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Intracellular survival of persistent Group A streptococci in cultured epithelial cells
Year:
2004
Authors :
Sela, Shlomo
;
.
Volume :
294
Co-Authors:
Marouni, M.J., Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Barzilai, A., Pediatric Infectious Diseases Unit, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Keller, N., Department of Clinical Microbiology, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Rubinstein, E., Unit of Infectious Diseases, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Sela, S., Department of Food Science, Institute of Technology and Storage, Volcani Center, P.O. Box 6, Beth-Dagan 50250, Israel
Facilitators :
From page:
27
To page:
33
(
Total pages:
7
)
Abstract:
Group A streptococcus (GAS) is the principle etiologic agent of bacterial pharyngotonsillitis and a wide range of other diseases. Failure to eradicate GAS from patients has been documented in 5-30% of patients with pharyngotonsillitis, in spite of the continued sensitivity of GAS to penicillin and other beta-lactams. It was recently proposed that eradication failure might be attributed to the ability of GAS to maintain an intracellular reservoir during antibiotic treatment. We have previously shown that strains derived from patients with bacterial eradication failure, despite antibiotic treatment (persistent strains), adhered to and were internalized by cultured epithelial cells more efficiently than strains that were successfully eradicated. Since, penicillin and other beta-lactams do not penetrate well into mammalian cells, intracellular survival of GAS is crucial in order to persist during prolonged antibiotic treatment. In this study, we compared the survival of GAS strains from cases of eradication failure and eradication success, using an epithelial cell culture model. We found that persistent strains show significantly increased intracellular survival, compared to the 'eradication success' strains. This finding supports the idea that an intracellular reservoir of GAS plays a role in the etiology of antibiotic eradication failure. © 2004 Elsevier GmbH. All rights reserved.
Note:
Related Files :
beta lactam antibiotic
epithelium cell
eradication therapy
Intracellular survival
pharyngitis
S. pyogenes
strain identification
Show More
Related Content
More details
DOI :
10.1016/j.ijmm.2004.01.001
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
29503
Last updated date:
02/03/2022 17:27
Creation date:
17/04/2018 00:47
Scientific Publication
Intracellular survival of persistent Group A streptococci in cultured epithelial cells
294
Marouni, M.J., Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Tel-Aviv, Israel
Barzilai, A., Pediatric Infectious Diseases Unit, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Keller, N., Department of Clinical Microbiology, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Rubinstein, E., Unit of Infectious Diseases, Chaim Sheba Medical Center, Tel-Hashomer Hospital, Israel
Sela, S., Department of Food Science, Institute of Technology and Storage, Volcani Center, P.O. Box 6, Beth-Dagan 50250, Israel
Intracellular survival of persistent Group A streptococci in cultured epithelial cells
Group A streptococcus (GAS) is the principle etiologic agent of bacterial pharyngotonsillitis and a wide range of other diseases. Failure to eradicate GAS from patients has been documented in 5-30% of patients with pharyngotonsillitis, in spite of the continued sensitivity of GAS to penicillin and other beta-lactams. It was recently proposed that eradication failure might be attributed to the ability of GAS to maintain an intracellular reservoir during antibiotic treatment. We have previously shown that strains derived from patients with bacterial eradication failure, despite antibiotic treatment (persistent strains), adhered to and were internalized by cultured epithelial cells more efficiently than strains that were successfully eradicated. Since, penicillin and other beta-lactams do not penetrate well into mammalian cells, intracellular survival of GAS is crucial in order to persist during prolonged antibiotic treatment. In this study, we compared the survival of GAS strains from cases of eradication failure and eradication success, using an epithelial cell culture model. We found that persistent strains show significantly increased intracellular survival, compared to the 'eradication success' strains. This finding supports the idea that an intracellular reservoir of GAS plays a role in the etiology of antibiotic eradication failure. © 2004 Elsevier GmbH. All rights reserved.
Scientific Publication
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