Viruses are among the most common causes of acute gastroenteritis. In recent years, new viruses causing outbreaks of acute gastroenteritis have been described. Among these, Aichi virus was identified in Japan in 1989. Aichi virus belongs to the Kobuvirus genus in the family Picornaviridae. This virus has been detected in outbreaks of gastroenteritis associated with oyster consumption and in pediatric stool samples, but little is known about its epidemiology or pathogenesis. In the present study, the prevalence of antibodies to Aichi virus in a Spanish population was determined between 2007 and 2008 by using an enzyme-linked immunosorbent assay (ELISA). As in previous studies, a high seroprevalence of antibodies to Aichi virus (70%) was observed, with levels differing according to age. We observed significant differences in titers of antibody to Aichi virus among different age groups, grouped by decades. We report high ELISA and neutralizing antibody titers, and both titers fitted a sigmoid curve significantly. However, this virus is seldom detected; therefore, further studies are needed to gain a better understanding of its importance as a pathogenic agent.Viruses are a common cause of gastroenteritis and affect humans of all ages. Rotavirus (mainly group A), calicivirus (including norovirus and sapovirus), adenovirus, and astrovirus are considered the major causes of viral gastroenteritis. However, in many cases of gastroenteritis, no specific pathogen can be identified, and other viruses, such as Aichi virus, may be involved. This virus was proposed as a probable cause of nonbacterial gastroenteritis associated with oyster consumption in Aichi, Japan, in 1989 (16). Aichi virus belongs to the genus Kobuvirus, in the family Picornaviridae (9, 19). The major differences between the genus Kobuvirus and other genera of the same family are found in the coding region of the L protein, in the absence of a VP0 cleavage site, and in the distinct morphology of the 2A protein (14).The Aichi virus genome is a single-stranded, positive-sense RNA molecule of 8,260 nucleotides and has a poly(A) tail. The single large open reading frame encodes a polyprotein of 2,432 amino acids. This polyprotein, like those of the other members of the family, is cleaved into the structural proteins VP0, VP3, and VP1 and the nonstructural proteins 2A, 2B, 2C, 3A, 3B, 3C, and 3D (11,19). Aichi virus has been classified into two genotypes (A and B) by phylogenetic analysis of a 519-bp sequence at the 3C-3D (3CD) junction (20) Little is known about the incidence of Aichi virus infection in humans. Aichi virus antigen or viral RNA was first detected in fecal samples collected in Japan (17). The virus was later isolated from patients with gastroenteritis, comprising Pakistani children and Japanese travelers from Southeast Asia (18), and among patients from Japan, Bangladesh, Thailand, and Vietnam (8). In 2006, the virus was isolated for the first time in the Americas (Brazil) and Europe (Germany) (7), and since then, Aichi virus has been detected i...

BackgroundPseudomonas aeruginosa is a common pathogen causing hospital-acquired infections. Carbapenem resistance in P. aeruginosa is either mediated via a combination of efflux pumps, AmpC overexpression, and porin loss, or through an acquired carbapenemase. Carbapenemase-producing P. aeruginosa (CPPA) strains are known to cause outbreaks and harbour a reservoir of mobile antibiotic resistance genes, however, few molecular surveillance data is available. The aim of this study was to analyse the prevalence and epidemiology of CPPA in three German medical centres from 2015 to 2017.MethodsIdentification and susceptibility testing were performed with VITEK 2 system. P. aeruginosa non-susceptible to piperacillin, ceftazidime, cefepime, imipenem, meropenem and ciprofloxacin (4MRGN according to the German classification guideline) isolated from 2015 to 2017 were analysed. A two-step algorithm to detect carbapenemases was performed: phenotypic tests (EDTA- and cloxacillin-combined disk tests) followed by PCR, Sanger sequencing, and eventually whole genome sequencing. CPPA isolates were further genotyped by RAPD and PFGE. In-hospital transmission was investigated using conventional epidemiology.ResultsSixty two P. aeruginosa isolates were available for further analysis, of which 21 were CPPA as follows: blaVIM-1 (n = 2), blaVIM-2 (n = 17), blaNDM-1/blaGES-5 (n = 1) and the newly described blaIMP-82 (n = 1). CPPA were mostly hospital-acquired (71.4%) and isolated on intensive care units (66.7%). All (except one) were from the tertiary care centre. PFGE typing revealed one large cluster of VIM-2-producing CPPA containing 13 isolates. However, using conventional epidemiology, we were only able to confirm three patient-to-patient transmissions, and one room-to-patient transmission, on several intensive care units.ConclusionsThese data give insight into the epidemiology of CPPA in three centres in Germany over a period of 3 years. Carbapenemases are a relevant resistance mechanism in 4MRGN-P. aeruginosa, illustrated by genetically related VIM-2-producing strains that seem to be endemic in this region. Our data suggest that infection control measures should especially focus on controlling transmission on the ICU and support the need for a local molecular surveillance system.

