Department of Pathology,

Faculty of Veterinary Medicine,

Zagazig University, Egypt.

Pathology of Respiratory SystemBY

Prof. Dr. Mohamed Hamed Mohamedmohamedelariny@yahoo.com

+201224067373

2012

Respiratory SystemThe respiratory tract is divided into three independent but

continuous systems:

1-Conducting system: It consists of the nasal cavity, sinuses, larynx,

trachea and bronchi. The mucosa of the conducting system is lined

by ciliated pseudostratified epithelium and goblet cells.

2-Transitional system: It is formed by the bronchioles that are lined

by a specialized mucosa containing several types of nonciliated and

secretory cells such as Clara cells.

NB: The normal bronchiolar mucosa contains no goblet cells.

3-Exchange system: This system is composed of the alveoli that are

lined externally by epithelial cells called pneumonocytes. The

type I (membranous) pneumonocytes are thin cells and

together with the capillary endothelium and basement

membrane constitute the air-blood barrier.

Type II pneumonocytes are cuboidal, progenitor of type I and

produce surfactant (This surfactant prevents alveolar collapse

during respiration).

Defense mechanisms:Overall, the most important defense mechanisms against inhaled particles

and particularly for bacteria are:

1-Air Filtration (conchae, bronchial bifurcation, turbulences,

attachment to mucus, coughing).

2-Mucociliary clearance*for the conducting system (nasal,

tracheal and bronchial mucosa).

3-Phagocytosis (alveolar macrophages for the exchange system

alveoli).

4-Innate and acquired immunity (Antibodies and cell-mediated

immunity).

*Each cell has 200 cilia and beating 25 time/second

Postmortem examination of the respiratory tract:

Nasal Cavity: Make transverse sections of the nasal cavity. Check

conchae, meatuses and sinuses and investigate the presence of

exudates, parasites, erosions, ulcers, edematous fluid, nodules, polyps

or tumors.

Larynx, Trachea and Bronchi: Open all these structures with scissors

and check the mucosa. Investigate the presence of exudates, erosions,

ulcers, parasites, nodules or tumors.

Thoracic Cavity: Check negative pressure by puncturing the

diaphragm and observing the retraction of the diaphragmatic muscle.

NB: Failure to retract suggests pneumothorax, pulmonary

inflammation, edema or emphysema.

Check for fluids or exudates as well as for fractured ribs.

Pathology of conducting systemNasal cavity and Sinuses:

Epistaxis (nose bleeding) and hemoptysis (blood in mouth, saliva or

sputum) are common findings in all species. Epistaxis is a common

problem in all animal species. It can be the result of trauma, foreign

body, nasal neoplasia, pulmonary hemorrhage (aneurism) or parasites.

Epistaxis is commonly seen in horse with:

Exercise induced pulmonary hemorrhage

Guttural pouch mycosis

Ethmoidal hematoma

Rhinitis and Sinusitis: characterized by unilateral or bilateral nasal

discharge.

According to exudate rhinitis and sinusitis can be classified as:

Serous: Mild irritants i.e., low levels of ammonia or chlorine

Catarrhal: Mucus i.e., viral infections

Purulent: Pyogenic bacteria i.e., Streptococcus equi

Fibrinous (Diphtheritic): Bacterial + potent bacterial toxins

Granulomatous: Foreign body, allergy, fungi

NB: Viral rhinitis is commonly seen in domestic animals but

infections generally are self-limiting unless complicated with bacteria

or mycoplasmas.

Examples of viral rhinitis in domestic animals:

Bovine Rhinotracheitis (IBR/BHV-1) Parainfluenza (PI-3)Equine Viral

Rhinopneumonitis

(EVR / EHV-4)

Feline Rhinotracheitis (FHV-1) and Feline

Calicivirus

Canine Distemper

(Morbillivirus)

Inclusion Body

Rhinitis piglets

(Cytomegalovirus

Guttural Pouches and Larynx:There are some important anatomical differences in domestic animals

(i.e., syrinx in birds, guttural pouches in horses).

Guttural Pouch Empyema: accumulation of pus in the equine guttural

pouches is a common and important disease. It is caused by pyogenic

bacteria such as Streptococci spp. Lesions: accumulation of purulent

exudates in guttural pouches.

