Determination of Human Pathogen Profiles in Food by Quality Assured Microbial Assays
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Human Illness Caused by E. Coli O157:H7 from Food and Non-Food Sources
FRI BRIEFINGS Human Illness Caused by E. coli O157:H7 from Food and Non-food Sources M. Ellin Doyle1*, John Archer2, Charles W. Kaspar1, and Ronald Weiss1 1Food Research Institute, University of Wisconsin–Madison, Madison, WI 53706 2Wisconsin Division of Public Health, Bureau of Communicable Diseases and Preparedness, Communicable Disease Epidemiology Section, Madison, WI 53702 Contents Introduction ...................................................................................................................................2 Epidemiology of E. coli O157:H7..................................................................................................2 Outbreak Data ........................................................................................................................2 Reservoirs of E. coli O157:H7 ..............................................................................................3 Cattle—the primary reservoir ........................................................................................3 Other ruminants .............................................................................................................4 Other animals .................................................................................................................4 Transport Hosts......................................................................................................................4 Routes of Human Infection ....................................................................................................5 -
How Do Pathogenic Microorganisms Develop Cross-Kingdom Host Jumps? Peter Van Baarlen1, Alex Van Belkum2, Richard C
Molecular mechanisms of pathogenicity: how do pathogenic microorganisms develop cross-kingdom host jumps? Peter van Baarlen1, Alex van Belkum2, Richard C. Summerbell3, Pedro W. Crous3 & Bart P.H.J. Thomma1 1Laboratory of Phytopathology, Wageningen University, Wageningen, The Netherlands; 2Department of Medical Microbiology and Infectious Diseases, Erasmus MC, University Medical Centre Rotterdam, Rotterdam, The Netherlands; and 3CBS Fungal Biodiversity Centre, Utrecht, The Netherlands Correspondence: Bart P.H.J. Thomma, Abstract Downloaded from https://academic.oup.com/femsre/article/31/3/239/2367343 by guest on 27 September 2021 Laboratory of Phytopathology, Wageningen University, Binnenhaven 5, 6709 PD It is common knowledge that pathogenic viruses can change hosts, with avian Wageningen, The Netherlands. Tel.: 10031 influenza, the HIV, and the causal agent of variant Creutzfeldt–Jacob encephalitis 317 484536; fax: 10031 317 483412; as well-known examples. Less well known, however, is that host jumps also occur e-mail: [email protected] with more complex pathogenic microorganisms such as bacteria and fungi. In extreme cases, these host jumps even cross kingdom of life barriers. A number of Received 3 July 2006; revised 22 December requirements need to be met to enable a microorganism to cross such kingdom 2006; accepted 23 December 2006. barriers. Potential cross-kingdom pathogenic microorganisms must be able to First published online 26 February 2007. come into close and frequent contact with potential hosts, and must be able to overcome or evade host defences. Reproduction on, in, or near the new host will DOI:10.1111/j.1574-6976.2007.00065.x ensure the transmission or release of successful genotypes. -
Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-By-Case Decision-Making
sustainability Review Genetic Engineering and Sustainable Crop Disease Management: Opportunities for Case-by-Case Decision-Making Paul Vincelli Department of Plant Pathology, 207 Plant Science Building, College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY 40546, USA; [email protected] Academic Editor: Sean Clark Received: 22 March 2016; Accepted: 13 May 2016; Published: 20 May 2016 Abstract: Genetic engineering (GE) offers an expanding array of strategies for enhancing disease resistance of crop plants in sustainable ways, including the potential for reduced pesticide usage. Certain GE applications involve transgenesis, in some cases creating a