2000 Richard J. Duma/NFID Annual Press Conference and Symposium on Infectious Diseases
Please Choose a Presenter
» Martin J. Blaser, M.D.
» J. Glenn Morris, Jr., M.D., MPH & TM
» Stephen M. Ostroff, M.D.
» Merle A. Sande, M.D.
Helicobacter pylori: Foe or Friend?
By Martin J. Blaser, M.D.
Until 1982, when Helicobacter pylori first was isolated, most physicians had considered the stomach to be sterile. However, there is increasing evidence that the human stomach has been normally inhabited by bacteria for millions of years, as are other parts of the gastrointestinal tract, the skin, the oral cavity, and vagina. Now, for probably the first time in human history, individuals are reaching adulthood and old age without H. pylori in their stomach. The reasons for this include changes in lifestyle, clean water, smaller families, and use of antibiotics. As a result, we now can assess the consequences of having H. pylori in the stomach, and of its absence. It now is clear that carriage of H. pylori is associated with increased risk for the development of peptic ulcer disease, and that elimination of it reduces the frequency of ulcer relapse. For these reasons, antibiotic treatment of patients with ulcers to eliminate H. pylori now is recommended. We also have learned that H. pylori is an important risk factor for the development of stomach cancer, much in the same way that smoking increases risk for lung cancer. Consistent with the decline of H. pylori in Western populations have come declines in the incidence of both peptic ulcer disease and of gastric cancer, especially the type involving the lower stomach.
However, diseases of the esophagus have been increasing. First described in the 1930's, gastro-esophageal reflux disease (GERD) has been increasing progressively in Western societies. A consequence of GERD, Barrettıs esophagus, which is a dysplastic condition induced by the inflammatory changes caused by the gastric acid reflux, was first described in 1950; Barrettıs esophagus also is rising dramatically. Most worrisome has been the rise in adenocarcinomas of the distal esophagus and proximal stomach, first observed in the 1970's. Once rarre, adenocarcinoma of the esophagus is rising at a rate of 11% a year in the U.S. population (16% in Australia, 17% in Norway) and is the fastest increasing cancer in the U.S. We now know that GERD is the major risk factor for those proximal (esophagus and gastric cardia) adenocarcinomas, and that their rise reflects the increases in GERD and Barrettıs over the past 50 years. These diseases have been rising when H. pylori has been disappearing. Is there any relationship?
Over the past four years, a body of evidence has been growing that the disappearance of H. pylori is related to the rise of these diseases. Evidence is from independent investigators and from different approaches, including epidemiologic, clinical, and pathophysiologic studies. In brief, persons without H. pylori in their stomach, especially one subtype of strains - the cagA+ variety - have higher rates of GERD, Barrett's, and esophageal adenocarcinoma. These data are consistent with the hypothesis that gastric colonization by H. pylori affects gastric physiology in a way that diminishes acid production. This phenomenon is the first, and highly important, example of a larger issue - that changes in our indigenous bacterial flora (microecology) have been occurring over the last century, and that these changes may have clinical consequences.
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Antimicrobial Resistance: Escalating Problems, and the Issue of Antibiotics in Agriculture
By J. Glenn Morris, Jr., M.D., MPH & TM
Within clinical medicine, the rising levels of antibiotic resistance among pathogens has cast a pall over old assumptions that bacterial infections could (almost always) be treated and cured. This rise in antibiotic resistance is being seen across all classes of bacteria, and reflects both an increase in the percentage of bacteria that are resistant to a specific antibiotic and in the number of antibiotics to which a bacterial strain may be resistant. With these increases in rates of resistance, we are also coming to recognize that we live within a single ecosystem, and that resistant bacteria may be seen in (and transmitted among) multiple settings, including hospitals, the general community, and agriculture.
Current trends suggest that, with enough time and sufficient antibiotic exposure, bacteria can develop resistance to virtually any antibiotic. In discussing new antibiotics, the key question would appear to be "how long before resistance develops," not "will resistance develop." Use (and overuse) of antibiotics in hospitals and by community physicians is clearly a major driving force for emergence of antibiotic resistance in human bacterial pathogens. At the same time, an estimated 40% of all antibiotic usage in the United States is in animals. While some of this is for treatment of specific animal diseases, antibiotics are also used as growth enhancers or growth promoters. For reasons which have never been well defined, inclusion of antibiotics in animal feeds results in marginal increases in growth rate. The impact of this use of antibiotics in agriculture on resistance in human pathogens (and, in turn, on human health) has been the subject of increasing public and scientific concern.
