The spectrum of legionnaires’ disease: a case series illustrating clinical diversity and outcomes

Introduction

Background

Respiratory infections remain a leading cause of death worldwide, with the burden expected to increase as global populations age and the prevalence of comorbid conditions rises (1). Legionella species cause two distinct clinical entities: Pontiac fever, a self-limited flu-like illness, and Legionnaires’ disease, a severe and potentially fatal atypical pneumonia (2). Legionella pneumophila is responsible for over 90% of Legionnaires’ disease cases, with serogroup 1 accounting for approximately 84% of all infections and being implicated in both sporadic cases and outbreaks (3-5).

The Centers for Disease Control and Prevention reports that Legionnaires’ disease incidence has steadily increased since the early 2000s, with current rates of 2 to 3 cases per 100,000 population in the United States (6). In 2021 alone, 8,442 cases of legionellosis were reported across the United States and territories (6). Retrospective analysis of 1,426 legionellosis cases revealed that 44% required intensive care unit admission, 27% required mechanical ventilation, and 9% died (7).

The disease is associated with substantial economic burden, with per-patient costs reaching $34,000 and total hospitalization costs exceeding $433,000 (8,9).

Rationale and knowledge gap

Despite being recognized for over 40 years, clinical awareness regarding the variable presentations of Legionnaires’ disease remains suboptimal among healthcare providers (10,11). The atypical presentation patterns, including gastrointestinal predominance and extrapulmonary manifestations, coupled with diagnostic limitations of standard urinary antigen testing (which only detects serogroup 1), contribute to underdiagnosis and delayed treatment initiation.

Objective

This case series describes the clinical presentation, diagnostic findings, laboratory abnormalities, imaging characteristics, and outcomes of five patients with confirmed Legionnaires’ disease to enhance clinical awareness and emphasize the importance of maintaining high clinical suspicion in patients presenting with atypical pneumonia. All patients presented to a community teaching hospital. Cases are summarized on Table 1.

This is a retrospective study of selected cases that have presented to an eastern Pennsylvania community hospital with data collection and analysis occurring between March and November 2025. We present this article in accordance with the AME Case Series reporting checklist (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0020/rc).

Case presentation

Case 1

A 70-year-old male with past medical history of peripheral artery disease, hypertension, alcohol use disorder, and tobacco abuse presented with a 3-week history of generalized weakness and poor oral intake due to anorexia. Notably, the patient did not report significant respiratory symptoms, denying cough, shortness of breath, or sputum production. Environmental exposures included a decorative pond in his yard, a swimming pool, a basement with a sump pump, and recent ductwork in an air conditioning unit.

On initial evaluation, the patient was hypotensive (70/50 mmHg), which improved with crystalloid administration. Physical examination revealed decreased breath sounds at the right base with rhonchi in the same region.

Laboratory findings demonstrated leukocytosis (white blood cell count 19.5×10³/µL with 40% bands), elevated lactic acid (2.2 mmol/L), hypokalemia (2.8 mEq/L), hypomagnesemia (1.5 mg/dL), and acute kidney injury (creatinine 1.5 mg/dL; baseline 0.9 mg/dL). Procalcitonin was elevated at 7.1 ng/mL. Chest imaging revealed bilateral ground glass opacities with right predominance concerning for pneumonia (Figure 1).

Figure 1 Case 1: chest X-ray with right-sided consolidation and bilateral ground-glass opacities concerning ARDS. ARDS, acute respiratory distress syndrome.

The patient was hospitalized and initiated on piperacillin-tazobactam. Legionella urinary antigen testing returned positive, prompting transition to intravenous levofloxacin. Despite initial improvement with fluid resuscitation, the patient rapidly developed recurrent hypotension and septic shock on day 1 with acute hypoxic respiratory failure requiring intubation and mechanical ventilation. He subsequently developed acute respiratory distress syndrome (ARDS) managed with lung-protective ventilation strategies. After a 10-day hospitalization, he was successfully extubated but experienced critical illness myopathy and hyperactive delirium. He was discharged to acute rehabilitation for further recovery after 10 days.

Case 2

An 83-year-old male with significant past medical history including hypertension, hyperlipidemia, diabetes mellitus, chronic obstructive pulmonary disease (COPD), heart failure with preserved ejection fraction (50%), mitral regurgitation, pulmonary hypertension, tricuspid regurgitation, and coronary artery disease status post coronary artery bypass grafting presented with generalized weakness, malaise, and a 3-day history of dyspnea requiring two pillows for sleep (orthopnea). He reported worsening sputum production.