metabolic pathway novel to the GE crop. In other cases, only cisgenessis is employed. In yet other cases, engineered genetic changes can be so minimal as to be indistinguishable from natural mutations. Thus, GE crops vary substantially and should be evaluated for risks, benefits, and social considerations on a case-by-case basis. Deployment of GE traits should be with an eye towards long-term sustainability; several options are discussed. Selected risks and concerns of GE are also considered, along with genome editing, a technology that greatly expands the capacity of molecular biologists to make more precise and targeted genetic edits. While GE is merely a suite of tools to supplement other breeding techniques, if wisely used, certain GE tools and applications can contribute to sustainability goals. Keywords: biotechnology; GMO (genetically modified organism) 1. Introduction and Background Disease management practices can contribute to sustainability by protecting crop yields, maintaining and improving profitability for crop producers, reducing losses along the distribution chain, and reducing the negative environmental impacts of diseases and their management. -
Differences in Innate Immune Response Between Man and Mouse
Institute of Medical Physics and Biophysics Medical Department, Leipzig University Author Manuscript © 2014. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/ Published in final edited form as: Critical Reviews™ in Immunology, 2014; 34:433-54. Available at: http://dx.doi.org/ 10.1615/CritRevImmunol.2014011600. DIFFERENCES IN INNATE IMMUNE RESPONSE BETWEEN MAN AND MOUSE Josefin Zschaler 1,2,*, Denise Schlorke 1,2,* & Juergen Arnhold 1,2 1 Institute for Medical Physics and Biophysics, Medical Faculty, Leipzig University, Leipzig, Germany 2 Translational Centre for Regenerative Medicine (TRM), Leipzig University, Leipzig, Germany * Both authors contributed equally to this work. Abstract Mouse strains are frequently used to model human disease states, to test the efficiency of drugs and therapeutic principles. However, the direct translation of murine experimental data to human pathological events often fails due to sufficient differences in the organization of the immune system of both species. Here we give a short overview of the principle differences between mice and humans in defense strategies against pathogens and mechanisms involved in response to pathogenic microorganisms and other activators of the immune system. While in human blood mechanisms of immune resistance are highly prevailed, tolerance mechanisms dominate for the defense against pathogenic microorganisms in mouse blood. Further on, species-related differences of immune cells mainly involved in innate immune response as well as differences to maintain oxidative homeostasis are also considered. A number of disease scenarios in mice are critically reflected for their suitability to serve as a model for human pathologies. -
Zoonotic Diseases Fact Sheet
ZOONOTIC DISEASES FACT SHEET s e ion ecie s n t n p is ms n e e s tio s g s m to a a o u t Rang s p t tme to e th n s n m c a s a ra y a re ho Di P Ge Ho T S Incub F T P Brucella (B. Infected animals Skin or mucous membrane High and protracted (extended) fever. 1-15 weeks Most commonly Antibiotic melitensis, B. (swine, cattle, goats, contact with infected Infection affects bone, heart, reported U.S. combination: abortus, B. suis, B. sheep, dogs) animals, their blood, tissue, gallbladder, kidney, spleen, and laboratory-associated streptomycina, Brucellosis* Bacteria canis ) and other body fluids causes highly disseminated lesions bacterial infection in tetracycline, and and abscess man sulfonamides Salmonella (S. Domestic (dogs, cats, Direct contact as well as Mild gastroenteritiis (diarrhea) to high 6 hours to 3 Fatality rate of 5-10% Antibiotic cholera-suis, S. monkeys, rodents, indirect consumption fever, severe headache, and spleen days combination: enteriditis, S. labor-atory rodents, (eggs, food vehicles using enlargement. May lead to focal chloramphenicol, typhymurium, S. rep-tiles [especially eggs, etc.). Human to infection in any organ or tissue of the neomycin, ampicillin Salmonellosis Bacteria typhi) turtles], chickens and human transmission also body) fish) and herd animals possible (cattle, chickens, pigs) All Shigella species Captive non-human Oral-fecal route Ranges from asymptomatic carrier to Varies by Highly infective. Low Intravenous fluids primates severe bacillary dysentery with high species. 16 number of organisms and electrolytes, fevers, weakness, severe abdominal hours to 7 capable of causing Antibiotics: ampicillin, cramps, prostration, edema of the days. -
