Foodborne diseases are associated with significant morbidity and mortality and high financial costs. Each year, approximately 48 million cases of foodborne disease occur in the United States, resulting in more than 56,000 hospitalizations and 1,350 deaths annually. The estimated economic burden is $6 billion each year through healthcare costs and lost productivity. Education campaigns and patient education strategies will be discussed in order to support efforts to prevent foodborne illness. In addition, the reporting process for foodborne illnesses will be described.

Education Category: Infection Control / Internal Medicine
Release Date: 01/01/2016
Expiration Date: 12/31/2018


This course is designed for physicians, physician assistants, nurse practitioners, and nurses seeking to enhance their knowledge of foodborne illness. The course is of particular importance for clinicians in the primary care and emergency settings.

Accreditations & Approvals

NetCE is accredited by the Accreditation Council for Continuing Medical Education to provide continuing medical education for physicians. NetCE is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation. NetCE is approved to offer continuing education through the Florida Board of Nursing Home Administrators, Provider #50-2405. NetCE is approved by the California Nursing Home Administrator Program as a provider of continuing education. Provider number 1622. NetCE is accredited by the International Association for Continuing Education and Training (IACET). NetCE complies with the ANSI/IACET Standard, which is recognized internationally as a standard of excellence in instructional practices. As a result of this accreditation, NetCE is authorized to issue the IACET CEU.

Designations of Credit

NetCE designates this enduring material for a maximum of 10 AMA PRA Category 1 Credit(s)™. Physicians should claim only the credit commensurate with the extent of their participation in the activity. NetCE designates this continuing education activity for 10 ANCC contact hour(s). NetCE designates this continuing education activity for 5 pharmacotherapeutic/pharmacology contact hour(s). NetCE designates this continuing education activity for 12 hours for Alabama nurses. Successful completion of this CME activity, which includes participation in the evaluation component, enables the participant to earn up to 10 MOC points in the American Board of Internal Medicine's (ABIM) Maintenance of Certification (MOC) program. Participants will earn MOC points equivalent to the amount of CME credits claimed for the activity. It is the CME activity provider's responsibility to submit participant completion information to ACCME for the purpose of granting ABIM MOC credit. Completion of this course constitutes permission to share the completion data with ACCME. This home study course is approved by the Florida Board of Nursing Home Administrators for 5 credit hour(s). This course is approved by the California Nursing Home Administrator Program for 10 hour(s) of continuing education credit - NHAP#1622010-5403/P. California NHAs may only obtain a maximum of 10 hours per course. NetCE is authorized by IACET to offer 1 CEU(s) for this program. AACN Synergy CERP Category A.

Individual State Nursing Approvals

In addition to states that accept ANCC, NetCE is approved as a provider of continuing education in nursing by: Alabama, Provider #ABNP0353, (valid through December 12, 2017); California, BRN Provider #CEP9784; California, LVN Provider #V10662; California, PT Provider #V10842; Florida, Provider #50-2405; Iowa, Provider #295; Kentucky, Provider #7-0054 through 12/31/2017.

Special Approvals

This activity is designed to comply with the requirements of California Assembly Bill 1195, Cultural and Linguistic Competency.

Course Objective

Physicians and other healthcare practitioners are integral to the prevention, identification, and treatment of foodborne diseases, and also play an important role in the control of foodborne disease outbreaks. The purpose of this course is to provide healthcare professionals with the information necessary to rapidly and effectively diagnose, manage, report, and prevent foodborne diseases, in the interest of individual patient care and protection of the public at large.

Learning Objectives

Upon completion of this course, you should be able to:

  1. List the bacterial and viral pathogens most often responsible for food-related illness in the United States.
  2. Identify the subset of the populations most at risk for a foodborne disease.
  3. Discuss the food sources of infectious and noninfectious pathogens.
  4. Outline key steps in the diagnosis of foodborne disease, including patient history, differential diagnosis, microbiologic testing, and considerations for non-English-proficient patients.
  5. Describe the general management principles and reporting requirements for cases of foodborne disease.
  6. Discuss the epidemiology, presentation, diagnosis, and treatment of foodborne bacterial infection.
  7. Identify viral foodborne pathogens, including associated diagnosis and treatment.
  8. Compare and contrast foodborne parasitic disease found in the United States.
  9. Describe marine toxins by source and the respective syndromes associated with food-related illness.
  10. List the symptoms and disease course of mushroom poisonings.
  11. Describe strategies to help individuals prevent foodborne disease.


Lori L. Alexander, MTPW, ELS, MWC, is President of Editorial Rx, Inc., which provides medical writing and editing services on a wide variety of clinical topics and in a range of media. A medical writer and editor for more than 30 years, Ms. Alexander has written for both professional and lay audiences, with a focus on continuing education materials, medical meeting coverage, and educational resources for patients. She is the Editor Emeritus of the American Medical Writers Association (AMWA) Journal, the peer-review journal representing the largest association of medical communicators in the United States. Ms. Alexander earned a Master’s degree in technical and professional writing, with a concentration in medical writing, at Northeastern University, Boston. She has also earned certification as a life sciences editor and as a medical writer.

Faculty Disclosure

Contributing faculty, Lori L. Alexander, MTPW, ELS, MWC, has disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

Division Planners

John M. Leonard, MD

Jane C. Norman, RN, MSN, CNE, PhD

Division Planners Disclosure

The division planners have disclosed no relevant financial relationship with any product manufacturer or service provider mentioned.

About the Sponsor

The purpose of NetCE is to provide challenging curricula to assist healthcare professionals to raise their levels of expertise while fulfilling their continuing education requirements, thereby improving the quality of healthcare.

Our contributing faculty members have taken care to ensure that the information and recommendations are accurate and compatible with the standards generally accepted at the time of publication. The publisher disclaims any liability, loss or damage incurred as a consequence, directly or indirectly, of the use and application of any of the contents. Participants are cautioned about the potential risk of using limited knowledge when integrating new techniques into practice.

Disclosure Statement

It is the policy of NetCE not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

Table of Contents

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#98621: Foodborne Disease

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Foodborne diseases are common, costly, and preventable. Based on public health surveillance data compiled from multiple sources, it is estimated that 48 million food-related illnesses occur in the United States each year. Of this total, about 9.4 million cases are caused by food contaminated with 31 known pathogens, resulting in 56,000 hospitalizations and 1,350 deaths [1].

The Foodborne Diseases Active Surveillance Network (FoodNet) was established in 1996 to monitor the incidence and trends of foodborne disease in the United States. FoodNet is a collaborative effort between the Centers of Disease Control and Prevention (CDC), the U.S. Food and Drug Administration (FDA), the U.S. Department of Agriculture (USDA), and state health departments in 10 selected geographic areas. Designed as a sentinel program, FoodNet conducts active, population-based surveillance for laboratory-confirmed infections caused by nine pathogens commonly transmitted through food. In 2014, FoodNet identified 19,542 cases, 4,445 hospitalizations, and 71 deaths attributable to foodborne diseases [2]. The incidence of foodborne disease is greatest among children younger than 5 years of age, while severe illness requiring hospitalization and deaths occur predominantly among persons older than 65 years of age.

Although most food-related illnesses are sporadic, regularly occurring foodborne disease outbreaks represent an ongoing, serious public health problem. Each year, approximately 800–900 linked clusters of cases (outbreaks) are reported through the CDC Foodborne Outbreak Reporting System. In 2013, 818 foodborne outbreaks were reported, resulting in 13,360 illnesses, 1,062 hospitalizations, and 16 deaths [3]. Norovirus accounted for the majority of outbreaks, followed by Salmonella, Escherichia coli, Campylobacter, and scombroid toxin.

Over the past decade, several national outbreaks of foodborne disease linked to a common source in the commercial food chain have heightened public awareness and illustrate the importance of a well-designed surveillance system. In 2008, two separate outbreaks of salmonellosis (serotypes Saintpaul and Typhimurium), affecting more than 1,400 persons in 44 states and Canada, were eventually traced to jalapeño and serrano peppers grown on farms in Mexico [4,5]. In 2008–2009, another outbreak of salmonellosis (serotype Typhimurium) affecting 600 people in 44 states and Canada was traced to a peanut butter producer in Georgia [6]. In 2011–2012, cantaloupes contaminated with Listeria caused the deadliest outbreak of a foodborne illness since 1973. During that time period, 146 illnesses, 30 deaths, and 1 miscarriage were reported in 28 states [7]. Another outbreak in 2012 was traced to Salmonella-infected yellowfin tuna, leading to more than 400 illnesses and 55 hospitalizations in 28 states and the District of Columbia [8]. One may conclude that despite advances in technology and food safety, foodborne disease remains a potentially serious public health threat. Physicians and other healthcare practitioners, by careful evaluation and prompt reporting of individual cases, play an important role in the early identification, control, and prevention of foodborne disease outbreaks.

Many factors account for the sustained threat of foodborne diseases. The global food supply, ease of travel and trade, changes in food preferences, increased consumption of fresh vegetables and fruits, changes in food production and distribution systems, a growing propensity to rely on food prepared in public places, and adaptation by microbial pathogens all contribute to the risk of contracting and spreading a foodborne disease [9,10,11,12]. These factors ensure continued infection with traditional foodborne pathogens as well as the emergence of novel pathogens [13].

Infectious agents (i.e., bacteria, viruses, parasites) are the cause of most confirmed cases of foodborne disease. The pathogens most commonly identified in reported foodborne outbreaks are norovirus (35%), Salmonella (34%), and Shiga toxin-producing E. coli (STEC) (7%) [3]. Parasitic causes of foodborne disease are rare in the United States but occur more frequently in developing countries. Also contributing to the incidence of foodborne disease are noninfectious agents such as heavy metals and natural toxins. Of the two, natural toxins, especially marine toxins, are responsible for the majority of foodborne toxin-mediated gastrointestinal illness.

For a variety of reasons, a large percentage of foodborne disease goes undiagnosed and unreported [13,15]. Under-reporting is a primary issue because many individuals with food-related gastrointestinal symptoms do not seek medical attention. Furthermore, healthcare providers may not pursue a specific diagnosis, take a careful travel and food exposure history, or recognize the potential link to additional cases in the community.

Trends in food consumption have had an impact on the particular source of foodborne disease. For example, the increased attention to the importance of a healthy diet has led to a greater consumption of fresh produce, and the proportion of outbreaks attributed to produce trended up from 1973 to 1997 [17]. Leafy greens, cut tomatoes, and cut melons have been responsible for 80% of outbreaks caused by fresh produce in recent years [18]. Of the outbreaks reported in 2013, fish (50 outbreaks), mollusks (23 outbreaks), chicken (21 outbreaks), and dairy (21 outbreaks, with 17 due to unpasteurized products) were the most common food categories implicated [3]. Knowledge of changing trends helps practitioners to better recognize the possibility of a foodborne infection.

Foodborne disease usually presents as an acute illness with clinical manifestations that are common and nonspecific. Gastrointestinal symptoms predominate (e.g., nausea, vomiting, diarrhea, abdominal discomfort). Varying degrees of fever may be seen depending on the pathogen, and neurologic symptoms are common with certain toxins. Because of potential public health implications, practitioners should consider a foodborne etiology when evaluating a patient who presents with such symptoms. A careful, directed history is key to the identification of a foodborne disease, and practitioners should be prepared with an approach designed to elicit pertinent information. Studies have identified gaps in healthcare practitioner knowledge of the epidemiology, etiology, diagnosis, and prevention of foodborne illnesses. A survey of practitioners in North Carolina showed that approximately one-third of respondents were not comfortable about their knowledge of foodborne disease or its diagnosis and treatment [19]. In addition, many practitioners did not adequately counsel patients about the prevention of foodborne illness.

This course provides an overview of infectious and noninfectious foodborne diseases in the United States. Topics to be covered include public health considerations and surveillance, common pathogens and toxins, clinical manifestations and evaluation, microbiologic testing, and management of infectious diarrhea. Emphasis is given to those foodborne pathogens and toxins that are encountered most frequently and that have the potential to cause widespread and severe disease. Pathogens and toxins are discussed in terms of their sources, the signs and symptoms they produce, the potential complications associated with infection, and the individuals who are at greatest risk. Toxins that can be deliberately introduced into a food or water supply as an act of terrorism are beyond the scope of this course.

The high incidence of foodborne disease also calls for increased education of the public at large, and healthcare professionals can play an integral role by discussing foodborne illness with their patients and providing educational resources. Media attention tends to focus on outbreaks stemming from food served in restaurants, but epidemiologic data demonstrate that a substantial proportion of food-related illness can be attributed to improper practices in food preparation in the home [20]. According to food safety experts, the importance of primary control factors in preventing foodborne infection varies according to the specific pathogen; the incidence of illness and the financial costs also vary according to pathogen [21,22]. The course concludes with a brief discussion of how healthcare professionals can help their patients better understand the need to change behaviors that put them at risk for foodborne diseases.


According to the World Health Organization, a foodborne disease is "a disease, usually either infectious or toxic in nature, caused by agents that enter the body through the ingestion of food" [23]. More than 250 specific pathogens or toxins have been identified as causes of human foodborne disease worldwide. In the United States, after combining the estimates for known pathogens and unspecified agents, the annual burden of foodborne diseases is estimated to be 48 million illnesses, 128,000 hospitalizations and 3,000 deaths [24]. The estimated annual economic burden is $77.7 billion, mainly due to healthcare costs and lost productivity [25]. Despite increased surveillance, intensified awareness/education campaigns, and improved food safety, the incidence of foodborne disease has not changed significantly since the late 1990s, and it may increase further as a result of the expanding global food economy and the increased threat of bioterrorism [26].

The landscape of food-related illness is continuously in flux as diseases emerge and re-emerge. For example, Campylobacter jejuni and STEC O157 were unknown pathogens in the 1970s [27]. By 2012, they were the first and third leading causes of foodborne infection, respectively, with Campylobacter accounting for more than 845,000 cases of laboratory-confirmed foodborne infections annually [28].

As noted, causative agents of foodborne disease may be infectious (i.e., bacteria, viruses, parasites) or noninfectious (e.g., heavy metals, natural toxins) [29]. Prions or transmissible spongiform encephalopathies—normal animal proteins that can become infectious through misfolding—also cause foodborne illness, but prion-related disease is extremely rare in the United States [30].


The incidence of foodborne diseases and trends over time are identified through passive and active surveillance programs of the CDC [31]. The National Notifiable Diseases Surveillance System, a passive system, relies on voluntary state reporting of diseases listed by the CDC as nationally notifiable [31]. As discussed, FoodNet, a component of the CDC's Emerging Infections Program, was established to help public health officials better understand the epidemiology of foodborne illnesses in the United States. FoodNet conducts population-based surveillance for laboratory-confirmed cases of infection with one of eight bacteria and two parasites [31]. In total, FoodNet monitors 47 million people, which represents approximately 15% of the U.S. population [33]. FoodNet also monitors the incidence of post-diarrheal hemolytic uremic syndrome (HUS), a potentially fatal complication of bacterial infection in children, through a network of pediatric nephrologists and infection-control practitioners housed in nine sites.

Many other foodborne surveillance programs contribute to the effort to enhance the detection, evaluation, and management of foodborne disease outbreaks. Among these programs are the Environmental Health Specialists Network (EHS-Net), a group of environmental health specialists and epidemiologists who partner with the CDC's National Center for Environmental Health, FoodNet, and the FDA to facilitate information exchanges about the environmental causes of foodborne illnesses, and PulseNet, a national network that conducts molecular surveillance using standardized pulse-field gel electrophoresis DNA fingerprinting, allowing for serotyping and subtyping of foodborne pathogens, which has been critical to the early detection and termination of outbreaks.

Despite improvements in health information technology and laboratory testing, foodborne disease surveillance is still limited by several factors [29,34,35]:

  • Under-reporting/delayed reporting of mild disease

  • Ill individuals not seeking treatment for acute gastroenteritis

  • Difficulties identifying causative factors

  • Confounding routes of foodborne transmission

  • Emerging/unrecognized food-related pathogens

  • Misdiagnosis of illness caused by noninfectious agents

  • Deaths caused by unknown foodborne agents attributed to other causes

  • Limited ability to identify virally contaminated food

Overcoming these barriers in the future will increase the capacity of surveillance programs to prevent the transmission of foodborne infections. Healthcare practitioners play a vital role in enhancing foodborne disease surveillance by accurately diagnosing food-related illness and reporting cases in a timely manner.


The CDC defines an outbreak of foodborne disease as "an incident in which two or more persons experience a similar illness resulting from the ingestion of a common food" [36]. After a healthcare practitioner has diagnosed a foodborne disease, he or she should notify the state health department about an outbreak (or potential outbreak). Epidemiologists then begin an investigation facilitated by the Foodborne Disease Surveillance and Outbreak Investigation Toolkit. This kit provides a guide to confirming a diagnosis of a foodborne disease, public health training network, standard questionnaires, and guidelines for specimen collection to investigate outbreaks [13]. Serotyping and genetic sequencing of pathogens enable investigators to link cases of an infection, sometimes across states, and a common source is then sought. State reports are published in Morbidity and Mortality Weekly Report, and the incidences are summarized at the end of the reporting year.

