scholarly journals Wild ciliates differ in susceptibility to Legionella pneumophila JR32

Microbiology ◽  
2021 ◽  
Vol 167 (8) ◽  
Author(s):  
Airi Kawashiro ◽  
Torahiko Okubo ◽  
Shinji Nakamura ◽  
Jeewan Thapa ◽  
Masaki Miyake ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Deletion Mutant ◽  
Virulence Genes ◽  
Reference Strain ◽  
Virulence Gene ◽  
Cyst Formation ◽  
Harsh Environments ◽  
Content Type ◽  
Pellet Production ◽  
Low Sensitivity

We investigated how Legionella pneumophila (Lp) JR32 interacts with Anteglaucoma CS11A and Colpoda E6, two ciliates that we isolated from sewage and sink trap sludge, respectively, using a handmade maze device containing a 96-well crafting plate. Our 18S rDNA-based phylogenetic analysis showed that Anteglaucoma CS11A and Colpoda E6 formed distinct clades. Scanning electron microscopy showed that Anteglaucoma CS11A had a bigger-sized body than Colpoda E6 and, unlike Tetrahymena IB (the reference strain), neither ciliate produced pellets, which are extracellular vacuoles. Fluorescence microscopic observations revealed that although the intake amounts differed, all three ciliates rapidly ingested LpJR32 regardless of the presence or absence of the icm/dot virulence genes, indicating that they all interacted with LpJR32. In co-cultures with Anteglaucoma CS11A, the LpJR32 levels were maintained but fell dramatically when the co-culture contained the LpJR32 icm/dot deletion mutant instead. Anteglaucoma CS11A died within 2 days of co-culture with LpJR32, but survived co-culture with the deletion mutant. In co-cultures with Colpoda E6, LpJR32 levels were maintained but temporarily decreased independently of the virulence gene. Concurrently, the Colpoda E6 ciliates survived by forming cysts, which may enable them to resist harsh environments, and by diminishing the sensitivity of trophozoites to Lp. In the Tetrahymena IB co-cultures with LpJR32 or Δicm/dot, the Lp levels were maintained, albeit with temporal decreases, and the Tetrahymena IB levels were also maintained. We conclude that unlike Tetrahymena IB with pellet production, Anteglaucoma CS11A can be killed by LpJR32 infection, and Colpoda E6 can resist LpJR32 infection through cyst formation and the low sensitivity of trophozoites to Lp. Thus, the two ciliates that we isolated had different susceptibilities to LpJR32 infection.

scholarly journals Indole Signaling at the Host-Microbiota-Pathogen Interface

mBio ◽  
2019 ◽  
Vol 10 (3) ◽  
Author(s):  
Aman Kumar ◽  
Vanessa Sperandio
Keyword(s):  
Gene Expression ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Enteric Pathogens ◽  
Bacterial Membrane ◽  
Gi Tract ◽  
Intestinal Tissue ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Membrane Bound

ABSTRACTMicrobial establishment within the gastrointestinal (GI) tract requires surveillance of the gut biogeography. The gut microbiota coordinates behaviors by sensing host- or microbiota-derived signals. Here we show for the first time that microbiota-derived indole is highly prevalent in the lumen compared to the intestinal tissue. This difference in indole concentration plays a key role in modulating virulence gene expression of the enteric pathogens enterohemorrhagicEscherichia coli(EHEC) andCitrobacter rodentium. Indole decreases expression of genes within the locus of enterocyte effacement (LEE) pathogenicity island, which is essential for these pathogens to form attaching and effacing (AE) lesions on enterocytes. We synthetically altered the concentration of indole in the GI tracts of mice by employing mice treated with antibiotics to deplete the microbiota and reconstituted with indole-producing commensalBacteroides thetaiotaomicron(B. theta) or aB. thetaΔtnaAmutant (does not produce indole) or by engineering an indole-producingC. rodentiumstrain. This allowed us to assess the role of self-produced versus microbiota-produced indole, and the results show that decreased indole concentrations promote bacterial pathogenesis, while increased levels of indole decrease bacterial virulence gene expression. Moreover, we identified the bacterial membrane-bound histidine sensor kinase (HK) CpxA as an indole sensor. Enteric pathogens sense a gradient of indole concentrations in the gut to probe different niches and successfully establish an infection.IMPORTANCEPathogens sense and respond to several small molecules within the GI tract to modulate expression of their virulence repertoire. Indole is a signaling molecule produced by the gut microbiota. Here we show that indole concentrations are higher in the lumen, where the microbiota is present, than in the intestinal tissue. The enteric pathogens EHEC andC. rodentiumsense indole to downregulate expression of their virulence genes, as a read-out of the luminal compartment. We also identified the bacterial membrane-bound HK CpxA as an indole sensor. This regulation ensures that EHEC andC. rodentiumexpress their virulence genes only at the epithelial lining, which is the niche they colonize.

