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Legionnaire's disease

Legionellosis is an infection caused by species of the bacterium Legionella, most notably L. pneumophila. At least 46 species and 70 serogroups have been identified. L. pneumophila, a ubiquitous aquatic organism that thrives in warm environments (25 to 45 °C with an optimum around 35 °C) causes over 90 % of Legionnaires Disease. more...

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The disease has two distinct forms:

  • Legionnaires' disease is the name for the more severe form of infection which includes pneumonia
  • Pontiac fever is a milder respiratory illness without pneumonia caused by the same bacterium

Legionnaires' disease acquired its name in 1976 when an outbreak of pneumonia occurred among persons attending a convention of the American Legion in Philadelphia. Later, the bacterium causing the illness was named Legionella.

On January 18, 1977 scientists identified a previously unknown bacterium as the cause of the mysterious "Legionnaires' disease."

An estimated 8,000 to 18,000 people get Legionnaires' disease in the United States each year. Some people can be infected with the Legionella bacterium and have mild symptoms or no illness at all.

Outbreaks of Legionnaires' disease receive significant media attention. However, this disease usually occurs as a single, isolated case not associated with any recognized outbreak. When outbreaks do occur, they are usually recognized in the summer and early fall, but cases may occur year-round. About 5% to 30% of people who have Legionnaires' disease die.


Patients with Legionnaires' disease usually have fever, chills, and a cough, which may be dry or may produce sputum. Some patients also have muscle aches, headache, tiredness, loss of appetite, and, occasionally, diarrhea. Laboratory tests may show that these patients' kidneys are not functioning properly. Chest X-rays often show pneumonia. It is difficult to distinguish Legionnaires' disease from other types of pneumonia by symptoms alone; other tests are required for diagnosis.

Persons with Pontiac fever experience fever and muscle aches and do not have pneumonia. They generally recover in 2 to 5 days without treatment.

The time between the patient's exposure to the bacterium and the onset of illness for Legionnaires' disease is 2 to 10 days; for Pontiac fever, it is shorter, generally a few hours to 2 days.


Intestinal Infections: These may only occur as part of respiratory infections, where gastrointestinal symptoms have on occasion been described.

Extraintestinal Infections: L. pneumophila is specifically considered as a pathogen of the respiratory tract, where it is a cause of atypical pneumonia, also known as Legionnaires' disease. Other infections have also been reported, including haemodialysis fistulae, pericarditis and wound and skin infections. Bacteraemia is often associated with Legionnaires' disease.

One species Legionella Longbeachae is contracted via inhaling infected compost or soil.


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The Radiologic Manifestations of Legionnaire's Disease - )
From CHEST, 2/1/00 by Michael J. Tan

Study objectives: To study the serial radiographic manifestations of Legionnaire's disease from the initial presentation on admission to recovery using strict criteria for the diagnosis of infection.

Materials and methods: We prospectively studied the chest radiographs of patients hospitalized with a diagnosis of community-acquired pneumonia in Summit County, Ohio between November 1990 and November 1992. Forty-three patients fulfilled strict criteria for legionellosis. The diagnosis of infection was based on the criteria of "definite" diagnosis as defined by the Ohio Community-Based Pneumonia Incidence Study Group report. The criteria included the isolation of the microorganism, the presence of a significant antibody rise, or the presence of Legionella antigen in the urine.

Results: Forty of 43 patients had admission radiographs interpreted as compatible with pneumonia. In spite of appropriate antimicrobial therapy, worsening of the infiltrates was found in more than half of the patients within the first week. Twenty-seven patients were observed to have pleural effusion during the course of hospitalization: 10 effusions were found on admission, another 14 developed during the first week, and 3 new effusions were discovered after the first week. Cavitation was found in only one patient. None of the patients had apical involvement.

Conclusion: This study confirms previous reports using less stringent etiologic diagnosis criteria that chest radiographic findings in Legionnaire's disease are not specific. Even with appropriate therapy, more than half of the patients will have worsening of the infiltrates during the first week. Pleural effusion is common among our patients, and it is frequently detected during the serial radiographic studies during the first week of hospitalization. Chest radiography in Legionnaire's disease is useful only for the monitoring of disease progression and not for diagnostic purposes. In addition, worsening of infiltrates and pleural effusion are seen in more than half of the patients in spite of appropriate therapy and clinical improvement.