The FDA, USDA, Environmental Protection Agency, and CDC support the efforts of state health departments as needed. In outbreak situations, state health departments commonly perform tasks such as antimicrobial susceptibility testing of submitted isolates, patient counseling, contact notification, and follow-up testing [9]. With the help of the CDC and other government agencies, state health departments may also attempt to identify the source of the illness, which could exist anywhere along the so-called farm-to-table continuum [13]. With outbreaks of bacterial and parasitic foodborne illnesses, a food source is the focal point. Because viral foodborne illnesses are usually transmitted through infected food handlers, a specific setting (e.g., restaurant, banquet) is usually the common denominator.

Identifying the source of an outbreak is associated with a variety of challenges. In 2008, the House Energy and Commerce Subcommittee on Oversight and Investigation were critical of the CDC and the FDA for not identifying rapidly and accurately that contaminated Mexico-grown jalapeño and serrano peppers were the cause of more than 1,000 cases of salmonellosis [38]. Because CDC epidemiologists determined that 84% of ill individuals ate tomatoes, tomatoes were initially targeted as the probable source [3,38]. During the search for contaminated tomatoes, the FDA found contaminated jalapeños in Texas, and investigators subsequently traced contaminated peppers back to two farms in Mexico [3].

As another example, between November 25, 2008, and January 28, 2009, 529 persons from 43 states and one person from Canada were reported to be infected with Salmonella (serotype Typhimurium) [6]. The source of the outbreak did not become apparent until after several weeks of detailed case interviews, investigations of local clusters of illness, and joint epidemiologic efforts across states. The source was a factory that made peanut butter and peanut paste for peanut butter-containing products (e.g., crackers, cookies, cereal, candy). The CDC refers to this type of outbreak as ingredient-driven, an outbreak in which a contaminated ingredient affected a variety of products that were distributed through different channels and consumed in various settings [6]. Tracing the first implicated product to its point of manufacture was crucial in defining the outbreak. The number of products and brands and the large quantities of some products recalled makes this one of the largest recalls in the United States [6].

On September 14, 2011, a farm in Colorado conducted a voluntary recall on cantaloupes that were potentially contaminated with Listeria. At the time of the recall, infected cantaloupes caused 146 illnesses, 30 deaths, and 1 miscarriage in 28 states [7]. In 2012, the common link for an outbreak of Salmonella Bareilly and Salmonella Nchanga among 425 people in 28 states was found in frozen and raw fresh yellowfin tuna products [8]. Even after the manufacturer recalled the product, infections developed in a substantial number of people, suggesting that food establishments were still serving the tuna during the recall [8].

Each year, the CDC provides a comprehensive list of outbreaks that have been reported through the Foodborne Disease Outbreak Surveillance System [3]. A review of select outbreaks since the mid-1990s demonstrates a range in causative pathogens, sources, and number of individuals affected (Table 1).


Pathogen/ToxinSourceNumber of CasesAction
Shiga toxin-producing Escherichia coli O121Wheat flour42 cases in 21 states, 11 hospitalizationsVoluntary recall of products
Salmonella (serotype Poona)Cucumbers imported from Mexico838 cases in 38 states, 165 hospitalizations, 4 deathsVoluntary recall of product
Multidrug-resistant Salmonella I 4,[5],12:i:- and Salmonella (serotype Infantis)Pork192 cases in 5 states, 30 hospitalizationsVoluntary recall of product
CyclosporaCilantro imported from Mexico207 cases in 19 states (mainly Texas)
Salmonella (serotype Newport)Cucumbers imported from Mexico275 cases in 29 statesVoluntary recall of product
CyclosporaPrepackaged salad mix served at restaurant chains400 cases in 16 states, 22 hospitalizations
Salmonella (serotype Saintpaul)Cucumbers imported from Mexico73 cases in 18 states, 14 hospitalizations
Salmonella (serotype Bredeney)Peanut butter and other products containing nuts and seeds30 illnesses in 19 states, 4 hospitalizations, no deathsVoluntary recall of product
Salmonella (serotypes Bareilly and Nchanga)Yellowfin tuna425 illnesses in 28 states, 55 hospitalizations, no deathsVoluntary recall of product
Listeria monocytogenesCantaloupes146 illnesses in 28 states, 30 deaths, 1 miscarriageVoluntary recall of produce
Salmonella (serotype Enteritidis)Eggs1,939 illnesses in 14 statesVoluntary recall of more than 500,000 eggs
Salmonella (serotype Saintpaul)Alfalfa sprouts (raw)228 in 13 states, 9 hospitalizations, no deathsSeed supplier voluntarily withdrew specific lots of seeds
Salmonella (serotype Typhimurium)Peanut butter and peanut-containing products (contamination at manufacturing plant)529 in 43 states, 116 hospitalizations, 8 deathsApproximately 54 companies recalled at least 431 different peanut butter-containing products
CiguateraAmberjack fish9 in 1 state
Clostridium botulinumBrand of canned hot dog chili sauce (deficiency in canning process)8 in 3 states, 8 hospitalizations
Salmonella (serotype Tennessee)Two commercial brands of peanut butter628 in 44 states, 125 hospitalizationsVoluntary recall of products, disposal of existing products in manufacturer's possession
Shiga toxin-producing Escherichia coli O157Prewashed, bagged spinach (growing field in California)199 illnesses in 26 states, 102 hospitalizations, 31 HUS cases, 3 deathsRecall of product
NorovirusInfected food-service workers (restaurant)364 in 1 state
Vibrio parahaemolyticusShellfish (oysters and clams)177 in 3 states, 3 hospitalizations
Hepatitis AGreen onions (used in foods at one restaurant)601 in 8 states, at least 124 hospitalizations, 3 deaths
Salmonella (serotype Typhimurium)Commercially prepared egg salad18 in 1 state, 2 hospitalizations

Outbreak data should be kept in perspective, because they represent only a portion of all food-related illness occurring over time. For example, the proportion of all food-related illnesses associated with outbreaks is low, and some small outbreaks may not be recognized or may not be reported [14]. Also, the specific etiology of an outbreak is not always confirmed. However, outbreak data serve three important functions [52]. First, the investigation of foodborne disease outbreaks leads to changes that help prevent contamination at all levels of food production. Second, outbreak data provide information on the impact of specific pathogens and help investigators recognize emerging pathogens and ongoing problems. Third, analysis of data over time enables public health authorities to monitor trends, providing a basis for regulatory and other changes to improve food safety.


The hallmark characteristics of an infectious food-related illness are gastrointestinal symptoms, most notably diarrhea, abdominal cramps, and vomiting. However, some individuals may be asymptomatic or only mildly ill. Approximately 36% of all cases of acute gastroenteritis are attributable to foodborne disease [29].

Foodborne diseases caused by bacteria and parasites are most often acquired by ingestion of food or water that has become colonized or contaminated. Viral pathogens capable of causing food-related illness do not replicate on foods; instead, their stable structure allows them to survive for prolonged periods in the environment and they are transmitted through the fecal-oral route. Such viruses replicate in the human intestinal tract, are shed through stool, and are transmitted to other humans through foods as a result of direct or indirect contamination with human feces [53]. Most infectious foodborne agents can also be spread through secondary and tertiary transmission [54]. These modes of transmission include droplet transmission (e.g., vomitus, respiratory secretions), vertical transmission (parent to child/fetus), and fomite contamination of objects.



Bacterial contamination of food can occur at any of a number of stages along the farm-to-table continuum: during growing, harvesting, processing, storing, shipping, or final preparation (in a restaurant or home). Most available information on the incidence of bacterial foodborne disease is derived from FoodNet surveillance of disease caused by the eight common foodborne bacterial pathogens [33]:

  • Salmonella

  • Campylobacter

  • Shigella

  • STEC O157

  • STEC non-O157

  • Yersinia

  • Listeria

  • Vibrio

In 2014, these bacteria were the cause of 19,542 cases of foodborne infections reported in FoodNet's 10 states (Table 2) [2]. One of the food safety objectives in Healthy People 2020 is to reduce the incidences of six bacterial infections—Salmonella, Campylobacter, STEC O157, Listeria, Vibrio, and Yersinia [2,55]. According to FoodNet data, there have been slight declines in the reported incidence of infections from Listeria, Campylobacter, Vibrio, Yersinia, and STEC 0157 [2]. However, cases of Salmonella have not declined in the past 15 years, and of these six bacterial infections, only Yersinia has met the target set in Healthy People 2020 [55].


PathogenNo. of CasesIncidence per 100,000
STEC non-O1576901.4
STEC O1574450.9
aAccording to FoodNet data.
STEC = Shiga toxin-producing Escherichia coli.


As discussed, while bacterial contamination of food can occur at several points, viral contamination usually occurs during food handling. Viruses may also be transmitted to humans through mollusks from contaminated waters [53]. Produce can be a vehicle if exposed to contaminated water. The pathogenicity of viruses is enhanced by their capacity to withstand dehydration, low pH, and other adverse, environmental conditions [53,56]. They endure on human hands, in fresh and dried fecal matter, in water, and on nonbiologic surfaces (fomites) such as kitchen counters and carpets [57].

More than 100 types of enteric viruses cause food-related illness, but in the United States, three types of viruses are most common [57]:

  • Noroviruses (and other caliciviruses)

  • Hepatitis A virus

  • Rotaviruses

Noroviruses and hepatitis A virus are the viruses most often transmitted through food [53]. Noroviruses are the most common cause of outbreaks of nonbacterial gastroenteritis; they accounted for 93% of outbreaks of viral gastroenteritis documented over a 3-year period in the United States [3,57].


Parasitic infection can be spread through food or water but is more commonly transmitted through contaminated water [58]. Parasitic protozoa do not multiply in foods, but they are able to survive in or on moist foods for months in a cool, damp environment [58]. Four parasites present the greatest risk of foodborne illness: Cryptosporidium, Cyclospora, Giardia, and Toxoplasma gondii [58]. Infections caused by Cryptosporidium and Cyclospora are monitored through FoodNet.


Crowding and poor hygiene are risk factors for food-related infectious illness. This accounts for the high rates found among closed populations, such as childcare centers and healthcare facilities [31]. A review of 75 enteric outbreaks in long-term care facilities found that 52% of bacterial infections were transmitted through food [59]. Other common risk factors for exposure to foodborne pathogens include [9,54]:

  • Eating raw/undercooked meats or fish

  • Ingesting raw/unpasteurized milk or dairy products

  • Working with animals or animal products

  • Traveling to developing countries

  • Abusing drugs

  • Having children in daycare or school


The complexity of the host-pathogen relationship creates a spectrum of individual responses to foodborne agents; some people remain asymptomatic whereas others develop severe illness [60]. In addition, the incubation period (time from acquisition to onset of symptoms) varies in relation to pathogen and certain host factors, such as age and comorbidities. Several characteristics of a foodborne agent have major roles in susceptibility, including pathogenicity, antigenicity, infective dose, mechanisms of disease production, and exposure route [61]. However, host-associated variables predominantly dictate the occurrence and severity of disease [61]. Determinants of individual susceptibility to a foodborne illness include [54,61]:

  • Extremes of age (especially children younger than 4 years of age)

  • Status of immune system at the time of exposure

  • Underlying medical conditions (e.g., diabetes, human immunodeficiency virus/acquired immunodeficiency syndrome [HIV/AIDS], cancer, organ transplantation)

  • Medications that alter normal flora (e.g., antimicrobial agents, corticosteroids, immunosuppressant drugs)

  • Pregnancy

  • Surgical procedures and radiation therapy

  • Low gastric acidity


The incidences of specific foodborne pathogens varies according to age of the patient, geographic location, the severity of illness caused, and susceptibility of common food sources to contamination by a given pathogen.

Bacterial Foodborne Outbreaks

The number of confirmed bacterial foodborne outbreaks has decreased slightly since the mid-2000s. In 2005, 188 outbreaks (4,348 illnesses) were reported. The number increased to 257 (6,410 illnesses) in 2007, then decreased to 239 outbreaks (5,001 illnesses) in 2013 (Table 3) [3]. Bacteria were the suspected cause of an additional 48 outbreaks in 2013 and were a component in several outbreaks with multiple confirmed or suspected etiologies [3].


Chemical and Toxina
Single Etiology
Multiple Etiologies
Unknown Etiology
All Known Outbreaks
aAgents causing outbreaks in the chemical category consisted primarily of marine toxins.

FoodNet surveillance data show that the highest incidence of bacterial foodborne disease is found among children younger than 5 years of age, followed by children 5 to 9 years of age (Table 4) [16]. The most common causative pathogens in these two age groups are Salmonella, Campylobacter, and Shigella [16,32]. Only Vibrio and Listeria infections occur more frequently in older individuals than in children. Among individuals 60 years of age or older, Salmonella and Campylobacter are the leading causes of bacterial foodborne infection.


PathogenIncidence (per 100,000)
<5 years of age5 to 9 years of age10 to 19 years of age20 to 59 years of age>60 years of age
Salmonella 69.521.412.312.217.0
Campylobacter 24.410.610.113.313.9
Shigella 16.411.
STEC O1573.
STEC non-O1575.
Cyclospora 0.10.1

Few studies have been conducted to evaluate differences in food-related illness according to race or ethnicity, but the available reports suggest that the rates of some bacterial infections are higher among black, Hispanic, and Asian populations than among the white population [62,63,64]. The infections occurring at higher rates are associated with food consumption habits specific to certain populations. For example, outbreaks of Yersinia have been associated with chitterlings (chitlins), a common food item in the black community, particularly in the South, and outbreaks of Listeria and Salmonella have been linked to Mexican-style cheeses and carnitas, respectively, in the Hispanic population [40,63,65]. These disparities call attention to the need for education on foodborne illnesses that is targeted to distinctive needs of specific populations.

The incidence of foodborne disease caused by bacterial pathogens also varies substantially according to geographic location. For example, the incidence of Campylobacter is more than three times higher in California (29.37 per 100,000) than in Maryland (8.34 per 100,000), while the incidence of Shigella ranges from 0.77 (per 100,000) in New York to 6.71 (per 100,000) in Georgia [16]. A survey of testing practices among laboratories in the FoodNet areas indicated that the regional differences in these incidences are not attributable to variations in stool culture practices [66].

Viral Foodborne Outbreaks

Viral pathogens, principally norovirus, are a leading cause of foodborne gastroenteritis outbreaks investigated since 2000. In 2013, a viral etiology was identified for 160 reported foodborne outbreaks affecting 4,021 persons [3]. In all of these outbreaks except six, the causative agent was a norovirus; hepatitis A accounted for four of the other six outbreaks [3]. More than two-thirds of outbreaks of norovirus are linked to a restaurant or a healthcare facility (e.g., hospital, nursing home) [67].

Viral gastroenteritis is the leading cause of food-related illness in the United States [28]. The illness may be caused by a number of viruses, but it is thought that noroviruses account for approximately one-third of the cases (excluding children 6 to 24 months of age) [28]. More than 5 million cases of foodborne noroviruses are reported each year [28,57,68].

Approximately 5% of the estimated 83,000 cases of hepatitis A infection each year are attributed to a food source [57]. Most individuals 18 years of age or older have lifelong protection against reinfection through immunity [28]. The percentage of adults with hepatitis A immunity increases with age, from 10% for individuals who are 18 to 19 years of age to 65% for individuals older than 50 years of age [28]. The incidence of hepatitis A virus is higher in western and southwestern states than in other states [56].

Rotavirus infection is the leading cause of severe acute diarrhea among infants and young children worldwide, but foodborne transmission represents only approximately 1% of cases [57,69]. Rotavirus occurs primarily in the winter in temperate areas but throughout the year in tropical areas [28].

Parasitic Foodborne Outbreaks

In the United States, parasites cause far fewer outbreaks or isolated incidences of foodborne infection than either bacteria or viruses. In 2013, a parasite was confirmed as the cause of six outbreaks (240 illnesses) [3]. The FoodNet surveillance program indicates that Cryptosporidium is the fourth-leading cause of foodborne disease [2,16]. The incidence of Cryptosporidium is highest among children younger than 5 years of age and children 5 to 9 years of age and is lowest among individuals 10 to 19 years of age [16]. The overall incidence of Cyclospora is low, with the highest incidence among individuals 60 years of age or older.

As with bacterial pathogens, the incidence of foodborne infection caused by Cryptosporidium and Cyclospora varies according to geographic location. In 2009, the incidence of Cryptosporidium ranged from 7.36 per 100,000 in New Mexico to 1.26 per 100,000 in Tennessee [16]. The incidence of Cyclospora was highest in Connecticut (0.51 per 100,000), and no cases were reported in California, Colorado, or Oregon [16].

The incidence of infection with Giardia attributable to a food or water source is not clear. In general, the infection is more prevalent among children than adults, which may be related to the potential for immunity after infection [28]. The parasite is believed to affect approximately 2% of the U.S. population [28]. From 2005 to 2007, there were approximately 65 cases of foodborne outbreaks associated with Giardia-infected food [28]. Toxoplasma gondii has been found in nearly one-third of the worldwide population [70]. In the United States, the seroprevalence of toxoplasmosis has decreased among U.S.-born individuals (12 to 49 years of age) from 14.1% in 1988–1994 to 9% in 1999–2004 [71,72]. The seroprevalence is higher in women of childbearing age (15 to 44 years of age), with a rate of 11% in 1999–2004 [71]. The number of infections transmitted through food is not well known.

