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Outbreak: Cases in Real-World Microbiology, 2nd Edition, is the newest edition of this fascinating textbook designed for introductory microbiology students and instructors. Thoroughly revised, this collection of case studies of real-world disease outbreaks, generously illustrated in full color, offers material that directly impacts college-level students, while the book's unique presentation offers instructors the flexibility to use it effectively in a number of ways.
More than 90 outbreak case studies, organized into six sections according to the human body system affected, illustrate the wide range of diseases caused by microbial pathogens. The studies are presented at differing levels of difficulty and can be taught at all undergraduate levels. Each case study includes questions for students to think about, discuss, and answer, and the book includes an appendix that directs students to the specific reference material on which each case was based, providing the opportunity to investigate further and to apply the reference content to the case being studied.
Each of the six sections of the book concludes with a College Perspective and a Global Perspective case study. The College Perspective provides a direct and practical link between the microbiology course and the daily lives of students. The Global Perspective connects students with outbreaks that have occurred in countries around the world to facilitate understanding of the social, religious, economic, and political values at play in the treatment and prevention of infectious disease. At the end of every section, detailed descriptions offer concise yet complete information on each disease involved in that section.
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Cover
Introduction
Content
Special Features
Case Studies in the Classroom
Features of
Outbreak, Second Edition
Recommendations for Using the Case Studies
Acknowledgments
About the Author
SECTION I: Outbreaks of Diseases of the Respiratory Tract
OUTBREAK I‐1 A Legionellosis Outbreak—Barceloneta
OUTBREAK I‐2 An Outbreak of Respiratory Syncytial Virus Infection—Arviat, Canada
OUTBREAK I‐3 A Tuberculosis Outbreak in a Prison Housing Inmates Infected with HIV—South Carolina
OUTBREAK I‐4 An Otitis Media Outbreak in a Child Care Center—Georgia
OUTBREAK I‐5 An Outbreak of a Rash—Venezuela and Colombia
OUTBREAK I‐6 Hantavirus Pulmonary Syndrome Outbreak—Vermont
OUTBREAK I‐7 A Diphtheria Outbreak—Newly Independent States of the Former Soviet Union
OUTBREAK I‐8 An Outbreak of Mycoplasmal Pneumonia—Ohio
OUTBREAK I‐9 A Pneumonia Outbreak in a Nursing Home—New Jersey
OUTBREAK I‐10 Past and Future Pandemics of Influenza A—Worldwide, 1918 to Present
OUTBREAK I‐11 A Pharyngitis Outbreak in the Marine Corps—San Diego
OUTBREAK I‐12 A Measles Outbreak in Kosovar Refugee Children—Albania
OUTBREAK I‐13 A Swimming Pool‐Related Outbreak of Pharyngitis and Conjunctivitis—Spain
OUTBREAK I‐14 A Cruise Ship‐Associated Legionnaires’ Disease Outbreak
OUTBREAK I‐15 A Pertussis Epidemic—Washington State
OUTBREAK I‐16 COLLEGE PERSPECTIVE
OUTBREAK I‐17 GLOBAL PERSPECTIVE
REFERENCE MATERIAL
SECTION II: Outbreaks of Disease of the Gastrointestinal Tract
OUTBREAK II‐1 A
Salmonella enterica
serovar Enteritidis Outbreak from Eating Eggs—Multistate
OUTBREAK II‐2 A Diarrhea Outbreak Associated with Swimming Pool Use—Ohio
OUTBREAK II‐3 Diarrhea among Attendees of the Washington County Fair—New York
OUTBREAK II‐4 An Amoebiasis Outbreak—Georgia
OUTBREAK II‐5 A Typhoid Fever Outbreak Linked with a Frozen Fruit Drink—Florida
OUTBREAK II‐6 A Diarrhea Outbreak in a Day Care Nursery—Juneau, Alaska
OUTBREAK II‐7 A Foodborne Outbreak of Bloody Diarrhea—Multistate
OUTBREAK II‐8 A Multistate Outbreak of Listeriosis—Northeastern United States
OUTBREAK II‐9 An Outbreak of Rotaviral Gastroenteritis among Children—Jamaica
OUTBREAK II‐10 Bloody Diarrhea Associated with Eating Ground Beef—United States
OUTBREAK II‐11 A Hepatitis Outbreak Associated with Restaurant Onions—Pennsylvania
OUTBREAK II‐12 A Rotavirus Outbreak among College Students—District of Columbia
OUTBREAK II‐13 A Cholera Outbreak in a Refugee Camp—Democratic Republic of the Congo
OUTBREAK II‐14 A Diarrhea Outbreak Associated with Raw Milk and Cheese Consumption—Pennsylvania
OUTBREAK II‐15 A Listeriosis Outbreak Associated with Pasteurized Milk—Massachusetts
OUTBREAK II‐16 An Outbreak Associated with Seasonal Consumption of Raw Ground Beef—Wisconsin
OUTBREAK II‐17 COLLEGE PERSPECTIVE A Diarrhea Outbreak Associated with an Adventure Race—Nevada
OUTBREAK II‐18 GLOBAL PERSPECTIVEA Case‐Control Study of an Outbreak of
Clostridioides difficile
at a Tertiary Care Medical Center—Amsterdam, The Netherlands
SECTION III: Pathogens and Diseases That Are Transmitted Sexually
OUTBREAK III‐1 An STD Outbreak among Teenagers—Georgia
OUTBREAK III‐2 An STD Outbreak among Hispanic Men—California
OUTBREAK III‐3 An Outbreak of HIV Disease in the Adult‐Film Industry—California
OUTBREAK III‐4 An Outbreak of Azithromycin‐Resistant Gonorrhea—Kansas City
OUTBREAK III‐5 Invasive Cervical Cancer among Women—United States
OUTBREAK III‐6 A Proctitis Outbreak among Men Who Have Sex with Men—Netherlands
OUTBREAK III‐7 A Syphilis Outbreak Connected to a Cybersex Chat Room—San Francisco
OUTBREAK III‐8 STDs in Operation Iraqi Freedom/Operation Enduring Freedom—Iraq
OUTBREAK III‐9 Herpes Simplex Virus Type 2 Infection among U.S. Military Service Members
OUTBREAK III‐10 COLLEGE PERSPECTIVE STD Risk Increased by Using the Internet To Find Casual Sexual Partners
OUTBREAK III‐11 GLOBAL PERSPECTIVE
REFERENCE MATERIAL
SECTION IV: Outbreaks of Diseases of the Skin, Soft Tissues, and Eyes
OUTBREAK IV‐1 An Outbreak of
Pseudomonas
Dermatitis from Hotel Pool and Hot Tubs—Colorado
OUTBREAK IV‐2 An Outbreak of Skin Lesions in a Wrestling Team—Alaska
OUTBREAK IV‐3 An Outbreak of Conjunctivitis at an Elementary School—Maine
OUTBREAK IV‐4 A Measles Outbreak among Internationally Adopted Children—United States
