Chapter 18 : : an Emerging and Model Pathogenic Fungus

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This chapter first reviews the evidence (i.e., clinical reports and incidence) that is an emerging opportunistic pathogen, how and why is found clinically (e.g., acquisition and host factors), and species identification and typing. The chapter describes the analysis (e.g., genetic, phenotypic, and experimental infections) of clinical isolates and clinically derived strains. In addition to making some specific comparisons of with other pathogenic fungi, the chapter describes classical genetic analysis of the ability of to survive in and kill mice. There is evidence that infections (and/or carriage) can be acquired nosocomially, through use in baking, sexually (and/or from person to person), and orally by direct ingestion. The tests used in clinical microbiology laboratories to distinguish different species of fungi, which include assimilation tests and microscopic examination, are not sufficient to distinguish the sensu stricto species, that is, the taxonomically accepted biological sibling species of which include , , , , and . The analysis of clinical (and nonclinical) isolates of benefits immensely from the use of sensitive, high-throughput genotyping technologies, such as the Affymetrix yeast genome arrays, that readily detect deletions, changes in gene copy numbers, and single-nucleotide polymorphisms across the entire genome.

Citation: Mccusker J. 2006. : an Emerging and Model Pathogenic Fungus, p 245-259. In Heitman J, Filler S, Edwards, Jr. J, Mitchell A (ed), Molecular Principles of Fungal Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555815776.ch18
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Image of Figure 1.
Figure 1.

High-temperature growth phenotypes of S288c, YJM145, and S288c-YJM145 diploid strains as determined by a qualitative colony size assay (a) and a quantitative growth assay (b). Reprinted from reference with permission.

Citation: Mccusker J. 2006. : an Emerging and Model Pathogenic Fungus, p 245-259. In Heitman J, Filler S, Edwards, Jr. J, Mitchell A (ed), Molecular Principles of Fungal Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555815776.ch18
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Image of Figure 2.
Figure 2.

Pseudohypha formation of a clinically derived strain, YJM309, determined using a casein-containing medium. Reprinted from reference with permission.

Citation: Mccusker J. 2006. : an Emerging and Model Pathogenic Fungus, p 245-259. In Heitman J, Filler S, Edwards, Jr. J, Mitchell A (ed), Molecular Principles of Fungal Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555815776.ch18
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Image of Figure 3.
Figure 3.

RHA is used to determine the contribution of each allele to a specific phenotype (in this case, high-temperature growth) and thereby identify quantitative-trait genes. Reprinted from reference with permission.

Citation: Mccusker J. 2006. : an Emerging and Model Pathogenic Fungus, p 245-259. In Heitman J, Filler S, Edwards, Jr. J, Mitchell A (ed), Molecular Principles of Fungal Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555815776.ch18
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Table 1.

Isolation of and from different patient and subject populations and from different body sites

Citation: Mccusker J. 2006. : an Emerging and Model Pathogenic Fungus, p 245-259. In Heitman J, Filler S, Edwards, Jr. J, Mitchell A (ed), Molecular Principles of Fungal Pathogenesis. ASM Press, Washington, DC. doi: 10.1128/9781555815776.ch18

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