Infective Endocarditis Caused by C. Sordellii: the First Case Report from India
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Gene Number Genera
Table 4. Location of the various genes Modified April 28, 2021 Originally modified from AAC 1999 43:2823-30 with permission from ASM Journals Gene Number Genera METHYLASES e erm(A) 11 AggregatibacterL,1, Bacteroides, Enterococcus , Haemophilusr, Helcococcus, Klebsiella, a a Listeria, Peptostreptococcus , Prevotella , Staphylococcus, Streptococcus erm(B) 39 Aggregatibacter1, Aerococcus, Bacillus, Bacteroidesa, Campylobacteraf, a Citrobacter, Corynebacterium, Clostridium , Clostridioides, Enterobacter, Escherichia, a a Eubacterium , Enterococcus, Fusobacterium , Gallibacteriumcp, Gemella, Haemophilus, Klebsiella, a Lactobacillus, Listeriacc, Micrococcus, Neisseria, Pantoea, Pediococcus, Peptostreptococcus , a a Porphyromonas , Proteus, Pseudomonas, Rothia, Ruminococcus , Salmonellacn, Serratia, Shigella ag, Staphylococcus, Streptococcus, UreaplasmaO, Wollinellaa, Treponemab, Trueperella1 a erm(C) 38 Aeromonasy, AggregatibacterL, Actinomyces, Bacillus, Bacteroides , Brevundimonas y, Burkholderia y, Campylobacter, Capnocytophagaa,ca ,Chryseomonasy, ,Corynebacterium, n a Clostridiuma,n Escherichia , Eubacterium , Enterococcus, Fusobacteriuma,br, Haemophilusr, y y Lactobacillus, Listeria, Macrococcus, Micrococcus, Neisseria, Paenibacillus , Pasteurella , a a Prevotella , Peptostreptococcus , Pseudomonasy, Pseudoramibactera,br, Rhizobiumy, Salmonella, y y y Serratia, Sinorhizobium , Sphingomonas , Stenotrophomans , Staphylococcus, Streptococcus, a Trueperella n, Wolinella erm(D) 2 Bacillus, Salmonella a a a a n erm(E) 7 Bacteroides , Eubacterium -
Toxic Shock Syndrome Contributors: Noah Craft MD, Phd, Lindy P
** no patient handout Toxic shock syndrome Contributors: Noah Craft MD, PhD, Lindy P. Fox MD, Lowell A. Goldsmith MD, MPH SynopsisToxic shock syndrome (TSS) is a severe exotoxin-mediated bacterial infection that is characterized by high fevers, headache, pharyngitis, vomiting, diarrhea, and hypotension. Two subtypes of TSS exist, based on the bacterial etiology: Staphylococcus aureus and group A streptococci. Significantly, the severity of TSS can range from mild disease to rapid progression to shock and end organ failure. The dermatologic manifestations of TSS include the following: • Erythema of the palms and soles that desquamates 1-3 weeks after the initial onset • Diffuse scarlatiniform exanthem that begins on the trunk and spreads toward the extremities • Erythema of the mucous membranes (strawberry tongue and conjunctival hyperemia) TSS was identified in and most commonly affected menstruating young white females using tampons in the 1980s. Current TSS cases are seen in post-surgical interventions in men, women, and children, as well as in other settings, in addition to cases of menstrual TSS, which have declined with increased public education on tampon usage and TSS. One study in Japanese patients found the highest TSS incidence to occur among children with burns, as Staphylococcus colonization is high in this subgroup and antibody titers are not yet sufficient to protect children from the exotoxins causing TSS. Staphylococcal TSS is caused by S. aureus strains that can produce the toxic shock syndrome toxin-1 (TSST-1). TSST-1 is believed to cause disease via direct effects on end organs, impairing clearance of gut flora derived endotoxins, with TSST-1 acting as a superantigen leading to massive nonspecific activation of T-cells and subsequent inflammation and vascular leakage. -
Investigation of Anthrax Associated with Intentional Exposure
