For the disease most commonly referred to as food poisoning, seeSalmonellosis.
Foodborne illness (also known asfoodborne disease andfood poisoning)[1] is anyillness resulting from thecontamination of food by pathogenicbacteria,viruses, orparasites,[2] as well asprions (the agents ofmad cow disease), andtoxins such asaflatoxins in peanuts,poisonous mushrooms, and various species ofbeans that have not been boiled for at least 10 minutes. While contaminants directly cause some symptoms, many effects of foodborne illness result from the body's immune response to these agents, which can vary significantly between individuals and populations based on prior exposure.[3]
Symptoms vary depending on the cause. They often includevomiting,fever, and aches, and may includediarrhea. Bouts of vomiting can be repeated with an extended delay in between. This is because even if infected food was eliminated from the stomach in the first bout,microbes, like bacteria (if applicable), can pass through thestomach into theintestine and begin to multiply. Some types of microbes stay in the intestine.
For contaminants requiring anincubation period, symptoms may not manifest for hours to days, depending on the cause and on the quantity of consumption. Longer incubation periods tend to cause those affected to not associate the symptoms with the item consumed, so they may misattribute the symptoms togastroenteritis, for example.
Foodborne illness usually arises from improper handling, preparation, orfood storage.[citation needed] However, many cases result from the immune system's response to unfamiliar microbes rather than from direct microbial damage, explaining why local populations often tolerate food that sickens travelers.[5]
Goodhygiene practices before, during, and after food preparation can reduce the chances of contracting an illness. There is a consensus in the public health community that regular hand-washing is one of the most effective defenses against the spread of foodborne illness.[citation needed] The action of monitoring food to ensure that it will not cause foodborne illness is known asfood safety.
In the past, bacterial infections were thought to be more prevalent because few places had the capability to test fornorovirus and no active surveillance was being done for this particular agent. Toxins from bacterial infections are delayed because the bacteria need time to multiply. As a result, symptoms associated with intoxication are usually not seen until 12–72 hours or more after eating contaminated food. However, in some cases, such as Staphylococcal food poisoning, the onset of illness can be as soon as 30 minutes after ingesting contaminated food.[7]
Salmonella
A 2022 study concluded that washing uncooked chicken could increase the risk ofpathogen transfer, and that specific washing conditions can decrease the risk of transfer.[8][9]
Salmonellaspp. – itsS. typhimurium infection is caused by consumption of eggs or poultry that are not adequately cooked or by other interactive human-animal pathogens[13][14][15]
Scandinavian outbreaks ofYersinia enterocolitica have recently increased to an annual basis, connected to the non-canonical contamination of pre-washed salad.[17]
Proper storage andrefrigeration offood help in the prevention of food poisoning.
Governments have the primary mandate of ensuring safe food for all, however all actors in the food chain are responsible to ensure only safe food reaches the consumer, thus preventing foodborne illnesses. This is achieved through the implementation of strict hygiene rules and a public veterinary and phytosanitary service that monitors animal products throughout thefood chain, from farming to delivery in shops and restaurants. This regulation includes:
traceability: the origin of the ingredients (farm of origin, identification of the crop or animal) and where and when it has been processed must be known in the final product; in this way, the origin of the disease can be traced and resolved (and possibly penalized), and the final products can be removed from sale if a problem is detected;
enforcement of hygiene procedures such asHACCP and the "cold chain";
power of control and of law enforcement ofveterinarians.
In August 2006, the United StatesFood and Drug Administration approvedphage therapy which involves spraying meat with viruses that infect bacteria, and thus preventing infection. This has raised concerns because withoutmandatory labeling, consumers would not know that meat and poultry products have been treated with the spray.[18]
At home, prevention mainly consists of goodfood safety practices. Many forms of bacterial poisoning can be prevented by cooking food sufficiently, and either eating it quickly or refrigerating it effectively.[2] Many toxins, however, are not destroyed by heat treatment.