OUTBREAK IV‐5 An Outbreak of “Flesh‐Eating Bacterium” Disease—Saint John, Brunswick, Canada
OUTBREAK IV‐6 An Outbreak of Invasive Group A
Streptococcus
at a Child Care Center—Boston
OUTBREAK IV‐7 An Outbreak of a Rash at a Camp for HIV‐Infected Children—Connecticut
OUTBREAK IV‐8 A Rubella Outbreak—Arkansas
OUTBREAK IV‐9 An Outbreak of Invasive Disease Associated with Varicella in a Child Care Center—Boston
OUTBREAK IV‐10 An Outbreak of Boils Associated with Footbaths at a Nail Salon—California
OUTBREAK IV‐11 An Outbreak of Boils Associated with Steam Bathing, Alaska
OUTBREAK IV‐12 A Skin Infection Outbreak at a Local School—Houston, Texas
OUTBREAK IV‐13 An Outbreak of MRSA at Surgical Sites—Paris
OUTBREAK IV‐14 An Outbreak of Necrotizing Fasciitis and Cellulitis Associated with Vein Sclerotherapy—Australia
OUTBREAK IV‐15 COLLEGE PERSPECTIVE Skin Infections among Tattoo Recipients—Ohio
OUTBREAK IV‐16 GLOBAL PERSPECTIVE A Gas Gangrene Outbreak after a Tsunami—Papua New Guinea
REFERENCE MATERIAL
SECTION V: Outbreaks of Diseases of the Cardiovascular and Lymphatic Systems
OUTBREAK V‐1 An Outbreak of Typhus—Burundi
OUTBREAK V‐2 An Outbreak of Cyclic Fevers—India
OUTBREAK V‐3 An Outbreak of Mononucleosis—Puerto Rico
OUTBREAK V‐4 Fever in a Traveler Returning from Venezuela—California
OUTBREAK V‐5 Cases of Rash and Fever, One Fatal, in a Family Cluster—Kentucky
OUTBREAK V‐6 An Outbreak of Ebola Hemorrhagic Fever—Uganda
OUTBREAK V‐7 An Outbreak of Leptospirosis during Eco‐Challenge—Malaysia
OUTBREAK V‐8 A Dengue Fever Outbreak—Puerto Rico
OUTBREAK V‐9 A Disease Outbreak Associated with International Travel—Chicago
OUTBREAK V‐10
Pseudomonas
Bloodstream Infections Associated with a Heparin‐Saline Flush—Missouri
OUTBREAK V‐11 A Brucellosis Outbreak Due to Unpasteurized Raw Goat Cheese—Andalusia, Spain
OUTBREAK V‐12 An Acute Respiratory Illness Associated with Dried Animal Hides—New York City
OUTBREAK V‐13 A Plague Outbreak—India
OUTBREAK V‐14 A Hepatitis Outbreak from a Pain Clinic—Oklahoma
OUTBREAK V‐15 An Outbreak of
Staphylococcus aureus
with Increased Vancomycin Resistance—Illinois
OUTBREAK V‐16 COLLEGE PERSPECTIVE An Outbreak of Lyme Disease—United States
OUTBREAK V‐17 GLOBAL PERSPECTIVEThe Zika Virus Spreads from Uganda to the United States
REFERENCE MATERIAL
SECTION VI: Outbreaks of Diseases of the Nervous System
OUTBREAK VI‐1 An Outbreak of Acute Flaccid Paralysis—Cape Verde
OUTBREAK VI‐2 An Outbreak of Paralysis from Eating Fermented Beaver Tails—Alaska
OUTBREAK VI‐3 Rabies Infections from Organ Donor Tissues—Multistate
OUTBREAK VI‐4 A Tetanus Outbreak—Puerto Rico
OUTBREAK VI‐5 An Outbreak of Aseptic Meningitis among Recreational Vehicle Campers—Connecticut
OUTBREAK VI‐6 A Mad Cow Disease Outbreak in Humans and Cattle—United States, Canada, Europe, and Japan
OUTBREAK VI‐7 Foodborne Paralysis from Eating Home‐Pickled Eggs—Illinois
OUTBREAK VI‐8 An Outbreak of Encephalitis—New York
OUTBREAK VI‐9 An Outbreak of
Haemophilus influenzae
Type b Meningitis—Alaska
OUTBREAK VI‐10 An Outbreak of Foodborne Botulism from Home‐Prepared Fermented Tofu—California
OUTBREAK VI‐11 Meningitis among Travelers Returning from Saudi Arabia—United States
OUTBREAK VI‐12 COLLEGE PERSPECTIVE Meningitis Outbreaks Traced to Raves and Clubs—Michigan and Argentina
OUTBREAK VI‐13 GLOBAL PERSPECTIVE An Outbreak of Pneumococcal Meningitis—Central African Republic
REFERENCE MATERIAL
APPENDIX: Selected Sources
Index
End User License Agreement
Chapter 1
Table I‐1 Selected outbreak‐causing respiratory pathogens
Chapter 2
Table II‐1 Selected outbreak‐causing pathogens of the GI tract
Table II‐3 Comparison of activities at the fair of cases and controls
Table II‐15 Characteristics of patients with listeriosis associated with past...
Table II‐17 Comparison of case patients with control subjects among participa...
Table II‐18 Crude ORs of potential risk factors for the development of CDI ri...
Chapter 3
Table III‐1 Selected STD‐causing pathogens
Table III‐8a Final diagnosis in female military personnel seeking gynecologic...
Table III‐8b Chief complaints in female military personnel seeking gynecologi...
Table III‐9 HSV‐2 seropositivity among case patients and controls
a
Chapter 4
Table IV‐1 Selected outbreak‐causing pathogens of skin and soft tissue
Table IV‐13 Demographic and clinical data of patients
a
Table IV‐15 Characteristics of tattoo‐associated MRSA skin infection clusters
Chapter 5
Table V‐9 Clinical and laboratory findings on hospital admission and treatmen...
Table V‐11 Case‐control study results
a
Chapter 6
Table VI‐9 Summary of four cases of Hib meningitis
a
Chapter 1
Figure I‐1a Micrograph of direct fluorescent‐antibody assay of
L. pneumophil
...
Figure I‐1b
L. pneumophila
growing on charcoal‐yeast extract agar.
Figure I‐2 Direct fluorescent‐antibody assay for respiratory syncytial virus...
Figure I‐3a Acid‐fast stain of the pathogen.
Figure I‐3b Chest X ray of a patient with tuberculosis.
Figure I‐4a Growth of the pathogen on blood agar.
Figure I‐4b Gram stain of the pathogen.
Figure I‐5a Maculopapular rash.
Figure I‐5b Koplik spots on the buccal mucosa.
Figure I‐6a Chest radiograph of a patient with hantavirus pulmonary syndrome...
Figure I‐6b Transmission electron micrograph of Sin Nombre virus.
Figure I‐6c A deer mouse.
Figure I‐7 Gram stain of the pathogen.
Figure I‐8 Transmission electron micrograph of
Mycoplasma
.
Figure I‐9a Chest X ray of a patient with pneumonia.
Figure I‐9b Growth of the pathogen on blood agar.
Figure I‐11a Gram stain of the pathogen.
Figure I‐11b Growth of the pathogen on blood agar.
Figure I‐12a Maculopapular rash.
Figure I‐12b Koplik spots on the buccal mucosa.
Figure I‐13 Cases of pharyngoconjunctival fever by date of disease onset (ac...
Figure I‐16 Number of mumps cases by week of illness onset.
Figure I‐17 DPT vaccination coverage in Cali for children <1 year old.
Chapter 2
Figure II‐1a Growth of the pathogen on MacConkey agar.
Figure II‐1b Growth of the pathogen on Hektoen enteric agar.
Figure II‐2 Light micrograph of an acid‐fast stain of a fecal smear.
