Exam 2 Flashcards
(159 cards)
Respiratory system
Learning Objective
Explain the portals of entry into the respiratory tract.
Diagnose and describe inflammation of the various parts of the respiratory tract. Explain and diagnose the types of transudates and exudates that commonly occur at these sites.
Explain the types of cells responsible for defense against pathogens and how they function in addition to the importance of the mucociliary apparatus.
Identify and describe lobulation vs lobation and the pathologic / physiologic significance of collateral ventilation
Diagnose respiratory anomalies/ diseases in domestic animals.
Brachycephalic airway syndrome
Tracheal hypoplasia /Tracheal collapse
Epiglottic entrapment
Dorsal displacement of the soft palate
Laryngeal hemiplegia
Diagnose nasal and sinus disease in domestic animals and describe the pathogenesis
Ethmoid hematomas
Streptococcus equi spp. Equi / gutteral pouch empyema
Gutteral pouch mycosis
Infectious bovine rhinotracheitis
Calf diphtheria
Oestrus ovis
Arophic rhinitis
Feline and canine upper respiratory diseases
Describe and diagnose types and causes of atelectasis
Describe, diagnose the mechanisms, lesions and characteristics of circulatory disturbances of the respiratory system (including specific mechanisms of edema formation)
Classify pneumonias based on distribution pattern and likely etiologic agent, portal of entry
Diagnose pneumonia in ruminants:
Bovine enzootic pneumonia (Pasteurella multocida)
Mannheimia haemolytica
Respiratory histophilosis
Mycoplasma bovis
Shipping Fever
Tuberculosis
IBR
BRSV
Atypical interstitial pneumonia
ARDS
Paraquat
OPP /CAE
Lung Anatomy
Lobes: defined by ramification of the bronchial tree. Ex: Cranial and caudal lobes.
Lobules: each pulmonary lobe is further subdivided by connective tissue into pulmonary lobules. Cattle and pigs prominent
Degree of lobation: external fissure
Degree of lobulation: connective tissue between lobules.
Lobated vs. Lobulated
Collateral ventilation: movement of air between lobules and between adjacent alveoli (PORES OF KOHN). Septae an connective tissue make it hard for air to pass through
Cattle and pigs are well lobated and well-lobulated: POOR COLLATERAL VENTILATION
Sheep and goats: well-lobated, poorly lobulated.
Horses: poor lobated, poor lobulated.
Dogs and cats: well lobated, not well lobulated. GOOD COLLATERAL VENTILATION
The degree of lobulation determined the degree of air movement between the lobules
Pulmonary interstitial compartments
-Bronchovascular
-Interlobular
-Alveolar
Pulmonary changes such as emphysema, edema, and inflammation may affect one or more of these compartments
Explain the portals of entry into the respiratory tract.
Diagnose and describe inflammation of the various parts of the respiratory tract. Explain and diagnose the types of transudates and exudates that commonly occur at these sites.
Explain the types of cells responsible for defense against pathogens and how they function in addition to the importance of the mucociliary apparatus.
Identify and describe lobulation vs lobation and the pathologic / physiologic significance of collateral ventilation
General Structure
- Conducting: includes nostrils, nasal cavity, paranasal sinuses, nasopharynx, larynx, trachea, extra and intra pulmonary bronchii.
All lined by PSEUDOSTRATIFIED CILIATED COLUMNAR epithelium.
-Goblet cells
-Serous cells
- Transitional: not as equally well developed in all species. Cilia begins to disappear
-Respiratory bronchioles
CLUB CELLS: contain numerous biosynthetic organelles detoxification and xenobiotics (foreign substances) role, similar to hepatocytes. Stem cells critical in remodeling and and repair.
-Primary, secondary, and tertiary bronchioles. - Exchange: Alveolar system. Millions of alveoli lined by
TYPE I cells: membranous pneumonocytes
TYPE II cells: granular pneumonocytes, which are precursor cells and more resistant to injury.
