Transcript Respiratory system

Introduction
 Disease of the respiratory system are some of the
leading causes of mortality and morbidity in
animal and a major source of economic losses
Structure and function
 Conducting , transitional and gas exchange system
 Conducting include nasal cavity ,paranasal sinuses ,pharynx
,larynx ,trachea and extra and intra pulmonary bronchi
 All of which are largely lined by pseudo stratified columnar
cells plus variable secretory goblet cells and serous cell
 Transitional system composed of bronchioles save as transition
zone between the conducting system (ciliated )and the gas
exchange alveolar system
 Normal bronchiole lack goblet cell but instate have other type
of secretory cells(Clara and neuroendocrine cells)
 Clara cells contain numerous biosynthetic organelles that play
role in detoxification of xenobiotics (foreign body)
 The gas exchange system of respiratory tract in all mammals is
formed by alveolar duct and million of alveoli .
 Alveoli are superficially lined by two distinct type of epithelial
cells ,known as the 1 pneumonocytes (membrane ) and type 2
pnemonocyes (granular)
 Vulnerability of respiratory system to aerogenous
(air borne ) injury is primarily because of
 1-extensive area of alveoli
 2-the large volume of the air passing continuously in to
lung
 3-the high consternation of noxious element that can
present in the air
 Surface of pulmonary alveoli is approximately 2000 m2 in
equine ,in human 200 m2,9000 liter \day ,
 9% of total blood volume within pulmonary vasculature
 right ventricle of cardiac goes in to lung , so lungs are also
susceptible to blood borne microbes ,toxin and emboli .
 capillary bed of the lung surface area of 70 m2 equal to 2400
km of capillaries with 1 ml of blood occupying up to 16 km of
capillary bed.
Normal bacterial flora of respiratory system
 The respiratory system has its own normal bacterial flora .
 Many spices of bacteria are found such as Mannheimia (pasteurella)
heamolytica in cattle ,pasteurella multocida in cat ,cattle and pigs,
bordetella bronchiseptica in dogs and pigs .
 The organism that consist the normal flora of respiratory tract are
restricted to proximal region (nasal cavity ,pharynx and larynx) .
 The thoracic portion of trachea ,bronchi ,lung are sterile.
 Type of bacteria in nasal flora very considerable among animal
species and geographic region.
Portal of entry in to respiratory system
 Microbe, toxin and pneumotoxicants can gain access in to respiratory
system by the following routes
1-airoginous
 The most common route in transmission of most respiratory infection in
domestic animals,
 bacteria ,mycoplasma and viruses along with toxic gas and foreign particles
include food can gain access to the respiratory system via inspired air.
2- hematogenous

via circulating blood, some viruses ,bacteria
inter the respiratory system
parasites and toxin can
3-directed extension ,

pathogenic organism can also reach the pleura and lung through
penetrating injury or rupture esophagus or perforated diaphragm.
Defense mechanism of respiratory tract
 Particles ,microbe ,toxic gas most be gain entry to a vulnerable
region of the respiratory system before it can have a
pathologic effect.
 Size ,shape ,dispersal ,and deposition of particles
 Clearance is process by which deposited particles are
destroyed ,neutralized and removed from the mucosal surface
 Removal by sneezing ,coughing ,mucocilliary transport and
phagocytosis
 Difference between deposit and clearance is referred to as
retention
 The anatomic configuration of the nasal cavity and bronchi in
the upper respiratory tract plays a unique role in preventing
or reducing the penetration of noxious material in to the lung
specially in to alveolar region .the narrow nasal meatuses and
the coiled arrangement of the nasal generate enormous
turbulences of air flow, slow Velocity, reduce centrifugal force
 . and as result physical forces are created that forcefully
impact particles larger than 10 um on to the surface of nasal
mucosa
 10 um and more in nasal mucosa
 2-10 um in bronchial mucosa
 2 um and smaller by gravitation
 o.1-2 um (bacteria ,virus)
 shape ,length ,electrical charge ,humidity
 200 um may reach lower region ,asbestos
Defense mechanism of conducting system
 Nose, trachea ,bronchi
 Mucocilliary clearance (the main defense )
 Mucus is complex mixture of (water ,glycoprotein,immunoglobulin
,lipid ,electrolyte) produce by goblet cell, serous cells ,submucosal
gland and fluid from transepithelial ion and water transport
 Mucus (thin double layer film of mucous is formed ,)outer layer is
in a viscous gel phase ,inner layer is in fluid or solution phase .100
ml of mucous daily ,250 cilia in each cell (each cilia 6 um long).
