ISO 22000:2018 Allergen Management

ISO 22000:2018 Allergen Prevention Requirements  

ISO 22000:2018 standard has only mentioned allergens on one occasion, where it tries to explain food safety hazards, since ISO 22000 considers allergen as a chemical hazard which includes allergens and radiological substances (3.22, note 2 for entry: Food safety hazards include allergens and radiological substances). Thus, the ISO 22000 standard has completely relied on its prerequisite programs to consider non-process preventive measures while considering process allergens to be considered in the category of significant food safety hazards. Hence, ISO 22000:2018 broadly consider allergen as a chemical hazard, without offering specific concerns or program requirements considered in private label standards such as SQF or BRC. However, one of ISO 22000 sister standards or the technical specification, ISO 22002-1:2009, specifies requirements for establishing, implementing, and maintaining an allergen management program. This program is prepared based on the scientific approach of risk analysis, the HACCP principles, by assessing allergen hazards. Thus, food manufacturers that have implemented their food safety systems in alignment with ISO 22000:2005 have already taken actions towards managing allergens as it is a prerequisite program required by the international standard, but the new classification of process preventive controls and non-process preventive controls has been introduced in the current version of ISO 22000:2018, which has created two types of actions base on the allergen cross-contact or intentional addition to the existing processes.  

 

Hence, an effective allergen management program depends on the physical segregation of allergenic foods and ingredients from all other products and ingredients at every step of the food production process, which starts from receiving raw materials to delivery of the final product. In addition to the elimination of unintentional presence of allergens in food products, education, and training of the staff on food allergen risks, management and communication must be a top priority for food manufacturers. The most applicable method is the declaration of allergens present in the product, either by design or by potential manufacturing cross-contact, which must be accurately indicated on labels for consumer products, or the accompanying documentation for products intended for further processing. Consequently, public health relevant to food allergies continues to grow, where the food industry has boosted its efforts to maintain the management of food allergens. Nonetheless, national legislations that regulate the labeling of food allergens in many countries, other international standards, and voluntary guidelines have been developed to help organizations effectively prevent food allergen incidents.   

    

Food Allergies 

Food allergies are the inappropriate immune responses generated due to constituents in the foods that are mostly protein substances causing allergic reactions when the same food is eaten again. There are many different types of allergic responses, but the primary concern in food allergen management is primarily focused on the greatest impact over humans or animals, where the immune system produces IgE antibodies to proteins in the food. Nonetheless, food allergy must be differentiated from food intolerance, such as lactose intolerance, which does not involve the immune system responses.

 

Food allergic reactions can be varied from very slight to severe impacts and occasionally fatal, depending on the dose and the individual as well as other factors, which affect a greater proportion of children than adults. The reactivity to some allergenic foods, such as milk and egg, tends to be largely outgrown, while allergy to others, such as peanuts, generally persists. When an IgE-mediated reaction occurs due to a constituent of food inside the body, a rapid release of chemicals such as histamine may occur resulting in symptoms within minutes, but occasionally it may take up to 2 or more hours after ingestion of the offending food. However, a severe systemic reaction may occur in rare cases, leading to a sudden drop in blood pressure, severe constriction of the airways, a generalized shock reaction, and multiple organ failure, which is known as an anaphylactic shock that can lead to death within minutes if not treated with adrenaline. There is a small number of people in each community with such risk of food allergies with serious reactions, and many documented cases of death resulting from accidental ingestion of an offending food. 

 

Presently, all the internationally recognized food standards require (all or some of) peanuts, tree nuts, milk, eggs, lupin, sesame seeds, fish, shellfish, crustaceans, soy, celery, mustard, Sulphites, and cereals (wheat, rye, barley) to be declared on labels whenever they are present as ingredients or as components of food additives or processing aids. Australia and New Zealand, the United States, the European Union, Canada, Japan, and other countries have similar requirements for these and other known food allergens, but the US considers big 8 allergens and the EU has 14 declared allergens while Canada has 13 priority allergens.  

 

Food allergies affect around 10% of children up to the age of 1, between 4 – 8% of children aged up to 5 and approximately 2% of adults, and hospitalization for severe allergic reactions/anaphylaxis have doubled over the last decade, where there is a five-fold increase for children aged between 0 to 4 years over hospital admissions. On the other hand, food allergies affect around 2 to 4% of the population in Europe, and an estimated 5-8% of children, where there is an estimated 10-20 million people suffer from food allergies in the 500 million population of the 27 EU Member States, who believe they have a food allergy is considerably higher at around 20% of the same population. Many children outgrow their allergies, such as those to milk and eggs by the age of 5-7 years. Other allergies, such as to fish and peanuts, tend to persist. Nonetheless, there is no practical cure exists for food allergy and allergic consumers must avoid foods that contain the ingredient(s) to which they are allergic. Hence, individuals with allergic conditions must rely on the information provided on the label to determine whether the ingredients include food that may be allergenic.