October 19, 2001 / Vol. 50 / No. 41 889 Update: Investigation of Anthrax Associated with Intentional Exposure and Interim Public Health Guidelines, October 2001 893 Recognition of Illness Associated with the Intentional Release of a Biologic Agent 897 Weekly Update: West Nile Virus Activity — United States, October 10–16, 2001 Update: Investigation of Anthrax Associated with Intentional Exposure and Interim Public Health Guidelines, October 2001 On October 4, 2001, CDC and state and local public health authorities reported a case of inhalational anthrax in Florida (1 ). Additional cases of anthrax subsequently have been reported from Florida and New York City. This report updates the findings of these case investigations, which indicate that infections were caused by the intentional release of Bacillus anthracis. This report also includes interim guidelines for postexposure pro- phylaxis for prevention of inhalational anthrax and other information to assist epidemi- ologists, clinicians, and laboratorians responding to intentional anthrax exposures. For these investigations, a confirmed case of anthrax was defined as 1) a clinically compatible case of cutaneous, inhalational, or gastrointestinal illness* that is laboratory confirmed by isolation of B. anthracis from an affected tissue or site or 2) other labora- tory evidence of B. anthracis infection based on at least two supportive laboratory tests. A suspected case was defined as 1) a clinically compatible case of illness without isola- tion of B. anthracis and no alternative diagnosis, but with laboratory evidence of B. anthracis by one supportive laboratory test or 2) a clinically compatible case of an- thrax epidemiologically linked to a confirmed environmental exposure, but without cor- roborative laboratory evidence of B. -
Toxic Shock-Like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection
Henry Ford Hospital Medical Journal Volume 37 Number 2 Article 5 6-1989 Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection Thomas J. Connolly Donald J. Pavelka Eugene F. Lanspa Thomas L. Connolly Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Connolly, Thomas J.; Pavelka, Donald J.; Lanspa, Eugene F.; and Connolly, Thomas L. (1989) "Toxic Shock- like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection," Henry Ford Hospital Medical Journal : Vol. 37 : No. 2 , 69-72. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol37/iss2/5 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Toxic Shock-like Syndrome Associated with Necrotizing Streptococcus Pyogenes Infection Thomas J. Connolly,* Donald J. Pavelka, MD,^ Eugene F. Lanspa, MD, and Thomas L. Connolly, MD' Two patients with toxic shock-like syndrome are presented. Bolh patients had necrotizing cellulitis due to Streptococcus pyogenes, and both patients required extensive surgical debridement. The association of Streptococcus pyogenes infection and toxic shock-like syndrome is discussed. (Henry Ford Hosp MedJ 1989:37:69-72) ince 1978, toxin-producing strains of Staphylococcus brought to the emergency room where a physical examination revealed S aureus have been implicated as the cause of the toxic shock a temperature of 40.9°C (I05.6°F), blood pressure of 98/72 mm Hg, syndrome (TSS), which is characterized by fever and rash and respiration of 36 breaths/min, and a pulse of 72 beats/min. -
Detection of ESKAPE Pathogens and Clostridioides Difficile in Simulated
bioRxiv preprint doi: https://doi.org/10.1101/2021.03.04.433847; this version posted March 4, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 1 Detection of ESKAPE pathogens and Clostridioides difficile in 2 Simulated Skin Transmission Events with Metagenomic and 3 Metatranscriptomic Sequencing 4 5 Krista L. Ternusa#, Nicolette C. Keplingera, Anthony D. Kappella, Gene D. Godboldb, Veena 6 Palsikara, Carlos A. Acevedoa, Katharina L. Webera, Danielle S. LeSassiera, Kathleen Q. 7 Schultea, Nicole M. Westfalla, and F. Curtis Hewitta 8 9 aSignature Science, LLC, 8329 North Mopac Expressway, Austin, Texas, USA 10 bSignature Science, LLC, 1670 Discovery Drive, Charlottesville, VA, USA 11 12 #Address correspondence to Krista L. Ternus, [email protected] 13 14 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.03.04.433847; this version posted March 4, 2021. The copyright holder for this preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under aCC-BY 4.0 International license. 15 1 Abstract 16 Background: Antimicrobial resistance is a significant global threat, posing major public health 17 risks and economic costs to healthcare systems. Bacterial cultures are typically used to diagnose 18 healthcare-acquired infections (HAI); however, culture-dependent methods provide limited 19 presence/absence information and are not applicable to all pathogens. -
