Antibiotic Therapy–Induced Collateral Damage: Iga Takes Center Stage in Pulmonary Host Defense

Total Page:16

File Type:pdf, Size:1020Kb

Antibiotic Therapy–Induced Collateral Damage: Iga Takes Center Stage in Pulmonary Host Defense Antibiotic therapy–induced collateral damage: IgA takes center stage in pulmonary host defense Juergen Lohmeyer, … , Rory E. Morty, Susanne Herold J Clin Invest. 2018;128(8):3234-3236. https://doi.org/10.1172/JCI122032. Commentary The use of broad-spectrum antibiotics in empirical antimicrobial therapy is a lifesaving strategy for patients in intensive care. At the same time, antibiotics dramatically increase the risk for nosocomial infections, such as hospital‑acquired pneumonia caused by Pseudomonas aeruginosa, and other antibiotic-resistant bacteria. In this issue of theJ CI, Robak and colleagues identified a mechanism by which depletion of resident gut and lung microbiota by antibiotic treatment results in secondary IgA deficiency and impaired anti–P. aeruginosa host defense. Impaired defenses could be improved by substitution of polyclonal IgA via the intranasal route in a mouse model of pneumonia. Importantly, antibiotic treatment caused lung IgA deficiency that involved reduced TLR-dependent production of a proliferation-inducing ligand (APRIL) and B cell–activating factor (BAFF) in intensive care unit patients. These patients might therefore benefit from future strategies to increase pulmonary IgA levels. Find the latest version: https://jci.me/122032/pdf COMMENTARY The Journal of Clinical Investigation Antibiotic therapy–induced collateral damage: IgA takes center stage in pulmonary host defense Juergen Lohmeyer,1 Rory E. Morty,1,2 and Susanne Herold1,3 1Department of Internal Medicine II, University of Giessen and Marburg Lung Center (UGMLC), member of the German Center for Lung Research (DZL), Justus-Liebig-University, Giessen, Germany. 2Department of Lung Development and Remodelling, Max Planck Institute for Heart and Lung Research, member of the German Center for Lung Research (DZL), Bad Nauheim, Germany. 3Division of Pulmonary and Critical Care, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA. biota changes induced by ABx treatment inhibit immunoglobulin A (IgA) produc- The use of broad-spectrum antibiotics in empirical antimicrobial therapy tion in the lung, thereby increasing suscep- is a lifesaving strategy for patients in intensive care. At the same time, tibility of ABx-treated patients to infection antibiotics dramatically increase the risk for nosocomial infections, such with P. aeruginosa (Figure 1). as hospital-acquired pneumonia caused by Pseudomonas aeruginosa, and other antibiotic-resistant bacteria. In this issue of the JCI, Robak and Microbiota-host immunity colleagues identified a mechanism by which depletion of resident gut and cross-talk lung microbiota by antibiotic treatment results in secondary IgA deficiency How do the findings of Robak et al. help and impaired anti–P. aeruginosa host defense. Impaired defenses could expand our understanding of the interplay be improved by substitution of polyclonal IgA via the intranasal route in between the microbiota and host defense a mouse model of pneumonia. Importantly, antibiotic treatment caused in lung infection, and thereby promote lung IgA deficiency that involved reduced TLR-dependent production of a development of new prophylactic or thera- proliferation-inducing ligand (APRIL) and B cell–activating factor (BAFF) in peutic strategies? It is well established that intensive care unit patients. These patients might therefore benefit from antimicrobial therapies inevitably cause future strategies to increase pulmonary IgA levels. dramatic and long-lasting collateral dam- age to the diverse populations of com- mensal bacterial species that are part of a patient’s intestinal microbiota. However, Antibiotic use and risk of risk factor for the normal microbiome to recent investigations have further revealed nosocomial infection turn into a so-called pathobiome, which is that composition of the microbiota also Broad-spectrum antibiotics (ABx) form diagnosed as hospital-acquired pneumo- crucially impacts systemic and pulmonary the backbone of empiric antimicrobial nia (HAP) and often associated with out- innate immune responses during bacterial treatment regimens, which are lifesav- growth of P. aeruginosa or other antibiotic- and viral infections (13–15). Considerably ing for those with severe infections such resistant bacteria (6, 7). Recent estimates less is known about how the microbiota as pneumonia, peritonitis, or sepsis, and indicate that in Europe, 2.6 million cases ecosystem and its depletion by ABx impact which constitute an integral part of treat- of hospital-acquired infections occur each adaptive immune responses. The gut ment guidelines (1). However, apart from year, and that HAP accounts for the high- microbiota is critical for regulating