Initial vital signs revealed hypotension (73/40 mmHg), tachycardia (127 beats per minute), and hypoxemia (oxygen saturation 75% on room air). Laboratory evaluation showed leukocytosis (18,000/µL with neutrophilic predominance), mild anemia (hemoglobin 10.8 g/dL; baseline 13 g/dL), hyponatremia (sodium 126 mEq/L; baseline 134 mEq/L), and elevated B-type natriuretic peptide (2,240 pg/mL). Procalcitonin was 2.6 ng/mL. Chest radiographs revealed right sided infiltrate in the lower lobe (Figure 2A,2B).

Figure 2 Case 2: chest X-rays on day 1. PA (A) and lateral (B) with right lower lobe consolidation. PA, posterior-anterior.

The patient was initiated on ceftriaxone and azithromycin. Legionella urinary antigen testing returned positive, and azithromycin was continued. Despite antimicrobial therapy and diuresis with intravenous furosemide, the patient developed worsening acute hypoxic and hypercapnic respiratory failure. He required intubation, mechanical ventilation, and pulmonary artery catheterization for hemodynamic monitoring. Progressive mixed septic and cardiogenic shock with severe mitral valve regurgitation ensued despite maximal vasopressor and inotropic support. Multiorgan dysfunction developed, culminating in pulseless electrical activity cardiac arrest. The patient expired on hospital day 3.

Case 3

A 76-year-old female with history of hypertension presented with a 2-day history of cough, dyspnea, and fever associated with generalized weakness, fatigue, malaise, and chills. Respiratory symptoms included dyspnea on exertion and predominantly dry cough. The patient denied sick contacts, recent travel, water leakages at home, or exposure to aerosolized water.

Physical examination revealed crackles in the right lung fields. Vital signs showed hypoxemia (oxygen saturation 88% on room air) but the patient was afebrile and hemodynamically stable.

Laboratory studies demonstrated leukocytosis (13,000/µL with neutrophilic predominance), hyponatremia (sodium 130 mEq/L), and procalcitonin elevation (3.1 ng/mL). Chest radiography showed a right middle lobe infiltrate (Figure 3A,3B).

Figure 3 Case 3: chest X-ray on day 1. PA (A) and lateral (B) with right middle lobe consolidation. PA, posterior-anterior.

The patient was hospitalized and initiated on ceftriaxone and azithromycin. Legionella urinary antigen testing returned positive, and she was transitioned to azithromycin monotherapy. She responded favorably to treatment and was discharged after 4 days of hospitalization.

Case 4

A 63-year-old female with past medical history of hypertension, rheumatoid arthritis on prednisone 10 mg daily, and gastroesophageal reflux disease presented with a 2-day history of profuse watery diarrhea associated with significant weakness, fatigue, and fever (103.5 ℉). She reported no prior dietary indiscretions except for a salad shared with friends, none of whom were symptomatic. Notably, she denied any respiratory symptoms.

On initial evaluation, the patient was febrile (103.5 ℉) and tachypneic (respiratory rate 20 breaths per minute) but hemodynamically stable with normal oxygen saturation (96% on room air). Laboratory studies were largely unremarkable; however, urinalysis revealed pyuria with negative urine culture. Arterial blood gas analysis showed mild alkalemia [pH 7.5, partial pressure of carbon dioxide (PCO₂) 24 mmHg, partial pressure of oxygen (PO₂) 70 mmHg]. Procalcitonin was mildly elevated at 0.9 ng/mL.

Despite no significant infiltrates on chest radiography (Figure 4A,4B), and abdominal computed tomography not revealing significant intra-abdominal pathology, that test incidentally visualized the lower chest demonstrating a right lower lobe consolidation (Figure 4C). Given this finding and the patient’s septic presentation, Legionella urinary antigen testing was obtained and returned positive. The patient was treated with intravenous levofloxacin with complete resolution of symptoms. She was discharged after 3 days.

Figure 4 Case 4: chest X-ray on day 1. PA (A) and lateral (B)—with no significant infiltrate; however, the upper slices of an abdominal CT (C) reveal a RLL consolidation. CT, computed tomography; PA, posterior-anterior; RLL, right lower lobe.

Case 5

A 38-year-old previously healthy male presented with productive cough and fever. He had presented to the emergency department 3 days prior with similar symptoms and was diagnosed with pneumonia as chest radiography was concerning for right middle and right lower lobe infiltrates (Figure 5A,5B), and initiated on amoxicillin-clavulanate. Despite adherence to the prescribed antibiotic course, he experienced no clinical improvement over 3 days, with persistent cough, sputum production, generalized weakness, and fatigue. He presented to the emergency department again with documented fever (102 ℉).

Figure 5 Case 5: chest X-ray on day 1. PA (A) and lateral (B) with evidence of right middle and right lower lobe pneumonia. PA, posterior-anterior.

Physical examination revealed crackles at the right hemithorax base.