scholarly journals Ciliates Expel Environmental Legionella-Laden Pellets To Stockpile Food

2012 ◽  
Vol 78 (15) ◽  
pp. 5247-5257 ◽  
Author(s):  
Fuhito Hojo ◽  
Daisuke Sato ◽  
Junji Matsuo ◽  
Masaki Miyake ◽  
Shinji Nakamura ◽  
...  
Keyword(s):  
Legionella Pneumophila ◽  
Lipid Accumulation ◽  
Membrane Integrity ◽  
Human Isolate ◽  
Dependent Manner ◽  
Optimal Conditions ◽  
Bacterial Strains ◽  
Content Type ◽  
Pellet Production ◽  
Morphological Studies

ABSTRACTWhenTetrahymenaciliates are cultured withLegionella pneumophila, the ciliates expel bacteria packaged in free spherical pellets. Why the ciliates expel these pellets remains unclear. Hence, we determined the optimal conditions for pellet expulsion and assessed whether pellet expulsion contributes to the maintenance of growth and the survival of ciliates. When incubated with environmentalL. pneumophila, the ciliates expelled the pellets maximally at 2 days after infection. Heat-killed bacteria failed to produce pellets from ciliates, and there was no obvious difference in pellet production among the ciliates or bacterial strains. Morphological studies assessing lipid accumulation showed that pellets contained tightly packed bacteria with rapid lipid accumulation and were composed of the layers of membranes; bacterial culturability in the pellets rapidly decreased, in contrast to what was seen in ciliate-free culture, although the bacteria maintained membrane integrity in the pellets. Furthermore, ciliates newly cultured with pellets were maintained and grew vigorously compared with those without pellets. In contrast, a humanL. pneumophilaisolate killed ciliates 7 days postinfection in a Dot/Icm-dependent manner, and pellets harboring this strain did not support ciliate growth. Also, pellets harboring the human isolate were resuscitated by coculturing with amoebae, depending on Dot/Icm expression. Thus, while ciliates expel pellet-packaged environmentalL. pneumophilafor stockpiling food, the pellets packaging the human isolate are harmful to ciliate survival, which may be of clinical significance.

scholarly journals Ethanolamine Controls Expression of Genes Encoding Components Involved in Interkingdom Signaling and Virulence in Enterohemorrhagic Escherichia coli O157:H7

mBio ◽  
2012 ◽  
Vol 3 (3) ◽  
Author(s):  
Melissa M. Kendall ◽  
Charley C. Gruber ◽  
Christopher T. Parker ◽  
Vanessa Sperandio
Keyword(s):  
Gene Expression ◽  
Escherichia Coli ◽  
Cell Signaling ◽  
Nitrogen Source ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Human Pathogen ◽  
Signaling Molecule ◽  
Content Type ◽  
Virulence Gene Expression