(CHEST 2000; 116:398-403)

Key words: Legionnaire's disease; Legionella; legionellosis; pleural effusion; pneumonia; radiograph);

Abbreviations: Lp1 = Legionella pneumophila serogroup 1

Legionnaire's disease is a febrile illness with pneumonia caused by Legionella spp. This illness presents both in outbreaks and sporadic situations.[1,2] This microorganism is responsible for 1 to 5% of community-acquired pneumonias requiring hospitalization.[3-6] The report from the Ohio Community-Based Pneumonia Incidence Study Group projected that the annual cases in a noninstitutionalized population range from 10,800 to 18,000 in the United States.[6]

There are [is greater than] 40 different Legionella spp, with Legionella pneumophila accounting for 90% of legionellosis.[7] Among the 14 serogroups of L pneumophila, L pneumophila serogroup 1 (Lp1) is responsible for 80% of reported cases.[7] Positive confirmation of Legionella infection has been traditionally based on the culture of sputum, paired serologic tests based on rising antibody titers, and antigen detection techniques such as urinary antigen or direct fluorescent antibody. Plouffe et al[8] reported that a single acute antibody titer [is greater than or equal to] 1:256 had a low positive predictive value (15%) for acute legionellosis.

Legionnaire's disease is often classified as an "atypical pneumonia" based on the dogma that chest radiographic findings are neither lobar nor consolidating, as in the classic pyogenic pneumonias. We report our experience with serial chest radiographs in patients with a diagnosis of Legionnaire's disease using stringent laboratory criteria to demonstrate the course of radiologic findings.


Patient Population: Summit County, Ohio residents who were [is greater than or equal to] 18 years old, who were not residents of institutions (nursing homes, long-term care facilities, or prisons), and who were admitted to Summa Health System (Akron City Hospital and St. Thomas Hospital), Akron General Medical Center, Cuyahoga Falls Medical Center, and Barberton Citizens Hospital with a diagnosis of community-acquired pneumonia were included as part of a prospective study of Ohio Community-Based Pneumonia Incidence Study Group.[6] Between November 1990 and November 1992, 2,750 patients were admitted with a confirmed diagnosis of community-acquired pneumonia. Serial chest radiographs were obtained on patients admitted with the diagnosis. These radiographs were read by a staff radiologist at each of the participating hospitals in addition to being reviewed by the authors, including a radiologist (RHH). Forty-three patients fulfilled the criteria for definite diagnosis of Legionnaire's disease. Two patients did not have a follow-up chest radiograph after admission.

Criteria for Diagnosis: The diagnosis of Legionnaire's disease was based on criteria defined by Marston et al[6] as a "definite" diagnosis: the isolation of Legionella from respiratory secretions, the presence of urine Lp1 antigens at a ratio [is greater than or equal to] 3 of sample-to-control, or a fourfold rise in antibody attaining 1:128 in paired acute and convalescent phase sera. Sputum samples were stored at 4 [degrees] C prior to culture for Legionella and were cultured at the microbiology laboratory of Summa Health System using a standard technique.[9] Sera from patients with pneumonia were stored at - 20 [degrees] C and were tested at the Centers for Disease Control and Prevention for antibodies to L pneumophila antigens by indirect immunofluorescent antibody assay.[10] Urine samples were stored at 4 [degrees] C at the Ohio State University laboratory and were tested for the Lp1 antigen at Ohio State University Medical Center using radioimmunoassay (Binax; South Portland, ME).[11]


Forty-three patients fulfilled the criteria for a definite diagnosis of Legionnaire's disease. Thirty-two patients fulfilled the fourfold antibody rise criterion. Among these 32 patients, 13 also had a positive urine Lp1 antigen and 9 had a positive culture for Legionella from respiratory secretions. Among 18 patients with a positive urine Lp1 antigen test, 13 had fourfold antibody rise and 3 had a positive culture. Two remaining patients with positive urine Lp1 antigen did not have an antibody rise or a positive culture. Legionella was isolated from nine patients, three of whom had a concomitant fourfold antibody rise and the presence of urine Lp1 antigen. Table 1 shows the demographic distribution. All of these patients received at least one antimicrobial agent with activity against Legionella during the hospitalization.

Table 1--Demographic Distribution of Patients With Legionnaire's Disease(*)

(*) Data presented denote white patients; data in parentheses denote African-American patients.

