Difference between revisions of "Lungs Inflammatory - Pathology"
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− | # | + | [[Pneumonia Overview]] |
+ | |||
+ | ==Pneumonia - Introduction and Classification== | ||
+ | [[Image:Acute fibrinous pneumonia.jpg|right|thumb|150px|<small><center>Acute fibrinous pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Pneumonia | ||
+ | **Inflammation that takes place in the '''alveoli and their walls''' | ||
+ | **Can be grouped either according to | ||
+ | ***Nature of the inflammatory process | ||
+ | ***Aetiological agent | ||
+ | ***Pattern of the lesion | ||
+ | |||
+ | *Patterns of lung inflammation vary depending on the aetiology, route and method of exposure and multiple host factors including age, general health, and immune status | ||
+ | **There are five general patterns of pneumonia: | ||
+ | ***[[Bronchopneumonia]] | ||
+ | ***[[Bronchointerstitial Pneumonia]] | ||
+ | ***[[Lobar Pneumonia]] | ||
+ | ***[[Interstitial Pneumonia]] | ||
+ | ***[[Embolic Pneumonia]] | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | =='''[[Bronchopneumonia]]'''== | ||
+ | |||
+ | =='''[[Bronchointerstitial Pneumonia]]'''== | ||
+ | |||
+ | |||
+ | |||
+ | =='''[[Lobar Pneumonia]]'''== | ||
+ | |||
+ | |||
+ | =='''Interstitial pneumonia'''== | ||
+ | [[Image:Interstitial pneumonia micro.jpg|right|thumb|150px|<small><center>Interstitial pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Lung inflammation that occurs primarily in '''alveolar walls''' rather than in alveolar spaces | ||
+ | *Can be widely distributed but is often most severe in '''caudal lung lobes''' | ||
+ | *Diffuse or patchy damage to alveolar septa, may be acute or chronic | ||
+ | *Lesions in most cases result from '''blood-borne insult''' and are more likely to involve the '''dorsocaudal regions''', although the damage is often diffuse | ||
+ | *No concentrated inflammatory response in the airway, only secondary to damage of alveolar walls | ||
+ | *As part of systemic infection | ||
+ | **[[Canine Distemper Virus|Canine distemper]] (in alveolar macrophages as inclusions) | ||
+ | **Salmonellosis | ||
+ | **Toxoplasmosis (in alveolar wall) | ||
+ | |||
+ | *Acute interstitial pneumonia is characterised by '''exudation into the alveolar lumen''' and in cattle is associated with [[Pulmonary Emphysema|interstitial emphysema]] | ||
+ | |||
+ | Examples: | ||
+ | ====Acute bovine pulmonary emphysema and oedema (ABPEE)==== | ||
+ | [[Image:Fog fever 1.jpg|right|thumb|150px|<small><center>Fog fever (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | [[Image:Fog fever 2.jpg|right|thumb|150px|<small><center>Fog fever (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | [[Image:Tracheal haemorrhage in fog fever.jpg|right|thumb|150px|<small><center>Tracheal haemorrhages in fog fever (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | |||
+ | *Synonym: '''fog fever''' | ||
+ | *Usually seen in adult beef cattle in the autumn as an outbreak | ||
+ | *Associated with a change in pasture (from dry to lush, green) | ||
+ | *Severe respiratory distress with laboured breathing and grunting on expiration | ||
+ | *Can result in [[Diffuse Fibrosing Alveolitis|diffuse fibrosing alveolitis]] | ||
+ | *Gross appearance is that of enlarged wet lungs, the interlobular septa are markedly widenedith [[Pulmonary Oedema|oedema]] and [[Pulmonary Emphysema|emphysema]] | ||
+ | *Underlying pathogenesis is ingestion of L-tryptophan in the pasture which is metabolised to 3-methylindole -> bloodstream -> lungs -> metabolised into a compound toxic to Type 1 pneumonocytes and non-ciliated bronchiolar epithelium | ||
+ | *Their loss allows massive flooding of the alveoli with a protein-rich fluid | ||
+ | *The sequence of events in the lung is as follows: | ||
+ | **Alveolar flooding with a protein-rich fluid due to the necrosis of Type 1 epithelium | ||
+ | **As the incoming air dries this fluid, fibrinous 'hyaline membranes' form | ||