Figure II‐3a Gram stain of the bloody‐diarrhea‐causing pathogen.
Figure II‐3b Growth of the pathogen on sorbitol MacConkey agar.
Figure II‐4 Light micrograph of a fecal smear.
Figure II‐5a Rose‐colored macular rash.
Figure II‐5b Growth of the pathogen on Hektoen enteric agar.
Figure II‐6 Light micrograph of a fecal smear.
Figure II‐7a Growth of the pathogen on MacConkey agar.
Figure II‐7b Light micrograph of a fecal sample.
Figure II‐8 Gram stain of the pathogen.
Figure II‐9 Transmission electron micrograph of rotavirus.
Figure II‐10a Gram stain of the pathogen.
Figure II‐10b Growth on MacConkey agar.
Figure II‐11 Transmission electron micrograph of the pathogen.
Figure II‐12a Transmission electron micrograph of the pathogen.
Figure II‐12b Rapid test for rotavirus.
Figure II‐13a Stool sample.
Figure II‐13b Dehydration caused by cholera.
Figure II‐13c Flagellar stain of the pathogen.
Figure II‐14 Number of cases of diarrheal illness caused by infection with
S
...
Figure II‐16a Gram stain of the pathogen.
Figure II‐16b Growth of the pathogen on sorbitol MacConkey agar.
Figure II‐17 Number of cases of illness among participants in a long‐distanc...
Chapter 3
Figure III‐1 Dark‐field microscopy of the pathogen.
Figure III‐2a Ulcer resulting from the pathogen.
Figure III‐2b Gram stain of an ulcer scraping.
Figure III‐3 Transmission electron micrograph of HIV.
Figure III‐4a Gram stain of pus discharge.
Figure III‐4b Pus discharge from urethra.
Figure III‐5a Genital warts.
Figure III‐5b Cervical cancer.
Figure III‐5c Incidence of localized invasive cervical cancer among Hispanic...
Figure III‐5d Incidence of advanced invasive cervical cancer among Hispanic ...
Figure III‐6 Positive DFA assay for
C. trachomatis
.
Figure III‐7a Ulcer on the penis.
Figure III‐7b Silver‐stained micrograph of tissue infected by the pathogen....
Figure III‐10a Syphilis chancre.
Figure III‐10b Pus discharge associated with gonorrhea.
Figure III‐11a A baby abandoned by his parents in a home for young HIV‐infec...
Figure III‐11b A student at a primary school in Africa where about one‐third...
Chapter 4
Figure IV‐1a Folliculitis.
Figure IV‐1b Gram stain of the pathogen.
Figure IV‐2a Skin lesion.
Figure IV‐2b Light micrograph of the pathogen (magnification, ×1,125).
Figure IV‐3a Conjunctivitis.
Figure IV‐3b Colony morphology on blood agar.
Figure IV‐3c Gram stain of the pathogen.
Figure IV‐4a Koplik spots on the buccal mucosa.
Figure IV‐4b Maculopapular rash.
Figure IV‐5a Growth of the pathogen on blood agar.
Figure IV‐5b Gram stain of the pathogen.
Figure IV‐6a Growth of the pathogen on blood agar.
Figure IV‐6b Gram stain of the pathogen.
Figure IV‐7 Vesicular rash. CDC, PHIL, 4493, 1975.
Figure IV‐8a Skin rash characteristic of rubella.
Figure IV‐8b Transmission electron micrograph of the pathogen.
Figure IV‐9 Cases of varicella and group A
Streptococcus
infection at a chil...
Figure IV‐10 Light micrograph of
M. fortuitum
(magnification, ×400). CDC/ Dr...
Figure IV‐11 Number of boils during the outbreak year.
Figure IV‐12a Growth of the pathogen on mannitol salt agar.
Figure IV‐12b Gram stain of the pathogen.
Figure IV‐14 Growth of the pathogen on blood agar.
Figure IV‐15 Pustules resulting from a MRSA skin infection in a tattoo recip...
Figure IV‐16 Gram stain of the pathogen.
Chapter 5
Figure V‐1a Rash caused by the pathogen.
Figure V‐1b Body louse.
Figure V‐1c Transmission electron micrograph of the intracellular pathogen....
Figure V‐2 Light micrograph of parasitized erythrocytes.
Figure V‐3a Blood smear showing atypical lymphocytes.
Figure V‐3b Blood smear showing atypical lymphocytes. μ, micrometers.
Figure V‐4a
Aedes
mosquito vector.
Figure V‐4b Transmission electron micrograph of the viral pathogen.
Figure V‐5a Rash caused by the pathogen.
Figure V‐5b Dog ticks.
Figure V‐6 Transmission electron micrograph of Ebola virus.
Figure V‐7 The pathogen in silver‐stained liver tissue.
Figure V‐8
A. aegypti
mosquito vector.
Figure V‐9 Light micrograph of the pathogen parasitizing erythrocytes.
Figure V‐10 Gram stain of
P. fluorescens
.
Figure V‐11 Cases per family as a function of the number of weeks from the b...
Figure V‐12 Light micrograph of
B. anthracis
.
Figure V‐13a Gram stain of
Y. pestis
in a blood smear.
Figure V‐13b Oriental rat flea.
Figure V‐13c A bubo.
Figure V‐14a Transmission electron micrograph of hepatitis B virus. CDC/Dr. ...
Figure V‐14b Transmission electron micrograph of hepatitis C virus. Gleiberg...
Figure V‐15 Gram stain of the pathogen.
Figure V‐16a Engorged
Ixodes
tick. CDC/ Dr. Gary Alpert / Urban Pests / Inte...
Figure V‐16b Skin rash seen in Lyme disease. CDC/ James Gathany, PHIL, 9872,...
Figure V‐16c Dark‐field light micrograph of the pathogen.
Figure V‐17a A digitally colorized transmission electron micrograph of Zika ...
Figure V‐17b Rash caused by Zika virus.
Figure V‐17c A female
A. aegypti
mosquito acquiring a blood meal.
Chapter 6
Figure VI‐1a Children affected with paralysis from the pathogen.
Figure VI‐1b Transmission electron micrograph of poliovirus.
Figure VI‐2 An endospore stain of the pathogen.
Figure VI‐3 Photomicrograph of a hematoxylin‐eosin‐stained brain tissue samp...
Figure VI‐4 Photomicrograph of a Gram‐stained specimen of the pathogen. CDC/...
Figure VI‐5 Attack rate for campsites with different numbers of campers.
Figure VI‐6a Light micrograph of spongiform brain tissues.
Figure VI‐6b Lack of muscle control in a cow with bovine spongiform encephal...
Figure VI‐7a Gram stain of the pathogen.
Figure VI‐7b Endospore stain of the pathogen. CDC/
Figure VI‐8 Computer‐colorized transmission electron micrograph of WNV. CDC/...
Figure VI‐10a Light micrograph of an endospore stain of
C. botulinum
.
Figure VI‐11a Rash associated with meningitis.
Figure VI‐11b Light micrograph of a Gram stain of
N. meningitidis
.
Figure VI‐12 Direct fluorescent‐antibody assay for
N. meningitidis
.
Figure VI‐13 Suspected and confirmed cases of meningitis.
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SECOND EDITION
Rodney P. Anderson
Department of Biological and Allied Health SciencesOhio Northern University, Ada, Ohio
Copyright © 2020 American Society for Microbiology. All rights reserved.