 

As for food recalls information, approximately 37% of food recalls occurred in Australia from 2008 to 2017 were due to undeclared allergens in the final product and 2% were due to mislabeling, where many foods recall still occur due to the incorrect labeling of allergens contained in the food. Hence, the common causes of these recalls can include changes in product formulation or changes in a supplier’s ingredient formulation.

 

Furthermore, oral allergy syndrome (OAS) is a form of food allergy in which people become allergic through inhaling pollen proteins (fruit and vegetables) and then react to similar proteins in foods, where the symptoms can only be felt by the allergic person, but severe reactions are extremely rare. The development of a food allergy or any other allergy depends on complex interactions between a person’s individual susceptibility and factors related to exposure and the circumstances in which it occurs. Besides, children born to allergic parents are more likely to become allergic themselves, as well as most food allergies, begin in childhood, but onset can also take place later in life.

 

Coeliac disease is considered as an adverse reaction to foods involving the immune system, which is an immunologically mediated, non-IgE reaction to gliadin, a prolamin (gluten protein) found in wheat, and similar proteins found in the crops of the genus Tritiaceae (barley, rye). Coeliac disease is considered an autoimmune disorder of the small intestine that occurs in genetically predisposed people of all ages from middle infancy onward. The symptoms include chronic diarrhea, failure to thrive at a young age, and fatigue, where longer-term impacts include osteoporosis and other severe health effects have been reported. 

 

Food intolerance refers to adverse reactions to foods, which do not involve the immune system and are not usually the result of inherent toxicity. However, food intolerance has some characteristic of the food involving pharmacological activity to the affected individual such as enzyme deficiency or the cause is sometimes unknown, which is not usually immediately life-threatening, but such reactions can make the sufferer feel extremely unwell and can have a major impact on working and social life. They may occur very rapidly and mimic an allergic reaction, or can develop over many hours until the offending substance has been removed, e.g. lactose intolerance.

 

The allergic reactions start with the recognition of the allergen constituent (protein), where any process that modifies the structure of a protein will have the potential to affect allergenicity. Thus, food processing is usually a rigorous process that induces several physicals, chemical, and biochemical changes, and nonetheless, certain methods may enhance, reduce, or eliminate the allergenic potential of food while potentially impact the allergenic potential of proteins. 0n the other hand, processing can be used to remove the protein fraction of the food that reduces the exposure to allergens to prevent allergic reactions, e.g. highly refined seed oils. Such foods have granted exemptions in the labeling legislation, but there are no general rules regarding how different allergenic foods respond to physical (thermal, mechanical), chemical, or biochemical processing methods. Consequently, if there is no sound evidence that a specific processing method reduces allergenicity, it should be assumed that the allergenic potential of processed food is identical to that of the food in its unprocessed form.

References:

ISO 22000:2018

https://www.fooddrinkeurope.eu/uploads/press-releases_documents/temp_file_FINAL_Allergen_A4_web1.pdf

https://multimedia.3m.com/mws/media/1648172O/food-safety-anz-edm-allergen-control-plan.pdf

https://erudus.com/14-major-food-allergens-for-eu-food-information-for-consumers/

https://www.iso.org/obp/ui/#iso:std:iso:ts:22002:-2:ed-1:v1:en

 

Common Foodborne Pathogens - X

Noroviruses Risk Profile 

Norovirus (NoV), or the winter vomiting bug, is the most common cause of gastroenteritis, which is characterized by non-bloody diarrhea, vomiting, and stomach pain. Noroviruses are environmentally hardy organisms that can be transmitted by food, water, and also can be easily transmitted through person-to-person contact or contact through environmental surfaces. The norovirus infection can infect the same person several times because there are many different types of noroviruses. Thus infection with one type of norovirus may not protect against other types, which is possible to develop immunity to (protection against) specific types and, it is not known exactly how long immunity lasts. Nonetheless, whether you are susceptible to norovirus infection or not is also determined in part by an individual’s genes.
 
NoV is a genetically diverse group of single-stranded positive-sense RNA, non-enveloped viruses belonging to the family Caliciviridae, which can be genetically classified into at least seven different genogroups (GI, GII, GIII, GIV, GV, GVI, and GVII), and further divided into different genetic clusters or genotypes. The strains are known to cause disease in humans, which exist primarily in genetic clusters within genogroups I, II, and IV, whereas the viruses belonging to the other genogroups have been shown to infect other animals such as cattle, swine, and mice. Norovirus in genogroups GI and GII alone can be divided into at least 15 genetic clusters. Thus, a genetic cluster of NoV is defined as strains that have at least 80% homology to a reference strain’s amino acid sequence. 
 
