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Acta Medica Okayama View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Okayama University Scientific Achievement Repository Acta Medica Okayama Volume 56, Issue 2 2002 Article 8 APRIL 2002 A study on intraalveolar exudates in acute mycoplasma pneumoniae infection. Takeo Yoshinouchi∗ Yuji Ohtsukiy Jiro Fujitaz Yoshiki Sugiura∗∗ Shogo Bannoyy Shigeki Satozz Ryuzo Uedax ∗Nagoya City University, yKochi Medical School, zKagawa Medical University, ∗∗Nagoya City University, yyNagoya City University, zzNagoya City University, xNagoya City University, Copyright c 1999 OKAYAMA UNIVERSITY MEDICAL SCHOOL. All rights reserved. A study on intraalveolar exudates in acute mycoplasma pneumoniae infection.∗ Takeo Yoshinouchi, Yuji Ohtsuki, Jiro Fujita, Yoshiki Sugiura, Shogo Banno, Shigeki Sato, and Ryuzo Ueda Abstract Pathologic features of Mycoplasma pneumoniae infection (M. pneumonia) are generally non- specific, and the literature regarding the pathologic features of M. pneumonia with intraalveolar exudates is limited. Clinical and histopathological studies were performed in 3 patients with M. pneumonia which did not respond to erythromycin and minocycline, but all rapidly recovered after corticosteroid therapy. In pathologic findings, we observed intraalveolar exudates and focal organi- zation in M. pneumonia, and its intraalveolar lesions were compared between M. pneumonia and bronchiolitis obliterans organizing pneumonia containing fibrin (BOOP). Immunohistochemical studies were performed using the streptavidin biotin peroxidase complex method with anti-alpha- smooth muscle actin antibody and anti-pancytokeratin AE1/AE3 antibody. In pathologic findings, more fibrin deposits in intaalveolar lesions were observed in M. pneumonia than in BOOP. In in- taalveolar lesions of M. pneumonia, a larger amount of nuclear debris, more neutrophils, and more erythrocytes were noted. Myofibroblasts were observed in the organization of BOOP, while in the intaalveolar lesions of M. pneumonia, myofibroblasts were not observed. These results suggest that M. pneumonia with intraalveolar exudates responds well to corticosteroid and its intraalveo- lar lesions apparently differed from those in BOOP. KEYWORDS: exudate, fibrin, Mycoplasma pneumonia, organizing pneumonia, steroid therapy ∗PMID: 12002617 [PubMed - indexed for MEDLINE] Copyright (C) OKAYAMA UNIVERSITY MEDICAL SCHOOL Yoshinouchi et al.: A study on intraalveolar exudates in acute mycoplasma ActaMed.Okayama,2002 Vol.56,No.2,pp.111-116 Copyrightｃ2002byOkayamaUniversityMedicalSchool. CaseReport http://www.lib.okayama-u.ac.jp/www/acta/ A StudyonIntraalveolarExudatesin AcuteMycoplasmaPneumoniaeInfection TakeoYoshinouchi,YujiOhtsuki,JiroFujita，YoshikiSugiura, ShogoBanno,ShigekiSato,andRyuzoUeda DepartmentofInternalMedicineII,NagoyaCityUniversity,MedicalSchool,Nagoya467-8601,Japan, DepartmentofPathologyII,KochiMedicalSchool,Nankoku783-8505,Japan,and DepartmentofInternalMedicineI,KagawaMedicalUniversity,Kagawa761-0793,Japan PathologicfeaturesofMycoplasmapneumoniaeinfection (M.pneumonia)aregenerally non- specific,andtheliteratureregardingthepathologicfeaturesofM.pneumoniawithintraalveolar