Portals of Entry
Hematogenous: blood-borne microbes, toxins, and emboli. 9% of total blood volume Rt ventricle goes to lung. Pulmonary capillary bed is largest in the body = human 2400 km, 1 ml occupying 16 km.
Aerogenous: airborne injury due to extensive alveolar area, large volume of air passing continuously, and high concentration of noxious elements that can be present in the air.
Direct injury: wounds, trauma.
Explain and diagnose the types of transudates and exudates that commonly occur at these sites.
Bronchitis can be
1. Fibrinous
2. Catarrhal
3. Purulent
4. fibrinonecrotic (diphtheric)
5. Granulomatous
6. Sputum (e.g., chronic smokers)
Club Cells Upper respiratory defense mechanism (Trachea, bronchus)
Secrete surfactant and collecting (protective proteins)
Mucociliary escalator: cilia, mucus.
Double layer: outer gel, inner in a fluid or sol phase
Lower respiratory defense mechanism (Bronchi, bronchioles, alveoli)
Mucociliary escalator, modified epithelial cell, at bifurcation of Bronchi and Bronchioles overlaying BALT.
Bronchioles: no cartilage.
Type I and Type II Pneumonocytes
Conductive system: Nose, paranasal sinuses, larynx, trachea, and bronchi
Example of viral infections that cause extensive mucosal ulceration
-Bovine herpesvirus 1 (Bovine rhinotracheitis)
-Feline rhinotracheitis (feline herpesvirus 1)
-Canine infectious respiratory disease group such as canine adenovirus 2 (CAV-2) and canine parainfluenza (CPIV)
-Injury to pseudo stratified columnar epithelium: viral infection, trauma, inhalation of toxic gases, cells swell, lose attachment to basement membrane and exfoliate, cell migration (conciliated secretory cells/preciliated cells), mitosis and finally attachment. TRANSIENT MILD EXUDATE: fluid, plasma proteins, and neutrophils.
-Injury to olfactory epithelium: limited capacity for regeneration, results in HYPOSMIA (reduction) ANOSMIA (loss of function), neurons regenerate but slow and less efficient.
-Injury to Squamous epithelium (MUCOCUTANEOUS JUNCTION) located in vestibular region of the nose, similar pattern of necrosis and inflammation as the oral mucosa.
Chronic Injury = Goblet cell hyperplasia leads to excessive mucus production (hyper secretion) and reduced mucociliary clearance, when there is loss of basement membrane then fibrosis repair and granulation tissue take place.
**Severe cases = Squamous cell metaplasia
What are some organisms normally present in the respiratory tract?
Laryngeal hemiplegia picture
Cattle: Mannheimia hemolytica (shipping fever)
Cats, cattle, and pigs: Pasteurella multicocida
Dogs and Pigs: Bordetella bronchiseptica
Defense mechanisms
Cells and secretions
Congenital Anomalies
Most commonly reported in cattle and sheep
-Accessory lungs are one of the most common anomalies and consist of distinctively lobulated masses of incompletely differentiated pulmonary tissue present in the thorax, abdominal cavity, or subcutaneous tissue virtually everywhere in the trunk.
-Ciliary dyskinesia (immotile cilia syndrome, Kartagener’s syndrome) defective ciliary movement = reduced mucociliary clearance. Chronic recurrent rhino sinusitis, pneumonia, and infertility in dogs.
-Congenital melanosis: common incidental findings in pigs and ruminants, usually seen at slaughter. It has no clinical significance.
-Congenital emphysema is sporadically seen in dogs.
-Brachycephalic Airway Syndrome: Stenotic airways. bulldog, boxers, pugs, pekingese.
-Tracheal collapse/stenosis: Toy, mini, brach dogs. Horse, cattle, goats. Dorsoventral flattening reverberation of tracheal membrane = decreased lumen. Most commonly the defect extends the entire length of the trachea and only rarely in cervical portions alone. Froth and even covered by diphtheric membrane In some cases is an acquired lesion that fallows trauma, compression caused by extraluminal masses, peritracheal inflammation, and flawed tracheotomy or transtracheal aspirate techniques.
