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Chronic Enzootic Pneumonia, Inhalation of the bacterium in fomites or…
Chronic Enzootic Pneumonia
Inhalation of the bacterium in fomites or fluid droplets @
Centrifugal and inertial turbulence
Bacteria deposited and trapped in the mucus layer of the mucosa of the conductive component
Opportunistic, commensal organisms that reside in the nasopharynx and tonsils of healthy animals
Alteration of the commensal relationship due to stressors such as adverse weather conditions
Allowing the bacteria to replicate in sufficient numbers to colonize the respiratory mucosa
Production of neuraminidase
Reduce the viscosity of the mucus making it less dense and a more fluidic layer
Allow better access to cell membranes via gravity and random Brownian movement
Cleaves sialic acid from the surface of cell membranes thus decreasing the net negative surface charge
Allowing closer contact of the bacterium with membranes
Bacteria adhere and binds to receptors using fimbria and pili by ligand-receptor interactions
Bacterial colonization of the mucosae
Replicate in large numbers in the conductive component of the respiratory system
Polysaccharide of the bacterial capsule inhibits phagocytsosis of the bacterium by neutrophils and mucosal macrophages
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Produce enzymes such as neuraminidase and toxins that injure and disrupt the function of the mucociliary apparatus
Ciliary dysfunction
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Produce leukotoxin
Attach to cells through passive adsorption and cell surface recepors
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Environmental factors such as high relative humidity
Mycoplasma spp. enters through milk of infected does, aerosol droplets or respiratory secretions
Impairment of pulmonary defense mechanisms
Secondary bacterial infection (
Pasteurella multocida, Mannheimia haemolytica
and
Escherichia coli
)
Escherichia coli
Normal flora that colonizes the intestinal tract of virtually all animals
Exposure to environmental stressors such as temperature extremes, and intercurrent infections
Attach to cells by a variety of pili or fimbriae
Bacterial endotoxin-induced, cGMP- and cGAMP-dependent kinase-induced sodium and chloride secretion into the intestinal lumen
Water drawn into the intestine to normalize the resultant sodium chloride
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Cytotoxins
Tissue necrosis and hemorrhage
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Hemolysins
Pasteurella multocida
Virulence determinates and mechanisms are similar to
M. haemolytica
Reduced bacterial pathogenicity
Slow onset and insidious inflammatory response
Nearly complete absence of cell necrosis, vasculitis, permeability changes and fibrinogenesis
Mechanism of injury is enhanced by environmental stressors and earlier or concurrent viral infections
Firm (consolidation) yellow-gray anterior-ventral lung lobes
Mannheimia haemolytica
Lesions
Necrotizing bronchiolitis, necrosis of type 1 pneumocytes with hyperplasia of type ii pneumocytes, mild interstitial and alveolar edema
Bronchointerstitial pneumonia (generally mild and transient)
Suppurative bronchopneumonia