be formed;
Fibrosis may cause polypoid projections into the
lumen (Brochiolitis obliterans).
Sequelae
i. Bronchi – Bronchiectasis.
ii. Lungs – Bronchopneumonia; atelectasis;
emphysema leads to greater strain on the
heart and chronic venous congestion occurs
ultimately.
THANKS

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Resp. tract -I, dvm3.pdf

  • 1. RESPIRATORY SYSTEM UPPER RESPIRATORY TRACT LOWER RESPIRATORY TRACT
  • 2. Congenital Anomalies CLEFT PALATE Abnormal connection between the nasal cavity and the mouth. It is otherwise called Palatoschisis. Fairly common defect seen in newborn animals – calf, lamb Affected animals do not survive long. Sequelae – Death of new born by starvation or aspiration pneumonia.
  • 3. EPISTAXIS (Syn. Nose bleeding) Occurrence - Infrequent in animals, seen in Horse, Dog Aetiology i. Physical - Trauma - Violent exercise induces pulmonary hemorrhage in horses ii. Infectious diseases like Anthrax, Glanders, purpura, IBR, MCF iii. Parasites-Eimeria canis in dogs; Oestrous ovis in sheep. iv. Erosion of vessels by pathological processes in nasal cavity v. Idiopathic – familial in certain race horses vi. Hemangioma - neoplasm vii. Poisoning by nitrates, bracken fern, sweet clover and mercurials. Clinical signs - Bleeding may be unilateral or bilateral
  • 4. RHINITIS - Inflammation of mucous membrane of nasal cavity/nose. • Classification : 1. Primary or Secondary. A. Primay rhinitis - occurs independently. B. Secondary rhinitis - manifestation of some of acute and chronic infectious diseases. 2. Based on the nature of exudate: i. Serous ii. Catarrhal iii. Purulent iv. Fibrinous • 3. Based on the age of lesion: i. Acute ii. Subacute iii. Chronic rhinitis • 4. Based on severity of insult: i. Mild ii. Moderate and iii. Severe rhinitis • 5. Based on aetiological agent: i. Bacterial ii. Viral iii. Mycotic and iv. Toxic rhinitis
  • 5. • Predisposing Factors • i. Environmental changes ii. Stress iii. Immunosuppression iv. Prolonged antibacterial therapy. Etiology: i. Physical causes a. Irritants – Dust, pollen b. Foreign bodies- wheat/rice chaff, insects, flies c. Injuries – horn, kicking ii. Chemical -Irritating gases i.e. Formalin and Ammonia gas arising from litter, smoke.
  • 6. iii. Bacterial Causes Bordetella bronchiseptica, Actinobacillus lignieresi, Actinomyces bovis, Mycobacterium tuberculosis, Fusobacterium necrophorum, Pasteurella multocida, Pseudomonas mallei, Staphylococci, Streptococcus equi, Hemophilus paragallinarum (Infectious coryza), Mycoplasma galliseptium, Pseudomonas aeruginosa,
  • 7. iv. Viruses - Common cold virus, Infectious bovine rhinotracheitis, Bovine malignant catarrhal fever, Rinderpest, Canine distemper, Equine rhinopneumonitis, Equine influenza, Swine influenza, Infectious laryngotracheitis and Fowl pox. v. Fungus - Aspergillus fumigatus, Cryptococcus neoformans, Rhinosporidium seeberi vi. Parasites - Oestrus ovis larvae - Sheep , Linguatula serrata - dog
  • 8. Route of infection - through inspired air. Sequelae - Rhinitis might extend to cause bronchitis and pneumonia Classification of rhinitis Rhinitis is classified as acute and chronic rhinitis. ACUTE RHINITIS - Acute inflammation of the nasal mucosa Causes – 1. Physical causes - Irritants – Dust, pollen, Foreign bodies – chaff, insects, flies ii. Chemical irritants iii. Infectious agents
  • 9. Gross lesions - Mucous membrane appear Congested, swollen, may be Dry /moist covered with Exudate which may be serous / mucous / mucopurulent /suppurative/ fibrinous in nature. Histopathology - Lumen contains inflammatory exudate with leucocytes. Mucosal epithelium shows hydropic degeneration; Lamina propria is hyperaemic and infiltration with inflammatory leucocytes-Neutrophil, Lymphocyte & macrophages
  • 10. CHRONIC RHINITIS: is usually a sequel of acute rhinitis Species affected - Jersey breed of cattle. Clinical signs - Nasal discharge - Mucous or muco- purulent, may be Nasal pruritis. Gross pathology – rough, mucosal surface with tiny nodules. Histopathology – Mucosa - Many closely packed tiny polyps covered by squamous epithelium projecting into the lumen. Lamina propria: contains oedema, engorged capillaries, fibroblasts, eosinophils, mast cells and plasma cells. May be ulceration of mucosa which is thickened and congested. .
