The lion's share of bacteria in various environments cannot be cloned in the laboratory and thus cannot be sequenced using existing technologies. A major goal of single-cell genomics is to complement gene-centric metagenomic data with whole-genome assemblies of uncultivated organisms. Assembly of single-cell data is challenging because of highly non-uniform read coverage as well as elevated levels of sequencing errors and chimeric reads. We describe SPAdes, a new assembler for both single-cell and standard (multicell) assembly, and demonstrate that it improves on the recently released E+V-SC assembler (specialized for single-cell data) and on popular assemblers Velvet and SoapDeNovo (for multicell data). SPAdes generates single-cell assemblies, providing information about genomes of uncultivatable bacteria that vastly exceeds what may be obtained via traditional metagenomics studies. SPAdes is available online ( http://bioinf.spbau.ru/spades ). It is distributed as open source software.

SPAdes, a new genome assembly algorithm and its applications to single-cell sequencing ( 7th Annual SFAF Meeting, 2012)

Acinetobacter baumannii has emerged as a highly troublesome pathogen for many institutions globally. As a consequence of its immense ability to acquire or upregulate antibiotic drug resistance determinants, it has justifiably been propelled to the forefront of scientific attention. Apart from its predilection for the seriously ill within intensive care units, A. baumannii has more recently caused a range of infectious syndromes in military personnel injured in the Iraq and Afghanistan conflicts. This review details the significant advances that have been made in our understanding of this remarkable organism over the last 10 years, including current taxonomy and species identification, issues with susceptibility testing, mechanisms of antibiotic resistance, global epidemiology, clinical impact of infection, host-pathogen interactions, and infection control and therapeutic considerations.

Acinetobacter baumannii: Emergence of a Successful Pathogen

https://www.cdc.gov/coronavirus/mers/downloads/Isolation2007.pdf

2007 Guideline for Isolation Precautions: Preventing Transmission of Infectious Agents in Health Care Settings.

INTRODUCTION 149 TAXONOMY 149 Historical Features 149 Current Taxonomic Status 149 Delineation of Species 149 Species of Clinical Importance 150 LABORATORY IDENTIFICATION 150 Isolation from Clinical Specimens 150 Morphological, Cultural, and Metabolic Characteristics 151 Species Identification 151 NOSOCOMIAL INFECTIONS CAUSED BY ACINETOBACTER SPP. 152 Overview 152 Respiratory Infection 152 Bacteremia 153 Meningitis 153 Urinary Tract Infection 154 Other Miscellaneous Infections 154 PATHOGENESIS OF ACINETOBACTER INFECTIONS 154 Predisposing Factors 154 Virulence of Acinetobacter spp. 154 EPIDEMIOLOGY 155 Human Carriage 155 Persistence in the Hospital Environment 155 TYPING SYSTEMS 156 Biotyping 156 Antibiograms 156 Serotyping 156 Phage Typing 157 Bacteriocin Typing 157 Protein Profiles 157 Multilocus Enzyme Electrophoretic Typing 157 Plasmid Profiles 157 Analysis by Pulsed-Field Gel Electrophoresis 157 Ribotyping 157 PCR-Based Methods 158 CLINICAL ANTIBIOTIC RESISTANCE 158 BIOCHEMICAL AND GENETIC MECHANISMS OF ANTIBIOTIC RESISTANCE 158 Genetics of Resistance 158 b-Lactams 159 Aminoglycosides 159 Quinolones 160 Other Antibiotics 160 THERAPY OF ACINETOBACTER INFECTIONS 160 CONCLUSIONS 160 ACKNOWLEDGMENTS 161 REFERENCES 161

/pdf/acinetobacter-spp-as-nosocomial-pathogens-microbiological-430u90opiv.pdf

Acinetobacter spp. as nosocomial pathogens: microbiological, clinical, and epidemiological features.

IOVS MS 11-7777 (Article 2207) Proofs Available _______________________ Dear Author: The proofs of your article above are available for your review. Please download the file located at this URLaddress: http://rapidproof.cadmus.com/RapidProof/retrieval/index.jsp Login: [your e-mail address]Password: 99S4UntgTcU9 You will need to have Adobe Acrobat Reader software to read this file. This is free software and is availablefor user downloading at http://www.adobe.com/products/acrobat/readstep.html. If you experience technical problems, please contact Tracey Ritchey(e-mail: ritcheyt@cadmus.com; phone: 717-721-2646) This file contains: -- Instructions to Author-- Adobe Acrobat Comments and Notes Instructions-- Publication Fees and Reprint Order Form-- Page Proofs for your article, table of contents precis blurb, and author queries - containing 5 pages Please insert your comments electronically (instructions enclosed), or print the PDF proofs and add yourcomments manually. Follow the enclosed instructions for emailing, faxing, or mailing your corrections.Return all materials within 48 hours (two business days) to assure quick publication of your article. NOTE: Effective with the January 2010 issue IOVS will be available online only. No printed issues will beproduced. Printed reprints may still be ordered using the file provided. If you have any questions regarding your article, please contact me. ALWAYS INCLUDE YOURARTICLE NO. (IOVS MS 11-7777) WITH ALL CORRESPONDENCE. Cathy FreyTel: 717-721-2616Fax: 717-738-9479 or 717-738-9478freyc@cadmus.com

/pdf/investigative-ophthalmology-and-visual-science-2azo1n1ewx.pdf

Investigative Ophthalmology and Visual Science

Since the 1970s, the spread of multidrug-resistant (MDR) Acinetobacter strains among critically ill, hospitalized patients, and subsequent epidemics, have become an increasing cause of concern. Reports of community-acquired Acinetobacter infections have also increased over the past decade. A recent manifestation of MDR Acinetobacter that has attracted public attention is its association with infections in severely injured soldiers. Here, we present an overview of the current knowledge of the genus Acinetobacter, with the emphasis on the clinically most important species, Acinetobacter baumannii.