-Laryngeal Hemiplegia: paralysis or roaring in horses, common disease characterized by atrophy of the dorsal and lateral cricoarytenoid muscles (abductor and adductor of the arytenoid cartilage), particularly on the left side. Primary denervation (recurrent laryngeal neuropathy) of unknown cause (idiopathic axonopathy) of cranial laryngeal nerve. Medial retropharyngeal lymph nodes are located immediately ventral to the floor of the guttural pouches. As a result of this close anatomic relationship, swelling or inflammation of the guttural pouches or retropharyngeal LNs often results in secondary damage to the laryngeal nerve. Grossly, muscle is pale, smaller than normal. It also occurs in dogs (Siberian Husky and bouvier Flanders), or secondary to choke chain trauma, or secondary to hepatic encephalopathy in horses.
-Epiglottic entrapment: undersized epiglottis entrapped below the arytenoepiglottic fold.
-Dorsal displacement of the soft palate: during exercise, narrows lumen of nasopharynx and creates abnormal air turbulence in the conducting system of horses.
Rhinitis
The occurrence of infectious rhinitis presupposes an upset in the imbalance of the normal microbial flora of the nasal cavity. Competitive exclusion maintains balance, but disruption caused by viruses, pathogenic bacteria, fungi, irritant gases, environmental changes, immunosuppression, local trauma, stress, or prolonged antibacterial treatment.
Bronchoaspiration of exudate leads to bronchopneumonia, chronic rhinitis leads to destruction of nasal concha, deviated septum, and eventually craniofacial deformations. Spread to sinus = sinusitis, can cause osteomyelitis through cribriform plate meningitis, otitis media or guttural pouch empyema in horses, otitis internal and vestibular syndrome. Severe cases present emaciation.
-Serous rhinitis: mildest form of inflammation, hyperemia, increased production of clear fluid produced by serous glands. Mild irritants and cold air culprits, or during early stage of viral infection. Upper respiratory tract infection, allergic reactions.
-Catarrhal Rhinitis: is a slightly more severe, additional increase in mucous production by hypersecretion of goblet cells. Mucous exudate is a thick, translucent, or slightly turbid viscous fluid, with exfoliated cells, leukocytes, cellular debris. Chronically = hyperplasia of goblet cells, as it becomes more severe inflammation with neutrophils give exudate cloudy appearance = MUCOPURULENT.
-Purulent (suppurative) rhinitis: neutrophilic exudate, nasal mucosa severe injury with necrosis and secondary bacterial infection. Cytokines, leukotrienes, complement activation, and bacterial products cause exudation of leukocytes, especially neutrophils. Thick, opaque, but it can vary from white to green to brown. In severe cases the nasal passages are completely blocked.
-Fibrinous rhinitis: reaction when nasal injury is severe in vascular permeability, resulting in abundant exudation of plasma fibrinogen, which coagulates into fibrin. Grossly, yellow, tan, gray, rubbery exudate mat on nasal mucosa “pseudomembrane.”diphtheric or fibrinonecrotic rhinitis presents destructive inflammatory process of the nasal, tonsil, pharyngeal, and laryngeal mucosa. Necrotic and ulcerated epithelium. fungal infections such as aspergillosis can cause fibrinonecrotizing rhinitis.
Ganulomatous Rhinitis/pneumonia
It is a reaction in the nasal mucosa and submucosa that is characterized by infiltration of numerous activated macrophages mixed with a few lymphocytes and plasma cells.
In come cases chronic inflammation leads to polyps nodules large enough to cause obstruction. It is associated with chronic allergic inflammation or infection such as fungal, tuberculosis, systemic mycosis and rhinosporidiosis.