The Public Health Impact of Prion Diseases1
10 Feb 2005 13:10 AR AR238-PU26-08.tex AR238-PU26-08.sgm LaTeX2e(2002/01/18) P1: IBD 10.1146/annurev.publhealth.26.021304.144536 Annu. Rev. Public Health 2005. 26:191–212 doi: 10.1146/annurev.publhealth.26.021304.144536 Copyright ©c 2005 by Annual Reviews. All rights reserved First published online as a Review in Advance on December 8, 2004 THE PUBLIC HEALTH IMPACT OF PRION DISEASES1 Ermias D. Belay and Lawrence B. Schonberger Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia 30333; email: [email protected] KeyWords transmissible spongiform encephalopathy, Creutzfeldt-Jakob disease, variant Creutzfeldt-Jakob disease, bovine spongiform encephalopathy, chronic wasting disease ■ Abstract Several prion disease–related human health risks from an exogenous source can be identified in the United States, including the iatrogenic transmission of Creutzfeldt-Jakob disease (CJD), the possible occurrence of variant CJD (vCJD), and potential zoonotic transmission of chronic wasting disease (CWD). Although cross- species transmission of prion diseases seems to be limited by an apparent “species barrier,” the occurrence of bovine spongiform encephalopathy (BSE) and its transmis- sion to humans indicate that animal prion diseases can pose a significant public health risk. Recent reports of secondary person-to-person spread of vCJD via blood products and detection of vCJD transmission in a patient heterozygous at codon 129 further illustrate the potential public health impacts of BSE. INTRODUCTION by IRMO/Information Center on 03/14/05. For personal use only. Prion diseases, also known as transmissible spongiform encephalopathies (TSEs), are a group of animal and human brain diseases that are uniformly fatal and often characterized by a long incubation period and a multifocal neuropathologic picture of neuronal loss, spongiform changes, and astrogliosis (3). -
Chapter 2 Disease and Disease Transmission
DISEASE AND DISEASE TRANSMISSION Chapter 2 Disease and disease transmission An enormous variety of organisms exist, including some which can survive and even develop in the body of people or animals. If the organism can cause infection, it is an infectious agent. In this manual infectious agents which cause infection and illness are called pathogens. Diseases caused by pathogens, or the toxins they produce, are communicable or infectious diseases (45). In this manual these will be called disease and infection. This chapter presents the transmission cycle of disease with its different elements, and categorises the different infections related to WES. 2.1 Introduction to the transmission cycle of disease To be able to persist or live on, pathogens must be able to leave an infected host, survive transmission in the environment, enter a susceptible person or animal, and develop and/or multiply in the newly infected host. The transmission of pathogens from current to future host follows a repeating cycle. This cycle can be simple, with a direct transmission from current to future host, or complex, where transmission occurs through (multiple) intermediate hosts or vectors. This cycle is called the transmission cycle of disease, or transmission cycle. The transmission cycle has different elements: The pathogen: the organism causing the infection The host: the infected person or animal ‘carrying’ the pathogen The exit: the method the pathogen uses to leave the body of the host Transmission: how the pathogen is transferred from host to susceptible person or animal, which can include developmental stages in the environment, in intermediate hosts, or in vectors 7 CONTROLLING AND PREVENTING DISEASE The environment: the environment in which transmission of the pathogen takes place. -
Innate Immunity Part I: the Immediate Response Deborah A