BackgroundA. baumannii is a common nosocomial pathogen known for its high transmission potential. A high rate of carbapenem-susceptible Acinetobacter calcoaceticus-Acinetobacter baumannii (ACB)-complex in clinical specimens led to the implementation of a pathogen-based surveillance on a 32-bed surgical intensive care unit (SICU) in a German tertiary care centre.MethodsBetween April 2017 and March 2018, ACB-complex isolates with an epidemiological link to the SICU were further assessed. Identification to the species level was carried out using a multiplex PCR targeting the gyrB gene, followed by RAPD, PFGE (ApaI) and whole genome sequencing (WGS, core genome MLST, SeqSphere+ software, Ridom). Additional infection prevention and control (IPC) measures were introduced as follows: epidemiological investigations, hand hygiene training, additional terminal cleaning and disinfection incl. UV-light, screening for carbapenem-susceptible A. baumannii and environmental sampling. Hospital-acquired infections were classified according to the CDC definitions.ResultsFourty four patients were colonized/infected with one or two (different) carbapenem-susceptible ACB-complex isolates. Fourty three out of 48 isolates were classified as hospital-acquired (detection on or after 3rd day of admission). Nearly all isolates were identified as A. baumannii, only four as A. pittii. Twelve patients developed A. baumannii infections. Genotyping revealed two pulsotype clusters, which were confirmed to be cgMLST clonal cluster type 1770 (n = 8 patients) and type 1769 (n = 12 patients) by WGS. All other isolates were distinct from each other. Nearly all transmission events of the two clonal clusters were confirmed by conventional epidemiology. Transmissions stopped after a period of several months. Environmental sampling revealed a relevant dissemination of A. baumannii, but only a few isolates corresponded to clinical strains. Introduction of the additional screening revealed a significantly earlier detection of carbapenem-susceptible A. baumannii during hospitalization.ConclusionsA molecular and infection surveillance of ACB-complex based on identification to the species level, classic epidemiology and genotyping revealed simultaneously occurring independent transmission events and clusters of hospital-acquired A. baumannii. This underlines the importance of such an extensive surveillance methodology in IPC programmes also for carbapenem-susceptible A. baumannii.

Here we report two cases of isolation of Aurantimonas altamirensis from pleural fluid and blood. The strains were identified by 16S rRNA gene sequencing. A. altamirensis appears to be a rare pathogen involved in unusual infectious processes, and must be isolated and studied at the molecular level for correct clinical diagnosis.

Genotype II.4 noroviruses (NoVs) are a leading cause of epidemic acute gastroenteritis in children and adults worldwide. The prevalence of different NoV genotypes causing outbreaks and sporadic cases of acute gastroenteritis in the region of Valencia, Spain, during a 4-year period (2008-11) was investigated. NoVs were detected in 42 out of 55 (76.3%) outbreaks and in 26 out of 332 (7.8%) sporadic cases of acute gastroenteritis. Genogroup GII strains were predominant in outbreaks and sporadic cases. Different genotype GII.4 variants were found (Yerseke_2006a, Den Haag_2006b, Apeldoorn_2007, and New Orleans_2009), with the latter variant detected most frequently (35.3%). A recombinant P domain of the NoV GII.4 Apeldoorn_2007 variant was produced in Escherichia coli and used as the coating antigen in an enzyme immunoassay to survey the IgG antibody seroprevalence against NoV GII.4 in a Spanish population. Baculovirus-expressed virus-like particles (VLPs) of NoV GII.4 Den Haag_2006b variant were also produced and used as antigen to compare seroreactivity. Of the 434 serum specimens analyzed, 429 (98.6%) had antibodies against the P domain. The comparison of reactivities of 30 serum samples to the NoV GII.4 P polypeptide and VLP showed reproducible results with a correlation coefficient of r = 0.794. Titers of antibodies to the P domain increased gradually and significantly with age, reaching the highest levels at the age group of 41-50 years. These results confirm the high prevalence of NoV GII.4 infections in Valencia from early childhood.

Antimicrobial resistance is a major health care problem, with the intensive use of heavy metals and biocides recently identified as a potential factor contributing to the aggravation of this situation. The present study investigated heavy metal susceptibility and genetic resistance determinants in Escherichia coli isolated from clinical urine samples from Sweden, Germany, and Spain. A total of 186 isolates were tested for their sodium arsenite, silver nitrate, and copper(II) sulfate MICs. In addition, 88 of these isolates were subjected to whole-genome sequencing for characterization of their genetic resistance determinants and epidemiology. For sodium arsenite, the isolates could be categorized into a resistant and a nonresistant group based on MIC values. Isolates of the resistant group exhibited the chromosomal ars operon and belonged to non-B2 phylogenetic groups; in contrast, within the B2 phylogroup, no ars operon was found, and the isolates were susceptible to sodium arsenite. Two isolates also harbored the silver/copper resistance determinant pco/sil, and they belonged to sequence types ST10 (phylogroup A) and ST295 (phylogroup C). The ST295 isolate had a silver nitrate MIC of ≥512 mg/liter and additionally produced extended-spectrum beta-lactamases. To our knowledge, this is the first study to describe the distribution of the arsenic resistance ars operon within phylogroups of E. coli strains isolated from patients with urinary tract infections. The arsenic resistance ars operon was present only in all non-B2 clades, which have previously been associated with the environment and commensalism in both humans and animals, while B2 clades lacked the ars operon.

No abstract

Trichosporon asahii fatal infection in a preterm newborn We present a case of Trichosporon asahii fatal infection recognized post mortem in a premature newborn baby of 685 g. Trichosporon asahii isolated from endovascular catheters and endotraqueal tube, is an opportunistic yeast described like an emergent pathogen in serious systemic infections and nosocomial infections in the neonatal intensive care units. The colonization and disease by this uncommon microorganism, usually is unspecific and has similar clinical presentation to other fungal infections with a bad prognosis.