The first edition of Bacterial Pathogenesis: A Molecular Approach was published in 1994 when the field of bacterial
pathogenesis research was still in the process of entering the molecular age. At the time, many scientists working
in the area advocated focusing on a few well-studied organisms, such as Escherichia coli and Salmonella typhimurium.
They believed that this strategy would furnish basic information about bacterial virulence strategies that would
be applicable to most, if not all, bacterial pathogens. This expectation was based on the highly successful use
of model organisms to understand such central life processes as DNA replication, transcription, and translation.
In retrospect, given what we now know about the mind-boggling diversity of microbes, it seems surprising that E.
coli and S. typhimurium proved to be such good models for the basic metabolic processes that are shared by all
free-living cells, including eukaryotes as well as bacteria and archaea.
In the intervening years, several things have happened that have forced scientists to question the model system
approach to pathogenesis research. First, although closely related species such as E.coli, S. typhimurium, Shigella
dysenteriae, and Yersinia enterocolitica (which today would have been classified as members of a single species)
did prove to have very similar virulence factors, the insights from studies of these species were not necessarily
applicable to more distantly related bacteria,such as the gram-positive cocci. Comparisons of genome sequences
across genus and phylum lines are revealing that, while there are core functions that are highly conserved � mostly
the basic life processes, such as DNA replication,transcription, translation, and the synthesis of amino acids
and nucleic acids � there is considerable variety in other genes. This is not surprising given that many of the
genes an organism carries are responsible for strategies required to occupy different niches, both inside and outside
the human body.
A second realization was that pathogenesis research, far more than basic molecular studies of the past, affects
human lives more immediately at the practical level. Given this, does it make sense to focus exclusively on a few
paradigm organisms such as E. coli and S. typhimurium when the biggest problem in hospitals today is the gram-positive
cocci? The answer, obviously, is to stay with the paradigm organisms but to branch out into areas that have been
relatively underdeveloped. Once one takes the position that pathogenesis research should focus on topics that could
become important at the practical level, either for preventing or for treating bacterial diseases, yet another
shift in perspective occurs: microbial ecology becomes very important.
How many examples do we need of cases in which changes in human practices are accompanied by the emergence of
new microbial pathogens before we realize that infectious disease patterns are a reflection of human and microbial
ecology? Especially when prevention of disease is the goal of a study, the ecology of the disease-causing microbe
and its interactions with potential human hosts become critical considerations. Also, as investigators began to
take the concept of host-parasite interactions seriously, more attention had to be given to understanding how microbial
interactions with the human body led to the pathology of the disease being studied. The use of cultured mammalian
cells as a model for the host side of the host-parasite interaction has been useful, but ultimately the most important
features to understand are the mode of entry of a pathogen into the body and why it infects some organs but not
others.
All of these influences have combined to produce a field of bacterial pathogenesis that looks very different
than it did when the first edition of this text was published. In the second edition, we have tried to capture
what we see as the new face of pathogenesis research by paying much more attention to the microbial ecology and
pathobiology of different bacterial diseases. When we embarked on this project, we thought that a second edition
of an existing book would be easy to write � add a few sections to existing chapters and update the references.
This proved to be a serious miscalculation. It soon became clear that we would have to rewrite the book completely
to capture not only new research findings but also the new perspective on the host-parasite interaction. In many
senses this book is not so much a second edition of the old Bacterial Pathogenesis book but the first edition of
a book that has the same title. A major problem we faced as authors was that not only had the feel of pathogenesis
research changed, but also the amount of published material had increased manyfold. It was a daunting task for
us to keep on top of the material that went into the first edition. The problem of information overload was much
worse this time around. We have tried to compensate for the inevitable errors and misunderstandings that we would
make if left to our own devices by having each chapter reviewed, often by several reviewers. The reviewers� comments
were most helpful, and virtually all of their suggestions have been incorporated into the final text. This is one
case in which reviewers can congratulate themselves for having a significant impact on what they spent precious
hours reviewing.
Features of the Text
Something that surprised us in the response to the first edition was that so many people liked the simple illustrations.
