Medical Microbiology

Mycobacterium 265

Thefurthercourseofthediseasedependsontheoutcomeofthebattlebe-

tweentheTBandthespecificcellularimmunedefenses.Postprimarydisse-

minationfociaresometimesobservedaswell,i.e.,developmentoflocaltis-

suedefectfociatotherlocalizations,typicallytheapicesofthelungs.Myco-

bacteriamayalsobetransportedtootherorgansviathelymphvesselsor

bloodstreamandproducedisseminationfocithere.Thehosteventuallypre-

vailsinover 90 %ofcases:thegranulomasandfocifibrose,scar,andcalcify,

andtheinfectionremainsclinicallysilent.

&Secondarytuberculosis.Inabout 10 %ofinfectedpersonstheprimary

tuberculosisreactivatestobecomeanorgantuberculosis,eitherwithin

months(5%)orafteranumberofyears(5%).Exogenousreinfectionis

rareinthepopulationsofdevelopedcountries.Reactivationbeginswitha

caseationnecrosisinthecenterofthegranulomas(alsocalledtubercles)

thatmayprogresstocavitation(formationofcaverns).Tissuedestruction

iscausedbycytokines,amongwhichtumornecrosisfactora(TNFa)appears

PossibleCoursesofPulmonaryTuberculosis

Miliary

tuberculosis

in cases of

compromised

immune

defenses

Primary tuberculosis Secondary tuberculosis

Localized foci

(frequently

apical focus)

Granuloma

(at primary

infection locus)

Open

tuberculosis

spread via

bronchial

system

Extrapul-

monary

tuberculosis

hematogenous

spread

aerogenic

Primary infection

Primary complex

(Ghon's complex)

Primary infection + lymph nodes

Scarification

Sclerotization

Scarification

Sclerotization

Silent infection (90%) or reactivation (10%)

endogenous

• immediate (5%)


• later (old scar: 5 %)

Caseation necrosis

Caverns

exoge-

nous

(super-

infection)

Fig.4. 13 Theprimarytuberculosisthatdevelopsimmediatelypostinfectionis

clinicallysilentinmostcasesthankstoaneffectiveimmuneresponse.However,

in 10 %ofcasesaso-calledsecondarytuberculosisdevelops,eitherimmediatelyor

yearslater,andmayspreadtotheentirebronchialsystemorotherorgansystems.

4

Kayser, Medical Microbiology © 2005 Thieme