An outbreak of amikacin- and ciprofloxacin-resistant Acinetobacter baumannii ST219 in Tokai University hospital's emergency intensive care unit was caused by its colonization in water systems and subsequent spread through oral care using tap water. The outbreak was successfully controlled after replacement of the water system and implementation as of daily cleaning of water taps and oral care with a dry method. It is important to strictly manage the water system in critical care areas.

A series of clinical isolates of drug-resistant (DR) Acinetobacter baumannii with diverse drug susceptibility was detected from eight patients in the emergency intensive care unit of Tokai University Hospital. The initial isolate was obtained in March 2010 (A. baumannii Tokai strain 1); subsequently, seven isolates were obtained from patients (A. baumannii Tokai strains 2–8) and one isolate was obtained from an air-fluidized bed used by five of the patients during the 3 months from August to November 2011. The isolates were classified into three types of antimicrobial drug resistance patterns (RRR, SRR and SSR) according to their susceptibility (S) or resistance (R) to imipenem, amikacin and ciprofloxacin, respectively. Genotyping of these isolates by multilocus sequence typing revealed one sequence type, ST208, whilst that by a DiversiLab analysis revealed two subtypes. All the isolates were positive for blaOXA-51-like and blaOXA-66, as assessed by PCR and DNA sequencing. A. baumannii Tokai strains 1–8 and 10 (RRR, SRR and SSR) had quinolone resistance-associated mutations in gyrA/parC, as revealed by DNA sequencing. The ISAba1 upstream of blaOXA-51-like and aminoglycoside resistance-associated gene, armA, were detected in A. baumannii Tokai strains 1–7 and 10 (RRR and SRR) as assessed by PCR. Among the genes encoding resistance–nodulation–division family pumps (adeB, adeG and adeJ) and outer-membrane porins (oprD and carO), overexpression of adeB and adeJ and suppression of oprD and carO were seen in isolates of A. baumannii Tokai strain 2 (RRR), as assessed by real-time PCR. Thus, the molecular characterization of a series of isolates of DR A. baumannii revealed the outbreak of ST208 and diverse antimicrobial drug susceptibilities, which almost correlated with differential gene alterations responsible for each type of drug resistance.

A 66-year-old female presented with progressive left-sided chest pain. The electrocardiogram (ECG) showed changes typical of an anterior wall myocardial infarction. She immediately underwent coronary angiography which revealed normal coronary arteries. Cardiac MRI (CMR) was then performed, which showed diffuse high intensity on T2-weighted images and transmural late gadolinium enhancement (LGE) in the apical wall. While transmural LGE was not typical for myocarditis, the patient was diagnosed with acute myocarditis based on the clinical and angiographic ndings in addition to the high intensity of T2-weighted image. During the course of the disease, the apical wall developed an aneurysm corresponding to the area of transmural LGE on CMR and an intraventricular thrombus formed in the aneurysm. She was given heparin and discharged after resolution of the thrombus. Further evaluation is warranted if this uncommon imaging nding is detected to prevent thromboembolic complications.

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