Severity of Illness

Most foodborne infections result in self-limited illness that resolves within a few days to a week. Severity of illness caused by bacterial foodborne disease varies by etiology, as evidenced by hospitalization rates reported by FoodNet for 2014 (Table 5) [2]. The case-fatality rate also varies by pathogen; mortality rates in 2014 were 15.3% for Listeria, 0.9% for Vibrio, 0.4% for Salmonella, and 0.2% for Campylobacter [2]. Hospitalization and mortality rates are somewhat higher among persons older than 65 years of age, and the case-fatality rate for children younger than 4 years of age ranges from 0.05% for Shigella to 12.7% for Listeria foodborne infections [16].


PathogenHospitalization Rate
STEC O15735%

According to statistics published in 1999, bacteria accounted for 72% of the deaths associated with foodborne disease; parasites accounted for 21%, and viruses for 7% [29]. The majority of deaths could be attributed to four pathogens: Salmonella (35%), Listeria (19%), Toxoplasma gondii (24%), and noroviruses (11%) [29,73]. Since 1999, Listeria has been the pathogen most likely to cause death from food-related illness, with 20% to 30% of infections in high-risk individuals being fatal [74,75].


There is a relationship between the food source and the pathogens most likely to cause contamination (Table 6). Food sources become contaminated with pathogens in a variety of ways. Raw foods and beverages pose the greatest risk because they have not been processed, cooked, or refrigerated/frozen, all of which reduce or destroy most pathogens. Produce (fruits and vegetables) may become contaminated in the field if soil or water is contaminated, leading to the growth of a variety of pathogens, such as Salmonella, STEC O157, Cyclospora, and hepatitis A [28]. If not pasteurized, milk or fruit juices may become the source for a variety of bacteria, most notably Listeria and Salmonella. Some pathogens, such as Campylobacter, E. coli, Toxoplasma gondii, and Yersinia, live in the intestinal tracts of animals, contaminating raw meat and poultry; this contamination can spread to other animals during slaughter. Eggs may become contaminated with Salmonella through infection of hens' ovaries.


Food SourcePathogens
Escherichia coli
Campylobacter jejuni
Toxoplasma gondii
Meat products, gravies
Clostridium perfringens
Bacillus cereus (diarrheal type)
Raw (unpasteurized) milk and dairy products (soft cheeses)
Campylobacter jejuni
Bacillus cereus (diarrheal type)
Raw and undercooked eggsSalmonella
Improperly canned goods; smoked or salted fishClostridium botulinum
Fresh or minimally processed produce (vegetables, fruit)
Escherichia coli
Bacillus cereus (diarrheal)
Hepatitis A virus
Shellfish (raw or undercooked)
Hepatitis A virus
Processed meats
Staphylococcus aureus
Escherichia coli (dry-cured salami)
Hepatitis A virus
Rice products and other starchy foods, including potato, pasta, and cheese productsBacillus cereus (emetic type)
Prepared salads (potato, tuna, macaroni, chicken) and sandwiches
Hepatitis A virus
Puddings, custards, pastries
Staphylococcus aureus
Bacillus cereus (emetic type)
Fruit juices (unpasteurized)
Escherichia coli
Hepatitis A virus

Freezing meat and poultry impedes bacterial replication, and cooking at an appropriate temperature serves to destroy remaining pathogens. Bacteria and parasites will not be destroyed unless the food is thoroughly cooked (at an appropriate cooking temperature and for an appropriate duration). Food may become contaminated again if left at room temperature for more than 2 hours [76]. Contamination may also occur during food preparation in a restaurant or a home kitchen through handling by an infected person or through exposure to contaminated surfaces or equipment. Norovirus is the pathogen most commonly transmitted through an intermediary food handler. Staphylococcus aureus and Cryptosporidium are also transmitted more often through an infected food handler than through direct contamination of a food product [28,76]. Rotavirus has not been isolated from any food associated with an outbreak [28].

The source of a food-related illness cannot always be identified; approximately 56% of cases have no known cause [14,52]. In 2013, an identifiable food source accounted for approximately 47% of outbreaks of known etiology [3,14]. The number of outbreaks and infected individuals associated with a food source varies over time. In 2006, fish was the leading source, causing 47 outbreaks; in 2008, poultry was the most common source, associated with 32 outbreaks [14,52]. The highest number of foodborne infections was associated with exposure to vegetables (1,596) in 2002, to poultry (1,355) in 2006, and to fruits and nuts (1,755) in 2008 [14,52]. Analysis of data from 2013 demonstrated that the pathogen-food source pairs representing the most outbreaks/illnesses were [3]:

  • Scombroid or ciguatoxin in fish (40 outbreaks, 118 illnesses)

  • Salmonella in poultry/pork/beef (23 outbreaks, 1,344 illnesses)

  • Vibrio parahaemolyticus in mollusks (13 outbreaks, 80 illnesses)

  • Norovirus in leafy vegetables (6 outbreaks, 196 illnesses)

  • Salmonella in seeded vegetables (5 outbreaks, 268 illnesses)


Heavy metals and natural toxins are the primary causes of noninfectious food-related illness [41,78]. Heavy metals, such as iron, lead, copper, and zinc, are primarily ingested through water contaminated by pipes or containers [78,79,80]. Food vessels, utensils, or containers are potential sources for ingestion of antimony, copper, and tin [13,78,80]. Water, soil, or food (including shellfish and finfish) may also be contaminated with arsenic, and fish and other seafood may be contaminated with methyl mercury [78,81]. Foodborne illness caused by heavy metals is extremely rare. One outbreak was reported in 2007, two outbreaks were reported in 2008, and none were reported in 2013 [3,14].

Naturally occurring toxic agents, principally marine and mushroom toxins, account for the great majority of noninfectious foodborne disease. Marine toxins include ciguatoxin, pufferfish toxin (tetrodotoxin), scombroid, and shellfish toxins. The sources of these toxins differ (Table 7) [28]. The CDC estimates that 30 cases of poisoning with marine toxins are reported each year in the United States and that one person dies from such poisoning every 4 years [82]. The frequency of illness caused by marine toxins is not well defined for several reasons: under-reporting (related primarily to the lack of a reporting requirement), the generally mild nature and short duration of the disease, and the paucity of medical information on the toxins [28]. However, illness caused by marine toxins can be severe and carries an annual healthcare cost burden in the United States of approximately $350 million [83].


CiguatoxinGrouper, snapper, amberjack, mackerel, triggerfish, barracuda
ScombroidTuna, mahi mahi, bluefish, sardines, mackerel, amberjack, abalone
Shellfish Toxins
ParalyticMussels, clams, cockles, scallops
DiarrheticMussels, oysters, scallops, clams
NeurotoxicShellfish harvested along the Florida coast and the Gulf of Mexico
AmnesicBivalve mollusks, crabs, lobsters

Mushroom toxins are found in several species of wild mushrooms, and poisoning occurs when the toxic mushrooms are misidentified as edible. Poisonous species of mushrooms grow in a range of habitats, from deep woods to suburban yards [28]. The frequency of mushroom poisoning is difficult to determine, but the number of reported cases is low, cases are sporadic, and large outbreaks are rare [28].


Accurate and efficient diagnosis and management is essential for minimizing the spread of a foodborne disease. In addition, rapid identification of a causative agent can help to control an outbreak. Diagnosis requires a comprehensive approach that includes a detailed clinical evaluation with attention to any history of suspect food exposures and appropriate cultures to identify the etiologic agent. Four clues can help in determining the etiology of a foodborne illness: period of incubation, duration of illness, predominant clinical symptoms, and the location of the individual or the ingested food (Table 8) [84].


Diagnostic ClueLikely Etiology
Incubation Period (Time to Onset of Symptoms)
Very short (hours)Toxin
Approximately one dayVirus
Several daysBacteria
Duration of Illness
ShortVirus or toxin
Predominant Clinical Symptoms
DiarrheaVirus or bacteria
Severe illnessBacteria
Location of Individual or Food
Closed population (school, healthcare facility)Virus
Large catered eventToxin or virus

The diagnosis and management of a food-related illness is challenged by several factors [9,54,85]:

  • Many symptoms are common among foodborne illnesses that require disparate treatments.

  • The cost of ordering multiple diagnostic laboratory tests is high.

  • Empirical treatments can lead to serious complications, secondary transmission, and emergence of drug-resistant pathogens.

Diarrhea is the symptom that prompts many individuals to seek medical attention. It is important to distinguish between inflammatory and noninflammatory diarrhea, as the pathogens for these two types differ. With inflammatory diarrhea, mucosal invasion, usually of the large intestine, causes stools to be bloody and often to contain many fecal leukocytes [13]. Inflammatory diarrhea is usually associated with fever, abdominal pain and tenderness, headache, nausea, vomiting, malaise, and myalgia. In contrast, noninflammatory diarrhea involves watery stool, which is sometimes severe, and fever and systemic symptoms are often absent. Such diarrhea is caused by mucosal hypersecretion or decreased absorption without mucosal destruction and usually involves the small intestine. Mild dehydration is typical, although severe dehydration may be present in children or individuals older than 65 years of age [13].

Evidence-based recommendations for the diagnosis and management of food-related illness have been established in a primer developed collaboratively by the American Medical Association (AMA), the CDC, the American Nurses Association (ANA), the FDA, and the USDA [13]. In addition, recognizing the increasing number of enteric pathogens associated with foodborne disease (and other gastrointestinal illnesses), the Infectious Diseases Society of America established practice guidelines for the management of infectious diarrhea [9]. These guidelines include five evidence-based recommendations [9]:

  • Carry out clinical/epidemiologic evaluation

  • Order microbiologic testing, as appropriate

  • Begin rehydration therapy

  • Treat severe disease empirically, when appropriate

  • Educate the patient about preventing secondary transmission

In addition to clinical evaluation, diagnosis, and treatment of the patient, suspected or confirmed cases of foodborne disease should be reported to local health departments so that a possible association with similar cases may be identified.

Most food-related illnesses are self-limited and require supportive care only (i.e., rest, rehydration). The routine use of antidiarrheal agents is not recommended, especially in infants and young children, as many agents have the potential for causing serious adverse effects [13]. Healthcare practitioners should ensure that patients understand the importance of checking with the practitioner before using an antidiarrheal.


The clinical presentation of a foodborne disease is often nonspecific and similar to that of viral syndromes unrelated to food exposure. In either case common symptoms are diarrhea, fever, and abdominal cramps. The presence of muscle aches or joint pain makes a viral syndrome more likely, but care should be taken to distinguish such symptoms from neurologic symptoms (e.g., weakness, paresthesias) that may be signs of food-related illnesses that target the neurologic system [13].

A clinical/epidemiologic evaluation of the patient is essential, and a directed history regarding travel, recent food exposures, and other illness among family and associates can help healthcare practitioners identify an illness as having a foodborne pathogen etiology (Table 9). A complete description of the patient's symptoms is an important key to diagnosis, and the healthcare practitioner should ask the patient to describe predominant symptoms as well as mild ones. The type of symptoms can help narrow the list of potential pathogens (Table 10) [13]. Noninfectious causative agents should be suspected for patients with nondescript gastrointestinal symptoms who became ill less than 12 hours after ingestion, especially if the onset of symptoms is within minutes after ingestion [13,26,86].


DomainSuggested Questions
TravelHave you traveled recently? If so, where (foreign country, coastal area, mountains, cruise)?
Where do you work?
Have you spent time recently at a childcare center? Dormitory? Farm? Petting zoo?
Have you had contact with animals recently? If so, what kind?
Have you recently spent time as an inpatient in a hospital, rehabilitation facility, or long-term care institution?
Eating habits
Have you recently eaten raw/undercooked food? Eggs? Soft cheeses? Shellfish or finfish? Fresh produce? Wild mushrooms?
Have you consumed raw/unpasteurized milk?
Did you drink water from an unknown source?
Have you eaten home-canned foods?
Have you eaten food that had a bitter or metallic taste, abnormal smell, unusual appearance?
Have you eaten at a buffet? At a banquet? At a picnic?
Do you know how the food you've eaten recently was prepared?
Symptom characteristics
When did your symptoms first occur, especially in relation to foods you've eaten?
What was your first symptom?
Did symptoms begin abruptly or develop gradually?
How long have you had your symptoms?
What are your stools like in terms of frequency, quantity, and characteristics (bloody, watery, febrile, mucoid, purulent)?
Do any family members, friends, coworkers, or classmates have similar symptoms?
Do you have a history of drug use? If so, what prescription and/or illicit drugs have you taken recently?
What do you think caused the illness?


SymptomPossible Diagnosis
Gastroenteritis, with vomiting as primary symptom (fever and/or diarrhea may also be present)
Viral gastroenteritis (rotavirus in infants and calicivirus in older children and adults)
Food poisoning with Bacillus cereus or Staphylococcus aureus
Ingestion of heavy metal
Noninflammatory diarrhea (acute watery diarrhea, usually without fever)
Can be caused by virtually all enteric pathogens (bacterial, viral, parasitic) but is a classic symptom of:
Enterotoxigenic Escherichia coli (traveler's diarrhea)
Vibrio cholerae
Enteric virus
Cyclospora cayetanensis
Inflammatory diarrhea (grossly bloody stool, fever, invasive gastroenteritis)
Enteroinvasive Escherichia coli
STECs (O157 and non-O157)
Vibrio parahaemolyticus
Yersinia enterocolitica
Persistent diarrhea (14 days or more)
Cyclospora cayetanensis
Neurologic symptoms (paresthesias, respiratory depression, bronchospasm, cranial nerve palsies)
Clostridium botulinum (botulism)
Marine toxins
Mushroom toxin
Guillain-Barré syndrome (associated with infectious diarrhea due to Campylobacter jejuni)
Systemic illness (fever, weakness, arthritis, jaundice)
Listeria monocytogenes
Toxoplasma gondii
Vibrio vulnificus
Hepatitis A virus

In addition, the patient's medical history or health record should be reviewed for underlying medical conditions and prescription medication use. Gastrointestinal symptoms may be related to a host of other conditions, such as irritable bowel syndrome, inflammatory bowel diseases, gastrointestinal surgery, malabsorption syndromes, and malignant disease, or as a side effect of antibiotics or other medications [13]. Particular attention should be paid to medical conditions that may increase the risk or severity of a foodborne illness.

Careful clinical evaluation of the patient is necessary, and the patient should be examined for signs of fever and abdominal tenderness and for indications of volume depletion, such as decreased skin turgor, thirst, reduced urination, tachycardia, orthostatic pulse, and dry mucous membranes.

Because specific details about the patient's history are crucial to diagnosing a foodborne illness, effective communication is required. Communicating effectively is more challenging when the patient's primary language differs from that of the practitioner. According to the U.S. Census Bureau, more than 59 million Americans speak a language other than English at home, and more than 25 million (nearly 9% of the total population) have limited English proficiency; that is, they speak English less than "very well" [87]. It has been suggested that when patients are first evaluated, they should be asked what language is spoken at home and if they speak English "very well" [88]. In addition, patients should also be asked what language they prefer for their medical care information, as some patients prefer their native language even though they have said they can understand and discuss symptoms in English [88]. Many studies have demonstrated that the lack of an interpreter for patients with limited English proficiency compromises the quality of care and that the use of professional interpreters improves communication (errors and comprehension), utilization, clinical outcomes, and patient satisfaction with care [89,90].

"Ad hoc" interpreters (untrained staff members, family members, friends) are often used instead of professional interpreters for a variety of reasons, including convenience and cost. However, the reliability and specificity of information obtained through ad hoc interpreters is less than with professional interpreters [91]. In addition, individuals with limited English language skills have indicated a preference for professional interpreters rather than family members [92]. A systematic review of the literature has shown that the use of professional interpreters facilitates a broader understanding and leads to better clinical care than the use of ad hoc interpreters [90].


The results of physician surveys have indicated a wide variation in practice with respect to requesting a stool culture from patients with acute diarrhea. The percentage of respondents who say they request this culture ranges from 38% to 71% [19,93,94]. Microbiologic studies should be done on the basis of the results of the clinical evaluation. In particular, testing of stool samples should be done if diarrhea has lasted more than 1 day or if any of the following signs and symptoms occur [13]:

  • Bloody diarrhea

  • Weight loss

  • Diarrhea leading to dehydration

  • Fever

  • Prolonged diarrhea (three or more unformed stools per day for several days)

  • Neurologic involvement (paresthesias, motor weakness, cranial nerve palsies)

  • Sudden onset of nausea, vomiting, and/or diarrhea

  • Severe abdominal pain

To better prevent and manage potential outbreaks, fecal studies are also recommended when the patient is a food handler, has contact with a childcare facility or other closed populations, has a compromised immune system, has traveled to a developing country, was recently hospitalized, or has recently taken antibiotics [13]. The appropriate fecal studies depend on the clinical presentation.

Routine stool culture examinations vary according to the particular suspected pathogens, and practitioners should be aware of pathogens that must be specifically requested. Many physicians surveyed have said they do not know whether stool culture examination includes testing for some specific species (e.g., Yersinia, Vibrio, STEC O157) [93]. A routine stool culture usually includes screening for Salmonella and Shigella species and Campylobacter jejuni or coli [13]. As such, if Vibrio, Yersinia, STEC O157, or Campylobacter species other than jejuni/coli is suspected, the practitioner should communicate this to, and consult with, the receiving clinical microbiology laboratory.