+ | **Proliferation of the more resistant cuboidal Type 2 epithelium which line the alveoli, called 'epithelialisation' | ||
+ | **Then either there is | ||
+ | ***Digestion of the hyaline membranes by macrophages which when completed, allows some of the proliferated Type 2 epithelium to differentiate into Type 1 and reconstitute the functional respiratory unit - a normal alveolus | ||
+ | **Or | ||
+ | ***Organisation of the fibrin into fibrous tissue in the lumen - destroying the alveolus or proliferation of fibrous tissue in the alveolar wall with retention of the epithelialised appearance to the alveolus | ||
+ | *Sequel | ||
+ | **Residual scarring if animal survives initial onslaught | ||
+ | **In chronic exposures there may be extensive fibroplasia | ||
+ | |||
+ | *Ingestion of sweet potatoes ifested with ''Fusarium solani'' mould or pasture contaminated with stinkweed or purple mint, rapeseed and kale also cause pulmonary oedema, emphysema and interstitial pneumonia | ||
+ | |||
+ | [[Image:Paraquat poisoning.jpg|right|thumb|150px|<small><center>Paraquat poisoning (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | |||
+ | ====Paraquat poisoning==== | ||
+ | *In dogs and cats | ||
+ | *Free radical release causes damage to air-blood barrier | ||
+ | *Depending on the dose, the lesions range from acute lesions (oedema, haemorrhage, hyaline membranes) -> chronic (fibroplasia of alveolar septae, replacement of alveolar cells with type II cells) | ||
+ | *Additional extrapulmonary lesions to note following paraquat intoxication are '''necrosis of the adrenal zona glomerulosa and renal tubular epithelium''' | ||
+ | |||
+ | ====Diffuse alveolitis==== | ||
+ | [[Image:Diffuse fibrosing alveolitis.jpg|right|thumb|150px|<small><center>Diffuse fibrosing alveolitis (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Chronic disease of adult cattle occuring sporadically | ||
+ | *Probably caused by repeated subclinical incidents of fog fever or farmer's lung | ||
+ | *[[Extrinsic Allergic Bronchio-Alveolitis|'''Farmer's Lung''']] | ||
+ | **Extrinsic allergic alveolitis | ||
+ | **Hypersensitivity of ingested or inhaled moulds | ||
+ | **May occur as an outbreak or sporadically in adult cattle | ||
+ | |||
+ | *'''Hypersensitivity diseases''' often cause an lymphocytic interstitial pneumonia | ||
+ | *Chronic interstitial pneumonia progresses to fibrosis | ||
+ | **Sometimes called '''pneumonitis''' | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | |||
+ | =='''Embolic pneumonia'''== | ||
+ | *Lung inflammation caused by '''haematogenous spread '''of infections into the lung | ||
+ | *No orientation around airways and can be in '''any''' lung region but most often affects '''caudal lobes''' | ||
+ | *The inflammation is oriented '''around blood vessels''', usually venules or alveolar capillaries in which septic emboli localise | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | =='''Granulomatous pneumonia'''== | ||
+ | [[Image:Granulomatous mycotic pneumonia.jpg|right|thumb|150px|<small><center>Granulomatous mycotic pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Variable number and distribution of caseous or non-caseous granulomas throughout the lung | ||
+ | *Must be distinguished from neoplasms | ||
+ | *Calcification may occur | ||
+ | *Caused by agents resistant to phagocytosis, mostly [[Respiratory Fungal Infections - Pathology#Blastomycosis|fungi]], [[Respiratory Bacterial Infections - Pathology#Tuberculosis|''Mycobacterium bovis'']], [[Respiratory Bacterial Infections - Pathology#Rhodococcus equi|''Rhodococcus equi'']], foreign material, [[Feline Infectious Peritonitis|FIP]] | ||
+ | *Micro: centre of necrotic tissue surrounded by macrophages, connective tissue and lymphocytes | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | |||
+ | =='''Verminous pneumonia'''== | ||
