Development and Characterization of a Caprine Aerosol Infection Model of Melioidosis 英文参考文献.docVIP

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Development and Characterization of a Caprine Aerosol Infection Model of Melioidosis 英文参考文献.doc

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Development and Characterization of a Caprine Aerosol Infection Model of Melioidosis 英文参考文献

DevelopmentandCharacterizationofaCaprineAerosol InfectionModelofMelioidosis CarlSoffler1,AngelaM.Bosco-Lauth2,TawfikA.Aboellail1,AngelaJ.Marolf3,RichardA.Bowen2* 1DepartmentofMicrobiology,Immunology,andPathology,CollegeofVeterinaryMedicineandBiomedicalSciences,ColoradoStateUniversity,FortCollins,Colorado, UnitedStatesofAmerica,2DepartmentofBiomedicalSciences,CollegeofVeterinaryMedicineandBiomedicalSciences,ColoradoStateUniversity,FortCollins,Colorado, United States of America, 3Department of Environmental and Radiological Health Sciences, College of Veterinary Medicine and Biomedical Sciences, Colorado State University,FortCollins,Colorado,UnitedStatesofAmerica Abstract Infection with Burkholderia pseudomallei causes the disease melioidosis, which often presents as a serious suppurative infectionthatistypicallyfatalwithoutintensivetreatmentandisasignificantemerginginfectiousdiseaseinSoutheastAsia. Despiteintensiveresearchthereisstillmuchthatremainsunknownaboutmelioidosispathogenesis.Newanimalmodelsof melioidosisareneededtoexaminenovelaspectsofpathogenesisaswellasfortheevaluationofnoveltherapeutics.The objectiveoftheworkpresentedherewastodevelopasubacutetochroniccaprinemodelofmelioidosisandtocharacterize the progression of disease with respect to clinical presentation, hematology, clinical microbiology, thoracic radiography, andgrossandmicroscopicpathology.Diseasewasproducedinallanimalsfollowinganintratrachealaerosolof104CFU delivered, with variable clinical manifestations indicative of subacute and chronic disease. Bronchointerstitial pneumonia wasapparentmicroscopicallybyday2andradiographicallyandgrosslyapparentbyday7postinfection(PI).Earlylesions of bronchopneumonia soon progressed to more severe bronchointerstitial pneumonia with pyogranuloma formation. Extrapulmonary dissemination appeared to be a function of pyogranuloma invasion of pulmonary vasculature, which peakedaroundday7PI.Histopathologyindicatedthatleukocytoclasticvasculitiswasthecentralstepindissemin