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Drug-Resistant Streptococcus Pneumoniae and Methicillin
NEWS & NOTES Conference Summary pneumoniae can vary among popula- conference sessions was that statically tions and is influenced by local pre- sound methods of data collection that Drug-resistant scribing practices and the prevalence capture valid, meaningful, and useful of resistant clones. Conference pre- data and meet the financial restric- Streptococcus senters discussed the role of surveil- tions of state budgets are indicated. pneumoniae and lance in raising awareness of the Active, population-based surveil- Methicillin- resistance problem and in monitoring lance for collecting relevant isolates is the effectiveness of prevention and considered the standard criterion. resistant control programs. National- and state- Unfortunately, this type of surveil- Staphylococcus level epidemiologists discussed the lance is labor-intensive and costly, aureus benefits of including state-level sur- making it an impractical choice for 1 veillance data with appropriate antibi- many states. The challenges of isolate Surveillance otic use programs designed to address collection, packaging and transport, The Centers for Disease Control the antibiotic prescribing practices of data collection, and analysis may and Prevention (CDC) convened a clinicians. The potential for local sur- place an unacceptable workload on conference on March 12–13, 2003, in veillance to provide information on laboratory and epidemiology person- Atlanta, Georgia, to discuss improv- the impact of a new pneumococcal nel. ing state-based surveillance of drug- vaccine for children was also exam- Epidemiologists from several state resistant Streptococcus pneumoniae ined; the vaccine has been shown to health departments that have elected (DRSP) and methicillin-resistant reduce infections caused by resistance to implement enhanced antimicrobial Staphylococcus aureus (MRSA). -
The Fine Structure of Diplococcus Pneumoniae
THE FINE STRUCTURE OF DIPLOCOCCUS PNEUMONIAE ALEXANDER TOMASZ, Ph.D., JAMES D. JAMIESON, M.D., and ELENA OTTOLENGtII, M.D. From The Rockefeller Institute and the New York University School of Medicine, New York ABSTRACT The fine structure of an unencapsulated strain of Diplococcus pneumoniae is described. A strik- ing feature of thcsc bacteria is an intracytoplasmic membrane system which appears to be an extension of septa of dividing bactcria. The possible function of these structures and their relationship to the plasma membrane and other types of intracytoplasmic membranes found in pncumococcus is discussed. INTRODUCTION Our main interest in the fine structure of Diplo- walls. Throughout this paper, such preparations will coccus pneumoniae stems from the fact that these be referred to as "spheroplasts." bacteria readily undergo genetic transformation. The bacteria were fixed and stained according to the method of Ryter and Kellenberger (4), embedded Prior to undertaking electron microscope studies in cross-linked methacrylate, and sectioned with a on this process, the fine structure of pneumococcal Porter-Blum mlcrotome using a diamond knife. The cells in thin sections was examined. During the sections were stained with lead according to the preliminary stage of these studies on a transform- method of Karnovsky (5) (method B) and were able strain, we observed some unique membranous examined in the RCA electron microscopes models structures which, to the best of our knowledge, 2B, 3F, or in the Siemens Elmiskop I. have not previously been described in bacteria. RESULTS MATERIALS AND METHODS The nuclear region of pneumococcus resembles that Unencapsulated strains of Diplocoecus pneumoniae R6, of other bacteria prepared by the method of R1, and some nutritional mutants derived from R6 Ryter and Kellenberger (4). -
Association Between Carriage of Streptococcus Pneumoniae and Staphylococcus Aureus in Children
