TY - JOUR
T1 - Intracellular survival of persistent Group A streptococci in cultured epithelial cells
AU - Marouni, Mehran J.
AU - Barzilai, Asher
AU - Keller, N.
AU - Rubinstein, Eitan
AU - Sela, Shlomo
N1 - Funding Information:
We are grateful to Itzhak Ofek and Gene H. Stollerman for continued interest and encouragement. This study was supported in part by Grant No. 3754 from the Chief Scientist's Office of the Ministry of Health, Israel, and by a grant from the Israel Science Foundation awarded to S. Sela.
PY - 2004/7
Y1 - 2004/7
N2 - 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.
AB - 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.
KW - Eradication failure
KW - Internalization
KW - Intracellular survival
KW - S. pyogenes
UR - http://www.scopus.com/inward/record.url?scp=1542416021&partnerID=8YFLogxK
U2 - 10.1016/j.ijmm.2004.01.001
DO - 10.1016/j.ijmm.2004.01.001
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C2 - 15293451
AN - SCOPUS:1542416021
SN - 1438-4221
VL - 294
SP - 27
EP - 33
JO - International Journal of Medical Microbiology
JF - International Journal of Medical Microbiology
IS - 1
ER -