Use of the Diagnostic Bacteriology Laboratory: a Practical Review for the Clinician
148 Postgrad Med J 2001;77:148–156 REVIEWS Postgrad Med J: first published as 10.1136/pmj.77.905.148 on 1 March 2001. Downloaded from Use of the diagnostic bacteriology laboratory: a practical review for the clinician W J Steinbach, A K Shetty Lucile Salter Packard Children’s Hospital at EVective utilisation and understanding of the Stanford, Stanford Box 1: Gram stain technique University School of clinical bacteriology laboratory can greatly aid Medicine, 725 Welch in the diagnosis of infectious diseases. Al- (1) Air dry specimen and fix with Road, Palo Alto, though described more than a century ago, the methanol or heat. California, USA 94304, Gram stain remains the most frequently used (2) Add crystal violet stain. USA rapid diagnostic test, and in conjunction with W J Steinbach various biochemical tests is the cornerstone of (3) Rinse with water to wash unbound A K Shetty the clinical laboratory. First described by Dan- dye, add mordant (for example, iodine: 12 potassium iodide). Correspondence to: ish pathologist Christian Gram in 1884 and Dr Steinbach later slightly modified, the Gram stain easily (4) After waiting 30–60 seconds, rinse with [email protected] divides bacteria into two groups, Gram positive water. Submitted 27 March 2000 and Gram negative, on the basis of their cell (5) Add decolorising solvent (ethanol or Accepted 5 June 2000 wall and cell membrane permeability to acetone) to remove unbound dye. Growth on artificial medium Obligate intracellular (6) Counterstain with safranin. Chlamydia Legionella Gram positive bacteria stain blue Coxiella Ehrlichia Rickettsia (retained crystal violet). -
Botulinum Toxin Ricin Toxin Staph Enterotoxin B
Botulinum Toxin Ricin Toxin Staph Enterotoxin B Source Source Source Clostridium botulinum, a large gram- Ricinus communis . seeds commonly called .Staphylococcus aureus, a gram-positive cocci positive, spore-forming, anaerobic castor beans bacillus Characteristics Characteristics .Appears as grape-like clusters on Characteristics .Toxin can be disseminated in the form of a Gram stain or as small off-white colonies .Grows anaerobically on Blood Agar and liquid, powder or mist on Blood Agar egg yolk plates .Toxin-producing and non-toxigenic strains Pathogenesis of S. aureus will appear morphologically Pathogenesis .A-chain inactivates ribosomes, identical interrupting protein synthesis .Toxin enters nerve terminals and blocks Pathogenesis release of acetylcholine, blocking .B-chain binds to carbohydrate receptors .Staphylococcus Enterotoxin B (SEB) is a neuro-transmission and resulting in on the cell surface and allows toxin superantigen. Toxin binds to human class muscle paralysis complex to enter cell II MHC molecules causing cytokine Toxicity release and system-wide inflammation Toxicity .Highly toxic by inhalation, ingestion Toxicity .Most lethal of all toxic natural substances and injection .Toxic by inhalation or ingestion .Groups A, B, E (rarely F) cause illness in .Less toxic by ingestion due to digestive humans activity and poor absorption Symptoms .Low dermal toxicity .4-10 h post-ingestion, 3-12 h post-inhalation Symptoms .Flu-like symptoms, fever, chills, .24-36 h (up to 3 d for wound botulism) Symptoms headache, myalgia .Progressive skeletal muscle weakness .18-24 h post exposure .Nausea, vomiting, and diarrhea .Symmetrical descending flaccid paralysis .Fever, cough, chest tightness, dyspnea, .Nonproductive cough, chest pain, .Can be confused with stroke, Guillain- cyanosis, gastroenteritis and necrosis; and dyspnea Barre syndrome or myasthenia gravis death in ~72 h .SEB can cause toxic shock syndrome + + + Gram stain Lipase on Ricin plant Castor beans S. -
The Sialidase Nans Enhances Non-Tcsl Mediated Cytotoxicity of Clostridium Sordellii
