Alphabetical Listing of Export Restricted Biological Items

Total Page:16

File Type:pdf, Size:1020Kb

Alphabetical Listing of Export Restricted Biological Items Alphabetical Listing of Export Restricted Biological Items There are two sets of regulations for export restricted biological items, the International Traffic in Arms Regulations (ITAR) from Dept. of State and the Export Administration Regulations from Dept. of Commerce. These items require export licenses to all countries. Licensing takes about 6 weeks. Fines are $250,000 to $1,094,010 per violation. See the Export Control website within the Office of Research at: https://research.uci.edu/ref/export-controls/index.html These listed items are controlled for export regardless of quantity or attenuation, genetic elements or genetically modified organisms for such agents or “toxins”, including small quantities or attenuated strains of select biological agents or “toxins” that are excluded from the lists of select biological agents or “toxins” by APHIS, CDC, or DHHS. Under the ITAR, Biological agents and biologically derived substances specifically developed, configured, adapted, or modified for the purpose of increasing their capability to produce casualties in humans or livestock, degrade equipment or damage crops are controlled under CATEGORY XIV—TOXICOLOGICAL AGENTS, INCLUDING CHEMICAL AGENTS, BIOLOGICAL AGENTS, AND ASSOCIATED EQUIPMENT. Please note that there are proposed regulations on this category that if they become final will impact the listing of biologicals. See Part 121 United States Munitions List Category XIV. Certain precursor chemicals, Biosafety gear, and lab equipment are also export restricted see Categories 1 & 2 of the Commerce Control List and Part 121 United States Munitions List Category XIV. Abrin Clavibacter michiganensis subspecies Diagnostic & food testing kits containing: sepedonicus (syn. Corynebacterium • Abrin; Aflatoxins michiganensis subspecies sepedonicum or • Aflatoxins; Corynebacterium sepedonicum); African horse sickness virus • Botulinum toxins; African Swine fever virus Clostridium argentinense (formerly known as • Cholera toxin; Clostridium botulinum Type G) botulinum • Clostridium perfringens alpha, beta 1, beta Andean potato latent virus (Potato Andean neurotoxin producing strains latent tymovirus) 2, epsilon and iota toxins; Clostridium baratii, botulinum neurotoxin • Conotoxin; Andes virus producing strains Avian influenza (AI) viruses with high • Diacetoxyscirpenol toxin; pathogenicity (HP), AI viruses that have an Clostridium botulinum • HT-2 toxin; intravenous pathogenicity index (IVPI) in 6- Clostridium butyricum, botulinum neurotoxin • Microcystin (Cyanginosin); week old chickens greater than 1.2; or AI producing strains • Modeccin toxin; viruses that cause at least 75% mortality in 4- Clostridium perfringens, epsilon toxin • Shiga toxin; to 8-week old chickens infected intravenously. producing types • Staphylococcus aureus enterotoxins, hemolysin alpha toxin, and toxic shock Note: Avian influenza (AI) viruses of the H5 or Clostridium perfringens alpha, beta 1, beta 2, syndrome toxin (formerly known as H7 subtype that do not have either of the epsilon and iota toxins Staphylococcus enterotoxin F); characteristics described in above should be Coccidioides immitis • T-2 toxin; sequenced to determine whether multiple basic Coccidioides posadasii • Tetrodotoxin; amino acids are present at the cleavage site of • Verotoxin and other Shiga-like ribosome Cochliobolus miyabeanus (Helminthosporium the haemagglutinin molecule (HA0). If the inactivating proteins; Viscum Album Lectin oryzae) amino acid motif is similar to that observed for 1 (Viscumin); or other HPAI isolates, then the isolate being Colletotrichum kahawae (Colletotrichum • Volkensin toxin tested should