Dissemination of ESBL-producing E. coli ST131 through wastewater and environmental water in Switzerland.

The E. coli lineage ST131 is a major cause of multidrug-resistant urinary tract and bloodstream infections worldwide. Recently emerged ST131 sublineages spread globally within few years, but their dissemination routes are incompletely understood. In this study, we investigate the potential role of wastewater and surface water in the spread of extended-spectrum ß-lactamase (ESBL)-producing ST131. Streams, lakes, and two wastewater treatment plants (WWTPs) in the canton of Zug, Switzerland, were consecutively sampled over 1.5 years. ST131 was detected in 38% of the samples taken downstream (1-5 km) of WWTP discharge sites, but usually absent in water bodies distant from urban areas or WWTP discharge. Specific strains were repeatedly isolated (≤5 pairwise cgSNP distance) from wastewater or river sites downstream of effluent discharge, indicating their repeated entry or persistence in WWTPs in large concentrations. Genetic characterization of the ESBL-producing water isolates revealed a predominance of clades A and C1 and an emerging ciprofloxacin-resistant sublineage with mutations in quinolone resistance determining regions (QRDR) within clade A. Multiple isolates belonged to internationally circulating sublineages, including C1-M27 and papGII + sublineages with chromosomally encoded ESBLs. This study demonstrates that the clinically relevant E. coli lineage ST131 pollutes river ecosystems, representing a significant challenge to public health and to technologies to minimize their entry into the water environment.

Complete Genome Sequence of Colistin-Resistant, mcr-10-Harboring, Enterobacter cloacae Isolate AVS0889, Recovered from River Water in Switzerland.

Here, we report the complete genome sequence of colistin-resistant Enterobacter cloacae sequence type 1 (ST1) isolate AVS0889, which was recovered from a river in Switzerland in 2021. The genome consists of a 4.95-Mbp chromosome and five plasmids, including a large plasmid (90.8 kb) harboring a disrupted mcr-10 gene.

Complete Genome Sequence of Hafnia paralvei Isolate AVS0177, Harboring mcr-9 on a Plasmid.

Here, we report the complete genome sequence of a Hafnia paralvei strain isolated from a lake in Switzerland in 2020. The genome consists of a 4.7-Mbp chromosome, a large plasmid (213 kb) harboring mcr-9, and a small plasmid (6 kb).

Complete Genome Sequence of Escherichia coli Sequence Type 1193 Isolate AVS0096, Recovered from River Water in Switzerland.

Escherichia coli sequence type 1193 (ST1193) is an important cause of multidrug-resistant extraintestinal infections. Here, we report the complete genome sequence of strain AVS0096, isolated from river water in Switzerland in 2020. The genome consists of a chromosome (4.9 Mbp), a multidrug resistance plasmid (101 kb), and two small plasmids.

Seizures, Systemic Inflammatory Response, and Rhabdomyolysis Associated With Laboratory-Confirmed 2C-I and 25-I Exposure.

The 2C drugs are hallucinogenic phenethylamines. They and their n-benzyloxymethyl analogs have become popular as "legal highs," and significant toxicity has been attributed to their use. We report on a case of seizures, systemic inflammatory response, and rhabdomyolysis associated with laboratory-confirmed 4-iodo-2,5-dimethoxyphenethylamine and 4-iodo-2,5-dimethoxy-N-(2-methoxybenzyl) phenethylamine exposure. A 17-year-old male teenager developed seizures after taking "2 strips of acid." The seizures resolved with midazolam, but he became apneic and was intubated. His head computed tomography was unremarkable. Initial creatinine level was 1.5 mg/dL, with a creatine kinase of 112 U/L. His urine immunoassay drug screen was negative. He was extubated within 12 hours but had elevated temperatures for 48 hours. He was treated with antibiotics, but no source of infection was identified. His creatinine level peaked at 2.46 mg/dL. His creatine kinase peaked 72 hours later at 14579 U/L. He was treated with intravenous fluids and did not require renal replacement therapy. He recovered fully and was discharged after 5 days. Serum and urine samples were tested using liquid chromatography time-of-flight mass spectrometry. We detected 4-iodo-2,5-dimethoxyphenethylamine and 4-iodo-2,5-dimethoxy-N-(2-methoxybenzyl) phenethylamine in both serum and urine. No other substances were detected. The 2C drugs and their n-benzyloxymethyl analogs are potent serotonergic agents. Their use has been associated with multiple adverse effects including seizures, rhabdomyolysis, and death. They should be considered in differential diagnosis for drug-induced seizures and as a cause for systemic inflammatory response. This case highlights the significant toxicity seen with these compounds.

Lemierre's syndrome: an unusual cause of sepsis and abdominal pain.

OBJECTIVE: To describe a patient with Lemierre's syndrome who presented with acute abdominal findings and to describe the evaluation and treatment of this syndrome. DESIGN: Case report. SETTING: A 38-bed, pediatric intensive care unit at a tertiary care children's hospital. PATIENT: One patient presenting with signs of severe sepsis and acute abdominal pain. INTERVENTIONS: Intravenous hydration, inotropic support, thoracostomy tube drainage of a pleural effusion, and prolonged antimicrobial therapy. MEASUREMENT AND MAIN RESULTS: The patient presented with severe sepsis and abdominal pain. After Fusobacterium necrophorum grew in blood cultures, anaerobic antimicrobial therapy was initiated. Doppler duplex ultrasonography and magnetic resonance venography demonstrated thrombus formation in the left internal jugular vein. Computed tomography of the chest demonstrated bibasilar lung nodules consistent with septic emboli. The patient was treated with ampicillin-sulbactam and metronidazole intravenously for 3 wks, followed by a 3-wk course of oral amoxicillin/clavulanate. He had a good recovery, and his thrombus had resolved at the time of discharge. CONCLUSION: Lemierre's syndrome occurs in young, otherwise healthy patients, and it thus needs to remain high on the differential diagnosis for this group of patients presenting with severe sepsis. The diagnosis can be confounded by a lack of symptoms of pharyngitis at the time of presentation and end-organ dysfunction associated with severe sepsis, suggesting alternative sources of infection.