intesti- driving the selection of multiresistant est disease burden and number of deaths nal IgA production, as IgA-secreting cells pathogens, ABx severely disrupt the host (8). HAP dramatically increases both the and IgA production are almost absent in microbiome, which has been increasingly length of the hospital stay and health care the gut of germ-free mice (16). Moreover, recognized as a critical factor in shaping costs, and is associated with a mortality of microbial signals are known to activate host immunity (2). Antibiotic stewardship up to 13% (9). TLRs on intestinal epithelial cells and DCs and improved point-of-care microbial The increased susceptibility of critical- to induce production of the crucial B cell diagnostics increasingly facilitate the opti- ly ill patients to infection with multidrug survival signals APRIL and BAFF, which mized use of specific antibiotics (3), but in resistant (MDR) gram-negative bacteria in turn, promote IgA production by plas- critically ill patients the empiric use of ABx was originally attributed to generation of ma cells (17–19). In addition, microbiota- will remain indispensable. Point-preva- a permissive niche with selection of MDR derived short-chain fatty acids have lence studies have documented that to pathogens that were not covered by the recently been demonstrated to positively date 64%–71% of all patients in intensive ABx regimen (10, 11). In this issue, Robak regulate IgA production (20). care units (ICUs) receive antibiotics (4, 5). and colleagues (12) identify an additional Previous antimicrobial therapy is a major mechanism by which lung and gut micro- IgA-mediated pulmonary host defense Related Article: p. 3535 What makes IgA so special for lung host defense? Immunoglobulin A has a criti- Conflict of interest: The authors have declared that no conflict of interest exists. cal role in immune defense, particularly Reference information: J Clin Invest. 2018;128(8):3234–3236. https://doi.org/10.1172/JCI122032. at mucosal surfaces, and IgA is specially 3234 jci.org Volume 128 Number 8 August 2018 The Journal of Clinical Investigation COMMENTARY Figure 1. Broad-spectrum antibiotic treatment exerts severe collateral damage by inhibiting microbiota-induced secretory IgA synthesis and IgA- dependent lung host defense toward P. aeruginosa. The lung and gut commensal microbiota induce IgA production at mucosal surfaces involving TLR-, APRIL-, and BAFF-dependent signaling. Lung secretory IgA (sIgA) binds P. aeruginosa and reduces host susceptibility to P. aeruginosa pneumonia. ABx treatment destroys luminal microbiota and severely reduces sIgA production by lung IgA-secreting plasma cells, thereby impairing anti-pseudomonas host defense, which can be reestablished by transnasal administration of sIgA. equipped to undertake this task through had not been investigated if and how dis- However, it is also conceivable that the the unique structural attributes of the turbances to this mechanism contribute to induction of IgA generation occurs in the IgA heavy chain and by virtue of its abil- the enhanced susceptibility to lung infec- intestinal tract and that IgA+ plasma cells ity to polymerize (16). Notably, more IgA tions following antibiotic treatment. The subsequently migrate to the lung, given antibodies are synthesized in mammals findings by Robak et al. explain how deple- that migration of plasma cells between per day than antibodies of all other iso- tion of the resident microbiota affects lung lung and intestine has been previously types combined. IgA plays a pivotal role host defense against P. aeruginosa and described (22). Second, the cellular com- in maintaining a homeostatic relation- represent a fundamental step in filling this partment responsible for the TLR-depen- ship between the host and the resident knowledge gap. To our knowledge, this is dent APRIL production and the specific microbiota of the intestine (21). Produc- the first study to demonstrate that deple- TLR member involved remain unknown. tion of high-affinity and antigen-specific tion of resident microbiota by ABx inhib- Third, the mechanism by which IgA exerts IgA in Peyer’s patches and mesenteric its TLR-dependent production of APRIL, antimicrobial properties directed against lymph nodes has been documented to be resulting in secondary IgA deficiency in P. aeruginosa (and most likely other bac- T cell dependent (16), whereas low-affin- the lungs of both mice and ICU patients terial species) in the lung is unknown, ity polyreactive IgA responses are mainly and increases susceptibility to subsequent but likely is similar to the gut, where IgA induced in isolated lymphoid follicles P. aeruginosa infection (Figure 1). There achieves neutralization of invasive patho- and in subepithelial B cells in a T cell– are several essential unresolved questions
Recommended publications
  • 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.