ABSTRACTBacterial pathogens must be able to both recognize suitable niches within the host for colonization and successfully compete with commensal flora for nutrients in order to establish infection. Ethanolamine (EA) is a major component of mammalian and bacterial membranes and is used by pathogens as a carbon and/or nitrogen source in the gastrointestinal tract. The deadly human pathogen enterohemorrhagicEscherichia coliO157:H7 (EHEC) uses EA in the intestine as a nitrogen source as a competitive advantage for colonization over the microbial flora. Here we show that EA is not only important for nitrogen metabolism but that it is also used as a signaling molecule in cell-to-cell signaling to activate virulence gene expression in EHEC. EA in concentrations that cannot promote growth as a nitrogen source can activate expression of EHEC’s repertoire of virulence genes. The EutR transcription factor, known to be the receptor of EA, is only partially responsible for this regulation, suggesting that yet another EA receptor exists. This important link of EA with metabolism, cell-to-cell signaling, and pathogenesis, highlights the fact that a fundamental means of communication within microbial communities relies on energy production and processing of metabolites. Here we show for the first time that bacterial pathogens not only exploit EA as a metabolite but also coopt EA as a signaling molecule to recognize the gastrointestinal environment and promote virulence expression.IMPORTANCEIn order to successfully cause disease, a pathogen must be able to sense a host environment and modulate expression of its virulence genes as well as compete with the indigenous microbiota for nutrients. Ethanolamine (EA) is present in the large intestine due to the turnover of intestinal cells. Here, we show that the human pathogenEscherichia coliO157:H7, which causes bloody diarrhea and hemolytic-uremic syndrome, regulates virulence gene expression through EA metabolism and by responding to EA as a signal. These findings provide the first information directly linking EA with bacterial pathogenesis.

scholarly journals Diverse Virulence Gene Content of Shiga Toxin-Producing Escherichia coli from Finishing Swine

2014 ◽  
Vol 80 (20) ◽  
pp. 6395-6402 ◽  
Author(s):  
Marion Tseng ◽  
Pina M. Fratamico ◽  
Lori Bagi ◽  
Sabine Delannoy ◽  
Patrick Fach ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Shiga Toxin ◽  
Virulence Genes ◽  
Genetic Relatedness ◽  
Virulence Gene ◽  
Health Concern ◽  
Limited Information ◽  
Content Type ◽  
Genes Encoding ◽  
Critical Public Health

ABSTRACTShiga toxin-producingEscherichia coli(STEC) infections are a critical public health concern because they can cause severe clinical outcomes, such as hemolytic uremic syndrome, in humans. Determining the presence or absence of virulence genes is essential in assessing the potential pathogenicity of STEC strains. Currently, there is limited information about the virulence genes carried by swine STEC strains; therefore, this study was conducted to examine the presence and absence of 69 virulence genes in STEC strains recovered previously from finishing swine in a longitudinal study. A subset of STEC strains was analyzed by pulsed-field gel electrophoresis (PFGE) to examine their genetic relatedness. Swine STEC strains (n= 150) were analyzed by the use of a high-throughput real-time PCR array system, which included 69 virulence gene targets. Three major pathotypes consisted of 16 different combinations of virulence gene profiles, and serotypes were determined in the swine STEC strains. The majority of the swine STEC strains (n= 120) belonged to serotype O59:H21 and carried the same virulence gene profile, which consisted of 9 virulence genes:stx2e,iha,ecs1763,lpfAO113,estIa(STa),ehaA,paa,terE, andureD. Theeae,nleF, andnleH1-2genes were detected in one swine STEC strain (O49:H21). Other genes encoding adhesins, includingiha, were identified (n= 149). The PFGE results demonstrated that swine STEC strains from pigs raised in the same finishing barn were closely related. Our results revealed diverse virulence gene contents among the members of the swine STEC population and enhance understanding of the dynamics of transmission of STEC strains among pigs housed in the same barn.

scholarly journals Klebsiella variicola Reference Strain F2R9 (ATCC BAA-830) Genome Sequence

2021 ◽  
Vol 10 (26) ◽  
Author(s):  
Ulises Garza-Ramos ◽  
Nadia Rodriguez-Medina ◽  
Luis Lozano-Aguirre ◽  
Jesús Silva-Sanchez ◽  
Margarita Sanchez-Arias ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Genome Sequence ◽  
Virulence Genes ◽  
Reference Strain ◽  
Sequence Type ◽  
Its Sequence ◽  
Plant Association ◽  
Content Type

Klebsiella variicola F2R9 was isolated from banana root, and its sequence has been deposited as ATCC BAA-830. It corresponds to sequence type 11 (ST11) and KL16 and contains no identifiable plasmids. The genome showed few antimicrobial resistance and virulence genes and several plant-association genes. The strain showed susceptibility to most antimicrobials and avirulent behavior.

scholarly journals Legionella pneumophila Transcriptional Response following Exposure to CuO Nanoparticles