+ | [[Image:Parasitic pneumonia.jpg|right|thumb|150px|<small><center>Parasitic pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Lesions in the lung may be due to: | ||
+ | **Parasites passing through the lung as part of their migration e.g. [[Respiratory Parasitic Infections - Pathology#Ascaris suum|''Ascaris suum'']] in the pig, aberrant migration in the case of flukes; | ||
+ | **Parasites for which the lung is the target tissue e.g. [[Respiratory Parasitic Infections - Pathology#Dictyocaulus viviparus|''Dictyocaulus viviparus'']] | ||
+ | *Lesions can vary from interstitial to [[Bronchitis|chronic bronchitis]] to [[Lungs Inflammatory - Pathology#Granulomatous pneumonia|granulomatous pneumonia]] | ||
+ | *May be infiltrate of eosinophils in pulmonary interstitium and bronchoalveolar spaces | ||
+ | *[[Atelectasis|Atelectasis]] and [[Pulmonary Emphysema|emphysema]] may result due to obstruction | ||
+ | |||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | |||
+ | =Stages of pneumonia= | ||
+ | [[Image:Acute exudative pneumonia.jpg|right|thumb|150px|<small><center>Acute exudative pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | [[Image:Acute exudative pneumonia - gross.jpg|right|thumb|150px|<small><center>Acute exudative pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Regardless of the pattern, all pneumonias pass through three stages: | ||
+ | **'''Exudative phase''' | ||
+ | ***In this initial stage inflammatory exudate pours into alveolar spaces and alveolar capillaries are congested | ||
+ | ***Type I alveolar epithelial cells are highly sensitive to injury and cannot proliferate in response to injury | ||
+ | ***Necrosis and sloughing of injured type I cells, denuding alveolar spaces of lining epithelium | ||
+ | ***[[Neutrophils|Neutrophils]] begin to enter alveolar spaces distended with inflammatory oedema | ||
+ | **'''Proliferative phase''' | ||
+ | ***Type II alveolar cells (less sensitive to and can proliferate in response to injury) begin to proliferate within 24 hours and eventually line the alveolar walls denuded of type I cells ***By 6 days cuboidal type II cells can completely line the alveoli | ||
+ | ***Proliferation of type II cells marks the shift from the exudative to the proliferative stage of pneumonia, also heralded by decreased blood flow in alveolar capillaries | ||
+ | ***Because the original squamous type I cells have been replaced by cuboidal type II cells, the microscopic appearance of pneumonic lungs at about 1 week has been described as “alveolar epithelialization”, “alveolar adenomatosis”, or “bronchiolisation of alveoli” | ||
+ | **'''Repair phase''' | ||
+ | ***Resolution of pneumonia is accomplished by transformation of type II cells to type I cells | ||
+ | |||
+ | |||
+ | |||
+ | =Pulmonary abscesses= | ||
+ | [[Image:Multiple pulmonary abscesses.jpg|right|thumb|150px|<small><center>Multiple pulmonary abscesses (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Commonly found post mortem | ||
+ | *Can be a consequence of: | ||
+ | # [[Pulmonary Embolism, Thrombosis and Infarction|'''Septic emboli''']] lodging in the pulmonary vessels | ||
+ | # '''Extension''' from severe focal suppurative [[Lungs Inflammatory - Pathology#Bronchopneumonia|bronchopneumonia]] | ||
+ | # '''Aspiration''' of foreign material (see [[Lungs Inflammatory - Pathology#Aspiration pneumonia|aspiration pneumonia]]) | ||
+ | # Direct '''penetration''' | ||
+ | *The pattern of abscessation can suggest the aetiology i.e. multiple widespread abscesses suggest a haematogenous origin; isolated cranioventral abscesses usually arise from suppurative pneumonia. | ||
+ | |||
+ | ='''Infectious causes of pneumonia'''= | ||
+ | {| cellpadding="5" cellspacing="0" border="1" | ||
+ | | . | ||
+ | | [[:Category:Respiratory Viral Infections|'''VIRAL''']] | ||
+ | | [[:Category:Respiratory Bacterial Infections|'''BACTERIAL''']] | ||
+ | | [[:Category:Respiratory Fungal Infections|'''FUNGAL''']] | ||
+ | | [[:Category:Respiratory Parasitic Infections|'''PARASITIC''']] | ||