Techniques that help prevent food borne illness in the kitchen are hand washing, rinsingproduce,[19] preventing cross-contamination, proper storage, and maintaining cooking temperatures. In general, freezing or refrigerating prevents virtually all bacteria from growing, and heating food sufficiently kills parasites, viruses, and most bacteria. Bacteria grow most rapidly at the range of temperatures between 40 and 140 °F (4 and 60 °C), called the "danger zone". Storing food below or above the "danger zone" can effectively limit the production of toxins. For storing leftovers, the food must be put in shallow containersfor quick cooling and must be refrigerated within two hours. When food is reheated, it must reach an internal temperature of 165 °F (74 °C) or until hot or steaming to kill bacteria.[20]
Enterotoxins are potent compounds produced by various microorganisms that specifically target and damage the intestines, causing many of the most rapid and severe forms of food poisoning. Unlike bacterial infections that require live organisms to multiply in the gut, enterotoxins (a type ofexotoxin) can cause illness even when the bacteria that produced them have been killed through cooking or other preservation methods.
Enterotoxins can produce illness even when the microbes that produced them have been killed. Symptom onset varies with the toxin but may be rapid in onset, as in the case of enterotoxins ofStaphylococcus aureus in which symptoms appear in one to six hours.[21] This causes intensevomiting including or not including diarrhea (resulting instaphylococcal enteritis), and staphylococcal enterotoxins (most commonlystaphylococcal enterotoxin A but also includingstaphylococcal enterotoxin B) are the most commonly reported enterotoxins although cases of poisoning are likely underestimated.[22] It occurs mainly in cooked and processed foods due to competition with other biota in raw foods, and humans are the main cause of contamination as a substantial percentage of humans are persistent carriers ofS. aureus.[22] The CDC has estimated about 240,000 cases per year in the United States.[23]
Traditional preservation methods like fermentation, sun-drying, and smoking have been used for centuries in non-Western cultures. These methods not only preserve food but also enhance nutritional value and can reduce foodborne illnesses by creating environments that inhibit harmful bacteria.[24]
The notion that Western food safety standards are universally applicable is challenged by the effectiveness of these traditional methods. In cultures without access to modern refrigeration, traditional preservation techniques adapted to local climates and resources have proven effective in preventing spoilage and illness.[25] Community knowledge and social practices can be as critical as technical standards in ensuring food safety, differing significantly from the regulatory focus in Western systems.[26]
The termalimentary mycotoxicosis refers to the effect of poisoning bymycotoxins through food consumption. The term mycotoxin is usually reserved for the toxic chemical compounds naturally produced by fungi that readily colonize crops under given temperature and moisture conditions. Mycotoxins can have important effects on human and animal health. For example, an outbreak which occurred in the UK during 1960 caused the death of 100,000 turkeys which had consumedaflatoxin-contaminated peanut meal. In theUSSR inWorld War II, 5,000 people died due toalimentary toxic aleukia (ALA).[27] In Kenya, mycotoxins led to the death of 125 people in 2004, after consumption of contaminated grains.[28] In animals, mycotoxicosis targets organ systems such as liver and digestive system. Other effects can include reduced productivity and suppression of the immune system, thus pre-disposing the animals to other secondary infections.[29]The common foodborneMycotoxins include:
Aflatoxins – originating fromAspergillus parasiticus andAspergillus flavus. They are frequently found in tree nuts, peanuts, maize, sorghum and other oilseeds, including corn and cottonseeds. The pronounced forms of aflatoxins are those of B1, B2, G1, and G2, amongst which Aflatoxin B1 predominantly targets the liver, which will result innecrosis,cirrhosis, andcarcinoma. Other forms of aflatoxins exist asmetabolites such as Aflatoxin M1.[30][31] In the US, the acceptable level of total aflatoxins in foods is less than 20μg/kg, except for Aflatoxin M1 in milk, which should be less than 0.5μg/kg The official document can be found atFDA's website.[32][33] The European union has more stringent standards, set at 10 μg/kg in cereals and cereal products. These references are also adopted in other countries.[34][35]
Ochratoxins – In Australia, The Limit of Reporting (LOR) level forochratoxin A (OTA) analyses in 20th Australian Total Diet Survey was 1 μg/kg,[44] whereas theEC restricts the content of OTA to 5 μg/kg in cereal commodities, 3 μg/kg in processed products and 10 μg/kg in dried vine fruits.[45]