2013 ◽  
Vol 79 (8) ◽  
pp. 2713-2720 ◽  
Author(s):  
Jingrang Lu ◽  
Ian Struewing ◽  
Helen Y. Buse ◽  
Jiahui Kou ◽  
Howard A. Shuman ◽  
...  
Keyword(s):  
Drinking Water ◽  
Legionella Pneumophila ◽  
Copper Ions ◽  
Virulence Gene ◽  
Copper Oxide Nanoparticles ◽  
Water Disinfection ◽  
Transcriptomic Response ◽  
Content Type ◽  
Cuo Nps ◽  
The Impact

ABSTRACTCopper ions are an effective antimicrobial agent used to control Legionnaires' disease and Pontiac fever arising from institutional drinking water systems. Here, we present data on an alternative bactericidal agent, copper oxide nanoparticles (CuO-NPs), and its efficacy onLegionella pneumophila. In broth cultures, the CuO-NPs caused growth inhibition, which appeared to be concentration and exposure time dependent. The transcriptomic response ofL. pneumophilato CuO-NP exposure was investigated by using a whole-genome microarray. The expression of genes involved in metabolism, transcription, translation, DNA replication and repair, and unknown/hypothetical proteins was significantly affected by exposure to CuO-NPs. In addition, expression of 21 virulence genes was also affected by exposure to CuO-NP and further evaluated by quantitative reverse transcription-PCR (qRT-PCR). Some virulence gene responses occurred immediately and transiently after addition of CuO-NPs to the cells and faded rapidly (icmV,icmW,lepA), while expression of other genes increased within 6 h (ceg29,legLC8,legP,lem19,lem24,lpg1689, andrtxA), 12 h (cegC1,dotA,enhC,htpX,icmE,pvcA, andsidF), and 24 h (legP,lem19, andceg19), but for most of the genes tested, expression was reduced after 24 h of exposure. Genes likeceg29andrtxAappeared to be the most responsive to CuO-NP exposures and along with other genes identified in this study may prove useful to monitor and manage the impact of drinking water disinfection onL. pneumophila.

scholarly journals Relationship between Vancomycin MIC and Virulence Gene Expression in Clonal Complexes of Methicillin-Susceptible Staphylococcus aureus Strains Isolated from Left-Sided Endocarditis

2020 ◽  
Vol 64 (3) ◽  
Author(s):  
Juan M. Pericàs ◽  
Carlos Cervera ◽  
Cristina Garcia-de-la-Mària ◽  
Batu K. Sharma-Kuinkel ◽  
Rachelle Gonzales ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Virulence Factors ◽  
Virulence Genes ◽  
Multivariable Analysis ◽  
Virulence Gene ◽  
Mortality Rates ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Vancomycin Mics ◽  
Genes Encoding

ABSTRACT Higher vancomycin MICs have been associated with more complicated courses and higher mortality rates in patients with Staphylococcus aureus bacteremia and infective endocarditis (IE). The aim of this study was to investigate whether the strains belonging to the cohort of 93 patients from a previously published study in which patients with strains with vancomycin MICs of ≥1.5 μg/ml presented higher mortality rates and systemic emboli than patients with strains with vancomycin MICs of <1.5 μg/ml had specific patterns of virulence factors, clonal complex (CC) types, or the ability to form biofilms. Vancomycin MICs were determined by Etest, and the isolates underwent spa typing to infer the CC, biofilm studies, a thrombin-induced platelet microbicidal assay, and multiplex PCR for the presence of virulence genes. We found no differences in genes encoding adhesins, toxins, or other putative virulence genes according to the vancomycin MIC group. CC30, CC34, and CC45 represented nearly half of the isolates, and there was no association with the vancomycin MIC. agr subgroups I and III predominated, with no association with the vancomycin MIC. Isolates with higher vancomycin MICs exhibited a poorer ability to form biofilms with and without the presence of vancomycin (2.03 versus 2.48 [P < 0.001], respectively, for isolates with higher vancomycin MICs and 2.60 versus 2.87 [P = 0.022], respectively, for isolates with lower vancomycin MICs). In the multivariable analysis, efb and V8 were risk factors for major emboli (adjusted odds ratio [aOR] = 7.5 and 95% confidence interval [CI] = 1.2 to 46.6 for efb, and aOR = 3.9 and 95% CI = 1.1 to 14.1 for V8), whereas no genotypic predictors of in-hospital mortality were found. No clear associations between genes encoding virulence factors, agr type, clonal complexes, mortality, and major embolic events according to vancomycin MIC group were found.

