The landscape of foodborne infections is in flux. New pathogens emerge, established pathogens may acquire new characteristics and appear in unexpected food vehicles, while many existing problems remain unsolved. Consumers want more fresh foods year round, populations age and migrate, and the technologies and trade practices that produce foods change. Protecting the public health and minimizing the burden of foodborne illness mean expecting the unexpected, and being prepared to understand it when it occurs, so that prevention can be improved. Public health surveillance is also constantly evolving, as new diseases emerge and are judged worthy of notification, as new diagnostic tests change the ease and specificity of routine diagnosis and as social interest in particular issues waxes and wanes. Accurate health information, including reliable estimates of the burden of foodborne disease, can improve foodborne disease prevention, foster global health security, promote economic growth and development and strengthen evidence-based policy making.

Improving the efficiency of outbreak investigation in restaurants is critical to reducing outbreak-associated illness and improving prevention strategies. Because clinical characteristics of outbreaks are usually available before results of laboratory testing, we examined their use for determining contributing factors in outbreaks caused by restaurants. All confirmed foodborne outbreaks reported to the Centers for Disease Control and Prevention (CDC) from 1982 to 1997 were reviewed. Clinical profiles were developed based on outbreak characteristics. We compared the percentage of contributing factors by known agent and clinical profile to their occurrence in outbreaks of unclassified aetiology. In total, 2246 foodborne outbreaks were included: 697 (31%) with known aetiology and 1549 (69%) with aetiology undetermined. Salmonella accounted for 65% of outbreaks with a known aetiology. Norovirus-like clinical profiles were noted in 54% of outbreaks with undetermined aetiology. Improper holding times and temperatures were associated with outbreaks caused by Clostridium perfringens, Bacillus cereus, Staphylococcus aureus, and Salmonella, and also with outbreaks of undetermined aetiology that fitted diarrhoea-toxin and vomiting-toxin clinical profiles. Poor personal hygiene was associated with norovirus, Shigella, and Salmonella, and also with outbreaks that fitted norovirus-like and vomiting-toxin clinical profiles. Contributing factors were similar for outbreaks with known aetiology and for those where aetiology was assigned by corresponding clinical profile. Rapidly categorizing outbreaks by clinical profile, before results of laboratory testing are available, can help identification of factors which contributed to the occurrence of the outbreak and will promote timely and efficient outbreak investigations.

Fresh produce increasingly is recognized as an important source of salmonellosis in the United States. In December 1999, the Centers for Disease Control and Prevention detected a nationwide increase in Salmonella serotype Newport (SN) infections that had occurred during the previous month. SN isolates recovered from patients in this cluster had indistinguishable pulsed-field gel electrophoresis (PFGE) patterns (which identified the outbreak strain), suggesting a common source. Seventy-eight patients from 13 states were infected with the outbreak strain. Fifteen patients were hospitalized; 2 died. Among 28 patients enrolled in the matched case-control study, 14 (50%) reported they ate mangoes in the 5 days before illness onset, compared with 4 (10%) of the control subjects during the same period (matched odds ratio, 21.6; 95% confidence interval, 3.53- infinity; P=.0001). Traceback of the implicated mangoes led to a single Brazilian farm, where we identified hot water treatment as a possible point of contamination; this is a relatively new process to prevent importation of an agricultural pest, the Mediterranean fruit fly. This is the first reported outbreak of salmonellosis implicating mangoes. PFGE was critical to the timely recognition of this nationwide outbreak. This outbreak highlights the potential global health impact of foodborne diseases and newly implemented food processes.