Copublication by the American Society for Microbiology and John Wiley & Sons, Inc.
No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means electronic, mechanical, photocopying, recording, scanning, or otherwise, except as permitted by law. Advice on how to reuse material from this title is available at http://wiley.com/go/permissions.
The right of Rodney P. Anderson to be identified as the author of this work/the editorial material in this work has been asserted in accordance with law.
Limit of Liability/Disclaimer of WarrantyWhile the publisher and author have used their best efforts in preparing this book, they make no representations or warranties with respect to the accuracy or completeness of the contents of this book and specifically disclaim any implied warranties of merchantability or fitness for a particular purpose. No warranty may be created or extended by sales representatives or written sales materials. The publisher is not providing legal, medical, or other professional services. Any reference herein to any specific commercial products, procedures, or services by trade name, trademark, manufacturer, or otherwise does not constitute or imply endorsement, recommendation, or favored status by the American Society for Microbiology (ASM). The views and opinions of the author(s) expressed in this publication do not necessarily state or reflect those of ASM, and they shall not be used to advertise or endorse any product.
Editorial CorrespondenceASM Press, 1752 N Street, NW, Washington, DC 20036-2904, USA
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Library of Congress Cataloging-in-Publication Data
Names: Anderson, Rodney P., author. | American Society for Microbiology, issuing body.Title: Outbreak : cases in real-world microbiology / Rodney P. Anderson.Description: Second edition. | Washington, DC : ASM Press ; Hoboken, NJ : Wiley, [2020] | Includes bibliographical references and index.Identifiers: LCCN 2019056743 (print) | LCCN 2019056744 (ebook) | ISBN 9781683670414 (paperback) | ISBN 9781683670421 (adobe pdf) | ISBN 9781683673552 (epub)Subjects: MESH: Disease Outbreaks | Communicable Diseases | Disease Reservoirs | Disease Transmission, Infectious | Environmental Microbiology | Case ReportsClassification: LCC RA643 (print) | LCC RA643 (ebook) | NLM WA 105 | DDC 616.9–dc23LC record available at https://lccn.loc.gov/2019056743LC ebook record available at https://lccn.loc.gov/2019056744
Cover and interior design: Susan Brown SchmidlerCover image credit: Shutterstock, spainter_vfx, https://www.shutterstock.com/image-illustration/connection-lines-around-earth-globe-theme-1075260245
For Tami, again and always
The science of microbiology is fascinating to those of us who have taken up the challenge of researching and teaching in this largely undiscovered and rapidly expanding field. One of the significant challenges faced by microbiology educators is to balance the need for providing a content foundation to students against the time required to demonstrate how microbiology affects their lives. The goal of Outbreak: Cases in Real‐World Microbiology is to help students make the important connections between the content of the course, their everyday lives, and the ways in which microbiology impacts society as a whole. These real‐world cases provide an opportunity for students to apply practical knowledge and to integrate their solutions to specific problems in cultures where customs, religion, public resources, and infrastructure influence the analysis.
The outbreaks featured in each section are preceded by one or two tables listing the significant pathogens that can cause the infectious disease outbreaks. The cases presented in that section include only diseases caused by pathogens listed in the table(s). The diseases and pathogens chosen are those that are often covered in an introductory microbiology course. Limiting the pool of possibilities helps the students learn the basics thoroughly without having to consider the myriad possible causes normally associated with a differential diagnosis, thus making the activity more appropriate for undergraduate students. Each chapter ends with a set of descriptions of the diseases covered in the case studies. The descriptions are meant to be used by students for reference, if necessary, to gather the information needed to develop appropriate answers to the questions at the end of each outbreak. Each disease description presents information on (i) the causative agent of the disease, (ii) the pathogen’s mode of transmission from its reservoir to a new host, (iii) pathogenesis, (iv) the clinical features of the disease, (v) clinical and laboratory diagnosis, (vi) treatment of the disease, and (vii) general principles of prevention of the disease. Throughout each section, there is a balance between outbreaks that allow students to integrate and apply their knowledge and those that also require students to diagnose the pathogenic agent on the basis of lab test data and the clinical features of the disease.
The Appendix directs students to specific reference materials that provide information relevant to the study questions and encourages the students to apply the reference content to the cases they are studying.
The last two outbreaks in each section are designated College Perspective and Global Perspective. The College Perspective presents outbreaks that directly impact the lives of students. The pathogens are typically spread easily in the college‐age population, or the outbreaks focus on issues important to students. The Global Perspective presents outbreaks that occur in non‐Western cultures. As a result, solutions developed by students for treatment and prevention require them to consider cultures in which differences in customs, religion, public resources, and infrastructure impact the analysis.
There are many ways in which case studies such as the outbreaks presented in this book can be integrated into a typical microbiology class. For example, they can be used as supplemental class readings and assignments to review application of content presented in class and to help students prepare for exams. They can be used to promote discussion to enhance lecture material. Students can become active participants in their learning by solving case studies that either review material already presented or introduce new material. Case studies can serve as the foundation for innovative approaches using cooperative learning groups. Cooperative learning groups can be used instead of lectures to allow students to investigate microbiological topics in depth. Case studies help students develop application, integration, and analysis skills. They can also be used as assessment tools to evaluate a course’s ability to develop integration and application skills. Therefore, they can be helpful in preparing for professional admission exams such as the MCAT, NCLEX, and GRE.
As with much of life, the most challenging parts are also the most rewarding. With much of science, learning the content base, although often challenging, is just the beginning. The real objective is to integrate and apply scientific concepts and principles to make a difference in the real world. The best education provides students with opportunities for both.
The content of the second edition of Outbreak has changed significantly. Twenty‐five of the 75 cases in this addition are newly developed. The remaining cases have been re‐edited based on classroom feedback. In addition, all cases have an expanded section of questions to allow the students to go into more depth in the analysis of each case or to allow faculty members to choose the questions that will most apply to either the level at which they present their material or where they are in the presenting course material. All reference material has been updated, so content on the epidemiology, diagnostic methods, pathogenesis, treatment, and prevention is current.
As in the first edition, all the case studies are real. When students in the biological sciences are asked to invest their time in analyzing a case study, it is important that the information that is given be real and factual. In no time in their careers as future professionals will current students be required to solve a fictional scenario that imitates real life but is designed to be solved with simple, straightforward answers. Real problems in the world of microbiology do not always agree with our initial expectations, nor do they often lend themselves to simple solutions. As a consequence, to best prepare students for their future careers, it is important to give them opportunities to solve real‐world problems where answers require not only knowledge about microbiology but also the realities of social, economic, and health care‐related issues.
Like all activities involved in the delivery of excellent health care in today’s world, the process requires a team approach. Consequently, when I integrate the case studies into my course, I have students work in collaborative learning groups when completing the case study assignments. The ability to work with others of diverse backgrounds and levels of ability is an important skill to develop for anyone choosing a career in health care. The collaborative learning groups also provide an opportunity for interprofessional education where the groups are composed of students whose goals are to pursue careers in various medical professions such as nursing, pharmacy, physicians, and physician assistants. In order to facilitate the teamwork process, it is important to introduce students to how to work successfully with others in their group by presenting some basic teamwork guidelines and rules. Teams that follow these straightforward guidelines are able to tap into others’ knowledge and expertise and present a case study analysis that is more concise and complete.