BRIEF REPORT Association Between Carriage of Streptococcus pneumoniae and Staphylococcus aureus in Children Gili Regev-Yochay, MD Context Widespread pneumococcal conjugate vaccination may bring about epidemio- Ron Dagan, MD logic changes in upper respiratory tract flora of children. Of particular significance may Meir Raz, MD be an interaction between Streptococcus pneumoniae and Staphylococcus aureus, in view of the recent emergence of community-acquired methicillin-resistant S aureus. Yehuda Carmeli, MD, MPH Objective To examine the prevalence and risk factors of carriage of S pneumoniae Bracha Shainberg, PhD and S aureus in the prevaccination era in young children. Estela Derazne, MSc Design, Setting, and Patients Cross-sectional surveillance study of nasopharyn- geal carriage of S pneumoniae and nasal carriage of S aureus by 790 children aged 40 Galia Rahav, MD months or younger seen at primary care clinics in central Israel during February 2002. Ethan Rubinstein, MD Main Outcome Measures Carriage rates of S pneumoniae (by serotype) and S aureus; risk factors associated with carriage of each pathogen. TREPTOCOCCUS PNEUMONIAE AND Results Among 790 children screened, 43% carried S pneumoniae and 10% car- Staphylococcus aureus are com- ried S aureus. Staphylococcus aureus carriage among S pneumoniae carriers was 6.5% mon inhabitants of the upper vs 12.9% in S pneumoniae noncarriers. Streptococcus pneumoniae carriage among respiratory tract in children and S aureus carriers was 27.5% vs 44.8% in S aureus noncarriers. Only 2.8% carried both Sare responsible for common infec- pathogens concomitantly vs 4.3% expected dual carriage (P=.03). Risk factors for tions. Carriage of S aureus and S pneu- S pneumoniae carriage (attending day care, having young siblings, and age older than moniae can result in bacterial spread and 3 months) were negatively associated with S aureus carriage. -
Streptococcus Pneumoniae Capsular Polysaccharide Is Linked to Peptidoglycan Via a Direct Glycosidic Bond to Β-D-N-Acetylglucosamine
Streptococcus pneumoniae capsular polysaccharide is linked to peptidoglycan via a direct glycosidic bond to β-D-N-acetylglucosamine Thomas R. Larsona and Janet Yothera,1 aDepartment of Microbiology, University of Alabama at Birmingham, Birmingham, AL 35294-2170 Edited by Emil C. Gotschlich, The Rockefeller University, New York, NY, and approved April 14, 2017 (received for review December 20, 2016) For many bacteria, including those important in pathogenesis, (Und-P). In S. pneumoniae serotype 2 CPS, Glcp-1-P is trans- expression of a surface-localized capsular polysaccharide (CPS) can ferred from UDP-Glcp (11), and this is followed by addition of be critical for survival in host environments. In Gram-positive the remaining sugars (12, 13) to form the complete repeat unit bacteria, CPS linkage is to either the cytoplasmic membrane or the (Fig. 1). Und-P-P-oligosaccharide repeat units are translocated cell wall. Despite the frequent occurrence and essentiality of these to the outer face of the cytoplasmic membrane by Wzx and po- polymers, the exact nature of the cell wall linkage has not been lymerized into high molecular weight (MW) polysaccharide by described in any bacterial species. Using the Streptococcus pneu- Wzy. Growth occurs at the reducing end, with single or multiple moniae serotype 2 CPS, which is synthesized by the widespread repeat units being transferred en bloc from Und-P-P to an ac- Wzy mechanism, we found that linkage occurs via the reducing ceptor Und-P-P-oligosaccharide repeat unit. Hydrolysis of the β N- end glucose of CPS and the -D- acetylglucosamine (GlcNAc) res- donor Und-P-P that remains after transfer yields Und-P, which is idues of peptidoglycan (PG). -
Universidade Do Algarve Investigation of Listeria Monocytogenes And
Universidade do Algarve Investigation of Listeria monocytogenes and Streptococcus pneumoniae mutants in in vivo models of infection Ana Raquel Chaves Mendes de Alves Porfírio Dissertação para a obtenção do Grau de Mestrado em Engenharia Biológica Tese orientada pelo Prof. Dr. Peter W. Andrew e coorientada pela Prof. Dr. Maria Leonor Faleiro 2015 I Investigation of Streptococcus pneumoniae and Listeria monocytogenes mutants in in vivo models of infection Declaro ser a autora deste trabalho, que é original e inédito. Autores e trabalhos consultados estão devidamente citados no texto e constam na listagem de referências incluída. Copyright © 2015, por Ana Raquel Chaves Mendes de Alves Porfírio A Universidade do Algarve tem o direito, perpétuo e sem limites geográficos, de arquivar e publicitar este trabalho através de exemplares impressos reproduzidos em papel ou de forma digital, ou por qualquer outro meio conhecido ou que venha a ser inventado, de o divulgar através