  • 11. SINUSES SINUSITIS – It is inflammation of sinus. Seen in birds in respiratory infections. Aetiology - Bacteria- Hemophilus/Avibacterium paragallinarum in chicken - Infectious coryza Route of entry – i. Inspired air. ii. Through wound produced by dehorning Gross pathology - The head will be swollen, eyelids may be closed, subcutis contains edematous fluid and sinus contains mucus or cheesy material. Sequelae - Spread to eustachian tubes in human being interfere with hearing.
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  • 13. Pharynx and Gutteral pouches Pharyngitis – is inflammation of pharynx. Pharynx is vulnerable to diseases of both upper respiratory tract and upper digestive tract. Causes - i. Penetrating wounds ii. Foreign bodies-bones, stick, syringe, wire etc iii. improper use of drenching or balling guns in cattle and sheep iv. Use of collars in dogs and cats cause choking injuries. Grossly - Local edema and thickening of wall due to fatal cellulitis. Foreign body may be present anywhere in pharynx, depending on its size and location, may cause dysphagia, regurgitation, dyspnoea and asphyxiation.
  • 14. Gutteral pouches are present in horses, as large ventral diverticula of Eustachian tubes. They are exposed to the same pathogens as is the pharynx. Because of anatomical closeness of guttural pouches to internal carotid arteries, cranial nerves, atlanto-occipital joint and middle ears, diseases of guttural pouches may involve these structures and cause a variety of clinical signs in horses.
  • 15. Gutteral pouch mycosis is caused by Aspergillus fumigatus, other Aspergillus sps. Infection is unilateral and begin with inhalation of spores from mouldy hay. Grossly – Dorsal and lateral surfaces of guttural pouch are covered with diphtheritic or fibrino-necrotic exudate.
  • 16. Microscopic lesions – Severe necrotic inflammation of mucosa and submucosa and widespread vasculitis. Fungal hyphae are present in lesions. Predilection of fungi for vessel walls can cause erosion/rupture of internal carotid artery (located adjacent to roof of guttural pouch)→Fatal bleeding into guttural pouches or in some cases, release of mycotic thrombo-emboli into carotid circulation resulting into multiple brain infarcts. May cause dysphagia due to damage to pharyngeal branches of Vagus and Glosso-pharyngeal nerves (lie on ventral aspect of pouches). Equine laryngeal hemiplegia (roaring) can result from involvement of laryngeal nerves
  • 17. Gutteral pouch empyema occurs as complication of suppurative inflammation of nasal cavity, most commonly to Streptococcus equi infection (strangles). In severe cases, entire guttural pouch can be filled with purulent exudate. Clinically, characterized by nasal discharge, enlarged retropharyngeal lymph nodes, dysphagia and respiratory distress. Other clinical effects caused are similar to guttural pouch mycosis, except that it does not produce erosion of internal carotid artery. Neoplasms – these are rare in horses, and are usually Squamous cell carcinoma
  • 18. Pathology of Larynx ROARING/Laryngeal hemiplegia Roaring is impaired sound due to laryngeal hemiplegia in horses. Etiology - Injury and degeneration of the left recurrent laryngeal nerve or secondary nerve damage by repeated trauma by pulsation in the aorta, lead poisoning, pressure on the nerve by aneurysms, enlarged lymph nodes, abscesses, tumours, oesophageal diverticula and other traumatic conditions.
