serovar Typhimurium in the laboratory of Professor Philip E. Hartman. He was a Helen Hay Whitney Postdoctoral Fellow in the laboratory of Professor Charles Yanofsky at Stanford University in Stanford, California, USA, where he reported the pausing mechanism in attenuation regulation of the tryptophan (trp) operon and used oligonucleotides to test the trp attenuation model. Thereafter, Dr. Winkler was a tenured faculty member at Northwestern University Medical School in Chicago, Illinois, and the University of Texas Houston Medical School in Houston, Texas, determining the pathway of vitamin B6 biosynthesis in Escherichia coli K-12 and studying the functions of tRNA modification enzymes encoded by complex operons in E. coli. He also worked on the physiological roles of the Hfq RNA chaperone and the post-transcriptional mechanisms that regulate MutHLS methyl-directed mismatch repair proteins in E. coli. Dr. Winkler next worked as a Research Advisor (Director) in antibiotic drug discovery at Eli Lilly and Company in Indianapolis, Indiana, where he changed his research program to understanding how the physiology, genetics, and cell biology of the Gram-positive human respiratory pathogen, Streptococcus pneumoniae, contribute to its pathogenesis and possibly reveal vulnerabilities that can be exploited as targets for new antibiotics and vaccines. Dr. Winkler’s laboratory is currently determining the composition, coordination, and chronology of the multiple-protein molecular machines that synthesize the pneumococcal peptidoglycan cell wall and the homeostatic and stress pathways that regulate peptidoglycan biosynthesis. Dr. Winkler is a Fellow of the American Academy of Microbiology (AAM) and a Fellow of the American Academy for the Advancement of Science (AAAS).
Brian Thomas Ho, PhD, is a Lecturer in Bacteriology at the Institute of Structural and Molecular Biology of the University College London and Birkbeck College, University of London, United Kingdom. He began his research training as an undergraduate researcher in the laboratory of Nancy Kleckner at Harvard University, where he studied changes in chromosome dynamics throughout the bacterial cell cycle. He then went on to earn his PhD degree in the laboratory of John J. Mekalanos at Harvard Medical School, where he studied various aspects of the structure and function of the type 6 secretion system (T6SS) and its effectors in Vibrio cholerae and Pseudomonas aeruginosa. Continuing as a postdoc, his research turned toward studying the T6SS and other contact-dependent secretion systems, such as DNA conjugation, in the context of in vivo microbial communities. His current research focuses on understanding how underlying bacterial cell-cell interactions shape larger macroscopic microbial population dynamics and microbial community structure.
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IN THIS CHAPTER
Why Are Bacteria So Much in the Public Health Spotlight Nowadays?
Bacteria, a Formidable Ancient Life Form
Pressing Current Infectious Disease Issues
Emerging and Reemerging Infectious Diseases
Foodborne and Waterborne Infections
Modern Medicine as a Source of New Diseases
Postsurgical and Other Wound Infections
Surveillance: An Early Warning System
Making Hospitals Safe for Patients
And Now for Some Good News: You’ve Got a Bacterial Infection!
The Helicobacter pylori Revolution
A Brave New World of Pathogenesis Research
Insights into Pathogen Evolution
Modeling the Host-Pathogen Interaction in Experimental Animals
CHAPTER 1
The Power of Bacteria
N ever underestimate a potential adversary that has had a 3-billion-year evolutionary head start.
Why Are Bacteria So Much in the Public Health Spotlight Nowadays?
Widespread clinical use of antibiotics first began in the 1950s. The availability of these “miracle drugs,” as they were called at the time, caused great excitement for both physicians and the public as a whole. They came at a time when the medical community was gaining greater control over infectious diseases than ever before. In clinics and hospitals, hygienic practices such as handwashing and disinfectant use were reducing the risk of disease transmission. In the community, improved nutrition made people better able to resist infections, while less crowded conditions and the availability of clean water helped reduce the spread of disease. Meanwhile, newly developed vaccines were protecting against some much-feared diseases. Despite all this, bacterial infections, such as pneumonia, tuberculosis, cholera, and syphilis, continued to take a heavy toll, and infectious diseases were still a leading cause of death. Antibiotics appeared to be the superweapon that would give humans the final decisive victory over bacteria.
In this early euphoria over the success of antibiotics, scientists and policy makers alike concluded that bacterial infections were no longer a threat and turned their attention to other problems, such as cancer, heart disease, and viral infections. For the next three decades, bacteria were of interest mainly as tractable model systems for studying physiology, genetics, and ecology, and as a source of tools for the new molecular biology and genetic engineering technologies that were revolutionizing
