Medical Microbiology

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Pseudomonas,Stenotrophomonas,Burkholderia 309

notablypneumoniasincysticfibrosis,colonizationofburnwounds,endocar-
ditisindrugaddicts,postoperativewoundinfection,urinarytractinfection,
sepsis.P.aeruginosafrequentlycontributestonosocomialinfections.Diagno-
sisrequiresidentificationofthepathogenincultures.Multipleresistanceto
anti-infectiveagentspresentsatherapeuticproblem.
NumerousotherPseudomonasspeciesandthespeciesofthegeneraBurk-
holderiaandStenotrophomonasareoccasionallyfoundinpathogenicrolesin
immunosuppressedpatients.B.malleicausesmalleus(glanders)andB.pseu-
domalleicausesmelioidosis. &

Pseudomonasaeruginosa


Occurrence,significance.Allpseudomonadsarewidespreadinnature.They
areregularlyfoundinsoils,surfacewater,includingtheocean,onplantsand,
insmallnumbers,inhumanandanimalintestines.Theycanproliferateina
moistmilieucontainingonlytracesofnutrientsubstances.Themostimpor-
tantspeciesinthisgroupfromamedicalpointofviewisP.aeruginosa,which
causesinfectionsinpersonwithimmunedefects.
Morphologyandculture.P.aeruginosaareplump, 2 – 4 lmlongrodswithone
toseveralpolarflagella.Somestrainscanproduceaviscousextracellular
slimelayer.Thesemucoidstrainsarefrequentlyisolatedinmaterialfromcys-
ticfibrosispatients.P.aeruginosapossessesanoutermembraneaspartofits
cellwall.Thearchitectureofthismembraneisresponsibleforthenatural
resistanceofthisbacteriumtomanyantibiotics.
P.aeruginosacanonlybegrowninculturemediumscontainingfreeO 2 as
aterminalelectronacceptor.Innutrientbroth,theorganismthereforegrows
atthesurfacetoformaso-calledpellicle.Coloniesonnutrientagaroftenhave
ametallicsheen(P.aeruginosa;Latin:aes=metalore).Givensuitablecon-
ditions,P.aeruginosacanproducetwopigments,i.e.,bothyellow-greenfluo-
resceinandblue-greenpyocyanin.
Pathogenesisandclinicalpictures.Thepathomechanismsinvolvedare
highlycomplex.P.aeruginosausuallyentersbodytissuesthroughinjuries.
Itattachestotissuecellsusingspecificattachmentfimbriae.Themostimpor-
tantvirulencefactorisexotoxinA(ADPribosyltransferase),whichblocks
translationinproteinsynthesisbyinactivatingtheelongationfactoreEF2.
TheexoenzymeS(alsoanADPribosyltransferase)inactivatescytoskeletal
proteinsandGTP-bindingproteinsineukaryoticcells.Theso-calledcytotoxin
damagescellsbycreatingtransmembranepores.Variousdifferentmetallo-
proteaseshydrolyzeelastin,collagen,orlaminin.TwotypeCphospholipases
showmembraneactivity.Despitethesepathogenicdeterminants,infections

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Kayser, Medical Microbiology © 2005 Thieme

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