+ | |- | ||
+ | | '''Dogs''' | ||
+ | | [[Canine Distemper Virus|Canine distemper]] | ||
+ | | usually secondary | ||
+ | | [[Blastomycosis|''Blastomyces dermatitidis'']] | ||
+ | | [[Angiostrongylus vasorum|''Angiostrongylus vasorum'']] | ||
+ | |- | ||
+ | | . | ||
+ | | [[Canine Infectious Tracheobronchitis|Infectious canine tracheitis]] | ||
+ | | bronchopneumonia: ''[[Bordetella bronchiseptica]], [[:Category:Staphylococcus species|Staphylococci]], [[:Category:Streptococcus species|Streptococci]], Coliforms'' | ||
+ | | [[Histoplasmosis|''Histoplasma capsulatum'']] | ||
+ | | ''[[Toxoplasma gondii]]'' | ||
+ | |- | ||
+ | | . | ||
+ | | [[Canine Herpesvirus 1|Herpes virus]] | ||
+ | | . | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | '''Cats''' | ||
+ | | [[Feline Calicivirus|Feline calicivirus]] | ||
+ | | bronchopneumonia: ''[[:Category:Pasteurella and Mannheimia species|Pasteurella sp.]], [[:Category:Streptococcus species|Streptococcus spp.]]'' | ||
+ | | . | ||
+ | | ''[[Aelurostrongylus abstrusus]]'' | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Chlamydiosis, Feline|Feline chlamydiosis]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | '''Horses''' | ||
+ | | [[Equine Rhinopneumonitis|Equine rhinopneumonitis]] | ||
+ | | [[Strangles|Strangles]] | ||
+ | | [[Pneumocystis carinii|''Pneumocystis carinii'']] | ||
+ | | ''[[Parascaris equorum]]'' | ||
+ | |- | ||
+ | | . | ||
+ | | [[Equine Influenza|Equine influenza]] | ||
+ | | [[Glanders|Glanders]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | [[Equine Viral Arteritis|Equine viral arteritis]] | ||
+ | | [[Rhodococcus equi|''Rhodococcus equi'']] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | '''Cattle''' | ||
+ | | [[Bovine Parainfluenza - 3|Parainfluenza- 3]] | ||
+ | | [[Necrotic Laryngitis]] | ||
+ | | . | ||
+ | | ''[[Dictyocaulus viviparus]]'' | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Pneumonic Pasteurellosis|Pneumonic pasteurellosis]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Contagious Bovine Pleuropneumonia|Contagious bovine pleuropneumonia]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Enzootic Pneumonia - Calves|Enzootic pneumonia of calves]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Acute Exudative Pneumonia|Acute exudative pneumonia]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Enzootic Pneumonia - Calves|''Mycoplasmal'' pneumonia]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Tuberculosis - Cattle|''Mycobacterium bovis'' - tuberculosis]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | bronchopneumonia: [[:Category:Pasteurella and Mannheimia species|''Pasteurella sp.'']], ''[[Corynebacterium pyogenes]]'' | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | '''Sheep''' | ||
+ | | [[Visna-Maedi Virus|Maedi Visna]] | ||
+ | | bronchopneumonia: ''[[Corynebacterium pyogenes]]'' | ||
+ | | . | ||
+ | | [[Muellerius|''Muellerius capillaris'']] | ||
+ | |- | ||
+ | | . | ||
+ | | [[Bovine Parainfluenza - 3|Parainfluenza- 3]] | ||
+ | | [[Enzootic Pneumonia - Lambs|Enzootic pneumonia of lambs]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | [[Sheep Pulmonary Adenomatosis]] | ||
+ | | [[Melioidosis|''Pseudomonas (Malleomyces) pseudomallei'']] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | '''Pigs''' | ||
+ | | [[Porcine Cytomegalovirus|Inclusion body rhinitis]] | ||
+ | | [[Enzootic Pneumonia - Pigs|Enzootic pneumonia of pigs]] | ||
+ | | . | ||
+ | | [[Ascaris suum|''Ascaris suum'']] | ||
+ | |- | ||
+ | | . | ||
+ | | [[Swine Influenza|Swine influenza]] | ||
+ | | [[Actinobacillus pleuropneumoniae|''Actinobacillus pleuropneumoniae'']] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | [[Porcine Reproductive and Respiratory Syndrome|Porcine reproductive and respiratory syndrome]] | ||
+ | | [[Necrotic Laryngitis]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | [[Porcine Circoviruses|Postweaning multisystemic wasting syndrome]] | ||