toxins Article The Sialidase NanS Enhances Non-TcsL Mediated Cytotoxicity of Clostridium sordellii Milena M. Awad, Julie Singleton and Dena Lyras * Infection and Immunity Program, Biomedicine Discovery Institute and Department of Microbiology, Monash University, Clayton 3800, Australia; [email protected] (M.M.A.); [email protected] (J.S.) * Correspondence: [email protected]; Tel.: +61-3-9902-9155 Academic Editors: Harald Genth, Michel R. Popoff and Holger Barth Received: 24 March 2016; Accepted: 7 June 2016; Published: 17 June 2016 Abstract: The clostridia produce an arsenal of toxins to facilitate their survival within the host environment. TcsL is one of two major toxins produced by Clostridium sordellii, a human and animal pathogen, and is essential for disease pathogenesis of this bacterium. C. sordellii produces many other toxins, but the role that they play in disease is not known, although previous work has suggested that the sialidase enzyme NanS may be involved in the characteristic leukemoid reaction that occurs during severe disease. In this study we investigated the role of NanS in C. sordellii disease pathogenesis. We constructed a nanS mutant and showed that NanS is the only sialidase produced from C. sordellii strain ATCC9714 since sialidase activity could not be detected from the nanS mutant. Complementation with the wild-type gene restored sialidase production to the nanS mutant strain. Cytotoxicity assays using sialidase-enriched culture supernatants applied to gut (Caco2), vaginal (VK2), and cervical cell lines (End1/E6E7 and Ect1/E6E7) showed that NanS was not cytotoxic to these cells. However, the cytotoxic capacity of a toxin-enriched supernatant to the vaginal and cervical cell lines was substantially enhanced in the presence of NanS. -
Vaginal and Rectal Clostridium Sordellii and Clostridium Perfringens Presence Among Women in the United States
View metadata, citation and similar papers at core.ac.uk brought to you by CORE HHS Public Access provided by CDC Stacks Author manuscript Author ManuscriptAuthor Manuscript Author Obstet Gynecol Manuscript Author . Author Manuscript Author manuscript; available in PMC 2018 February 01. Published in final edited form as: Obstet Gynecol. 2016 February ; 127(2): 360–368. doi:10.1097/AOG.0000000000001239. Vaginal and Rectal Clostridium sordellii and Clostridium perfringens Presence Among Women in the United States Erica Chong, MPH, Beverly Winikoff, MD, MPH, Dyanna Charles, MPH, Kathy Agnew, BS, Jennifer L. Prentice, MS, Brandi M. Limbago, PhD, Ingrida Platais, MS, Karmen Louie, MPH, Heidi E. Jones, PhD, MPH, Caitlin Shannon, PhD, and for the NCT01283828 Study Team* Gynuity Health Projects, the City University of New York School of Public Health and Hunter College, and EngenderHealth, New York, New York; the University of Washington, Seattle, Washington; and the Centers for Disease Control and Prevention, Atlanta, Georgia Abstract OBJECTIVE—To characterize the presence of Clostridium sordellii and Clostridium perfringens in the vagina and rectum, identify correlates of presence, and describe strain diversity and presence of key toxins. METHODS—We conducted an observational cohort study in which we screened a diverse cohort of reproductive-aged women in the United States up to three times using vaginal and rectal swabs analyzed by molecular and culture methods. We used multivariate regression models to explore predictors of presence. Strains were characterized by pulsed-field gel electrophoresis and tested for known virulence factors by polymerase chain reaction assays. RESULTS—Of 4,152 participants enrolled between 2010 and 2013, 3.4% (95% confidence interval [CI] 2.9–4.0) were positive for C sordellii and 10.4% (95% CI 9.5–11.3) were positive for C perfringens at baseline. -
Germinants and Their Receptors in Clostridia
JB Accepted Manuscript Posted Online 18 July 2016 J. Bacteriol. doi:10.1128/JB.00405-16 Copyright © 2016, American Society for Microbiology. All Rights Reserved. 