Thank you to Ohio Northern University for providing the sabbatical time that made this work possible. I also thank the staff of and the contributors to the Centers for Disease Control and Prevention’s journals and image library. The journals and images are a rich resource of information for educators and the public to use. All images credited to CDC PHIL can be located at https://phil.cdc.gov/default.aspx by using the PHIL numbers provided.
Rodney P. Anderson received his PhD in biological sciences from the University of Iowa in 1989. His doctoral work centered on protein synthesis mechanisms in Escherichia coli. After graduate school, he began his academic career at Ohio Northern University, where he continues to teach undergraduates in the Department of Biological and Allied Health Sciences. He teaches courses in microbiology for both majors and allied health students as well as courses in genetics. He has also introduced nonmajors to microbiology through interdisciplinary seminars in disease and society.
Dr. Anderson has been actively involved in microbiology education. He is a past chair of the American Society for Microbiology (ASM) Conference for Undergraduate Educators, which developed the core curriculum for undergraduate microbiology courses, and has organized and spoken at a number of education division symposia at the ASM annual meetings. His outreach activities have included microbial presentations at local elementary schools. His interest in microbiology education has resulted in another undergraduate microbiology textbook, Visualizing Microbiology, Second Edition (John Wiley & Sons, Inc.), and in a children’s book, The Invisible ABCs (ASM Press). The Invisible ABCs emphasizes to children the benefits of the microbial world, rather than the incomplete message that all microbes cause disease.
Dr. Anderson and his wife, Tami, are parents of two adult children, Isaac and Graetel, who are both using their microbiology knowledge in their nursing careers. He loves classic cars, hunting, and traveling.
For full indeed is earth of woes, and full the sea; and in the day as well as night diseases unbidden haunt mankind, silently bearing ills to men.
Hesiod, Works and Days, ca. line 101(Trans., J. Banks, 1856)
Among those who require a visit to a physician, infections of the respiratory system are the most common reason for the visit. These respiratory infections account for an average of ~80 physician visits per 100 persons each year. Infections of the lower respiratory tract, such as pneumonia and influenza, are also the leading cause of death by infectious disease worldwide. Pneumonia, influenza, and tuberculosis result in about 4.3 million deaths per year.
Containment of a respiratory outbreak can be complicated by a pathogen’s ability to survive outside the body. For example, some cold‐causing viruses can remain infective on an environmental surface for several hours. This makes classroom desks and doorknobs potential fomites for the spread of disease. Pathogens on the hands can be inoculated into the eyes and drain into the nose. There they can attack and initiate a respiratory tract infection. Consequently, one important way to decrease spread of respiratory pathogens is to wash hands frequently and to avoid touching the eyes.
The primary method of spread for respiratory tract pathogens is via airborne particles and mucus droplets. Airborne particles can travel over 1 meter through the air and still remain infectious, while mucus droplets travel less than 1 meter through the air. As a result, respiratory pathogens are highly contagious and spread rapidly through a community. Outbreaks of respiratory pathogens are common in colleges. Students who occupy college residence halls usually share rooms with one or more students and are in contact with hundreds of students at sporting events, in recreational facilities, and in classrooms. As a result, the number of opportunities for transmission of respiratory pathogens is greatly increased relative to others who live at home. The frequency of transmission of respiratory pathogens is significantly higher during cold‐weather periods, when students are restricted to indoor activities. Therefore, annual winter outbreaks of colds, influenza, strep throat, and bronchitis in this setting are common.
Although several thousand microbes are inhaled each day, the defenses of the respiratory system are very efficient and regularly prevent infection and disease. Mucus is secreted by goblet cells within the respiratory epithelium. This mucus traps most microbes before they travel deep into the respiratory tract. It helps to inhibit attachment of microbes to host cell receptors. Microbes that are trapped in the mucus are swept out of the respiratory system by cilia on the surface of the pseudostratified epithelium. The mucus is swallowed, and the microbes are destroyed in the digestive system. In addition, the mucus has a high concentration of dissolved solutes. The hypertonic environment thus created inhibits the growth of most cellular microbes—bacteria, fungi, and protozoa. In the alveoli of the lungs, macrophages are present to phagocytize microbes that escape the other defenses.
Microbial pathogens have evolved strategies to bypass these defenses. Adhesins on the surfaces of microbes allow pathogens to attach to receptors on epithelial cells so that the microbes are not swept out of the respiratory tract. These adhesins are highly specific and at times limit infections to certain parts of the respiratory tract. For example, rhinoviruses attach to receptors located in the upper respiratory tract and are thus limited to causing a common cold. Influenza A virus, however, attaches all along the respiratory mucosa and can cause a wide range of respiratory diseases, from a common cold to life‐threatening pneumonia.
Microbes that can survive in the alveoli of the lungs are the most dangerous, causing a life‐threatening infection that blocks gas exchange. Streptococcus pneumoniae has an antiphagocytic capsule that inhibits phagocytosis by alveolar macrophages. Strains with a capsule cause pneumonia, while those without a capsule are nonpathogenic. Mycobacterium tuberculosis, the causative agent of tuberculosis, a chronic infection of the lungs, and Legionella pneumophila, the causative agent of Legionnaires’ disease, avoid being digested after being phagocytized by alveolar macrophages.
The outbreaks described in this chapter emphasize the serious nature of respiratory tract infections, the difficulty in consistently and effectively implementing basic disease control measures, and the rapid spread of microbes that travel through the air.
Table I‐1 Selected outbreak‐causing respiratory pathogens
Organism
Key Physical Properties
Disease Characteristics
Bacteria
Bordetella pertussis
Fastidious, Gram‐negative coccobacillus
Whooping cough in unvaccinated individuals
Chlamydophila pneumoniae
Obligate intracellular bacterium; very small; Gram negative
Pneumonia, bronchitis
Corynebacterium diphtheriae
Gram‐positive, club‐shaped bacillus
Diphtheria in unvaccinated individuals
Streptococcus pyogenes
Gram‐positive streptococcus; beta‐hemolytic on blood agar; group A surface antigen
Strep throat, scarlet fever, rheumatic fever
Legionella pneumophila
Fastidious, Gram‐negative bacillus
Pneumonia (Legionnaires' disease)
Mycobacterium tuberculosis
Acid‐fast bacillus found in chains or cords; cell wall contains mycolic acid, which results in drug and disinfectant resistance
Tuberculosis
Mycoplasma pneumoniae
Wall‐less bacterium; variable shape
Walking pneumonia
Streptococcus pneumoniae
Gram‐positive diplococcus; alpha‐hemolytic on blood agar
Otitis media, sinusitis, conjunctivitis, pneumonia
Viruses
Adenovirus
Nonenveloped polyhedral capsid with double‐stranded DNA
Pharyngitis, bronchiolitis, pneumonia, conjunctivitis
Epstein‐Barr virus
Enveloped polyhedral capsid with double‐stranded DNA
Mononucleosis
Hantavirus
Enveloped helical capsid with negative‐sense single‐stranded RNA
Hantavirus pulmonary syndrome; zoonotic disease carried by rodents
Influenza viruses (A, B, and C)
Enveloped pleomorphic capsid with segmented negative‐sense single‐stranded RNA
Influenza, pneumonia; predisposes to secondary bacterial pneumonia
Mumps virus
Enveloped pleomorphic capsid with negative‐sense single‐stranded RNA
Mumps
Parainfluenza viruses
Enveloped pleomorphic capsid with negative‐sense single‐stranded RNA
Croup, bronchiolitis, pneumonia, laryngitis
Respiratory syncytial virus
Enveloped helical capsid with negative‐sense single‐stranded RNA
Bronchiolitis and pneumonia, primarily in infants
Rhinoviruses
Nonenveloped polyhedral capsid with negative‐sense single‐stranded RNA
Common cold
Rubella virus
Enveloped polyhedral capsid with positive‐sense single‐stranded RNA
German measles; can cause significant birth defects when pregnant women are infected
Rubeola virus
Enveloped helical capsid with negative‐sense single‐stranded RNA
Measles in unvaccinated individuals
Varicella‐zoster virus
Enveloped polyhedral capsid with double‐stranded DNA
Chickenpox in unvaccinated individuals; shingles as a latent manifestation
In the fishing neighborhood of Barceloneta, Spain, on the Mediterranean waterfront, 33 people were hospitalized in respiratory distress. Four of the victims were in serious condition. The area is predominantly inhabited by elderly people. The youngest victim was 49, while the oldest was 92. The common signs and symptoms were fatigue, malaise, high fever, shortness of breath, and coughing. Examination revealed rales (crackling sounds heard during breathing, indicating fluid in the lungs) and bilateral shadowing in the lungs on X ray (indicating fluid accumulation in both lungs).