  • 19. Pathogenesis Hyaline degeneration and fibrosis of the left dorsal and lateral cricoarytenoideus muscle, atrophy and paralysis leads to incomplete dilatation of larynx. The arytenoids cartilage cannot open and so will stand in the way of air passing freely into the wind pipe. This condition is accentuated when animal is exercised. A noise is heard by brushing of air with the arytenoid cartilage and noise is called roaring
  • 20. Gross pathology – Affected cricoarytenoideus muscle is pale and atrophic. Histopathology - Left recurrent laryngeal nerve show Demyelination and Wallerian degeneration, Atrophic changes of muscle fibres (neurogenic atrophy).
  • 21. LARYNGITIS It is the inflammation of the laryngeal mucosa. Aetiology : i. Extension of infection from nasal cavity and pharynx in infectious diseases - Canine distemper in dog; Strangles and Glanders in horses; Infectious laryngo- tracheitis in poultry. ii. Irritant vapours of chemicals. iii. Mechanical injury by kicks, bites, grass awns, horn, Injuries while passing probes or stomach tube. iv. Excessive barking in dogs.
  • 22. v. Specific diseases – Calf diphtheria, Tuberculosis, Glanders and Actinomycosis. Gross pathology - Mucosa of larynx is swollen, hemorrhagic and dry at first, later becomes coated with mucus or muco-purulent discharge. Histopathology - Mucosa is covered with exudate, may be mucus, blood or necrotic material. Lamina propria is infiltrated with leucocytes like N, M, L.
  • 23. TRACHEITIS Tracheitis means inflammation of the trachea. Causes – a. Bacterial - Escherichia coli and Mycoplasma gallisepticum. b. Viruses - Ranikhet disease virus, IBV, ILTV c. Parasite: Syngamus trachea. Gross pathology - Tracheal mucosa is congested, its lumen contains mucus or blood tinged mucus containing red worms.
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  • 26. Histopathology The mucosal epithelium is denuded and the lamina propria is infiltrated with leucocytes. Sequelae : In heavy worm infections, asphyxia leads to death.
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  • 28. ACUTE TRACHEO-BRONCHITIS Condition usually encountered along with upper respiratory disease and pneumonia. Route of infection - i. Nasal cavity ii. Aspiration into trachea iii. Extension from pharynx and sinuses Causes – i. Inhalation of irritants like industrial fumes, smokes, feed particles and dust. ii. Faulty drenching of medicaments. iii. Bacterial – Pasteurellosis. iv. Viral – Infectious bovine rhinotracheitis, Ranikhet disease, ILT and IBV of fowls. v. Parasites - Lung worms.
  • 29. Gross pathology - Mucosa is covered by exudate which may be catarrhal, fibrinous or purulent type. Tracheal mucosa is thick and reddish. In gangrenous tracheitis, there is extensive necrosis of the mucosa which becomes sloughed. Histopathology - Lumen contains mucus, leucocytes, dead epithelial cells, lung worms and their ova. Mucosal epithelium shows necrotic changes. Lamina propria congested and infiltrated with inflammatory cells of which neutrophils predominate. Sequelae - Recovery may occur in mild cases. In severe cases, may result in Bronchiectasis, Chronic bronchitis, peribronchitis and bronchopneumonia. Abscess may develop, if infected by pyogenic organisms.