Laryngeal Hemiplegia("Roaring"): It is a disease of horses characterized by

paralysis of the intrinsic muscles of the larynx resulting in audible inspiratory

dyspnea. The condition is usually associated with injury to the left recurrent

laryngeal nerve (which is the motor nerve to the intrinsic muscles of the larynx).

The condition may be mild or severe, unilateral or bilateral.

Causes: have been suggested to explain laryngeal hemiplegia (pounding of the

heart and aorta on the recurrent laryngeal nerve, inflammatory lesions,

trauma, toxins, abscesses, neoplasms, etc.).

Results:1-Paralysis and atrophy of the muscles and drops the arytenoid cartilage

(epiglottis) inward into the lumen of the larynx upon inspiration.

2-During the act of inspiration, the arytenoid cartilage and the relaxed

vocal cords vibrate in the air stream, resulting in the sound referred to as

roaring.

Necrotic laryngitis (calf diphtheria): caused by Fusobacterium

necrophorum . Lesions: Exuberant plaques of fibrinonecrotic exudate

on top of deep ulcers.

Trachea and Bronchi:Tracheobronchitis: it caused by

1-Canine Infectious Tracheobronchitis (Kennel Cough)

Kennel Cough: Acute, self-limiting tracheobronchitis (cough) of

complex etiology (Canine Adenovirus-2, Canine Parainfluenza

virus, Bordetella bronchiseptica, Mycoplasmas). Lesions:

necrosis, inflammation and repair are the same as for rhinitis.

2-Parasitic Tracheobronchitis: (Oslerus – Filaroides - osleri)

PATHOLOGY OF THE TRANSITIIONAL SYSTEMSThe bronchioles is unlike bronchi, the walls of the bronchioles do

NOT contain cartilage and the mucosa does not normally have goblet

cells. The pseudo-stratified epithelium in bronchi gradually flattens and

looses their cilia in bronchioles.

Progressive branching of the major bronchi forms bronchioles.

Further branching of bronchioles lead to the terminal bronchioles

called the acinus or the terminal respiratory unit.

Acini: contain alveoli and are thus the site of gaseous exchange.

An acinus is composed of

1-Respiratory bronchioles (terminal ones) which is

surrounded by several alveoli.

2-Alveolar ducts

3-The alveolar sac (the blind end of the respiratory

passage).

whose walls are formed entirely of alveoli. A cluster of 3 to 5

terminal bronchioles, each with its appended acinus, is usually

referred to as the pulmonary lobule.

Remember:The functional unit of the lungs in mammals is the acinus (not

the alveolus); thus, disease of the lungs usually affect acinar units

rather than just alveoli.

Bronchitis: inflammation of bronchus.

Bronchiolitis: inflammation of bronchiole.

Acute Bronchitis:

Causes:

1-Exposure to cold weather particularly in young age or

recently sheared animals.

2-Parasitic infestation as Dictyocaulus viviparous in cattle.

3Aspiration of foreign bodies.

4-Extension from tracheitis or pneumonia.

5-Secondary to some specific diseases as strangles, IB, HS.

Microscopic Pictures:

1-Congested blood vessels (active hyperemia).

2-Leukocytic infiltrations.

3-Edema in the wall of the bronchi.

4-Hyperplasia and desquamation of the lining epithelium.

5-Thickening of the basement membrane.

6-Loss of the cilia.

7-Metaplasia of the epithelium into goblet cells and mucus.

Macroscopic Picture:

1-The mucous membrane is red and swollen.

2-The m.m. show petechial hemorrhages and covered by mucus

3-Presence of parasite if it is the cause of bronchitis.

Chronic bronchitis:

Causes:

1-Follow the acute one.

2-Inhalation of dust (feeding on dusty food).

3-Lung-worm in calves.

4-Persistent venous congestion.

Microscopic Picture:

1-Hyperplasia of the lining epithelium with loss of cilia.

2-Thickening of the basement membrane.

3-The mucosa is replaced by granulation tissue.

4-Perivascular and peribronchial aggregation of lymphocytes.

5-Destruction of elastic and smooth muscle fibers.

6-Dilation or narrowing of the bronchial lumen.

Macroscopic Picture:1-Grayish-red or grayish brown m.m. with irregular surface.

2-Villous or nodular formation of c.t.