Testing for norovirus and rotavirus is not typically done, but the viruses can be detected in stool specimens, if necessary. Hepatitis A virus is confirmed through serologic testing.

Stool specimens should be examined for parasites if a patient has a travel history that suggests parasitic infection, when diarrhea has been chronic or persistent, when diarrhea has not responded to appropriate antimicrobial therapy, and when the incubation period for the diarrhea/illness has been long [13]. Usually, a request for an ova and parasite examination of a stool specimen allows for the identification of Giardia lamblia, whereas examination for Cryptosporidium, Cyclospora cayetanensis, and Toxoplasma gondii must be requested specifically. Because routine procedures for parasite detection vary among laboratories, it is helpful to contact the testing laboratory to confirm the appropriate procedures according to the parasites suspected.

Some bacteria, viruses, and parasites can be identified rapidly with direct antigen detection tests and molecular biology techniques. In some cases, vomitus or food samples should be submitted to the laboratory for testing [13]. Other diagnostic evaluations, such as serum chemistry analysis, urinalysis, complete blood cell count, blood culture, abdominal radiograph, and flexible endoscopy may also be considered when appropriate [9,13]. Consultation with an infectious disease specialist, a clinical microbiologist, or a state public health official can be beneficial in some cases.

If microbiologic testing identifies the causative pathogen as a nationally notifiable disease, the healthcare practitioner should report the illness promptly [37]. Reporting requirements for each state or territory are available on the Council of State and Territorial Epidemiologists website. Practitioners should also report suspected outbreaks to the local or state health department.

All public health laboratories have resources to serotype Salmonella and Shigella and subtype Listeria and STEC isolates using pulsed-field gel electrophoresis, which helps to determine antimicrobial susceptibility [9]. The use of specialized laboratories for diagnostic needs is arranged through the state health department [54].


Rehydration Therapy

Diarrhea and vomiting can lead to intravascular volume depletion, dehydration, and electrolyte imbalance. Oral rehydration should be started for patients who have mild or moderate fluid losses. An oral rehydration solution should be used rather than a sports drink, which does not replace fluid and sodium losses correctly. Intravenous therapy should be used for severe dehydration and for debilitated patients. Studies have indicated that for children with mild-to-moderate volume depletion caused by gastroenteritis, oral rehydration is as effective as intravenous therapy [95]. For young children (i.e., 5 to 33 months of age), rice-based oral fluid therapy plus recombinant human lactoferrin and lysozyme has been shown to reduce the duration of diarrhea better than reduced-osmolarity oral hydration therapy [96].

Empirical Antimicrobial Therapy

The use of antimicrobial therapy should be limited, as antibiotic resistance has increased for many enteric pathogens [13]. Empirical antimicrobial therapy is usually reserved for patients with severe illness. Antibiotics should not be administered to reduce secondary transmission risk.

The decision to treat and selection of antimicrobial therapy should be based on clinical considerations and epidemiologic clues or positive identification of the causative pathogen, such as [13]:

  • Clinical signs and symptoms

  • Organism detected in clinical specimens

  • Antimicrobial susceptibility tests

The antimicrobial selection for specific foodborne infections will be discussed in detail later in the course.

Education about Secondary Transmission

Healthcare practitioners should educate the patient or parents about what actions he or she should take to prevent secondary transmission, emphasizing the importance of appropriate hand hygiene, the use of disinfectant cleaner to wash surfaces, and the need to remain out of work, school, or daycare until symptoms have resolved. Many educational resources are available, and efforts should be made to provide resources that are language and culture appropriate.


Because healthcare professionals are often the first to identify foodborne illnesses, they are the frontline protection for the public against many foodborne disease outbreaks [13]. Prompt and accurate disease reporting to the local or state health department is necessary for the prevention and control of outbreaks as well as for accurate surveillance [9,13]. Healthcare practitioners should be familiar with the list of nationally notifiable diseases and check with the CDC for the most recent list, as it is updated annually [37].

The CDC recommends that suspected foodborne-illness outbreaks or sporadic illnesses that may be caused by a nationally notifiable disease should be reported as soon as possible [13]. Because early intervention is crucial, definitive diagnoses are unnecessary [9,13]. Links to state health department websites, which include contact information for local health departments, are available on the CDC website. When reporting, the practitioner should provide the following information to the local or state health department [97,98]:

  • Date of illness(es)

  • Age, sex, and full residence address and phone number for patient(s)

  • Symptom complexes (especially unusual symptoms)

  • Disease patterns

Local or state health departments may communicate additional requests or requirements to practitioners under their jurisdiction.

Many practitioners leave the reporting responsibilities up to the clinical laboratory [97,98]. However, the practitioner should report the illness because he or she is the one who is uniquely able to describe symptomatic clusters and communicate other specific information [97]. Practitioner failure to report foodborne illnesses has led to missed opportunities for the implementation of early prevention measures and postexposure prophylaxis [97].


Misdiagnosing a foodborne illness or beginning empirical treatment to which the responsible pathogen is resistant may prolong illness and lead to complications. Thus, it is important for healthcare practitioners to be familiar with key characteristics of the most common foodborne pathogens and toxins.

The bacterial foodborne pathogens discussed in this section include the 10 agents tracked by FoodNet as well as other bacteria that are significant because of either the incidence or severity of disease they cause.


Salmonella are rod-shaped, non-spore-forming, gram-negative enterobacteria that have become the most common bacterial cause of foodborne illness in the United States [2,3,16,33]. One serotype, Salmonella typhi, causes systemic infections and typhoid fever; many other serotypes cause gastroenteritis and are referred to as nontyphoid Salmonella [56]. Typhoid (or enteric) fever is rare in the United States. Of the more than 6,371 isolate serotypes of Salmonella, 10 are responsible for most cases (73.1%) of Salmonella infection in the United States (Table 11) [16]. As few as 200 cells may cause infection [56].


SerotypeNo. of CasesPercent of Reported Infections
I 4,[5],12:i:-1973.1%

National Salmonella surveillance systems from France, England and Wales, Denmark, and the United States have identified the emergence of multidrug-resistant isolates of Salmonella enterica (serotype Kentucky) with a demonstrated high-level resistance to ciprofloxacin [99]. Between 2000 and 2008, 679 S. enterica serotype Kentucky isolates were reported to the CDC. Poultry flocks have been identified as the primary vector. Samples of spices imported from North Africa are also being investigated [100].


Salmonella infection, or salmonellosis, is the leading cause of bacterial foodborne disease. According to preliminary FoodNet data for 2014, the incidence was 15.5 per 100,000 [2]. Compared with 2011–2013, the 2014 incidence was significantly lower for Salmonella serotype Typhimurium, but overall the rate of foodborne salmonellosis has not declined in recent years [2].

The highest incidence of salmonellosis occurs among children, with a rate of 72.93 cases per 100,000 in children younger than 4 years of age [16]. However, the population affected can vary according to the food source of infection; the 2008 Salmonella (Saintpaul) outbreak caused by contaminated Mexican peppers primarily affected adults 20 to 29 years of age [3]. The incidence of Salmonella infection is highest in the summer and fall [101].

Contamination and Transmission

Transmission of Salmonella is generally animal-to-human, caused by human ingestion of food that has been exposed to the gastrointestinal systems or fecal matter of animals (e.g., birds, reptiles, mammals) or contact with pet reptiles (especially turtles), baby chicks, and ducklings [54]. Contaminated foods are typically eggs and raw/processed meats [54]. Although modern disinfection practices render eggshell contamination rare, egg yolks may harbor Salmonella from the ovaries of infected hens [102]. In the northeastern United States, one in 10,000 eggs is contaminated [102]. Raw fruits and vegetables (e.g., cantaloupe, tomatoes, alfalfa sprouts) are usually externally contaminated, although Salmonella can infect the inside of a growing fruit or vegetable [54].

Clinical Presentation and Disease Course

The onset of symptoms is usually 1 to 3 days after ingestion of contaminated food [13]. Salmonellosis is characterized by diarrhea, abdominal cramps, vomiting, and nausea that typically lasts 4 to 7 days [13,54]. Some individuals with infection may be asymptomatic, and others may present with colitis, bacteremia (sustained or intermittent), and/or focal infections (e.g., meningitis, osteomyelitis) [54].

Diagnostic Testing and Treatment

Salmonella infection is diagnosed with a routine stool culture and is a nationally notifiable disease [13]. Antimicrobial treatment is avoided in the usual case of gastrointestinal salmonellosis, as this often leads to antimicrobial resistance and prolongs the carrier state. If the patient is at increased risk for the invasive form of the disease (i.e., not isolated to the gastrointestinal tract), antimicrobial agents such as fluoroquinolones or expanded-spectrum cephalosporins are suggested [9]. In addition, ampicillin, gentamicin, and trimethoprim-sulfamethoxazole (TMP-SMX) have been effective [13,54].

The use of fluoroquinolones is not recommended for children if safe and effective alternatives are available; physicians should weigh the benefits of therapy against potential adverse musculoskeletal events, such as tendinitis and tendon rupture [9,54]. In July 2008, the FDA requested the addition of a boxed warning to fluoroquinolone prescribing information emphasizing these risks [103].


Campylobacter jejuni is a spiraled, motile, thermophilic, gram-negative rod considered unique among other foodborne pathogens because of its microaerophilic growth needs (i.e., 5% O2, 10% CO2) [54,60]. Campylobacter jejuni are more sensitive to low pH, heat, and arid conditions than other common foodborne pathogens [104]. The infective dose is 400 cells [28].


Campylobacter infection, campylobacteriosis, is the second leading cause of infectious foodborne illness in the United States, with an incidence of 13.6 per 100,000 [2]. Compared with 2006–2008, the incidence of reported Campylobacter foodborne infections increased 13% in 2014 [2]. Most cases of campylobacteriosis are sporadic and not associated with an outbreak. However, in 2008, 25 outbreaks were reported (21 confirmed and 4 suspected), affecting 615 individuals [14]; and in 2013, 27 known or suspected outbreaks were reported, causing 287 illnesses and 23 hospitalizations [3]. In 2012, a multistate outbreak of Campylobacter infections resulting in 147 illnesses was associated with ingestion of unpasteurized milk. The common source traced to a single dairy holding a permit to produce unpasteurized milk [106].

Contamination and Transmission

Campylobacter is associated with poultry, livestock, flies on farms, wild and caged animals, and pets [107,108]. Most cases of foodborne Campylobacter infection are caused by the consumption of undercooked poultry or from cross-contamination of other foods by these items. Outbreaks are most often associated with unpasteurized dairy products, poultry, and produce irrigated with contaminated water [106,108].

Clinical Presentation and Disease Course

Symptoms usually occur 2 to 5 days after consumption of contaminated food [13]. The classic symptoms of campylobacteriosis are similar to those associated with acute appendicitis. Symptoms include so-called sticky diarrhea with blood/fecal leukocytes, abdominal pain, fever, nausea, and muscular pain; vomiting is rare [13,54]. Symptoms generally last for 2 to 10 days [13].

Acute Campylobacter infection may cause intestinal hemorrhage, toxic colitis, meningitis, bacteremia, and HUS [54]. HUS is characterized by renal impairment, microangiopathic hemolytic anemia, and thrombocytopenia and most frequently affects children with campylobacteriosis [28,54]. Other potential long-term complications of campylobacteriosis include reactive arthritis (1% to 7%), irritable bowel syndrome (25%), and Guillain-Barré syndrome (0.1%) [54,109,110]. The mortality rate associated with campylobacteriosis is 0.1% [28].

Diagnostic Testing and Treatment

Most clinical laboratories can isolate Campylobacter spp. on request. Treatment is recommended only for severe cases of Campylobacter infection or for individuals who have a compromised immune system. When antimicrobial therapy is warranted, macrolides, such as erythromycin, or fluoroquinolones are the preferred drugs; however, resistance to these agents has increased with the use of antibiotics in chickens (as therapeutic agents or growth promoters) [9,111]. In general, Campylobacter is susceptible to chloramphenicol and clindamycin [111].


Shigella spp. are highly infectious, gram-negative, non-spore-forming, facultative anaerobes [28]. Unlike pathogenic Salmonella and Campylobacter, Shigella is nonmotile [28]. Four species (with more than 40 serotypes) have been identified: Shigella dysenteriae, Shigella flexneri, Shigella boydii, and Shigella sonnei [54]. These species are also known as groups A, B, C, and D, respectively [60]. Because Shigella is enteroinvasive in the large intestine, it is commonly mistaken for an enteroinvasive E. coli [60]. In experimental situations, as few as 10 organisms has caused disease in 10% of volunteers, and 500 organisms has routinely caused disease in 50% of volunteers [56].


According to preliminary data from 2014, Shigella is the third leading cause of foodborne illness in the United States, with an incidence of 5.8 per 100,000 [2]. The most prevalent pathogenic species is Shigella sonnei, which has been isolated in 75% to 80% of Shigella infections [112,113,114]. Outbreaks may continue for months in closed populations [115]. The other Shigella spp. isolated in association with outbreaks are Shigella flexneri (18%), Shigella boydii (1%), and Shigella dysenteriae (<1%) [113]. In 2013, Shigella accounted for only four reported outbreaks and 31 illnesses [3].

Contamination and Transmission

Typically, only primates harbor Shigella [28,54]. The pathogen is transmitted via the fecal-oral route through person-to-person contact, ingestion of contaminated food/water, and fomite contamination [28,54]. Because incidence rates peak in the late summer, the most common routes of Shigella exposure may differ from Salmonella and Campylobacter [101].

Clinical Presentation and Disease Course

Shigellosis manifests as diarrhea (usually mucoid, possibly bloody), which may be accompanied by abdominal cramps/pain, fever, and tenesmus; symptoms usually occur within 8 to 48 hours after ingestion of the contaminated food and last 4 to 7 days [13,28]. Symptoms vary by Shigella species. For example, Shigella flexneri, Shigella boydii, and Shigella dysenteriae typically present with bloody diarrhea and severe systemic symptoms, whereas Shigella sonnei typically causes watery stools [54].

As with STECs, Shigella dysenteriae type I produces Shiga toxins, which cause HUS [54,28]. However, the development of HUS is delayed with Shigella dysenteriae, with a median of 7 days from the onset of Shigella-induced diarrhea to the development of HUS, compared with the typical 4 days for HUS caused by STEC infections [28,116].

Reactive arthritis will develop in approximately 7% of individuals with shigellosis, and Reiter syndrome will develop in 3% [60,117]. The mortality rate associated with the infection is less than 1% in the United States [16,118].

Diagnostic Testing

Stool samples or rectal swabs should be obtained during the acute phase of the disease and cultured for Shigella [54]. Blood samples should be examined for signs of bacteremia in patients who are severely ill, are malnourished, or have a compromised immune system [54]. Shigella infection is a nationally notifiable disease.

Shigella dysenteriae type I Shiga toxins are often identified with use of enzyme-linked immunosorbent assays [54]. Shigella-induced neutrophilia is typically greater than that caused by STECs; the degree of neutrophilia at the onset of disease may be used to predict the development and potential severity of HUS [118].


Antimicrobial therapy is not advised for most cases of infection with Shigella spp. because of high rates of resistance [28,54]. These resistance rates have been reported to be approximately 78% for ampicillin, 56% for streptomycin, 47% for sulfisoxazole, and 46% for TMP-SMX [113]. In addition, resistance to both ampicillin and TMP-SMX has been found in 38% of cases [113].

For patients with severe disease, most resistant Shigella strains can be treated with azithromycin (oral) or ceftriaxone (intramuscular) [54]. Fluoroquinolones may be effective for adults with suspected shigellosis who have fever, tenesmus, and inflammation [9]. Early and appropriate antimicrobial treatment of Shigella dysenteriae type I infections may prevent HUS [54,60].


E. coli is a motile gram-negative rod common to the human gastrointestinal tract. Although most E. coli are nonpathogenic and beneficial, some are diarrheagenic [60]. Six diarrheagenic virotypes have been identified, of which the primary ones are STEC (Shiga toxin-producing or enterohemorrhagic E. coli) and enterotoxigenic E. coli (traveler's diarrhea). Enteropathogenic E. coli (infantile diarrhea) occurs primarily in developing countries. The remaining three virotypes—enteroaggregative, enteroinvasive, and diffusely adherent E. coli—are not as well-established as the others [112,119]. The incubation period is 1 to 8 days for STEC and 1 to 3 days for enterotoxigenic E. coli [13].

STECs (STEC O157:H7 and Others)

STECs adhere to and efface the wall of the large intestine [60]. The infective dose has been reported to be as low as 20 organisms, ranging to 700 organisms [56].


STEC O157 is the most virulent as well as the most commonly identified STEC [32,119]. In 2010, STEC O157 was the fifth leading bacterial cause of foodborne illness in the United States [16]. In 2014, the reported incidence of STEC 0157 was 0.92 cases per 100,000, a 32% decrease over that reported for 2006–2008 [2]. Infection with STEC non-O157 is more frequent than infection with STEC O157 [2]. Non-O157 serogroups in the United States include O26 (22%), O11 (16%), and O103 (12%) [32,54]. In 2013, 28 confirmed outbreaks of STEC O157 were reported, affecting approximately 400 individuals [3].