 1000 strokes / minute ,Mucus move 20 mm /minute
 If cilliary transport is reduced (Loss of cilia) or mucous
production is excessive ,coughing becomes an important
mechanism for clearance the air way
 M cell( microfold cells ) modified epithelial cells covering the
(BALT)
 By M cell ,macrophage ,dendritic cell (APCs) and B ,T cell , IgA
and less IgG and IgM
Defense mechanism of alveoli
 Lack ciliated and mucus
 Phagocytosis by alveolar macrophages ,capillary macrophages
 Transferrin ,anionic peptide ,pulmonary surfactant

Defense mechanism of alveoli
 Lack ciliated and mucus
 Phagocytosis by alveolar macrophages ,capillary macrophages
 Innate immunity :Transferrin ,anionic peptide ,pulmonary surfactant.
 Humeral immunity :IgA in the nasal and tracheal secretion ,IgG and
lesser IgE and IgM in alveolar surface .
 Cellular immunity :Pulmonary alveolar macrophage ,pnemocyte
,endothelial cell ,lymphocyte , plasma cell ,Dentric cell
,(macrophage receptor ,Fc ,C3b ,C3a ,C5a,TNF,CD40,TLR, FAS)
Defense mechanism against blood borne pathogens (intra
vascular space )
 In ruminant ,cat, horse ,pigs ,pulmonary intra vascular macrophage
are the cell responsible for the removable of circulating particles,
pathogen bacteria and endotoxin from the blood
 Defense mechanism against oxidant induced lung injury
 Existing in an oxygen rich in environment and being site of
numerous metabolic reaction
 This form of damage is caused by inhaled oxidant gases example
nitrogen dioxide ,ozon ,sulfur di oxide ,tobacco smoking ,and by
xenobiotic toxic metabolite produced locally or by reaching the lung
via the blood stream ,example (paraquat) ,or by free radical (reactive
oxygen species ) released by phagocytic cells during inflammation.
 Oxygen and free radical scavengers such as catalase
,superoxide dismutase ,and vitamin E are largely responsible
for production pulmonary cells against peroxidation ,these
scavenger are present in alveolar and bronchiolar epithelial and
in the extra cellular space of the lung .
 The defense mechanism are so effective in trapping ,
destroying and removal bacteria that under normal condition
,animal can be exposed to aerosol containing massive number
of bacteria without any ill effect. If defense mechanism are
impaired ,inhaled bacteria colonized and multiply in bronchi,
bronchiole and alveoli and produce infection, similarly when
air born and blood born pathogen ,inhaled toxicant or free
radicals impairment the protective defense mechanism of
respiratory system and causing injury and serious respiratory
disease
Impairment of defense mechanism in the respiratory
system
 1-viral infection: viral agent are notorious in predisposing
animal to secondary bacterial pneumonia by what in known as
viral -bacterial synergism .e.g. influenza virus .
 The mechanism of the synergistic effect of viral- bacterial
infection by destruction of the mucociliary blanket and
reduction of mucociliary clearance. Also the phagocytic
function of pulmonary alveolar macrophage is notably
impaired.
 2-Toxic Gases
 Hydrogen sulfide and ammonia ,poor ventilation ,polluted
cities ,impaired respiratory defense mechanism and increase
susceptibility to bacterial pneumonia
 Immunodeficiency: Immunodeficiency disorder whether
acquired or congenital are often associated with increased
susceptibility to viral- bacterial and protozoal pneumonia .
 Large dose of chemotherapeutic agents such as steroids
and alkylating agent causes immunosuppression .
 Other condition that predispose to secondary bacterial
pneumonia
 Uremia ,endotoxemia, dehydration ,starvation, hypoxia
,acidosis ,pulmonary edema ,anesthesia ,ciliary dyskinesia
,and stress
 Hypoxia and pulmonary edema decrease phagocytic
function of pulmonary alveolar macrophages and alter the
production of surfactant by type 11 pneumonocytes .
 Dehydration is thought to increase the viscosity of mucous
,reducing or stopping mucocillary movement .
 Anesthesia induced cilliostasis with concurrent loss of
mucocilliary function .