Innate Immunity Part I: The Immediate Response Deborah A. Lebman, Ph.D. OBJECTIVES 1. Describe three mechanisms present at epithelial surfaces that protect the host from pathogens. 2. List 3 functions of complement proteins in innate immunity 3. Know the primary functions of macrophages and neutrophils 4. List the receptors on macrophages involved in recognition of pathogens 5. List the key toxic products of phagocytes READING • Parham, The Immune System, pg 227-238. TERMS • Defensin: antibacterial peptide produced by the host at epithelial surfaces • Complement: ubiquitously present proteins synthesized primarily in the liver that mediate a variety of responses to pathogens • Opsonin (opsonization): alteration of cell surface that facilitates phagocytosis • Phagocytosis: internalization of particulate matter by cells • CD14: LPS receptor • TLR-4: toll like receptor 4 I. Introduction A. The first response to pathogens occurs immediately B. The early response employs both mechanical and cell mediated mechanisms C. There is no cellular expansion, but there is cell recruitment D. A wide array of soluble mediators with both positive and negative effects, i.e. remove the pathogen but hurt the host, is released II. Overview of Pathogens A. There are four types of pathogen: bacteria, virus, fungus, parasite B. Table I: Examples of the Four Types of Common Human Pathogen Table 1: Examples of the Four Types of Common Human Pathogen Table 1 (Continued): Examples of the Four Types of Common Human Pathogen C. Pathogens can be intracellular or extracellular Table 2: Examples of intracellular and extracellular pathogens. Notice that both innate and adaptive mechanisms are involved in the response to both types of pathogen. -
Ask a Scientist: How Do People Become Infected with Germs?
One way to think about how living things get sick is to imagine a triangle. The three corners represent the environment... ...the host... All three aspects of this triangle must come ...and the cause of the disease, together for disease to occur. Disease the Agent. agents can be non-infectious or infectious. Non-infectious agents are non-living things that are toxic to the host, like radiation or chemicals... ...while infectious agents are organisms that invade a host to survive. Only infectious agents can spread, or transmit, between hosts. Infectious disease agents, otherwise known as pathogens, A person can become infected with a must infect a host pathogen when in the same environment in order to grow, or as the agent... replicate. Human pathogens, like viruses, bacteria, and parasites, evolved to infect people. Their survival is dependent on quickly invading, making more of themselves, and efficiently transmitting to others. If a pathogen gets past a host’s defenses, it will attempt to infect the host and begin replicating itself. ...and don’t have enough protection in the form The subsequent battle between Many cells will be destroyed as of physical barriers or the germs and the body’s germs kill them through replicating pre-existing immunity. immune system will cause the and as collateral damage from the symptoms of illness. activated immune cells. That’s just how one person gets infected, but how does disease spread? Well, if sick people go around sneezing and coughing without covering their mouth or frequently washing their hands... ...they are actually spreading pathogens all over the environment around them. -
Supporting Information
Supporting Information Rosenberg et al. 10.1073/pnas.1307243110 SI Results and Discussion domestic ungulates (horses, cows, sheep, goats, camels, and pigs) Of the 83 arboviruses, nonhuman vertebrate hosts have been and rodents in both groups might be a consequence of spatial identified for 70 (84%); the remaining 13 are presumed to be proximity to humans. Sentinel monkeys were often used in pro- zoonoses because there is no indication they can be transmitted cedures to isolate arboviruses, which might account for their directly between humans by vectors (Table S1). Animal hosts have higher representation among arboviruses. In contrast, there are been identified for at least 57 (44%) of the 130 nonarboviruses; an few published records of bats being routinely sampled during additional 5 (8%) are presumed on epidemiological evidence to arbovirus studies, and only two arboviruses (3%) have been iso- have nonhuman reservoirs (Table S1). A number of viruses infect lated from bats. The reason a much larger number of arbovirus more than one nonhuman vertebrate host species and it is likely species (n = 16) have been isolated from birds than have that the variety of hosts is wider than has been recorded. The nonarbovirus species (n = 1) might, however, be characteristic of predominant host groups for arboviruses (n = 70) are nonhuman the pathogenicity of the togaviruses and flaviviruses, which are primates (31%), rodents (29%), ungulates (26%), and birds (23%); much more common among the arboviruses. The most prominent for the nonarboviruses (n = 57), they are rodents (30%), ungu- vectors of arboviruses were mosquitoes (67%), ticks (19%), and lates (26%), bats (23%), and primates (16%). -
