Comparative Pathogenicity of a Wild-Type Strain and Respiratory Mutants of Candida albicans in Mice
Abstract
The pathogenicity of a parent wild-type strain and three respiratory mutants of Candida albicans was examined in intravenously infected mice. The wild-type strain K grew well in the kidney and caused severe candidosis, and the 21-day LD50 value was 7.2 x 10(6) cells/mouse. A mutant with a low rate of respiration (KRD-8) whose growth rate in vitro was somewhat lower than that of the wild type, produced germ tubes in vitro to the same extent as the wild-type strain and was associated with mortality rates similar to those of the wild-type strain. Two respiration-deficient (petite) mutants (KRD-19 and KRD-51), whose growth rates in vitro were far lower than that of the wild-type strain, could neither colonize the kidney nor cause fatal infection, even at a dose of 10(8) cells/mouse. Formation of germ tubes and hyphal growth in vitro of the petite mutants were less extensive than those of the wild-type strain or KRD-8. Extracellular proteinase was produced at pH 3.5 by the wild-type strain and by KRD-8 but not by the petite mutants. From these results, it is most likely that the nonlethality of infection by the petite mutants in mice results primarily from the low capacity of growth of these mutants, even though the inability of the petite mutants to produce extracellular proteinase may be also related to some extent to their avirulence.
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Most other described C. albicans petite strains are induced by harsh chemical treatments, making correlations of specific mitochondrial dysfunctions with azole resistance difficult to interpret.
“Other C. albicans petite strains have been described, but most are induced by harsh chemical treatments, and therefore, correlations of specific mitochondrial dysfunctions with azole resistance are more difficult to interpret (15–17).”
From Azole Susceptibility and Transcriptome Profiling in Candida albicans Mitochondrial Electron Transport Chain Complex I Mutants (2013) · cites this paper as [16]
Respiration deficiency leads to attenuated virulence in C. albicans, C. glabrata, and A. fumigatus.
“respiration deficiency leads to attenuated virulence in the fungal pathogens C. albicans (Aoki et al. 1990), C. glabrata (Brun et al. 2005) and Aspergillus fumigatus (Grahl et al. 2012).”
From The potential of respiration inhibition as a new approach to combat human fungal pathogens (2019) · cites this paper as Aoki et al. 1990
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References 27 · Cited by 71
- Authors
- Aoki, S., Ito-Kuwa, S., Nakamura, Y., & Masuhara, T.
- Affiliations
- Nippon Dental University (JP)
- ORCID
- Nakamura, Yasunori
- Venue
- Zentralblatt für Bakteriologie
- Publisher
- Elsevier BV
- Published
- 1990-08
- Volume
- 273
- Issue
- 3
- Pages
- 332-343
- ISSN
- 0934-8840 (ISSN-L)
- OpenAlex
- W2014766562
- Cited by
- 71
- References
- 27
- Citations by year
- 2026: 1 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 2 · 2021: 1 · 2020: 4 · 2019: 3 · 2018: 3 · 2017: 3 · 2015: 1 · 2014: 6 · 2013: 1 · 2012: 2
- FWCI
- 1.43
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Zentralblatt für Bakteriologie (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Antifungal resistance and susceptibility
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
- Health Sciences › Medicine › Epidemiology › Fungal Infections and Studies
- Keywords
- Candida albicans, pathogenicity, respiratory mutants, petite mutants, respiration-deficient mutants, candidiasis, kidney colonization, germ tube formation, hyphal growth, extracellular protease, virulence, mouse infection model
- MeSH terms
- Animals, Body Weight, Candida albicans, Candidiasis, Kidney, Liver, Male, Mutation, Endopeptidases, Colony Count, Microbial, Mice
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