zithromax and baicalin

The ability to form biofilms on surfaces makes Staphylococcus saprophyticus (S. saprophyticus) becomes the main pathogenic factor in nosocomial infections. Previously, we demonstrated that baicalin (Bac) inhibited azithromycin-resistant S. saprophyticus (ARSS) biofilm formation. This investigation aims to explore the influence of baicalin on primary adhesion and aggregation phases of biofilm formation, and the treatment effect of baicalin and azithromycin on ARSS biofilm-associated infection. Crystal violet (CV) staining and scanning electron microscope (SEM) observations clearly showed that sub-inhibitory concentration baicalin inhibited ARSS biofilm formation when baicalin was added before the adhesion and aggregation phases. Baicalin significantly increased the relative adhesion inhibition rate and decreased the rate of bacteria aggregation in a dose-dependent manner. Moreover, CLSM and cell lysis assays revealed that baicalin inhibited the production of surface proteins and cell autolysis in bacteria adhesion and aggregation phases of biofilm formation. Meanwhile, the relative expressions of adhesion-related and autolysis-related genes were down-regulated by baicalin. In vivo, the combination of baicalin and azithromycin succeeded in eradicating ARSS from the mouse cutaneous infection model and decreasing the pathological injuries, the expressions of cytokines in infected tissue, and the number of inflammatory cells in the blood. Simultaneously, baicalin decreased the bacterial burdens in tubes, the level of TNF-α, and the number of monocytes and neutrophils compared with that of the SS and azithromycin groups. Based on these results, baicalin inhibited the adhesion and aggregation phases of biofilm formation by influenced the production of surface proteins and cell autolysis. Baicalin and azithromycin synergetically treated ARSS biofilm-associated infection.

Topics: Animals; Azithromycin; Bacterial Adhesion; Biofilms; Flavonoids; Membrane Proteins; Mice; Staphylococcus saprophyticus

Francolins ophthalmia is often caused by resistant conditional pathogenic bacteria. Conditional pathogenic Staphylococcus saprophyticus is a potential reservoir of macrolides antibiotics resistance gene. Baicalin has been reported as a potential agent to synergistically inhibit the replication of Staphylococcus. The objective of this study was to isolate the pathogen of the francolins ophthalmia, identify the antibiotic resistance profile of isolated S. saprophyticus, and investigate the effect of baicalin combined with azithromycin (Azm) against azithromycin resistant S. saprophyticus (ARSS). The ARSS was isolated and identified from francolins suffered from ophthalmia by phenotypic and molecular biology methods. The antibiotic resistance profile was identified by Kirby-Bauer method. Then the minimal inhibitory concentration (MIC) of Azm in absence and presence of a sub-inhibitory concentration baicalin/verapamil was determined to assess the effect that baicalin combined with Azm against ARSS. ARSS was isolated and identified from francolins experienced ophthalmia. The isolated ARSS was resistant to 11 among the 13 antibiotics that were tested. The synergistic effect of baicalin and Azm was noticed with a reduction rate varied from 2 to 128-fold. It appears from this study that S. saprophyticus can cause francolins ophthalmia and baicalin may be used as a natural agent resistance inhibitor for ARSS.

Topics: Animals; Anti-Bacterial Agents; Azithromycin; Drug Resistance, Microbial; Drug Synergism; Endophthalmitis; Flavonoids; Galliformes; Poultry Diseases; Staphylococcus saprophyticus