Contamination and Transmission

Human STEC infection typically follows consumption of fecally contaminated food/water or person-to-person contact with infected (usually symptomatic) individuals [54,119]. Undercooked ground beef or cattle contact causes most STEC O157 outbreaks; however, contaminated raw milk, dry-cured salami, unpasteurized fruit juice, vegetables, and petting zoos have also been associated with STEC O157 outbreaks [32,119].

Clinical Presentation and Disease Course

Symptoms typically begin 1 to 8 days after consumption of contaminated food [11]. Initially, individuals experience severe abdominal cramping/pain, watery diarrhea, vomiting, and/or low-grade fever [60,119]. Medical attention is usually sought during the second stage, when diarrhea becomes visibly bloody [54]. In most cases, the disease is self-limiting, with symptoms resolving within 5 to 10 days [13,119].

Diagnostic Testing

Stool samples for culture should be obtained as close to the onset of symptoms as possible, and testing for STEC O157 must be specifically requested [13,54]. In some clinical laboratories, immunoassays are used to detect Shiga toxins [32,54]. Physicians should request that STEC strains be identified for patients and their contacts who have bloody diarrhea, HUS, and/or thrombotic thrombocytopenia purpura (TTP) [54].


Nonspecific supportive treatment approaches, including hydration, are used for patients with STEC infections. Antimicrobial therapy is not recommended [119]. It was once thought that antimicrobial agents promoted the development of HUS, but a meta-analysis has shown that this is not the case [120]. Nevertheless, STECs cause approximately 90% of all cases of HUS, and the syndrome will develop in 8% of children infected with STEC [118]. Patients should be monitored for potential HUS development with measurements of complete blood cell count with differential and blood urea nitrogen and creatinine levels [54]. HUS is unlikely to develop in patients with no indication of hemolysis, nephropathy, and thrombocytopenia 3 days after infection [54]. TTP, which is characterized by HUS, neurologic abnormalities, and fever, typically affects adults, especially individuals older than 65 years of age [54].

Enterotoxigenic Escherichia coli

In contrast to STECs, enterotoxigenic E. coli adheres to and effaces the small intestine [60]. The infective dose is 108 cells [60].


Enterotoxigenic E. coli is a major cause of bacteria-related diarrhea in individuals who travel outside the United States, especially to developing countries [112,121]. The infection has become more frequently identified as a cause of foodborne illness in the United States [122].

Contamination and Transmission

Enterotoxigenic E. coli is spread through fecally contaminated food or water. Infected food handlers may also be a source of contamination [60,121].

Clinical Presentation and Disease Course

Symptoms usually occur 1 to 3 days after ingestion of contaminated food or water [13,121]. Symptoms include watery diarrhea for 3 to 7 days, abdominal cramps, nausea, and malaise; low-grade fever is an infrequent symptom [13,54,121]. Manifestation of the infection ranges from minor discomfort to a severe cholera-like syndrome [60].

Diagnostic Testing

Distinguishing enterotoxigenic E. coli from nonpathogenic E. coli is difficult for most clinical laboratories, but enterotoxigenic E. coli can be identified in research laboratories accessed through the state health department [54,121]. Testing for the organism must be specifically requested [13,121].


Treatment with antibiotics is not routinely needed for enterotoxigenic E. coli infection [13]. For severe illness, recommended antimicrobial agents are TMP-SMX, ciprofloxacin, and azithromycin [54]. Fluoroquinolones may also decrease the duration of illness caused by enterotoxigenic E. coli and other travel-related bacterial pathogens from 3 to 5 days to 1 to 2 days [9,121].


Listeria monocytogenes is an aerobic, gram-positive, usually pathogenic bacillus [28,54]. Although non-spore-forming, Listeria is resistant to freezing, drying, and heat, and it multiplies in refrigerated foods [28,54]. The organism attacks the gastrointestinal epithelium and then enters the bloodstream to replicate; it can enter the brain and placenta by infecting circulating phagocytes [28,60]. The infective dose is fewer than 1,000 cells [28].


Since 2000, the incidence of listeriosis has decreased considerably, by 34% between 1989 and 1993 and by 36% from 1996 to 2006 [112]. In 2008, 33 individuals were affected by three confirmed outbreaks [14]. In 2013, six reported foodborne listeriosis outbreaks resulted in 34 illnesses, 30 hospitalizations, and 6 deaths [3]. In 2011, health officials in Colorado notified the CDC of seven cases of listeriosis associated with consumption of cantaloupe from the same farm [123].

Pregnant women are at high risk for the disease, but symptoms are nonspecific and diagnosis is difficult [124]. Maternal infection leads to premature birth or spontaneous abortion in many cases [28,125,126]. The mortality rate associated with Listeria infection is approximately 20% to 30% [74,75].

Contamination and Transmission

Ubiquitous in the environment, Listeria is found in many species of mammals (particularly herd animals), birds, and marine life [28,54]. Contaminated soil or water can cause contamination of fruits and vegetables or farm animals. Raw (unpasteurized) milk is a primary source. As many as 10% of humans are carriers of the pathogen [28].

Clinical Presentation and Disease Course

Foodborne listeriosis often begins with fever, muscle aches, nausea, and possibly diarrhea; gastrointestinal symptoms usually begin within 9 to 48 hours after ingestion [13]. In pregnant women, infection usually manifests as mild flu-like symptoms [13]. Potential complications include bacteremia and meningitis [13]. Listeriosis-related meningitis is associated with a mortality rate of approximately 70% [28]. Invasive disease typically manifests 2 to 6 weeks after ingestion [13].

Diagnostic Testing and Treatment

Samples of blood, cerebrospinal fluid, gastric washings, meconium, placental tissue, and other infected tissue are appropriate for culture and gram stain [28,54]. Infection with Listeria is a nationally notifiable disease. Since 2004, the CDC has requested that patients with listeriosis be interviewed with use of a standardized Listeria Initiative questionnaire. Use of this tool provides timely exposure information for case-control analyses [126].

Intravenous ampicillin, penicillin, or TMP-SMX is recommended for invasive disease; cephalosporins are ineffective [13,54]. Patients with meningitis should be treated with antibiotics for 14 to 21 days [54].


Vibrio are gram-negative, motile, comma-shaped rods [65,71]. Commonly found in aquatic environments, they are salt-tolerant, facultative anaerobes [71]. Pathogens in this species/class include Vibrio cholerae and noncholera Vibrio spp.

Vibrio cholerae

Vibrio cholerae is classified into two serotypes: O1 and non-O1 [127]. O1 is further subdivided into two biotypes: classical and El Tor. El Tor is the major cholera-causing biotype [54,128,129]. Of the non-O1 serotypes, O139 and O141 cause clinical cholera [54,129,130]. The infective dose is 107 cells [28].


Cholera is rare in the United States (one outbreak was reported in 2011) as well as in other industrialized nations [131]. However, it is still common in some parts of the world, including the Indian subcontinent and sub-Saharan Africa [112]. Of the 221,226 cholera cases reported to the World Health Organization in 2009, 99% were reported from Africa [129].

Contamination and Transmission

The ingestion of fecally contaminated water or food is the most common mode of transmission [60,112,129]. Person-to-person transmission is rare.

Clinical Presentation and Disease Course

Symptom onset is 1 to 3 days after ingestion [13]. Most patients with cholera will experience minimal or no symptoms [112]. However, the disease can be associated with profuse, watery diarrhea that lasts 3 to 7 days; there is usually no abdominal pain or fever [54,129]. Stool is colorless with flecks of mucus—sometimes referred to as "rice water"—and the initial stool may exceed one liter [54,129]. In approximately 5% to 10% of cases, the individual becomes severely dehydrated and metabolic acidosis and hypokalemia may develop within hours [13,54,129]. Vibrio cholerae infection can progress to hypovolemic shock, seizures, coma, and death, particularly in children [54].

Diagnostic Testing

Vibrio cholerae can be detected in culture of stool or vomitus, but the test must be specifically requested [13,129]. Isolates should be forwarded to the state health department for serogrouping [54]. Cholera is a nationally notifiable disease.


Rehydration should begin as soon as cholera is suspected and should be aggressive [13,54,129]. If possible, antimicrobial susceptibility testing is recommended because many Vibrio cholerae type O139 strains are resistant to TMP-SMX [54]. Oral doxycycline (single dose) or tetracycline (3-day regimen) is recommended, especially for adults [13]. Although tetracycline stains developing teeth in children younger than 8 years of age, the American Association of Pediatrics has noted that the benefit of tetracycline therapy outweighs the risks for children with severe cholera [54]. Tetracycline-resistant strains may be effectively treated with ciprofloxacin, ofloxacin, or TMP-SMX [13,54].

Noncholera Vibrio spp.

Noncholera Vibrio is commonly found in all seawater [28,54]. The species of noncholera Vibrio that cause gastroenteritis include Vibrio parahaemolyticus and Vibrio vulnificus [13]. Vibrio parahaemolyticus naturally inhabits coastal waters in the United States and Canada and is present in higher concentrations during the summer [112]. Vibrio vulnificus normally inhabits warmer seawater [112,129]. The infective dose is 107 cells [28].


According to preliminary data from 2014, the incidence of Vibrio infection is 0.45 per 100,000, and the incidence is highest among individuals 60 years of age and older [2]. The risk for infection is greatest for individuals who consume raw/undercooked seafood (especially oysters, shrimp, and crabs) and individuals who have liver disease [54]. In 2008, one confirmed outbreak of Vibrio parahaemolyticus and one suspected outbreak of another Vibrio species were reported, affecting five individuals [14].

Contamination and Transmission

Ingestion of raw or undercooked seafood (e.g., mollusks, crustaceans) is the primary mode of transmission [13,28,129].

Clinical Presentation and Disease Course

The time from ingestion to onset of symptoms can be as short as 2 to 48 hours (Vibrio parahaemolyticus) or 1 to 7 days (Vibrio vulnificus) [13]. Unlike cholera, noncholera Vibrio infection, or vibriosis, causes abdominal cramps along with watery diarrhea [28,54]. More than half of patients have a fever, chills, and headache, and at least 25% experience vomiting [54]. Bacteremia may develop in individuals with a compromised immune system [54].

Diagnostic Testing

Vibriosis can be diagnosed by culture of stool or vomitus samples, and the test must be specifically requested [13,28,54,129]. Vibrio infection became a nationally notifiable disease in January 2007 [112].


Treatment is recommended only for severe disease. Recommended antimicrobial agents include tetracycline and doxycycline, as well as gentamicin and cefotaxime (Vibrio parahaemolyticus) and ceftazidime (Vibrio vulnificus) [13].


Yersinia are pleomorphic, gram-negative rods [54]. Only Yersinia enterocolitica and Yersinia pseudotuberculosis are associated with gastroenteritis [28]. The infective dose is unknown, but is estimated to be between 104 to 106 organisms [28].


In 2014, the incidence of yersiniosis was 0.3 per 100,000, a decrease of 22% compared with that reported for 2006–2008 [2]. The incidence is highest among children younger than 5 years of age. Yersinia enterocolitica O:3 is the most frequently identified serotype [28,54].

Contamination and Transmission

Pigs are the primary reservoirs for Yersinia [132]. However, humans may be carriers for several months after infection [54,132]. Commonly associated foods are raw/undercooked pork, oysters, fish, unpasteurized milk, and ice cream [28,54]. The organism can grow at 4°C, which means that refrigerated meats can be sources of infection [28,56]. Waterborne infections are rare [54].

Clinical Presentation and Disease Course

Symptoms associated with Yersinia infection usually occur within 24 to 48 hours after ingestion of contaminated food [13]. The clinical presentation of yersiniosis is age-specific. In infants and young children, mucoid diarrhea with blood and leukocytes, as well as fever, is common, whereas in adolescents and adults, an appendicitis-like syndrome (i.e., diarrhea, vomiting, fever, abdominal pain) usually occurs [28,54]. Yersinia enterocolitica may lead to reactive arthritis in 2% to 3% of individuals with infection, even in the absence of obvious symptoms [28,54]. Bacteremia is a potential complication among children with excessive iron storage or who have compromised immune systems [54].

Diagnostic Testing and Treatment

Yersinia can be detected in a stool, vomitus, or blood culture, if specifically requested [13,28]. Serology testing is available in some research and reference laboratories.

Antimicrobial therapy is recommended if septicemia or invasive disease develops [13]. Options for antimicrobial agents include gentamicin, cefotaxime, doxycycline, and ciprofloxacin [13].


Clostridium perfringens are anaerobic, gram-positive spore-forming rods that are widely distributed in the environment. Spores exist in soil, sediments, and areas subject to human or animal fecal pollution [28]. The infective dose is more than 108 vegetative cells [28]. Related disease is caused by toxins excreted by the bacteria rather than infection.


The CDC has attributed nearly 1 million domestically acquired foodborne illnesses to Clostridium perfringens [133]. In 2008, Clostridium perfringens accounted for the second greatest number of illnesses (1,409) in 40 reported outbreaks (21 confirmed and 19 suspected) of foodborne disease [14]. More recently, these numbers have declined somewhat. In 2013, 27 known or suspected outbreaks of Clostridium perfringens were reported, causing 601 illnesses [3].

Contamination and Transmission

Small numbers of Clostridium perfringens are present in some foods after cooking and multiply to the level of an infective dose if cooked foods are cooled or stored at inappropriate temperatures [28,133]. Common sources for the bacteria are meat, meat products, and gravy [38,133].

Clinical Presentation and Disease Course

Symptoms of Clostridium perfringens poisoning include watery diarrhea, abdominal cramps, and nausea; fever is rare [13,28]. The onset of symptoms is usually 8 to 22 hours after ingestion of contaminated food. Illness is usually relatively mild and rarely leads to hospitalization. Symptoms usually resolve within 24 to 48 hours, although less severe symptoms may last for 1 to 2 weeks in some patients (i.e., older individuals, individuals with compromised immune systems) [13,28,133].

Diagnostic Testing and Treatment

Perfringens poisoning is diagnosed primarily by the clinical presentation, but the toxin can be detected in stool samples. A stool culture can also be done to detect Clostridium perfringens, but because these bacteria are normally found in stool, a quantitative analysis should be done [13,133]. Food can also be cultured, and an exceptionally high number of the bacteria indicates contamination [28]. Antimicrobial therapy is not indicated for perfringens poisoning, as it is ineffective against the toxin [13,133].


Clostridium botulinum is ubiquitous in soil, and under anaerobic conditions, the rod-shaped bacteria form spores that allow them to survive in a dormant state until they are exposed to conditions that support their growth [112]. The bacteria produce neurotoxins; human disease is typically caused by neurotoxins A, B, and E; F rarely causes disease in humans [28,54]. The infective dose is an extremely small amount (i.e., several nanograms) [28].


Foodborne botulism is relatively rare, primarily due to the improvements in commercial canning processes, which have reduced the incidence of botulism. However, outbreaks do occur. A small outbreak (eight cases) in 2007 involved a commercial brand of canned chili sauce [43]. During 2008 and 2009, the CDC and state and local health departments in Ohio and Washington investigated three outbreaks of botulism caused by unsafe home canning of vegetables [134]. In 2011, consumption of commercially produced (and then improperly stored) potato soup was associated with toxin type A botulism in two individuals in separate states [135]. There were no reported foodborne outbreaks of Clostridium botulinum in 2013 [3].

The incidence of foodborne botulism in Alaska remains more than 800 times the overall U.S. rate [136]. Approximately 27% of all foodborne botulism cases in the United States have occurred in that state [137]. Between 1950 and 2000, 114 outbreaks (226 cases) of foodborne botulism were recorded in Alaska and involved Alaska Natives [137,138]. In 2010, 112 confirmed cases of botulism were reported to the CDC, with foodborne botulism accounting for nine of the cases (8%) [139]. Infant botulism was more common than foodborne botulism, with 85 cases (76%) reported in 2010 [139]. Most cases of infant botulism have occurred in breastfed babies when nonhuman-milk foods were introduced [54,56]. The rate of mortality associated with the disease is approximately 5% [112].

Contamination and Transmission

Botulism is caused by ingestion of Clostridium botulinum toxin produced in food [112]. The most common source is home-canned foods that have been prepared in an unsafe manner. Infant botulism occurs when Clostridium botulinum spores germinate and produce toxin in the gastrointestinal tract of infants. The risk of infant botulism is high among infants who eat honey before the age of 1 year, as honey is a source of the spores that produce Clostridium botulinum [54].

Clinical Presentation and Disease Course

Symptoms of foodborne botulism typically occur within 12 to 72 hours after ingestion of contaminated food but may occur as late as 10 days following ingestion [13,140]. Characteristic symptoms include weakness with disproportionate involvement of cranial nerves (diplopia, dysarthria, dysphagia) and symmetric descending flaccid paralysis in the absence of sensory changes that usually accompany other disorders with similar symptoms, such as stroke or Guillain-Barré syndrome [28,54,56]. If symptoms of muscle paralysis are left untreated, they may progress to cause permanent paralysis of the arms, legs, trunk, and respiratory muscles.

Infant botulism is characterized by constipation, lethargy, lack of appetite, drooling, and weakness, which begin 1 to 30 days after ingestion of contaminated food [13]. Subsequent symptoms include descending symmetrical paralysis manifested as bulbar palsies (e.g., poor head and muscle control, flat affect, ptosis, impaired swallow reflexes, sluggish pupillary reaction) [13]. Intubation and ventilatory support are necessary in the vast majority of cases [54].