Patulin – Currently, this toxin has been advisably regulated on fruit products. TheEC and theFDA have limited it to under 50 μg/kg for fruit juice and fruit nectar, while limits of 25 μg/kg for solid-contained fruit products and 10 μg/kg for baby foods were specified by the EC.[45][46]
Trichothecenes – sourced fromCephalosporium,Fusarium,Myrothecium,Stachybotrys, andTrichoderma. The toxins are usually found in molded maize, wheat, corn, peanuts and rice, or animal feed of hay and straw.[48][49] Four trichothecenes,T-2 toxin,HT-2 toxin,diacetoxyscirpenol (DAS), anddeoxynivalenol (DON) have been most commonly encountered by humans and animals. The consequences of oral intake of, or dermal exposure to, the toxins will result in alimentary toxic aleukia,neutropenia,aplastic anemia,thrombocytopenia and/or skin irritation.[50][51][52] In 1993, theFDA issued a document for the content limits of DON in food and animal feed at an advisory level.[53] In 2003, US published a patent that is very promising for farmers to produce a trichothecene-resistant crop.[54]
Viral infections make up perhaps one third of cases of food poisoning in developed countries. In the US, more than 50% of cases are viral andnoroviruses are the most common foodborne illness, causing 57% of outbreaks in 2004. Foodborne viral infection are usually of intermediate (1–3 days)incubation period, causing illnesses which are self-limited in otherwise healthy individuals; they are similar to the bacterial forms described above.[citation needed]
Hepatitis A is distinguished from other viral causes by its prolonged (2–6 week) incubation period and its ability to spread beyond the stomach and intestines into theliver. It often results injaundice, or yellowing of the skin, but rarely leads to chronic liver dysfunction. The virus has been found to cause infection due to the consumption of fresh-cut produce which has fecal contamination.[55][56]
Several foods can naturally containtoxins, many of which are not produced by bacteria. Plants in particular may be toxic; animals which are naturally poisonous to eat are rare. In evolutionary terms, animals can escape being eaten by fleeing; plants can use only passive defenses such as poisons and distasteful substances, for examplecapsaicin inchili peppers and pungentsulfur compounds ingarlic andonions. Most animal poisons are not synthesised by the animal, but acquired by eating poisonous plants to which the animal is immune, or by bacterial action.[citation needed]
Ptomaine poisoning was a myth that persisted in the public consciousness, in newspaper headlines, and legal cases as an official diagnosis, decades after it had been scientifically disproven in the 1910s.[65]
In the 19th century, the Italian chemistFrancesco Selmi, of Bologna, introduced the generic nameptomaine (from Greekptōma, "fall, fallen body, corpse") foralkaloids found in decaying animal and vegetable matter, especially (as reflected in their names)putrescine andcadaverine.[66] The 1892Merck's Bulletin stated, "We name such products of bacterial origin ptomaines; and the specialalkaloid produced by thecomma bacillus is variously named Cadaverine, Putrescine, etc."[67] whileThe Lancet stated, "The chemical ferments produced in the system, the... ptomaines which may exercise so disastrous an influence."[68] It is now known that the "disastrous... influence" is due to the direct action ofbacteria and only slightly due to the alkaloids. Thus, the use of the phrase "ptomaine poisoning" is now largely obsolete.[citation needed]
At aCommunist political convention inMassillon, Ohio,[69] and aboard a cruise ship in Washington, D.C., hundreds of people were sickened in separate incidents by taintedpotato salad, during a single week in 1932, drawing national attention to the dangers of so-called "ptomaine poisoning" in the pages of the American news weekly,Time.[70] In 1944, another newspaper article reported that over 150 people in Chicago were hospitalized with ptomaine poisoning, apparently fromrice pudding served by a restaurant chain.[71]
The delay between the consumption of contaminated food and the appearance of the firstsymptoms of illness is called theincubation period. This ranges from hours to days (and rarely months or even years, such as in the case oflisteriosis orbovine spongiform encephalopathy), depending on the agent, and on how much was consumed. If symptoms occur within one to six hours after eating the food, it suggests that it is caused by a bacterial toxin or a chemical rather than live bacteria.[citation needed]
The long incubation period of many foodborne illnesses tends to cause those affected to attribute their symptoms togastroenteritis.[72]
During the incubation period,microbes pass through thestomach into theintestine, attach to thecells lining the intestinal walls, and begin to multiply there. Some types of microbes stay in the intestine, some produce atoxin that is absorbed into thebloodstream, and some can directly invade the deeper body tissues. The symptoms produced depend on the type of microbe.[73]