Initial Radiographic Presentation

Among the 43 patients included in the study, 40 patients had positive findings (infiltrates) on the initial chest radiograph (Table 2). The infiltrates of 33 were patchy (76.7%), 7 were confluent or lobar in character (16.3%), and 3 were interpreted as having no acute pneumonic infiltrate (7%). One was interpreted as pleural effusion (by day 3, the chest radiograph showed confluent infiltrates with a cavity); the second was interpreted as "changes compatible with chronic lung disease" (this patient later had both a positive Legionella culture and a positive urinary Lp1 antigen); and the third was interpreted as compatible with congestive heart failure and was later interpreted as inflammatory infiltrate. Twenty-six infiltrates were unilobar, 12 were multilobar, and 7 were bilateral in distribution. Thirty-two patients had infiltrates involved the lower lung fields. The right upper lobe infiltrates were found in 11 patients, whereas 5 patients had left upper lobe involvement (lingula involvement excluded). One patient had perihilar infiltrate with sparing of the periphery. He died on day 10. None of the patients had apical involvement. Ten patients presented with pleural effusion on admission.

Table 2--Admission and Serial Chest Radiographic Findings of Patients With Confirmed Diagnosis of Legionnaire's Disease(*)

(*) Data are presented as No.

([dagger]) Some patients listed as having multilobar distribution also had bilateral involvement.

([double dagger]) Includes one patient who progressed from having unilateral effusion with bulging fissure.

Radiographic Findings From Days 1 and 2

Sixteen patients had follow-up chest radiograph studies during days 1 and 2 of hospitalization. Eight patients had minimal or no change, two progressed from patchy to unilateral confluent infiltrates, three had progression of patchy infiltrates unilaterally, and none who had unilateral disease had contralateral progression. Six patients who had no pleural effusion on admission had an effusion on day 2: one bilateral effusion, two left-sided effusions, and three right-sided effusions, including one with a bulging fissure. Three patients with new effusion did not have increasing pulmonary infiltrates.

Radiographic Findings From Days 3 to 6

Twenty-six patients had chest radiography between days 3 and 6 of hospitalization (Fig 1). We were not able to show any correlation between the worsening of radiologic findings and the clinical course. Ten patients had minimal or no change, 1 had reduction of infiltrate size, and 15 showed worsening (1 developed confluent infiltrates and 11 had progression of infiltrates unilaterally to other lobes, 5 of which involved the contralateral lung). One patient who had small bilateral pleural effusion on admission improved to undetectable on day 3; eight patients had new pleural effusion during this time: four patients on day 3, three patients on day 4, and one patient on day 5. Three effusions were on the right, one was on the left, and three were bilateral. A patient with bilateral effusion started with the right-sided bulging fissure on day 2.


Radiographic Findings From Day 7 and Later

Twenty-seven patients had follow-up chest radiography after day 6. Only one patient had increased infiltrates, which most likely were due to superinfection. Four patients were observed to have new effusion.

Pleural Effusion

Twenty-seven (62.8%) had pleural effusion. Figure 2 shows the number of patients with pleural effusion detected by chest radiography. On admission, only 10 patients had detectable pleural effusion (7 on the left, 1 on the right, and 2 bilateral). An additional 17 patients developed effusion during hospitalization. Six more patients had pleural effusion detected on day 2. Eleven more patients developed pleural effusion subsequently. Five patients had bilateral effusion, 11 had effusion on the left side, and 11 had effusion on the right side. Most effusions were small and were detected based on the blunting of the costophrenic angle.


Other Findings

Cavitation and pulmonary infiltrates were found on day 3 in a 70-year-old woman who had pleural effusion but no infiltrates on admission. This patient had no known immunosuppressive disease or medication. By day 7, the cavitation was smaller; by day 10, it had completely resolved. Perihilar infiltrate was observed in one patient. Hilar and mediastinal lymphadenopathy were not observed.

Course of Illness and Correlation With Anti-Legionella Antibiotic Treatment

Among 37 patients with serial radiographs beyond day 2, 24 patients had worsening of radiologic findings during the first week. Radiologic improvement was observed most commonly after 6 days. Three patients showed improvement after [is greater than] 10 days. Five patients had no significant change from the admission radiograph by day 14. The radiographic changes lagged behind clinical improvement and were not related to the antimicrobial agent used. All but six patients received antimicrobial agents with anti-Legionella activity. Three patients who were treated with [Beta]-lactam alone had resolution of infiltrates within the first week. The other three patients treated with [Beta]-lactam alone showed resolution after the first week. None of the six patients died. One patient received anti-Legionella agent on day 3; this patient on admission had a small left pleural effusion but had no pulmonary infiltrate. Cavity with air fluid was detected on day 3. Follow-up on day 7 showed that the cavity had decreased in size, and on day 10 the cavity was not seen on radiograph.


Two patients died during the follow-up. One patient had progressive worsening of pulmonary infiltrates on day 4 with involvement of the perihilar area. This patient died on day 10. Another patient died on day 39 with the diagnosis of congestive heart failure. The chest radiograph findings of this patient were consistent with the diagnosis of heart failure.