Diagnostic Testing

Serum, stool, gastric fluid, vomitus, or food samples can be used to detect botulism neurotoxins [112]. Because its clinical presentation is similar to neurologic conditions, diagnostic testing should be done to rule out these conditions [112,140]. For example, the incremental increase of evoked muscle potentials at high frequency 20–50 Hz nerve stimulation may distinguish botulism from Guillain-Barré syndrome or myasthenia gravis [54,56]. Clostridium botulinum is a category A bioterrorism agent, and infection is a nationally notifiable disease [112].


Treatment should begin when botulism is suspected on the basis of symptoms and should not be delayed while waiting for confirmation from laboratory results [54]. If diagnosed early, foodborne botulism can be treated with an equine antitoxin that will prevent worsening of the disease. Antitoxins can be obtained from the CDC Drug Service [140]. Induced vomiting, gastric lavage, rapid purgation, or high enema can remove contaminated food in the gut [13,54]. A respirator is often needed, and complete recovery can take many weeks to months.

Infant botulism can be treated with botulism immune globulin, which can be obtained from the Infant Botulism Prevention Program, California Department of Public Health [140].


Bacillus cereus are gram-positive, aerobic spore-forming rods [28]. A large-molecular-weight protein is the cause of the diarrheal type illness, and a low-molecular-weight, heat-stable peptide is the cause of the emetic type illness [28]. The infective dose is thought to be greater than 106 organisms per gram of food [28].


Infection with Bacillus cereus is infrequent. In 2008, 15 outbreaks of the illness were reported (three confirmed and 12 suspected), affecting a total of 73 individuals [14]. By 2013, this number had declined to five reported foodborne outbreaks and 25 illnesses [3].

Contamination and Transmission

Bacillus cereus food poisoning is transmitted through ingestion of contaminated food, and there is a broad range of potential food sources, including meats, milk, vegetables, and fish (diarrheal-type illness) and rice products and other starchy foods, such as potato, pasta, and cheese products (emetic-type illness) [28]. Outbreaks have often involved food mixtures, such as sauces, puddings, soups, casseroles, and pastries. Bacillus cereus is heat resistant and can survive cooking (even at recommended temperatures). In addition to contaminated food, transmission of infection can also occur with improper food handling or storage; person-to-person transmission is rare [28].

Clinical Presentation and Disease Course

The symptoms caused by the diarrheal type of Bacillus cereus food poisoning are similar to those of Clostridium perfringens infection. Symptoms include watery diarrhea and abdominal cramps that may be accompanied by nausea but usually not vomiting. The onset of symptoms is typically 6 to 16 hours after ingestion of contaminated food [13,28]. Symptoms usually resolve within 24 to 48 hours [13].

The enteric type of Bacillus cereus food poisoning causes symptoms similar to those associated with foodborne Staphylococcus aureus infection. The onset of nausea and vomiting occurs within 1 to 6 hours after ingestion of contaminated food and may be accompanied by diarrhea and/or abdominal cramps [13,28]. Symptoms usually resolve within 24 hours.

Diagnostic Testing and Treatment

The diagnosis of either type of Bacillus cereus food poisoning is based primarily on the clinical presentation. Laboratories do not routinely identify the enteric type of Bacillus cereus; testing for the toxin in food and stool samples should be considered if an outbreak is suspected [13]. Antimicrobial therapy is not indicated for Bacillus cereus food poisoning [13].


Brucella spp. are gram-negative, nonmotile coccobacilli [54]. Brucella melitensis and Brucella ovis are found in sheep and goats, Brucella abortus is found in cattle, and Brucella suis is found in pigs [112]. The infective dose for aerosolized infection is 10–100 organisms [56].


Brucellosis is rare in the United States, with an incidence of less than 0.5 per 100,000 [105,141]. Most cases are caused by Brucella melitensis, the majority of which are reported from California, Florida, Texas, and Virginia [112]. In 2013, there were no reported outbreaks [3,14].

Contamination and Transmission

In the United States, milk or dairy products from contaminated animals are the most common sources of infection with Brucella [112,141]. Transmission through person-to-person contact is extremely rare.

Clinical Presentation and Disease Course

Symptoms typically occur 7 to 21 days after ingestion of contaminated food [13]. The clinical presentation of brucellosis is nonspecific and includes fever with chills, sweating, malaise, headache, and myalgia as well as diarrhea, which may be bloody during the acute stage of disease [13]. Symptoms may last for weeks. Meninges, bone, and/or the heart may be involved, which can lead to such complications as meningitis, osteomyelitis, and endocarditis [54,141]. Disease is usually more severe in adults than in children [54].

Diagnostic Testing and Treatment

Samples of blood, bone marrow, or other tissues are tested for the bacteria and must be incubated for 4 weeks before testing [54,141]. The CDC has designated Brucella as a category B bioterrorism agent, and infections are nationally notifiable [112].

Recommended therapy for brucellosis is doxycycline and rifampin for at least 6 weeks [141]. Individuals who have complications should be treated with the combination of rifampin, tetracycline, and an aminoglycoside [13].


Staphylococcus aureus is a gram-positive, catalase-positive coccus that grows in grape-like clusters or chains when cultured [28]. Pathogenicity is caused by eight heat-stable enterotoxins (A, B, C1, C2, C3, D, E, and F) [28,54]. Of these, staphylococcal enterotoxin A is usually responsible for foodborne-illness outbreaks [54]. The infective dose is 1.0 mcg of toxin [28].


In 2013, Staphylococcus aureus enterotoxin was implicated in six reported outbreaks involving 263 illnesses and 27 hospitalizations [3].

Contamination and Transmission

Staphylococcus aureus is transmitted through person-to-person contact, usually as a result of a food handler who is infected with the bacteria [112]. The bacteria will multiply on improperly stored foods, especially pastries, custards, salad dressings, cheeses, meat products, and expressed human milk [54,112]. Staphylococcal toxins are resistant to heat and cannot be destroyed by cooking [112].

Clinical Presentation and Disease Course

Staphylococcal food poisoning is characterized by the rapid onset of nausea and vomiting, which may occur within 30 minutes of ingestion (range: 1 to 6 hours) [13,112,142]. Other symptoms include abdominal pain, diarrhea, and fever [13,142]. The disease is usually mild, with recovery within 1 to 3 days [13,112].

Diagnostic Testing and Treatment

Staphylococcus aureus toxins can be identified from stool, vomitus, and food, but microbiologic testing is not usually done [13,142]. Staphylococcal enterotoxin B is classified as a category B bioterrorism agent and is nationally notifiable [112].

Antimicrobial agents should not be used to treat foodborne Staphylococcus aureus infection, as they are not effective against the toxins [142].


As noted previously, the three viruses associated with foodborne illness are caliciviruses (e.g., norovirus), hepatitis A virus, and rotavirus. Astroviruses and enteric adenoviruses have been implicated in isolated cases and outbreaks of viral gastroenteritis but are much less common. Treatment of viral foodborne illnesses consists primarily of rehydration and supportive therapy.


Caliciviruses are nonenveloped ribonucleic acid (RNA) viruses [56]. The two caliciviruses most likely to cause foodborne illness are norovirus and sapovirus. There are six recognized norovirus genogroups divided into 25 different genotypes. Three of the genogroups (GI, GII, and GIV) affect humans [143]. Sapovirus also consists of five genogroups (GI–GV), and all except GIII cause infection in humans [144,145]. The infective dose for both types of viruses is 10–100 viral particles [56,143,147].


Norovirus is the leading cause of gastroenteritis and foodborne disease outbreaks in the United States. According to estimates derived from surveillance data, norovirus causes 2 million illnesses, 56,000 to 71,000 hospitalizations, and 570 to 800 deaths annually [105,143]. In 2013, norovirus was the most common cause of confirmed single-etiology foodborne outbreaks, accounting for 154 (35%) outbreaks and 3,758 (40%) illnesses; moreover, it was the suspect etiologic agent for an additional 103 outbreaks and 1,241 food-related illnesses [3]. The incidence of norovirus infection increases during the winter months, and periodic outbreaks tend to occur in association with the emergence of new GII strains that evade population immunity [147].

In 2009, the CDC launched CaliciNet, an outbreak surveillance network for noroviruses in the United States [148,149]. The CDC uses the information to link norovirus outbreaks, monitor trends, and identify emerging strains. As of 2012, 25 state public health laboratories have been certified by the CDC to participate in CaliciNet [149].

Between 2009 and 2012, norovirus was the etiologic pathogen identified in 1,008 foodborne outbreaks, accounting for 48% of all reported outbreaks with a single known cause [146]. Eating in restaurants was the most common setting (65%), and food handlers were implicated as the source in 70% of outbreaks in which factors contributing to contamination could be identified. Other factors included contamination of food during preparation (92%) and consumption of raw food (75%) [146]. Specific food categories were implicated in only 67 outbreaks, the most frequent being leafy vegetables (30%), fruits (21%), and mollusks (19%) [146].

Contamination and Transmission

Foodborne infection with either norovirus or sapovirus is transmitted via the fecal-oral route through infected food handlers, exposure to contaminated surfaces, consumption of contaminated food, or rarely, ingestion of contaminated water [143,146,147]. Aerosolized norovirus particles in vomitus can also contribute to spread of the disease, and these particles can travel a distance of up to 3 feet [143,150,151]. The most common sources are prepared foods (e.g., sandwiches, salads) and raw produce [68].

Clinical Presentation and Disease Course

The symptoms associated with infection with either norovirus or sapovirus are nausea, vomiting, abdominal cramps, diarrhea (usually watery), fever, myalgia, and headache [13,143]. Diarrhea is more common among adults, and vomiting is more common among children [13,143]. The onset of disease is 24 to 48 hours but may be as few as 12 hours [13,143]. Symptoms usually resolve within 24 to 72 hours [143]. Viral shedding lasts 2 weeks in otherwise healthy individuals and longer in individuals with compromised immune systems [56,147].

Diagnostic Testing

The diagnosis of norovirus or sapovirus is usually made on the basis of the clinical presentation and the lack of positive results on stool cultures for bacteria [13]. The absence of white blood cells in the stool is also an indicator of the virus [13]. Reference/research laboratories can identify norovirus or sapovirus in stool with reverse transcriptase polymerase chain reaction (RT-PCR), immunoassays, or electron microscopy [56,143,147].


Hepatitis A is an RNA virus with only one serotype, and seven genotypes (I–VII); genotypes I, II, III, and VII cause disease in humans [54]. In North America, most hepatitis A infections are caused by subtype IA [56]. The infective dose is believed to be 10–100 viral particles [28]. The virus replicates in the liver and is shed (in high concentrations) in the stool [152]. Unlike other forms of hepatitis, hepatitis A infection is self-limited and does not cause chronic infection or chronic liver disease [152].


The hepatitis A vaccine, which became available in 1995, has led to a 92% decrease in the incidence of the disease [152]. In 2009, the incidence of hepatitis A was 1.0 per 100,000 [152]. The highest incidence is found among young adults, especially those in lower socioeconomic classes [54]. Four confirmed outbreaks of foodborne hepatitis A (172 individuals) were reported in 2013 [3]. Outbreaks of hepatitis A have been caused by fruits (strawberries) and vegetables (green onions) that were contaminated during packing or shipping from farms outside the United States; one of these outbreaks involved 601 individuals who had consumed green onions at a single restaurant in Pennsylvania [44].

Contamination and Transmission

Foodborne hepatitis A is transmitted via person-to-person contact (fecal-oral); waterborne transmission is rare in the United States and other developed countries [152]. The virus is destroyed if heated to 185°F for 1 minute; however, the virus may be spread from cooked food if it is contaminated after cooking [54]. Because children with hepatitis A are often asymptomatic, they play a key role in transmission [56].

Clinical Presentation and Disease Course

The incubation period of hepatitis A is 2 to 5 weeks (average: 4 weeks) [153]. Jaundice occurs in most infected older children and adults [13]. In children younger than 6 years of age, jaundice is uncommon; only 30% of children are symptomatic at this age [13]. Other common symptoms among children and adults are dark urine, fever, malaise, and loss of appetite [13,54].

Symptoms persist for several days to months [13,54]. Communicability extends from 1 to 2 weeks before the onset of disease to about 1 week after the development of jaundice [56]. The risk for severe illness is higher for individuals with chronic liver disease or clotting-factor disorders [54,152]. Hepatitis A-induced acute liver failure is uncommon (0.4%) and is most likely to manifest in people with chronic liver disease [54].

Diagnostic Testing

The presence of anti-hepatitis A immunoglobulin (Ig) M in serum represents current or recent infection; anti-hepatitis IgG in the absence of IgM indicates past infection [54]. Increases in serum levels of bilirubin and alanine aminotransferase are also indicators of infection [13].


"Rota" (Latin for wheel) describes the wheel-like structure of these viruses, which is made up of 11 double-stranded RNA segments surrounded by a distinctive two-layered protein capsid [28]. Six serologic groups have been identified, three of which (groups A, B, and C) infect humans [28]. The infective dose is believed to be 10–100 viral particles [13].


In the United States, annual epidemics of rotavirus spread from the Southwest to the Northeast between fall and spring [54]. Prior to introduction of the rotavirus vaccine in 2006, almost all children in the United States had been infected by 5 years of age [154]. By extension, the virus affects approximately 20% of adults having close contact with an infant [54].

Contamination and Transmission

Rotavirus is transmitted via the fecal-oral route through person-to-person contact or fomites. Rotavirus is stable in the environment [154].

Clinical Presentation and Disease Course

The primary symptoms of rotavirus infection are vomiting, watery diarrhea, and low-grade fever, all of which occur 1 to 3 days after infection [13]. Temporary lactose intolerance may occur [28]. Symptoms typically last 4 to 8 days and are milder in adults than in children [13]. Infection can become persistent in individuals who have compromised immune systems [54].

Diagnostic Testing

Diagnosis of rotavirus infection is made primarily on the basis of the clinical presentation and the nondetection of bacteria in stool cultures. The virus can be detected in a stool sample with use of a radioimmunoassay [154].


Astroviruses are nonenveloped single-stranded RNA viruses with a star-like morphology; eight antigenic types cause human disease [28,54]. Adenoviruses, which contain double-stranded DNA, usually cause respiratory infection, but serotypes 40 and 41 are enteric [28]. Adenoviruses are unusually stable, allowing them to survive outside the body for prolonged periods [155]. The infective doses are not known but are thought to be low [28].


Astroviruses and adenoviruses infect children more often than adults, and the incidence is highest among children younger than 4 years of age [54,155]. According to the most recent data, no outbreaks of astrovirus have occurred in the United States [14].

Contamination and Transmission

Astroviruses and adenoviruses are transmitted via the fecal-oral route through an infected food handler or exposure to a contaminated surface [54]. Enteric adenovirus may also be transmitted via respiratory secretions [28].

Clinical Presentation and Disease Course

The incubation period for these viruses ranges from 10 to 70 hours [13]. Associated symptoms include diarrhea, nausea, vomiting, abdominal pain, fever, malaise, and headache [13,54]. Symptoms typically resolve within 2 to 9 days, and the virus is shed for a median of 5 days after the onset of symptoms [13,54]. In individuals with a compromised immune system, viral shedding is often persistent [54].

Diagnostic Testing

Commercial assays are available to detect astroviruses and adenoviruses in stool samples, although testing is uncommon [13].


As with bacterial and viral infections, most parasitic infections are self-limiting. Treatment with only rehydration is often adequate.


Cryptosporidium are obligate intracellular coccidia with an infective oocyst stage [56]. Oocysts are excreted by an infected host through feces and possibly other routes (e.g., respiratory secretions) [156]. Human disease is caused by Cryptosporidium hominis and Cryptosporidium parvum[156]. The infective dose for healthy adults is 30 oocysts; the dose is greater (100–1,000 oocysts) for reinfection after 1 year [56]. Cryptosporidium targets the jejunum and terminal ileum [56].


The prevalence of cryptosporidiosis in North America is estimated to be 2% of the population; serologic surveys have indicated that 80% of the population has had the infection [28]. Three confirmed outbreaks of foodborne infection with Cryptosporidium were reported in 2013, affecting 29 individuals [3]. The incidence of Cryptosporidium was 2.4 per 100,000 in 2014, ranking it fourth among the infectious foodborne pathogens monitored in the FoodNet program [2]. Rates of cryptosporidiosis peak strongly in the late summer [101].

Contamination and Transmission

Acquisition of cryptosporidiosis usually occurs by way of food contamination by an infected food handler [13]. Animals raised for food may also serve as vehicles for transmission, and the parasite most commonly infects herd animals (e.g., cows, goats, sheep) [28]. Fresh produce may also become contaminated [28].

Clinical Presentation and Disease Course

Infection with Cryptosporidium causes noninflammatory, profuse watery diarrhea, and stomach cramps, upset stomach, and slight fever may also be present [13,56,157]. Some individuals may be asymptomatic [54,56,157]. The onset of symptoms is usually within 2 to 10 days [13,157]. Although infection is self-limiting in otherwise healthy individuals (10 to 14 days), it can become chronic in individuals with compromised immune systems [56,157].

Diagnostic Testing

Acid-fast staining of stool samples is a common means of testing [56]. Four commercial enzyme immunoassays are available for detecting oocyst antigens in stool specimens [54,56]. These tests must be ordered specifically [13]. Because shedding may be intermittent, three stool samples collected on different days should be tested before suspected cryptosporidiosis can be ruled out [54]. Cryptosporidium infection is a nationally notifiable disease.