de repositórios científicos e de admitir a sua copia e distribuição com objetivos educacionais ou de investigação, não comerciais, desde que seja dado crédito ao autor e editor. II “I was taight that the way of progress was neither swift nor easy” – Marie Curie III Acknowledgements First of all I would like to thank the University of Algarve and the University of Leicester for providing me with the amazing opportunity of doing my dissertation project abroad. I wish to particularly express my deepest gratitude to my supervisors Prof. Peter Andrew and Prof. Maria Leonor Faleiro for their continuous guidance and support throughout this project. Their useful insight and feedback was thoroughly appreciated. -
Streptococcus Pneumoniae Technical Sheet
technical sheet Streptococcus pneumoniae Classification On necropsy, a serosanguineous to purulent exudate Alpha-hemolytic, Gram-positive, encapsulated, aerobic is often found in the nasal cavities and the tympanic diplococcus bullae. The lungs can have areas of firm, dark red consolidation. Fibrinopurulent pleuritis, pericarditis, Family and peritonitis are other changes seen on necropsy of animals affected by S. pneumoniae. Histologic Streptococcaceae lesions are consistent with necropsy findings, Affected species and bronchopneumonia of varying severity and fibrinopurulent serositis are often seen. Primarily described as a pathogen of rats and guinea pigs. Mice are susceptible to infection. Agent of human Diagnosis disease and human carriers are a likely source of An S. pneumoniae infection should be suspected if animal infections. Zoonotic infection is possible. encapsulated Gram-positive diplococci are seen on a smear from a lesion. Confirmation of the diagnosis is Frequency via culture of lesions or affected tissues. S. pneumoniae Rare in modern laboratory animal colonies. Prevalence grows best on 5% blood agar and is alpha-hemolytic. in pet and wild populations unknown. The organism is then presumptively identified with an optochin test. PCR assays are also available for Transmission diagnosis. PCR-based screening for S. pneumoniae Transmission is primarily via aerosol or contact with may be conducted on respiratory samples or feces. nasal or lacrimal secretions of an infected animal. S. PCR may also be useful for confirmation of presumptive pneumoniae may be cultured from the nasopharynx and microbiologic identification or confirming the identity of tympanic bullae. bacteria observed in histologic lesions. Clinical Signs and Lesions Interference with Research Inapparent infections and carrier states are common, Animals carrying S. -
158273443.Pdf
Cover: A single cell from a mouse embryo, moving about on a glass slide. The cell was fixed and then stained with antibody to actomyosin, a contractile protein complexof muscle cells. The antibody was visualized by fluorescence, and its pattern revealed thatthe embryo cell contained actomyosin in sheaths, even though it was not a muscle cell. (Photo by B. Pollack, K. Weber, G. Felsten) ANNUAL REPORT 1974 COLD SPRING HARBOR LABORATORY COLD SPRING HARBOR, NEW YORK COLD SPRINGHARBOR LABORATORY Cold Spring Harbor, Long Island,New York OFFICERS OF THE CORPORATION Chairman: Robert H. P. Olney Secretary: Dr. Bayard Clarkson 1st Vice Chairman: Edward Pulling Treasurer: Angus P. McIntyre 2nd Vice Chairman: Arthur Trottenberg Assistant Secretary-Treasurer: William R. Udry Laboratory Director: Dr. James D. Watson Administrative Director: William R. Udry BOARD OF TRUSTEES INSTITUTIONAL TRUSTEES Albert Einstein College of Medicine New York University MedicalCenter Dr. Harry Eagle Dr. Milton R. J. Salton The City University of New York Princeton University Dr. Norman R. Eaton Dr. Bruce Alberts Columbia University The Rockefeller University Dr. James E. Darnell, Jr. Dr. Rollin Hotchkiss Duke UniversityMedical Center Sloan-Kettering Institute Dr. Robert E. Webster Dr. Bayard Clarkson Harvard MedicalSchool University of Chicago Dr. Charles A.Thomas, Jr. Dr. Robert Haselkorn Long IslandBiological Association University of Wisconsin Mr. Edward Pulling Dr. Julian Davies Massachusetts Wawepex Society Institute of Technology J. Knight Dr. HermanEisen Mr. Townsend INDIVIDUALTRUSTEES Dr. DavidP. Jacobus Colton P. Wagner Watson Mrs. GeorgeN. Lindsay Dr. James D. White Angus P.McIntyre Mrs. Alex M. A. Woodcock RobertH. P. Olney Mr. William WalterII. Page Honorary Trustees: Hollaender CharlesS. -