Sinusitis
Nasal Amyloidosis
It occurs sporadically in domestic animals and is frequently combined with rhinitis (rhinosinusitis) or it occurs as a sequela to penetrating or septic wounds of the nasal frontal sinus, maxillary tooth infection in horses and dogs. It can be serous, catarrhal, fibrinous (rare), purulent, or granulomatous. Paranasal sinuses have poor drainage, exudate tends to accumulate causing mucocele (accumulation of mucus) or empyema (accumulation of pus). chronic sinusitis may extend to adjacent bone (osteomyelitis) or through ethmoidal conchae into meninges and brain (meningitis and encephalitis)
Nasal Amyloidosis
The deposition of Amyloid Protein (fibrils with a Beta-pleated configuration) in various tissues localized in lesion of the nasal cavity in horses AMYLOID AL, opposite of the common amyloid AA. Affected horses have epistaxis and reduced athletic performance. Large firm nodules resembling neoplasm can be observed in the alar folds, rostral nasal septum, and floor of nasal cavity. Confirmed by Congo-REd.
Diagnose pulmonary diseases/ pneumonia in horses:
EIPH
COPD
Rhodococcus equi
Equine influenza
Equine viral rhinopneumonitis
Hendra virus
EVA
African horse sickness
Equine multinodular pulmonary fibrosis
Circulatory disturbances
-Progressive ethmoidal hematoma: single soft, tumor-like, pedunculate, dark, red mass arising from mucosa of ethmoidal concha. Important in older horses C/S: chronic, progressive, often unilateral nasal bleeding. Microscopically abundant macrophages. Unilateral epistaxis.
-Equine viral rhinopneumonitis: aerogenous viral transient infection. Caused by Equine herpesvirus 1 (EHV-1). Mild respiratory disease in weanling foals and young race horses as neurologic disease (myeloencephalopathy) or abortion in mares. Lesions in lungs not seen in necropsy unless secondary bacterial infection rhinitis, pharyngitis, or bronchopneumonia. Stress, immunosuppression, susceptible (latency).
-Equine influenza: highly contagious and self-limiting type A. (H7N7) and H3N8. High morbidity, low mortality. Occasionally severe pneumonia with pulmonary edema. Often conjunctivitis, serous nasal discharge, fever. 2-3 year old horses mostly at racetrack. Opportunistic secondary infections (Streptococcus zooepidemicus, Staphylococcus aureus, or Bacteroides sp.) found in the normal flora. H3N8 jumped to canine.
-Strangles: Streptococcus equi (NOT NORMAL FLORA).
Mucopurulent rhinitis, lymphadenitis. Bastard Strangles: metastatic abscesses in the lungs, liver, spleen, kidneys, brain or joints. It is often fatal. Sequela: bronchopneumonia, horners, roaring, purport hemorrhagic, guttural pouch empyema. Horner’s syndrome results from damage to the cranial cervical ganglion and sympathetic fibers located in the caudodorsal aspect of the pouches (guttural pouch mycosis, Aspergillus spp.) Empyema of guttural pouches is a sequale to suppurative inflammation of the nasal cavities, most commonly from Streptococcus equi infection. Purulent exudate in severe cases, possible internal carotid artery erosion. Nasal discharge, enlarged retropharyngeal lymph node, painful swelling of the parted region, dysphagia, and respiratory distress.
-Glanders/Pseudoglanders: Glanders eradicated in most countries. Burkholderia mallei, Gram (-) It can be fatal in humans from eating infected horse meat. Pyogranulomatous -stellate scars. skin: farcy
Notifiable disease
Pyolgranulomatous nodules in the submucosa, lesions ulcerate releasing copious amounts of Burkholderia mallei.
Severe suppurative lymphangitis nodular thickening lymph vessels in subcutaneous tissue, eventually rupture.
-Pseudoglanders: (meliodiosis) similar to ganders but disseminated. Lots of species affected. Abscesses in organs, liver, spleen, kidneys, lymph nodes.
-Rhinosporidium seeberi: Granulomatous rhinitis in horses and dogs. AQUATIC PROTISTAN.
Polypoid nodules that may be mistaken as tumors present in nasal mucosa close to nares.
Notifiable disease horses’s infected meat = human infection?
Glanders
Burkholderia mallei gram negative bacteria.
Bovine/Small ruminant Upper Respiratory Diseases
Bovine Herpesvirus-1
-“Red nose”
-Bovine abortion
-Infectious pustular vulvovaginitis (IPV)
-Infectious balanoposthitis (IBP).
