Statistical method for testing the neutral mutation hypothesis by DNA polymorphism.

FRED C. TENOVER,* ROBERT D. ARBEIT, RICHARD V. GOERING, PATRICIA A. MICKELSEN, BARBARA E. MURRAY, DAVID H. PERSING, AND BALA SWAMINATHAN National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333; Veterans Affairs Medical Center, Boston, Massachusetts 02130; Creighton University, Omaha, Nebraska 68178; Stanford University Medical Center, Stanford, California 94305; University of Texas Medical School, Houston, Texas 77030; and Mayo Clinic, Rochester, Minnesota 55905

https://courses.washington.edu/pabio568/files/tenover.pdf

Interpreting chromosomal DNA restriction patterns produced by pulsed-field gel electrophoresis: criteria for bacterial strain typing.

The 11th edition of Harrison's Principles of Internal Medicine welcomes Anthony Fauci to its editorial staff, in addition to more than 85 new contributors. While the organization of the book is similar to previous editions, major emphasis has been placed on disorders that affect multiple organ systems. Important advances in genetics, immunology, and oncology are emphasized. Many chapters of the book have been rewritten and describe major advances in internal medicine. Subjects that received only a paragraph or two of attention in previous editions are now covered in entire chapters. Among the chapters that have been extensively revised are the chapters on infections in the compromised host, on skin rashes in infections, on many of the viral infections, including cytomegalovirus and Epstein-Barr virus, on sexually transmitted diseases, on diabetes mellitus, on disorders of bone and mineral metabolism, and on lymphadenopathy and splenomegaly. The major revisions in these chapters and many

Harrison's Principles of Internal Medicine

Lionel A. Mandell, Richard G. Wunderink, Antonio Anzueto, John G. Bartlett, G. Douglas Campbell, Nathan C. Dean, Scott F. Dowell, Thomas M. File, Jr. Daniel M. Musher, Michael S. Niederman, Antonio Torres, and Cynthia G. Whitney McMaster University Medical School, Hamilton, Ontario, Canada; Northwestern University Feinberg School of Medicine, Chicago, Illinois; University of Texas Health Science Center and South Texas Veterans Health Care System, San Antonio, and Michael E. DeBakey Veterans Affairs Medical Center and Baylor College of Medicine, Houston, Texas; Johns Hopkins University School of Medicine, Baltimore, Maryland; Division of Pulmonary, Critical Care, and Sleep Medicine, University of Mississippi School of Medicine, Jackson; Division of Pulmonary and Critical Care Medicine, LDS Hospital, and University of Utah, Salt Lake City, Utah; Centers for Disease Control and Prevention, Atlanta, Georgia; Northeastern Ohio Universities College of Medicine, Rootstown, and Summa Health System, Akron, Ohio; State University of New York at Stony Brook, Stony Brook, and Department of Medicine, Winthrop University Hospital, Mineola, New York; and Cap de Servei de Pneumologia i Allergia Respiratoria, Institut Clinic del Torax, Hospital Clinic de Barcelona, Facultat de Medicina, Universitat de Barcelona, Institut d’Investigacions Biomediques August Pi i Sunyer, CIBER CB06/06/0028, Barcelona, Spain.

/pdf/infectious-diseases-society-of-america-american-thoracic-1cn65eiqga.pdf

Infectious Diseases Society of America/American Thoracic Society Consensus Guidelines on the Management of Community-Acquired Pneumonia in Adults

Micrococcus, which, when limited in its extent and activity, causes acute suppurative inflammation (phlegmon), produces, when more extensive and intense in its action on the human system, the most virulent forms of septicaemia and pyaemia.1 In an elegant series of clinical observations and laboratory studies published in 1880 and 1882, Ogston described staphylococcal disease and its role in sepsis and abscess formation.1,2 More than 100 years later, Staphylococcus aureus remains a versatile and dangerous pathogen in humans. The frequencies of both community-acquired and hospital-acquired staphylococcal infections have increased steadily, with little change in overall mortality. Treatment of these infections . . .

https://www.nejm.org/doi/pdf/10.1056/NEJM199808203390806?articleTools=true

Staphylococcus aureus infections.

Role of lipids in the pathogenesis of coagulase-negative staphylococcal bacteremia in neonates.

77 – Myositis, Pyomyositis, and Necrotizing Fasciitis

A variety of bacterial species are associated with acute respiratory tract infections, including Gram-positive, Gram-negative, and atypical pathogens. The most common pathogens include Streptococcus pneumoniae, Mycoplasma pneumoniae, Chlamydia pneumoniae, Legionella species, Haemophilus influenzae, and Moraxella catarrhalis. Because of cost considerations and specimen collection difficulties, primary care physicians seldom attempt to identify the causative pathogen. As a result treatment is necessarily empiric with agents including: the 13-lactams, macrolides, tetracyclines, and trimethoprim-sulfamethoxazole (TMP-SMX). However, antimicrobial resistance among the most common respiratory tract pathogens to these agents is increasing [1-5]. Specifically, the growing problem of multidrug resistant pneumococci has been the catalyst for the development of fluoroquinolones such as levofloxacin, gatifloxacin, which are effective against this resistant organism. However, there are reports of fluoroquinolone resistance emerging among pneumococci from a number of countries including: Canada, Spain, Hong Kong, Eastern and Central Europe, and Northern Ireland Figure 1. In Canada, Chen et al. [6] found that the prevalence of ciprofloxacin-resistant pneumococci (MIC >_ 4.ug/ml) increased from 0% in 1993 to 1.7% in 1997-1998 (p = 0.01). In adults, the prevalence increased from 0% in 1993 to 3.7% in 1998.

Fluoroquinolones for the treatment of respiratory tract infections other than pneumonia

/pdf/ll-37-at-the-local-site-of-streptococcal-skin-and-soft-2xl6we664g.pdf

LL-37 at the local site of streptococcal skin and soft-tissue infections

Streptococcal toxic shock syndrome (STSS) and necrotizing fasciitis caused by group A streptococcus (GAS) are rapidly-progressive invasive diseases that are associated with high mortality rates, ranging from 30% to 80% despite prompt antibiotic therapy and surgical debridement (1). Intense research in the field of GAS pathogenesis has unraveled complex host-pathogen interplay and provided an impetus for the design of novel therapeutic strategies to attenuate or prevent these diseases. One of the more promising therapeutic strategies is the intravenous administration of polyspecific immunoglobulin (IVIG) to patients with severe invasive GAS infections. In this chapter, we will review the mechanistic actions and use of IVIG as adjunctive therapy for severe invasive GAS infections. In doing so, we will also highlight epidemiological and pathogenic aspects of invasive GAS infections and show how IVIG acts, in part, by attenuating the inflammatory cytokine cascade in these patients.

Donald E. Low

Papers

Role of lipids in the pathogenesis of coagulase-negative staphylococcal bacteremia in neonates.

77 – Myositis, Pyomyositis, and Necrotizing Fasciitis

Fluoroquinolones for the treatment of respiratory tract infections other than pneumonia

LL-37 at the local site of streptococcal skin and soft-tissue infections

Intravenous Immunoglobulin Adjunctive Therapy in Patients with Streptococcal Toxic Shock Syndrome and Necrotizing Fasciitis