Bacillus toyonensis is widespread in nature. Multidrug-resistant B. toyonensis strain 4HC1 was isolated from polyethylene submerged in the water column near a beach in Øygarden, Norway. see more We analysed the whole genome sequence of strain 4HC1 in order to understand the genetic basis of the observed phenotypic antibiotic resistance. Whole-genome sequencing of B. toyonensis strain 4HC1 was performed on Illumina MiSeq platform using 2×300 bp chemistry. The genome sequence was assembled using SPAdes v.3.13.0 and was annotated using the NCBI Prokaryotic Genome Annotation Pipeline (PGAP). The draft genome of strain 4HC1 is 6 156 259 bp (133 contigs) in size with a GC content of 34.95%. The genome comprises 6089 protein-coding genes, 86 tRNAs and 24 rRNAs. Strain 4HC1 is resistant to cefotaxime, trimethoprim and ampicillin and carries various antibiotic resistance genes (ARGs), including several β-lactamases, aminoglycoside 6-adenylyltransferase, a TetM family tetracycline resistance gene, two different tetracycline efflux pumps, and a bleomycin resistance gene. Several virulence genes including genes involved in immune evasion, iron acquisition and toxins were also detected in strain 4HC1. The draft genome sequence of B. toyonensis strain 4HC1 released here shows the presence of various ARGs and virulence genes in a multidrug-resistant strain isolated from marine plastic.The draft genome sequence of B. toyonensis strain 4HC1 released here shows the presence of various ARGs and virulence genes in a multidrug-resistant strain isolated from marine plastic.Recent COVID-19 (coronavirus disease 2019) host genetics studies suggest enrichment of mutations in genes involved in the regulation of type I and type III interferon (IFN) immunity in patients with severe COVID-19 infection. We performed whole-genome sequencing analysis of samples obtained from patients participating in the ongoing ODYSSEY phase 3 study of hospitalised patients with severe COVID-19 infection receiving supplemental oxygen support. We focused on burden testing of categories of rare and common loss-of-function (LOF) variants in all of the IFN pathway genes, specifically with MAF less then 0.1% and MAF less then 1%. In a model including LOF and missense variants (MAF less then 1%), we report a significant signal in both INFAR1 and IFNAR2. We report carriers of rare variants in our COVID-19 cohort, including a stop-gain IFNAR2 (NM_000874exon9c.C966Ap.Y322X) amongst carriers of several other IFNAR rare nonsynonymous variants. Furthermore, we report an increased allelic frequency of common IFNAR2 variants in our data, reported also by the COVID-19 Host Genetics Initiative. There is currently no consensus on the most effective treatment protocol for necrotizing otitis externa (NOE). This article aims to produce a NOE treatment protocol from the literature and clinical experience. A total of 26 case series from the literature were reviewed in combination with a retrospective case series of inpatients from Hull University Teaching Hospitals NHS Trust from 2013-2018. Over 5 years, 40 patients were identified, with only 29 being analysed due to unavailable or incomplete case notes. In the literature review, the most common bacterial species causing NOE was Pseudomonas aeruginosa. Resistance to ciprofloxacin was prevalent, however multidrug resistance was rare. Ciprofloxacin and ceftazidime were the most widely used antibiotics. No ceftazidime resistance was reported in the literature or in our cohort. The average age of the patients in our cohort was 80 years. Moreover, 62% had either diabetes mellitus or were immunosuppressed. One patient died directly due to NOE-related sepsis. Intravenous ceftazidime monotherapy was mostly used. The duration of treatment was 6-7 weeks, with no relapses documented. Ceftazidime monotherapy was an effective empirical treatment in our cohort, and a total duration of 6-7 weeks of antibiotics was sufficient. We have created a standardised treatment protocol based on our findings that will need to be validated in a larger cohort of patients.Ceftazidime monotherapy was an effective empirical treatment in our cohort, and a total duration of 6-7 weeks of antibiotics was sufficient. We have created a standardised treatment protocol based on our findings that will need to be validated in a larger cohort of patients. Brucella anthropi is a Gram-negative, aerobic, motile, oxidase-positive, non-fermentative Alphaproteobacteria belonging to the family Brucellaceae. It is most commonly found in soil but is an emerging, opportunistic, nosocomial human pathogen. The objective of this study was to understand the genome features of a drug-resistant B. anthropi (SOA01) isolated from a blood culture of a 4-day-old neonate and to determine its antimicrobial resistance and pathogenic potential. Hybrid genome assembly of B. anthropi strain SOA01 was generated using quality-trimmed short Illumina and long MinION reads. Identification and antimicrobial susceptibility profile were determined by MALDI-TOF, in silico ribosomal multilocus sequence typing (rMLST) and VITEK®2, respectively. PATRIC webserver and VFDB were used to identify antimicrobial resistance (AMR), virulence factor (VF) and transporter genes. Multidrug-resistant B. anthropi strain SOA01 has a genome of 4 975 830 bp with a G+C content of 56.29%. Several AMR, VF and tmary habitat of soil to the human system. Since it is often misidentified as Brucella melitensis or Brucella suis, genome characterisation and detailed understanding of its biology are crucial.Alzheimer's disease (AD) is the most common neurodegenerative disorder where the accumulation of amyloid plaques and the formation of tau tangles are the prominent pathological hallmarks. Increasing preclinical and clinical studies have revealed that different components of the immune system may act as important contributors to AD etiology and pathogenesis. The recognition of misfolded Aβ and tau by immune cells can trigger a series of complex immune responses in AD, and then lead to neuroinflammation and neurodegeneration. In parallel, genome-wide association studies have also identified several immune related loci associated with increased - risk of AD by interfering with the function of immune cells. Other immune related factors, such as impaired immunometabolism, defective meningeal lymphatic vessels and autoimmunity might also be involved in the pathogenesis of AD. Here, we review the data showing the alterations of immune cells in the AD trajectory and seek to demonstrate the crosstalk between the immune cell dysfunction and AD pathology.