The patient was hospitalized with presumed community-acquired pneumonia and initiated on ceftriaxone and azithromycin. Laboratory studies revealed normal white blood cell count and normal chemistry panel. Procalcitonin was mildly elevated at 1.3 ng/mL. Legionella urinary antigen testing returned positive. He was switched to intravenous levofloxacin and improved significantly. He was discharged after an uneventful hospitalization course of 3 days.

Ethical statement

All procedures performed in this article were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case series was not obtained from the patients or their relatives after all reasonable attempts were made to contact them.

Discussion

Key findings

This case series encompasses five patients with confirmed Legionnaires’ disease, demonstrating the heterogeneity of clinical presentation while reinforcing established epidemiologic, clinical, and diagnostic principles reported in the medical literature (Table 1).

The cases presented align closely with existing literature regarding disease epidemiology and microbiology (12,13). In most instances, identifiable environmental exposure to water sources was documented (Cases 1, 3, and 5), consistent with the established understanding that Legionella species preferentially colonize warm, stagnant water environments including water distribution systems, biofilms on pipes, showers, ponds, whirlpool spas, cooling towers, and air-conditioning systems (14). Person-to-person transmission remains exceptionally rare, with only a single case reported in the literature (15).

Clinical presentations aligned with established patterns: patients demonstrated combinations of respiratory symptoms (cough, dyspnea), systemic manifestations (high-grade fever, fatigue, myalgia), and extrapulmonary features (diarrhea, hyponatremia, headache) (16,17). Imaging findings of unilateral or bilateral infiltrates on chest radiography or computed tomography with rapid progression to consolidation were consistent with typical Legionnaires’ disease presentations (16,17).

Laboratory abnormalities observed in this series paralleled literature findings. Leukocytosis, elevated inflammatory markers, and hyponatremia were frequently encountered. Notably, hyponatremia occurred in 40% of our cases (Cases 2, and 3), which is in line with the baseline prevalence of hyponatremia in Legionnaires’ disease (44.8%) and significantly exceeds rates in other pneumonia types (8.2%) (18). This finding underscores the importance of electrolyte screening in suspected Legionnaires’ disease.

Diagnostic confirmation in all cases was achieved via urinary antigen testing [enzyme immunoassay (EIA) method], detecting Legionella pneumophila serogroup 1, consistent with current practice patterns. The urinary antigen test remains the most widely utilized diagnostic method due to its high sensitivity (69–100%), excellent specificity (99–100%), ease of performance, and rapid turnaround time (19-21). However, a critical limitation is its detection of only serogroup 1. Serogroup 1 accounts for about 80% of disease cases; thus, about 20% of cases caused by other clinically significant serotypes or other Legionella species (L. micdadei, L. longbeachae) may be missed. In addition to that, a large multicenter study found 44.4% of urine antigen test (UAT)-negative results were actually Legionella-positive by polymerase chain reaction (19,22).

Unique aspects and atypical presentations

While our cases generally aligned with established literature, they also demonstrated important variations and atypical features. Most notably, Case 4 presented primarily with gastrointestinal symptoms (profuse diarrhea and constitutional symptoms) without significant respiratory complaints at initial evaluation, with pneumonia identified only incidentally on imaging obtained for abdominal pathology evaluation. This presentation, while less common, has been documented in the literature and represents an important clinical pearl regarding the variable presentation patterns of Legionnaires’ disease (16,17).

Case 5 represented an atypical clinical scenario wherein a previously healthy young adult (38 years old) without significant comorbidities developed Legionnaires’ disease and did not respond to community-acquired pneumonia coverage with beta-lactam/beta-lactamase inhibitor combination therapy. This case highlights the importance of considering atypical pathogens, particularly Legionella, when community-acquired pneumonia fails to improve with standard beta-lactam therapy.

Strengths and limitations

Strengths of this series include institutional confirmation of Legionella disease in five patients, detailed clinical, laboratory, and radiographic documentation for each case, and identification of environmental exposures in most instances. The series captures the full spectrum of disease outcomes, from uncomplicated pneumonia to fatal septic and cardiogenic shock.

Limitations include the retrospective nature of case documentation, reliance solely on urinary antigen testing (which detects only serogroup 1, potentially missing other Legionella infections), inability to perform serotyping or additional molecular testing in most cases, lack of respiratory cultures, and lack of bronchoalveolar lavage data. The limited sample size (n=5) restricts generalization of findings. Additionally, Case 2’s fatal outcome involved multiple complex comorbidities, making attribution of death specifically to Legionella infection versus overwhelming infection in a fragile host with cardiac disease challenging.

Comparison with similar research

Our findings align with epidemiologic data demonstrating that advanced age and multiple comorbidities substantially increase mortality risk from Legionnaires’ disease (7). The case with fatal outcome (Case 2) involved an 83-year-old with extensive comorbidities including advanced heart failure, coronary artery disease, COPD, and diabetes, consistent with literature identifying advanced age and multiple comorbidities as predictors of poor outcomes (7,23).

