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Legionnaires' Disease Pneumonia

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Legionnaires' Disease Pneumonia ANNALS OF CLINICAL AND LABORATORY SCIENCE, Vol. 9, No. 5 Copyright © 1979, Institute for Clinical Science, Inc. Legionnaires’ Disease Pneumonia: Histopathologic Features and Comparison with Microbial and Chemical Pneumonias* GARY L. LATTIMER, M.D.,f RAYMOND A. RACHMAN, M.D.,* and MICHAEL SCARLATO, M.D.f t Infectious Diseases Section and \ Department of Pathology, Allentown and Sacred Heart Hospital Center, Allentown, PA 18105 ABSTRACT The histopathologic findings in lung tissue are reported from five cases of Philadelphia Legionnaires’ Disease and the results are compared to pneumonias caused by other microbial and chemical agents. Histopathology of lung tissue was similar in all cases, despite the fact that death occurred between the fourth and 14th day of clinical illness. The inflammatory re­ sponse was almost totally limited to the lower respiratory tract and primarily involved respiratory bronchioles, alveolar ducts and alveoli. Major bronchial branches and pulmonary interstices showed little or no involvement. There was considerable variation in the extent and nature of the consolidation, but the overall reaction pattern was highly characteristic of diffuse alveolar damage. Most involved areas showed intra-alveolar, fibrinocellular mono­ nuclear cell predominant exudates, associated with pneumocytic hyper­ plasia and slough. These findings plus the presence of erythroleucophago- cytosis by macrophages and paucity of polymorphonuclear leucocytes are commonly associated with psittacine pneumonia, and much less so with classic patterns of bacterial, viral, fungal or rickettsial pneumonias. Of the toxic inhalants, nickel carbonyl, phosgene, nitrous oxide, cadmium oxide and some halogenated hydrocarbons have been associated with this tissue reaction pattern. Bacteria were notably absent in lung tissue stained by methods used to demonstrate the Legionnaires’ Disease agent. Introduction epidemiologic and laboratory investiga­ tion, the Center for Disease Control An unusually severe pneumonia, (CDC) reported the isolation of a Gram- Legionnaires’ Disease (LD), resulting in negative bacterium from lung tissue of 182 cases and 29 deaths, occurred in disease victims and identified it as the Philadelphia during July and August of putative agent by demonstrating immuno- 1976.4 After five months of intensive fluorescent antibodies in serum of pa­ tients surviving the illness.5 Findings in Send request for reprints to: Gary L. Lattimer, the lungs of 14 autopsied victims were M.D., Allentown and Sacred Heart Hospital Center,1200 S. Cedar Crest Blvd., Allentown, initially reported as non-specific and PA 18105. probably produced by a toxic substance.22 353 0091-7370/79/0900-0353 $01.20 © Institute for Clinical Science, Inc. 354 LATTIMER, RACHMAN AND SCARLATO Most showed areas of extensive pneu­ study of lung tissue did not reveal changes monitis with some areas of mild inter­ seen in acute bacterial pneumonia.910 In­ stitial reaction. Special stains revealed stead, the present authors found a fibrino- no fungi, bacteria or other microorganisms cellular, mononuclear cell predominant, except in one case with disseminated intra-aveolar exudative process more candidiasis.4 More recently, the pul­ commonly described in psittacosis,14 but monary tissue reaction pattern was de­ also seen in toxic, viral, fungal and myco­ scribed as “similar to those associated plasma pneumonia. To compare, in with a lobar pneumonia,” with acute further details, the histopathologic fea­ fibrinopurulent pneumonia in 21 cases tures of these clinically similar entities, and diffuse alveolar disease in 13 cases.3 tissue sections were studied from five In 19 of 26 LD victims, bacilli were read­ fatal LD cases and from two fatal cases ily demonstrated in lung tissue by the of psittacosis and our findings were com­ Dieterle silver-impregnation method and pared with those seen in other microbial found inconsistently with conventional or toxic pneumonias. histopathologic stains for micro­ organisms.3 Material and Methods The epidemiologic features and clinical findings of progressive atypical In table I are given the sex, age, days of pneumonia associated with fever and rela­ clinical illness at the time of death, under­ tive bradycardia, with apparent response lying disease process, antibiotic therapy to tetracycline therapy, suggest the clini­ and summary of the gross description of cal diagnosis of a zoonosis, particularly the lung noted at the time of autopsy. All psittacosis. 