    [Show full text]
  • The Resistance to Host Antimicrobial Peptides in Infections Caused by Daptomycin-Resistant Staphylococcus Aureus
    antibiotics Communication The Resistance to Host Antimicrobial Peptides in Infections Caused by Daptomycin-Resistant Staphylococcus aureus Md Saruar Bhuiyan 1,† , Jhih-Hang Jiang 1,† , Xenia Kostoulias 1, Ravali Theegala 1, Graham J. Lieschke 2 and Anton Y. Peleg 1,3,* 1 Infection and Immunity Program, Monash Biomedicine Discovery Institute, Department of Microbiology, Monash University, Clayton, VIC 3800, Australia; [email protected] (M.S.B.); [email protected] (J.-H.J.); [email protected] (X.K.); [email protected] (R.T.) 2 Australian Regenerative Medicine Institute, Monash University, Clayton, VIC 3800, Australia; [email protected] 3 Department of Infectious Diseases, The Alfred Hospital and Central Clinical School, Monash University, Melbourne, VIC 3004, Australia * Correspondence: [email protected] † These authors contributed equally to this work. Abstract: Daptomycin is an important antibiotic for the treatment of infections caused by Staphylococcus aureus. The emergence of daptomycin resistance in S. aureus is associated with treatment failure and persistent infections with poor clinical outcomes. Here, we investigated host innate immune responses against clinically derived, daptomycin-resistant (DAP-R) and -susceptible S. aureus paired isolates using a zebrafish infection model. We showed that the control of DAP-R S. aureus infections was attenuated in vivo due to cross-resistance to host cationic antimicrobial Citation: Bhuiyan, M.S.; Jiang, J.-H.; peptides. These data provide mechanistic understanding into persistent infections caused by DAP-R Kostoulias, X.; Theegala, R.; Lieschke, S. aureus and provide crucial insights into the adaptive evolution of this troublesome pathogen. G.J.; Peleg, A.Y. The Resistance to Host Antimicrobial Peptides in Keywords: S.
    [Show full text]
  • 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.
    [Show full text]
  • STD (Sexually Transmitted Disease) Or STI (Sexually Transmitted Infection): Should We Choose? Janet Byron Anderson, Phd
    STD (sexually transmitted disease) or STI (sexually transmitted infection): Should we choose? Janet Byron Anderson, PhD 1. Clinical foundation of the problem Another surprise: Documented incidence had shown Each of the terms—“sexual(ly)”, “transmitted”, “disease”, that the two routes of sexual transmission were male-to- and “infection”—is problematic independently, as this female and male-to-male. However, on 15 July 2016 the study will show. Moreover, co-occurring variants, used CDC reported the first case of suspected female-to-male as synonyms in English medical articles worldwide, ag- sexual transmission in New York City [4]. Since 2008, gravate the problem. The purpose of this study is to pro- then, the Zika virus has shown that it is now sexually pose a single term that can stimulate discussion about transmissible. “Transmissible” denotes a potential, and is whether the co-occurring variants are clinically and lin- distinct from “transmitted”, which denotes a reality. guistically justifiable—especially now, when STDs/STIs To say that Zika has proved to be transmissible through have become a global health problem, and public health sexual contact means that it can be transmitted through agencies in every country are scrambling to educate their sex but that it need not be (Zika remains a chiefly vec- citizens. [Until the presentation advances to the point tor-borne disease). However, cases reported since 2008 where the question posed in the title can be definitively document the reality of transmittedness through sexual answered, I’ll use the expression “STD/STI” or the terms contact. “illness(es)” and “condition(s)”.] The predisposing epidemiologic context will first be clar- This carefully differentiated language is used by the ified, for it sheds light on two of the problematic terms: European Centre for Disease Prevention and Control chiefly “transmitted” but also “sexual(ly)”.
