Legionella species are gram-negative rod-shaped γ-proteobacteria that are ubiquitously found in freshwater environments, as well as in moist soil and composted material[1]. Human infection most commonly occurs as a consequence of inhaling Legionella-containing aerosols generated by contaminated manmade water sources, such as showers, hot tubs, plumbing networks, and air-conditioning systems[2]. Individuals at higher risk for developing Legionnaires’ disease are males older than 50 years, smokers, and people with an underlying medical condition such as diabetes, cancer, or immuno suppression[3]. Summer and early fall are the most common times of the year for Legionella infection to occur.
The genus Legionella contains about 65 species and is organized in more than 70 serogroups. However, not all of them are equally responsible for the laboratory-confirmed cases of Legionnaires’ disease (LD) worldwide[4, 5]. The overwhelming majority of clinical infections (~90%) are caused by a single species, L. pneumophila, and strains of serogroup 1 are responsible for approximately 90% of cases. The next most common etiological agents of LD are L. longbeachae, L. bozemanii and L. micdadei, which account for 2–7% of infections worldwide[6]. L. longbeachae is the leading cause of LD (~30%) in Australia and New Zealand and is the only species naturally found in soil[7]. In comparison to L. pneumophila, pneumonia caused by non-pneumophila Legionella (non-Lpn) species are rare and almost exclusively nosocomial[6].
Legionella species are ubiquitous in the environment, and amoebae are their natural hosts[8]. Amoebae serve a dual role for Legionella by providing both a niche for intracellular replication and protection from harsh conditions of the environment including antibiotics, chemicals, heat, and osmotic stress[9]. Legionella’s environmental persistence is also due to colonization of interspecies biofilms in both natural and built freshwater environments. The phenotypic variation in biofilms is controlled by Legionella quorum sensing (Lqs) system along with a transcription factor, LvbR, and the temperature[10].
Legionella species encode a highly conserved type IVB secretion system (T4SS) called Dot/Icm (defective for organelle trafficking/intracellular multiplication)[11]. The Dot/Icm T4SS is essential for intracellular replication, and functions to translocate hundreds of bacterial virulence factors, termed effector proteins, directly into host cells. Dot/Icm-translocated effectors have diverse functions and biochemical activities but broadly act to subvert lysosomal bacterial degradation and acquire nutrients from the host cell. Despite conservation of the Dot/Icm T4SS and relative abundance of effector genes, there is extensive interspecies variation in translocated effector repertoires[11].
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[1] Newton H J, Ang D K, van Driel I R, et al. Molecular pathogenesis of infections caused by Legionella pneumophila[J]. Clin Microbiol Rev, 2010, 23(2): 274-98.
[2] Blatt S P, Parkinson M D, Pace E, et al. Nosocomial Legionnaires' disease: aspiration as a primary mode of disease acquisition[J]. Am J Med, 1993, 95(1): 16-22.
[3] Cunha C B, Cunha B A. Legionnaire's Disease Since Philadelphia: Lessons Learned and Continued Progress[J]. Infect Dis Clin North Am, 2017, 31(1): 1-5.
[4] Laura G V, Alvaro C O, Iñaki C, et al. Evolutionary Dissection of the Dot/Icm System Based on Comparative Genomics of 58 Legionella Species[J]. Genome Biology and Evolution, 2019, (9): 9.
[5] Khodr A, Kay E, Gomez-Valero L, et al. Molecular epidemiology, phylogeny and evolution of Legionella[J]. Infection Genetics & Evolution Journal of Molecular Epidemiology & Evolutionary Genetics in Infectious Diseases, 2016, 43: 108-122.
[6] Muder R R, Yu V L. Infection due to Legionella species other than L. pneumophila[J]. Clin Infect Dis, 2002, 35(8): 990-8.
[7] Mondino S, Schmidt S, Rolando M, et al. Legionnaires' Disease: State of the Art Knowledge of Pathogenesis Mechanisms of Legionella[J]. Annu Rev Pathol, 2020, 15: 439-466.
[8] Chauhan D, Shames S R. Pathogenicity and Virulence of Legionella: Intracellular replication and host response[J]. Virulence, 2021, 12(1): 1122-1144.
[9] Hoffmann C, Harrison C F, Hilbi H. The natural alternative: protozoa as cellular models for Legionella infection[J]. Cell Microbiol, 2014, 16(1): 15-26.
[10] Personnic N, Striednig B, Hilbi H. Quorum sensing controls persistence, resuscitation, and virulence of Legionella subpopulations in biofilms[J]. Isme j, 2021, 15(1): 196-210.
[11] Gomez-Valero L, Rusniok C, Carson D, et al. More than 18,000 effectors in the Legionella genus genome provide multiple, independent combinations for replication in human cells[J]. Proc Natl Acad Sci U S A, 2019, 116(6): 2265-2273.