In the first edition, the simplicity of the figures was dictated by our desire to keep the cost of the book as
low as possible. We now realize that students appreciate simple figures because they focus attention on critical
points and principles. Ever ready to learn from our readers and students, we have kept the same style of illustration
in this volume.
Two new features have been added to the chapters in this edition. One appears at the beginning of each chapter
that covers a particular bacterium or group of bacteria � a short snapshot of the organism(s) covered in that chapter.The
purpose of this feature is to present the organism as an intact entity associated with a particular disease before
the student dives into the detailed material presented in the text of the chapter. With so much material available,
it is easy for students to get lost in the details and to lose sight of the organism and its niche. This feature
was suggested to us by Anne Morris Hooke.
A second new feature is the changed form of the summary section at the end of each chapter. In the first edition,
the summary section had a narrative form. We have since concluded that this form of summary is not only of little
use to students but even encouraged some of them to think that it can replace the chapter text. In this edition,
we have presented the summaries in outline and table form, a summary format that in our experience is much more
useful to students and encourages students to process the material covered in the chapter in a slightly different
way. For the most part, the comments of reviewers on the content and organization of the book were positive, but
there was one complaint we found a little disturbing � that we had dropped what little bacterial physiology there
was in the first edition. This complaint arose from the fact that there was no chapter entitled �bacterial physiology.�
We strongly disagree with this way of organizing text material. If we have learned anything over the past few decades,
it is that bacterial physiology is not an isolated topic that can be summarized neatly in a chapter or two but
varies widely depending on the microorganism and its environmental setting. In our view, the physiology of each
microorganism should be woven into the chapter that covers that microorganism or presented along with such topics
as the action of antibiotics and the characteristics of the host defense systems. Bacterial physiology makes much
more sense when it is presented in a real-world context. We also take issue with those who see �bacterial physiology
� as synonymous with glycolysis, the tricarboxylic acid (TCA) cycle,and amino acid biosynthetic pathways. In our
opinion, toxin production, pilin production, and peptidoglycan synthesis are more appropriate and imortant aspects
of the physiology of bacteria that cause human disease.Also, we have noticed that the minute the subject of glycolysis
and the TCA cycle comes up, independent of any relevance to disease, students start to nod off, perhaps never to
return to consciousness.
Teamwork
This book has two authors listed on the cover, but as anyone who has gone through the process of book production
knows, a book is a group effort that involves not only the authors but also members of the publisher's staff and
the reviewers. We are particularly grateful to Jeff Holtmeier and Susan Birch for keeping us on the right path,
sometimes with great difficulty, and for always being there to answer our many questions. We also appreciate their
patience. It must have been frustrating for them to watch our fits and starts of composition as we came to the
daunting realization that it was necessary to completely rewrite this book to bring it up-to-date. We have a new
sympathy for publishers who have to fit sometimes-unreliable authors into some sort of rational business plan.
We now know why Prozac had to be invented. We also thank Mary McKenney, our copy editor. She has been an all-around
good sport and an excellent copy editor. Cathy Balogh deserves thanks for patiently incorporating our many changes
into the manuscript.