In cases of foodborne illness, particularly traveler's diarrhea, symptoms often result from the immune system's response rather than direct pathogen damage. This inflammatory response can lead to post-infectious irritable bowel syndrome (PI-IBS), where 3-20% of affected individuals develop chronic gastrointestinal symptoms even after the pathogen is cleared.[74] This suggests that the body's immune reaction, particularly inflammation, plays a significant role in both acute symptoms and long-term effects of foodborne illness.[75]
Theinfectious dose is the amount of agent that must be consumed to give rise to symptoms of foodborne illness, and varies according to the agent and the consumer's age and overall health. Pathogens vary in minimum infectious dose; for example,Shigella sonnei has a low estimated minimum dose of < 500colony-forming units (CFU) whileStaphylococcus aureus has a relatively high estimate.[76]
Importantly, prior exposure to pathogens can significantly increase an individual's tolerance to subsequent exposures. Locals in a region may tolerate pathogen levels that would cause illness in travelers due to immune memory developed from repeated low-level exposures.[77] This helps explain why locals often consume food without illness that might sicken visitors.
In the case ofSalmonella a relatively large inoculum of 1million to 1billion organisms is necessary to produce symptoms in healthy human volunteers,[78] asSalmonellae are very sensitive to acid. An unusually high stomachpH level (low acidity) greatly reduces the number of bacteria required to cause symptoms by a factor of between 10 and 100.[citation needed]
Foodborne illness often occurs astravelers' diarrhea in persons whosegut microbiota is unaccustomed to organisms endemic to the visited region. This effect of microbiologic naïveté is compounded by anyfood safety lapses in the food's preparation.[citation needed]
Locals develop immunity to local food pathogens through repeated exposure, explaining why they often don't get sick from food that affects travelers. This immune adaptation involves developing specific defenses against common local bacteria, viruses, and parasites.[79] Through this process, locals' immune systems produce a measured response that eliminates pathogens without triggering excessive inflammatory reactions, while travelers' immune systems often mount exaggerated responses to novel pathogens.[80]
Globally, infants are a group that is especially vulnerable to foodborne disease. The World Health Organization has issued recommendations for the preparation, use and storage of prepared formulas. Breastfeeding remains the best preventive measure for protection from foodborne infections in infants.[81]
A CDC report[82] for the period 2017–2019 found that 41% of outbreaks at restaurants were caused by a sick employee. Contributory factors identified included lack of written policy compliance with FDA recommendations for identifying red-flag symptoms, glove use, and hand washing; lack ofpaid sick leave at the majority of establishments; and social pressure to come to work even while sick.[83] The remaining outbreaks had a variety of causes, including inadequate cooking, improper temperature, and cross-contamination[citation needed].
In the United States, using FoodNet data from 2000 to 2007, the CDC estimated there were 47.8million foodborne illnesses per year (16,000 cases for 100,000 inhabitants)[84] with 9.4million of these caused by 31 known identified pathogens.[85]
127,839 were hospitalized (43 per 100,000 inhabitants per year).[86][87][88]
3,037 peopledied (1.0 per 100,000 inhabitants per year).[87][88]
According to a 2012 report from theFood Standards Agency, there were around a million cases of foodborne illness per year (1,580 cases for 100,000 inhabitants).[89]
20,000 people were hospitalised (32 per 100,000 inhabitants);[89][90]
This data pertains to reported medical cases of 23 specific pathogens in the 1990s, as opposed to total population estimates of all foodborne illness for the United States.[91]
In France, for 735,590 to 769,615 cases of infection identified as being with the 23 specific pathogens, 238,836 to 269,085 were estimated to have been contracted from food:
between 12,995 and 22,030 people were hospitalized (10,188 to 17,771 estimated to have contracted their infections from food);
between 306 and 797 people died (228 to 691 estimated to have contracted their infections from food).[91]
A study by the Australian National University published in 2022 for Food Standards Australia New Zealand estimated there are 4.67 million cases of food poisoning in Australia each year that result in 47,900 hospitalisations, 38 deaths and a cost to the economy of $2.1 billion.[93]