15Furthermore, our initial cases were listed as LD victims by the T A B L E I Clinical Data with Gross Pulmonary Pathology Age, Day of Yr/ Illness Cause of Underlying Antibiotic Autopsy Findings Patient Sex At Death Death Disease Therapy Gross Description of Lung 1 41/M 5 Acute Diabetes Penicillin Plum colored pleural surface. Pneumonitis Mellitus Ampicillin Fibrinous pleuritis. Diffuse consolidated - all lobes. Appearance of red hepatization on cut surface. 2 55/F Bilateral ASCVD* Cephalothin Extensive consolidation 75 percent left Pneumonia Angina upper, 90 percent right upper lobe. Pectoris Variegated reddish-gray pattern on Old myocar­ cut surface. dial infarct 3 54/M Pulmonary Folic Acid Penicillin Bilateral straw-colored pleural effusion Edema deficiency (400ccc) . Pneumonia Anemia Edema and congestion - all lobes. Pylonephritis Consolidation right lower lobe. 4 66/F Pulmonary ASCVD* Cephalothin Petechial hemorrhage pleural surface. edema with Angina Gentamicin Bilateral hemorrhagic pleural effusion hemorrhage Pectoris (500 cc). Pneumonia Diffuse severe edema and patchy pneumonia all lobes. 5 49/M Bilateral Congestive Penicillin Diffuse bilateral pneumonia, edema and Pneumonia Heart Cephalothin congestion all lobes. Failure ♦Arteriosclerotic cardiovascular disease LEGIONNAIRES’ PNEUMONIA HISTOPATHOLOGY 355 Pennsylvania State Department of tive patterns of involvement were recog­ Health,23 were over 40 years of age, had nized. Dense consolidation, extending significant underlying disease and ex­ into uninvolved area by direct alveolar pired between the fourth and 14th day spread, was most commonly seen (figure 1). after the clinical illness was noted. The In other sections, dilated alveolar ducts, immediate cause of death was ascribed to some filled with exudates, were found respiratory failure (4 cases) and cardiac scattered throughout normal appearing failure (1 case). lung (figure 2). Septal and interstitial Formalin-fixed, paraffin embedded tis­ areas were congested with red blood cells sue specimens from lung (5 cases), liver but contained few inflammatory cells. and spleen (4 cases) were stained by the Those alveoli located at the periphery of haematoxylin and eosin, periodic acid- the inflammatory reaction contained Shiff, Gridley’s reticulin, Verhoeff-Van fewer numbers of inflammatory cells; Gieson, Peris’ prussian blue and phospho- however, the components of the exuda­ tungstic acid-hematoxylin methods. To tive response were similar to those found compare staining characteristics of micro­ in central dense areas of inflammation. bial agents, sequential sections of lung Hypertrophied alveolar lining cells, many tissue specimens were stained by the of which were desquamating in cohesive Brown-Brenn, Giemsa, Dieterle silver- sheets, were frequently found at the mar­ impregnation methods27 and direct fluo­ gin of the inflammatory response (figure rescent antibody (FA) technique.6 Lung 3). The contents of the alveolar exudate tissues in cases 1 and 5 were also commonly varied from field to field. Most examined with an electron microscope. involved alveoli contained a fibrinocel- Finally, haematoxylin and eosin and lular exudate composed of large, occasion­ Giemsa stained lung tissue slides from ally vacuolated mononuclear cells, red fatal cases of human psittacosis infected blood cells, polymorphonuclear cells, with the Epizootic Bovine Abortion1 and lymphocytes and alveolar epithelial cells Borg2 strains of Chlamydia psittaci were in various proportions (figure 4). Erythro- compared directly to LD victim speci­ phagocytosis and leukophagocytosis by mens. Control tissue for the Dieterle stain macrophages was frequently encountered and specific conjugate for fluorescent (figure 5). The polymorphonuclear leuco­ staining was kindly supplied by the CDC. cyte content varied, but they were in the main fewer in number than the mono­ Results nuclear cells. Fibrin, where present, was The histopathology of lung tissue was in the form of intra-alveolar meshwork similar in all five cases regardless of the with entrapped cells, not splayed on the day of illness prior to death. The inflam­ septa as a hyaline membrane (figure 5). matory response was almost totally lim­ Interstitial fibrosis, or organizing oblitera- ited to the lower respiratory tract and in­ tive alveolitis, was not seen. Pulmonary volved respiratory bronchioles, alveolar arterial and venous thrombi or emboli ducts and alveoli. The bronchial branches were absent. often had light chronic inflammatory infil- Hepatic and splenic tissue showed trates within their walls, consisting marked acute congestion. There was mainly of lymphocytes, but destruction of moderate hepatic steatosis and moderate the mucosa was rare or absent even in Kupffer cell hypertrophy. Occasional those with lumenal cellular exudates. hepatic Kupffer cells and macrophages in There was considerable variation in the the splenic red pulp showed erythrocytic extent and nature of the consolidation, and leucocytic phagocytosis. There were often within the same lobule.
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