Cell Structure and Function in the Bacteria and Archaea
4 Chapter Preview and Key Concepts 4.1 1.1 DiversityThe Beginnings among theof Microbiology Bacteria and Archaea 1.1. •The BacteriaThe are discovery classified of microorganismsinto several Cell Structure wasmajor dependent phyla. on observations made with 2. theThe microscope Archaea are currently classified into two 2. •major phyla.The emergence of experimental 4.2 Cellscience Shapes provided and Arrangements a means to test long held and Function beliefs and resolve controversies 3. Many bacterial cells have a rod, spherical, or 3. MicroInquiryspiral shape and1: Experimentation are organized into and a specific Scientificellular c arrangement. Inquiry in the Bacteria 4.31.2 AnMicroorganisms Overview to Bacterialand Disease and Transmission Archaeal 4.Cell • StructureEarly epidemiology studies suggested how diseases could be spread and 4. Bacterial and archaeal cells are organized at be controlled the cellular and molecular levels. 5. • Resistance to a disease can come and Archaea 4.4 External Cell Structures from exposure to and recovery from a mild 5.form Pili allowof (or cells a very to attach similar) to surfacesdisease or other cells. 1.3 The Classical Golden Age of Microbiology 6. Flagella provide motility. Our planet has always been in the “Age of Bacteria,” ever since the first 6. (1854-1914) 7. A glycocalyx protects against desiccation, fossils—bacteria of course—were entombed in rocks more than 3 billion 7. • The germ theory was based on the attaches cells to surfaces, and helps observations that different microorganisms years ago. On any possible, reasonable criterion, bacteria are—and always pathogens evade the immune system. have been—the dominant forms of life on Earth. -
Bacterial Size, Shape and Arrangement & Cell Structure And
Lecture 13, 14 and 15: bacterial size, shape and arrangement & Cell structure and components of bacteria and Functional anatomy and reproduction in bacteria Bacterial size, shape and arrangement Bacteria are prokaryotic, unicellular microorganisms, which lack chlorophyll pigments. The cell structure is simpler than that of other organisms as there is no nucleus or membrane bound organelles.Due to the presence of a rigid cell wall, bacteria maintain a definite shape, though they vary as shape, size and structure. When viewed under light microscope, most bacteria appear in variations of three major shapes: the rod (bacillus), the sphere (coccus) and the spiral type (vibrio). In fact, structure of bacteria has two aspects, arrangement and shape. So far as the arrangement is concerned, it may Paired (diplo), Grape-like clusters (staphylo) or Chains (strepto). In shape they may principally be Rods (bacilli), Spheres (cocci), and Spirals (spirillum). Size of Bacterial Cell The average diameter of spherical bacteria is 0.5- 2.0 µm. For rod-shaped or filamentous bacteria, length is 1-10 µm and diameter is 0.25-1 .0 µm. E. coli , a bacillus of about average size is 1.1 to 1.5 µm wide by 2.0 to 6.0 µm long. Spirochaetes occasionally reach 500 µm in length and the cyanobacterium Accepted wisdom is that bacteria are smaller than eukaryotes. But certain cyanobacteria are quite large; Oscillatoria cells are 7 micrometers diameter. The bacterium, Epulosiscium fishelsoni , can be seen with the naked eye (600 mm long by 80 mm in diameter). One group of bacteria, called the Mycoplasmas, have individuals with size much smaller than these dimensions. -
Streptococci
STREPTOCOCCI Streptococci are Gram-positive, nonmotile, nonsporeforming, catalase-negative cocci that occur in pairs or chains. Older cultures may lose their Gram-positive character. Most streptococci are facultative anaerobes, and some are obligate (strict) anaerobes. Most require enriched media (blood agar). Streptococci are subdivided into groups by antibodies that recognize surface antigens (Fig. 11). These groups may include one or more species. Serologic grouping is based on antigenic differences in cell wall carbohydrates (groups A to V), in cell wall pili-associated protein, and in the polysaccharide capsule in group B streptococci. Rebecca Lancefield developed the serologic classification scheme in 1933. β-hemolytic strains possess group-specific cell wall antigens, most of which are