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Legionnaires' Disease

Infectious Diseases · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

An acute, sometimes fatal, pneumonia-like bacterial infection characterized by high fever, malaise, muscle aches, respiratory disorders and headache.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (657 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

An acute, sometimes fatal, pneumonia-like bacterial infection characterized by high fever, malaise, muscle aches, respiratory disorders and headache. It is named for an outbreak at the 1976 Philadelphia convention of the American Legion.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Disease, Legionnaires'; Legionnaire's Disease; Legionnaires Disease; Legionnaire Disease; Disease, Legionnaire; Infections, Legionella pneumophila; Infection, Legionella pneumophila; Legionella pneumophila Infection.

Where it fits in the MeSH classification

Broader topics
Legionellosis

Research landscape

PubMed indexes 5,258 records tagged with the MeSH heading “Legionnaires' Disease” (counts retrieved 2026-10-29). 547 of them (10.4%) were published from 2020 onward, and the busiest period so far is through 1999 with 2,623 records.

Reviews account for 556 records (10.6%) and meta-analyses for 5. Randomized controlled trials number 12 (0.2%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 2,623 records; 2000-2009: 1,075 records; 2010-2019: 1,013 records; 2020 onward: 547 records2,623through 19991,0752000-20091,0132010-20195472020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19992,623
2000-20091,075
2010-20191,013
2020 onward547
Share of records by publication typeReviews: 10.6 percent; Meta-analyses: 0.1 percent; Randomized controlled trials: 0.2 percentReviews10.6% (556)Meta-analyses0.1% (5)Randomized controlled trials0.2% (12)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 5,258 PubMed records
TypeRecordsShare
Reviews55610.6%
Meta-analyses50.1%
Randomized controlled trials120.2%

Method: PubMed query "Legionnaires' Disease"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in infectious diseases

Infectious disease evidence combines microbiology, epidemiology and clinical trials. Laboratory studies identify pathogens and how they cause harm; surveillance and outbreak investigations describe who is affected and how infection spreads; trials establish whether treatments and vaccines work. Results depend on place and time, because pathogens evolve and resistance patterns and population immunity change. Check when and where the data were collected, how cases were defined and how up to date the evidence is.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
IFNs Modify the Proteome of Legionella-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid
Naujoks J, Tabeling C, Dill BD, Hoffmann C, Brown AS, Kunze M, et al.
2016Research article
Design not recorded in structured metadata
231cc by
PMID 26829557 · DOI · PMC4734697
Legionnaires' disease in Europe, 2011 to 2015
Beauté J, The European Legionnaires' Disease Surveillance Network
2017Research article
Design not recorded in structured metadata
96cc by
PMID 28703097 · DOI · PMC5508329
Pathogenicity and Virulence of Legionella: Intracellular replication and host response
Chauhan D, Shames SR
2021Review article
Design not recorded in structured metadata
90cc by
PMID 33843434 · DOI · PMC8043192
Clinical, laboratory, and radiological features of community-acquired pneumonia due to Chlamydia psittaci and Legionella pneumophila confirmed using next-generation sequencing
Cheng R, Deng Z, Lin F, Zhang B, Liang J, Lu M
2026Research article
Design not recorded in structured metadata
2cc by
PMID 41684123 · DOI · PMC12912205

IFNs Modify the Proteome of Legionella-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid [1]

Research article Naujoks J, Tabeling C, Dill BD, Hoffmann C, Brown AS, Kunze M, et al. · · 2016 · cited 231 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Macrophages can be niches for bacterial pathogens or antibacterial effector cells depending on the pathogen and signals from the immune system.
Closing excerpt
IRG1 or its product itaconic acid might be therapeutically targetable to fight intracellular and drug-resistant bacteria.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (158 words)

Macrophages can be niches for bacterial pathogens or antibacterial effector cells depending on the pathogen and signals from the immune system. Here we show that type I and II IFNs are master regulators of gene expression during Legionella pneumophila infection, and activators of an alveolar macrophage-intrinsic immune response that restricts bacterial growth during pneumonia. Quantitative mass spectrometry revealed that both IFNs substantially modify Legionella-containing vacuoles, and comparative analyses reveal distinct subsets of transcriptionally and spatially IFN-regulated proteins. Immune-responsive gene (IRG)1 is induced by IFNs in mitochondria that closely associate with Legionella-containing vacuoles, and mediates production of itaconic acid. This metabolite is bactericidal against intravacuolar L. pneumophila as well as extracellular multidrug-resistant Gram-positive and -negative bacteria. Our study explores the overall role IFNs play in inducing substantial remodeling of bacterial vacuoles and in stimulating production of IRG1-derived itaconic acid which targets intravacuolar pathogens. IRG1 or its product itaconic acid might be therapeutically targetable to fight intracellular and drug-resistant bacteria.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 26829557 · DOI · PMC4734697

