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Skin Fungi from Colonization to Infection

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  • Authors: Sybren de Hoog1, Michel Monod2, Tom Dawson3, Teun Boekhout4, Peter Mayser5, Yvonne Gräser6
  • Editor: Joseph Heitman7
  • VIEW AFFILIATIONS HIDE AFFILIATIONS
    Affiliations: 1: Westerdijk Fungal Biodiversity Institute, 3584 CT Utrecht, The Netherlands; 2: Department of Dermatology, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland; 3: Institute of Medical Biology, Agency for Science, Technology, and Research, Singapore 138648; 4: Westerdijk Fungal Biodiversity Institute, 3584 CT Utrecht, The Netherlands; 5: Universitätsklinikum Giessen Hautklinik, 35392 Giessen, Germany; 6: Nationales Konsiliarlabor für Dermatophyten, Institut für Mikrobiologie und Hygiene, 12203 Berlin, Germany; 7: Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710
    • Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
  • Received 03 June 2016 Accepted 12 May 2017 Published 14 July 2017
  • Sybren de Hoog, [email protected]
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  • Abstract:

    Humans are exceptional among vertebrates in that their living tissue is directly exposed to the outside world. In the absence of protective scales, feathers, or fur, the skin has to be highly effective in defending the organism against the gamut of opportunistic fungi surrounding us. Most (sub)cutaneous infections enter the body by implantation through the skin barrier. On intact skin, two types of fungal expansion are noted: (A) colonization by commensals, i.e., growth enabled by conditions prevailing on the skin surface without degradation of tissue, and (B) infection by superficial pathogens that assimilate epidermal keratin and interact with the cellular immune system. In a response-damage framework, all fungi are potentially able to cause disease, as a balance between their natural predilection and the immune status of the host. For this reason, we will not attribute a fixed ecological term to each species, but rather describe them as growing in a commensal state (A) or in a pathogenic state (B).

  • Citation: de Hoog S, Monod M, Dawson T, Boekhout T, Mayser P, Gräser Y. 2017. Skin Fungi from Colonization to Infection. Microbiol Spectrum 5(4):FUNK-0049-2016. doi:10.1128/microbiolspec.FUNK-0049-2016.

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2017-07-14
2020-10-30

Abstract:

Humans are exceptional among vertebrates in that their living tissue is directly exposed to the outside world. In the absence of protective scales, feathers, or fur, the skin has to be highly effective in defending the organism against the gamut of opportunistic fungi surrounding us. Most (sub)cutaneous infections enter the body by implantation through the skin barrier. On intact skin, two types of fungal expansion are noted: (A) colonization by commensals, i.e., growth enabled by conditions prevailing on the skin surface without degradation of tissue, and (B) infection by superficial pathogens that assimilate epidermal keratin and interact with the cellular immune system. In a response-damage framework, all fungi are potentially able to cause disease, as a balance between their natural predilection and the immune status of the host. For this reason, we will not attribute a fixed ecological term to each species, but rather describe them as growing in a commensal state (A) or in a pathogenic state (B).

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Skin Fungi from Colonization to Infection
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Citation: de Hoog S, Monod M, Dawson T, Boekhout T, Mayser P, Gräser Y. 2017. Skin fungi from colonization to infection. microbiolspec 5(4): doi:10.1128/microbiolspec.FUNK-0049-2016
/content/microbiolspec/10.1128/microbiolspec.FUNK-0049-2016.fig1
FIGURE 1
Overview of basic types of fungal occurrence on human skin and modes of transmission.
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FIGURE 1

Overview of basic types of fungal occurrence on human skin and modes of transmission.

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
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FIGURE 2
Maximum likelihood phylogenetic tree (RAxML v.8.0.0) based on ITS and partial LSU, TUB, and 60S L10 sequences of species using GTRCAT as model, with 1,000 bootstrap replications, shown as collapsed when bootstrap values >70%. was selected as outgroup. Reprinted from de Hoog et al. ( 13 ).
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FIGURE 2

Maximum likelihood phylogenetic tree (RAxML v.8.0.0) based on ITS and partial LSU, TUB, and 60S L10 sequences of species using GTRCAT as model, with 1,000 bootstrap replications, shown as collapsed when bootstrap values >70%. was selected as outgroup. Reprinted from de Hoog et al. ( 13 ).

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
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FIGURE 3
species tree was constructed using concatenated sequences of 164 core eukaryotic genes that are present in all , , and genomes. Sequences were aligned using MUSCLE and the phylogeny constructed using a maximum likelihood (ML) approach by RAxML. RAxML was run using “–f a –m PROTGAMMAJTT” with 400 bootstraps.
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FIGURE 3

species tree was constructed using concatenated sequences of 164 core eukaryotic genes that are present in all , , and genomes. Sequences were aligned using MUSCLE and the phylogeny constructed using a maximum likelihood (ML) approach by RAxML. RAxML was run using “–f a –m PROTGAMMAJTT” with 400 bootstraps.

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
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FIGURE 4
Synthesis of indole-derived pigments by one enzymatic step (TAM1) and possible intervention by TAM inhibitors.
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FIGURE 4

Synthesis of indole-derived pigments by one enzymatic step (TAM1) and possible intervention by TAM inhibitors.

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
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Skin Fungi from Colonization to Infection
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Citation: de Hoog S, Monod M, Dawson T, Boekhout T, Mayser P, Gräser Y. 2017. Skin fungi from colonization to infection. microbiolspec 5(4): doi:10.1128/microbiolspec.FUNK-0049-2016
/content/microbiolspec/10.1128/microbiolspec.FUNK-0049-2016.T1
TABLE 1
Selected Trp-derived indole compounds and their potential relationship to clinical phenomena in PV
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TABLE 1

Selected Trp-derived indole compounds and their potential relationship to clinical phenomena in PV

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016
/content/microbiolspec/10.1128/microbiolspec.FUNK-0049-2016.T2
TABLE 2
genome statistics
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TABLE 2

genome statistics

Source: microbiolspec July 2017 vol. 5 no. 4 doi:10.1128/microbiolspec.FUNK-0049-2016

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