The variable clinical presentation observed in our series mirrors literature findings emphasizing that Legionnaires’ disease encompasses a spectrum of severity ranging from mild disease to life-threatening pneumonia with septic shock, ARDS, and multiorgan dysfunction (12,16). The occurrence of ARDS in Case 1, while representing severe disease, has been well-documented in the literature and represents approximately 20–30% of severe Legionnaires’ disease cases (24).

The treatment responses in our series were consistent with current evidence demonstrating equivalent efficacy between macrolides (azithromycin) and fluoroquinolones (levofloxacin) in Legionnaires’ disease (25). Most patients responded favorably to these agents, with the notable exception of Case 2, where death resulted from overwhelming septic and cardiogenic shock despite appropriate antimicrobial coverage—a scenario that aligns with literature findings that treatment failure occurs predominantly in elderly patients with severe underlying comorbidities (25,26).

Explanations of findings

The predominance of right lower lobe infiltrates observed in our cases (Cases 1, 2, 4, 5) likely reflects the gravitational effect on bacterial seeding during aspiration or inhalation, consistent with typical pneumonia distributions. The variable clinical presentations reflect the pleomorphic nature of Legionnaires’ disease pathogenesis, whereby the organism triggers both direct infectious pneumonitis and inflammatory host responses affecting multiple organ systems.

Hyponatremia, observed in 40% of our patients in our series, was in the past believed to be secondary to Legionella-induced inappropriate antidiuretic hormone (SIADH) secretion, however recent literature challenges that as patients with hyponatremia in the setting of Legionnaires’ disease often have normal CT-ProVasopressin levels (18). Currently an alternative explanation for the observed hyponatremia would be renal salt wasting due to direct proximal tubular disfunction leading to Fanconi syndrome (27). This is an important consideration given that, unlike SIADH, this type of hyponatremia should improve with crystalloid fluids which are typically given during early stages of sepsis resuscitation.

Implications and actions needed

These cases underscore several critical clinical implications. First, heightened clinical suspicion for Legionnaires’ disease should be maintained when encountering atypical presentations of pneumonia, particularly in patients with risk factors (advanced age, immunosuppression, comorbidities) or identifiable water exposure. Second, community-acquired pneumonia coverage with beta-lactams alone may not be sufficient – when treating pneumonia, the clinician should consider atypical pathogen coverage either with macrolides or respiratory fluoroquinolones, particularly if clinical response is inadequate. Guidelines for community-acquired pneumonia already emphasize the need for atypical coverage particularly in patients with comorbidities (28). Third, comprehensive metabolic panels should be obtained in suspected Legionnaires’ disease, with attention to hyponatremia as a marker of disease severity. Fourth, environmental investigation and remediation are warranted when Legionnaires’ disease is confirmed, particularly in healthcare or hospitality settings, to prevent additional cases.

Future research should prioritize expanded diagnostic testing beyond urinary antigen detection, including routine polymerase chain reaction (PCR) or molecular methods that can identify non-serogroup 1 Legionella species and thereby reduce underdiagnosis. Public health agencies should maintain heightened surveillance for Legionella outbreaks, particularly in settings with complex water systems prone to colonization and aerosolization.

Conclusions

This case series illustrates the significant clinical heterogeneity of Legionnaires’ disease while reinforcing critical diagnostic and management principles. The variable clinical presentations—ranging from predominantly gastrointestinal symptoms to severe septic shock with ARDS—highlight the importance of maintaining a high index of clinical suspicion when evaluating patients with atypical pneumonia, particularly those with risk factors including advanced age, immunosuppression, comorbid conditions, or environmental exposures to aerosolized water sources.

Early diagnostic testing with urinary antigen detection, despite its limitations regarding serotype specificity, remains essential for confirming Legionella infection. Prompt initiation of appropriate antimicrobial therapy with respiratory fluoroquinolones or macrolides significantly improves outcomes in most patients; however, severe comorbidities and advanced age substantially increase mortality risk, as exemplified by Case 2.

Continued clinical awareness, appropriate diagnostic vigilance, and timely antimicrobial intervention are paramount to reducing morbidity and mortality associated with this potentially fatal infection.

Acknowledgments

We would like to thank the nursing and respiratory therapy staff who provided exceptional care for these patients. We acknowledge the clinical microbiology laboratory personnel whose prompt identification and reporting of Legionella antigen results facilitated timely diagnosis and treatment modification.

Footnote

Reporting Checklist: The authors have completed the AME Case Series reporting checklist. Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0020/rc

Peer Review File: Available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0020/prf

Funding: None.

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://acr.amegroups.com/article/view/10.21037/acr-2026-0020/coif). The authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this article were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Declaration of Helsinki and its subsequent amendments. Written informed consent for publication of this case series was not obtained from the patients or their relatives after all reasonable attempts were made to contact them.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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