+ | | [[Pasteurellosis - Pigs|''Pasteurella multocida'']] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | [[Porcine Respiratory Coronavirus|Porcine respiratory coronavirus]] | ||
+ | | [[Contagious Porcine Pleuropneumonia|Contagious porcine pleuropneumonia]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Glasser's Disease|Glasser's disease]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | [[Atrophic Rhinitis|''Bordetella bronchiseptica'']] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | | . | ||
+ | | . | ||
+ | | bronchopneumonia: [[:Category:Pasteurella and Mannheimia species|''Pasteurella'' spp.]], ''[[Corynebacterium pyogenes]]'', also [[:Category:Streptococcus species |''Streptococcus'' spp.]], [[Tuberculosis - Pigs|Tuberculosis]] | ||
+ | | . | ||
+ | | . | ||
+ | |- | ||
+ | |} | ||
+ | |||
+ | |||
+ | |||
+ | ='''Other forms of pneumonia'''= | ||
+ | |||
+ | |||
+ | ===Aspiration pneumonia=== | ||
+ | [[Image:Acute necrotising pneumonia.jpg|right|thumb|150px|<small><center>Acute necrotising pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | [[Image:Inhalation pneumonia.jpg|right|thumb|150px|<small><center>Aspiration pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Response of the lungs to aspirated foreign material will depend on the nature of the material (e.g. food), the bacterial load and the distribution of the material within the lungs | ||
+ | *Mild bronchopneumonia can develop into a severe necrotising pneumonia and in very severe cases can progress to gangrenous pneumonia (below) | ||
+ | *In Cattle | ||
+ | **Associated with poor husbandry | ||
+ | **Regurgitated ruminal content | ||
+ | **Cranio-ventral distribution | ||
+ | **Respiratory insufficiency secondary to [[:Category:Cardiovascular System - Developmental Pathology|congenital cardiac disease]] | ||
+ | *In Horses | ||
+ | **Most commonly in right ventral lung lobe (most rostral secondary bronchus leads to right accessory lobe) | ||
+ | **Risk factors: | ||
+ | ***[[Oesophagus - Anatomy & Physiology|Oesophageal]] obstruction | ||
+ | ***Spontaneous reflux (GI obstruction, equine grass sickness) | ||
+ | ***[[Respiratory System Clinical Signs - Pathology#Dysphagia|Dysphagia]] | ||
+ | ***Iatrogenic | ||
+ | ****Nasogastric tube in the wrong place | ||
+ | *In Dogs | ||
+ | **Most commonly [[Control of Feeding - Anatomy & Physiology#The Vomit Reflex|vomited]]/regurgitated material or contrast medium introduced into airways | ||
+ | **In severe acute cases may die from septic shock | ||
+ | **In chronic cases -> [[Lungs Inflammatory - Pathology#Bronchopneumonia|bronchopneumonia]] | ||
+ | **Common sequel to [[Myasthenia Gravis|myasthenia gravis]], [[Megaoesophagus|megaoesophagus]] or [[Persistent Right Aortic Arch|persistent right aortic arch]] | ||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | ===Gangrenous pneumonia=== | ||
+ | [[Image:Gangrenous pneumonia.jpg|right|thumb|150px|<small><center>Gangrenous pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Can occur following severe infections in which tissue becomes necrotic and is then invaded by putrefactive saprophytes, however this is rare. | ||
+ | *The usual cause is administration of medicines (intended for the oesophagus!) or as a sequel to aspiration pneumonia | ||
+ | *The dead tissue undergoes liquefactive necrosis forming a cavity which is surrounded by intense hyperaemia and inflammation | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | ===Lipid pneumonia=== | ||
+ | [[Image:Lipid pneumonia.jpg|right|thumb|150px|<small><center>Lipid pneumonia (Image sourced from Bristol Biomed Image Archive with permission)</center></small>]] | ||
+ | *Associated with inhalation of oil, paraffin, etc. | ||
+ | *Reaction dominated by macrophages which fill the alveoli and interstitial thickening (mononuclear cells and fibrosis) | ||
+ | *Tends to acumulate in ventral regions bilterally | ||