-Fibronecrotizing tracheitis (IBR)
Calf Diphtheria
-Necrotic Laryngitis: common disease of feedlot cattle and cattle affected with nutritional deficiencies, or housed under unsanitary conditions.
-Fusobacterium necrophorum causes necrotic laryngitis = NECROTIC SSTOMATITIS, lesions in cheeks, palate, tongue, and pharynx.
-Opportunistic organism produces potent ends and exotoxins.
Entry through lesions of viral infections or feed or careless use of specula or balling guns
-Necrotizing ulcerative laryngitis
-It occurs periodically in sheep and pigs
-Sequela: overwhelming fusobacterimia. Sometimes copious exudate can cause obstruction asphyxiation or be aspirated and cause bronchopneumonia.
-Fever, anorexia, depression, halitosis, moist painful cough, dysphagia, inspiratory dyspnea and ventilation failure because of fatigue muscles.
Nasal Bots Myiasis (Oestrus Ovis)
Diptera: Oestridae; nasal bot
Brownish fly about the size of a honeybee deposits first stage larvae in the nostrils of sheep in most areas of the world. Myiasis = parasitism in which larvae invades live tissue
It can affect dogs and humans.
-Mucopurulent rhinitis and sinusitis, rarely penetrate cranial vault and cause bacterial meningitis.
Diagnose pneumonia in pigs:
Pasteurella multocidea
Porcine pleuropneumonia
Haemophilus parasuis
Streptococcus suis
Porcine enzootic pneumonia
PRRS
PCV-2
Porcine Inclusion Body Rhinitis
Disease of young pigs < 5weeks old
High morbidity, low mortality
Virus: porcine cytomegalovirus said herpivirus-2 (PHV-2)
Incidental findings in euthanized animals, transient viremia.
Lesions: hyperemia of nasal mucosa, secondary bacterial infections, mucopurulent rhinitis with giant basophilic intranuclear inclusion bodies in nasal epithelium.
Atrophic rhinitis
-6-12 weeks old, obligate nasal breather.
-Inflammation and atrophy of nasal conchae (turbinates)
-Facial deformities in growing pigs because of deviation of nasal septum and nasal bones.
-Environmental factors and nutritional deficiencies
-Osteoclastic hyperplasia and osteopenia of the conchae are key microscopic features.
-Mucopurulent exudate. Hyperplastic or metaplastic changes can occur.
-Sneezing, coughing, nasal discharge. Accumulation of secretions on the skin inferior to the medial cants of the eye from obstruction of the nasolacrimal duct.
Bordetella bronchiseptica
Pasteurella multicocida type A and D, cytotoxins, destruction of turbinate.
Diagnose pneumonia in dogs and cats:
Canine distemper
Canine parvovirus
CHV-1
Endogenouus lipid pneumonia
Feline Asthma syndrome
Diagnose granulomatous pneumonia in domestic animals to include: Higher order bacteria
Fungal agents
Parasitic agents
Diagnose the types and causes of thoracic transudates and exudates in domestic species
Diagnose nasopharyngeal polyps in cats.
Diagnose the most common primary and secondary respiratory and pleural neoplasms.
Viral infections: dogs do not have specific viral infections affecting exclusively the nasal cavity or sinuses. Acute rhinitis and sinusitis occurs as part of the canine infectious respiratory disease (CIRD) caused by
-Canine distemper virus
-CAV-1, 2
-Canine parainfluenza virus
-Reovirus
-Canine Herpesvirus (CHV)
Bacterial infections: secondary to rhinitis, sinusitis, and pneumonia.
-Bordetella bronchiseptica
-Escherichia coli
-Pasteurella multicocida
-Protozoal: Rhinosporidium seeberi
-Fungal: Aspergillus
-Parasitic: Oslerus (Filaroides) osleri. Nematode parasite that causes characteristic protruding nodules into the lumen at the tracheal bifurcation. Seen in endoscopic examination or necropsy. When the parasite dies an intense foreign body reaction develops with neutrophils and giant cells. From asymptomatic to Chronic cough that can be exacerbated by exercise or excitement. Dyspnea, cyanosis, exercise intolerance, emaciation, even death in young dogs.
