Legionnaires’ Disease: Postmortem Pathologic Findings of 20 Cases

Abstract

From March 1977 to December 1978, postmortem examination was performed at Wadsworth Veterans Administration Medical Center for 20 patients who had had nosocomially acquired Legionnaires' disease. Seventeen patients died during the acute illness due to Legionnaires' disease, and three patients died after clinical resolution of the acute process. The only consistent postmortem findings were limited to the lungs. Confluent bronchopneumonia, and less frequently lobar pneumonia, was present in most cases. Although a spectrum of microscopic pulmonary findings was observed, the characteristic histologic features of acute Legionnaires' disease were an extensive intra-alveolar exudation of macrophages and neutrophils in varying proportions, erythrocytes, and fibrin. Lysis of the inflammatory cells was frequently found. Areas of coagulative necrosis of the lung parenchyma and edematous thickening of the alveolar septa were typically seen. Microscopy of lung tissue from the three patients who died after clinical resolution of the acute process revealed organized pneumonia, with patchy organization of the intra-alveolar exudate and focal obliteration of the alveolar septal framework. Associated postmortem findings were fibrinous endocarditis in one case and hemorrhagic infarction of the adrenal glands in two cases. Electron-microscopic examination of the lungs revealed as many as 23 separate bacillary profiles within a single macrophage. Septate binary fission or spore-like structures were not observed.

The Bacterial Peptide N-Formyl-Met-Leu-Phe Inhibits Killing of Staphylococcus epidermidis by Human Neutrophils in Fibrin Gels

“…In contrast, PMN stimulated with leukotriene B 4 (LTB 4 ) or IL-8 form zones of loose apposition on fibrin and migrate effectively into these gels. In addition, fMLP or TNF-␣ inhibited PMN migration through fibrin gels in response to LTB 4 or IL-8. These findings suggested that fMLP might exert an inhibitory effect on PMN killing of bacteria at sites of fibrin deposition by blocking PMN migration into and in these sites.…”

“…Following wounding or invasion of tissues by bacteria, fibrinogen-rich exudates lead to the formation of fibrin gels to which bacteria bind or in which they become embedded (3,4). Fibrin also is deposited on prosthetic devices such as venous catheters, making them attractive substrates for adhesins expressed by Staphylococci and other bacteria (5).…”

Cryptogenic organising pneumonia

“…Radiation-primed organising pneumonia is thus quite similar to COP. Interestingly, this peculiar iatrogenic organising pneumonia provides some insight into the pathogenesis of Chlamydia pneumoniae [184,185] Coxiella burnetii [186,187] Legionella pneumophila [95,[188][189][190][191][192][193][194] Mycoplasma pneumoniae [95,189,[195][196][197] Nocardia asteroides [198,199] Pseudomonas aeruginosa [200] Serratia marcescens [201]; in lung transplant recipient [200] Staphylococcus aureus In lung transplant recipient [200] Streptococcus pneumoniae [5,6,202] Viruses Adenovirus [203] Cytomegalovirus [203,204] Herpes virus In lung transplant recipient [200] HIV [205][206][207][208][209][210]; in a pregnant patient using cocaine [205]; following highly active antiretroviral therapy introduction [211] Influenza virus [189,[212][213][214] Parainfluenza virus [215] Human herpes virus-7 …”

Serial Bronchoalveolar Lavage Studies in a Patient with Intra-Alveolar Fibrosis Following Legionnaires' Disease.

“…The clinical features of Legionnaires' disease (LD) range from an asymptomatic course to fatal pneumonia. Although there have been no properly controlled studies of prolonged sequelae, a few case reports have noted a permanent pulmonary sequelae including pulmonary fibrosis following LD (2)(3)(4)(5)(6)(7)(8)(9).…”