+ | *Occurs subclinically in cats, sometimes dogs, unrelated to aspiration | ||
+ | *Gross lesion: | ||
+ | **Multifocal, firm, white nodules | ||
+ | *Microscopic lesions: | ||
+ | **Macrophages full of lipid forming foam within alveoli | ||
+ | **Interstitial lymphocyte and plasma cell infiltration, fibrosis | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | ===Uraemic pneumonia=== | ||
+ | *Severe uraemia causes increased permeability of the blood-air barrier and therefore can cause [[Pulmonary Oedema|pulmonary oedema]] | ||
+ | *In addition to the oedema, there may also be degeneration and calcification of smooth muscle and connective tissue fibres | ||
+ | *Lungs do not collapse on opening the thorax in severe cases | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | ===Foetal pneumonia=== | ||
+ | *Especially foals and farm species | ||
+ | *Due to aspiration of amniotic fluid contaminated with meconium and bacteria | ||
+ | **Secondary to fetal distress | ||
+ | **Microscopic lesions of [[Lungs Inflammatory - Pathology#Bronchopneumonia|bronchopneumonia]] | ||
+ | **Involves all lobes (versus postnatal bronchopneumonia) | ||
+ | *Haematogenous spread | ||
+ | **Causes [[Lungs Inflammatory - Pathology#Interstitial pneumonia|interstitial pneumonia]] | ||
+ | **Often caused by ''Listeria monocytogenes'', ''Salmonella'' spp. or ''Chlamydia psittaci'' | ||
+ | *In viral abortions | ||
+ | **Cause [[Lungs Inflammatory - Pathology#Bronchointerstitial pneumonia|bronchointerstitial pneumonia]] | ||
+ | **E.g.: [[Infectious Bovine Rhinotracheitis|IBR]], [[Bovine Parainfluenza - 3|PI-3]] and [[Equine Rhinopneumonitis|equine viral rhinopneumonitis]] | ||
+ | |||
+ | |||
+ | [[Category:Pneumonia]] | ||
+ | |||
+ | |||
+ | |||
+ | =Test yourself with the Lungs Pathology Flashcards= | ||
+ | |||
+ | [[Lungs_Flashcards_-_Pathology|Lungs Pathology Flashcards]] |
Revision as of 18:04, 19 February 2011
Pneumonia - Introduction and Classification
- Pneumonia
- Inflammation that takes place in the alveoli and their walls
- Can be grouped either according to
- Nature of the inflammatory process
- Aetiological agent
- Pattern of the lesion
- Patterns of lung inflammation vary depending on the aetiology, route and method of exposure and multiple host factors including age, general health, and immune status
- There are five general patterns of pneumonia:
Bronchopneumonia
Bronchointerstitial Pneumonia
Lobar Pneumonia
Interstitial pneumonia
- Lung inflammation that occurs primarily in alveolar walls rather than in alveolar spaces
- Can be widely distributed but is often most severe in caudal lung lobes
- Diffuse or patchy damage to alveolar septa, may be acute or chronic
- Lesions in most cases result from blood-borne insult and are more likely to involve the dorsocaudal regions, although the damage is often diffuse
- No concentrated inflammatory response in the airway, only secondary to damage of alveolar walls
- As part of systemic infection
- Canine distemper (in alveolar macrophages as inclusions)
- Salmonellosis
- Toxoplasmosis (in alveolar wall)
- Acute interstitial pneumonia is characterised by exudation into the alveolar lumen and in cattle is associated with interstitial emphysema
Examples:
Acute bovine pulmonary emphysema and oedema (ABPEE)
- Synonym: fog fever
- Usually seen in adult beef cattle in the autumn as an outbreak
- Associated with a change in pasture (from dry to lush, green)
- Severe respiratory distress with laboured breathing and grunting on expiration
- Can result in diffuse fibrosing alveolitis
- Gross appearance is that of enlarged wet lungs, the interlobular septa are markedly widenedith oedema and emphysema
- Underlying pathogenesis is ingestion of L-tryptophan in the pasture which is metabolised to 3-methylindole -> bloodstream -> lungs -> metabolised into a compound toxic to Type 1 pneumonocytes and non-ciliated bronchiolar epithelium
- Their loss allows massive flooding of the alveoli with a protein-rich fluid