Treatment is usually reserved for severe disease, and paromomycin (7-day course) is the recommended drug [13]. Treatment with nitazoxanide (3-day course) is suggested for children 1 to 11 years of age [13].


Cyclospora cayetanensis is an oocyst-forming, unicellular coccidium [54,156,158]. This species is the cause of all cyclosporiasis in humans [156,158]. Unlike Cryptosporidium, the oocyst of Cyclospora shed in stools is not infective [156].


Cyclosporiasis occurs most commonly in tropical and subtropical areas [77,156]. The disease is not known to be endemic in the United States; however, since 1990, at least 11 foodborne outbreaks of cyclosporiasis, affecting approximately 3,600 persons, have been documented in the United States and Canada [156,158]. In 2009, 141 cases of Cyclospora were reported to the CDC [158]. In 2014, FoodNet surveillance identified 26 cases of Cyclospora foodborne disease, an incidence rate of 0.05 per 100,000 persons [2]. During the period of 1997–2008, the CDC was notified of 1,110 laboratory-confirmed cases of sporadic cyclosporiasis, occurring in 37 states, including seven in which cyclosporiasis is not an explicitly reportable disease. More than one-third of the case-patients had a documented history of international travel [77].

Contamination and Transmission

Individuals become infected with Cyclospora by ingesting oocysts that have become environmentally contaminated [158]. Direct person-to-person transmission of Cyclospora is unlikely because shed oocysts are noninfectious [156]. Washing of contaminated produce decreases, but does not eliminate, the risk of transmission [54]. A large outbreak of Cyclospora on imported raspberries demonstrates the potential risk for transmission from contaminated water or infected food handlers [45].

Clinical Presentation and Disease Course

The onset of symptoms of cyclosporiasis is typically at least 1 week after ingestion of contaminated food (range: 2 to 14 days) [13,158]. Symptoms include profuse, usually watery diarrhea, loss of appetite with resultant weight loss, stomach cramps, nausea and vomiting, and fatigue [13,158]. Illness may become persistent (10 to 12 weeks) and relapsing if left untreated [13,158].

Diagnostic Testing and Treatment

Oocysts can be detected in stool samples, but testing must be specifically requested [13,158]. Cyclosporiasis is a nationally notifiable infection. The recommended treatment is oral TMP-SMX for 7 to 10 days [13,156,158].


Giardia infects the small intestine and biliary tract [56]. The parasite survives best in cool moist conditions, and the infective dose is one cyst [28].


Giardiasis affects approximately 2% of the U.S. adult population [28,159]. In 2008, one outbreak of laboratory-confirmed giardiasis affected eight individuals [14]. Similar to cryptosporidiosis, the incidence of giardiasis peaks in late summer [101].

Contamination and Transmission

Transmission of giardiasis is most commonly waterborne. However, infection can be transmitted through ingestion of cysts in food or by the fecal-oral route [28,159].

Clinical Presentation and Disease Course

The onset of symptoms is usually 1 week after ingestion of contaminated food [13,159]. Symptoms of giardiasis include watery diarrhea, abdominal pain, bloating, nausea, and vomiting, which usually last for 1 to 3 weeks or longer [156]. However, many individuals with giardiasis are asymptomatic [54,159]. Disaccharide intolerance develops in approximately 40% of individuals [28]. Lasting immunity after infection is common [28]. Chronic, debilitating giardiasis may occur and affects more adults than children [28,54].

Diagnostic Testing

Diagnosis can be determined through the identification of cysts in stained fecal smears, of trophozoites in a smear of stool or duodenal fluid, or of antigens in stool samples [28,54]. The sensitivity of diagnostic testing is higher when samples of diarrhea are tested and when testing is done on specimens obtained on alternating days [54]. At least three stool specimens may be needed for accurate results [13]. Giardiasis is a nationally notifiable disease.


Metronidazole is the recommended agent for treatment, although it is not FDA-approved for this indication [13,156]. Other options include tinidazole, nitazoxanide, paromomycin, furazolidone, or quinacrine [156].


Toxoplasma gondii is a protozoan parasite that infects most species of warm-blooded animals, including humans [156]. The parasite forms tissue cysts, most commonly in skeletal muscle, myocardium, and brain, and these cysts may remain throughout the life of the host [156].


Toxoplasmosis is one of the most common human infections worldwide. An estimated 22.5% of the population 12 years of age and older has been infected with the parasite [160]. It is more common in warm climates and at lower altitudes [156].

Contamination and Transmission

Cats are the main reservoirs of Toxoplasma gondii, and they become infected through carnivorism [56,156,160]. Although cats shed oocysts for only 1 to 2 weeks, large numbers may be shed, and they can survive in the environment for several months, with considerable resistance to disinfectants, freezing, and drying [156]. Humans become infected by ingesting raw or undercooked, cyst-contaminated meat (primarily pork) or by ingesting oocysts from fecally contaminated hands or food [54,156,160,161]. Congenital toxoplasmosis develops as a result of maternal infection during pregnancy [156,160].

Clinical Presentation and Disease Course

The incubation period for Toxoplasma gondii is 5 to 23 days [13]. Infected individuals are usually asymptomatic or have nonspecific symptoms [56,160]. Lymphadenopathy, with or without flu-like symptoms, will develop in approximately 10% to 20% of affected individuals [156]. Symptoms usually resolve within a few months to a year. Fetuses (infected through maternal transmission) and individuals with AIDS are the most susceptible to complications [54,160]. Although not evident at birth, mental retardation, visual impairment, and learning disabilities are likely to develop in children born with congenital toxoplasmosis [54,56,160].

Diagnostic Testing

Serologic testing for Toxoplasma gondii antibodies is the most commonly used diagnostic test [54,56,160]. It is important to note that chronic Toxoplasma gondii is difficult to diagnose in patients with HIV, as serologic tests are considered unreliable in this population [54].


Treatment is not necessary for individuals with healthy immune systems who are not pregnant. Pyrimethamine plus sulfadiazine has been used to treat central nervous system toxoplasmosis in individuals with HIV infection [156].


The natural toxins most associated with foodborne illness are marine toxins and mushroom toxins.


Ocean and gulf algal blooms that occur along coastal areas are capable of producing many marine toxins that lead to foodborne "shellfish poisoning." These blooms were previously known as "red tides" because of the red discoloration they cause in the ocean. Contrary to common belief, however, red tides are not well correlated to outbreaks of shellfish poisoning. Red tide refers to the phenomenon by which pigmented phytoplankton reproduce to such a high concentration that it turns the water red or dark brown. However, nontoxic algae can also cause red tides. With the hope of clarifying this, the scientific community has adopted the term harmful algae bloom (HAB) for toxic red tides. It should also be noted that most production of toxic algae is not accompanied by the red coloration of seawater [162].

Different types of blooms occur in various geographic locations in the United States, and the toxins produced differ according to the bloom (Table 12) [163]. Pyrodinium bahamense from harmful algal blooms have caused toxic pufferfish exclusively in the waters off the coast of Florida. Another toxin, tetrodotoxin, is also found in pufferfish, but in species that inhabit the shallow waters of the temperate and tropical zones [164]. These fish (e.g., ocean sunfishes, porcupine fishes, pufferfish [fugu]) are considered to be a delicacy in some cultures but are the most poisonous of all marine life [165]. Tetrodotoxin is among the most potent poisons known [166; 167].


Region of the United StatesHarmful Algal Bloom OrganismToxinHuman Illness
Gulf of Mexico (Florida, Texas), Hawaii, Pacific Islands, Puerto Rico, U.S. Virgin IslandsGambierdiscus spp., Prorocentrum spp.,Ostreopsis spp.Ciguatoxin, gambiertoxin, maitotoxinCiguatera fish poisoning
Northeast, Pacific Coast, AlaskaAlexandrium spp.SaxitoxinsParalytic shellfish poisoning
New England, Gulf of Mexico, Pacific CoastDinophysis spp.Okadaic acidDiarrheic shellfish poisoning
Gulf of Mexico, South-Atlantic CoastKarenia spp.BrevetoxinsNeurotoxic shellfish poisoning
Pacific Coast, Alaska, Gulf of Mexico, Northeast, Mid-Atlantic CoastPseudo-nitzschia spp.Domoic acidAmnesic shellfish poisoning
South-Atlantic Coast (Florida) Pyrodinium bahamense SaxitoxinsPufferfish poisoning

An additional toxin, scombroid, is caused by an elevated level of histamine in fish, most frequently tuna, albacore, and mackerel. The growth of certain bacteria and their decarboxylase enzyme activity causes this histamine formation [12]. The CDC has also identified non-scombroid fish (e.g., mahi-mahi) as a source of scombroid toxicity. Scombroid poisoning is the principal chemical agent type of foodborne disease found in the United States [168,169].

Some mouse bioassays are available as diagnostic tools to identify marine toxins [167,170]. However, testing with these assays is usually available only in specialized laboratories. Tetrodotoxin may be detected by fluorescent spectrometry [167]. Diagnosis of marine toxin poisoning is typically based on the clinical presentation and a history of recent ingestion of a particular type of seafood. If a portion of the type of seafood eaten is still available, it can be tested for the presence of the toxin. However, treatment does not depend on the type of toxin, so such testing is not essential.



Ciguatera fish poisoning is endemic in tropical and subtropical regions of the Pacific basin, Indian Ocean, and Caribbean [46,171]. The illness occurs much less frequently in the United States, with 178 single exposures reported in 2010 [171]. However, the CDC estimates that 2% to 10% of poisonings may not be reported [170]. Worldwide, an estimated 50,000 cases of ciguatera poisoning occur each year [46,172].

Clinical Presentation and Disease Course

Gastrointestinal symptoms (e.g., diarrhea, vomiting, abdominal pain) occur in more than 50% of individuals within 2 to 6 hours after ingestion of the toxin and may last 1 to 2 days; neurologic symptoms, which include reversal of temperature sensations, distal and perioral numbness and/or tingling, and dizziness, usually occur within a few hours to 3 days and can be persistent, lasting weeks to several months [13,170,171]. Within 2 to 5 days, cardiovascular symptoms (less common but potentially severe), such as bradycardia, hypotension, and T wave abnormalities, may appear [13,171].

Muscular weakness, paresthesias, and fatigue may last for weeks to months [170,171]. Women of childbearing age may have increased pain during menses, and intercourse may be painful for both men and women [46,173]. Among individuals with chronic symptoms, relapse may occur after stressful conditions or ingestion of fish (any type), alcohol, caffeine, or nuts, 3 to 6 months after the initial poisoning [170,174].

Serious illness may involve severe hypotension with bradycardia, respiratory difficulties, and paralysis [171,174]. Death as a result of respiratory and cardiovascular failure occurs in approximately 2% of infected individuals [175]. Children are most vulnerable to severe illness [176].


Intravenous mannitol should be given within 24 to 48 hours to relieve neurologic symptoms [13,170,176]. Gut emptying and charcoal decontamination is recommended acutely; however, gastrointestinal symptoms may prohibit this measure [170]. Atropine may be necessary for bradycardia, and dopamine or calcium gluconate may be administered for shock [171]. Amitriptyline (and similar medications) may be effective in relieving chronic symptoms of fatigue and paresthesias [170]. Opiates and barbiturates should be avoided, as they may interact with the toxin and cause hypotension [170].

Shellfish Toxins


Seven outbreaks of foodborne disease attributed to shellfish poisoning (three neurotoxic, four paralytic) were reported in 2007 [172]. In 2011, health officials in Alaska identified a total of eight confirmed and 13 probable cases of paralytic shellfish poisoning from consumption of noncommercially harvested Alaskan shellfish [177]. Children are particularly sensitive to paralytic shellfish toxins, and the mortality rate is particularly high in children [178]. Individuals older than 65 years of age are predisposed to the severe neurologic effects of amnesic shellfish poisoning [13]. The incidence of shellfish poisoning has been declining as a result of careful monitoring, beach closures, and improved public awareness [162].

Clinical Presentation and Disease Course

The shellfish toxins differ according to the timing from ingestion of the toxin to the onset of symptoms, the symptoms caused, and the severity of illness [13,170].

Paralytic shellfish poisoning is the most severe type of illness. It has a mortality rate of 6% worldwide (higher in developing countries) [162]. This toxin (e.g., saxitoxin) causes tingling, burning, numbness, drowsiness, incoherent speech, and respiratory paralysis within 15 minutes to 3 hours after ingestion [162,170]. Other symptoms may include headache, dizziness, nausea, vomiting, rapid-onset pain, and anuria [170]. With severe illness, respiratory paralysis is common, occurring within 2 to 12 hours in severe poisoning, and persisting for as long as 72 hours to one week. Death may occur if respiratory support is not provided [162,170]. Patients surviving 9 hours usually recover, and recovery begins 12 hours after the onset of symptoms and may take a few days to resolve completely [170].

With diarrheic shellfish poisoning, symptoms occur 30 minutes to 12 hours after ingestion of the toxin [162,170]. Diarrhea occurs in almost all affected individuals (92%), and nausea and vomiting are also common (80% and 79%, respectively) [170]. Other symptoms may include abdominal pain, chills, headache, and fever [13]. Illness usually resolves within 2 to 3 days, and recovery is complete, with no aftereffects [13,170]. No cases of death from diarrheic shellfish poisoning have been reported [162].

Symptoms of neurotoxic shellfish poisoning occur within a few minutes to 3 hours. The toxin (e.g., brevetoxin) causes both gastrointestinal and neurologic symptoms, generally mild and self-limited [162,179]. Gastrointestinal symptoms may include diarrhea and vomiting. Neurologic symptoms may include tingling and/or numbness of the lips, tongue, and throat; muscle aches; dizziness; and reversal of temperature sensations [13,162,180]. Neurotoxic shellfish poisoning is the least common of the shellfish poisonings and is less severe than ciguatera poisoning. Recovery is complete within hours to 2 to 3 days [13,170]. No fatalities have been reported [179].

Amnesic shellfish poisoning (e.g., domoic acid poisoning) causes symptoms of gastroenteritis (nausea, vomiting, abdominal cramps, diarrhea) within 24 hours after ingestion [170]. Although a potentially serious poisoning, only one human outbreak has been reported [181]. The primary symptom was vomiting, occurring in approximately 76% of infected individuals; abdominal cramps occurred in about half of those affected [170,181]. In cases of severe poisoning, neurologic symptoms (i.e., dizziness, headache, seizures, disorientation, short-term memory loss, respiratory difficulty, coma) occur within 48 hours [170]. Cognitive dysfunction is most likely to be permanent in individuals who have neurologic symptoms within 48 hours after ingestion of the toxin, in men older than 60 years of age, and in individuals who have pre-existing conditions such as renal disease, diabetes, and hypertension with a history of transient ischemic attacks [170]. All reported fatalities associated with this toxin have involved individuals older than 65 years of age [170].


Gut decontamination and administration of activated charcoal or dilute bicarbonate solution is recommended when shellfish poisoning is diagnosed during the early stage of illness [170]. Treatment should include oral rehydration therapy, as it may enhance renal excretion of the toxin [170]. Respiratory support is recommended for individuals with moderately severe cases [13]. Anticholinesterase agents are not advised and may be harmful [170,182]. If seizures occur, intravenous diazepam or phenobarbital is recommended; the seizures may be resistant to phenytoin [170,183].

Tetrodotoxin and Saxitoxin (Pufferfish Toxins)


Foodborne illness caused by ingestion of pufferfish (tetrodotoxin [TTX]) is rare in the United States [162]. Most reports of pufferfish poisoning occur due to unskilled preparation by unlicensed cooks. The FDA allows importation into the United States through a single certified Japanese importer, but illegal importation continues and has resulted in multiple poisonings [184; 185]. The minimum lethal dose of TTX is estimated to be 2 mg but can vary depending on age and existing comorbidities. Reports of toxicity with consumption of 0.25–1.5 ounces of incorrectly prepared pufferfish has been reported by the CDC [162].

Clinical Presentation and Disease Course

Symptoms typically occur 5 to 45 minutes after ingestion of the toxin but may be observed as late as several hours later [13,28,162]. Higher toxin ingestion is associated with a more rapid onset of symptoms [162]. Pufferfish poisoning is characterized by slight numbness of the lips and tongue, followed by increasing paraesthesia in the face and extremities and sensations of lightness or floating [28,180]. Gastrointestinal symptoms (vomiting, diarrhea, abdominal pain) and difficulty walking may occur. As paralysis increases, patients are unable to move and have respiratory distress. Decreased levels of consciousness, seizures, and death have occurred in as few as 17 minutes [162]. Without treatment, death occurs in 4 to 8 hours [13,28]. Patients are conscious and often lucid until shortly before death [180]. The mortality rate has been reported to be nearly 60% [186]. If treatment is begun before poisoning becomes severe, life-threatening effects are highly unlikely after 24 hours [166].


There is no known antidote for pufferfish poisoning [180]. Intravenous therapy, gastric lavage, and activated charcoal are recommended to reduce absorption of the toxin [165]. Individuals who have moderate-to-severe reactions to tetrodotoxin should be admitted to an intensive care unit, and respiratory support may be needed for 24 to 72 hours [162,166,180]. Atropine can be used to treat bradycardia in severe cases [187].