be considered as HPAI and the coffeanum var. virulans) virus is export restricted Conotoxins Dobrava-Belgrade virus Bacillus anthracis SARS-associated coronavirus (SARS-CoV) Eastern Equine Encephalitis virus Bluetongue virus Coxiella burnetii Ebolavirus (includes all members of the Botulinum toxins Ebolavirus genus) Crimean-Congo hemorrhagic fever virus Brucella abortus Enterohaemorrhagic Escherichia coli (E Coli), Dengue virus Shiga toxin producing Escherichia coli (STEC) Brucella melitensis Diacetoxyscirpenol toxin of serogroups O26, O45, O103, O104, O111, Brucella suis O121, O145, O157, and other shiga toxin producing serogroups Burkholderia mallei (Pseudomonas mallei) Note: Shiga toxin producing Escherichia coli (STEC) is also known as enterohaemorrhagic Burkholderia pseudomallei (Pseudomonas E. coli (EHEC) or verocytotoxin producing E. pseudomallei) coli (VTEC). Chapare virus Equine Morbillivirus (Hendra Virus) Chikungunya virus Foot-and-mouth disease virus Chlamydophila psittaci (formerly Chlamydia Francisella tularensis psittaci) Choclo virus Cholera toxin Classical swine fever virus (Hog cholera virus). Rev 6/23/21 “Genetic elements” or genetically modified Junin virus organisms that contain nucleic acid sequences Puccinia striformis (syn. Puccinia glumarum) associated with the pathogenicity of the Kyasanur Forest disease virus Rabies virus and all other members of the microorganisms controlled by 1C351.a to .c, Laguna Negra virus Lyssavirus genus 1C352, 1C354, items in this alphabetical list. Ralstonia solanacearum, race 3, biovar 2 Lassa virus “Nucleic acid sequences associated with the Louping ill virus Rathayibacter toxicus; pathogenicity of any of the microorganisms Lujo virus Reconstructed 1918 influenza virus controlled by 1C351.a to .c, 1C352, or 1C354” Ricin means any sequence specific to the relevant Lumpy skin disease virus controlled microorganism that: in itself or Rickettsia prowazekii Lymphocytic Choriomeningitis virus (LCV) through its transcribed or translated products Rift Valley fever virus represents a significant hazard to human, Lyssa virus (aka Rabies) Rinderpest virus animal or plant health; or is known to enhance Machupo virus the ability of a microorganism controlled by Rocio virus 1C351.a to .c, 1C352, or 1C354, or any other Magnaporthe oryzae (Pyricularia oryzae) Sabia virus organism into which it may be inserted or Marburgvirus (includes all members of the otherwise integrated, to cause serious harm to Marburgvirus genus) Salmonella typhi human, animal or plant health. Medical products containing: Severe acute respiratory syndrome-related • Abrin; coronavirus (SARS-related coronavirus) “Genetically modified organisms” include • Aflatoxins; Saxitoxin organisms in which the genetic material • Cholera toxin; Sclerophthora rayssiae var. zeae; (nucleic acid sequences) has been altered in a • Clostridium perfringens alpha, beta 1, beta way that does not occur naturally by mating 2, epsilon and iota toxins; Seoul virus and/or natural recombination, and • Diacetoxyscirpenol toxin; Sheeppox virus encompasses those produced artificially in • HT-2 toxin; whole or in part. • Microcystin (Cyanginosin); Shiga toxin • Modeccin toxin; “Genetic elements” include, inter alia, Shigella dysenteriae • Shiga toxin; chromosomes, genomes, plasmids, Sin Nombre virus transposons, and vectors, whether genetically • Staphylococcus aureus enterotoxins, St. Louis encephalitis virus modified or unmodified, or chemically hemolysin alpha toxin, and toxic shock synthesized in whole or in part. syndrome toxin (formerly known as Staphylococcus aureus enterotoxins, Staphylococcus enterotoxin F); hemolysin alpha toxin, and toxic shock “Genetic elements” or genetically modified • T-2 toxin; syndrome toxin (formerly known as organisms that contain nucleic acid