The old truths seem to crumble away. Reactivation tb has always been thought to be associated with a cxr of upper lobe infiltrates, with or without cavitation and typically upper lobe volume loss with hilar retraction while primary tb is typically associated with hilar nodes , middle and lower lobe parenchymal disease and pleural effusion. Molecular diagnostic techniques have caused an amendment to this venerable distinction.
An article in a recent issue of JAMA points to HIV infection playing an important role in the radiographic appearance of tuberculosis. The authors state "The altered radiographic appearance of pulmonary tuberculosis in HIV is due to altered immunity rather than recent acquisition of infection and progression to active disease."and "... radiographic findings have implications regarding host immune status...but whether a patient's disease is due to remotely acquired infection cannot be determined from them."
An earlier article also found no difference in cxr patterns in primary and reactivation tb. Both articles used restriction fragment length polymorphism (RFLP) analysis to define clusters of cases and made observations of cxr patterns in clustered and non-clustered (presumed to be reactivation) cases. There were clustered cases-presumably due to recent infection- which had upper lobe infiltrates.Reference is made by the authors in the earlier article to cases of documented recent infection with radiographic finding suggestive of reactivation. Well, I guess I shouldn't be surprised. We used to treat CHF (now HF) with bed rest, now we recommend exercise.We used to risk malpractice if we gave a CHF patient a beta blocker,now we risk it when we don't. Heraclitus had it right. All is flux.