scholarly journals Effect of Rubusoside, a Natural Sucrose Substitute, on Streptococcus mutans Biofilm Cariogenic Potential and Virulence Gene Expression In Vitro

2020 ◽  
Vol 86 (16) ◽  
Author(s):  
Chunru Guan ◽  
Faai Che ◽  
Huoxiang Zhou ◽  
Yiwei Li ◽  
Yaru Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dental Caries ◽  
Streptococcus Mutans ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Extracellular Polysaccharides ◽  
Bacterial Viability ◽  
Content Type ◽  
Virulence Gene Expression ◽  
The Impact

ABSTRACT Dental caries is a biofilm-mediated disease in which Streptococcus mutans is the main pathogenic microorganism, and its incidence is closely related to sucrose. Rubusoside is a natural nonnutritive sweetener isolated from Rubus suavissimus S. Lee. This study was designed to determine the effect of this sucrose substitute on the cariogenic properties and virulence gene expression of S. mutans biofilms. S. mutans was exposed to brain heart infusion (BHI) medium (as a control), 1% sucrose-supplemented medium, 1% rubusoside-supplemented medium, and 1% xylitol-supplemented medium. The growth curve of the biofilm was monitored by crystal violet staining, and the pH was measured every 24 h. After 5 days, the biofilms formed on the glass coverslips were recovered to determine the biomass (dry weight and total amount of soluble proteins), numbers of CFU, and amounts of intra- and extracellular polysaccharides. Biofilm structural imaging was performed using a scanning electron microscope (SEM). Virulence gene expression (gtfB, gtfC, gtfD, ftf, spaP, gbpB, ldh, atpF, vicR, and comD) was determined by reverse transcription-quantitative PCR. Growth in rubusoside resulted in lower levels of acid production than observed during growth in sucrose, xylitol, and the control, while it also reduced the level of biofilm accumulation and bacterial viability and even reduced the level of production of extracellular polysaccharides. By SEM, the levels of biofilm formation and extracellular matrix during growth in rubusoside were lower than these levels during growth in sucrose and xylitol. From the perspective of virulence genes, growth in rubusoside and xylitol significantly inhibited the expression of virulence genes compared with their levels of expression after growth in sucrose. Among these genes, gtfB, gtfC, gbpB, ldh, and comD downregulation was found with growth in rubusoside compared with their expression with growth in xylitol. Therefore, rubusoside appears to be less potentially cariogenic than sucrose and xylitol and may become an effective sucrose substitute for caries prevention. Further studies are needed to deepen these findings. IMPORTANCE Dental caries is a major public health challenge and places heavy biological, social, and financial burdens on individuals and health care systems. To palliate the deleterious effect of sucrose on the virulence factors of S. mutans, massive commercial efforts have been oriented toward developing products that may act as sucrose substitutes. Rubusoside, a natural sucrose substitute, is a plant extract with a high level of sweetness. Although some studies have shown that rubusoside does not produce acids or inhibit the growth of S. mutans, little attention has been paid to its effect on dental biofilm and the underlying mechanisms. Our study focuses on the effect of rubusoside on the formation and structure of biofilms and the expression of virulence genes. The results confirm that rubusoside can inhibit accumulation, bacterial viability, polysaccharide production by the biofilm, and related gene expression. These results provide further insight into the cariogenicity of S. mutans biofilms and demonstrate a new perspective for studying the impact of sucrose substitutes on caries.

scholarly journals Polyphosphate Kinase Antagonizes Virulence Gene Expression inFrancisella tularensis

2017 ◽  
Vol 200 (3) ◽  
Author(s):  
Amy E. Rohlfing ◽  
Kathryn M. Ramsey ◽  
Simon L. Dove
Keyword(s):  
Gene Expression ◽  
Rna Polymerase ◽  
Virulence Genes ◽  
Virulence Gene ◽  
Dna Binding Protein ◽  
Polyphosphate Kinase ◽  
Prior Work ◽  
Content Type ◽  
Virulence Gene Expression ◽  
Regulatory Effects