City health officials carried out bacterial analyses of a ventilation system in the neighborhood located in a seaside building which uses a water tower as part of the cooling system for air conditioning. They isolated Legionella pneumophila, a Gram‐negative, rod‐shaped bacterium (Fig. I‐1a and I‐1b).
Figure I‐1a Micrograph of direct fluorescent‐antibody assay of L. pneumophila (magnification, ×400).
Source: CDC/ Dr. William Cherry, PHIL, 2015, 1978.
Figure I‐1bL. pneumophila growing on charcoal‐yeast extract agar.
Source: CDC/ Dr. Jim Feeley, PHIL, 2137, 1978.
How is
Legionella pneumophila
transmitted?
What is an appropriate way to manage the disease?
How is legionellosis diagnosed?
What are the physical characteristics of the pathogen?
Besides
Legionella
, list four possible microbial causes of pneumonia.
How would you prevent future outbreaks of the disease?
An outbreak of respiratory syncytial virus (RSV) disease sent 50 sick babies from the town of Arviat to hospitals in the south. Arviat is a remote community of 1,700 people that is located on the southwestern shore of Hudson Bay. For 2 weeks, the waiting room at the small clinic staffed by Arviat's nurses had as many as 70 sick people looking for treatment, half of them with coughing, crying infants. Nurses worked around the clock with no backup to care for the ill and to decide which children to send out, in medevac batches of three, to Churchill or Winnipeg. The disease was characterized initially as a cold or influenza, but children then developed coughing, fast breathing, wheezing, and difficulty breathing.
Lab tests of respiratory fluids were positive for RSV, an enveloped virus with a helical capsid and single‐stranded RNA (Fig. I‐2).
Arviat's nursing station was built in 1938 and is no longer adequate for Arviat's population. There is no resident physician in the community and no hospital facilities to treat seriously ill patients. Community leaders have called for better medical services for Arviat, including a full‐time doctor, a suggestion that the hard‐pressed Keewatin Regional Health Board had not yet acted on. In the year of the outbreak, Arviat was expected to see its population of 1,700 grow by 75 new babies. With a growth rate of more than 4% a year, Arviat was one of the fastest growing communities in the region.
Although the population of Arviat was small at the time of the outbreak, overcrowding was common. It was not unusual for many individuals to live in very small homes. In addition, the public schools and community center were considered too small. In addition, 82 new Nunavut government jobs were planned for Arviat. As a result, the community's population was expected to jump to more than 2,000 residents, and problems with overcrowding would worsen.
At the time of the outbreak, city officials worried that the outbreak would be compounded in the following week by hundreds of Christians from around Nunavut and Nunavik who would be traveling to the area to attend a Holy Spirit Crusade. Arviat’s mayor, Mr. Hicks, expressed his concern: “Sitting elbow to elbow, with the lights on, in the heat, makes a great incubator for disease.”
Figure I‐2 Direct fluorescent‐antibody assay for respiratory syncytial virus.
Source: CDC/ Dr. H. Craig Lyerla, PHIL, 6484, 1977.
How is this pathogen transmitted?
How would you treat individuals affected by this disease?
What are the physical characteristics of the pathogen?
What specimen is used to test for the pathogen?
How do you test for the pathogen in the medical science laboratory?
What public health actions should be taken to stop the outbreak and prevent future occurrences?
What age group is most susceptible to RSV bronchiolitis? Why?
An outbreak of drug‐susceptible tuberculosis (TB) occurred in a state correctional facility housing human immunodeficiency virus (HIV)‐infected inmates. Before entry, inmates are tested for HIV status. They are then segregated in three dormitories of one prison, with each dormitory partitioned into right and left sides. On admission to the facility, all inmates are also screened for TB infection and disease with a tuberculin skin test and chest radiography.
In early July, an HIV‐infected man aged 34 years housed in dormitory A was taken to the prison hospital with a 2‐week history of fever, abdominal pain, and cough. His chest radiograph was normal; however, sputum specimens were not obtained for culture, and no acid‐fast staining was done to detect acid‐fast bacilli (AFB). As a result, he was not placed in respiratory isolation. The inmate was returned to the prison in mid‐July without a definitive diagnosis. In mid‐August, the man was evaluated at a community hospital. A lab test of his sputum was positive for AFB (Fig. I‐3a), and he was diagnosed with active pulmonary TB. Later that year, the medical student who examined the inmate during the initial hospitalization developed active TB with cavities within the lungs (Fig. I‐3b).
A contact investigation of dormitory A inmates identified 31 current or former inmates who had signs and symptoms of active TB. They were transferred from dormitory A to the hospital for respiratory isolation and medical evaluation. The exposed group comprised 323 men who had spent 1 to 152 days (median, 135 days) in dormitory A during that period. Of the 31 case patients, 27 (87%) resided on the right side of dormitory A during the exposure period; four (13%) resided on the left.
All case patients were non‐Hispanic black men born in the United States and were infected with HIV. The median age was 36 years (range, 23 to 56 years). All of the isolates of the pathogen tested were identical based on DNA fingerprinting analysis. Five case patients had TB diagnosed after being released from prison; all five were released before the source case patient had TB diagnosed in August.
Figure I‐3a Acid‐fast stain of the pathogen.
Source: Lewis L. Tomalty and Gloria Delisle, Queen’s University.
Figure I‐3b Chest X ray of a patient with tuberculosis.
Source: Giller Boris, Public Domain Wikimedia Commons.
How is the pathogen transmitted?
What is the pathogenesis of the microbe?
What type of results would be expected in a chest X ray of a person who has active TB?
What color do AFB stain? Why?
What color do non‐AFB stain? Why?
What is a tuberculin skin test?
What does a positive test indicate?
What pathogen is causing this outbreak?
How would you have prevented the spread of the pathogen through the prison?
What characteristic of AFB makes them difficult to treat?
What characteristics of the pathogen result in the requirement for long‐term multidrug therapy?
How did the inmates on the opposite side of the dormitory contract TB?
How does a person’s HIV status influence the risk of developing TB?
