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Cited by 23Vibrio bacteria research studiesBacterial Infections and VaccinesInfections and bacterial resistance

Use of a marker plasmid to examine differential rates of growth and death between clinical and environmental strains of Vibrio vulnificus in experimentally infected mice

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Starks, Angela M., Bourdage, Keri L., Thiaville, Patrick C., Gulig, Paul A.·2006·Molecular Microbiology
DOI 10.1111/j.1365-2958.2006.05227.x
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Abstract

Summary: Vibrio vulnificus is Gram‐negative bacterium that contaminates oysters, causing highly lethal sepsis after consumption of raw oysters and wound infection. We previously described two sets of V. vulnificus strains with different levels of virulence in subcutaneously inoculated iron dextran‐treated mice. Both virulent, clinical strains and attenuated, environmental strains could be recovered in high numbers from skin lesions and livers; however, the attenuated environmental strains required significantly higher numbers of colony‐forming units (cfu) in the inoculum to produce lethal infection. Using some of these strains and an additional clinical strain, we presently asked if the different abilities to cause infection between the clinical and environmental strains were due to differences in rates of growth or death of the bacteria in the mouse host. We therefore constructed a marker plasmid, pGTR902, that functions as a replicon only in the presence of arabinose, which is not present in significant levels in animal tissues. V. vulnificus strains containing pGTR902 were inoculated into iron dextran‐treated and untreated mice. Measuring the proportion of bacteria that had maintained the marker plasmid recovered from mice enabled us to monitor the number of in vivo divisions, hence growth rate; whereas measuring the number of marker plasmid‐containing bacteria recovered enabled the measurement of death of the vibrios in the mice. The numbers of bacterial divisions in vivo for all of the strains over a 12–15 h infection period were not significantly different in iron dextran‐treated mice; however, the rate of death of one environmental strain was significantly higher compared with the clinical strains. Infection of non‐iron dextran‐treated mice with clinical strains demonstrated that the greatest effect of iron dextran‐treatment was increased growth rate, while one clinical strain also experienced increased death in untreated mice. V. vulnificus inoculated into iron dextran‐treated mice replicated extremely rapidly over the first 4 h of infection with doubling times of approximately 15–28 min. In contrast, one of the environmental strains exhibited a reduced early growth rate. These results demonstrate that differences in virulence among naturally occurring V. vulnificus can be explained by diverse abilities to replicate rapidly in or resist defences of the host. The marker plasmid pGTR902 should be useful for examining virulence of bacteria in terms of differentiating growth verses death in animal hosts for most Gram‐negative bacteria.

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  • The plasmid pGTR905 replicates only when arabinose is present, and arabinose is absent from mouse tissues.

    “The plasmid replicates only in the presence of arabinose, which is not found in mouse tissues.”

    From Hepcidin-Induced Hypoferremia Is a Critical Host Defense Mechanism against the Siderophilic Bacterium Vibrio vulnificus (2015) · cites this paper as Starks et al., 2006

    The Construction of marker plasmid pGTR902 section says that pGTR902 replicates in the presence of arabinose and does not replicate without it. The Discussion says arabinose was not present in mice at levels high enough to initiate replication, but does not claim absolute absence. The source identifies the plasmid as pGTR902, not pGTR905; page numbers are unavailable in our copy. (LLM, conf=0.88)

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Research works printed but not linked: 1

  1. Gerhardt, P., Murray, R.G.E., Costilow, R., Nester, E.W., Wood, W.A., Krieg, N.R., and Phillips, G.B. (eds). Washington, DC: American Society for Microbiology, pp. 243-265.

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Authors
Starks, A. M., Bourdage, K. L., Thiaville, P. C., & Gulig, P. A.
Affiliations
University of Florida Health (US)
Corresponding author
Gulig, Paul A.
ORCID
Starks, Angela M.
Venue
Molecular Microbiology
Publisher
Wiley
Published
2006-06-15
Volume
61
Issue
2
Pages
310-323
ISSN
  • 0950-382X (ISSN-L)
  • 1365-2958
DOI
10.1111/j.1365-2958.2006.05227.x
OpenAlex
W2037635337
Cited by
23
References
41
Citations by year
2023: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 1 · 2015: 3 · 2013: 1 · 2012: 1
FWCI
1.78
Type
journal article
Language
en
Open access
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations
  • Molecular Microbiology (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Agriculture
  • American Heart Association
  • National Institutes of Health
  • National Institute of Allergy and Infectious Diseases (T32 AI-07110, R01-AI1056056-01, T32AI007110)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Vibrio bacteria research studies
  • Life Sciences › Immunology and Microbiology › Microbiology › Bacterial Infections and Vaccines
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Infections and bacterial resistance
Keywords
Vibrio vulnificus, virulence, clinical strains, environmental strains, bacterial growth rate, bacterial cell death, iron dextran, experimental infection in mice, sepsis, wound infection, host defense
MeSH terms
Animals, Disease Models, Animal, Environment, Female, Genetic Markers, Humans, Iron, Iron-Dextran Complex, Mice, Inbred ICR, Plasmids, Skin, Vibrio Infections, Vibrio vulnificus, Cell Proliferation, Mice

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