3-The lumen contains mucus, purulent or caseated material.

4-Dilation or narrowing such lumen.

Sequellae:

1-Resolution (if the cause is removed)

2-Bronchopneumonia.

3-Bronchiolitis obliterans where there is complete

obstruction of the bronchioles. It either

A-Partial obstruction Emphysema.

B-Complete obstruction Collapse.

4-Changes in the bronchial lumen:

1-Bronchostenosis (stenosis= narrowing).

2-Bronchiectasia (ectasia =dilation).

Bronchostenosis: it is the narrowing of the bronchial lumen

due to changes in the bronchial wall.

Pathogenesis:

Causes and Pathogenesis: it is due to

1-Pressure from outside by tumor, TB nodules, enlarged Lns.

2-Thickening in the wall due to chronic bronchitis.

3-Presence of caseated material, parasites or foreign bodies.

Bronchiectasia: it is dilation of the bronchi which may be

Cylindrical form Saccular form

Fusiform form Irregular form

Causes and Pathogenesis: it is due to 3 factors

1-Destruction of elastic and smooth muscle fibers in chronic

bronchitis with loss of elasticity of wall to become dilated.

2-Chronic peribronchitis induce fibrosis, contracted and pull

the wall outside (dilation).

3-persence of the caseated material for long time stretches and

dilates the lumen.

Microscopic Picture:

1-Overdilation of the bronchial lumen.

2-Chronic inflammatory cells infiltration.

3-Dstruction of elastic and smooth muscle fibers.

4- The wall replaced by fibrous c.t.

Macroscopic Picture:

1-The mucosa is gray and thin.

2-The lumen is filled with mucopurulent material.

3-The bronchial wall is thickened .

4-Dilation of the bronchial lumen.

Lungs:Hypostatic Congestion: it is the gravitation of the blood to the lowest

parts of the body including lungs in recumbent or diseased animals due

to cardiac weakness or gravity (in dead animals).

Hemoptysis: it is a hemorrhage from the lungs (frothy).

Changes in the air content of the lungs:

Congenital

1-Atelectasis

Acquired

2-Emphysema

Congenital Atelectasis: it is a failure of the alveoli to open to contain

air. It either localized or generalized (in the newly born animals).

Causes:

Causes:

1-It may be nervous.

2-The bronchi and bronchioles may be plugged by mucus, pus or

amniotic fluid.

Microscopic Picture:

1-The alveoli are compressed to form parallel slits-like.

2-They are lined by cuboidal epithelium.

Macroscopic Picture:

1-The lungs or the affected areas are dark red in color (dull).

2-Depressed under the level of the surrounding normal tissue.

3-Sink under the water (floating test).

Acquired Atelectasis (collapse): it is loss of air content from

previously functioning alveoli (acquired airless alveoli).

Causes: pressure on the alveoli which may be due to

1-Intrathoracic causes as hydrothorax, hydropericardium

2-Intrapulmonary causes as lesions in the lungs (tumor, cysts, TB)

3-Intra-abdominal causes as ascites and tympany.

Microscopic Picture:

Microscopic Picture:

1-The alveoli appeared slits-like.

2-They are lined by flat epithelium.

Macroscopic Picture:

1-The affected areas are depressed under the surface.

2-Dark red in color.

3-Firm in consistency.

4-Float over the water.

Sequellae:

1-If the cause is removed the affected areas return to the normal.

2-If the cause is persist leads to

i-Chronic edema.

ii-Interstitial pulmonary fibrosis (splenized lungs).

Emphysema (Inflation): it is the accumulation of gasses or air in the

tissues. It is the inflation of tissues by gasses or air.

Types of Emphysema:

1-Pulmonary Emphysema.

2-Subcutaneous Emphysema. 3-Postmortem Emphysema.

Pulmonary Emphysema:

It is the overdistention of the alveoli or interstitial tissues of the

lungs with air.

Types of Pulmonary Emphysema: Focal

1-Acute

Diffuse

I-Alveolar Emphysema Focal

2-Chronic

Diffuse

Focal

1-Acute

Diffuse

II-Interstitial Emphysema

Focal

2-Chronic

Diffuse

Acute Focal Alveolar Emphysema: it is usually compensatory in

case of atelectasis, tumor, pneumonia.

