A ciprofloxacin-resistant Escherichia coli isolate, isolate 1B, was obtained from a urinary specimen of a Canadian patient treated with norfloxacin for infection due to a ciprofloxacin-susceptible isolate, isolate 1A. Both isolates harbored a plasmid-encoded sul1-type integron with qnrA1 and bla VEB-1 genes. Isolate 1B had amino acid substitutions in gyrase and topoisomerase.Plasmid-mediated resistance to the quinolones was reported first in 1998 from a Klebsiella pneumoniae isolate from the United States (7). The plasmid-encoded protein QnrA protects DNA gyrase and topoisomerase IV from the inhibitory activity of quinolones (15,16). Another plasmid-mediated quinolone resistance determinant, QnrS, sharing 59% amino acid identity with QnrA, has been identified in Japan from a single Shigella flexneri isolate (3). These Qnr determinants confer resistance to quinolones and reduced susceptibility to fluoroquinolones (9). Several studies showed a worldwide dissemination of QnrA determinants among enterobacterial isolates that often also produced extended-spectrum ␤-lactamases (ESBLs), such as SHV-5, SHV-7, CTX-M-9, and VEB-1 (9, 12, 13).Our study was initiated by the observation of in vivo selection of fluoroquinolone resistance in Escherichia coli. Strains 1A and 1B were isolated in December 2000 and April 2001, respectively, from urine samples from a patient with community-acquired urinary tract infections in Calgary, Canada. After isolation of strain 1A, the patient received norfloxacin for five days. Resistance to quinolones and fluoroquinolones and production of ESBL were evaluated as previously described and interpreted according to Clinical and Laboratory Standards Institute guidelines (1, 10). Both isolates had an identical ESBL-mediated ␤-lactam resistance phenotype, whereas isolate 1A had reduced susceptibility to nalidixic acid and ciprofloxacin and isolate 1B was resistant to nalidixic acid and ciprofloxacin (Table 1). Pulsed-field gel electrophoresis analysis showed that strains 1A and 1B were clonally related (data not shown). Since isolate 1A had reduced susceptibility to quinolones, the qnrA and qnrS genes were searched for by using a PCR protocol as described previously (6) with specific primers for qnrA (6) and qnrS (primers QnrS-A2 [5Ј-AGTGATCTCA CCTTCACCGC-3Ј] and QnrS-B2 [5Ј-CAGGCTGCAATTTT GATACC-3Ј]). Total DNAs of E. coli Lo (qnrA) (6) and plasmid PBC-H2.6 (qnrS) (gift from M. Hata) were used as controls. PCR and sequencing revealed that isolates E. coli 1A and 1B possessed the qnrA1 gene (9), being the first identification of plasmid-mediated quinolone resistance in Canada and also the first evidence of such a determinant in a clear community-acquired isolate.To explain the difference in fluoroquinolone resistance between the two isolates, the quinolone resistance-determining regions of subunit gyrA of the DNA gyrase gene (primers gyrA6 and gyrA631R) and of subunit parC of the topoisomer-

The central autonomic response to autonomic challenges is altered in patients with Takotsubo cardiomyopathy, thus suggesting a dysregulation of the central autonomic nervous system network. Subsequent studies are needed to unveil whether these alterations are causal or predisposing factors to Takotsubo cardiomyopathy.

Detection of right heart thrombi (RHT) in the context of pulmonary thromboembolism (PE) is uncommon (4–18%) and increases the risk of mortality beyond the presence of PE alone. Type A thrombi are serpiginous and highly mobile and are thought to be originated from large veins and captured in-transit within the right heart. Optimal management of RHT is still uncertain. A 79-year-old woman, with a history of recent total hysterectomy with adnexectomy and a Wells procedure, presented to the emergency department following an episode of syncope. Computed tomography revealed bilateral PE and the presence of a right atrial thrombus. Transthoracic echocardiography demonstrated a free-floating type A thrombus in the right atrium, protruding into the right ventricle, and signs of pulmonary hypertension and right ventricle dysfunction. Considering the recent surgery and clinical stability, treatment with heparin alone was decided. Subsequent clinical improvement was observed and echocardiographic follow-up revealed complete thrombus dissolution and complete recovery of right ventricle function. Most authors recommend treatment of PE with RHT with thrombolysis or embolectomy followed by anticoagulation, although evidence is scarce. Individual risk of hemorrhage and operatory-related mortality should be taken into account when defining the treatment strategy especially when benefit is not firmly established.

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We report the case of a 37-year-old male patient admitted to the cardiac intensive care unit for acute pulmonary edema. He had a history of excessive alcoholic consumption and had had a viral syndrome in the preceding 10 days. A transthoracic echocardiogram revealed severe biventricular dysfunction, mild dilatation of the left heart chambers, and severe dilatation of the right chambers. Nonsustained ventricular tachycardia with a left bundle branch block morphology was detected during electrocardiographic monitoring. In the follow-up, he underwent a contrast-enhanced transthoracic echocardiogram and a cardiac resonance which were compatible with the diagnosis of arrhythmogenic right ventricular cardiomyopathy with biventricular involvement. Molecular analysis detected the mutation c.1423+2T>G (IVS10 ds +2T>G) in intron 10 of the gene DSG2 (desmoglein-2) in heterozygosity. To our knowledge, this mutation has not been previously described in arrhythmogenic right ventricular cardiomyopathy.

The image shows a pseudoaneurysm of the mitral-aortic intervalvular fibrosa and a fistula between the non-coronary sinus and the left atrium.

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