Legionnaires' disease in Europe, 2011 to 2015 [2]

Research article Beauté J, The European Legionnaires' Disease Surveillance Network · · 2017 · cited 96 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Under the coordination of the European Centre for Disease Prevention and Control (ECDC), the European Legionnaires' disease Surveillance Network (ELDSNet) conducts surveillance of Legionnaires' disease (LD) in Europe.
Closing excerpt
5/100,000 population.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (198 words)

Under the coordination of the European Centre for Disease Prevention and Control (ECDC), the European Legionnaires' disease Surveillance Network (ELDSNet) conducts surveillance of Legionnaires' disease (LD) in Europe. Between 2011 and 2015, 29 countries reported 30,532 LD cases to ECDC (28,188 (92.3%) confirmed and 2,344 (7.7%) probable). Four countries (France, Germany, Italy and Spain) accounted for 70.3% of all reported cases, although their combined populations represented only 49.9% of the study population. The age-standardised rate of all cases increased from 0.97 cases/100,000 population in 2011 to 1.30 cases/100,000 population in 2015, corresponding to an annual average increase of 0.09 cases/100,000 population (95%CI 0.02-0.14; p = 0.02). Demographics and infection setting remained unchanged with ca 70% of cases being community-acquired and 80% occurring in people aged 50 years and older. Clinical outcome was known for 23,164 cases, of whom 2,161 (9.3%) died. The overall case fatality ratio decreased steadily from 10.5% in 2011 to 8.1% in 2015, probably reflecting improved reporting completeness. Five countries (Austria, Czech Republic, Germany, Italy, and Norway) had increasing age-standardised LD notification rates over the 2011-15 period, but there was no increase in notification rates in countries where the 2011 rate was below 0.5/100,000 population.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 28703097 · DOI · PMC5508329

Pathogenicity and Virulence of Legionella: Intracellular replication and host response [3]

Review article Chauhan D, Shames SR · · 2021 · cited 90 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Bacteria of the genus Legionella are natural pathogens of amoebae that can cause a severe pneumonia in humans called Legionnaires' Disease.
Closing excerpt
pneumophila, the implications of Legionella genome diversity and future avenues for the field.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (116 words)

Bacteria of the genus Legionella are natural pathogens of amoebae that can cause a severe pneumonia in humans called Legionnaires' Disease. Human disease results from inhalation of Legionella-contaminated aerosols and subsequent bacterial replication within alveolar macrophages. Legionella pathogenicity in humans has resulted from extensive co-evolution with diverse genera of amoebae. To replicate intracellularly, Legionella generates a replication-permissive compartment called the Legionella-containing vacuole (LCV) through the concerted action of hundreds of Dot/Icm-translocated effector proteins. In this review, we present a collective overview of Legionella pathogenicity including infection mechanisms, secretion systems, and translocated effector function. We also discuss innate and adaptive immune responses to L. pneumophila, the implications of Legionella genome diversity and future avenues for the field.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33843434 · DOI · PMC8043192

Clinical, laboratory, and radiological features of community-acquired pneumonia due to Chlamydia psittaci and Legionella pneumophila confirmed using next-generation sequencing [4]

Research article Cheng R, Deng Z, Lin F, Zhang B, Liang J, Lu M · · 2026 · cited 2 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Background and objectiveChlamydia psittaci and Legionella pneumophila are common atypical pathogens that cause severe community-acquired pneumonia (CAP).
Closing excerpt
The observational finding that both pathogens respond to azithromycin and cause severe disease when left undetected underscore the value of guideline-recommended β-lactams/macrolide combination therapy in CAP settings, particularly where these intracellular pathogens remain undiagnosed without NGS.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (185 words)

