Medical Microbiology

Host–PathogenInteractions 15

piliatahighrate(Fig. 1. 2 ).Theborreliaethatcauserelapsingfevershavethe

capacitytochangethestructureofoneoftheadhesionproteinsintheirouter

membrane(vmp=variablemajorprotein),resultinginthetypical“recur-

rences”offever.Similarly,meningococcicanchangethechemistryoftheir

capsulepolysaccharides(“capsuleswitching”).

&IgAproteases.Mucosalsecretionscontainthesecretoryantibodiesofthe

sIgA 1 classresponsibleforthespecificlocalimmunityofthemucosa.Classic

mucosalparasitessuchasgonococci,meningococciandHaemophilusinflu-

enzaeproduceproteasesthatdestroythisimmunoglobulin.

ClinicalDisease.........................................

Theclinicalsymptomsofabacterialinfectionarisefromtheeffectsofdama-

gingnoxaeproducedbythebacteriaaswellasfromexcessivehostimmune

responses,bothnonspecificandspecific.Immunereactionscanthuspoten-

tiallydamagethehost’shealthaswellasprotectit(seeImmunology,p. 1 03ff.).

&Cytopathiceffect.Obligateintracellularparasites(rickettsiae,chlamy-

diae)maykilltheinvadedhostcellswhentheyreproduce.

&Exotoxins.Pathogenicbacteriacanproduceavarietyoftoxinsthatare

eithertheonlypathogenicfactor(e.g.,indiphtheria,cholera,andtetanus)

oratleastamajorfactorintheunfoldingofthedisease.Oneaspecttheclas-

sificationandnomenclatureofthesetoxinsmustreflectisthetypeofcell

affected:cytotoxinsproducetoxiceffectsinmanydifferenthostcells;neu-

rotoxinsaffecttheneurons;enterotoxinsaffectenterocytes.Thestructures

andmechanismsofactionofthetoxinsarealsoconsideredintheirclassifica-

tion(Table 1. 5 ):

— ABtoxins.Theyconsistofabindingsubunit“B”responsibleforbindingto

specificsurfacereceptorsontargethostcells,andacatalyticsubunit“A”

representingtheactiveagent.Onlycellspresentingthe“B”receptorsare

damagedbythesetoxins.

— Membranetoxins.Thesetoxinsdisruptbiologicalmembranes,eitherby

attachingtothemandassemblingtoformpores,orintheformofphos-

pholipasesthatdestroymembranestructureenzymatically.

— Superantigens(seep. 7 2).TheseantigensstimulateTlymphocytesand

macrophagestoproduceexcessiveamountsofharmfulcytokines.

&Hydrolyticexoenzymes.Proteases(e.g.,collagenase,elastase,nonspecific

proteases),hyaluronidase,neuraminidase(synonymouswithsialidase),lec-

ithinaseandDNasescontributeatvaryinglevelstothepathogenesisofan

infection.

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Kayser, Medical Microbiology © 2005 Thieme