Complicationsofpneumoniainclude(1)tissuedestructionandnecrosis,causingabscess formation;(2)spreadofinfectiontothepleuralcavity,causingtheintrapleuralfibrinosuppurativereactionknownasempyema;and(3)bacteremic dissemination totheheartvalves,pericardium,brain,kidneys,spleen,orjoints,causingmetastaticabscesses,endocarditis,meningitis,orsuppurativearthritis.
The major symptoms of typical community-acquired acute bacterial pneumonia are abrupt onset of high fever, shaking chills, and cough producing mucopurulent sputum; occasional patients have hemoptysis. When pleuritis is present, it is accompanied by pleuritic pain and pleural friction rub. The whole lobe is radiopaque in lobar pneumonia, whereas there are focal opacities in bronchopneumonia.
The clinical picture is markedly modified by the administration of effective antibiotics. Treated patients may be relatively afebrile with few clinical signs 48 to 72 hours after the initiation of antibiotics. The identification of the organism and the determination of its antibiotic sensitivity are the keystones of therapy. Less than 10% of patients with pneumonia severe enough to merit hospitalization now succumb, and in most such instances death results from a complication, such as empyema, meningitis, endocarditis, or pericarditis, or to some predisposing influence, such as debility or chronic alcoholism.
The most common causes of community-acquired viral pneumonias are influenza types A and B, the respiratory syncytial viruses, human metapneumovirus, adenovirus, rhinoviruses, rubeola virus, and varicella virus (see 13.5 ). Nearly all of these agents also cause upper-respiratory tract infections (“common cold”).
These pathologic viruses share a propensity to infect and damage resspiratory epithelium, producing an inflammatory response. When the process extends to alveoli, there is usually interstitial inflammation, but some outpouring of fluid into alveolar spaces may also occur, so that on chest films the changes may mimic those of bacterial pneumonia. As a result, it is not possible to distinguish bacterial and viral pneumonia based on radiologic appearance alone. Moreover, damage leading to necrosis of the respiratory epithelium inhibits mucociliary clearance and predisposes to secondary bacterial infections. Such serious complications of viral infection are more likely in infants, older adults, malnourished patients, alcoholics, and immunosuppressed individuals.
MORPHOLOGYThemorphologicpatternsinviralpneumoniasaresimilar.Theprocessmaybepatchy,oritmayinvolvewholelobesbilaterallyorunilaterally.Macroscopically,theaffectedareasarered-blue,congested,andsubcrepitant.Onhistologicexamination,the inflammatory reaction is largely confined to the walls of the alveoli (
Fig.13.32 ).Theseptaarewidenedandedematous;theyusuallycontainamononuclearinflammatoryinfiltrateoflymphocytes,macrophagesand,occasionally,plasmacells.Intheclassiccase,alveolarspacesinviralpneumoniasarefreeofcellularexudate.Inseverecases,however,full-blowndiffusealveolardamagewithhyalinemembranesmaydevelop.Inlesssevere,uncomplicatedcases,subsidenceofthediseaseisfollowedbyreconstitutionofthenormalarchitecture.Superimposedbacterialinfection,asexpected,resultsinamixedhistologicpicture.
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