Enfermedades infecciosas y microbiologia clinica · 2006
Isolation of Chlamydophila pneumoniae from atheromas of the carotid artery and their antibiotics susceptibility profile.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Cuffini Cecilia, Alberto Guzmán Luis, Villegas Néstor, Eduardo Alonso Carlos, Martínez-Riera Leandro, Rodríguez-Fermepín Marcelo, Carolina Entrocassi Andrea, Pilar Adamo María, Pedranti Mauro, Zapata Marta
Аннотация
BACKGROUND: Atherosclerosis is pathogenically similar to a chronic inflammatory response. Peripheral arterial disease (PAD) is a common manifestation of atherosclerosis. Chlamydophila pneumoniae has been suggested to play a role in the origin of PAD.
OBJECTIVE: To determine whether C. pneumoniae is present in atherosclerosis lesions of the carotid artery wall in patients with PAD through several diagnostic methods and to characterize C. pneumoniae susceptibility profiles.
METHODS: The presence of C. pneumoniae in 9 tissue samples from atherosclerotic lesions obtained by carotid endarterectomy was investigated by 3 methods. Karnofsky-fixed specimens were examined by transmission electron microscopy (TEM), isolation of C. pneumoniae was attempted in LLCMK2 cell structure (ICC), and the presence of chlamydial DNA was investigated by polymerase chain reaction (PCR). The in vitro activities of azithromycin, roxithromycin and penicillin were tested in 4 isolations and the reference strain of C. pneumoniae (AR39).
RESULTS: C. pneumoniae was detected in atherosclerotic plaques from 4 patients with PAD. The pathogen was identified by TEM, PCR and ICC. We report data of the in vitro susceptibility of 4 strains. These strains did not differ from respiratory AR39 strain in their susceptibility patterns to azithromycin, roxithromycin and penicillin.
CONCLUSIONS: C. pneumoniae is frequently found in the advanced carotid atherosclerotic lesions of patients undergoing endarterectomy. Although these findings do not establish causality in carotid artery atherosclerosis, they should stimulate investigation of the possible causal or pathogenic role of C. pneumoniae. Notably, the profiles of antibiotic susceptibility of C. pneumoniae isolated from 4 of the patients did not differ from those of the reference strain.
OBJECTIVE: To determine whether C. pneumoniae is present in atherosclerosis lesions of the carotid artery wall in patients with PAD through several diagnostic methods and to characterize C. pneumoniae susceptibility profiles.
METHODS: The presence of C. pneumoniae in 9 tissue samples from atherosclerotic lesions obtained by carotid endarterectomy was investigated by 3 methods. Karnofsky-fixed specimens were examined by transmission electron microscopy (TEM), isolation of C. pneumoniae was attempted in LLCMK2 cell structure (ICC), and the presence of chlamydial DNA was investigated by polymerase chain reaction (PCR). The in vitro activities of azithromycin, roxithromycin and penicillin were tested in 4 isolations and the reference strain of C. pneumoniae (AR39).
RESULTS: C. pneumoniae was detected in atherosclerotic plaques from 4 patients with PAD. The pathogen was identified by TEM, PCR and ICC. We report data of the in vitro susceptibility of 4 strains. These strains did not differ from respiratory AR39 strain in their susceptibility patterns to azithromycin, roxithromycin and penicillin.
CONCLUSIONS: C. pneumoniae is frequently found in the advanced carotid atherosclerotic lesions of patients undergoing endarterectomy. Although these findings do not establish causality in carotid artery atherosclerosis, they should stimulate investigation of the possible causal or pathogenic role of C. pneumoniae. Notably, the profiles of antibiotic susceptibility of C. pneumoniae isolated from 4 of the patients did not differ from those of the reference strain.