A previous study using different methodology and published in November 2014, found in 2010 that there were an estimated 4.1 million cases of foodborne gastroenteritis acquired in Australia on average each year, along with 5,140 cases of non-gastrointestinal illness.[94]
The main causes were norovirus, pathogenicEscherichia coli,Campylobacter spp. and non-typhoidalSalmonella spp., although the causes of approximately 80% of illnesses were unknown. Approximately 25% (90%CrI: 13%–42%) of the 15.9 million episodes of gastroenteritis that occur in Australia were estimated to be transmitted by contaminated food. This equates to an average of approximately one episode of foodborne gastroenteritis every five years per person. Data on the number of hospitalisations and deaths represent the occurrence of serious foodborne illness. Including gastroenteritis, non-gastroenteritis and sequelae, there were an estimated annual 31,920 (90% CrI: 29,500–35,500) hospitalisations due to foodborne illness and 86 (90% CrI: 70–105) deaths due to foodborne illness circa 2010. This study concludes that these rates are similar to recent estimates in the US and Canada.[citation needed]
A main aim of this study was to compare if foodborne illness incidence had increased over time. In this study, similar methods of assessment were applied to data from circa 2000, which showed that the rate of foodborne gastroenteritis had not changed significantly over time. Two key estimates were the total number of gastroenteritis episodes each year, and the proportion considered foodborne. In circa 2010, it was estimated that 25% of all episodes of gastroenteritis were foodborne. By applying this proportion of episodes due to food to the incidence of gastroenteritis circa 2000, there were an estimated 4.3 million (90% CrI: 2.2–7.3 million) episodes of foodborne gastroenteritis circa 2000, although credible intervals overlap with 2010. Taking into account changes in population size, applying these equivalent methods suggests a 17% decrease in the rate of foodborne gastroenteritis between 2000 and 2010, with considerable overlap of the 90% credible intervals.[citation needed]
This study replaces a previous estimate of 5.4 million cases of foodborne illness in Australia every year, causing:[95]
18,000 hospitalizations
120 deaths (0.5 deaths per 100,000 inhabitants)
2.1 million lost days off work
1.2 million doctor consultations
300,000 prescriptions for antibiotics.
Most foodborne disease outbreaks in Australia have been linked to raw or minimally cooked eggs or poultry.[96] TheAustralian Food Safety Information Council estimates that one third of cases of food poisoning occur in the home.[97]
The vast majority of reported cases of foodborne illness occur as individual or sporadic cases. The origin of most sporadic cases is undetermined. In the United States, where people eat outside the home frequently, 58% of cases originate from commercial food facilities (2004 FoodNet data). An outbreak is defined as occurring when two or more people experience similar illness after consuming food from a common source.[citation needed]
Often, a combination of events contributes to an outbreak, for example, food might be left at room temperature for many hours, allowing bacteria tomultiply which is compounded by inadequate cooking which results in a failure to kill the dangerously elevated bacterial levels.[citation needed]
Outbreaks are usually identified when those affected know each other. Outbreaks can also be identified bypublic health staff when there are unexpected increases in laboratory results for certain strains of bacteria. Outbreak detection and investigation in the United States is primarily handled by local health jurisdictions and is inconsistent from district to district. It is estimated that 1–2% of outbreaks are detected.[citation needed]
In Aberdeen, in 1964, a large-scale (>400 cases) outbreak oftyphoid occurred, caused by contaminatedcorned beef which had been imported fromArgentina.[98] The corned beef was placed in cans and because the cooling plant had failed, cold river water from thePlate estuary was used to cool the cans. One of the cans had a defect and the meat inside was contaminated. That meat was then sliced using a meat slicer in a shop in Aberdeen, and a lack of machinery-cleaning led to the spreading of the contamination to other meats cut in the slicer. Those meats were eaten by people in Aberdeen who then became ill.[citation needed]
Serious outbreaks of foodborne illness since the 1970s prompted key changes in UKfood safety law. The outbreaks included the deaths of 19 patients in the Stanley Royd Hospital outbreak[99] and thebovine spongiform encephalopathy (BSE, mad cow disease) outbreak identified in the 1980s. The deaths of 21 people in the1996 Wishaw outbreak ofE. coli O157[100][101] was a precursor to the establishment of theFood Standards Agency which, according toTony Blair in the 1998white paperA Force for Change Cm 3830, "would be powerful, open and dedicated to the interests of consumers".[102]