 Cilliary dyskinesia ,an inherited defect in cilia causes
abnormal mucus transport
 Starvation ,hypothermia and stress can reduce humeral
and cellular immune response .
Disease of respiratory system
 Rhinitis :Inflammation of nasal cavity
 Rhinitis ,Sinusitis .these conditions usually occur together .
 Disturbance in the balance of the normal and pathogenic flora
,caused by viruses ,fungi ,bacteria ,gases ,environmental
changes and immunosuppression ,local trauma ,stress ,prolong
antibacterial therapy, lead to inflammation of the nasal cavity.
 -Based on nature of exudate ,Rhinitis classified as serous
,catarrhal ,purulent ,fibrinous , or granulomatous , this type of
inflammatory reaction can progress from one to another.
 Acute, subacute or chronic according to the age of the lesion
,mild, moderate, severe according to the severity .
 Other types are hemorrhage, ulcers, mucosal hyperplasia .
 Serous Rhinitis is the mildest form of inflammation characterized by
hyperemia and increased production of a clear fluid , caused by mild
irritants or cold air or it occurs during early stages of viral infection.
 Catarrhal Rhinitis is slightly more sever process increase in mucous
production by increase activity of goblet cells and mucous glands .
 Mucous exudate is a thick translucent slightly turbid viscous fluids .some
time containing a few exfoliated cells , leucocyte and cellular debris .
 In chronic case hyperplasia of goblet cell ,infiltrated with neutrophil giving
the exudate a cloudy mucopurulent appearance .
 Purulent Rhinitis :this inflammation characterized by a neutrophilic
exudate .sever injury that is accompanied by mucosal necrosis and
secondary bacterial infection .
 Cytokine leukotrienes, complement activation ,and bacterial product
cause exudation of leukocyte specially neutrophil.
 Grossly the exudate is thick and opaque and vary from white to green to
brown depending on the types of bacteria and type of leukocytes(neutrophils
or eosinophils) present in the exudate .
 Fibrinous Rhinitis :this reaction occur when nasal injury and sever
increase in vascular permeability ,resulting in abundant exudation of plasma
fibrinogen which coagulates into fibrin (yellow or gray ). Some times forms
pseudomembrane.
 Granulomatous Rhinitis :this reaction in the nasal mucosa and sub
mucosa is characterized by infiltration of numerous activated macrophages
mixed with few lymphocyte and plasma cells .
 In some cases lead to the formation of polypoid nodules .
 Granulomatous Rhinitis is generally associated with chronic allergic or
with systemic mycosis ,tuberculosis or foreign bodies .
 Acute Rhinitis lead to chronic and destruction of nasal conchae - deviation of
the septum and craniofacial deformation -, otitis media and interna ,and
vestibular syndrome (abnormal head tilt and abnormal gait which may lead to
emaciation .
 Sinusitis
 Sinusitis occur frequently accompanied with Rhinitis or as sequel to
penetrating or septic wound of the cranium improper dehorning in cattle, or
tooth infection .
 Para nasal sinuous have poor drainage ,there for exudate tends to accumulate
causing mucocele or empyema ,sinusitis – osteomyelitis –meningitis .
 Specific disease of the nasal Cavity and sinuous :
 equine viral infection (equine viral Rhino pneumonitis ,equine Influenza ,
 equine bacterial infection (strangles and glanders ).
 Infectious Bovine Rhinotrichitis .
 Pharyngitis ,laryngitis and tracheitis
 Pharynx, larynx and trachea are important because of their
potential to obstructed air flow and lead to aspiration
pneumonia
 The pharynx is effected by disease of the upper respiratory
tract and upper digestive tract .
 Obstruction of pharynx can be caused by masses in
surrounding tissues such as neoplasm of thyroid gland ,thymus
and Parathyroid gland .
 Eg. Calf diphtheria
Trachea can be involved by extension from both the lung and
larynx .the most common causes of tracheitis are viral infection.
According to the exudate tracheitis is classified as catarrhal
,purulent ,fibrinous or granulomatous
 Lungs
 Each lung is subdivided into various number of pulmonary lobe.
 Left lung is composed of cranial and caudal lobe .
 Right lung is composed of cranial ,middle (absent in horse), caudal
and accessory lobe.
 In dog ,cat ,cattle and pigs ,the lung are well – lobated and well
lobulated
 Goat, sheep are well lobated and poorly lobulated .