/pdf/an-increasing-threat-in-hospitals-multidrug-resistant-4mki9sim2r.pdf

An increasing threat in hospitals: multidrug-resistant Acinetobacter baumannii.

In the past decade, various methods have been developed for the identification and typing of prokaryotic and eukaryotic organisms at the DNA level. These methods differ in their taxonomic range, discriminatory power, reproducibility, and ease of interpretation and standardization ([62][1], [67][2

Amplified-Fragment Length Polymorphism Analysis: the State of an Art

Thirty-one Acinetobacter baumannii strains, comprising 14 strains from 14 outbreaks in different northwestern European cities and 17 sporadic strains, were compared by investigating various properties of the strains including biotype, antibiogram, cell envelope protein electrophoretic profile, ribotype pattern, and the band pattern generated by a novel genomic fingerprinting method, named AFLP, which is based on the selective amplification of restriction fragments. Results showed that 12 strains from unrelated outbreaks were linked together in two clusters according to their similarities by these typing methods, whereas sporadic strains were more heterogeneous. Outbreak strains appeared to be markedly more resistant to antibiotics than nonoutbreak strains. The uniformity of typing characters in two sets of outbreak strains suggests that strains in each cluster have a common clonal origin.

Comparison of outbreak and nonoutbreak Acinetobacter baumannii strains by genotypic and phenotypic methods.

Following characterisation by phenotypic tests and amplified ribosomal DNA restriction analysis (ARDRA), 50 tetracycline-resistant (MIC≥165mumg/L) Acinetobacter strains from clinical (n=35) and aquatic (n=15) samples were analysed by PCR for tetracycline resistance (Tet) determinants of classes A–E. All the clinical strains were A. baumannii; most (33 of 35) had Tet A (n=16) or B (n=17) determinants, and only two did not yield amplicons with primers for any of the five tetracycline resistance determinants. The aquatic strains belonged to genomic species other than A. baumannii, and most (12 of 15) did not contain determinants Tet A–E. Strains negative for Tet A–E were also negative for Tet G and M; further analysis of two aquatic strains with specific primers for Tet O and Tet Y and degenerate primers for Tet M-S-O-P(B)-Q also showed negative results. Transfer of tetracycline resistance was tested for 20 strains with three aquatic Acinetobacter strains and Escherichia coli K-12 as recipients. Transfer of resistance was demonstrated between aquatic strains from distinct ecological niches, but not from clinical to aquatic strains, nor from any Acinetobacter strain to E. coli K-12. Most transconjugants acquired multiple relatively small plasmids (<36 kb). Transfer did not occur when DNA from the donor strains was added to the recipient cultures and was not affected by deoxyribonuclease I, suggesting a conjugative mechanism. It is concluded that Tet A and B are widespread among tetracycline-resistant A. baumannii strains of clinical origin, but unknown genetic determinants are responsible for most tetracycline resistance among aquatic Acinetobacter spp. These differences, together with the inability of clinical strains to transfer tetracycline resistance in vitro to aquatic strains, contra-indicate any important flow of tetracycline resistance genes between clinical and aquatic acinetobacter populations.

Distribution and in-vitro transfer of tetracycline resistance determinants in clinical and aquatic Acinetobacter strains

The taxonomic status of two recently described phenetically distinctive groups within the genus Acinetobacter, designated phenon 1 and phenon 2, was investigated further. The study collection included 51 strains, mainly of clinical origin, from different European countries with properties of either phenon 1 (29 strains) or phenon 2 (22 strains). DNA-DNA hybridization studies and DNA polymorphism analysis by AFLP revealed that these phenons represented two new genomic species. Furthermore, 16S rRNA gene sequence analysis of three representatives of each phenon showed that they formed two distinct lineages within the genus Acinetobacter. The two phenons could be distinguished from each other and from all hitherto-described Acinetobacter (genomic) species by specific phenotypic features and amplified rDNA restriction analysis patterns. The names Acinetobacter ursingii sp. nov. (type strain LUH 3792T = NIPH 137T = LMG 19575T = CNCTC 6735T) and Acinetobacter schindleri sp. nov. (type strain LUH 5832T = NIPH 1034T = LMG 19576T = CNCTC 6736T) are proposed for phenon 1 and phenon 2, respectively. Clinical and epidemiological data indicate that A. ursingii has the capacity to cause bloodstream infections in hospitalized patients.

/pdf/acinetobacter-ursingii-sp-nov-and-acinetobacter-schindleri-2pt5qcvuhy.pdf

L. Dijkshoorn

Papers

An increasing threat in hospitals: multidrug-resistant Acinetobacter baumannii.

Amplified-Fragment Length Polymorphism Analysis: the State of an Art

Comparison of outbreak and nonoutbreak Acinetobacter baumannii strains by genotypic and phenotypic methods.

Distribution and in-vitro transfer of tetracycline resistance determinants in clinical and aquatic Acinetobacter strains

Acinetobacter ursingii sp. nov. and Acinetobacter schindleri sp. nov., isolated from human clinical specimens.