sequences Staphylococcus enterotoxin F) coding for any of the “toxins” controlled by • Tetrodotoxin; 1C351.d or “sub-units of toxins” thereof. • Verotoxin & other Shiga-like ribosome Suid herpesvirus 1 (Pseudorabies virus; inactivating proteins; Viscum Album Lectin Aujeszky’s disease) Goatpox virus 1 (Viscumin); or Swine fever virus (Hog cholera virus) • Volkensin toxin Guanarito virus Swine vesicular disease virus Microcyclus ulei (syn. Dothidella ulei) Hantaan virus Synchytrium endobioticum; Microcystin (Cyanginosin) Hendra virus (Equine morbillivirus) T-2 toxin Modeccin toxin Herpes virus (Aujeszky’s disease) Tetrodotoxin (TTX) Hog cholera virus (Swine fever virus) Monkeypox virus Tick-borne encephalitis complex viruses (Russian Spring-Summer encephalitis virus HT-2 toxin Murray Valley encephalitis virus aka Far Eastern subtype) and (Siberian Immunotoxins containing: Mycoplasma capricolum subspecies subtype, formerly West Siberian virus) • Abrin; capripneumoniae (“strain F38”). • Aflatoxins; Thecaphora solani Mycoplasma mycoides subspecies mycoides • Botulinum toxins; Tilletia indica • Cholera toxin; SC (small colony) (a.k.a. contagious bovine pleuropneumonia); Vaccines against items in this alphabetical list • Clostridium perfringens alpha, beta 1, beta (ECCNs1C351, 1C353, or 1C354) 2, epsilon and iota toxins; Newcastle disease virus Variola virus (Smallpox virus) • Conotoxin; Nipah virus Venezuelan Equine Encephalitis virus • Diacetoxyscirpenol toxin; Omsk hemorrhagic fever virus • HT-2 toxin; Verotoxin & other Shiga like ribosome • Microcystin (Cyanginosin); Oropouche virus inactivating proteins • Modeccin toxin; Peronosclerospora philippinensis (a.k.a. Vesicular stomatitis virus • Ricin; Peronosclerospora sacchari); Vibrio cholerae • Saxitoxin; Peste-des-petits ruminants virus Viscum Album Lectin 1 (Viscumin) • Shiga toxin; Phoma glycinicola (formerly Pyrenochaeta Volkensin toxin • Staphylococcus aureus enterotoxins, glycines) hemolysin alpha toxin, and toxic shock Western equine encephalitis virus syndrome toxin (formerly known as Porcine herpes virus (Aujeszky's
Recommended publications
  • Assessing Neurotoxicity of Drugs of Abuse
    National Institute on Drug Abuse RESEARCH MONOGRAPH SERIES Assessing Neurotoxicity of Drugs of Abuse 136 U.S. Department of Health and Human Services • Public Health Service • National Institutes of Health Assessing Neurotoxicity of Drugs of Abuse Editor: Lynda Erinoff, Ph.D. NIDA Research Monograph 136 1993 U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES Public Health Service National Institutes of Health National Institute on Drug Abuse 5600 Fishers Lane Rockville, MD 20857 ACKNOWLEDGMENT This monograph is based on the papers and discussions from a technical review on “Assessing Neurotoxicity of Drugs of Abuse” held on May 20-21, 1991, in Bethesda, MD. The technical review was sponsored by the National Institute on Drug Abuse (NIDA). COPYRIGHT STATUS NIDA has obtained permission from the copyright holders to reproduce certain previously published material as noted in the text. Further reproduction of this copyrighted material is permitted only as part of a reprinting of the entire publication or chapter. For any other use, the copyright holder’s permission is required. All other material in this volume except quoted passages from copyrighted sources is in the public domain and may be used or reproduced without permission from the Institute or the authors. Citation of the source is appreciated. Opinions expressed in this volume are those of the authors and do not necessarily reflect the opinions or official policy of the National Institute on Drug Abuse or any other part of the U.S. Department of Health and Human Services. The U.S. Government does not endorse or favor any specific commercial product or company.