 Horse and human have both poorly lobated and lobulated .
 Pores of kohn :this pore between lobule and adjacent alveoli ,poor in
cattle and pigs and good in dog .
 Atelectasis
 The term atelectasis means incomplete distention of alveoli and lung that
have failed to expand with air at the time of birth or lungs that have
collapsed after inflation .
1. Acquired (Compressive and obstructive )
a. Compressive –space occupying masses in plural cavity such as
abscesses and tumor or bloat ,hydrothorax ,heamothorax and empyma,
pneumothorax.
b. Obstructive occur when there is reduction in the diameter of air ways
caused by mucosal edema and inflammation or blocked by mucous
plugs ,exudate ,aspirated foreign material or lung worm.
 Atelectasis also occur when large animal are kept recumbent
for prolonged period such as during anesthesia, milk fever .
 The lung with atelectasis appear depressed below the surface of
the normally inflated lung .the color is generally dark , blue
,and the texture is flabby or firm.
Pulmonary emphysema
 Abnormal permanent enlargement of air space distal to
terminal bronchiole, accompanied by destruction of
alveolar walls ((alveolar emphysema must separate from
simple air space enlargement or hyper inflation in which
there is no destruction of alveolar wall can occur
congenitally (Down syndrome) or acquired with aged)) .
 An imbalance between protease released by phagocytes
and anti protease produce in the lung as a defense
mechanism suggests that causes destruction of alveolar
wall .
 The destructive process is markedly accelerated by any factor
such as cigarette smoking ,pollution or defect in synthesis of
anti protease.
 In animal ,emphysema occur always secondary to abstraction
of out flow of air by exudate plugging bronchi and bronchiole
causes imbalance between the volume of air entering than
leaving the lung .
 Classified of emphysema depending on effected area of the
lung (alveolar emphysema and interstitial emphysema) .
Circulating disturbance of the lung
 Lungs are extremely well vascularized organ ,disturbance
in pulmonary circulation have a notable effect on gases
exchange result in hypoxemia and acidosis ,also can have
an impact on other organ such as the heart and liver .
 Hyperemia and congestion
 Hyperemia is an active process that is a part of acute
inflammation .
 Congestion is the passive process ,resulting from
decreased outflow of venous blood.
 Pulmonary congestion caused by heart failure result in
stagnation of blood in pulmonary vessel lead to edema and
egression of erythrocyte in to alveolar space lead to
phagocytosed by pulmonary alveolar macrophage
(erythrophagocytosis ). Brown cytoplasm ,hemosiderin
,iron pigment ,siderophages ,heart failure.
 Hypostatic congestion result from gravity and poor
circulation ,may be followed by hypostatic edema and
hypostatic pneumonia .
 Pulmonary hemorrhage
 Pulmonary hemorrhage can occur as a result of trauma
,coagulopathies ,pulmonary thromboembolism .
 Pulmonary edema in normal lung ,fluid from the vascular
space slowly but continuously passes into the interstitial tissue
where it is rapidly drained by the pulmonary lymphatic vessel .
 Cardiogenic (hydrostatic ,hemodynamic ) and non cardiogenic
(permeability types )
 Neurogenic pulmonary edema(head injury ,brain edema ,brain
tumor ,cerebral hemorrhage ) massive sympathetic stimulation
released catecholamines , also in sever excitement ,sever
stress.
 Pulmonary embolism

With it is vast capillary bed and position in the
circulation ,the lung act as a safety net to catch emboli
before they reach the brain and other tissue ,septic
bacterial emboli ,fat emboli ,tumor cell emboli
,thromboemboli
 Pulmonary infarction
 Because of a dual arterial supply to the lung ,pulmonary
infarction is rare .
 Bronchi
 The pattern of necrosis ,inflammation and repair in intrapulmonary
bronchi are similar to nasal and tracheal epithelium.
 Injury to ciliated bronchial epithelium may result in degeneration
,detachment and exfoliation of necrotic cell . cellular exfoliation is
promptly followed by inflammation .
 Mitosis ,cell proliferation and cell differentiation and finally repair .
 Depending on the type of exudate ,bronchitis can be fibrinous
,catarrhal ,purulent ,fibrinonecrotic (diphtheritic) and some time
granuloma .
 In chronic bronchitis ,production of mucous is increased
via goblet cell hyperplasia ,chronic catarrhal inflammation
in smoker who continuously coughing out excessive
mucous secretion (sputum).