exudatesislimited.Clinicalandhistopathologicalstudieswereperformedin3patientswithM. pneumoniawhichdidnotrespondtoerythromycinandminocycline,butallrapidlyrecoveredafter corticosteroid therapy. In pathologicfindings, weobserved intraalveolarexudatesand focal organizationinM.pneumonia,anditsintraalveolarlesionswerecomparedbetweenM.pneumonia andbronchiolitisobliteransorganizingpneumoniacontainingfibrin(BOOP).Immunohistochemical studieswereperformedusingthestreptavidinbiotinperoxidasecomplexmethodwithanti-α-smooth muscleactinantibodyandanti-pancytokeratinAE1/AE3antibody.Inpathologicfindings,more fibrindepositsinintaalveolarlesionswereobservedinM.pneumoniathaninBOOP.Inintaalveolar lesionsofM.pneumonia,alargeramountofnucleardebris,moreneutrophils,andmoreeryth- rocyteswerenoted.Myofibroblastswereobservedin theorganization ofBOOP,whilein the intaalveolarlesionsofM.pneumonia,myofibroblastswerenotobserved.Theseresultssuggestthat M.pneumoniawithintraalveolarexudatesrespondswelltocorticosteroidanditsintraalveolar lesionsapparentlydieredfrom thoseinBOOP. Keywords:exudate，fibrin,Mycoplasmapneumonia,organizingpneumonia,steroidtherapy ycoplasmapneumoniaeinfection(M.pneumonia) limited.RollinsS.reportedthatM.pneumoniashowed M isamilddiseasewithafavorableprognosisasa apolymorpho-nuclearleukocyte-richexudateinthebron- rule,butrecently,severecasesshowingacuterespiratory chiolarluminaandalymphoplasmacyticbronchiolarwall insuciencyhavebeenreported［1,2］.Reporteddata infiltrate［7］.Wereportheretheclinicalfeaturesand suggestthatthepathologicfeaturesofM.pneumoniaare histopathologicalfindingsof3patientswithM.pneumo- notspecificingeneral,andarefrequentlysimilartothose niawhichdidnotrespondtoerythromycinandminocy- ofbronchiolitisorinterstitialpneumonia［3-6］.The cline,butallrapidlyrecoveredaftercorticosteroidther- literatureonthepathologicfeaturesofM pneumoniais apy. Additionally, the pathological findings of intraalveolarlesionswerecomparedbetweenM.pneumo- niaandidiopathicbronchiolitisobliteransorganizingpneu- ReceivedJune18,2001;acceptedSeptember4,2001. moniaassociatingfibrinexudation(BOOP)becausewe Correspondingauthor.Phone:＋81-052-853-8216;Fax:＋81-052-852-0849 observedcharacteristicintraalveolarexudatesandonly Produced by The Berkeley Electronic Press, 2002 1 Acta Medica Okayama, Vol. 56 [2002], Iss. 2, Art. 8 112 Yoshinouchietal. ActaMed.Okayama Vol.56,No.2 focalorganizationinM.pneumoniacomparedtothoseof 10.1mg/dl.ChestX-rayrevealedinfiltrativeshadows BOOP. partlyincludingparticulateshadowsintherightupper lungfieldandleftlowerlungfield(Fig.1A).Sputum Methods examinationshowednormalfindings.Coldagglutinintiter was1:128,andMycoplasmaantibodytiter(CF)was1: Lung specimens obtained by transbronchiallung 256(atadmission)and1:1.024(20dayslater).Although biopsy(TBLB)oropenlungbiopsywerefixedin10 erythromycinwasadministeredfor12days,symptoms bueredformalin,thenstainedwithH-E andphos- persisted,andtherewasnochangeininfiltrativeshadows photungsticacid-hematoxylin(PTAH)forfibrin.Im- onchestX-rayfilms.TBLBwasperformedforaccurate munohistochemicalstudiesofdewaxedlungsectionswere diagnosis. Pathologicfindingsofbiopsied specimens performedusingthestreptavidinbiotinperoxidasecom- takenfromtheleftS10revealedanumberofintraalveolar plexmethod(ABC method)accordingtoakitmanual