On December 18, public health officials in southwest Georgia contacted the Georgia Division of Public Health about a child aged 11 months hospitalized for otitis media. Eight days before hospitalization, a culture of drainage obtained from the child’s middle ear revealed Gram‐positive cocci arranged in chains. The bacteria were resistant to penicillin, clindamycin, erythromycin, trimethoprim/sulfamethoxazole, and tetracycline. The child attended a local child care center.
The child care center was located in a rural county (population, 6,318) in southwest Georgia and served approximately 54 children (age range, 9 months to 10 years). The children were divided into two groups on the basis of age (<18 months and >18 months), and the two groups had separate rooms. Nasopharyngeal (NP) swabs were collected and sent to the Centers for Disease Control and Prevention (CDC) for identification and antimicrobial susceptibility testing.
NP swabs were obtained from 5 of the 12 children who had shared a room at the child care center with the child who was hospitalized; NP swabs also were obtained from 17 of the 42 children from the other room. The pathogen was grown on blood agar under anaerobic conditions (Fig. I‐4a). Alpha‐hemolytic colonies were Gram stained (Fig. I‐4b). The bacterium was isolated from 90% of the NP cultures; of these, 79% were penicillin nonsusceptible (i.e., they had intermediate or high‐level resistance and were resistant to more than one antibiotic or class of antibiotics).
A questionnaire was distributed to evaluate risk factors that might be associated with infection. Eighty‐two percent of the children in the child care center had had an illness for which they received antibiotic treatment during the 2 months preceding the questionnaire.
Figure I‐4a Growth of the pathogen on blood agar.
Source: Nathan Reading, Halesowen, UK, CC‐BY 2.0.
Figure I‐4b Gram stain of the pathogen.
Source: CDC, PHIL, 2170, 1970.
How is this pathogen commonly transmitted in a child care setting?
How would you treat those infected with the multidrug‐resistant pathogen?
What pathogen is most likely affecting the children at the day care center?
What are the physical characteristics of the pathogen?
What other disease(s) can this pathogen cause?
Why are children in day care and their mothers particularly susceptible to infections from drug‐resistant pathogens?
How would you stop this outbreak and reduce the risk of similar outbreaks in the future?
In January, a girl aged 7 months received medical care at a hospital near her home. Her illness started with a fever and the appearance of a maculopapular rash (a rash of flat red spots). She infected a nurse, who then transmitted the disease to several other contacts, some of whom visited a popular tourist site in Falcón, Venezuela. Of the 165 persons that were infected during this outbreak, 52% had visited the same tourist site.
The first rash case in Zulia, Colombia, occurred in a woman aged 27 years who was an auxiliary nurse in a physician's office that provided care to residents of Falcón. The nurse had had onset of rash on October 25 of the year previous to the outbreak and subsequently infected four other persons. During the next 3 months, the outbreak spread to all municipalities in Zulia; 2,074 cases had been confirmed as of July 24. For several chains of transmission, the index case was in a health care worker. Beginning in February, the outbreak spread to 14 additional states in Venezuela, including four states bordering Colombia. By July, Venezuela reported 6,380 cases.
Two years before the outbreaks, routine measles, mumps, and rubella vaccination coverage in Venezuela was 84%. By September of the year before the outbreaks, estimated coverage had decreased to 58% and was lower in Venezuelan states near the border with northern Colombia (Falcón, 44%; Zulia, 34%).
Affected persons first experienced a fever lasting about 2 to 4 days that peaked at about 104°F (40°C). This was followed by a cough, runny nose, and the outbreak of a macular rash (Fig. I‐5a) that began at the hairline and then proceeded down throughout the body. In addition, tiny white dots surrounded by a red halo appeared on the inflamed mucosa inside the cheeks (Koplik spots) (Fig. I‐5b). The rash lasted about 5 days.
Figure I‐5a Maculopapular rash.
Source: CDC, PHIL, 4499, 1963.
Figure I‐5b Koplik spots on the buccal mucosa.
Source: CDC, PHIL, 6111, 1975.
How is the pathogen transmitted?
How does this pathogen cause a rash?
How would you treat a patient who contracted this disease?
What pathogen caused this outbreak?
What are the physical characteristics of the pathogen?
What is the disease?
In order to minimize the number of cases of the disease, how would you manage the outbreak?
On February 17, a 61‐year‐old previously healthy Vermont resident was hospitalized following three episodes of chills and fever (102°F [39°C]), nausea, vomiting, and anorexia. On examination, the lungs were clear and a 2‐ by 2‐cm nontender lymph node was identified at the angle of the left jaw. Chest radiographs were also clear. However, 1 day after admission, the patient's condition deteriorated, with onset of respiratory failure, profound hypoxemia (lack of oxygen), and hypotension (low blood pressure), requiring mechanical ventilation. Subsequent chest radiographs revealed fluid in the lungs consistent with acute respiratory distress syndrome (Fig. I‐6a). The patient also developed disseminated intravascular coagulation (blood clots forming throughout the body) and renal insufficiency.
During the 2 months preceding hospitalization, the patient, who resided in a house on four rural acres, had cleaned a mouse nest from a woodpile, observed mice in the basement, and trapped two mice under the kitchen counters.
Lab tests for bacterial pathogens, protozoal pathogens, influenza virus, adenovirus, and coronaviruses were negative. An enzyme‐linked immunosorbent assay detected antibodies to Sin Nombre virus (Fig. I‐6b) in the patient’s serum. Forty‐three rodents were trapped around the home and also tested for signs of hantavirus infection; two of five deer mice (Fig. I‐6c) were positive for hantaviral antibodies, while all other rodents were negative.
Figure I‐6a Chest radiograph of a patient with hantavirus pulmonary syndrome.
Source: CDC/ D. Loren Ketai, MD; PHIL, 6076, 1994.
Figure I‐6b Transmission electron micrograph of Sin Nombre virus.
Source: CDC/ Cynthia Goldsmith, PHIL, 1136, 1993.
Figure I‐6c A deer mouse.
Source: National Center for Infectious Diseases, CDC, PHIL, 92, 1997.
How does the Sin Nombre virus cause respiratory distress?
How is infection with this organism most commonly acquired?
What are the physical characteristics of Sin Nombre virus?
How does an enzyme‐linked immunosorbent assay detect antibodies to a specific pathogen?
How would you prevent an outbreak of this disease from occurring?
How would you reduce the risk of a similar outbreak in the future?
A diphtheria epidemic began in Russia and spread to all of the other newly independent states (NIS) of the former Soviet Union. More than 150,000 cases and 5,000 deaths were reported from the NIS in 8 years. Diphtheria is caused by the bacterial pathogen Corynebacterium diphtheriae (Fig. I‐7).
As a consequence of the fall of the Soviet Union, the health care system and public health infrastructure were extremely underfunded, resulting in the loss of health care professionals and significant interruption of health care supplies. The dire state of Russia’s public health system created what President Vladimir Putin called a national emergency: during the 4‐year outbreak, life expectancy at birth fell by over 5 years to 58.5, the lowest level in the developed world. Only one child in five was born healthy according to official statistics, which many experts said understated the problem. The death rate rose by 20%, an increase with no modern precedent.
After the collapse of the former Soviet Union, doctors no longer had the medicine, equipment, or money to deal with standard health care. Many physicians at the time were pessimistic about any improvements in the near future. Almost half of the medical school graduating class—doctors who are practicing throughout Russia today—could not even read an electrocardiogram on the day they got their diplomas, according to the Russian Academy of Sciences. On average during this time, doctors earned less money than drivers or baby sitters—about $145 each month.
