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Respiration metabolism of Group B Streptococcus is activated by environmental haem and quinone and contributes to virulence
Abstract
Summary: Group B Streptococcus (GBS) is a common constituent of the vaginal microflora, but its transmission to newborns can cause life‐threatening sepsis, pneumonia and meningitis. Energy metabolism of this opportunist pathogen has been deduced to be strictly fermentative. We discovered that GBS undergoes respiration metabolism if its environment supplies two essential respiratory components: quinone and haem. Respiration metabolism led to significant changes in growth characteristics, including a doubling of biomass and an altered metabolite profile under the tested conditions. The GBS respiratory chain is inactivated by: (i) withdrawing haem and/or quinone, (ii) treating cultures with a respiration inhibitor or (iii) inactivating the cydA gene product, a subunit of cytochrome bd quinol oxidase, in all cases resulting in exclusively fermentative growth. cydA inactivation reduced GBS growth in human blood and strongly attenuated virulence in a neonatal rat sepsis model, suggesting that the animal host may supply the components that activate GBS respiration. These results suggest a role of respiration metabolism in GBS dissemination. Our findings show that environmental factors can increase the flexibility of GBS metabolism by activating a newly identified respiration chain. The need for two environmental factors may explain why GBS respiration metabolism was not found in previous studies.
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“For bacteria that do not synthesize heme, heme acquisition allows them to aerobically respire or activate catalases, which protect against the oxidative burst of host phagocytes (29, 129).”
From Overcoming the Heme Paradox: Heme Toxicity and Tolerance in Bacterial Pathogens (2010) · cites this paper as [129]
In the citing paper
“This is exemplified by the inactivation of the S. agalactiae cytochrome bd quinol oxidase cydA , which prevents acquired heme from activating aerobic respiration reducing bacterial fitness in a murine model (129).”
From Overcoming the Heme Paradox: Heme Toxicity and Tolerance in Bacterial Pathogens (2010) · cites this paper as [129]
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Self-citation
Metadata
- Authors
- Yamamoto, Y., Poyart, C., Trieu‐Cuot, P., Lamberet, G., Gruss, A., & Gaudu, P.
- Venue
- Molecular Microbiology
- Publisher
- Wiley
- Published
- 2005-03-07
- Volume
- 56
- Issue
- 2
- Pages
- 525-534
- ISSN
- 0950-382X
- 1365-2958
- Cited by
- 109
- References
- 47
- Language
- en
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