Secondary tuberculosis should always be an important consideration in HIV-positive patients who present with pulmonary disease. Of note, although an increased risk for tuberculosis exists at all stages of HIV disease, the manifestations differ depending on the degree of immunosuppression. For example, patients with less severe immunosuppression (CD4+ T cell counts >300 cells/µL) present with “usual” secondary tuberculosis (apical disease with cavitation) while those with more advanced immunosuppression (CD4+ T cell counts below 200 cells/µL) present with a clinical picture that resembles progressive primary tuberculosis (lower and middle lobe consolidation, hilar lymphadenopathy, and noncavitary disease). The extent of immunosuppression also determines the frequency of extrapulmonary involvement, rising from 10% to 15% in mildly immunosuppressed patients to greater than 50% in those with severe immune deficiency.
MORPHOLOGYTheinitiallesionusuallyisasmallfocusofconsolidation,lessthan2cmindiameter,within1to2cmoftheapical pleura. Suchfociaresharplycircumscribed,firm,gray-whitetoyellowareasthathaveavariableamountofcentralcaseationandperipheralfibrosis.Infavorablecases,theinitialparenchymalfocusundergoesprogressivefibrousencapsulation,leavingonlyfibrocalcificscars.Histologically,theactivelesionsshowcharacteristiccoalescenttubercleswithcentralcaseation.Althoughtuberclebacillicanbedemonstratedbyappropriatemethodsinearlyexudativeandcaseousphasesofgranulomaformation,itisusuallyimpossibletofindtheminthelate,fibrocalcificstages.
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Fig. 13.36 Secondarypulmonarytuberculosis.Theupperpartsofbothlungsareriddledwithgray-whiteareasofcaseationandmultipleareasofsofteningandcavitation.
Localized,apical,secondarypulmonarytuberculosismayhealwithfibrosiseitherspontaneouslyoraftertherapy,orthediseasemayprogressandextendalongseveraldifferentpathways.Inprogressive pulmonary tuberculosis, theapicallesionenlargesandtheareaofcaseationexpands.Erosionintoabronchusevacuatesthecaseouscenter,creatingaragged,irregular cavity lined by caseous material thatispoorlywalledoffbyfibroustissue(
Fig.13.36 ).Erosionofbloodvesselsresultsinhemoptysis.Withadequatetreatment,theprocessmaybearrested,althoughhealingbyfibrosisoftendistortsthepulmonaryarchitecture.Irregularcavities,nowfreeofcaseousnecrosis,mayremainintactorcollapseandbecomefibrotic.Ifthetreatmentisinadequateorhostdefensesareimpaired,theinfectionmayspreadbydirectextensionandbydisseminationthroughairways,lymphaticchannels,andthevascularsystem.Miliary pulmonary disease occurswhenorganismsreachthebloodstreamthroughlymphaticvesselsandthenrecirculatetothelungviathepulmonaryarteries.Thelesionsappearassmall(2-mm)fociofyellow-whiteconsolidationscatteredthroughthelungparenchyma(thewordmiliary isderivedfromtheresemblanceofthesefocitomilletseeds).Withprogressivepulmonarytuber-culosis,thepleuralcavityisinvariablyinvolvedandserouspleural effusions, tuberculous empyema, orobliterative fibrous pleuritis maydevelop.