    [Show full text]
  • Biosafety Level 1 and Rdna Training
    Biosafety Level 1and rDNA Training Office of Biological Safety Biosafety Level 1 and rDNA Training • Difference between Risk Group and Biosafety Level • NIH and UC policy on recombinant DNA • Work conducted at Biosafety Level 1 • UC Code of Conduct for researchers Biosafety Level 1 and rDNA Training What is the difference between risk group and biosafety level? Risk Groups vs Biosafety Level • Risk Groups: Assigned to infectious organisms by global agencies (NIH, CDC, WHO, etc.) • In US, only assigned to human pathogens (NIH) • Biosafety Level (BSL): How the organisms are managed/contained (increasing levels of protection) Risk Groups vs Biosafety Level • RG1: Not associated with disease in healthy adults (non‐pathogenic E. coli; S. cerevisiae) • RG2: Cause diseases not usually serious and are often treatable (S. aureus; Legionella; Toxoplasma gondii) • RG3: Serious diseases that may be treatable (Y. pestis; B. anthracis; Rickettsia rickettsii; HIV) • RG4: Serious diseases with no treatment/cure (Hemorrhagic fever viruses, e.g., Ebola; no bacteria) Risk Groups vs Biosafety Level • BSL‐1: Usually corresponds to RG1 – Good microbiological technique – No additional safety equipment required for biological work (may still need chemical/radiation protection) – Ability to destroy recombinant organisms (even if they are RG1) Risk Groups vs Biosafety Level • BSL‐2: Same as BSL‐1, PLUS… – Biohazard signs – Protective clothing (lab coat, gloves, eye protection, etc.) – Biosafety cabinet (BSC) for aerosols is recommended but not always required – Negative airflow into room is recommended, but not always required Risk Groups vs Biosafety Level • BSL‐3: Same as BSL‐2, PLUS… – Specialized clothing (respiratory protection, Tyvek, etc.) – Directional air flow is required.
    [Show full text]
  • Biosafety Manual 2017
    Biosafety Manual 2017 Revised 6/2017 Policy Statement It is the policy of Northern Arizona University (NAU) to provide a safe working environment. The primary responsibility for insuring safe conduct and conditions in the laboratory resides with the principal investigator. The Office of Biological Safety is committed to providing up-to-date information, training, and monitoring to the research and biomedical community concerning the safe conduct of biological, recombinant, and acute toxin research and the handling of biological materials in accordance with all pertinent local, state and federal regulations, guidelines, and laws. To that end, this manual is a resource, to be used in conjunction with the CDC and NIH guidelines, the NAU Select Agent Program, Biosafety in Microbiological and Biomedical Laboratories (BMBL), and other resource materials. Introduction This Biological Safety Manual is intended for use as a guidance document for researchers and clinicians who work with biological materials. It should be used in conjunction with the Laboratory-Specific Safety Manual, which provides more general safety information. These manuals describe policies and procedures that are required for the safe conduct of research at NAU. The NAU Personnel Policy on Safety 5.03 also provides guidance for safety in the workplace. Responsibilities In the academic research/teaching setting, the principal investigator (PI) is responsible for ensuring that all members of the laboratory are familiar with safe research practices. In the clinical laboratory setting, the faculty member who supervises the laboratory is responsible for safety practices. Lab managers, supervisors, technicians and others who provide supervisory roles in laboratories and clinical settings are responsible for overseeing the safety practices in laboratories and reporting any problems, accidents, and spills to the appropriate faculty member.