Feline
-FHV-1
-Feline Calcivirus
Examples of suppurative rhinitis and conjuctivitis in cats
Viral
-Feline calicivirus: acute, multifocal vesicular glossitis. Infections cause ulcerative stomatitis (ulcers and inflammation of the oral cavity), glossitis (vesicles, ulcers, and inflammation in tongue), conjunctivitis and interstitial pneumonia. Lesions vary from subclinical to lethal depending on the strain of the virus and include rhinitis, conjunctivitis, acute diffuse interstitial pneumonia with necrotizing bronchiolitis. “Limping kitten syndrome” self-limiting arthritis. High mortality 50% and febrile hemorrhagic syndrome. Laboratory tests are always required for a definitive diagnosis.
-Feline Viral Rhinotracheitis: FeHV-1 causes impairment of pulmonary defense mechanisms predisposing cats to secondary bacterial pneumonia. Low maternal immunity, stress, kittens. Lesions are fully REVERSIBLE. Secondary interstitial pneumonia can occur.
Bacterial
-Bordatella bronchiseptica
-Escherichia coli
-Streptococcus spp.
-Mycoplasma felis
Sequela can be severe suppurative rhinitis and also conjunctivitis. Intranuclear inclusion bodies are rarely seen in cats with FVR bc they are only present during the early stages of viral infection. Conchal atrophy, permanent damage to olfactory epithelium, and secondary bacterial pneumonia can occur
Mycotic
-Cryptococcus neoformas: lesions are characterized by mucosal granulomas containing acid-Schiff (PAS)-positive fungal organisms, and the infection is clinically characterized by mucopurulent nasal discharge. Lesions vary from nasal granulomas to large confluent masses of mucopurulent exudate entire nasal cavity and paranasal sinuses. PAS-positive organisms.
Viral rhinitis in cats often together with conjuctivitis. Note exudate in nostrils and conjunctiva.
Feline Chlamydiosis
-Persistent respiratory infection caused by Chlamydophila feels. Conjunctivitis, mucopurulent rhinitis, bronchointerstitial pneumonia.
Patterns of Pneumonia
Debate on classification, but roughly
- By cause: viral, bacterial, ex Pasteurella pneumonia, distemper pneumonia
- Type of exudate, ex suppurative pneumonia, fibrinous and pyogranulomatous pneumonia.
- Morphologic features, ex gangrenous, proliferative, and embolic
- Distribution of lesions, ex focal, diffuse, cranioventral, lobar
- Epidemiological attributes, ex Montana progressive pneumonia
- Miscellaneous, farmer’s lung, etc.
Inflammatory lesion of the lungs regardless of whether it is exudative, proliferative, alveolar or interstitial in this chapter
On the basis of texture, appearance, and exudation pneumonias can be grossly diagnosed into four
- Bronchopneumonia
- Interstitial pneumonia
- Embolic Pneumonia
- Granulomatous pneumonia
overlapping of this four types is possible but helps predict most likely etiology
The distribution of the inflammatory lesions can be
- Cranioventral
- Multifocal
- Diffuse
- Locally extensive
Texture
- Firm
- Hard
- Rubbery (elastic)
- Nodular feeling
Consolidation is comparable to the texture of the forehead = firm or hard lung filled with exudate.
What are the types of Atelectasis?
- Congenital
-Aspiration of meconium
-Decreased quantity or quality of surfanctant - Acquired
-Obstructive: edema, inflammation, mucus plugs, exudate, foreign material, parasites.
-Compressive: space occupying masses, transferred pressure (bloat, pnuemothorax, etc). Alveolar collapses
Pores of Kohn
The pores of Kohn are apertures in the alveolar septum, which allow the communication of two adjacent alveoli. Their existence has been most disputed, but was lastly supported in man and adult mammalians by observations from electron microscopy
What is Emphysema? What type of gross lesions can be present and seen during necropsy?