 Chronic bronchial irritation causes squamous metaplasia,
in which highly functional ciliated epithelium is replaced
by non functional .
 Bronchiectasis is one of the most devastating sequel that
follows chronic bronchitis ,permanent dilatation of
bronchus as a result of accumulation of exudates in the
lumen and partial rupture of bronchial wall.
 Bronchioles
 The epithelial lining of bronchiolar region is susceptible
to injury particularly respiratory viruses
(A deno virus, Canine distemper ), and oxidant gases.
 The prone to injury may due to :
1. It is highly vulnerability to oxidant and free radical
2. Clara cells rich in oxidase which generate toxic
metabolite.
3. The tendency for macrophage and leukocytes to
accumulate in this region
 Depending on the types of injury band inflammatory response
,bronchiolitis is classified as catarrhal ,supportive , necrotizing
or granulomatous .
 In sever injury ,exudate can not be removed from the basement
membrane and the exudate become infiltrated by fibroblast
which form small masses of fibrovascular tissues and
developed in to polyps.
 Air way hyperresponsiveness following transient viral
infection of the lower respiratory tract or exposure to certain
allergens lead to increased number of mast cell ,eosinophil's
and T lymphocyte in air way mucosa .
 Clinically ,air way hyperresponsiveness is characterized by an
exaggerated bronchoconstriction following exposure to mild
stimuli such as cold air or exposed to aerosols of histamine .
 Alveoli
 Three layer composed of blood air barrier (vascular endothelium,basal
lamina and alveolar interstitium
 Injury of type 1 pneumonocytes causes swelling and vacuolation .when
cellular damage has become irreversible ,type 1 cells detach ,resulting in
denudation of the basement membrane ,increased alveolar permeability and
edema .
 Alveolar repair is possible as long as the basement membrane remain intact
.when alveolar injury is diffuse ,proliferation of type 2 pneumonocytes, and
interfere in gas exchange and causes hypoxemia.
 When sever injury, fibroblast proliferate in alveolar wall (alveolar
interstitium )casing alveolar fibrosis .
 In more sever injury ,fibroblast actively migrate from the interstitium to
alveolar space causing intra alveolar fibrosis.
 These two types of fibrosis are most commonly seen in toxic and allergic
pulmonary disease
 General aspects of lung inflammation
 Pulmonary inflammation is highly regulated process that involve a
complex interaction between cells important from the blood
(neutrophil ,eosinophil ,mast cell and lymphocyte ) and pulmonary
cells type 1 and type 2 pneumonocyte and endothelial, Clara and
stromal interstitial cells).
1. Complement (c3a,c3b,c5a),Coagulation factor (v1 ,v2),Arachidonic
acid ,metabolites(leukotriene and
prostaglandins),Cytokines(interleukin ,monokines, chemokinase
),Enzymes and enzyme inhibiter (elastase, antitrypsin ),Oxygen
metabolites(O2,OH,H2O2),Antioxidant,Nitric oxide
2. Pulmonary macrophage (alveolar ,intravascular and interstitial )
which have an immense biologic armamentarium .
 Feature of pulmonary injury:
1. Leukocyte can exit the vascular system through the
alveolar capillaries –unlike other tissues where post
capillary venules are the site of leukocyte diapedesis
(extravasation ).
2. The intact lung contain within alveolar capillaries a
large pool of resident leukocyte
3. Additional neutrophil are sequestered within alveolar
capillaries within minutes of local or systemic
inflammatory response.
 Nitric oxide has bee identified as a major regulatory molecules
of inflammation in lung producing locally by macrophages
,pulmonary endothelium and pneumonocytes .
 nitric oxide regulate the vascular and bronchial tone ,modulate
the production of cytokine ,trafficking of neutrophil ,switches
on/off genes involved in inflammation and immunity .
 As alveolar injury is transient and there is no interference with
the normal host response ,the entire process of injury
,,degeneration ,necrosis ,inflammation and repair can occur vin
less than 1 week.