carbohydrates. These antigens can be detected by immunologic assays and have been useful for the rapid identification of some important streptococcal pathogens. The most important groupable streptococci are A, B and D. Among the groupable streptococci, infectious disease (particularly pharyngitis) is caused by group A. Group A streptococci have a hyaluronic acid capsule. Streptococcus pneumoniae (a major cause of human pneumonia) and Streptococcus mutans and other so-called viridans streptococci (among the causes of dental caries) do not possess group antigen. Streptococcus pneumoniae has a polysaccharide capsule that acts as a virulence factor for the organism; more than 90 different serotypes are known, and these types differ in virulence. Fig. 1 Streptococci - clasiffication. Group A streptococci causes: Strep throat - a sore, red throat, sometimes with white spots on the tonsils Scarlet fever - an illness that follows strep throat. It causes a red rash on the body. -
Laboratory Harbor Spring Cold Annual Report 1990
YEAR CENTENNIAL THE LABORATORY HARBOR SPRING COLD ANNUAL REPORT 1990 COLD SPRING HARBOR LABORATORY THE CENTENNIAL YEAR ANNUAL REPORT 1990 Cold Spring Harbor Laboratory Box 100 1 Bungtown Road Cold Spring Harbor, New York 11724 Book design Emily Harste Editors Dorothy Brown, Lee Martin Photography Margot Bennett, Herb Parsons, Edward Campodonico Typography Marie Sullivan Front cover: Jones Laboratory, during the Centennial fireworks dis- play. This building, completed in 1893, was the first structure built expressly for science at Cold Spring Harbor. (Photograph by Ross Meurer and Margot Bennett.) Back Cover: (Top) Centennial reenactment of the first biology class at Cold Spring Harbor on board the launch "Rotifer." (Inset) The original class of 1890. Reenactments for the Centennial were directed by Rob Gensel. (Photograph by Randy Wilfong.) (Bottom) Centennial reenactment of the Laboratory's first biology class on the Jones Laboratory porch. (Inset) The original 1890 class on the porch of the old Fish Hatchery building before the completion of Jones Laboratory. (Photograph by Margot Bennett.) Contents Officers of the Corporation/Board of Trustees v Governance and Major Affiliations vi Committees vii Edward Pulling (1898-1991)viii DIRECTOR'S REPORT DEPARTMENTAL REPORTS 21 Administration 23 Buildings and Grounds 25 Development 28 Library Services 30 Public Affairs 32 RESEARCH 35 Tumor Viruses 37 Molecular Genetics of Eukaryotic Cells 93 Genetics 155 Structure and Computation 197 Neuroscience 213 CSH Laboratory Junior Fellows217 COLD SPRING -
Pneumococcal Disease (Sickness Caused by Streptococcus Pneumoniae)
Pneumococcal Disease (Sickness Caused by Streptococcus pneumoniae) What is pneumococcal disease? Pneumococcal disease is an infection caused by the bacteria Streptococcus pneumoniae. It's also called pneumococcus and can cause ear infections, pneumonia, infections in the blood and meningitis. When does it happen? Children can get pneumococcal disease any time of the year. What are the symptoms? Fever and increased fussiness or irritability are common Meningitis symptoms include fever, trouble bending or moving the neck, increased fussiness or irritability, and headache in anyone over age 2. In babies, the only symptoms may be that the baby is less active, fussy or crying more than usual, throwing up, or not eating normally. Pneumonia symptoms in children include fever, cough, working hard to breathe, breathing faster than usual or grunting. Ear infection symptoms are ears that hurt, crying or pulling on ears, sore throat or pain when swallowing. Children may also be sleepy, have a fever, and be fussy. Is it contagious? How is it spread? Pneumococcus is spread by contact with people who either have a pneumococcal illness or who carry the bacteria in their throats without being sick. It can be spread by droplets in the air from coughing or sneezing. It can also be spread if you touch something that has the droplets on it, and then touch your own nose, mouth or eyes. How bad is pneumococcal disease? Pneumococcal disease can be very bad for young children and is the most common cause of meningitis and bacterial pneumonia in children. How can pneumococcal disease be avoided in children? There is a vaccine that can help stop serious pneumococcal disease, such as meningitis and blood infections.