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This work aimed to determine the presence of Arcobacter spp. in shellfish and to determine its susceptibility to quinolones. One hundred samples (41 mussels, 37 clams, and 22 cockles) were purchased from different local retail shops in Valencia, Spain, from September 2013 to June 2015. All samples were analyzed simultaneously by culture, after an enrichment step, and by polymerase chain reaction (PCR), directly and after enrichment. The susceptibility to levofloxacin and ciprofloxacin of the isolates was tested using the disk-diffusion test and E-test strips method. To clarify the mechanism of quinolone resistance, a fragment of the quinolone resistance-determining region of the gyrA gene was sequenced. Thirty-seven samples were positive and 49 isolates were obtained by culture, and Arcobacter spp. DNA was detected in 32% of the samples by PCR. However, after 48-h enrichment, the number of positive samples increased, and 68 of the 100 samples yielded the specific Arcobacter spp. PCR product. In addition, 49 isolates were identified by PCR-restriction fragment length polymorphism. The most commonly found species was Arcobacter butzleri (25 isolates, 51.03%) followed by Arcobacter cryaerophilus (19 isolates, 38.77%) and Arcobacter defluvii (5 isolates, 10.20%). Only three isolates of A. butzleri were resistant to both antibiotics. A mutation C to T transition in the position 254 of the gyrA gene was present in the three resistant isolates. This study confirms that pathogenic arcobacters are frequently found in edible shellfish samples. Moreover, this is the first time that A. butzleri and A. cryaerophilus have been isolated from cockles.
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Subunits of DNA gyrase (GyrA and GyrB) proteins of M. pneumoniae FH were separately expressed as His-tagged proteins in Escherichia coli Chaperone Competent Cell BL21 by IPTG induction of plasmids containing the respective gyrA and gyrB genes. The inhibitory activities of garenoxacin, moxifloxacin, gatifloxacin and levofloxacin against DNA gyrase were evaluated by the inhibition of supercoiling activity (n = 3).
During 1999-2000, 5015 isolates were collected from 13 countries and tested against levofloxacin. Overall, levofloxacin resistance minimum inhibitory concentration (MIC>or =8 mg/l) was found in 40 isolates (0.8%). The highest resistance rates were in Hong Kong (8.0%), China (3.3%) and Spain (1.6%). Levofloxacin retained an MIC(90) of 1 mg/l in all countries. Pulsed-field gel electrophoresis analysis of resistant isolates demonstrated the presence of clones in countries where levofloxacin resistance exceeded 1%, suggesting that the elevated resistance rates could result from resistant clones within participating hospitals. DNA-sequence analysis of the quinolone-resistance-determining regions of gyrA, gyrB, parC and parE genes showed that the most common mutations were in GyrA (Ser81Phe), ParC (Ser79Phe, Lys137Asn) and ParE (Ile460Val), accounting for 40% of the isolates tested. Levofloxacin-resistant isolates were generally non-susceptible to other fluoroquinolones tested. Future studies to characterise resistant isolates by other molecular methods may ensure that the appropriate counter-measures can be taken to control the spread of resistant isolates.
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Millions of assays are performed each year to monitor for substance abuse in various settings. When common medications cross-react with frequently used testing assays, false-positive results can lead to invalid conclusions.
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Fluoroquinolones are widely recommended as empirical monotherapy for community-acquired pneumonia. Since 1999, case reports of failure of levofloxacin therapy due to levofloxacin-resistant strains of Streptococcus pneumoniae have started to appear. Most worrying is that, in some cases, levofloxacin resistance has been acquired by pneumococci within days of the initiation of therapy. Because use of current clinical antimicrobial resistance breakpoints fail to identify the majority of S. pneumoniae isolates with only first-step mutations, current treatment guidelines not only may have implications with regard to the ability of surveillance programs to detect emerging resistance but may have therapeutic implications as well.
This analysis from the global Tigecycline Evaluation and Surveillance Trial (T.E.S.T.) reports on 24 784 isolates collected from integumentary culture sources between 2004 and 2009.
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Surface temperature measured by an infrared temperature-scanning thermometer was used to evaluate disease severity and predict imminent death in a murine model of pneumococcal pneumonia. We showed that a decrease in temperature was associated with increasing severity of disease and concomitant histological changes and also that a temperature of 30 degrees C or less was a predictor of death. Furthermore, viable bacterial counts in the lungs of mice euthanized at a temperature of < or = 30 degrees C were not significantly different from those seen in the lungs of mice allowed to die without intervention. These data support temperature change as a more subtle indicator of outcome than death and demonstrate that this could be used as a reliable end point for euthanasia. To test the utility of our model in a drug trial, we examined the efficacies of moxifloxacin and levofloxacin by using temperature as a measure of disease severity prior to and during treatment. Regardless of the antibiotic used, mice assessed as moderately ill (temperature > or = 32 degrees C) at the start of treatment had better clinical and bacteriological outcomes than mice assessed as severely ill (temperature < 32 degrees C). However, moxifloxacin offered better protection and greater bacterial clearance than did levofloxacin in all infected mice independent of disease severity. This model not only allows a more subtle evaluation of drug efficacy but also ensures a better degree of standardization and a more humane approach to drug efficacy studies involving animals.
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Majocchi's granuloma (MG) is a rare deep skin dermatophyte infection that can occur either in immunocompetent or in immunocompromised individuals. Oral itraconazole or terbinafine is considered to be the first choice of treatment. We report an immunocompetent man with deep nodular form of MG, the form which is generally found in immunosuppressed individuals. Previous treatment with either oral itraconazole or terbinafine yielded no apparent improvement. After a series of examination, the man was diagnosed as having Trichophyton rubrum-induced MG mixed with bacterial infection as evidenced by growth of Klebsiella pneumoniae in tissue bacterial culture. The patient was treated with a combination of cefoselis and levofloxacin for bacterial clearance followed by voriconazole treatment. After approximately 4 months of voriconazole treatment, the lesions completely resolved. Alternative medicine (voriconazole) can be considered in case of refractory infections during MG treatment.