 When alveolar injury become persistent or when capacity of
the host for repair is impaired ,lesion can progress to an
irreversible stage –lesion progress to a stage of terminal
alveolar fibrosis
 Classification of pneumonia based on:
 1-Causes :Viral pneumonia, Pasteurella pneumonia ,Verminous pneumonia,
chemical pneumonia ,hypersensitivity pneumonia
2- Type of exudate :Suppurative pneumonia ,Fibrinous pneumonia ,
Pyogranulomatous pneumonia
3-Morphologic feature :Gangerenous pneumonia , Proliferative
pneumonia ,Embolic pneumonia
4-Distribution of lesion :Focal pneumonia , cranioventral pneumonia
,diffuse pneumonia , lobar pneumonia
5-Epidemiologic attributes :Enzootic pneumonia, contagious bovine
pleuropnemonia


6-Geographic region ,Montana pneumonia
7 -Miscellaneous attributes : a typical pneumonia ,cuffing pneumonia ,
aspiration pneumonia ,progressive pneumonia ,farmers lung
 Pneumonia in domestic animal can be classified on
texture ,distribution appearance and exudation in to 4
morphologically distinct type :
 1-broncho pneumonia 2- interstitial pneumonia 3-embolic
pneumonia
 4- granulomatous pneumonia
 1-Bronchopneumonia
 Bronchopneumonia refer to a particular type of
pneumonia in which injury and the inflammatory process
take place primarily in the bronchial ,bronchiolar and
alveolar lumens ,and it is the most common type of
pneumonia seen in domestic animal.
 Factor contributing to topographic selectivity within the lungs
include:
1. Gravitational sedimentation of the exudate
2. Greater deposition of infectious organism
3. Inadequate defence mechanism
4. Reduced vascular perfusion
5. Shortness and abrupt branching of airways
6. Regional differences in ventilation
 Bronchopneumonia are caused by bacteria and mycoplasma .the
lesion tend to spread centripetally by kohn pores
 Consolidation is used when the texture of pneumonic lung becomes
firmer or harder than normal because of exudation and atelectasis .
 2-Fibrinous bronchopneumonia : are the result of more sever
pulmonary injury and thus are more life threatening than suppurative
bronchopneumonia.

Early stage of fibrinous bronchopneumonia are characterized by
severe congestion and hemorrhage . A few hours later ,fibrin starts to
accumulate on the plural surface ,giving the pleura a ground glass
appearance and forming plagues of fibrinous exudate over a red
dark lung .
 Marbled appearance :the distention of intralobular septa by
edema and dilation and thrombosis of lymphatic vessels .
 Pulmonary sequestra :pulmonary necrosis develop when
isolated pieces of necrotic lung in capsulated by connective tissues
caused by sever ischemia or necrotizing toxin released by
pathogenic bacteria . Fibrin is chemotactic for neutrophil, these type of leukocyte are
always present
a few hours' after the onset of fibrinous inflammation .
 3-Interstitial pneumonia
 The inflammatory process take place primarily in any of the three
layer of the alveolar wall .
 Erogenous inhalation of toxic gases ,toxic fumes (smoke inhalation )
,and infectious agent (viruses).
 Fungal spore (antigen ) combine with antibody and deposits in
alveolar wall ,
 a cascade of inflammatory response occur (allergic alveolitis ) .
 When the source of alveolar injury persist ,the proliferative and
infiltrative lesion progress to chronic interstitial pneumonia and the
hallmark of chronic interstitial pneumonia is fibrosis of alveolar wall
and accumulation of mononuclear inflammatory cells and lead to
granuloma and hyperplasia of smooth muscles in air ways of
pulmonary vasculature .
 4-Embolic pneumonia
 The injury is hematogenous , and the inflammatory response is
typically centered in pulmonary arterioles and alveolar
capillaries .to caused pulmonary infection ,circulating bacteria
must first attached to the pulmonary endothelium with specific
binding proteins or simply attach to intravascular fibrin and
then evade phagocytosis by intravascular macrophage or
leukocyte.
 Infected thrombi ,because of there size facilitate entrapment of
bacteria in the pulmonary vessels and provide a favorable
environment to escape phagocytosis .
 Omphalophlebitis ,skin or hoof infection ,valvular or mural
endocarditis.
 5-Granulomatous pneumonia

Granulomatous pneumonia refer to type of
pneumonia in which aerogenous or hematogenous injury
is caused by organism or particles that can not be normally
eliminated by phagocytosis and that evoke a local
inflammatory reaction with numerous alveolar and
interstitial macrophage ,lymophocyte , a few neutrophil
and some time giant cell . systemic fungal disease
,cryptococcus coccidioidimycosis ,tuberculosis
,inhalation starch ,foreign bodies.