To better quantify the impact of foodborne diseases on health in the United States, we compiled and analyzed information from multiple surveillance systems and other sources. We estimate that foodborne diseases cause approximately 76 million illnesses, 325,000 hospitalizations, and 5,000 deaths in the United States each year. Known pathogens account for an estimated 14 million illnesses, 60,000 hospitalizations, and 1,800 deaths. Three pathogens, Salmonella, Listeria, and Toxoplasma, are responsible for 1,500 deaths each year, more than 75% of those caused by known pathogens, while unknown agents account for the remaining 62 million illnesses, 265,000 hospitalizations, and 3,200 deaths. Overall, foodborne diseases appear to cause more illnesses but fewer deaths than previously estimated.

similar to Campylobacter than to Salmonella ratios? The total estimated cases of these illnesses would increase by a factor of 40. The inadequacy of simply applying a Salmonellabased multiplier to the number of cases reported from outbreaks can be demonstrated by applying that multiplier to the total number of cases reported in all foodborne disease outbreaks, typically 15,000 to 20,000 per year (3,4). On the basis of these estimates, the number of foodborne illnesses would range from 5.7 million to 7.6 million, including illnesses caused by unknown agents. The authors make similar assumptions for hospitalizations and deaths: unknown agents are estimated to account for 81% of hospitalizations and 65% of deaths due to foodborne illnesses. In a retrospective review of death certificate data similar to that used by Mead and colleagues, Perkins et al. projected the number of unexplained deaths possibly due to infectious diseases they expected to find in the Emerging Infections Program sites (5). Prospectively, a much smaller number of unexplained deaths was actually found, because known causes were identified through a detailed review of the death certificates and cases (6). A prospective examination of death certificates for foodborne diseases might also result in a smaller than expected yield. The need to rely on assumptions to generate estimates highlights the gaps in our understanding of foodborne diseases. A dozen different studies could address these data gaps. However, once the 76 million figure is agreed upon, the perceived need for these studies will decrease. Finally, if these estimates are accepted as reasonable, do current food safety efforts represent sound public policy? If 82% of foodborne illnesses, 81% of hospitalizations, and 65% of deaths are caused by agents we have not yet identified, where is the commitment of resources needed to identify them? If eradicating Campylobacter, Salmonella, Escherichia coli O157:H7, and Listeria would reduce the number of foodborne illnesses by only 5%, hospitalizations by 10%, and deaths by 25%, why are these agents the primary focus of our national foodborne disease control efforts? Overestimating the occurrence of foodborne diseases caused by unknown agents may lead us to undervalue the public health importance of these and other well-known agents. Estimating the occurrence of foodborne diseases is daunting. The numerous efforts, including this one by Mead et al., to provide estimates have serious shortcomings. The real challenge is to identify the gaps in our knowledge so that they can be systematically addressed and updated estimates of foodborne illness can be provided to guide prevention efforts and assess the effectiveness of current food safety measures (2).