Sources 

The major source of NoV outbreaks have been associated with the drinking of contaminated water, including municipal water, well water, stream water, commercial ice, lake water, and swimming pool or recreational surface-water exposure, as well as floodwater. The second most implicated source was salad ingredients, fruit, and oysters are the foods most often implicated in norovirus outbreaks. However, any ready-to-eat food that has been handled by an ill food worker may be contaminated. Molluscan shellfish, particularly oysters, have been commonly identified in NoV-related gastroenteritis outbreaks worldwide. However, this represents a different etiology that does not necessarily involve a contaminated food worker. The rapid spread of secondary infections is particularly evident in areas where a large population is enclosed within a static environment, such as in institutions, college campuses, schools, military operations, hotels, restaurants, recreational camps, hospitals, nursing homes, day-care facilities, and cruise ships, and after natural disasters, such as hurricanes and earthquakes. Nonetheless, nearly 29% of all NoV foodborne outbreaks from 1997-2004 could be attributed to food purchased or served at a restaurant or delicatessen.
 
Disease 
Norovirus infections occur more commonly during winter months, which is often occur in outbreaks, especially among those living in close quarters, which are a leading cause of foodborne infection in the United States. 
 

Mortality

The infections approximately account for 26% of hospitalizations and 11% of deaths associated with food consumption. 

 

Infective dose

The infective dose is considered very low, which is estimated to be as low as 1 to 10 viral particles. The viral particles are excreted at high levels as high as 1 x 10¹² million viral particles of 1g feces by both symptomatic and asymptomatic people. 

Onset

Mild, brief symptoms usually develop between 24 and 48 hours after contaminated food or water is consumed, but onset times within 12 hours of exposure have been reported.

 

Complications

Norovirus infection is self-limiting, which can be very debilitating as a result of the high rate of vomiting, where recovery is usually complete without evidence of long-term effects. The most common complication is dehydration, particularly among the very young, the elderly, and patients with underlying medical conditions, where no specific therapy exists for viral gastroenteritis or NoV infection. Treatment for NoV infection is consisted primarily of oral rehydration and, if needed, intravenous replacement of electrolytes. There is no antiviral medication or vaccine is available, and antibiotics are not effective for treating NoV infection. Prevention involves proper hand washing and disinfection of contaminated surfaces, and alcohol-based hand sanitizers can be used as an alternative, but they are less effective than hand washing. There is no vaccine or specific treatment for norovirus, where management involves supportive care, such as drinking sufficient fluids or intravenous fluids.

 

Symptoms

Explosive, projectile vomiting usually is the first sign of infection and is often used to characterize the infection. Symptoms usually present as acute-onset explosive often vomiting, watery, non-bloody diarrhea with abdominal cramps, and nausea, headache, low-grade fever, chills, and muscle aches may also occur. Thus, the severity of symptoms appears to be higher in hospitalized patients, immunocompromised people, and elderly people, compared with younger adults and other groups. Nonetheless, there is about 30% of people infected with NoV display no gastrointestinal illness or associated symptoms, though they are still excreted high levels of virus in their stool, and such distinctive groups of people are considered to be silent shedders of NoV. 

Duration

Symptoms generally persist for 12 to 60 hours, with a mean period of 24 to 48 hours, where most patients report feeling better within 1 to 2 days. However, immunocompromised or elderly people and hospitalized patients may retain symptoms as vomiting and diarrhea continue for a while, and generally resolve within 72 to 96 hours, where the non-specific symptoms, such as headache, thirst, and vertigo, could persist up to 19 days.

 

Route of entry

Though the virus is usually spread by the fecal-oral route, foodborne norovirus infections have been epidemiologically linked into three distinctive segments:  

Cases associated with the consumption of ready-to-eat (RTE) foods contaminated by food workers; 

Environmental contamination of produce; 

Consumption of molluscan shellfish harvested from contaminated water. 

In rare cases, transmission can occur through vomit and is often associated with improper sanitation controls or their application. Secondary transmission following the foodborne illness is common, due to the high levels of virus that are excreted. 

 

Pathway

Norovirus infection causes gastroenteritis, an inflammation of the stomach and the small and large intestines, but the precise pathogenic pathway of infection is unknown. 

 
Frequency 

Norovirus infections annually result in about 685 million cases of disease and 200,000 deaths globally, which is common both in the developed and developing worlds. Infants under the age of five are most often affected, which results in about 50,000 deaths in the developing world. According to the Centers for Disease Control and Prevention (CDC) estimates that noroviruses cause 5.5 million infections annually in the United States with an estimated range of 3.2 million to 8.3 million cases of foodborne infections, which accounts for 58% of all foodborne illnesses, including approximately about 0.03% (14,663) require hospitalization, and less than 0.1% of these illnesses results in death (149). 
 
