MORPHOLOGYIncountriesinwhichbovinetuberculosisandinfectedmilkhavelargelydisappeared,primarytuberculosisalmostalwaysbeginsinthelungs.Theinhaledbacilliusuallyimplantinthedistalairspacesofthelowerpartoftheupperlobeorintheupperpartofthelowerlobe.Theyaretypicallyclosetothepleura.Duringthedevelopmentofsensitization,a1-cmto1.5-cmareaofgray-whiteinflammatoryconsolidationemerges.ThisiscalledtheGhon focus. Inthemajorityofcases,thecenterofthisfocusundergoescaseousnecrosis.Tuberclebacilli,eitherfreeorwithinphagocytes,travelviathelymphaticvesselstotheregionallymphnodes,whichalsooftencaseate.ThiscombinationofparenchymalandnodallesionsiscalledtheGhon complex (
Fig.13.34 ).Lymphaticandhematogenousdisseminationtootherpartsofthebodyalsooccursduringthefirstfewweeks.Developmentofcell-mediatedimmunitycontrolstheinfectioninapproximately95%ofcases.Therefore,theGhoncomplexundergoesprogressivefibrosis,andcalcificationoftenfollows(detectableasaRanke complex onradiograph).Despiteseedingofotherorgans,nolesionsdevelop.Histologically,sitesofinfectionareinvolvedbyacharacteristicinflammatoryreactionmarkedbythepresenceofcaseatingandnoncaseatinggranulomas,whichconsistofepithelioidhistiocytesandmultinucleategiantcells (Fig.13.35AtoC
Secondary tuberculosis is the pattern of disease that arises in a previously sensitized host. It may appear shortly after primary tuberculosis, but more commonly arises from reactivation of dormant primary lesions many decades after initial infection, particularly when host resistance is weakened. It also may result from reinfection, which may occur either because the protection afforded by the primary disease has waned or because of exposure to a large inoculum of virulent bacilli. Whatever the source of the organism, only a few patients (<5%) with primary disease subsequently develop secondary tuberculosis.
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Fig. 13.35 Themorphologicspectrumoftuberculosis.Acharacteristictubercleatlowmagnification(A)andathigherpower(B)showscentralgranularcaseationsurroundedbyepithelioidandmultinucleategiantcells.Thisistheusualresponseinindividualswhodevelopcell-mediatedimmunitytotheorganism.(C)Occasionally,eveninimmunocompetentpatients,tuberculargranulomasmaynotshowcentralcaseation;hence,irrespectiveofthepresenceorabsenceofcaseousnecrosis,useofspecialstainsforacid-fastorganismsisindicatedwhengranulomasarepresent.(D)Inthisspecimenfromanimmunosuppressedpatient,sheetsofmacrophagespackedwithmycobacteriaareseen(acid-faststain).
Secondary pulmonary tuberculosis is classically localized to the apex of one or both upper lobes. The reason is obscure but may relate to high oxygen tension in the apices. Because of the preexistence of hypersensitivity, the bacilli excite a prompt and marked tissue response that tends to wall off the focus. As a result of this localization, the regional lymph nodes are less prominently involved early in the disease than they are in primary tuberculosis. On the other hand, cavitation occurs readily in the secondary form, leading to erosion into and dissemination along airways. Such changes become an important source of infectivity, because the patient now produces sputum containing bacilli.