Scombroid toxin was the causative agent in 25 foodborne outbreaks reported in the United States in 2013 (22 confirmed and 3 suspected), affecting a total of 68 individuals [14].

Clinical Presentation and Disease Course

Symptoms are immediate, usually occurring within 1 minute to 3 hours [13,188]. Symptoms include flushing, rash on the upper body, dizziness, and burning sensation of the skin, mouth, and throat [13,188]. Other symptoms may include throbbing headache and an unusual taste in the mouth, frequently described as peppery or pungent, but in some cases bitter or metallic [188]. Symptoms usually last about 3 to 6 hours but may persist for several days [13,189]. Patients with comorbidities such as coronary artery disease may experience acute coronary syndrome caused by scombroid-associated tachycardia and hypotension [28]. Death is rare.


Treatment with antihistamine medication is recommended, and rehydration therapy (oral or intravenous) may also be needed [13,188].


Mushrooms can contain one or more of several toxins, including amanitin, gyromitrin, orellanine, muscarine, ibotenic acid/muscimol, and psilocybin, which are produced by the mushrooms themselves [28,190]. Poisonous mushrooms are referred to as toadstools.

Mushroom poisoning is caused by the ingestion of raw or cooked toadstools. Most mushrooms that cause human poisoning cannot be made nontoxic by cooking, canning, freezing, or any other means of processing [28,190]. The chemical composition of most mushroom toxins is unknown, and poisonings are therefore categorized according to their physiologic effects: protoplasmic poisons (amanitin, gyromitrin, orellanine), neurotoxins (muscarine, ibotenic acid/muscimol, psilocybin), gastrointestinal irritants, and disulfiram-like toxins.

As with marine toxins, the diagnosis of mushroom poisoning is based on the clinical presentation and a history of mushroom ingestion. A commercial radioimmunoassay is available to detect mushroom toxin in urine and plasma, but the time needed for incubation and testing may not be warranted. Identification of the mushroom species ingested is important; however, this it is not often possible. Other food sources should be ruled out before the mushroom is definitively determined to be the cause [28].


The American Association of Poison Control Centers reported 5,644 mushroom exposures in 2008, with 39 major outcomes and four deaths [191]. Poisonings usually result from a novice misidentifying a wild mushroom, a non-native of the United States picking (and consuming) a mushroom that appears similar to one in his or her native country, or a person seeking to consume a mushroom with psychoactive compounds [28,191]. Children, the elderly, and persons with disabilities are at highest risk for the development of serious complications from mushroom poisoning [190].

Clinical Presentation and Disease Course

The clinical presentation and disease course vary according to the toxin. Diagnosis relies on the timing between ingestion, the onset of symptoms, and the amount of mushrooms ingested (Table 13) [28,190].


SymptomsOnsetCauseDisease Course
Nausea, abdominal discomfort (sometimes with diarrhea and vomiting)15 minutes to 2 hoursUnknown toxins (from numerous genera)Rapid and complete recovery; severe illness may cause symptoms to last 2 to 3 days and require fluid replacement
Excessive sweating, lacrimation, salivation15 to 30 minutesMuscarineComplete recovery within approximately 2 hours; death is rare but may result from cardiac or respiratory failure
Inebriation or hallucinations without drowsiness or sleep15 minutes to 2 hoursPsilocybinComplete and spontaneous recovery occurs within 5 to 10 hours; if large amount of toxin ingested, recovery may take up to 24 hours; more severe in children
Delirium with sleepiness or coma1 to 2 hoursIbotenic acid/ muscimolAlternating periods of drowsiness and excitement occur for several hours, followed by total recovery
Feeling of abdominal fullness, severe headache, vomiting (no diarrhea)6 to 10 hoursGyromitrinComplete recovery occurs within 2 to 6 days; correction of metabolic acidosis may be required; some deaths have occurred as a result of liver failure
Persistent and intense vomiting; abdominal pain; profuse, watery diarrhea6 to 12 hoursAmanitinApparent recovery occurs a few hours after onset of symptoms, followed by a symptom-free period of 3 to 5 days, and subsequently by a period of jaundice, loss of strength, coma, and often death
Intense, burning thirst and frequent urination, followed by gastrointestinal disturbances, headache, pain in the limbs, spasms, and loss of consciousness3 to 21 daysOrellanineRecovery (including recovery of renal function) may require several months in cases of less severe poisoning; death from kidney failure may occur in cases of severe poisoning
Flushing; palpitations; rapid heartbeat; rapid, labored breathing within 30 minutes to 2 hours after consuming alcoholWithin 72 hoursCoprineRecovery is spontaneous and complete within a few to several hours after onset of symptoms


The treatment of most mushroom poisonings consists primarily of supportive care. For severe cases (as with ingestion of amanitin), life-support measures may be necessary [190].


The prevention of foodborne illness is essential to maintaining the health of individuals as well as protecting overall public health. Although infectious foodborne diseases usually produce mild symptoms and are self-limited in most people, the course of disease can be complicated in many, especially young children, older individuals, and people with a compromised immune system. The ease with which many foodborne pathogens can be transmitted heightens the need to prevent secondary transmission. Preventive measures are also important to avoid illness from natural toxins. The prevention of foodborne illness involves three main features: food safety, vaccination, and education.


Prevention of foodborne illness requires a focus on food safety at every point on the farm-to-table continuum. Several government agencies, including the USDA, the FDA, and the CDC, collaborate to ensure the safety of all foods for human consumption and to investigate and analyze foodborne-illness outbreaks.

Food safety depends on safeguards at several key points on the continuum, including:

  • Pre-harvest

  • Slaughter and processing

  • Food distribution

  • Food preparation/consumption

Both the USDA and the FDA regulate the safety of the food supply. These government agencies inspect food products, develop and enforce food safety regulations, test suspect foods, and work with industry to improve safety practices. The USDA oversees meat, poultry, and processed egg products, and the FDA is responsible for nonmeat products such as seafood, fruits, vegetables, and shell eggs. Initiatives and research efforts regarding food safety can be found at the Food Safety website, which provides links to news and research reports from these agencies and the state and local regulatory departments with which they collaborate.

In mid-2009, the House Energy and Commerce Committee passed legislation to reform the U.S. food safety system, granting the FDA more authority and funding. The bill also calls for a new focus on prevention, with a shared responsibility between the FDA and food manufacturers. The FDA Food Safety Modernization Act (FSMA), which was enacted in January 2011, is intended to help reduce foodborne illness by means of a paradigm shift from responding to contamination of the U.S. food supply to preventing contamination. The law establishes new prevention measures for food regulated by the FDA [192,193].

State and local health departments collaborate with federal organizations to prevent the transmission of infectious and noninfectious foodborne illnesses. These departments have issued requirements about food handlers in a variety of settings (e.g., farm work, food distribution, food service), the primary source of viral foodborne illnesses. For example, many state and local health departments require that food handlers who have gastroenteritis refrain from working until 2 or 3 days after symptoms have resolved [146]. State and local health departments also issue policies and guidelines regarding such preventive measures as proper food storage and heating temperatures, appropriate hand hygiene, the cleaning and disinfection of food preparation surfaces, and the disposal of any food or nonfood items that may have been contaminated. Routine inspections are carried out to ensure compliance with these guidelines.

Prevention of infection with marine toxins is a major concern. To ensure that commercially available shellfish are safe for consumption, rigorous shellfish monitoring programs are established in all states. When harmful algal blooms (the source of shellfish poisoning) become high, state alerts are given to ban shellfish harvesting. Monitoring of blooms also helps to reduce the likelihood of ciguatera poisoning. In addition, the Ecology and Oceanography of Harmful Algal Blooms Program and the Monitoring and Event Response for Harmful Algal Blooms Program have funded approximately $100 million in marine research to gain a better understanding of harmful algae blooms [163].

The commercial and personal importation of pufferfish into the United States is heavily restricted to avoid tetrodotoxin poisoning, and the state of Florida bans commercial and recreational harvesting of pufferfish from the waters of most counties on the East Coast because of persistent saxitoxin toxicity [194]. The FDA advises that tetrodotoxin has not been found in northern pufferfish from the mid-Atlantic coastal waters (typically between Virginia and New York), but potential risk still exists without routine toxin screening [194].


Vaccines have been developed for two viruses that can be transmitted through food: rotavirus and hepatitis A. Two vaccines are now available for rotavirus: RV5 (RotaTeq) was approved for use in 2006, and RV1 (Rotarix) was approved in 2008. The American Academy of Pediatrics recommends routine vaccination with either vaccine, without noting a preference for either one [195]. RV5 is given orally in a three-dose series, at 2, 4, and 6 months of age. RV1 is given orally in a two-dose series, at 2 and 4 months of age [195]. Studies have shown that the vaccines provide 85% to 95% protection against severe rotavirus and 74% to 87% protection against any rotavirus illness [195,196].

Vaccines are also available for hepatitis A virus. The CDC and the American Academy of Pediatrics recommend that vaccination against hepatitis A be included in the early childhood immunization schedule [197]. The vaccine is given (intramuscularly) in a two-dose series, with the first dose given at 12 months and the second dose given 6 to 18 months later, depending on the vaccine. The rate of hepatitis A in the United States was 88% lower in 2003 than the rate in 1996 before immunization was initiated [198].

Among individuals who were not vaccinated in childhood, those at increased risk of the virus should receive the vaccine. This includes individuals traveling to or living in areas with an intermediate or high endemicity for the infection, men who have sex with men, users of either injectable or noninjectable illicit drugs, individuals treated with clotting factors, and individuals who work with hepatitis A virus in the laboratory setting [198].


Education about preventing foodborne illness requires a multifaceted approach that includes heightening awareness and enhancing knowledge about foodborne illnesses at the individual level and supporting broad public education campaigns. In addition, physicians and other healthcare professionals are encouraged to remain up-to-date on foodborne illnesses and their diagnosis and management.

Patient Education

Healthcare practitioners should take every available opportunity to provide their patients with information about the prevention of foodborne illnesses in the home and while traveling, focusing on the specific needs of certain populations. For example, pregnant women should be cautioned about the potential risks of infection with Listeria and Toxoplasma gondii. Parents should be advised of the need to avoid secondary transmission of viruses by keeping children with gastroenteritis out of daycare or school until symptoms have resolved. Individuals preparing for international travel (especially to developing countries) should receive appropriate immunizations and will benefit from a description of ways to prevent traveler's diarrhea.

Educational resources for patients are available online, and some websites offer downloadable fact sheets and posters. The USDA Food Safety and Inspection Service website offers fact sheets on food safety for the general population as well for as a wide range of target populations, including ethnic minorities, older individuals, pregnant women, and individuals with cancer, diabetes, or HIV. Fact sheets are also available for preparing food for large groups, such as church suppers and other community meals. Consumer brochures and posters are commonly available in English and Spanish, and some are tailored to consumers' cultural food practices.

Individuals in high-risk groups are often confused about proper safe handling processes and are resistant to many food safety recommendations [199]. The findings of studies suggest that the primary barrier to accepting recommendations is the lack of understanding about the importance of the precautions [199,200]. Cultural and economic factors as well as simple food hygiene habits have also been shown to be barriers [201,202]. When discussing foodborne illnesses with high-risk individuals, healthcare professionals should emphasize why certain foods should be avoided or be prepared in a designated manner [199,203]. Providing consistent information in a patient-friendly form is key to patient compliance [204].

It has been suggested that education on food safety is most effective when it is targeted to changing behaviors that most likely result in foodborne illness [22]. The following behaviors have been recommended as the primary focus of education on food safety [22,205]:

  • Handwashing

  • Use of a thermometer to cook foods adequately

  • Avoidance of cross-contamination

Also recommended (of secondary importance) are keeping foods at safe temperatures and avoidance of foods likely to be contaminated [22]. These behaviors were also emphasized by food experts who were asked to identify and rank food-handling and consumption behaviors as being of primary or secondary importance in preventing infection with 13 foodborne pathogens [21]. According to these experts, the following are of primary importance [21]:

  • Keeping foods at safe temperatures (Bacillus cereus and Clostridium perfringens)

  • Use of a thermometer to cook foods adequately (Campylobacter jejuni,Salmonella, STEC O157, Toxoplasmagondii, and Yersinia)

  • Hand washing (Shigella)

  • Avoidance of certain foods that are likely to be contaminated (Listeria, noroviruses, and Vibrio)

In addition, the experts indicated that keeping foods at safe temperatures were of secondary importance in preventing foodborne infection with Staphylococcus aureus, and avoidance of cross-contamination was of secondary importance in preventing infection with most pathogens [21].

Public Education Campaigns

The key messages identified as being of primary importance for education form the core of public health education campaigns on food safety. The most prominent campaigns have included "BAC Down!," "Be Safe," and "Ounce of Prevention."

"BAC Down!" is a collaborative initiative of the FDA and the Partnership for Food Safety Education. Its primary objective is to urge consumers to keep their refrigerators at 40°F or below to prevent foodborne illness such as listeriosis. "BAC Down!" uses the media, the Partnership's website, and eye-catching strategies for information dissemination at grocery stores. The Partnership also manages "Be Safe," which emphasizes four basic safe food-handling behaviors: Clean, Separate, Cook, and Chill. In addition, education on six steps to safer fresh fruits and vegetables and other topics are available in Spanish on the website.

The popular and successful "Ounce of Prevention" campaign is led by the National Center for Infectious Diseases, the CDC's coordinating center for infectious diseases, in partnership with Reckitt Benckiser, Inc. This campaign provides health educators and consumers with information and tips to prevent infectious diseases, including how to handle, store, and cook foods safely.

Education for Healthcare Professionals

Practitioners are urged to seek supplemental information regarding foodborne agents, particularly agents that are prevalent in their geographic location. There is a variety of print and Internet information available on infectious foodborne agents (Resources). Many cases of foodborne illness affect individuals in the community, but outbreaks, especially of viral etiology, often occur in hospitals and long-term care facilities. Nevertheless, no foodborne illness risk management guidelines exist specifically for U.S. hospitals [206]. Because of this, healthcare professionals should also be familiar with the evidence-based isolation and control guidelines for infectious diseases developed by the Healthcare Infection Control Practices Advisory Committee [61].


A variety of infectious and noninfectious foodborne diseases cause substantial morbidity and mortality in the United States each year. In addition to the high number of sporadic cases and cases related to outbreaks, researchers estimate that thousands of cases are unreported or undiagnosed annually. Although a steady decline in the incidence of several foodborne infections was observed between 1996 and 2007, the composite annual rate of foodborne disease has remained stable since that time [207]. Several foodborne-illness outbreaks in the last several decades are continued evidence of the threat to public health and the need for improved food safety.

Bacteria (especially Salmonella) and viruses (especially norovirus) are the primary causes of most foodborne illness and outbreaks. Parasitic causes are rare in the United States. Noninfectious agents, especially natural toxins, are also important causes of foodborne disease. Among natural toxins, marine toxins and mushroom toxins are responsible for most cases and outbreaks of foodborne disease. Although uncommon, these toxin-related illnesses can be severe and life-threatening.

The diagnosis of foodborne disease can be challenging because the symptoms are often similar to those associated with other conditions. The patient history is key to the identification of an illness with a foodborne etiology, and practitioners should know the appropriate questions to elicit the information essential to making an accurate diagnosis. Physicians and other healthcare practitioners should also be familiar with the mechanisms of contamination and transmission of foodborne pathogens and toxins, the characteristic symptoms of food-related illnesses, and the appropriate reporting procedures. Healthcare professionals play a key role in preventing foodborne disease by providing education and resources on food safety and secondary transmission.


Centers for Disease Control and Prevention:
"An Ounce of Prevention" Campaign
Provides information and tips on preventing infectious diseases.
Centers for Disease Control and Prevention: Epidemic Information Exchange (Epi-X)
Portal through which state and local health departments, poison control centers, and other public health professionals can access and share preliminary health surveillance information.
Centers for Disease Control and Prevention: Food Safety
Information on food safety, prevention of illness for high-risk populations, and outbreaks.
Centers for Disease Control and Prevention: Outbreak Response Team
Collaborates with network of epidemiologists and other public health officials who investigate outbreaks of foodborne, waterborne, and other enteric illnesses in the United States.
Centers for Disease Control and Prevention: Traveler's Health
Current information regarding outbreaks in worldwide destinations.
Council of State and Territorial Epidemiologists
Represents public health epidemiologists.
Fight BAC! Partnership for Food Safety Education
Provides information about protecting health through safe food handling and hygiene.
Consumer advice, information on foodborne pathogens, news on outbreaks and recalls.
Pathogen Portal: The Bioinformatics Resource Centers Portal
Sponsored by the National Institute of Allergy and Infectious Diseases. Provides resources to members of the scientific community conducting research on organisms causing emerging or re-emerging diseases.
American Academy of Pediatrics
Red Book: 2012 Report of the Committee on Infectious Diseases
U.S. Food and Drug Administration: Bad Bug Book (2nd Edition)
Provides current information about the major known agents that cause foodborne illness.
U.S. Food and Drug Administration: Foods
Information on foodborne illness, news on outbreaks, alerts and recalls.
USDA Food Safety and Inspection Service (FSIS)
Variety of downloadable fact sheets on food safety, with some targeted to specific populations and others describing appropriate preparation of specific foods.

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Evidence-Based Practice Recommendations Citations

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