    [Show full text]
  • STEC) Detection in Food Shiga Toxin-Producing Escherichia Coli (STEC) Are Synonymous with Verocytotoxigenic Escherichia Coli (VTEC)
    Report of the Scientific Committee of the Food Safety Authority of Ireland 2019 Advice on Shiga toxin-producing Escherichia coli (STEC) detection in food Shiga toxin-producing Escherichia coli (STEC) are synonymous with verocytotoxigenic Escherichia coli (VTEC). Similarly, stx genes are synonymous with vtx genes. The terms STEC and stx have been used throughout this report. Report of the Scientific Committee of the Food Safety Authority of Ireland Advice on Shiga toxin-producing Escherichia coli (STEC) detection in food Published by: Food Safety Authority of Ireland The Exchange, George’s Dock, IFSC Dublin 1, D01 P2V6 Tel: +353 1 817 1300 Email: [email protected] www.fsai.ie © FSAI 2019 Applications for reproduction should be made to the FSAI Information Unit ISBN 978-1-910348-22-2 Report of the Scientific Committee of the Food Safety Authority of Ireland CONTENTS ABBREVIATIONS 3 EXECUTIVE SUMMARY 5 GENERAL RECOMMENDATIONS 8 BACKGROUND 9 1. STEC AND HUMAN ILLNESS 11 1.1 Pathogenic Escherichia coli . .11 1.2 STEC: toxin production.............................................12 1.3 STEC: public health concern . 13 1.4 STEC notification trends . .14 1.5 Illness severity ....................................................16 1.6 Human disease and STEC virulence ..................................17 1.7 Source of STEC human infection . 22 1.8 Foodborne STEC outbreaks .........................................22 1.9 STEC outbreaks in Ireland . 24 2. STEC METHODS OF ANALYSIS 28 2.1 Detection method for E. coli O157 in food . .29 2.2 PCR-based detection of STEC O157 and non-O157 in food.............29 2.3 Discrepancies between PCR screening and culture-confirmed results for STEC in food ............................................32 2.4 Alternative methods for the detection and isolation of STEC .
    [Show full text]
  • Neutralizing Equine Anti-Shiga Toxin
    al of D urn ru Jo g l D a e Yanina et al., Int J Drug Dev & Res 2019, 11:3 n v o e i l t o International Journal of Drug Development a p n m r e e e e t n n n n n I I t t t a n h d c r R a e e s and Research Research Article Preclinical Studies of NEAST (Neutralizing Equine Anti-Shiga Toxin): A Potential Treatment for Prevention of Stec-Hus Hiriart Yanina1,2, Pardo Romina1, Bukata Lucas1, Lauché Constanza2, Muñoz Luciana1, Berengeno Andrea L3, Colonna Mariana1, Ortega Hugo H3, Goldbaum Fernando A1,2, Sanguineti Santiago1 and Zylberman Vanesa1,2* 1Inmunova S.A., San Martin, Buenos Aires, Argentina 2National Council for Scientific and Technical Research (CONICET) Center for Comparative Medicine, Institute of Veterinary Sciences of the Coast (ICiVetLitoral), Argentina 3National University of the Coast (UNL)/Conicet, Esperanza, Santa Fe, Argentina *Corresponding author: Zylberman Vanesa, Inmunova S.A. 25 De Mayo 1021, CP B1650HMP, San Martin, Buenos Aires, Argentina, Interno 6053, Tel: +54-11- 2033-1455; E-mail: [email protected] Received July 29, 2019; Accepted August 30, 2019; Published Sepetmber 07, 2019 Abstract STEC-HUS is a clinical syndrome characterized by the triad of thrombotic microangiopathy, thrombocytopenia and acute kidney injury. Despite the magnitude of the social and economic problems caused by STEC infections, there are currently no specific therapeutic options on the market. HUS is a toxemic disorder and the therapeutic effect of the early intervention with anti-toxin neutralizing antibodies has been supported in several animal models.