- The sequence of events in the lung is as follows:
- Alveolar flooding with a protein-rich fluid due to the necrosis of Type 1 epithelium
- As the incoming air dries this fluid, fibrinous 'hyaline membranes' form
- Proliferation of the more resistant cuboidal Type 2 epithelium which line the alveoli, called 'epithelialisation'
- Then either there is
- Digestion of the hyaline membranes by macrophages which when completed, allows some of the proliferated Type 2 epithelium to differentiate into Type 1 and reconstitute the functional respiratory unit - a normal alveolus
- Or
- Organisation of the fibrin into fibrous tissue in the lumen - destroying the alveolus or proliferation of fibrous tissue in the alveolar wall with retention of the epithelialised appearance to the alveolus
- Sequel
- Residual scarring if animal survives initial onslaught
- In chronic exposures there may be extensive fibroplasia
- Ingestion of sweet potatoes ifested with Fusarium solani mould or pasture contaminated with stinkweed or purple mint, rapeseed and kale also cause pulmonary oedema, emphysema and interstitial pneumonia
Paraquat poisoning
- In dogs and cats
- Free radical release causes damage to air-blood barrier
- Depending on the dose, the lesions range from acute lesions (oedema, haemorrhage, hyaline membranes) -> chronic (fibroplasia of alveolar septae, replacement of alveolar cells with type II cells)
- Additional extrapulmonary lesions to note following paraquat intoxication are necrosis of the adrenal zona glomerulosa and renal tubular epithelium
Diffuse alveolitis
- Chronic disease of adult cattle occuring sporadically
- Probably caused by repeated subclinical incidents of fog fever or farmer's lung
- Farmer's Lung
- Extrinsic allergic alveolitis
- Hypersensitivity of ingested or inhaled moulds
- May occur as an outbreak or sporadically in adult cattle
- Hypersensitivity diseases often cause an lymphocytic interstitial pneumonia
- Chronic interstitial pneumonia progresses to fibrosis
- Sometimes called pneumonitis
Embolic pneumonia
- Lung inflammation caused by haematogenous spread of infections into the lung
- No orientation around airways and can be in any lung region but most often affects caudal lobes
- The inflammation is oriented around blood vessels, usually venules or alveolar capillaries in which septic emboli localise
Granulomatous pneumonia
- Variable number and distribution of caseous or non-caseous granulomas throughout the lung
- Must be distinguished from neoplasms
- Calcification may occur
- Caused by agents resistant to phagocytosis, mostly fungi, Mycobacterium bovis, Rhodococcus equi, foreign material, FIP
- Micro: centre of necrotic tissue surrounded by macrophages, connective tissue and lymphocytes
Verminous pneumonia
- Lesions in the lung may be due to:
- Parasites passing through the lung as part of their migration e.g. Ascaris suum in the pig, aberrant migration in the case of flukes;
- Parasites for which the lung is the target tissue e.g. Dictyocaulus viviparus
- Lesions can vary from interstitial to chronic bronchitis to granulomatous pneumonia
- May be infiltrate of eosinophils in pulmonary interstitium and bronchoalveolar spaces
- Atelectasis and emphysema may result due to obstruction
Stages of pneumonia
- Regardless of the pattern, all pneumonias pass through three stages:
- Exudative phase
- In this initial stage inflammatory exudate pours into alveolar spaces and alveolar capillaries are congested
- Type I alveolar epithelial cells are highly sensitive to injury and cannot proliferate in response to injury
- Necrosis and sloughing of injured type I cells, denuding alveolar spaces of lining epithelium
- Neutrophils begin to enter alveolar spaces distended with inflammatory oedema
- Proliferative phase
- Type II alveolar cells (less sensitive to and can proliferate in response to injury) begin to proliferate within 24 hours and eventually line the alveolar walls denuded of type I cells ***By 6 days cuboidal type II cells can completely line the alveoli