    [Show full text]
  • Sexually Transmitted Infections Treatment Guidelines, 2021
    Morbidity and Mortality Weekly Report Recommendations and Reports / Vol. 70 / No. 4 July 23, 2021 Sexually Transmitted Infections Treatment Guidelines, 2021 U.S. Department of Health and Human Services Centers for Disease Control and Prevention Recommendations and Reports CONTENTS Introduction ............................................................................................................1 Methods ....................................................................................................................1 Clinical Prevention Guidance ............................................................................2 STI Detection Among Special Populations ............................................... 11 HIV Infection ......................................................................................................... 24 Diseases Characterized by Genital, Anal, or Perianal Ulcers ............... 27 Syphilis ................................................................................................................... 39 Management of Persons Who Have a History of Penicillin Allergy .. 56 Diseases Characterized by Urethritis and Cervicitis ............................... 60 Chlamydial Infections ....................................................................................... 65 Gonococcal Infections ...................................................................................... 71 Mycoplasma genitalium .................................................................................... 80 Diseases Characterized
    [Show full text]
  • Transmission of SARS-Cov-2: Implications for Infection Prevention Precautions
    Transmission of SARS-CoV-2: implications for infection prevention precautions Scientific brief 9 July 2020 This document is an update to the scientific brief published on 29 March 2020 entitled “Modes of transmission of virus causing COVID-19: implications for infection prevention and control (IPC) precaution recommendations” and includes new scientific evidence available on transmission of SARS-CoV-2, the virus that causes COVID-19. Overview This scientific brief provides an overview of the modes of transmission of SARS-CoV-2, what is known about when infected people transmit the virus, and the implications for infection prevention and control precautions within and outside health facilities. This scientific brief is not a systematic review. Rather, it reflects the consolidation of rapid reviews of publications in peer-reviewed journals and of non-peer-reviewed manuscripts on pre-print servers, undertaken by WHO and partners. Preprint findings should be interpreted with caution in the absence of peer review. This brief is also informed by several discussions via teleconferences with the WHO Health Emergencies Programme ad hoc Experts Advisory Panel for IPC Preparedness, Readiness and Response to COVID-19, the WHO ad hoc COVID-19 IPC Guidance Development Group (COVID-19 IPC GDG), and by review of external experts with relevant technical backgrounds. The overarching aim of the global Strategic Preparedness and Response Plan for COVID-19(1) is to control COVID-19 by suppressing transmission of the virus and preventing associated illness and death. Current evidence suggests that SARS-CoV-2, the virus that causes COVID-19, is predominantly spread from person-to-person.
    [Show full text]
  • Supporting North Carolina's Vaccination Efforts
    Supporting North Carolina’s Vaccination Efforts Toolkit for Partner Organizations Updated June 17th, 2021 Current State of North Carolina COVID-19 Vaccinations: COVID-19 vaccines are available for free in North Carolina to everyone ages 12 and older. Those 18 and over can receive any of the three approved vaccines, while youth aged 12-17 may only receive the Pfizer vaccine. Individuals and CBOs may use the CDC Vaccine Finder to find locations that carry the Pfizer vaccine. While walk-in vaccinations are available, some locations may require appointments. In North Carolina, anyone can get vaccinated regardless of immigration status – getting vaccinated will not affect your immigration. No government-issued ID or insurance is required. Everyone can read the frequently asked questions on the DHHS website to learn more about vaccinations and what you can do after you’re vaccinated. Earning the Trust of North Carolinians: The injustices that drive the disparate impact of COVID-19 on historically marginalized populations (HMP)1 can also cause very legitimate reasons for community members to have questions about vaccines. That is why NCDHHS are working to partner with trusted leaders and organizations to provide accurate information to communities. NCDHHS is committed to earning the trust of North Carolinians related to the COVID-19 vaccine and beyond and building upon already established relationships. Organizations can consider the following strategies to support North Carolina’s vaccination efforts: 1. Share information about the COVID-19 vaccine: • Use the NCDHHS COVID-19 vaccine communications toolkit to make sure all North Carolinians have accurate and up-to-date information on the vaccine.