ABSTRACTThe alarmone ppGpp is a critical regulator of virulence gene expression inFrancisella tularensis. In this intracellular pathogen, ppGpp is thought to work in concert with the putative DNA-binding protein PigR and the SspA protein family members MglA and SspA to control a common set of genes. MglA and SspA form a complex that interacts with RNA polymerase (RNAP), and PigR functions by interacting with the RNAP-associated MglA-SspA complex. Prior work suggested that ppGpp indirectly exerts its regulatory effects inF. tularensisby promoting the accumulation of polyphosphate in the cell, which in turn was required for formation of the MglA-SspA complex. Here we show that inEscherichia coli, neither polyphosphate nor ppGpp is required for formation of the MglA-SspA complex but that ppGpp promotes the interaction between PigR and the MglA-SspA complex. Moreover, we show that polyphosphate kinase, the enzyme responsible for the synthesis of polyphosphate, antagonizes virulence gene expression inF. tularensis, a finding that is inconsistent with the notion that polyphosphate accumulation promotes virulence gene expression in this organism. Our findings identify polyphosphate kinase as a novel negative regulator of virulence gene expression inF. tularensisand support a model in which ppGpp exerts its positive regulatory effects by promoting the interaction between PigR and the MglA-SspA complex.IMPORTANCEInFrancisella tularensis, MglA and SspA form a complex that associates with RNA polymerase to positively control the expression of key virulence genes. The MglA-SspA complex works together with the putative DNA-binding protein PigR and the alarmone ppGpp. PigR functions by interacting directly with the MglA-SspA complex, but how ppGpp exerts its effects was unclear. Prior work indicated that ppGpp acts by promoting the accumulation of polyphosphate, which is required for MglA and SspA to interact. Here we show that formation of the MglA-SspA complex does not require polyphosphate. Furthermore, we find that polyphosphate antagonizes the expression of virulence genes inF. tularensis. Thus, ppGpp does not promote virulence gene expression in this organism through an effect on polyphosphate.

scholarly journals Virulence Phenotypes of Legionella pneumophila Associated with Noncoding RNA lpr0035

2012 ◽  
Vol 80 (12) ◽  
pp. 4143-4153 ◽  
Author(s):  
Deepak Jayakumar ◽  
Julie V. Early ◽  
Howard M. Steinman
Keyword(s):  
Legionella Pneumophila ◽  
Noncoding Rna ◽  
Deletion Mutant ◽  
Acanthamoeba Castellanii ◽  
Direct Repeat ◽  
Repeat Sequence ◽  
Open Reading Frames ◽  
Causative Organism ◽  
Content Type ◽  
Intracellular Multiplication

ABSTRACTThe Philadelphia-1 strain ofLegionella pneumophila, the causative organism of Legionnaires' disease, contains a recently discovered noncoding RNA, lpr0035. lpr0035 straddles the 5′ chromosomal junction of a 45-kbp mobile genetic element, pLP45, which can exist as an episome or integrated in the bacterial chromosome. A 121-bp deletion was introduced in strain JR32, a Philadelphia-1 derivative. The deletion inactivated lpr0035, removed the 49-bp direct repeat at the 5′ junction of pLP45, and locked pLP45 in the chromosome. Intracellular multiplication of the deletion mutant was decreased by nearly 3 orders of magnitude inAcanthamoeba castellaniiamoebae and nearly 2 orders of magnitude in J774 mouse macrophages. Entry of the deletion mutant into amoebae and macrophages was decreased by >70%. The level of entry in both hosts was restored to that in strain JR32 by plasmid copies of two open reading frames immediately downstream of the 5′ junction and plasmid lpr0035 driven by its endogenous promoter. When induced from atacpromoter, plasmid lpr0035 completely reversed the intracellular multiplication defect in macrophages but was without effect in amoebae. These data are the first evidence of a role for noncoding RNA lpr0035, which has homologs in six otherLegionellagenomes, in entry ofL. pneumophilainto amoebae and macrophages and in host-specific intracellular multiplication. The data also demonstrate that deletion of a direct-repeat sequence restricts the mobility of pLP45 and is a means of studying the role of pLP45 mobility inLegionellavirulence phenotypes.

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