In parts of Europe, these concerns have been sufficient to result in a ban on use of antibiotics as growth promoters, and restrictions on therapeutic use of key antibiotic classes in animals. These restrictions have, in turn, resulted in demonstrable decreases in levels of resistance in certain pathogens. In the United States, use of antibiotics as growth promoters has continued, and certain new classes of antibiotics (such as the quinolones) have been recently approved for therapeutic use in animals. This has been paralleled by increasing problems with resistance in certain food borne pathogens, such as Campylobacter: 1999 data from the National Antimicrobial Resistance Monitoring System suggest that 21% of human Campylobacter isolates are now resistant to ciprofloxacin (a key quinolone antibiotic). Substantive questions have also been raised about the importance of transfer of bacterial antimicrobial resistance genes from animals into enterococci and other potential human pathogens.
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Unraveling the Mystery of the West Nile Virus
By Stephen M. Ostroff, M.D.
In the last year, vectorborne and zoonotic diseases have come to the forefront in the arena of emerging infectious diseases. During 1999, additional cases of locally-acquired malaria were seen in Georgia and Long Island, New York. An outbreak of dengue fever occurred in south Texas involving 56 cases and one fatality, with 17 of the cases acquired within the United States. Internationally, three cases of Lassa fever have been imported to Europe, a large outbreak of tularemia has occurred in Kosovo, and hantavirus pulmonary syndrome has been diagnosed in Panama for the first time.
The outbreak which generated the most attention in the past year involves West Nile encephalitis in the New York Metropolitan area. This outbreak marked the first recognition of this virus in the Western hemisphere, demonstrating the ease of movement of microbes in an era of global travel and commerce. West Nile virus is a flavivirus first recognized in Uganda in 1937; before 1999 it was limited to the Middle East, and some parts of Europe and Asia. Illness due to West Nile is generally mild and self-limited, however in one in every 100-300 cases it produces a severe encephalitis/meningitis; severe illness tends to be more frequent in the elderly and immunocompromised. Like its close relative, St. Louis encephalitis virus, West Nile has a natural cycle in birds and mosquitoes; humans and other mammals are innocent bystanders who become infected when bitten by an infected mosquito.
The 1999 outbreak in New York was recognized when an astute physician noted a cluster of encephalitis cases in Queens in late August. Rapid investigation by the New York City Department of Health identified additional cases, and CDC was consulted. Initially suspected to be botulism, the cases were identified as arboviral in the New York laboratory, and were confirmed initially as St. Louis encephalitis in early September, prompting City-wide pesticide application over the Labor Day weekend. Excess mortality in birds was observed during the same period, and specimens from birds, mosquitoes, and humans were tested in various laboratories. In mid-September, West Nile infection was confirmed in these specimens.
Eventually, 62 cases of encephalitis/meningitis and seven fatalities were identified in New York City and adjacent regions of Westchester County and Long Island. Serosurveys showed that in the hardest hit area of Queens, 2.5% of the population had been infected. West Nile positive birds/horses/mosquitoes were found in Connecticut, New York State, New York City, New Jersey, and Maryland. Viral persistence was found in overwintering mosquitoes collected in New York City during January and February. Laboratory analysis of the outbreak strain showed high sequence analogy to one circulating in Israeli geese in 1998.
It remains unclear how or when the virus moved from Israel to New York. However, the outbreak highlights the need for more capacity to address vectorborne diseases, and the need for better communication between the medical, public health, and veterinary communities. Resources have been made available to strengthen monitoring and diagnostics for West Nile virus, and active campaigns are underway to reduce mosquito populations.
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The World With HIV Without a Vaccine in 2010
By Merle A. Sande, M.D.
The AIDS epidemic is for practical purposes now twenty years old. Therapies have become available that effectively control progression and markedly reduce mortality for those who can afford the medication, which is less than 5% of those who could benefit from it. I propose that we are entering a dangerous period. The total number of patients infected or dead from this virus infection reached 50 million as we entered into the new millennium. However while the infection rate clearly is dropping in the western industrial world, it is exploding elsewhere. The current hot spots include Southeast Asia and particularly India and China, the states of the former Soviet Union and today in the southern part of the African continent. There appears to be no effective vaccine on the horizon.
In a recent report from the National Security Council of the Clinton Administration, several scenarios have been proposed, the most likely of which will be that this epidemic will continue to expand for at least the next ten years and that it will leave possibly hundreds of millions infected and dead and nearly 50 million orphans. It will destabilize struggling democracies in the emerging world with a marked reduction in economic productivity-a combination which has the potential to lead to chaos. There appears to be lethargy on the part of the western societies even in the face of the exploding epidemic in the emerging world. The impact of this infectious disease could significantly alter progress that has been made in our civilization in the next ten years.