 Granulomatous pneumonia is characterized by the
presence of variable number of caseous or non caseous
granulomas randomly disturbed in the lung
 Pleura and thoracic cavity
 The thoracic wall and mediastinum are lined by the
parietal pleura .
 Hilus :where bronchi and blood vessels inter the lung .
 Pleural space :the space between the lung and chest.
 Degeneration and disturbance
 Pleural calcification
 In chronic uremia :lesion appear as white streaks in parietal
pleura ,mainly over the intercostal nephritic muscles of the
cranial part of the thoracic cavity.
 The lesion are not functionally significant but indicate a severe
underlying renal problem.
 Vitamin D toxicity(hypervitaminosis D) and ingestion of
hypercalcemic substance ,such as vitamin D analogs.
 Pneumothorax
 Presence of air in the thoracic cavity where there should normally be
negative pressure to facilitate inspiration .
 there are two types of Pneumothorax
-
In spontaneous Pneumothorax ,air leaking into the pleural cavity occurs
without any known underlying disease or trauma.
-
In secondary Pneumothorax ,movement of air into pleural cavity results
from an underlying pulmonary or thoracic wall disease
 most common causes of secondary Pneumothorax in veterinary medicine
are penetrating wounds ,ruptured esophagus , biopsy.
 Clinical signs of Pneumothorax include respiratory distress and the lesion is
simply a collapsed ,atelectasis lung .
 The air is readily reabsorbed from the cavity if the site of entry is sealed
 Circulatory and lymphatic disturbance
 Pleural effusion
 General term is used to described accumulation of any
fluid (transudate ,modified transudate ,exudate ,blood
,lymph ,or chyle ) in the thoracic cavity .
 Cytological and biochemical evaluations of pleural
effusions are some times helpful in suggesting possible
pathogenesis .
 Based on protein concentration and total number of
nucleated cells , pleural effusions are cytological divided
into transudates , modified transudate and exudate
 Hydrothorax
 When the fluid is serous ,clear and odorless ,and fails to coagulate when
exposed to air ,the condition is referred to as hydrothorax(transudates).
Cause :
 Edema in other organs :increased hydrostatic pressure (heart failure)
,decreased oncotic pressure (hypoprotenima ,as in liver disease ), alteration
in vascular permeability, obstruction of lymph drainage (neoplasia ).
 In case where the leakage is corrected , if the fluid is a transudate ,it is
rapidly reabsorbed . if the fluid persist ,it irritates pleura and causes
mesothelial hyperplasia and fibrosis which thickens the pleura .
 Excessive fluid in the thorax causes compressive atelectasis ,resulting in
respiratory distress .
 Congestive heart failure, chronic hepatic disease , nephrotic syndrome.
 Hemothorax
 Blood in the thoracic cavity (exudate with a sanguineous
component )
 Causes
 Rupture of major blood vessel as a result of severe
thoracic trauma( hit by car ) ,erosion of a vascular wall by
malignant cell or inflammation, rupture aortic aneurysms
,clotting defects (warfarin toxicity ), thrombocytopenia
bone marrow suppression .
 Hemothorax is generally acute and fatal .
 Chylothorax
 The accumulation of chyle (lymph rich in
triglycerides ) in thoracic cavity .
 Causes :
 Rupture of major lymph vessel (thoracic neoplasia ),
trauma ,fungal infection ,congenital lymph vessel
anomalies.
 Pleuritis or pleurisy : Inflammation of pleura
 Pleural tissue is readily susceptible to injury caused by
direct implantation of an organism through a penetrating
thoracic or abdominal wounds, by hematogenous
dissemination of infectious organism in septicemias ,
direct extension from an adjacent inflammatory process ,
such as in fibrinous bronchopneumonia or from
perforated esophagus .
 Chronic injury typically results in serosal fibrosis and
tight adhesions between visceral and parietal pleura . in
severe case ,these adhesion can obliterate the pleural
space.
 according to the type of exudate ,can be fibrinous
,suppurative ,granulomatous ,hemorrhagic or
combination .
 Pyothorax (thoracic empyema ) accumulation of
purulent exudate in the cavity in suppurative pleuritis
.
 Clinical signs :pain ,severe toxemia ,interfere with
inflation of the lungs .
 Pleurtitis can occur as an extenion of pneumonia
(fibrinous bronchopnemonia