During this period, Russia budgeted slightly less than 1% percent of its resources to health care, about the same as the poorest African nations. During the outbreak, the Russian Health Ministry said that half of the country’s 21,000 hospitals did not have hot water, a quarter had no sewage systems, and several thousand had no water at all.
The collapse of the previous economic system and civil wars in parts of the former Soviet Union seriously impaired the social and health situation. During the period of the outbreak, in some of the NIS, over 65% of the population were estimated to be below the poverty level. Health services at this time were free of charge only for emergency situations; otherwise, drug treatment and hospital care had to be paid for by the patient.
Figure I‐7 Gram stain of the pathogen.
Source: CDC, PHIL, 1943.
What are the clinical features of diphtheria?
How can the disease be fatal?
How is diphtheria usually prevented?
What specimen is used to test for the pathogen?
What laboratory test(s) is used to identify the pathogen?
How would you prevent the disease from spreading to tourists and travelers to the NIS?
Why are infants particularly at risk for acquiring diphtheria?
How would you arrest this outbreak?
From June 15 through September 5, an acute respiratory illness caused by Mycoplasma pneumoniae occurred among 47 (12%) of 403 staff members and clients of a sheltered workshop for developmentally disabled adults in Ohio. The disease was characterized by acute onset of cough and fever. The median age of patients was 35 years (range, 20 to 60 years); seven (15%) required hospitalization, and 31 (66%) had chest X rays showing fluid in the lungs—evidence of pneumonia. One workshop participant died on June 30 from complications of pneumonia.
Specimens of blood, sputum, and nasopharyngeal secretions were analyzed in the clinical laboratory.
Results of the Gram stain of a sputum sample were inconclusive; however, abundant cells that fight off infection (polymorphonuclear leukocytes) were observed. Serologic and microbiologic studies were negative for acute viral infections. No bacteria were present in the blood sample. An antigenic test was able to identify the pathogen as Mycoplasma pneumoniae (Fig. I‐8).
Figure I‐8 Transmission electron micrograph of Mycoplasma.
Source: Reprinted from Yanez A, et al, Emerg Infect Dis5:164–167, 1999.
How is
Mycoplasma pneumoniae
transmitted?
How would you treat those affected by this pathogen?
What are the physical characteristics of
Mycoplasma pneumoniae
?
What specimen is used to test for the pathogen?
What laboratory test(s) is used to identify the pathogen?
What are three other viral or bacterial pathogens that can cause primary pneumonia?
Why is an institutional setting a common place for such an outbreak?
What physical property makes
Mycoplasma
different from all other pathogens that cause bacterial pneumonia?
To which group of antibiotics would
Mycoplasma pneumoniae
be resistant?
How would you reduce the risk of future outbreaks?
On April 24, nine cases of pneumonia among residents of a nursing home were investigated by the Hamilton Township Department of Health, New Jersey. Illness onset among the residents occurred from April 3 to24. Four residents died. Pneumonia was characterized by one or more lobes filled with fluid and pleural effusions (pus in the pleural space) (Fig. I‐9a).
The nursing home is a 114‐bed facility that employs approximately 200 staff, including nurses, restorative aides, and other administrative and support personnel. None of the employees was known to have pneumonia during this period.
Seven of the residents lived in the same wing of the nursing home. All nine patients had blood cultures that grew alpha‐hemolytic colonies on blood agar (Fig. I‐9b). Sputum samples were Gram stained to identify the pathogen. All isolates were penicillin sensitive and resistant to erythromycin.
Figure I‐9a Chest X ray of a patient with pneumonia.
Source: CDC/ Dr. Thomas Hooten, PHIL, 5803, 1973.
Figure I‐9b Growth of the pathogen on blood agar.
Source: Nathan Reading, Halesowen, UK, CC‐BY 2.0.
How would you treat a patient who contracted this disease?
What physical property does this pathogen have that enables it to avoid phagocytosis by the macrophages in the lungs?
How is the pathogen transmitted?
What pathogen is causing this outbreak?
What are the physical characteristics of the pathogen?
In order to minimize the number of cases of the disease, how would you manage the outbreak?
How would you reduce the risk of a similar outbreak in the future?
The golden age of microbiology began with Louis Pasteur and his development of the anthrax and rabies vaccines and saving of the French wine industry. It continued with Robert Koch, who established the germ theory of disease and discovered the causative agents of anthrax, cholera, and tuberculosis. The first time knowledge from the new field of microbiology was practically applied to attempt to control a major epidemic was the influenza pandemic of 1918, probably the world’s worst epidemic of all time.
Some modern epidemiologists estimate that the influenza pandemic caused 50 to 100 million deaths, with about one‐half occurring in men and women in their 20s and 30s. The flu killed 8% of all young adults then living. The 2‐year epidemic spread rapidly, with two‐thirds of deaths occurring in 24 weeks and over half occurring from mid‐September to early December of 1918 (Fig. I‐10).
Figure I‐10 1918 influenza pandemic record.
Source: National Museum of Health and Medicine, Armed Forces Institute of Pathology, Washington, DC; Reeve, 3143.
Past and present plagues fall far short of the influenza pandemic of 1918. The flu killed more people in 24 weeks than AIDS has killed in 24 years. It killed more people in a year than the Black Death of the Middle Ages killed in a century.
In 1997, the partial sequences of five influenza virus genes were recovered from the preserved lung tissue of a U.S. soldier who died from influenza in 1918. The sequence data now suggest that the hemagglutinin gene (coding for the H antigen) of the 1918 virus was a composite of a stretch of nucleotides from a pig virus flanked by nucleotides from a human virus.
The current version of the bird flu also has a unique combination of H and N antigens (H5N1) found in no other version of the virus. Fortunately for the world, this version of influenza A virus has not been effectively spread via respiratory droplets. In most cases, it has been spread by direct contact with infected birds. Like the 1918 version, this new strain appears to result in extremely high mortality. Over 50% of those who are infected die.
In an interview with author Michael Spector (February 28, 2005, issue of The New Yorker), Scott Dowell, the director of the Centers for Disease Control and Prevention’s Thailand office, stated, “The world just has no idea what it’s going to see if this thing comes. When, really. It's when. I don't think we can afford the luxury of the word ‘if’ anymore. … The clock is ticking. We just don't know what time it is.”
John S. Marr, M.D., former director of the Bureau of Preventable Diseases and a principal epidemiologist in the New York City Department of Public Health, is also concerned about a future influenza pandemic. In a 1999 interview, he stated, “The spread of the ‘Spanish Flu’ in 1918–19 took four months to circle the world. A new strain of influenza could cause a pandemic in four days. … Sadly, many people believe that ‘flu’, a household word, is nothing much to be concerned about, but a new strain could kill tens of millions of people quite easily, within weeks. That is the one I worry about.”
When Tommy Thompson announced his resignation as Secretary of Health and Human Services in December of 2004, he cited a bird flu epidemic as one of the greatest dangers the United States faces. Governmental estimates of the cost of an influenza epidemic have been made. Without large‐scale immunization, the estimates of the total economic impact in the United States of an influenza pandemic range from 71.3 billion to 166.5 billion dollars.
How is the influenza virus transmitted?
How can influenza be treated?