- Proliferation of type II cells marks the shift from the exudative to the proliferative stage of pneumonia, also heralded by decreased blood flow in alveolar capillaries
- Because the original squamous type I cells have been replaced by cuboidal type II cells, the microscopic appearance of pneumonic lungs at about 1 week has been described as “alveolar epithelialization”, “alveolar adenomatosis”, or “bronchiolisation of alveoli”
- Repair phase
- Resolution of pneumonia is accomplished by transformation of type II cells to type I cells
- Exudative phase
Pulmonary abscesses
- Commonly found post mortem
- Can be a consequence of:
- Septic emboli lodging in the pulmonary vessels
- Extension from severe focal suppurative bronchopneumonia
- Aspiration of foreign material (see aspiration pneumonia)
- Direct penetration
- The pattern of abscessation can suggest the aetiology i.e. multiple widespread abscesses suggest a haematogenous origin; isolated cranioventral abscesses usually arise from suppurative pneumonia.
Infectious causes of pneumonia
Other forms of pneumonia
Aspiration pneumonia
- Response of the lungs to aspirated foreign material will depend on the nature of the material (e.g. food), the bacterial load and the distribution of the material within the lungs
- Mild bronchopneumonia can develop into a severe necrotising pneumonia and in very severe cases can progress to gangrenous pneumonia (below)
- In Cattle
- Associated with poor husbandry
- Regurgitated ruminal content
- Cranio-ventral distribution
- Respiratory insufficiency secondary to congenital cardiac disease
- In Horses
- Most commonly in right ventral lung lobe (most rostral secondary bronchus leads to right accessory lobe)
- Risk factors:
- Oesophageal obstruction
- Spontaneous reflux (GI obstruction, equine grass sickness)
- Dysphagia
- Iatrogenic
- Nasogastric tube in the wrong place
- In Dogs
- Most commonly vomited/regurgitated material or contrast medium introduced into airways
- In severe acute cases may die from septic shock
- In chronic cases -> bronchopneumonia
- Common sequel to myasthenia gravis, megaoesophagus or persistent right aortic arch
Gangrenous pneumonia
- Can occur following severe infections in which tissue becomes necrotic and is then invaded by putrefactive saprophytes, however this is rare.
- The usual cause is administration of medicines (intended for the oesophagus!) or as a sequel to aspiration pneumonia
- The dead tissue undergoes liquefactive necrosis forming a cavity which is surrounded by intense hyperaemia and inflammation
Lipid pneumonia
- Associated with inhalation of oil, paraffin, etc.
- Reaction dominated by macrophages which fill the alveoli and interstitial thickening (mononuclear cells and fibrosis)
- Tends to acumulate in ventral regions bilterally
- Occurs subclinically in cats, sometimes dogs, unrelated to aspiration
- Gross lesion:
- Multifocal, firm, white nodules
- Microscopic lesions:
- Macrophages full of lipid forming foam within alveoli
- Interstitial lymphocyte and plasma cell infiltration, fibrosis
Uraemic pneumonia
- Severe uraemia causes increased permeability of the blood-air barrier and therefore can cause pulmonary oedema
- In addition to the oedema, there may also be degeneration and calcification of smooth muscle and connective tissue fibres
- Lungs do not collapse on opening the thorax in severe cases
Foetal pneumonia
- Especially foals and farm species
- Due to aspiration of amniotic fluid contaminated with meconium and bacteria
- Secondary to fetal distress
- Microscopic lesions of bronchopneumonia
- Involves all lobes (versus postnatal bronchopneumonia)
- Haematogenous spread
- Causes interstitial pneumonia
- Often caused by Listeria monocytogenes, Salmonella spp. or Chlamydia psittaci
- In viral abortions
- Cause bronchointerstitial pneumonia
- E.g.: IBR, PI-3 and equine viral rhinopneumonitis