Microscopic Picture:

1-The affected alveoli are distended and with thin wall.

2-Some alveoli may be ruptured on each other forming large space

3-The perialveolar capillaries are empty from the blood.

4-The interalveolar septa are thick.

5-The smooth muscles around the alveolar ducts are hyperplastic;

but those around the bronchi are normal.

Macroscopic Picture:

1-The affected areas are projected above the surface.

2-Pale or white in color.

3-Float over the surface of water.

4-It can be compressed by finger but does not pit.

5-On Pressure, crepitation may occurs.

Acute diffuse alveolar emphysema:

It is only occur in guinea pigs suffered anaphylactic shock (Type I

hypersensitivity). It causes severe bronchial spasm (constriction).

Chronic focal alveolar emphysema:

Causes: it is usually accompanied by bronchostenosis as in case of

i-Lung worm infestation.

ii-Continuous coughing.

iii-After parturition and long standing vomition.

Microscopic Picture:

1-The alveoli are dilated with thin wall.

2-The interalveolar septa are thin.

3-Bronchostenosis or lungworms may be present.

4-The peribronchial smooth muscles and lymphoid tissues

are hyperplastic.

Macroscopic Picture:

1-The affected areas are raised on the surface and pale in color

2-The emphysematous areas are cone-shaped with their base at

the pleura and their apex at the narrowed bronchus.

Differentiate between acute and chronic alveolar emphysema

Criteria Acute Chronic

Interalveolar septa Thick thin

Bronchostenosis or lungworm - ve + ve

Hyperplasia of bronchial smooth muscle and lymphoid tissue

normal present

Chronic diffuse alveolar emphysema (Heaves, Broken wind disease, Poor man disease or Asthma of horse)

It is abnormal prominent overdistention of the alveoli with air

without changes in the interstitial tissue (affects the drought horse).

Causes:1-Heavy work with non-nourished food (dusty hay) poor man disease

2-Prolonged spasmodic cough.

3-Chronic bronchitis. 4-Bad ventilation

5-The animal has no rest after meal.

Pathogenesis:-The weakened alveolar elastic fibers (congenitally) or due to chronic

bronchitis with an increased respiratory efforts leads to ballooning of

the alveoli and interference with the pulmonary circulation. The

disease induces double expiratory effort (broken wind disease).

Microscopic Picture:1-The alveoli are ballooned with thin wall.

2-Diffuse thickening of the bronchial mucosa.

3-Empty of the perialveolar capillaries.

4-Hyperplasia of the peribronchial lymphoid tissues.

Macroscopic Picture:1-The affected lungs are pale and voluminous.

2-Crepitation may occur by pressure or cut.

3-The cut surface is smooth and dry.

4-Float over the surface of water.

5-Numerous translucent miliary foci represent the lymphoid follicles

Sequellae:1-Cardiac hypertrophy. 2-Congestive heart failure.

3-General passive hyperemia, edema, death.

Interstitial Emphysema:It is the collection of air in the interstitial septa, under the pleura and in

the interstitial pulmonary tissues.

Causes:1-Chronic alveolar emphysema with violent cough lead to rupture

of alveoli and escaping the air into the interstitial tissue.

2-Traumatic due to broken ribs.

3-Heavy lung worm infestation (during migration).

Microscopic Picture:1-The interalveolar septa are thickened due to separation of the

fibers by air without any increase in the tissue elements.

Macroscopic Picture:1-Presence of air in the subpleural space and interlobular septa.

2-The interlobular septa appeared thick.

3-Atelectasis are seen in the adjacent alveoli.

Sequellae:1-Right heart hypertrophy (core pulmonal).

2-Tricuspid valve insufficiency.

3-Hydropericardium and general venous congestion.

NB: Pneumothorax: it is the presence of air in the thoracic

cavity which leads to collapse of the lungs.

Parasites of the lungs:1-Hydatid cysts in camel, sheep, cattle, horse.

2-Lngworms larval stage of metastrongyloidae.

3-Larva migrans in the paratenic hosts

Pneumonia (Pneumonitis)Definition: It is the inflammation of the pulmonary tissue.

Causes:I-Predisposing Causes:

1-Damp drafty stable. 2-Malnutrition.

3-Fatigue after shipping or work.

4-Dipping for external parasites in cold weather.