1 Germinants and their receptors in clostridia 2 Disha Bhattacharjee*, Kathleen N. McAllister* and Joseph A. Sorg1 3 4 Downloaded from 5 Department of Biology, Texas A&M University, College Station, TX 77843 6 7 Running Title: Germination in Clostridia http://jb.asm.org/ 8 9 *These authors contributed equally to this work 10 1Corresponding Author on September 12, 2018 by guest 11 ph: 979-845-6299 12 email: [email protected] 13 14 Abstract 15 Many anaerobic, spore-forming clostridial species are pathogenic and some are industrially 16 useful. Though many are strict anaerobes, the bacteria persist in aerobic and growth-limiting 17 conditions as multilayered, metabolically dormant spores. For many pathogens, the spore-form is Downloaded from 18 what most commonly transmits the organism between hosts. After the spores are introduced into 19 the host, certain proteins (germinant receptors) recognize specific signals (germinants), inducing 20 spores to germinate and subsequently outgrow into metabolically active cells. Upon germination 21 of the spore into the metabolically-active vegetative form, the resulting bacteria can colonize the 22 host and cause disease due to the secretion of toxins from the cell. Spores are resistant to many http://jb.asm.org/ 23 environmental stressors, which make them challenging to remove from clinical environments. 24 Identifying the conditions and the mechanisms of germination in toxin-producing species could 25 help develop affordable remedies for some infections by inhibiting germination of the spore on September 12, 2018 by guest 26 form. -
Identification and Antimicrobial Susceptibility Testing of Anaerobic
antibiotics Review Identification and Antimicrobial Susceptibility Testing of Anaerobic Bacteria: Rubik’s Cube of Clinical Microbiology? Márió Gajdács 1,*, Gabriella Spengler 1 and Edit Urbán 2 1 Department of Medical Microbiology and Immunobiology, Faculty of Medicine, University of Szeged, 6720 Szeged, Hungary; [email protected] 2 Institute of Clinical Microbiology, Faculty of Medicine, University of Szeged, 6725 Szeged, Hungary; [email protected] * Correspondence: [email protected]; Tel.: +36-62-342-843 Academic Editor: Leonard Amaral Received: 28 September 2017; Accepted: 3 November 2017; Published: 7 November 2017 Abstract: Anaerobic bacteria have pivotal roles in the microbiota of humans and they are significant infectious agents involved in many pathological processes, both in immunocompetent and immunocompromised individuals. Their isolation, cultivation and correct identification differs significantly from the workup of aerobic species, although the use of new technologies (e.g., matrix-assisted laser desorption/ionization time-of-flight mass spectrometry, whole genome sequencing) changed anaerobic diagnostics dramatically. In the past, antimicrobial susceptibility of these microorganisms showed predictable patterns and empirical therapy could be safely administered but recently a steady and clear increase in the resistance for several important drugs (β-lactams, clindamycin) has been observed worldwide. For this reason, antimicrobial susceptibility testing of anaerobic isolates for surveillance -
Blackleg and Clostridial Diseases
BCM – 31 Blackleg and Clostridial Diseases The Clostridial diseases are a group of mostly Malignant Edema fatal infections caused by bacteria belonging to Malignant edema is a disease of cattle of any age the group called Clostridia. These organisms caused by CI. septicum is found in the feces of have the ability to form protective shell-like forms most domestic animals and in large numbers in called spores when exposed to adverse the soil where livestock populations are high. The conditions. This allows them to remain potentially organism gains entrance to the body in deep infective in soils for long periods of time and wounds and can even be introduced into deep present a real danger to the livestock population. vaginal or uterine wounds in cows following Many of the organisms in this group are also difficult calving. The symptoms are those normally present in the intestines of man and primarily of depression, loss of appetite and a wet animals. doughy swelling around the wound which often gravitates to lower portions of the body. Black Leg Temperatures of 106° or more are associated Blackleg is a disease caused by Clostridium with the infection with death frequently occurring chauvoei and primarily affects cattle under two in twenty-four to forty-eight hours. years of age and is usually seen in the better doing calves. The organism is taken in by mouth. Post mortem lesions seen are those of necrotic, Symptoms first noted are those of lameness and darkened foul smelling areas under the skin, depression. A swelling caused by gas bubbles, often extending into muscle.