Each year in the United States, foodborne diseases affect millions of persons, who become ill after exposure to any of a growing spectrum of identified agents and toxins. Typhoid fever and other foodborne diseases common a century ago have been controlled by measures that prevent contamination of food and water with human sewage and by technologies (such as milk pasteurization) that eliminate any remaining pathogens. Many recently identified foodborne diseases are caused by contamination with animal feces and can be prevented by measures that reduce contamination and eliminate residual pathogens. In the future, growing attention will need to be directed to the safety of the food and water the animals themselves consume. New foodborne diseases emerge for many reasons, including changes in the pathogens themselves, increasingly centralized and concentrated food production, globalization of the food supply, and increases in populations at higher risk. Better surveillance and investigation now detect outbreaks that a few years ago would have been missed. The continuing challenges are to identify new pathogens as they emerge, understand how foodborne pathogens contaminate food and cause illness, and define and implement the best prevention strategies. Many efforts are now under way to improve food safety in the United States. In 1997, the National Food Safety Initiative outlined an interagency effort to enhance foodborne disease surveillance, research, and prevention. The Centers for Disease Control and Prevention (CDC) and state and local health departments have begun to implement improved surveillance strategies, including additional resources for basic surveillance and investigation, an active surveillance network called FoodNet, surveillance for antimicrobial resistance, and a network for molecular subtyping called PulseNet. Basic research at the National Institutes of Health (NIH) is clarifying virulence mechanisms and developing prevention tools. Dennis Lang, National Institute of Allergy and Infectious Diseases, emphasized that NIH-supported investigators who study the organisms responsible for foodborne illness represent a national resource that can be used to address food safety questions more effectively. New approaches to prevention are now being implemented by the food regulatory agencies, and more approaches, including irradiation, have been approved for industry use. Barbara Herwaldt, CDC, reported that Cyclospora cayetanensis is an archetypical emerging foodborne pathogen. This recently described parasitic pathogen sprang to national attention in nationwide outbreaks in 1996, which were traced to raspberries imported from Guatemala. Outbreaks recurred in 1997, leading to a suspension of importation, despite efforts of the Guatemalan raspberry industry to reduce potential contamination. With improved surveillance, other outbreaks were detected, investigated, and traced to mesclun lettuce and basil. CDC investigation has now documented C. cayetanensis as a common cause of springtime diarrhea among children in Guatemala. Critical gaps in our understanding of the biology and epidemiology of this parasite, particularly in the raspberry farm environment, need to be closed before effective control measures can be developed. B. Swaminathan, CDC, described a new subtyping strategy for public health surveillance of Escherichia coli O157:H7 that will become available electronically later this year. This strategy depends on standardized molecular fingerprinting in public health and food regulatory agency laboratories by pulsed-field gel electrophoresis (PFGE). With standardized methods and equipment, excellent interlaboratory comparability of DNA fingerprint patterns has been achieved. Twenty-four states, the U.S. Department of Agriculture, and the Food and Drug Administration are now equipped to use CDC’s PFGE method for E. coli O157:H7. These New Approaches to Surveillance and Control of Emerging Foodborne Infectious Diseases

The epidemiology of foodborne disease is changing. New pathogens have emerged, and some have spread worldwide. Many, including Salmonella, Escherichia coli O157:H7, Campylobacter, and Yersinia enterocolitica, have reservoirs in healthy food animals, from which they spread to an increasing variety of foods. These pathogens cause millions of cases of sporadic illness and chronic complications, as well as large and challenging outbreaks over many states and nations. Improved surveillance that combines rapid subtyping methods, cluster identification, and collaborative epidemiologic investigation can identify and halt large, dispersed outbreaks. Outbreak investigations and case-control studies of sporadic cases can identify sources of infection and guide the development of specific prevention strategies. Better understanding of how pathogens persist in animal reservoirs is also critical to successful long-term prevention. In the past, the central challenge of foodborne disease lay in preventing the contamination of human food with sewage or animal manure. In the future, prevention of foodborne disease will increasingly depend on controlling contamination of feed and water consumed by the animals themselves.

ceftriaxone and convenience of outpatient parenteral therapy, this antibiotic was continued to complete a 10-day course. On extensive questioning, the patient denied contact with any cat, dog, or other animal. He had recently traveled to Nigeria but denied even transient animal contact. Since 1966, three cases of P. multocida epiglottitis have been reported (2-4). Although no direct culture of the epiglottis was performed in the present case, the clinical syndrome and the absence of any other focus accounting for P. multocida bacteremia strongly suggest that this organism caused the epiglottitis. Including the present case, three of the four reported cases have occurred since 1993, which suggests that either earlier cases were not recognized or the incidence of this condition may be increasing. In all three previous cases of P. multocida epiglottitis, the patients had cats as pets. As in the current case, the clinical features of P. multocida epiglottitis were indistinguishable from epiglottitis secondary to more common bacterial pathogens. However, the cases were all associated with positive blood cultures. In contrast, a 23% rate of bacteremia was reported in a series of epiglottitis cases in adults (including patients with blood cultures positive for Haemophilus influenzae type b or Group A streptococci)(5). The vehicle of infection for this patient remains unknown, as human-to-human transmission has not been documented. This case demonstrates that epiglottitis due to P. multocida, a rare condition that may be increasing in frequency, need not be accompanied by recognized exposure to animals.