Background and objectiveChlamydia psittaci and Legionella pneumophila are common atypical pathogens that cause severe community-acquired pneumonia (CAP). This study aimed to compare the clinical features and outcomes of Chlamydia psittaci pneumonia (CPP) and Legionella pneumophila pneumonia (LPP) identified using next-generation sequencing (NGS) for accurate identification.MethodsThis retrospective study included 68 patients with CPP and 42 patients with LPP. All cases were confirmed by metagenomic or targeted next-generation sequencing (mNGS/tNGS) of bronchoalveolar lavage fluid, serum, or sputum samples.ResultsPatients with LPP had a higher prevalence of diabetes and were predominantly male. Poultry contact was common in CPP (64.7% vs. 14.3%), whereas recent travel was associated with LPP (47.6% vs. 2.9%). LPP presented with increased extrapulmonary symptoms. Inflammatory marker levels were higher in LPP, including leukocytosis, neutrophilia, C-reactive protein, and procalcitonin (all p ConclusionLPP demonstrated greater initial clinical and laboratory severity compared to CPP. Under NGS-guided targeted therapy, both groups achieved comparable outcomes. The observational finding that both pathogens respond to azithromycin and cause severe disease when left undetected underscore the value of guideline-recommended β-lactams/macrolide combination therapy in CAP settings, particularly where these intracellular pathogens remain undiagnosed without NGS.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 41684123 · DOI · PMC12912205

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Legionella and Legionnaires' disease: 25 years of investigation [5]
    Fields BS, Benson RF, Besser RE · Clin Microbiol Rev · 2002 · cited 1,112 times (Europe PMC)
  • Research article Legionnaires' disease [6]
    Cunha BA, Burillo A, Bouza E · Lancet · 2016 · cited 411 times (Europe PMC)
  • Research article Legionellosis [7]
    Stout JE, Yu VL · N Engl J Med · 1997 · cited 324 times (Europe PMC)
  • Research article Epidemiology and clinical management of Legionnaires' disease [8]
    Phin N, Parry-Ford F, Harrison T, Stagg HR, Zhang N, Kumar K, et al. · Lancet Infect Dis · 2014 · cited 302 times (Europe PMC)
  • Research article Differentiate to thrive: lessons from the Legionella pneumophila life cycle [9]
    Molofsky AB, Swanson MS · Mol Microbiol · 2004 · cited 252 times (Europe PMC)
  • Research article Current and emerging Legionella diagnostics for laboratory and outbreak investigations [10]
    Mercante JW, Winchell JM · Clin Microbiol Rev · 2015 · cited 222 times (Europe PMC)

References

  1. Naujoks J, Tabeling C, Dill BD, Hoffmann C, Brown AS, Kunze M, et al.. IFNs Modify the Proteome of Legionella-Containing Vacuoles and Restrict Infection Via IRG1-Derived Itaconic Acid. . 2016. PMID 26829557 · DOI · PMC4734697
  2. Beauté J, The European Legionnaires' Disease Surveillance Network. Legionnaires' disease in Europe, 2011 to 2015. . 2017. PMID 28703097 · DOI · PMC5508329
  3. Chauhan D, Shames SR. Pathogenicity and Virulence of Legionella: Intracellular replication and host response. . 2021. PMID 33843434 · DOI · PMC8043192
  4. Cheng R, Deng Z, Lin F, Zhang B, Liang J, Lu M. Clinical, laboratory, and radiological features of community-acquired pneumonia due to Chlamydia psittaci and Legionella pneumophila confirmed using next-generation sequencing. . 2026. PMID 41684123 · DOI · PMC12912205
  5. Fields BS, Benson RF, Besser RE. Legionella and Legionnaires' disease: 25 years of investigation. Clin Microbiol Rev. 2002. PMID 12097254 · DOI · PMC118082
  6. Cunha BA, Burillo A, Bouza E. Legionnaires' disease. Lancet. 2016. PMID 26231463 · DOI
  7. Stout JE, Yu VL. Legionellosis. N Engl J Med. 1997. PMID 9278466 · DOI
  8. Phin N, Parry-Ford F, Harrison T, Stagg HR, Zhang N, Kumar K, et al.. Epidemiology and clinical management of Legionnaires' disease. Lancet Infect Dis. 2014. PMID 24970283 · DOI
  9. Molofsky AB, Swanson MS. Differentiate to thrive: lessons from the Legionella pneumophila life cycle. Mol Microbiol. 2004. PMID 15225301 · DOI · PMC13218203
  10. Mercante JW, Winchell JM. Current and emerging Legionella diagnostics for laboratory and outbreak investigations. Clin Microbiol Rev. 2015. PMID 25567224 · DOI · PMC4284297

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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At a glance

5,258
PubMed records on this heading
10%
published since 2020
556
review articles
12
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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