Diagnosis 
Clinical diagnosis, without the diagnostic tests used to identify NoV-associated infections, include the following four criteria: 1) vomiting in more than 50% of affected persons in an outbreak; 2) a mean (or median) incubation period of 24 to 48 hours; 3) a mean (or median) duration of illness of 12 to 60 hours, and 4) lack of identification of a bacterial pathogen in stool culture. The clinical diagnosis of NoV infection is carried out using analytical tests on serum, stool, and in some instances, vomitus. Diagnosis also can be achieved by examining blood serum samples for a rise in virus-specific serum antibody titers, measured by enzyme immunoassay (i.e., ELISA or EIA). However, this method has had only a 55% level of accuracy when compared with a reverse transcription-polymerase chain reaction (RT-PCR) approach. The applicability of these assays is also limited by the requirement to collect stool specimens from acute or convalescent patients for accurate determination. Examination of stool specimens for norovirus can be performed by microscopy through direct electron microscopy or immunoelectron microscopy to visualize viral capsids, which requires high densities (generally >106 /g). Thus, RT-PCR is the preferred method of diagnosis since it is significantly more sensitive than microscopy; does not require a large, expensive electron microscope with highly skilled personnel; and has the ability to rapidly differentiate genogroups, which could be instrumental in follow-up epidemiologic investigations, to determine the route and distribution of NoV in the community. 
 
Target Populations 

NoV may impact people of any age, but it is more prevalent among the elderly and children under the age of 5. According to the research data, there is a genetic predisposition to acquiring an infection that is dependent on the patient’s blood type (ABO phenotype). Nonetheless, the previous infection of Norovirus does not provide long-term immunity, and reinfection by the same strain can occur several months after the initial infection. On the other hand, the rapid spread of secondary infections through congested areas where a large population is enclosed within a static environment, such as in institutions, college campuses, schools, military operations, hotels, restaurants, recreational camps, hospitals, nursing homes, day-care facilities, and cruise ships, or after natural disasters, such as hurricanes and earthquakes. 
 
Food Analysis 

Assays using RT-PCR technology for NoV detection and quantitation are commercially available, but quantitative RT-PCR (qRT-PCR) is the most sensitive method for NoV detection in food extracts, which is an improvement over conventional RT-PCR due to its increased specificity and sensitivity. NoV has been successfully detected and isolated from oysters, irrigation, and groundwater, as well as deli meats.
 
 
Reference:
FDA Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins. Second Edition. 2013
Preventive Controls for Human Foods. 2016
www.cdc.gov 

Common Foodborne Pathogens - IX

Clostridium perfringens Risk Profile 

Clostridium perfringens is an anaerobic and aero-tolerant, gram-positive, spore-forming rod that is relatively cold-tolerant and produces enterotoxins, where its spores are heat-resistant. Nonpathogenic C. perfringens is widely distributed in the environment and is frequently found in the intestines of humans and many domestic and feral animals. The spores persist in soil, sediments, and areas subject to human or animal fecal pollution. Isotype A almost always contains the “cpe” gene or the enterotoxin gene, which causes food poisoning, and types B, C, D, and E sometimes contain this gene among many C. perfringens isotypes found in nature. 
 
Sources 
The actual cause of poisoning happens due to temperature abuse of cooked foods in most instances. C. perfringens can be present in small numbers often after the food is cooked due to germination of its spores, which can survive high heat and can multiply rapidly as a result of a fast doubling time (<10 minutes for vegetative cells), depending on temperature and food matrix. Therefore, during cool-down (109-113°F) and storage of prepared foods, this organism can reach levels that cause food poisoning much more quickly than can other bacteria. Meats (especially beef and poultry), meat-containing products (e.g., gravies and stews), and Mexican foods are important vehicles for C. perfringens foodborne illness, although it is also found on vegetable products, including spices and herbs, and in raw and processed foods. Spores of some C. perfringens strains can survive boiling water for an hour or longer in a relatively protective medium (e.g., a cooked-meat medium, <10 minutes for vegetative cells) depending on temperature and food matrix. Hence, C. perfringens can reach levels that cause food poisoning much more quickly than can other bacteria, during cool-down (109-113°F) and storage of prepared foods.
 

Especially beef and poultry are implicated, other meat varieties and meat-containing products such as gravies and stews, as well as Mexican foods are important vehicles for C. perfringens foodborne infections. C. perfringens is also found on vegetable products, including spices and herbs, and in raw and processed foods, where spores of some C. perfringens strains can survive boiling water for an hour or longer in a relatively protective medium e.g., a cooked-meat medium. 