    [Show full text]
  • Enterohemolysin Operon of Shiga Toxin-Producing Escherichia Coli
    FEBS 26317 FEBS Letters 524 (2002) 219^224 View metadata, citation and similar papers at core.ac.uk brought to you by CORE Enterohemolysin operon of Shiga toxin-producing Escherichiaprovided by coliElsevier :- Publisher Connector a virulence function of in£ammatory cytokine production from human monocytes Ikue Taneike, Hui-Min Zhang, Noriko Wakisaka-Saito, Tatsuo Yamamotoà Division of Bacteriology, Department of Infectious Disease Control and International Medicine, Niigata University Graduate School of Medical and Dental Sciences, 757 Ichibanchou, Asahimachidori, Niigata, Japan Received 5 April 2002; revised 14 June 2002; accepted 19 June 2002 First published online 8 July 2002 Edited by Veli-Pekka Lehto Stx [6]. In the case of the outbreak strains in Japan in 1996, Abstract Shiga toxin-producing Escherichia coli (STEC) is associated with hemolytic uremic syndrome (HUS). Although more than 98% of STEC were positive for enterohemolysin most clinical isolates ofSTEC produce hemolysin (called en- [8]. terohemolysin), the precise role ofenterohemolysin in the patho- Enterohemolysin and K-hemolysin (which is produced from genesis ofSTEC infectionsis unknown. Here we demonstrated approximately 50% of E. coli isolates from extraintestinal in- that E. coli carrying the cloned enterohemolysin operon (hlyC, fections [9], or from porcine STEC strains [6]) are members of A, B, D genes) from an STEC human strain induced the pro- the RTX family, associated with the ATP-dependent HlyB/ duction ofinterleukin-1 L (IL-1L) through its mRNA expression HlyD/TolC secretion system through which hemolysin K but not tumor necrosis factor- from human monocytes. No (HlyA) is secreted across the bacterial membranes. Both the L IL-1 release was observed with an enterohemolysin (HlyA)- enterohemolysin and K-hemolysin operons consist of the hlyC, negative, isogenic E.
    [Show full text]
  • Safe Handling of Acutely Toxic Chemicals Safe Handling of Acutely
    Safe Handling of Acutely Toxic Chemicals , Mutagens, Teratogens and Reproductive Toxins October 12, 2011 BSBy Sco ttBthlltt Batcheller R&D Manager Milwaukee WI Hazards Classes for Chemicals Flammables • Risk of ignition in air when in contact with common energy sources Corrosives • Generally destructive to materials and tissues Energetic and Reactive Materials • Sudden release of destructive energy possible (e.g. fire, heat, pressure) Toxic Substances • Interaction with cells and organs may lead to tissue damage • EfftEffects are t tilltypically not general ltllti to all tissues, bttbut target tdted to specifi c ones • Examples: – Cancers – Organ diseases – Inflammation, skin rashes – Debilitation from long-term Poison Acute Cancer, health or accumulation with delayed (ingestion) risk reproductive risk emergence 2 Toxic Substances Are All Around Us Pollutants Natural toxins • Cigare tte smo ke • V(kidbt)Venoms (snakes, spiders, bees, etc.) • Automotive exhaust • Poison ivy Common Chemicals • Botulinum toxin • Pesticides • Ricin • Fluorescent lights (mercury) • Radon gas • Asbestos insulation • Arsenic and heavy metals • BPA ((pBisphenol A used in some in ground water plastics) 3 Application at UNL Chemicals in Chemistry Labs Toxin-producing Microorganisms • Chloro form • FiFungi • Formaldehyde • Staphylococcus species • Acetonitrile • Shiga-toxin from E. coli • Benzene Select Agent Toxins (see register) • Sodium azide • Botulinum neurotoxins • Osmium/arsenic/cadmium salts • T-2 toxin Chemicals in Biology Labs • Tetrodotoxin • Phenol
    [Show full text]
  • Shiga Toxin E. Coli Detection Differentiation Implications for Food
    SL440 Shiga Toxin-Producing Escherichia coli: Detection, Differentiation, and Implications for Food Safety1 William J. Zaragoza, Max Teplitski, and Clifton K. Fagerquist2 Introduction for the effective detection of the Shiga-toxin-producing pathogens in a variety of food matrices. Shiga toxin is a protein found within the genome of a type of virus called a bacteriophage. These bacteriophages can There are two types of Shiga toxins—Shiga toxin 1 (Stx1) integrate into the genomes of the bacterium E. coli, giving and Shiga toxin 2 (Stx2). Stx1 is composed of several rise to Shiga toxin-producing E. coli (STEC). Even though subtypes knows as Stx1a, Stx1c, and Stx1d. Stx2 has seven most E. coli are benign or even beneficial (“commensal”) subtypes: a–g. Strains carrying all of the Stx1 subtypes affect members of our gut microbial communities, strains of E. humans, though they are less potent than that of Stx2. Stx2 coli carrying Shiga-toxin encoding genes (as well as other subtypes a,c, and d are frequently associated with human virulence determinants) are highly pathogenic in humans illness, while the other subtypes affect different animals. and other animals. When mammals ingest these bacteria, Subtypes Stx2b and Stx2e affect neonatal piglets, while STECs can undergo phage-driven lysis and deliver these target hosts for Stx2f and Stx2g subtypes are not currently toxins to mammalian guts. The Shiga toxin consists of an known (Fuller et al. 2011). Stx2f was originally isolated A subunit and 5 identical B subunits. The B subunits are from feral pigeons (Schmidt et al. 2000), and Stx2g was involved in binding to gut epithelial cells.