5-Unhyeigenic ventilation.

II-Main Causes:

A-Primary Pneumonia:1-Chemical agents (inhalation of hot gasses).

2-Physical causes (smoking).

3-Bacterial causes (staph, Coryne, Pasteurella).

4-Viral causes (pneumotropic as MCF, IBR)

5-Mycotic causes (Asperigellosis).

6-Parasitic causes (lungworms).

B-Secondary Pneumonia: secondary to some generalized

diseases.

Pathogenesis:It depends upon the route of entry of the causative agents.

1-Bronchogenic route: The way of infection through the upper

respiratory tract (rhinitis, laryngitis, tracheitis, bronchitis,

bronchioleitis, pneumonia (bronchopneumonia = lobular pneumonia).

2-Hematogenic route: it occurs in septicemic and pyemic diseases,

where the causative agent circulate in the blood (Lobar pneumonia).

3-Lymphogenic route: Similar to hematogenic route.

Classification of PneumoniaI-According to the naked eye appearance (anatomical):

1-Lobar Pneumonia:i-One or more whole lobes are involved.

ii-Caused by Diplococcus pneumoniae.

iii-The infection occurs through hematogenic route.

iv-Not present in animals.

V-It is usually acute fibrinous type.

2-Lobular Pneumonia:i-Only scattered individual lobules are involved.

ii-The infection through the bronchogenic route

iii-It usually occurs in the animals.

iv-It is acute or chronic catarrhal type.

3-Interstitial Pneumonia:i-The lesions of this type are present in the interlobular,

peribronchial and perivascular tissues.

ii-It is caused by infectious diseases as CBPP, lungworms.

iii-It is usually acute or chronic interstitial pneumonia.

-The acute type is characterized by Edema.

-The chronic type is characterized by Fibrosis

II-According to the causative agents:

1-Viral Pneumonia:-It is common in young animals.

-It is usually Proliferative bronchopneumonia.

Microscopic Picture:1-Loss of the cilia. 2-Extensive lymphocytic infiltrations.

3-Necrosis of the bronchial epithelium.

4-Cyncytial giant cells and inclusion bodies.

2-Bacterial Pneumonia:It is generally exudative and mostly fibrinous (pasteurella) or suppurative

(pyogenic m.o.) bronchopneumonia.

3-Mycotic Pneumonia:It is granulomatous pneumonia as in case of Aspergillosis.

4-Parasitic Pneumonia (verminous Pneumonia):

It induces catarrhal bronchopneumonia.

5-Mycoplasma Pneumonia:It is characterized by fibrinous pneumonia with marbling feature and

thickening of the interlobular septa as in case of CBPP.

III-According to the predominant exudates:Serous Pneumonia Catarrhal Pneumonia

Fibrinous Pneumonia Hemorrhagic Pneumonia

Suppurative Pneumonia Eosinophilic and lymphocytic

General Picture of Pneumonia:

Gangrenous Pneumonia:-It is a putrefactive decomposition of the necrotic pulmonary tissue

-It is caused by saprophytic bacteria either from bronchogenic or

hematogenic route.

Embolic Pneumonia:-It is usually suppurative type and hematogenous route.

-Focally distributed allover the pulmonary tissue

(pneumonic foci), particularly around the blood vessels.

-The lesions are numerous under the pleura because it

contains greatest number of small arteries and arterioles.

Hypostatic Pneumonia:-It occurs in sick recumbent animals.

-There is congestion in the lower parts of the lungs with

exudation in the alveoli.

Pulmonary Granuloma:

Granuloma: It is chronic inflammatory reaction consisting

of macrophages or macrophages and giant cells. Several

diseases induce granulomatous lesions as TB, Actinomycosis,

Actinobacillosis, Glanders, Mycotic disease. Some granuloma

show central necrosis and encapsulated by fibrous c.t.

Stages of Fibrinous PneumoniaThey include: 1-Stage of Congestion 2-Stage of Red Hepatization

3-Stage of Gray Hepatization 4-Stage of Resolution

Stage of Congestion:

Microscopic Picture:1-The perialveolar and peribronchial capillaries are congested.

2-The alveoli are filled with eosinophilic granular material.

3-Very few or no leukocytes infiltration.

Macroscopic Picture:1-The affected lungs are swollen and congested.