Growth Factors 

Temperature:

Minimum – 10°C Maximum – 47.1°C Optimum (43 – 47°C)

pH:

Minimum – 5 .0 Maximum – 9.0 Optimum (7.2)

Water Activity (aW):

Minimum – 0.93 Maximum – >0.99 Optimum (0.95 – 0.96)

Water Phase Salt:

Maximum – 7%       

 
Disease 
C. perfringens can cause two types of foodborne infections, and the gastroenteritis form is very common and often is mild and self-limiting. However, it may also develop as more severe gastroenteritis depending on the strain, which leads to damage of the small intestine and, potentially, but rarely, fatality. The second form C. perfringens is enteritis necroticans or “pig-bel disease” or characteristic swollen bellies and other severe symptoms, which is rare in the developed world, but more severe than the other form of the infection, and often fatal. As C. perfringens can replicate much more rapidly than most other bacteria that result in the ingestion of a large number of vegetative cells from both infection forms. Hence, C. perfringens will more quickly reach pathogenic levels in contaminated food left unrefrigerated than other bacteria, and the consumers who eat the food may ingest large doses of the bacterium. 

Mortality 

There were an estimated 26 annual deaths in the United, States according to the Centers for Disease Control and Prevention (CDC) and C. perfringens annually accounts for: 

Common gastroenteritis form - A few deaths resulting from diarrhea-induced dehydration and other complications have been reported, and usually were among debilitated or elderly people. 

Pig-bel form (enteritis necroticans) - This disease is often fatal, and it is extremely rare in the U.S. 

 

Infective dose 

Symptoms are caused by ingestion of large numbers of (> 106) vegetative cells or >106 spores/g of food, where toxin production in the digestive tract (or in vitro) is associated with sporulation, which is characterized as a food infection. 

 

Onset 

Symptoms occur about 16 hours after consumption of foods infected with C. perfringens serotypes that are capable of producing the enterotoxin and containing large numbers of (>106) live vegetative cells or (>106) spores. 

Complications 

Complications are rare in the typical, mild gastroenteritis form of the disease, particularly among people under 30 years of age. However, elderly people are more likely to have prolonged or severe symptoms, as are immunocompromised people. The more severe form of the disease may cause necrosis of the small intestine, peritonitis, and septicemia. 

 

Symptoms 

Gastroenteritis form – Common characteristics include watery diarrhea and mild abdominal cramps. 

Pig-bel form (enteritis necroticans) – Abdominal pain and distention, diarrhea (sometimes bloody), vomiting, and patchy necrosis of the small intestine. 

 

Duration 

The milder form of the disease generally lasts 12 to 24 hours, but symptoms may last 1 to 2 weeks in the elderly or infants. 

 

Route of entry 

Oral. 

 

Pathway 

CPE protein usually is released into the intestines when the vegetative cells lyse on completion of sporulation, where this enterotoxin is responsible for clinical presentation in humans. The enterotoxin induces fluid and electrolyte losses from the GI tract, where the principal target organ for CPE is believed to be the small intestine.

 

Pig-bel disease involves the production of the beta toxin, which is highly trypsin-sensitive, where the effects of low gastrointestinal levels of trypsin appear to have contributed to the progression of the disease. It has been demonstrated that when starvation and high levels of potato consumption which generally contain trypsin inhibitor contributed to low levels of this enzyme in the population. 

 
Frequency 

C. Perfringens poisoning is the second most commonly reported foodborne infection in the U.S, which second only to Salmonella when considering bacterial causes of foodborne infection. The CDC estimates that 965,958 domestically acquired cases occur annually in the United States, where there were 34 outbreaks in 2006 included 1,880 cases excluding isolated cases with an average of 50 to 100 people are affected in one outbreak. Many outbreaks probably go unreported, because the implicated foods and patients’ feces are not tested routinely for C. perfringens or its toxin. 
 
Diagnosis 
C. perfringens poisoning is diagnosed by its symptoms and the typical delayed onset of infection, which is confirmed by detection of the toxin in patients’ feces. The presence of exceptionally large numbers of the bacteria in implicated foods or patients’ fecal samples is also used for bacteriological confirmation. 
 
Target Populations 
Institutional settings, where large quantities of food are prepared several hours before serving such as school cafeterias, hospitals, nursing homes, prisons, etc. are the most common circumstance in which C. perfringens poisoning occurs. The young and elderly are the most frequent victims of C. perfringens poisoning, whereas immunocompromised people are at higher risk of severe infection than are others, such as those with HIV/AIDS or undergoing cancer chemotherapy or immunosuppressive drugs for rheumatoid arthritis or other inflammatory conditions.
 
Food Analysis 

Standard bacteriological culturing methods are applied to determine the C. perfringens in implicated foods and feces of patients, and the serological assays are used for detecting enterotoxin in the feces of patients and for testing the ability of strains to produce toxin. Further identifications are carried out using PCR based methods in modern identification techniques. 