    [Show full text]
  • Cationic Host Defense (Antimicrobial) Peptides Kelly L Brown and Robert EW Hancock
    Cationic host defense (antimicrobial) peptides Kelly L Brown and Robert EW Hancock Members of the cationic host defense (antimicrobial) peptide Peptides are expressed with elements of immunity family are widely distributed in nature, existing in organisms Innate immunity is the most ancient form of immune from insects to plants to mammals and non-mammalian defense, conserved throughout the animal kingdom and vertebrates. Although many demonstrate direct antimicrobial vital to invertebrate host defenses. More recently dis- activity against bacteria, fungi, eukaryotic parasites and/or covered aspects of innate immunity — most notably, the viruses, it has been established that cationic peptides have a family of Toll-like receptors (TLRs) — have illuminated key modulatory role in the innate immune response. More the previously unrecognized complexity and heterogene- recent evidence suggests that host defense peptides are ity within the innate immune system. Many factors sup- effective adjuvants, are synergistic with other immune port important and diverse roles for antimicrobial effectors, polarize the adaptive response, and support wound peptides in immunity: the robust membership, broad healing. In addition, the mechanisms of action are being diversity in sequence and structure, thematic similarity unraveled, which support more effective implementation of of vertebrate and invertebrate antimicrobial peptides, derivatives of these endogenous peptides as therapeutic wide distribution in cells of the immune system (leuko- agents. cytes, Paneth
    [Show full text]
  • Emerging Infectious Diseases
    EMERGING INFECTIOUS DISEASES Javier Garau Hospital Universitari Mutua de Terrassa Universitat de Barcelona Spain Roma, 9-10 October 2008 Outline •Importance and impact of EIDs •Some definitions •Host range and EIDs and REIDs •Global trends •Getting ready for the future Leading causes of death worldwide. About 15 million (>25%) of 57 million annual deaths worldwide are the direct result of infectious disease. (http://www.who.int/whr/en) Not included the additional millions of deaths that occur as a consequence of past infections (for example, streptococcal rheumatic heart disease), or because of complications associated with chronic infections, such as liver failure and hepatocellular carcinoma in people infected with hepatitis B or C viruses. EIDS: PREPARING FOR THE FUTURE •IDs account for a quarter of all human mortality and a similar fraction of morbidity (www.who.int/whr/2005/en/) •IDs of crops and livestock cost the global economy many billions of euros every year •Sudden epidemics of IDs can deliver humanitarian and economic shocks on a scale diffricult to absorb. * United Nations, The Millenium Development goals Report 2005, New York 2005 WB Report 2003: SARS epidemic, which killed < 1000 people, was responsible for an estimated fall of 2% in GDP across East Asia •Outbreaks of livestocks (FMD, BSE, CSF, AI… ) and crop diseases (Soybean rust, Southern corn leaf blight) costing individual countries billions of euros The UN Millenium Development goals* for reducing the burden of IDs (HIV, TB, malaria), poverty and hunger (compromised by livestock and crop diseases) are gloomy: in most developing regions, where the impacts of IDs are greatest, little hope of meeting any of these goals by 2015 *United Nations, The Millenium Development goals Report 2005, New York 2005 EMERGING INFECTIONS “infections that have newly appeared in a population or have existed previously but are rapidly increasing in incidence or geographic range” Morse, S.