    [Show full text]
  • National Shiga Toxin-Producing Escherichia Coli (STEC) Surveillance
    National Enteric Disease Surveillance: STEC Surveillance Overview Surveillance System Overview: National Shiga toxin-producing Escherichia coli (STEC) Surveillance Shiga toxin-producing Escherichia coli (STEC) are estimated to cause more than 265,000 illnesses each year in the United States, with more than 3,600 hospitalizations and 30 deaths (1). STEC infections often cause diarrhea, sometimes bloody. Some patients with STEC infection develop hemolytic uremic syndrome (HUS), a severe complication characterized by renal failure, hemolytic anemia, and thrombocytopenia that can be fatal. Most outbreaks of STEC infection and most cases of HUS in the United States have been caused by STEC O157. Non- O157 STEC have also caused US outbreaks. Although all STEC infections are nationally notifiable, for several reasons many cases are likely not recognized (2). Not all persons ill with STEC infection seek medical care, healthcare providers may not obtain a specimen for laboratory diagnosis, or the clinical diagnostic laboratory may not perform the necessary diagnostic tests. Accounting for under-diagnosis and under-reporting, an estimated 96,534 STEC O157 and 168,698 non-O157 infections occur each year (1). STEC transmission occurs through consumption of contaminated foods, ingestion of contaminated water, or direct contact with infected persons (e.g., in child-care settings) or animals or their environments. Colored scanning electron micrograph (SEM) of Escherichia coli bacteria. National STEC surveillance data are collected through passive surveillance of laboratory-confirmed human STEC isolates in the United States. Clinical diagnostic laboratories submit STEC O157 isolates and Shiga toxin-positive broths to state and territorial public health laboratories, where they are further characterized.
    [Show full text]
  • Combined Action of Shiga Toxin Type 2 and Subtilase Cytotoxin in the Pathogenesis of Hemolytic Uremic Syndrome
    toxins Article Combined Action of Shiga Toxin Type 2 and Subtilase Cytotoxin in the Pathogenesis of Hemolytic Uremic Syndrome Romina S. Álvarez 1, Fernando D. Gómez 1, Elsa Zotta 1,2, Adrienne W. Paton 3, James C. Paton 3, Cristina Ibarra 1 , Flavia Sacerdoti 1 and María M. Amaral 1,* 1 Laboratorio de Fisiopatogenia, Departamento de Fisiología, Instituto de Fisiología y Biofísica Bernardo Houssay (IFIBIO Houssay-CONICET), Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires 1121, Argentina; [email protected] (R.S.Á.); [email protected] (F.D.G.); [email protected] (E.Z.); [email protected] (C.I.); [email protected] (F.S.) 2 Cátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, Universidad de Buenos Aires, Buenos Aires 1113, Argentina 3 Research Centre for Infectious Diseases, Department of Molecular and Biomedical Science, University of Adelaide, Adelaide 5005, Australia; [email protected] (A.W.P.); [email protected] (J.C.P.) * Correspondence: [email protected]; Tel.: +54-11-5285-3280 Abstract: Shiga toxin-producing E. coli (STEC) produces Stx1 and/or Stx2, and Subtilase cytotoxin (SubAB). Since these toxins may be present simultaneously during STEC infections, the purpose of this work was to study the co-action of Stx2 and SubAB. Stx2 + SubAB was assayed in vitro on monocultures and cocultures of human glomerular endothelial cells (HGEC) with a human proximal tubular epithelial cell line (HK-2) and in vivo in mice after weaning. The effects in vitro of both toxins, co-incubated and individually, were similar, showing that Stx2 and SubAB contribute similarly to renal cell damage.