Neglected Tropical Diseases in The
Qian et al. Infectious Diseases of Poverty (2019) 8:86 https://doi.org/10.1186/s40249-019-0599-4 SCOPING REVIEW Open Access Neglected tropical diseases in the People’s Republic of China: progress towards elimination Men-Bao Qian1, Jin Chen1, Robert Bergquist2, Zhong-Jie Li3, Shi-Zhu Li1, Ning Xiao1, Jürg Utzinger4,5 and Xiao-Nong Zhou1* Abstract Since the founding of the People’s Republic of China in 1949, considerable progress has been made in the control and elimination of the country’s initial set of 11 neglected tropical diseases. Indeed, elimination as a public health problem has been declared for lymphatic filariasis in 2007 and for trachoma in 2015. The remaining numbers of people affected by soil-transmitted helminth infection, clonorchiasis, taeniasis, and echinococcosis in 2015 were 29.1 million, 6.0 million, 366 200, and 166 100, respectively. In 2017, after more than 60 years of uninterrupted, multifaceted schistosomiasis control, has seen the number of cases dwindling from more than 10 million to 37 600. Meanwhile, about 6000 dengue cases are reported, while the incidence of leishmaniasis, leprosy, and rabies are down at 600 or fewer per year. Sustained social and economic development, going hand-in-hand with improvement of water, sanitation, and hygiene provide the foundation for continued progress, while rigorous surveillance and specific public health responses will consolidate achievements and shape the elimination agenda. Targets for poverty elimination and strategic plans and intervention packages post-2020 are important opportunities for further control and elimination, when remaining challenges call for sustainable efforts. Keywords: Control, Elimination, People's Republic of China, Neglected tropical diseases Multilingual abstracts deprived urban settings [1, 2]. -
Spillback in the Anthropocene: the Risk of Human-To-Wildlife Pathogen Transmission for Conservation and Public Health
Spillback in the Anthropocene: the risk of human-to-wildlife pathogen transmission for conservation and public health Anna C. Fagre*1, Lily E. Cohen2, Evan A. Eskew3, Max Farrell4, Emma Glennon5, Maxwell B. Joseph6, Hannah K. Frank7, Sadie Ryan8, 9,10, Colin J Carlson11,12, Gregory F Albery*13 *Corresponding authors: [email protected]; [email protected] 1: Department of Microbiology, Immunology, and Pathology, College of Veterinary Medicine and Biomedical Sciences, Colorado State University, Fort Collins, CO 2: Icahn School of Medicine at Mount Sinai, New York, NY 10029 3: Department of Biology, Pacific Lutheran University, Tacoma, WA, 98447 USA 4: Department of Ecology & Evolutionary Biology, University of Toronto 5: Disease Dynamics Unit, Department of Veterinary Medicine, University of Cambridge, Cambridge CB3 0ES, UK 6: Earth Lab, University of Colorado Boulder, Boulder, CO 80309 7: Department of Ecology and Evolutionary Biology, Tulane University, New Orleans, LA, 70118 USA 8: Quantitative Disease Ecology and Conservation (QDEC) Lab Group, Department of Geography, University of Florida, Gainesville, FL, 32610 USA 9: Emerging Pathogens Institute, University of Florida, Gainesville, FL, 32610 USA 10: School of Life Sciences, University of KwaZulu-Natal, Durban, 4041, South Africa 11: Center for Global Health Science and Security, Georgetown University Medical Center, Washington, DC, 20057 USA 12: Department of Microbiology and Immunology, Georgetown University Medical Center, Washington, DC, 20057 USA 13: Department of Biology, Georgetown University, Washington, DC, 20057 USA 1 Abstract The SARS-CoV-2 pandemic has led to increased concern over transmission of pathogens from humans to animals (“spillback”) and its potential to threaten conservation and public health.