This report is a prospective study on the chest radiographic findings of community-acquired Legionnaire's disease proven by strict diagnostic criteria. The initial presenting chest radiographic findings among our patients reviewed are comparable, to those reported in earlier studies that were retrospective and based on less stringent criteria.[12,13] Eighty-six percent of our patients presented with patchy infiltrates, and more than two thirds of these patients had unilobar involvement. Figure 3 shows the chest radiograph of a patient with right upper lobe consolidation. This observation is comparable to that of Kroboth et al,[14] who noted that 76% of 34 patients had initial patchy alveolar infiltrates and more than three fourths of their patients had a single lobe disease at presentation. Three of our patients did not have active pulmonary infiltrate on admission; however, the nonspecific findings may have represented an earlier pneumonia. The lack of active pulmonary findings during the early phase of illness is not unique. Kirby et al,[15] in their report of 35 patients, noted that 3 patients had no infiltrates on admission. Both Kirby et al,[15] in their study of Legionella infection in California, and Pedro-Botet et al,[16] in their study of immunosuppressed hosts in Barcelona, Spain, reported that 71% of their patients had unilobar patchy infiltrates. Dietrich et al[17] noted that 68% of patients had unilateral left lung infiltrates initially, whereas the Barcelona study[16] found that 73% of their patients presented with unilateral distribution. Pleural effusion was noted in 62.8% of our patients, compared to 35 to 63% as reviewed by Kroboth et al.[14] Bulging fissure sign, as described in a single case report by Lucas et al,[18] was noted in one of our patients.


In most cases, in spite of clinical improvement, chest radiographic findings continued to worsen between days 2 and 6 in the form of increasing consolidation of the same lobe, involvement of a contiguous lobe or ipsilateral noncontiguous lobe, infiltration of the contralateral lung, and development of pleural effusion. Lower lobe involvement was more common in our study. Sixty-seven percent of our patients had lower lobe involvement, compared to 79% reported by Kroboth et al[14] and 92% in the study of Storch et al.[19] Cavitation is found rarely in immunocompetent hosts,[2,20-26] and it was noted in only one of our patients. Cavitation and air fluid level improved rapidly after therapy. Fairbank et al[22] estimated that cavitation is found in 4.3% of patients with the disease. Storch et al[19] reported a patient with cavity formation that on biopsy showed signs of a necrotizing pneumonia. Perihilar involvement or mediastinal node involvement was not reported in many of the large studies.[14,15,17,27,28] As a rule, perihilar involvement is not commonly reported. Perihilar involvement was observed in one of our patients on day 4 of hospitalization. He died on day 10 due to the infection. Storch et al[19] reported 1 of their 17 patients with hilar lymphadenopathy. The diagnosis was based on a fourfold antibody rise using indirect fluorescent antibody titer. Cavitation is uncommon among immunocompetent hosts. However, among the immunocompromised host, cavitation is fairly common.[29-34] Perihilar infiltrates have been reported but are rarely encountered. Our only patient with hilar infiltrate died of progressive pneumonia. Apical involvement was not observed among our patients and was rarely observed in other reports. Pleural effusion may be found on admission. Many patients developed effusion during the first week of hospitalization. Figure 4 shows an example of the delayed progression of pleural effusion. The development of new effusion after the first week is uncommon.



We report our prospective study of chest radiographic findings in patients with laboratory-proven Legionnaire's disease. Our study showed that three fourths of our patients with Legionnaire's disease had patchy pneumonic infiltrates. Lobar distribution was observed in the minority of the patients. Only 16% of patients had lobar distribution of infiltrate on admission, and this increased to 28% after hospitalization. Pleural effusion, usually small, was found in about 23% of the patients on admission and increased to 63% of the patients during the hospitalization. Despite radiographic deterioration, most patients improved clinically. Although it has been suggested that radiographic findings may be helpful in differentiating Legionnaire's disease from other forms of pneumonia,[35] reports from many investigators, including the present study, did not support this contention.[14,15,17,27,28] When pneumonia is suspected, we recommend that chest radiography be obtained to confirm the presence of pneumonia and effusion but not to guide antimicrobial therapy. Consequently, in immunocompetent hosts, antimicrobial therapy should be directed to treat the common etiologic agents, namely, Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, L pneumophila, Mycoplasma pneumoniae, and Chlamydia pneumoniae. Among immunocompromised hosts, every effort should be made to identify the infecting agent. Chest radiographs are clinically useful to confirm the diagnosis of pneumonia and to monitor the disease progression.