    [Show full text]
  • Toxins and the Gut: Role in Human Disease a Fasano
    iii9 PAPER Gut: first published as 10.1136/gut.50.suppl_3.iii9 on 1 May 2002. Downloaded from Toxins and the gut: role in human disease A Fasano ............................................................................................................................. Gut 2002;50(Suppl III):iii9–iii14 Bacterial enteric infections exact a heavy toll on the TOXINS THAT ACTIVATE ENTEROCYTE human population, particularly among children. Despite SIGNAL PATHWAYS Intestinal cells operate through three well estab- the explosion of knowledge on the pathogenesis of lished intracellular signal transduction pathways enteric diseases experienced during the past decade, to regulate water and electrolyte fluxes across the the number of diarrhoeal episodes and human deaths intestinal mucosa: cyclic adenosine monophos- phate (cAMP); cyclic guanosine monophosphate reported worldwide remains of apocalyptic dimensions. (cGMP); and calcium dependent pathways (fig However, our better understanding of the pathogenic 1). Recently, a fourth pathway involving nitric mechanisms involved in the onset of diarrhoea is finally oxide (NO) has been described. leading to preventive interventions, such as the cAMP development of enteric vaccines, that may have a An extremely heterogeneous group of microor- significant impact on the magnitude of this human ganisms, Escherichia coli encompass almost all features of possible interaction between intestinal plague. The application of a multidisciplinary approach microflora and the host, ranging from a role of to study bacterial pathogenesis, along with the recent mere harmless presence to that of highly patho- sequencing of entire microbial genomes, have made genic organisms. In fact, the E coli species is made up of many strains that profoundly differ from possible discoveries that are changing the way scientists each other in terms of biological characteristics view the bacterium–host interaction.
    [Show full text]
  • Effects of Bacterial Lipopolysaccharide and Shiga Toxin on Induced
    bioRxiv preprint doi: https://doi.org/10.1101/2021.09.07.459335; this version posted September 7, 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-NC 4.0 International license. Effects of bacterial lipopolysaccharide and Shiga Toxin on induced Pluripo- tent Stem Cell-derived Mesenchymal Stem Cells Daiana Martire-Greco a;d∗‡ Alejandro La Greca b∗ Luis Castillo Montanez˜ a Celeste Biani b Antonella Lombardi b Federico Birnberg-Weiss a Alessandra Norris b Flavia Sacerdoti c;d Mar´ıa Marta Amaral c;d Nahuel Rodrigues-Rodriguez a Jose Ramon´ Pittaluga a Veronica´ Alejandra Furmento b Veronica´ Ines´ Landoni a;d Santiago Gabriel Miriuka b;d Carlos Luzzani b;d Gabriela Cristina Fernandez´ a;d aLaboratorio de Fisiolog´ıa de los Procesos Inflamatorios. Instituto de Medicina Experimental (IMEX-CONICET). Academia Nacional de Medicina, Buenos Aires, Argentina. bLaboratorio de Investigacion´ Aplicada a Neurociencias (LIAN), FLENI-CONICET, Buenos Aires, Argentina. cLaboratorio de Fisiopatogenia, Instituto de Fisiolog´ıa y Biof´ısica Bernardo Houssay (IFIBIO Houssay-CONICET), Departamento de Fisiolog´ıa, Facultad de Medicina, Buenos Aires (Ar- gentina). dConsejo Nacional de Investigaciones Cient´ıficas y Tecnicas´ (CONICET), Buenos Aires, Ar- gentina. ∗ These authors contributed equally to this work z Corresponding author: [email protected] Lead Contact Daiana Martire-Greco Running title iPSC-MSC response to LPS and Stx. Competing interest The authors declare no competing interest. 1 bioRxiv preprint doi: https://doi.org/10.1101/2021.09.07.459335; this version posted September 7, 2021.
    [Show full text]