The permanent enlargment of air spaces distal to terminal bronchioles
Secondary to obstruction of outflow of aour or agonal at time of slaughter. More air entering than leaving.
Lesions:
-Equine emphysematous bullae
Bronchopneumonia Suppurative Lobar
What is the portal of entry?
Distribution of lesions?
Texture of the lung?
Gross visible exudate?
Disease Example
Common pulmonary Sequela
Aerogenous (Bacteria)
Cranioventral consolidation
Hard lung
Purulent exudate in bronchi
Enzootic pneumonia
Cranioventral abscesses, adhesions, bronchiectasis (chronic inflammatory or degenerative condition of the bronchi marked by dilation and loss of elasticity)
-The inflammatory process takes place in the bronchial, bronchiolar, and alveolar lumens. It is the most common type of pneumonia in domestic animals and with a few exceptions is characterized by cranioventral consolidation of the lungs.
-As a rule the pathogen arrives at the lungs via aerosols or via nasal flora. The initial injury is centered on the mucosa of bronchioles. Exudate accumulates in lumen and leaves the interstitium unchanged except for hyperemia and possible edema.
The lesion tends to spread centrifugally, with older lesions in the center, an exudate can be coughed up and then aspirated into other lobules, where the inflammatory process starts again.
Bronchopneumonias are generally caused by bacteria and mycoplasmas, by bronchioaspiration of feed or gastric contents, or by improper tubing.
-The initial injury is centered on the mucosa of bronchioles; then spreads downward to distal portions of the alveoli and upward to the bronchi.
-Alveolar interstitium typically unchanged except for possible hyperemia and edema.
-Consolidated lungs sink to the bottom of container when placed in fixative due to replacement of air by exudate. Texture firm or harder than normal. HEPATIZATION bc the texture is firm like the liver and hyperemia present.
-It can be suppurative or fibrinous bronchopneumonia
Cattle and pigs obvious pattern CHECKBOARD due to admixture of normal and abnormal (consolidated) lobules
-First 12 hours: hyperemic and edematous
-By 48 hours: parenchyma starts to consolidate, firm in texture
-By 3-5 days: neutrophils and macrophages fill, lung sinks when placed in formalin. Gray-pink color lung at this stage, purulent exudate at cut surface from bronchi.
-Resolution face when infection regresses, 1-2 weeks.
-Chronic phase, 7-10 days after infection, pale gray lungs “fish flesh” appearance. Purulent and catarrhal inflammation, obstructive atelecsis, mononuclear cell infiltration, peribronchial and peribronchiolar lymphoid hyperplasia, and early alveolar fibrosis
Complete resolution is unusual and lungs scar, pleural and pulmonary fibrosis. Bronchioectasis as a consequence of chronic destructive bronchitis, atelectasis, pleural adhesions, abscesses may remain unresolved for a long time
ENZOOTIC PNEUMONIA of ruminant and pigs = chronic suppurative bronchopneumonias
Chronic bronchopneumonia, Pleural adhesions
Hyperplasia of BALT (bronchial associated lymphoid tissue) is also seen in chronic suppurative bronchopneumonia. It appears as conspicuous white nodules (cuffs) around bronchial walls (cuffing pneumonia). Hyperplastic change indicates normal reaction of lymphoid tissue to infection.
Bronchiectasis: affected bronchus is dilated and has lost its normal projections of the mucosa into the lumen, loss of mucosa, destruction of bronchial wall, fibrosis with atrophy of cartilage and bronchial glands
-Pulmonary abscesses
-Pleural adhesions
-Atelactasis
-Emphysema from bronchioectasis
Most common pathogens associated with chronic suppurative bronchopneumonias
-Pateurella multocida
-Bordatella bronchiseptica
-Trueperella pyogenes
-Streptococcus spp.
-Escherichia coli
-Several species of mycoplasmas
Mostly secondary pathogens, initial preceding impairment of pulmonary defense
It can also result from aspiration of bland material (e.g., milk), pulmonary gangrene may ensue when lungs invaded by saprophytic bacteria