Reference:
FDA Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins. Second Edition. 2013
Preventive Controls for Human Foods. 2016
www.cdc.gov

Common Foodborne Pathogens - VIII

Shigella spp. Risk Profile

Shigella infection (shigellosis) is an intestinal infection caused by a family of bacteria known as shigella. Shigella is very contagious and the main sign of shigella infection is diarrhea with blood, which is caused by Shigella sonnei, S. boydii, S. flexneri, and S. dysenteriae. Shigellae are Gram-negative, non-motile, non-spore-forming, rod-shaped bacteria. Some strains produce enterotoxins and Shiga toxin, where the latter is very similar to the toxins produced by E. coli O157:H7. Humans are the only host of Shigella, but it has also been isolated from higher primates and it is frequently found in water polluted with human feces. 

Shigellae are very sensitive to environmental conditions die rapidly and heat-sensitive, hence do not survive the pasteurization and cooking temperatures. Shigella species are tolerant to low pH and are able to transit the harsh environment of the stomach. These pathogens can grow in low pH foods, such as some fruits and vegetables, or survive on produce commodities packaged under vacuum or modified atmosphere and can also survive in water, with a slight decrease in numbers.
 
Growth Factors

Temperature:

            Minimum – 6.1°C     Maximum – 47.1°C 

pH:

Minimum – 4.8         Maximum – 9.3        

Water Activity (aW):

Minimum – 0.96       Maximum – -            

Water Phase Salt:

Maximum – 5.2%    

 
Disease

The infection caused by Shigella is shigellosis and also called bacillary dysentery, where diarrhea may range from watery stool to severe, life-threatening dysentery. All Shigella spp. can cause acute, bloody diarrhea, and can spread rapidly through a population under unsanitary conditions with mass populations. S. dysenteriae type 1 causes the most severe disease and is the only serotype that produces the Shiga toxin, which may be partially responsible for cases in which hemolytic uremic syndrome (HUS) develops. On the other hand, S. sonnei produces the mildest form of shigellosis, which is usually watery diarrhea; S. flexneri and S. boydii infections can be either mild or severe.
 

Mortality

The disease usually is self-limiting in healthy people, although some strains are associated with fatality rates as high as 10-15%.

 

Infective dose

As few as 10 to 200 cells can cause disease, depending on the age and condition of the host.

 

Onset

Eight to 50 hours.

 

Complications

The disease usually consists of self-limiting diarrhea in healthy people and the symptom includes fever and stomach cramps, but severe cases, which tend to occur primarily in immunocompromised or elderly people and young children, are associated with mucosal ulceration, rectal bleeding, and potentially drastic dehydration. Potential sequelae of shigellosis include reactive arthritis and hemolytic uremic syndrome.

 

Symptoms

May include abdominal pain; cramps; diarrhea; fever; vomiting; blood, pus, or mucus in stools; tenesmus (straining during bowel movements).

 

Duration

Uncomplicated cases usually resolve in 5 to 7 days. Most of the time, the illness is self-limiting. In some circumstances, antibiotics are given, such as trimethoprim-sulfamethoxazole, ceftriaxone, or ciprofloxacin.

 

Route of entry

The fecal-oral route is the primary means of human-to-human transmission of Shigella. However, the contamination of foods is often due to an infected food handler with poor personal hygiene.

 

Pathway

The disease is caused when Shigella cells attach to, and penetrate, colonic epithelial cells of the intestinal mucosa and they multiply intracellularly while spreading into contiguous epithelial cells, resulting in tissue destruction.

 
Frequency

According to the US Centers for Disease Control and Prevention (CDC), there are about 15,000 domestically acquired foodborne infections of laboratory-confirmed isolates are reported each year, with estimates of actual occurrence ranging from 24,511 to 374,789 cases (average of 131,243) and about 31% of them estimated to be foodborne. Nonetheless, most of the foodborne infections are caused by 31 different pathogens, where Shigella is ranked as the sixth most frequent cause after norovirus, Salmonella species, Clostridium perfringens, Campylobacter, and Staphylococcus aureus. Shigellosis appears to follow seasonal variations, and the highest incidences generally occur during the warmer months of the year in developed countries.
  
Diagnosis
Diagnosis is by serological or molecular identification of cultures isolated from the stool, but Shigella may be more difficult to cultivate if stool samples are not processed within a few hours. However, cultivating Shigella spp is relatively difficult and depends on the amount of time within which stool or food samples are collected and processed. In terms of growth, shigellae are not particularly fastidious in their requirements and, in most cases, the organisms are routinely cultivated in the laboratory, on artificial media.
 
Target Populations
Everyone in the community is susceptible to shigellosis, but children 1 to 4 years old, the elderly, and the immunocompromised are most at risk to some degree. Further, Shigellosis is very common among people with AIDS and AIDS-related complex.
 
Food Analysis

A molecular-based method (PCR) that targets a multi-copy virulence gene has been developed and implemented by the FDA. Improvements in the bacterial isolation method continue as Shigellae remain a challenge to isolate from foods. The window for collecting and processing Shigella from foods, for cultivation, maybe days rather than hours, as is the case with stool, depending on the food matrix and storage conditions, such as temperature. Shigella species can be outgrown by the resident bacterial populations found in foods, which may reflect the usual low numbers of the organism present in foods, or a very large number of non-Shigella bacteria in some foods. The physiological state of the pathogen at the time of analysis may be another factor that reduces the chance of isolating Shigella from foods. Environmental conditions could affect its ability to either grow or survive in any food matrix.

