Biofilm formation by saprophytic and pathogenic leptospires

Ristow, Paula; Bourhy, Pascale; Kernéis, Sophie; Schmitt, Christine; Prévost, Marie‐Christine; Lilenbaum, Walter; Picardeau, Mathieu

doi:10.1099/mic.0.2007/014746-0

Cited by 133 publications

(125 citation statements)

References 18 publications

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“…5.0 to 7.0 mg cm −2 ). A fast increase in wet weight was also observed in 2007 (data not shown); contrary to this, in artificial systems (such as a reactor system) and on substrata (glass tubes, and glass and Teflon cylinders) longer periods (20 d-78 d) are required to obtain a stationary biofilm (26,34,35). The bare reed surface exposed to lake water just after the removal of the biofilm seems to be a competitive site for microbial attachment and growth; this may be related to the high activity of bacteria and the rapid increase in bacterial numbers, as discussed below.…”

Section: Biofilm Wet Weightmentioning

confidence: 91%

Analysis of How a Biofilm Forms on the Surface of the Aquatic Macrophyte Phragmites australis

et al. 2009

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The process by which a biofilm forms on the surface of the aquatic macrophyte Phragmites australis was investigated over a period of about two months (from mid-May to late-July, 2008) in Lake Biwa. The biofilm formed relatively quickly, its wet weight per unit area after seven day being that of a mature biofilm. This speed can be attributed to the many active bacteria in the early stage of its formation and the extracellular polymeric substances (EPS) they produce. The EPS carried electric charges that attracted nutrient ions from surrounding lake water, which, by electrostatic interaction, reached a high concentration as early as day 7 of the formation process. This significantly affected the biofilm community, which differed greatly from that of the lake water even at the beginning of biofilm formation. Brown amorphous compounds (a complex of organic and inorganic substances), covered the biofilm in the second half of its formation process producing a different community structure from that initially. This study revealed a fast and dynamic process of biofilm formation on the reed surface of reed.

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Section: Biofilm Wet Weightmentioning

confidence: 91%

Analysis of How a Biofilm Forms on the Surface of the Aquatic Macrophyte Phragmites australis

et al. 2009

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“…Furthermore, LipL32 is absent in the saprophytic species Leptospira biflexa, which has only an environmental existence (28). L. interrogans has been shown to form biofilms (30), but the role of LipL32 in this process is unknown.…”

Section: Discussionmentioning

confidence: 99%

Major Surface Protein LipL32 Is Not Required for Either Acute or Chronic Infection with Leptospira interrogans

Murray¹,

Srikram²,

Hoke³

et al. 2009

Infect Immun

110

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Leptospira interrogans is responsible for leptospirosis, a zoonosis of worldwide distribution. LipL32 is the major outer membrane protein of pathogenic leptospires, accounting for up to 75% of total outer membrane protein. In recent times LipL32 has become the focus of intense study because of its surface location, dominance in the host immune response, and conservation among pathogenic species. In this study, an lipL32 mutant was constructed in L. interrogans using transposon mutagenesis. The lipL32 mutant had normal morphology and growth rate compared to the wild type and was equally adherent to extracellular matrix. Protein composition of the cell membranes was found to be largely unaffected by the loss of LipL32, with no obvious compensatory increase in other proteins. Microarray studies found no obvious stress response or upregulation of genes that may compensate for the loss of LipL32 but did suggest an association between LipL32 and the synthesis of heme and vitamin B 12 . When hamsters were inoculated by systemic and mucosal routes, the mutant caused acute severe disease manifestations that were indistinguishable from wild-type L. interrogans infection. In the rat model of chronic infection, the LipL32 mutant colonized the renal tubules as efficiently as the wild-type strain. In conclusion, this study showed that LipL32 does not play a role in either the acute or chronic models of infection. Considering the abundance and conservation of LipL32 among all pathogenic Leptospira spp. and its absence in saprophytic Leptospira, this finding is remarkable. The role of this protein in leptospiral biology and pathogenesis thus remains elusive.

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“…Cells were then harvested at 4, 8, 12, 20, or 24 h by centrifugation, washed once in PBS, and resuspended in cacodylate buffer (0.1 M; pH 7.2) supplemented with 2.5% glutaraldehyde. Samples were then processed for electron microscopy experiments as described previously (49). For cell length measurements, 50 to 100 cells were randomly chosen in the micrographs, and the distance between two ends was manually calculated using the ImageJ program (http://rsb.info.nih.gov/ij/).…”

Section: Lbl_2647 Lepbia0257mentioning

confidence: 99%

Deciphering Morphological Determinants of the Helix-Shaped Leptospira

et al. 2011

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Leptospira spp. are thin, highly motile, slow-growing spirochetes that can be distinguished from other bacteria on the basis of their unique helical shape. Defining the mechanisms by which these bacteria generate and maintain this atypical morphology should greatly enhance our understanding of the fundamental physiology of these pathogens. In this study, we showed that peptidoglycan sacculi from Leptospira spp. retain the helical shape of intact cells. Interestingly, the distribution of muropeptides was different from that in the Escherichia coli model, indicating that specific enzymes might be active on the peptidoglycan macromolecule. We could alter the shape of Leptospira biflexa with the broad-spectrum ␤-lactam antibiotic penicillin G and with amdinocillin and aztreonam, which are ␤-lactams that preferentially target penicillin-binding protein 2 (PBP2) and PBP3, respectively, in some species. Although genetic manipulations of Leptospira spp. are scarce, we were able to obtain mutants with alterations in genes encoding PBPs, including PBP3. Loss of this protein resulted in cell elongation. We also generated an L. biflexa strain that conditionally expresses MreB. Loss of the MreB function was correlated with morphological abnormalities such as a localized increased diameter and heterogeneous length. A prolonged depletion of MreB resulted in cell lysis, suggesting that this protein is essential. These findings indicate that important aspects of leptospiral cell morphology are determined by the cytoskeleton and the murein layer, thus providing a starting point for a better understanding of the morphogenesis in these atypical bacteria.

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Biofilm formation by saprophytic and pathogenic leptospires

Cited by 133 publications

References 18 publications

Analysis of How a Biofilm Forms on the Surface of the Aquatic Macrophyte Phragmites australis

Analysis of How a Biofilm Forms on the Surface of the Aquatic Macrophyte Phragmites australis

Major Surface Protein LipL32 Is Not Required for Either Acute or Chronic Infection with Leptospira interrogans

Deciphering Morphological Determinants of the Helix-Shaped Leptospira

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