exudateswithmarkedfibrindepositionandfocalorganiza- employinganti-α-smoothmuscleactin(α-SMA)antibody tion,inwhichfibroblasticspindlecellproliferationwas todetectmyofibroblastinintraalveolarspaces(DAKO, observed, containing many erythrocytes, neutrophils, CA,USA,1:200)andanti-pancytokeratinAE1/AE3 andmuchnucleardebris.Inthesurroundinglungfield, antibodytodetectalveolarepithelialcellproliferation markedhyperplasiaofthealveolarepitheliumwasnoted. (Boehringer-Mannheim,Biochemica,Mannheim,Ger- Therapywithoralpredonisone(PSL20mg)wasadminis- many,1:400). tered.Asaresult,subjectivesymptomsdramatically improved,andshadowsonchestX-rayfilmsandcomput- Results edtomographyofthelungs(CT)disappeared(Fig.1B). Case2:A 37-year-oldmalewasadmittedtothe CaseReport.Case1:A44-year-oldmalewasadmit- hospitalbecauseof7dayshistoryofhighfever,cough, tedtothehospitalbecauseof8dayshistoryofhighfever and dyspnea. Physicalexamination demonstrated ta- andcough.Physicalexaminationrevealedtachycardiaand chycardia,hyperpnea,highfever(38.7°C),andfine highfever(38.4°C).Laboratoryfindingsonadmission crackle.Laboratoryfindingsonadmissionwereasfol- wereasfollows:Hb13.2g/dl;whitebloodcell(WBC) lows:Hb13.9g/dl;WBC7,800/μl(neutrophils88 , count,10,300/μl(neutrophils61 ,lymphocytes22 , lymphocytes8 ,eosinophils2 ,monocytes2 ); eosinophils2 ,monocytes12 );erythrocytesedimen- ESR 80mm/h;CRP 6mg/dl;PO54.5 Torr;and tationrate(ESR),77mm/h;C-reactiveprotein(CRP), PCO37.4 Torr. ChestX-ray revealed infiltrative A B Fig.1 A,achestroentgenogramobtainedonadmissionrevealsinfiltrativeshadowspartlyincludingparticulateshadowsintherightupper andleftlowerlungfieldsofcase1.B,achestroentgenogramaftercorticosteroidtherapyrevealedamarkedimprovementincase1. http://escholarship.lib.okayama-u.ac.jp/amo/vol56/iss2/8 2 Yoshinouchi et al.: A study on intraalveolar exudates in acute mycoplasma April2002 IntraalveolarExudateinM.Pneumonia 113 shadowspartlyincludingparticulateshadowsinthebilat- Table1 ComparisonofpathologicalfindingsofbothM.pneumo- erallowerlungfields.Allresultsofatuberculintestand niawithintraalveolarexudatesandBOOP sputumexaminationwerenegative.Mycoplasmaantibody M.pneumonia BOOP titer(CF)was1:128(atadmission)and1:2,048(14days Intraalveolarexudates later).Thepatientwastreatedwitherythromycinand Fibrin ＋＋ ＋～－ flomoxefsodiumfor10days,buthighfeveranddyspnea Nucleardebris ＋ － persistedandinfiltrativeshadowsonchestX-rayfilms Neutrophil ＋ － wereaggravated.Openlungbiopsywascarriedoutfor Redbloodcell ＋ ＋～－ precisediagnosis.Pathologicfindingsoftissuespecimens Plasmacell － ＋～－ Macrophage ＋ ＋～－ takenfromrightS10revealedanumberofintraalveolar Myofibroblast － ＋～－ exudatescontainingfibrindepositionwithfocalorganiza- CoveringbytypeIIepithelium － ＋ tion. Corticosteroid pulsetherapy wasadministered, TypeIIepithelium proliferation ＋＋ ＋ resultingindramaticimprovementofthesubjectivesymp- insurroundings toms,anddisappearanceofshadowsonchestX-raysand CT. Case3:A 28-year-oldfemalewasadmittedtothe pneumoniathaninintraalveolarlesionsofBOOP(Figs. hospitalbecauseof5dayshistoryofhighfeverand 2B,3B).AsshowninFig.3C,withregardtofibro- cough.Physicalexaminationshowedhighfever(38.5°C). blastsintheintraalveolarlesions,stainingwithα-SMA
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