  • 30. Pathology of Bronchi/Bronchiole BRONCHOSTENOSIS/ Bronchiolostenosis It is Narrowing of the bronchial lumen due to obstruction or peripheral pressure. Aetiology – i. Aspiration of foreign bodies ii. Accumulation of exudate and infiltration in to the wall causing reduction of diameter of the bronchus iii. Parasites within the lumen iv. Pressure from outside the bronchial wall by abscesses, enlarged lymph nodes, tumors and exudate of pleural cavity. v. Spasms of the muscles of the bronchi as in allergy. Sequelae – i. A partial closure of the bronchi or bronchioles results in ballooning of the alveoli as air that enters during inspiration is not expelled. Repeated inspiration will therefore lead to ballooning of the alveoli - Emphysema ii. Complete obstruction of bronchus results in collapse of lung - ATELECTASIS
  • 31. BRONCHIECTASIS It means dilatation of the bronchus. Aetiology and pathogenesis – i. Chronic bronchitis - Due to destruction of the elastic tissue of the bronchial wall, contractile power of the bronchus is lost and so the bronchus dilates. At the place of dilatation, exudate accumulates, thereby further dilating the bronchus. ii. In chronic pneumonia, the bronchial wall is weak. The fibrous tissue on contraction, pulls the bronchial wall which gets dilated. iii. In bronchostenosis, air accumulates during inspiration below the level of obstruction and causes dilatation of the bronchus. When the bronchi are completely closed resulting in atelectasis, the negative pressure in the pleural cavity pulls the bronchial wall and cause dilatation. Clinical signs - Persistent cough and Debilitation.
  • 32. Gross pathology: i. Cylindrical form of bronchiectasis is more common in cattle and cause uniform dilatation of the bronchus. ii. Saccular form is less common in which there is an out pouching of the bronchial wall due to focal necrosis as occurs in lung worm infections in cattle and sheep. Histopathology - Destruction and disappearance of the elastic tissue, musculature and even the cartilage of bronchus, Mucosa: disappearance of lining epithelium, Lamina propria infiltrated with mononuclear cells, Lung: collapsed and carnified; pleural adhesions may develop. Sequelae - Prognosis: course is chronic and unfavorable Complications – i. Development of abscesses with metastasis ii. Bronchiolitis with emphysema iii. Bronchopneumonia iv. Secondary amyloidosis
  • 33. BRONCHITIS/Bronchiolitis It means inflammation of the bronchial mucosa. Causes - Viral – Canine tracheo-bronchitis and infectious bronchitis in fowls. Gross Pathology - Trachea is congested and contains mucus exudate. Bronchial lumen is obstructed by yellow plugs of caseous material. Histopathology - Bronchial mucosa is thickened due to edema and cellular infiltration. Bronchial lumen may contain neurophil or heterophil rich exudate.
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  • 36. CHRONIC BRONCHITIS Causes -i. Mild, continuous irritant like smoke &dust ii. Extension of chronic infection of upper respiratory tract as in chronic sinusitis. iii. Most common cause in animals is Lung worm infection, abscess, tuberculosis. iv. Pathological – bronchiectasis – open tract v. Chronic venous congestion – as in heart diseases. Gross pathology – Bronchus may be dilated, lumen may contain exudate – Mucoid or mucopurulent mixed with worms, Pale (sometimes congested), mucosa is thickened.
  • 37. Histopathology Lumen contains worms and eggs in case of parasitic bronchitis. Mucosal glands may be atrophic; ciliated epithelium replaced by cuboidal epithelium. Lamina propria is infliltration by lymphoid cells. Peribronchial glands are hyperplastic (resemble goblet cells). Walls: Lymphoid follicles may be formed; Fibrosis may cause polypoid projections into the lumen (Brochiolitis obliterans).
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  • 39. Sequelae i. Bronchi – Bronchiectasis. ii. Lungs – Bronchopneumonia; atelectasis; emphysema leads to greater strain on the heart and chronic venous congestion occurs ultimately.