[1] England AC III, Fraser DW, Plikaytis BD, et al. Sporadic legionellosis in the United States: the first thousand cases. Ann Intern Med 1981; 94:164-170

[2] Fraser DW, Tsai TR, Orenstein W, et al. Legionnaires disease: description of an epidemic of pneumonia. N Engl J Med 1977; 297:1189-1197

[3] British Thoracic Society Research Committee. The etiology, management and outcome of severe community-acquired pneumonia on the intensive care unit. Respir Med 1992; 86:7-13

[4] Fang GD, Fine M, Orloff J, et al. New and emerging etiologies for community-acquired pneumonia with implications for therapy: a prospective multicenter study of 359 cases. Medicine (Baltimore) 1990; 69:307-316

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[10] Wilkinson HW, Cruce DD, Broome CV. Validation of Legionella pneumophila indirect immunofluorenscense assay with epidemic sera. J Clin Microbiol 1981; 13:139-146

[11] Kohler RB, Zimmerman SE, Wilson E, et al. Rapid radioimmunoassay diagnosis of Legionnaires disease. Ann Intern Med 1981; 94:601-605

[12] Coletta FS, Fein AM. Radiological manifestations of Legionella/ Legionella-like organisms. Semin Respir Infect 1998; 13:109-115

[13] Muder RR, Yu VL, Parry MF. The radiologic manifestations of Legionella pneumonia. Semin Respir Infect 1987; 2:242-254

[14] Kroboth FJ, Yu VL, Reddy SC, et al. Clinicoradiographic correlation with the extent of Legionnaire disease. AJR Am J Roentgenol 1983; 141:263-268

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[16] Pedro-Botet ML, Sabria-Leal M, Sopena N, et al. Role of immunosuppression in the evolution of Legionnaire's disease. Clin Infect Dis 1998; 26:14-19

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[19] Storch GA, Sagel SS, Baine WB. The chest roentgenogram in sporadic cases of Legionnaire's disease. JAMA 1981; 245:587-590

[20] Edelstein PH, Meyer RD, Finegold SM. Long-term follow-up of two patients with pulmonary cavitation caused by Legionella pneumophila. Am Rev Respir Dis 1981; 124:90-93

[21] Hughes JA, Anderson PB. Pulmonary cavitation, fibrosis and Legionnaire's disease. Eur J Respir Dis 1985; 66:59-61

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[23] Lewin S, Brettman LR, Goldstein EJ, et al. Legionnaire's disease: a cause of severe abscess-forming pneumonia. Am J Med 1979; 67:339-342

[24] Gump DW, Frank RO, Winn WC, Jr, et al. Legionnaire's disease in patients with associated serious disease. Ann Intern Med 1979; 90:538-542

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[27] Macfarlane JT, Miller AC, Roderick Smith WH, et al. Comparative radiographic features of community acquired Legionnaire's disease, pneumococcal pneumonia, mycoplasma pneumonia, and psittacosis. Thorax 1984; 39:28-33

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[30] Bauling PC, Weil R, III, Schroter GP. Legionella lung abscess after renal transplantation. J Infect 1985; 11:51-55

[31] Moore EH, Webb WR, Gamsu G, et al. Legionnaire's disease in the renal transplant patient: clinical presentation and radiographic progression. Radiology 1984; 153:589-593

[32] Copeland J, Wieden M, Feinberg W, et al. Legionnaire's disease following cardiac transplantation. Chest 1981; 79: 669-671

[33] Gombert ME, Josephson A, Goldstein EJ, et al. Legionnaire's pneumonia: nosocomial infection in renal transplant recipients. Am J Surg 1984; 147:402-405

[34] Meenhorst PL, Mulder JD. The chest X-ray in Legionella pneumoniae (Legionnaire's disease). Eur J Radiol 1983; 3:180-186

[35] Miller AC. Early clinical differentiation between Legionnaire's disease and other sporadic pneumonias. Ann Intern Med 1979; 90:526-528

(*) From the Departments of Internal Medicine (Drs. Tan, Tan, and File) and Radiology (Dr. Hamor), Summa Health System, Akron, OH; and the Centers for Disease Control and Prevention (Dr. Breiman), Atlanta, GA.

Manuscript received April 15, 1999; revision accepted August 9, 1999.

Part of this study was supported by a grant from the Centers for Disease Control and Prevention.

Correspondence to: James S. Tan, MD, 75 Arch St, Suite 105, Akron, OH 44304; e-mail:

COPYRIGHT 2000 American College of Chest Physicians
COPYRIGHT 2000 Gale Group

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