2-Blood-stained fluid is oozed from cut surface.

3-The lung is floated (does not sink) on the water surface.

Stage of Red Hepatization (hepar = liver) :

Microscopic Picture:1-The alveoli are filled with erythrocytes, fibrinous or serous exudate

2-The perialveolar and peribronchial capillaries are congested.

3-Few leukocytes are seen.

Macroscopic Picture:The affected lungs are similar to the liver (hepatized). It include:

1-Dark red in color. 2-Firm in consistency

3-Heavy and enlarged. 4-Sink under the water

5-The plural surface is dull due to pleuritis.

Stage of Gray Hepatization:Microscopic Picture:

1-The alveoli are filled with inflammatory cells (to phagocytize

the remnant of hemolysed erythrocytes and fibrin).

2-Few or no intact erythrocytes.

3-The congestion of the pulmonary capillaries is decrease due to

pressure of exudate inside the alveoli and they appeared empty.

Macroscopic Picture:1-The affected lungs are enlarged. 2-Gray in color

3-Firm in consistency 4-Sink under the water

5-Purulent fluid runs from cut surface

Stage of Resolution:

Microscopic Picture:1-The pulmonary capillaries and blood vessels appear normal.

2-Complete lysis of the fibrin and cellular debris.

3-Regeneration of the alveolar epithelium.

4-The exudate is completely absorbed (normal picture).

Macroscopic Picture:-The pulmonary tissue appeared normal.

The complete resolution is not occur in animals due to:1-The severe damage of the peribronchial, perivascular and

subpleural lymphatics which is essential in resorption of the exudate

2-Thrombosis, infarctions, necrosis and suppuration are rapidly

occur with organization of the exudate.

3-Myocardial degeneration may occur due to the release of toxic

substances from the pneumonia.

If The Resolution did not occur, some chronic stages are seen:

1-Fetalization: It is chronic inflammatory condition in which the

alveolar epithelium become cuboidal (resembling to the fetal lung).

2-Adenomatosis: It is the sequella of fetalization where there is

hyperplasia of the cuboidal alveolar epithelium, particularly in viral

infection (resembling papillary adenoma).

3-Carnification: It is the organization of the fibrinous exudate into

permanent fibrous tissue.

NB: Cornification: Excessive keratin formation (corn).

Interstitial Pneumonia:

Causes: viral infection.

Types or Classification of the Interstitial Pneumonia:

1-Interstitial-Intralobular Pneumonia

2-Interstitial-Interlobular Pneumonia

3-Interstitial-Peribronchia Pneumonia

Microscopic Picture:Acute Type: it is characterized by inflammatory edema (serous).

-Thickening of the alveolar wall by cellular infiltration.

Chronic Type: it is characterized by fibrosis (splenized lung).

PleuraPneumothorax: it is the presence of air or gasses in the thoracic cavity.

Hydrothorax: it is abnormal accumulation of fluid in the thoracic cavity.

Hematothorax: it is abnormal accumulation of blood in the thoracic cavity.

Pyothorax: it is the presence of pus in the thoracic cavity.

Chylothorax: abnormal accumulation of lymph in the thoracic cavity

Pleuritis (Pleurisy)

It is the inflammation of the pleura (serous, fibrinous or purulent).

Causes:1-CBPP 2-HS 3-Canine distemper

Macroscopic Picture:1-The pleura is dull (loss of glistening).

2-Congestion of the serous membrane.

3-Hydrothorax (serous) or gray membrane (fibrin).

Microscopic Picture:1-Blood vessels are congested.

2-Leukocytic infiltration.

3-Exudate either albumen (serous), fibrin (fibrinous) or both.

Sequellae:1-Absorbed exudate and healing by regeneration.

2-Unabsorbed exudate, organization and adhesion between

parietal and visceral layers of pleura.

Purulent (suppurative) Pleuritis:1-Focal Type: It occurs in case of Coryne pyogenes (focal abscess).

2-Diffuse Type: Extension from suppurative pneumonia.

Tuberculous Pleuritis:1-Pearl disease

Granulomatous Pleuritis

2-Grap’s disease

Tumors of Pleura:-Primary Tumor: Mesothelioma (fibrosarcoma or

adenocarcinoma like).

-Secondary Tumors: metastatic carcinoma, others