A major contribution to this text and the original edition was made by the legion of reviewers who patiently
read drafts of the chapters and made a number of very useful suggestions.With a few exceptions,we did not know
the identity of the reviewers. ASM Press has consented to release this previously confidential list to honor those
who selflessly gave their time to make both editions of this book as accurate as possible. We thank the following
reviewers enthusiastically: Alan G. Barbour, University of California, Irvine; Stephen B.Calderwood, Massachusetts
General Hospital, Boston; Virginia L.Clark, University of Rochester, Rochester, N.Y.; P. Patrick Cleary, University
of Minnesota, Minneapolis; R. John Collier, Harvard Medical School, Boston, Mass.; John Davies, Monash University,
Clayton, Victoria, Australia; Michael P. Doyle, University of Georgia, Griffin; B. Brett Finlay, University of
British Columbia, Vancouver; Vincent A. Fischetti, Rockefeller University, New York, N.Y.; Frank C. Gherardini,
Rocky Mountain Labs, Hamilton, Mont.; Peter H.Gilligan, University of North Carolina Hospitals, Chapel Hill; Paul
A.Gulig, University of Florida, Gainesville; Stuart Hazell, University of Southern Queensland, Toowoomba, Australia;
Anne Morris Hooke, Miami University, Oxford, Ohio; Barbara H. Iglewski, University of Rochester Medical Center,
Rochester, N.Y.; Ralph R. Isberg, Tufts University School of Medicine, Boston, Mass.; James R. Johnson, University
of Minnesota, Minneapolis; David M. Lyerly, Techlab Inc., Blacksburg, Va.; Anthony T. Maurelli, Uniformed Services
University of the Health Sciences, Bethesda, Md.; Jeffery F. Miller, University of California, Los Angeles; Virginia
L. Miller, Washington University School of Medicine, St.Louis, Mo.; Stephen A. Morse, Centers for Disease Control
and Prevention, Atlanta, Ga.; Steve L. Moseley, University of Washington, Seattle; Irving Nachamkin, University
of Pennsylvania, Philadelphia; Alison D. O�Brien, Uniformed Services University of the Health Sciences, Bethesda,
Md.; Todd Patrick, Mayo Clinic, Rochester, Minn.; David H. Persing, Corixa Corporation, Seattle, Wash.; Daniel
A. Portnoy, University of California, Berkeley; Steven Projan, Wyeth-Ayerst Research, Pearl River, N.Y.; Thomas
M. Shinnick, Centers for Disease Control and Prevention, Atlanta, Ga.; Susan Straley, University of Kentucky, Lexington;
Richard A. Strugnell, The University of Melbourne, Parkville, Victoria, Australia; Ronald K. Taylor, Dartmouth
Medical School, Hanover, N.H.; Elaine Tuomanen, St. Jude�s Children�s Research Hospital, Memphis, Tenn.; Janis
J.Weis, University of Utah, Salt Lake City; Susan E.H. West, University of Wisconsin, Madison; Tracy D. Wilkins,
Virginia Polytechnic Institute and State University, Blacksburg.
We also want to thank two local reviewers, Brenda Wilson and Stanley Maloy, both colleagues at the University
of Illinois, who stepped into the breach when we needed specific advice or reviews on an emergency basis. D.W.thanks
Greg, whose eyes only occasionally became glazed during what must have seemed at times to be somewhat excessive
discussions about �the book.�
Finally, we want to thank the many undergraduate and graduate students who have contributed to this edition
and the first edition by telling us of their experiences with the text. We have found that, if asked, students
are quite willing to express opinions about their textbooks and often make insightful comments.
Summary
Completely revised and updated to capture new research findings and the new perspective on the host-parasite
interaction, the second edition of this best-selling text is designed to provide a comprehensive introduction to
bacterial pathogenesis for both students and researchers. The authors integrate material from pathogenic microbiology,
molecular biology, immunology, and human physiology to provide a complete but accessible overview of the field.
Bacterial Pathogenesis, Second Edition includes two new features. Key Features at the beginning of each chapter
in Section II provide a short snapshot of the organism(s) covered. These snapshots present the organisms as intact
entities associated with a particular disease while the detailed material is presented in the text of the chapter.
In addition, the summary sections at the end of each chapter have been reformatted and now present the information
as outlines and tables, an arrangement that is more useful to students.
The text is engagingly written with more than 175 straightforward and clear diagrams that help students easily
understand the molecular mechanisms of pathogenesis. Boxed highlights in all of the chapters cover material of
special clinical and historical interest. A highly extensive and detailed glossary is also included.
What�s New in this Edition?
Completely revised and updated
Reflects the new face of pathogenesis research with coverage of microbial ecology and pathobiology of different
bacterial diseases
Snapshots of each organism appear at the beginning of the chapter in which it is covered
Summary sections are presented as outlines and tables
An expanded glossary that rivals many medical dictionaries