 
Reference:
FDA Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins. Second Edition. 2013
Preventive Controls for Human Foods. 2016

Common Foodborne Pathogens - VII

Clostridium botulinum Risk Profile 

Clostridium botulinum is gram-positive, spore-forming rod-shaped, an anaerobic bacterium that produces a protein, which has characteristic neurotoxicity. The spores are heat-resistant and can survive in foods that are incorrectly or minimally processed. C. botulinum may grow in foods under certain conditions while producing toxin(s), where a severe form of food poisoning (botulism) results when the toxin-containing foods are ingested. Although it is rare, its mortality rate is high. 
 
There are seven serotypes of C. botulinum have been identified (A, B, C, D, E, F, and G), based on the antigenic specificity of the toxin produced by each strain. Further, types A, B, E, and F cause human botulism, and types C and D cause botulism in animals including birds and fish. Besides, type G outbreaks have never been reported yet. Although most strains produce only one type of toxin, dual toxin-producing strains also been reported. 
 
Spores produced by the C. botulinum are heat-resistant, and both bacterium and the spores are widely distributed in nature. The spores germinate in the absence of oxygen, grow, and excrete toxins. They are found in both cultivated and forest soils, bottom sediments of streams, lakes, and coastal waters as well as in the intestinal tracts of fish and mammals, and on the gills and viscera of crabs and other shellfish.
 
Growth Factors
Temperature:
            Minimum – 10°C      Maximum – 48°C     (Optimum 35 - 40°C)
pH:
            Minimum – 4.6         Maximum – 9.0         (Optimum -)
Water Activity (aW):
            Minimum – 0.93       Maximum – -            (Optimum -)
Water Phase Salt:
            Maximum – 10%     
 
Sources

The food types that are susceptible to botulism vary according to the specific food preservation and cooking practices. Almost any food that is not very acidic, where pH is above 4.6 can be susceptible to the proliferation, growth, and toxin production by C. botulinum. Hence, 4% to 5% salt concentration is required for inhibition of its spores (especially regarding type E), while a 5% salt concentration can completely inhibiting growth. Salt concentrations slightly lower than those providing inhibition tend to extend spore outgrowth time at low temperatures.
 
Thus, any food that is conducive to outgrowth and toxin production of C. botulinum can be associated with botulism, when inadequate food processing practices that will allow survival of spores and that are not subsequently heated before consumption, to eliminate any live cells. A variety of foods, such as canned corn, peppers, green beans, soups, beets, asparagus, mushrooms, ripe olives, spinach, tuna fish, chicken and chicken livers, liver pate, luncheon meats, ham, sausage, stuffed eggplant, lobster, and smoked and salted fish have been associated with botulinum toxin.
 
Infant botulism can be caused due to various potential environmental sources, such as soil, cistern water, dust, and foods, honey is the one dietary reservoir of C. botulinum spores linked to infant botulism by both laboratory and epidemiologic studies. 
 
Disease

Botulism is a serious and sometimes fatal, rare non-transmittable foodborne infection caused by C. botulinum due to a potent neurotoxin formed during growth. The recommended treatment for foodborne botulism includes early administration of botulinum antitoxin, and intensive supportive care, including mechanical breathing assistance. An antitoxin for infant botulism (Botulism Immune Globulin Intravenous or BIG-IV) also is available, which should be administered as early in the illness as possible. However, antimicrobial therapy is not recommended, due to concerns about increased toxin release as a result of cell lysis. 
 

Mortality: 

The general fatality of botulinum is in-between 5% to 10% of the cases, but the mortality rate is high if treatment is not immediately administered. 

 

Infective dose: 

An extremely small amount such as “a few nanograms” of the toxin can cause infection.

 

Onset:

Adult – Usually 18 to 36 hours after ingesting food containing the toxin, although times have varied from 4 hours to 8 days.

Infant – Generally follows a period of normal development.

Complications: 

The infection results in flaccid paralysis of muscles due to neurotoxin, including those of the respiratory tract. The botulinum causes flaccid paralysis due to toxin by blocking motor nerve terminals at the neuromuscular junction, which progresses symmetrically downward, usually starting with the eyes and face, to the throat, chest, and extremities. Once the diaphragm and chest muscles become fully involved, respiration is inhibited and death can result from asphyxia without intervention. 

 

There are three major types of botulism are to be known and foodborne botulism and infant botulism, which also is foodborne. The third type, wound botulism, is not a foodborne infection. Nonetheless, there is a fourth undecided category, which might be the result of intestinal colonization in adults, with in vivo production of toxin. 

