Fluoroquinolone use in poultry production may select for resistant Escherichia coli that can be transmitted to humans. To define the prevalence and virulence potential of poultry-associated, quinolone-resistant E. coli in the United States, 169 retail chicken products from the Minneapolis-St. Paul area (1999 to 2000) were screened for nalidixic acid (Nal)-resistant E. coli. Sixty-two (37%) products yielded Nal-resistant E. coli. From 55 products that yielded both Nal-resistant and susceptible E. coli, two isolates (one resistant, one susceptible) per sample were further characterized. Twenty-three (21%) of the 110 E. coli isolates (13 resistant, 10 susceptible) satisfied criteria for extraintestinal pathogenic E. coli (ExPEC), i.e., exhibited >2 of pap (P fimbriae), sfa/foc (S/F1C fimbriae), afa/dra (Dr binding adhesins), iutA (aerobactin receptor), and kpsMT II (group 2 capsule synthesis). Compared with other isolates, ExPEC isolates more often derived from virulence-associated E. coli phylogenetic groups B2 or D (74% versus 32%; P < 0.001) and exhibited more ExPEC-associated virulence markers (median, 10.0 versus 4.0; P < 0.001). In contrast, the Nal-resistant and -susceptible populations were indistinguishable according to all characteristics analyzed, including pulsed-field gel electrophoresis profiles. These findings indicate that Nal-resistant E. coli is prevalent in retail poultry products and that a substantial minority of such strains represent potential human pathogens. The similarity of the Nal-resistant and -susceptible populations suggests that they derive from the same source population, presumably the avian fecal flora, with Nal resistance emerging by spontaneous mutation as a result of fluoroquinolone exposure.

Seventeen Escherichia coli isolates from dogs with urinary tract infection (UTI) were characterized with respect to phylogenetic background and virulence genotype and were compared with the E. coli reference (ECOR) collection and with human clinical isolates with similar serotypes from patients with diverse extraintestinal infections. Most of the canine urine isolates were from (virulence-associated) E. coli phylogenetic groups B2 or D, expressed papG allele III, and exhibited numerous other putative virulence genes that are characteristic of human extraintestinal pathogenic E. coli (ExPEC). Close phylogenetic and pathotypic correspondence was documented within 5 clonal groups among individual canine and human isolates, including archetypal human ExPEC strains CFT073 (O6:K2:H1), 536 (O6:K15:H31), and J96 (O4:K-:H5). These findings suggest that canine UTI isolates, rather than being dog-specific pathogens, as previously suspected, may pose an infectious threat to humans. Commonality between canine and human ExPEC has potentially important implications for disease prevention, antibiotic resistance avoidance, and studies of pathogenesis.

Among 1,102 recent Escherichia coli clinical isolates, clonal group A was identified in 17 of 20 (U.S. and non-U.S.) geographic locales, mainly among U.S. isolates (9% vs. 3%; p < 0.001) and those resistant to trimethoprim-sulfamethoxazole (10% vs. 1.7%; p < 0.001). The extensive antimicrobial resistance and virulence profiles of clonal group A may underlie its recent widespread emergence.

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Schizophrenia has existed as a distinct disorder for nearly a century, and, ever since this disorder was first described and studied, cognitive impairment has been recognized as a prominent feature. However, the positive symptoms of schizophrenia moved to the forefront of clinical and research attention in the latter half of the twentieth century. With the new movement toward functional recovery in schizophrenia, cognitive dysfunction has become an important treatment target. This shift in focus has been prompted by our evolving knowledge of brain changes associated with schizophrenia and by the mounting body of evidence indicating that cognition is closely related to functional outcome. Cognitive assessments can enhance the evaluation and treatment of all patients with schizophrenia, and clinicians may select from a variety of valid and reliable scales and assessment measures.

Practice parameters recommend systematic assessment of depression symptoms over the course of treatment to inform treatment planning; however, there are currently no guidelines regarding how to use symptom monitoring to guide treatment decisions for psychotherapy. The current study compared two time points (week 4 and week 8) for assessing symptoms during interpersonal psychotherapy for depressed adolescents (IPT-A) and explored four algorithms that use the symptom assessments to select the subsequent treatment. Method: Forty adolescents (aged 12À17 years) with a depression diagnosis began IPT-A with an initial treatment plan of 12 sessions delivered over 16 weeks. Adolescents were randomized to a week 4 or week 8 decision point for considering a change in treatment. Insufficient responders at either time point were randomized a second time to increased frequency of IPT-A (twice per week) or addition of fluoxetine. Measures were administered at baseline and weeks 4, 8, 12, and 16. Results: The week 4 decision point for assessing response and implementing treatment augmentation for insufficient responders was more efficacious for reducing depression symptoms than the week 8 decision point. There were significant differences between algorithms in depression and psychosocial functioning outcomes. Conclusion: Therapists implementing IPT-A should routinely monitor depression symptoms and consider augmenting treatment for insufficient responders as early as week 4 of treatment.

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Multiple characteristics of pretherapy Escherichia coli urine isolates from 39 children with acute, uncomplicated cystitis (including specific virulence genes and phylogenetic groups) identified an increased risk for recurrent bacteriuria after 3-day (but not 10-day) therapy with amoxicillin-clavulanate. Rapid testing conceivably could facilitate rational selection of treatment duration for pediatric cystitis. Certain traits might represent good targets for preventive interventions.