    [Show full text]
  • Prioritizing Zoonotic Diseases for Multisectoral, One Health Collaboration in the United States Workshop Summary
    Prioritizing Zoonotic Diseases for Multisectoral, One Health Collaboration in the United States Workshop Summary CS29887A ONE HEALTH ZOONOTIC DISEASE PRIORITIZATION WORKSHOP REPORT, UNITED STATES Photo 1. A brown bear in the forest. ii ONE HEALTH ZOONOTIC DISEASE PRIORITIZATION WORKSHOP REPORT, UNITED STATES TABLE OF CONTENTS Participating Organizations ........................................................................................................................................................... iv Executive Summary ............................................................................................................................................................................. 1 Background ............................................................................................................................................................................................ 21 Workshop Methods ....................................................................................................................................................................... 30 Recommendations for Next Steps ........................................................................................................................................... 35 APPENDIX A: Overview of the One Health Zoonotic Disease Prioritization Process ................................ 39 APPENDIX B: One Health Zoonotic Disease Prioritization Workshop Participants for the United States ...............................................................................................................................................................................
    [Show full text]
  • Understanding Basic Food Safety 30 After Completing This Lesson
    Understanding Basic Food Safety Foodborne illness is transmitted to humans by eating food that has been contaminated. This contamination is from unwanted microbes and pathogens, the microorganisms that cause foodborne illness. This lesson will explain many common pathogens and microbes causing foodborne illnesses. After completing this lesson, participants will be able to: x Define key vocabulary terms relating to foodborne illness x Understand common food pathogens and where they are found x Learn how to preventSAMPLE common foodborne illnesses FOCUS x PowerPoint Presentations Slide 8 1. Prepare to show Presentation Slide 8 5 - 10 minutes x Foodborne Illness Key Vocabulary 2. Print/photocopy the Foodborne Illness handout Key Vocabulary handout (one per x Foodborne Illness Key Vocabulary participant) Definitions LEARN x Research Graphic Organizer 1. Print/photocopy the Research Graphic 60 – 90 minutes x Internet access Organizer (one per participant) x Common Pathogens Known to Cause 2. Ensure Internet access for participants Foodborne Illness 3. Common Pathogens Known to Cause Foodborne Illness handout (one per participant) REVIEW x Foodborne Illness Vocabulary Quiz 1. Print/photocopy the Foodborne Illness 5 - 10 minutes x Foodborne Illness Vocabulary Quiz Vocabulary Quiz (one per participant) Answer Key 30 Understanding Basic Food Safety 5 – 10 minutes Purpose: Students will learn to define key vocabulary terms that relate to foodborne illnesses in order to recognize and prevent against food contamination. Materials: x PowerPoint Presentation Slide 8 x Foodborne Illness Key Vocabulary handout x Foodborne Illness Key Vocabulary Definitions Facilitation Steps: 1. Show Presentation Slide 8. Share the following statistic with participants: The CDC estimates that 48 million Americans get sick each year, 128,000 are hospitalized, and up to 3000 die of foodborne diseases each year.
    [Show full text]
  • Origins of the COVID-19 Pandemic
    Updated June 11, 2021 Origins of the COVID-19 Pandemic In late 2019, a new coronavirus, SARS-CoV-2, was transmitted it to humans. No intermediate hosts have been identified in Wuhan, China. The virus, which causes identified. Coronavirus Disease 2019 (COVID-19), has contributed to significant morbidity (illness) and mortality (death), as well (2) Direct zoonotic spillover, a “possible-to-likely” as severe public health and economic effects, among other pathway through which SARS-CoV-2 could have been impacts. Several Members of Congress have made public transmitted from an animal reservoir host to a human. Bats are seen as a likely reservoir host, as several studies have statements and introduced legislation calling for an investigation into the origin of SARS-CoV-2. Determining identified high genetic similarity between SARS-CoV-2 the origin and pathway by which a zoonotic disease (i.e., and coronaviruses found in certain bat species found in China and elsewhere in South Asia. one that originated in animals) emerges and is transmitted to humans can help scientists prevent further outbreaks, (3) Introduction through cold/food-chain products, a inform the public health response, and aid in the “possible” hypothesis positing that people contracted development of therapeutics and vaccines. Further, such SARS-CoV-2 through contact with contaminated food, knowledge may guide the development of policies and potentially including frozen, imported foodstuffs. SARS- practices that reduce the potential for the emergence of CoV-2 has been identified on frozen food, its packaging, other zoonotic diseases. Determining the origin of zoonotic and cold-chain products (items stored at controlled diseases can take years, and in some cases, an origin may temperatures to preserve and extend shelf life).
    [Show full text]