 

Foodborne botulism – A severe type of food poisoning caused by the ingestion of foods contaminated with the toxin produced by C. botulinum, which mostly develops symptoms often after consumption of improperly processed and inadequately cooked home-preserved foods. Home-canned or, occasionally, commercially produced foods have been involved in botulism outbreaks. Foodborne botulism is a rare occurrence in most commercially produced food products, but of considerable concern, because of its high mortality rate if not treated immediately and properly. 

 

Infant botulism – Colonization of C. botulinum in the intestinal tracts of infants due to the ingestion of spores that produce toxin is a serious infection such as intestinal toxemia botulism. 

 

Wound botulism - The rarest form of botulism and it does not involve food, which occurs when C. botulinum colonizes in a wound and produces toxins. The toxins are transported through the bloodstream. Whereas foodborne botulism is limited to the amount of toxin ingested, C. botulinum in wounds produce toxin in situ (gas gangrene) until the pathogen is gone. 

Symptoms:

Adult – Early signs of intoxication consist of marked lassitude, weakness, and vertigo, usually followed by double vision and progressive difficulty in speaking and swallowing. Initial symptoms may include double vision, blurred vision, drooping eyelids, slurred speech, difficulty swallowing, dry mouth, and muscle weakness. If the disease is not treated, symptoms may progress to paralysis of the arms, legs, trunk, and respiratory muscles. Difficulty in breathing, weakness of other muscles, abdominal distention, and constipation may also be common symptoms. 

 

Infant – Constipation is often the first sign of normal development of infant botulism, which is followed by flat facial expression; poor feeding (weak sucking); weak cry; decreased movement; trouble swallowing, with excessive drooling; muscle weakness; and breathing problems.

 

Duration: 

Patients with severe cases that involve paralysis of the respiratory muscles may need mechanical ventilation and intensive care for weeks or months.

 

Route of entry: 

Oral, botulinum toxins are ingested through improperly processed food in which the bacteria or the spores survive, then grow and produce the toxins. Though mainly a foodborne intoxication, human botulism can also be caused by intestinal infection with C. botulinum in infants, wound infections, and inhalation.

 

Pathway: 

Clinical symptoms develop after a person ingests the pre-formed toxin, or if the organisms grow in the intestines or in-wounds, followed by toxin release. The ingested botulinum toxin, which is an endopeptidase enzyme, blocks peripheral cholinergic neurotransmission at the neuromuscular junction and cholinergic autonomic nervous system. The toxin acts by binding presynaptically to high-affinity recognition sites on the cholinergic nerve terminals and decreasing the release of acetylcholine, causing a neuromuscular blocking effect. 

 

C. botulinum produces the toxin as a complex of proteins, among which is the neurotoxic moiety. The toxin is synthesized as a relatively inactive single-chain polypeptide. It becomes an active toxin by selective proteolytic cleavage to yield the heavy and light chains that are linked by a single disulphide bond and non-covalent interactions. The toxin’s light chain is a Zn⁺⁺ containing endopeptidase that blocks acetylcholine-containing vesicles from fusing with the terminal membrane of the neuron, resulting in flaccid muscle paralysis. 

 
Frequency
Although this food illness is rare, its mortality rate is high if the disease is not treated immediately and properly. There are 962 recorded botulism outbreaks in the United States from 1899 to 1990 involved 2320 cases and 1036 deaths. In outbreaks in which the toxin type was determined, 384 were caused by type A, 106 by type B, 105 by type E, and 3 by type F. In two outbreaks, the foods implicated contained both types A and B toxins. Some cases of botulism may go undiagnosed because symptoms are transient or mild or are misdiagnosed as Guillain-Barré syndrome.
 
Target Populations
All people are believed to be susceptible to botulism.
 
Diagnosis

Botulism can be diagnosed by clinical symptoms alone, but differentiation from other diseases may be difficult. Hence, the most direct and effective way in a laboratory to confirm the clinical diagnosis of botulism is to demonstrate the presence of toxin in the serum or feces of the patient or in the food he consumed. The most sensitive and widely used method for detecting toxin is the mouse neutralization test, which takes 48 hours, and the culturing of specimens takes 5 to 7 days.

Food Analysis
Determination of the source of an outbreak is usually based on the detection and identification of toxin in the food since botulism results from the ingestion of preformed C. botulinum toxin. Hence, the most widely accepted method is the mouse neutralization test, where extracts of the food injected into passively immunized mice, and results can be obtained in 48 hours. The mouse neutralization is followed by culturing of all suspected food in an enrichment medium, to detect and isolate the causative organism.

Reference:

FDA Bad Bug Book, Foodborne Pathogenic Microorganisms and Natural Toxins. Second Edition. 2013
Preventive Controls for Human Foods. 2016
www.cdc.gov