Evaluation of microorganisms cultured from injured and repressed tissue regeneration sites in endangered giant aquatic Ozark Hellbender salamanders

Cheryl Nickerson, C. Mark Ott, Sarah L. Castro, Veronica M. Garcia, Thomas C. Molina, Jeffrey T. Briggler, Amber L. Pitt, Joseph J. Tavano, J. Kelly Byram, Jennifer Barrila, Max A. Nickerson

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Investigation into the causes underlying the rapid, global amphibian decline provides critical insight into the effects of changing ecosystems. Hypothesized and confirmed links between amphibian declines, disease, and environmental changes are increasingly represented in published literature. However, there are few long-term amphibian studies that include data on population size, abnormality/injury rates, disease, and habitat variables to adequately assess changes through time. We cultured and identified microorganisms isolated from abnormal/injured and repressed tissue regeneration sites of the endangered Ozark Hellbender, Cryptobranchus alleganiensis bishopi, to discover potential causative agents responsible for their significant decline in health and population. This organism and our study site were chosen because the population and habitat of C. a. bishopi have been intensively studied from 1969-2009, and the abnormality/injury rate and apparent lack of regeneration were established. Although many bacterial and fungal isolates recovered were common environmental organisms, several opportunistic pathogens were identified in association with only the injured tissues of C.a. bishopi. Bacterial isolates included Aeromonas hydrophila, a known amphibian pathogen, Granulicetella adiacens, Gordonai terrae, Stenotrophomonas maltophilia, Aerococcus viridans, Streptococcus pneumoniae and a variety of Pseudomonads, including Pseudomonas aeruginosa, P. stutzeri, and P. alcaligenes. Fungal isolates included species in the genera Penicillium, Acremonium, Cladosporium, Curvularia, Fusarium, Streptomycetes, and the Class Hyphomycetes. Many of the opportunistic pathogens identified are known to form biofilms. Lack of isolation of the same organism from all wounds suggests that the etiological agent responsible for the damage to C. a. bishopi may not be a single organism. To our knowledge, this is the first study to profile the external microbial consortia cultured from a Cryptobranchid salamander. The incidence of abnormalities/injury and retarded regeneration in C. a. bishopi may have many contributing factors including disease and habitat degradation. Results from this study may provide insight into other amphibian population declines.

Original languageEnglish (US)
Article numbere28906
JournalPLoS One
Volume6
Issue number12
DOIs
StatePublished - Dec 19 2011

Fingerprint

Urodela
Ozarks
Tissue regeneration
Amphibians
Pathogens
tissue repair
salamanders and newts
Microorganisms
amphibians
Regeneration
Ecosystem
microorganisms
organisms
Wounds and Injuries
Biofilms
pathogens
Streptococcus viridans
Aerococcus
Ecosystems
Aerococcus viridans

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

Cite this

Evaluation of microorganisms cultured from injured and repressed tissue regeneration sites in endangered giant aquatic Ozark Hellbender salamanders. / Nickerson, Cheryl; Ott, C. Mark; Castro, Sarah L.; Garcia, Veronica M.; Molina, Thomas C.; Briggler, Jeffrey T.; Pitt, Amber L.; Tavano, Joseph J.; Byram, J. Kelly; Barrila, Jennifer; Nickerson, Max A.

In: PLoS One, Vol. 6, No. 12, e28906, 19.12.2011.

Research output: Contribution to journalArticle

Nickerson, Cheryl ; Ott, C. Mark ; Castro, Sarah L. ; Garcia, Veronica M. ; Molina, Thomas C. ; Briggler, Jeffrey T. ; Pitt, Amber L. ; Tavano, Joseph J. ; Byram, J. Kelly ; Barrila, Jennifer ; Nickerson, Max A. / Evaluation of microorganisms cultured from injured and repressed tissue regeneration sites in endangered giant aquatic Ozark Hellbender salamanders. In: PLoS One. 2011 ; Vol. 6, No. 12.
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