Growth Inhibition of Trichophyton Species by Pseudomonas aeruginosa

Treat, James R.; James, William D.; Nachamkin, Irving; Seykora, John T.

doi:10.1001/archderm.143.1.61

Cited by 18 publications

(7 citation statements)

References 9 publications

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“…aeruginosa inhibited the growth of all Candida species tested, some of the yeast species were in turn capable of inhibiting Ps. aeruginosa (Bandara et al , 2010; Treat et al , 2007). Therefore, the factors contributing to the inhibition by Ps.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of co-colonizing cystic fibrosis-associated pathogens by Pseudomonas aeruginosa and Burkholderia multivorans

et al. 2014

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Cystic fibrosis (CF) is a recessive genetic disease characterized by chronic respiratory infections and inflammation causing permanent lung damage. Recurrent infections are caused by Gramnegative antibiotic-resistant bacterial pathogens such as Pseudomonas aeruginosa, Burkholderia cepacia complex (Bcc) and the emerging pathogen genus Pandoraea. In this study, the interactions between co-colonizing CF pathogens were investigated. Both Pandoraea and Bcc elicited potent pro-inflammatory responses that were significantly greater than Ps. aeruginosa. The original aim was to examine whether combinations of pro-inflammatory pathogens would further exacerbate inflammation. In contrast, when these pathogens were colonized in the presence of Ps. aeruginosa the pro-inflammatory response was significantly decreased. Real-time PCR quantification of bacterial DNA from mixed cultures indicated that Ps. aeruginosa significantly inhibited the growth of Burkholderia multivorans, Burkholderia cenocepacia, Pandoraea pulmonicola and Pandoraea apista, which may be a factor in its dominance as a colonizer of CF patients. Ps. aeruginosa cell-free supernatant also suppressed growth of these pathogens, indicating that inhibition was innate rather than a response to the presence of a competitor. Screening of a Ps. aeruginosa mutant library highlighted a role for quorum sensing and pyoverdine biosynthesis genes in the inhibition of B. cenocepacia. Pyoverdine was confirmed to contribute to the inhibition of B. cenocepacia strain J2315. B. multivorans was the only species that could significantly inhibit Ps. aeruginosa growth. B. multivorans also inhibited B. cenocepacia and Pa. apista. In conclusion, both Ps. aeruginosa and B. multivorans are capable of suppressing growth and virulence of co-colonizing CF pathogens.

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Section: Discussionmentioning

confidence: 99%

Inhibition of co-colonizing cystic fibrosis-associated pathogens by Pseudomonas aeruginosa and Burkholderia multivorans

et al. 2014

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“…39 Cellulose production was followed using the Calcofluor White qualitative assay with modification. 73 Strains were grown onto a coverslip immersed in M63 medium containing different Pi concentrations at 30 C during 48 h. After incubation attached cells were washed twice with distilled water and stained with 15 ml of Calcofluor White for 10 min. Celullose were visualized under a fluorescence microscope Olympus BX51TF equipped with an Olympus QColor5 digital camera (Q-imaging, Surrey, BC, Canada) at excitation and emission wavelengths of 395 and 440 nm, respectively.…”

Section: Microscopic Analysismentioning

confidence: 99%

Environmental phosphate differentially affects virulence phenotypes of uropathogenicEscherichia coliisolates causative of prostatitis

et al. 2015

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“…As the skin surface is never sterile, dermatophytes also come into contact with bacteria immediately. Interactions between dermatophytes and bacteria have not yet been studied extensively, but Pseudomonas aeruginosa can inhibit growth of Trichophyton rubrum and Trichophyton mentagrophyes [21]. Possibly, a certain bacterial flora may – in the face of an intact epidermis – prevent the development of tinea and thus contribute to nonspecific defense mechanisms.…”

Section: Nonspecific Defensesmentioning

confidence: 99%

Pathogenesis of tinea

Brasch

2010

J Deutsche Derma Gesell

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SummaryDermatophytes are hyphomycetes that can degrade keratin. This puts them in a position to cause infections of the keratin-containing superficial skin. The resulting clinical picture is called tinea. The pathogenesis and course of tinea is decisively determined by pathogen-related factors and by the defense mechanisms of the host. An infection starts with an adherence of fungal propagules, followed by the formation of hyphae that can spread within the tissue. This process is accompanied by a release of fungal enzymes and other pathogenic factors. Next keratinocytes are activated, the epidermal barrier is destroyed, epidermal proliferation is enhanced and defensins are expressed within the epidermis. In addition, innate and specific immune responses are initiated, involving neutrophilic granulocytes, macrophages, antibodies and T cells. The cellular mechanisms are thought to be crucial for healing. Special conditions apply to nail infections, because within nail plates the fungi are not accessible to effective defense mechanisms, as well as to infections of hair follicles that contain specific concentrations of steroid hormones. Dermatophytes that penetrate into the dermis can cause granulomatous inflammatory reactions and systemic immune reactions are supposed to be a trigger of so-called id reactions.

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Growth Inhibition of Trichophyton Species by Pseudomonas aeruginosa

Cited by 18 publications

References 9 publications

Inhibition of co-colonizing cystic fibrosis-associated pathogens by Pseudomonas aeruginosa and Burkholderia multivorans

Inhibition of co-colonizing cystic fibrosis-associated pathogens by Pseudomonas aeruginosa and Burkholderia multivorans

Environmental phosphate differentially affects virulence phenotypes of uropathogenicEscherichia coliisolates causative of prostatitis

Pathogenesis of tinea

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