In May 2015, for the second year running, England's Food Standards Agency devoted its annual Food Safety Week to "The Chicken Challenge". The focus was on the handling of raw chicken in the home and in catering facilities in a drive to reduce the high levels of food poisoning from thecampylobacter bacterium. Anne Hardy argues that widespread public education of food hygiene can be useful, particularly through media (TV cookery programmes) and advertisement. She points to the examples set byScandinavian societies.[103]
None of the US Department of Health and Human Services targets[105] regarding incidence of foodborne infections were reached in 2007.[106]
A report issued in June 2018 by NBC's Minneapolis station using research by both the CDC and the Minnesota Department of Health concluded that foodborne illness is on the rise in the U.S.[107]
In India,Entamoeba is the most common cause of food illness, followed byCampylobacter bacteria,Salmonella bacteria,E. coli bacteria, andnorovirus.[108] According to statistics, food poisoning was the second most common cause of infectious disease outbreak in India in 2017. The numbers of outbreaks have increased from 50 in 2008 to 242 in 2017.[108]
TheWorld Health Organization Department of Food Safety and Zoonoses (FOS) provides scientific advice for organizations and the public on issues concerning the safety of food. Its mission is to lower the burden of foodborne disease, thereby strengthening the health security and sustainable development of Member States. Foodborne and waterborne diarrhoeal diseases kill an estimated 2.2million people annually, most of whom are children. WHO works closely with the Food and Agriculture Organization of the United Nations (FAO) to address food safety issues along the entire food production chain—from production to consumption—using new methods of risk analysis. These methods provide efficient, science-based tools to improve food safety, thereby benefiting both public health and economic development.[citation needed]
International Food Safety Authorities Network (INFOSAN)
The International Food Safety Authorities Network (INFOSAN) is a joint program of the WHO and FAO. INFOSAN has been connecting national authorities from around the globe since 2004, with the goal of preventing the international spread of contaminated food and foodborne disease and strengthening food safety systems globally. This is done by:[citation needed]
Promoting the rapid exchange of information during food safety events;
Sharing information on important food safety issues of global interest;
Promoting partnership and collaboration between countries; and
Helping countries strengthen their capacity to manage food safety risks.
Membership to INFOSAN is voluntary, but is restricted to representatives from national and regional government authorities and requires an official letter of designation. INFOSAN seeks to reflect the multidisciplinary nature of food safety and promote intersectoral collaboration by requesting the designation of Focal Points in each of the respective national authorities with a stake in food safety, and a single Emergency Contact Point in the national authority with the responsibility for coordinating national food safety emergencies; countries choosing to be members of INFOSAN are committed to sharing information between their respective food safety authorities and other INFOSAN members. The operational definition of a food safety authority includes those authorities involved in: food policy; risk assessment; food control and management; food inspection services; foodborne disease surveillance and response; laboratory services for monitoring and surveillance of foods and foodborne diseases; and food safety information, education and communication across thefarm-to-table continuum.[citation needed]
The Food and Agriculture Organization of the United Nations and The World Health Organization have published a global ranking of foodborne parasites using a multicriteria ranking tool concluding thatTaenia solium was the most relevant, followed byEchinococcus granulosus,Echinococcus multilocularis, andToxoplasma gondii.[109] The same method was used regionally to rank the most important foodborne parasites in Europe rankingEchinococcus multilocularis of highest relevance, followed byToxoplasma gondii andTrichinella spiralis.[110]
Food may be contaminated during all stages of food production and retailing. In order to prevent viral contamination, regulatory authorities in Europe have enacted several measures:[citation needed]
European Commission Regulation (EC) No 2073/2005 of November 15, 2005
European Committee for Standardization (CEN): Standard method for the detection of norovirus and hepatitis A virus in food products (shellfish, fruits and vegetables, surfaces and bottled water)
CODEX Committee on Food Hygiene (CCFH): Guideline for the application of general principles of food hygiene for the control of viruses in food[111]
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