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Year : 2019  |  Volume : 3  |  Issue : 3  |  Page : 135-139

Insight to foodborne diseases: Proposed models for infections and intoxications

Department of Microbiology, School of Life Sciences, Independent University Bangladesh, Dhaka, Bangladesh

Date of Submission18-Jun-2019
Date of Decision25-Jul-2019
Date of Acceptance12-Aug-2019
Date of Web Publication10-Sep-2019

Correspondence Address:
Dr. Rashed Noor
School of Life Sciences, Independent University Bangladesh, Plot 16, Block B, Aftabuddin Ahmed Road, Bashundhara, Dhaka 1229
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bbrj.bbrj_86_19

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Disclosure of microbial prevalence in different food items around the globe is very much likely due to the pathogenic microbial propagation, as well as due to lack of sufficient understanding on food poisoning mechanism. A line of microbiological analyses of foods unstitched the promulgation of Escherichia coli and their toxins, Staphylococcus spp., Vibrio spp., Aeromonas spp., and Listeria spp. While the cases of food poisoning are handled frequently basically with the treatment strategies, the inner mechanism of the food poisoning by microorganisms remains unraveled. In the present review, author attempted to formulate models for the foodborne infections, intoxications, and toxicoinfections. Understanding of these models and pathogenesis would be useful to combat foodborne diseases using the accurate strategies to resolve the complications and to improve the public health as well.

Keywords: Foodborne infections, foodborne intoxications, foodborne toxicoinfections, public health

How to cite this article:
Noor R. Insight to foodborne diseases: Proposed models for infections and intoxications. Biomed Biotechnol Res J 2019;3:135-9

How to cite this URL:
Noor R. Insight to foodborne diseases: Proposed models for infections and intoxications. Biomed Biotechnol Res J [serial online] 2019 [cited 2023 May 30];3:135-9. Available from: https://www.bmbtrj.org/text.asp?2019/3/3/135/266568

  Introduction Top

Foodborne complications posed by microorganisms

Foods are frequently contaminated with various bacterial species and fungal population during different stages of handling.[1],[2],[3],[4],[5],[6],[7],[8],[9],[10],[11] A line of microorganisms are known to gain access into the foods of different groups, resulting in food poisoning with some commonly known symptoms to more serious complications.[12],[13],[14],[15],[16] To the global knowledge, in perspective of the types of foods prone to microbial attack, the red meats, poultry, and seafood products have been reported to be more likely to cause illness than fruits and vegetables.[17]

Major types of bacteria causing the foodborne illnesses include (1)  Salmonella More Details spp., contaminating raw and undercooked meat, poultry, dairy products, and sea-foods; (2) Campylobacter jejuni, contaminating the raw or undercooked chicken and unpasteurized milk; (3) Shigella spp., mostly contaminating the water used for food processing; (4)  Escherichia More Details spp., principally contaminating raw or undercooked meat, unpasteurized fruit juices and milk, and fresh vegetables and fruits; (5) Listeria monocytogenes, contaminating raw and undercooked meats, unpasteurized milk, soft cheeses, etc.; (6) Vibrio spp., mostly contaminating fish or shellfish; (7) Clostridium botulinum, contaminating improperly canned foods and smoked and salted fish; (8) Alicyclobacillus acidoterrestris, heat-resistant mold, Penicillium expansum contaminating fruits especially apples; (9) Bacillus cereus from infant foods; and (10) the fungal genus Wallemia from dried, salted, or highly sugared foods.[18],[19],[20],[21],[22],[23] Shiga toxin-producing Escherichia coli, including O157 and many non-O157 serogroups, are also known to be the important causes of foodborne complications. Approximately 400 STEC serotypes are considered to be implicated in the disease.[12] Apart from bacterial spoilage of foods, the major food-contaminating viruses include Norovirus causing inflammation of the stomach and intestines and the hepatitis A virus causing inflammation of the liver.[24] Among the food-spoiling parasites, Cryptosporidium parvum, Giardia intestinalis, and Trichinella spiralis are well known.[15]

Rationale of the current review

Apparently foodborne diseases (FBDs) are known to be triggered by microbial attack; however, the mechanism of causing the spoilage is not well established although the information on foodborne toxins is adequate.[25] While the information on inhibiting the toxicological potential of natural toxins excreted by the microorganisms is also known, the mechanism of actual pathogenesis is still unclear. In the current review, the possible modes of the FBDs are discussed with the proposed models. These models may contribute to the chronicle understanding of possible ways of food poisoning, which may aid to the invention of new treat strategies of the cases of food poisoning.

Foodborne illnesses: Infections, intoxications. and toxicoinfections

FBDs are a prime public health issue round the globe.[26] A line of data from 2000 to 2008 showed that the microbial pathogens that were implicated in most FBDs were Norovirus, nontyphoidal Salmonella spp., Clostridium perfringens (1.0 million, 10%), and Campylobacter spp.[26] Foodborne illness is usually known as “FBD,” “foodborne infection,” or “food poisoning.”[3],[15] Foodborne microbial hazards are principally grouped into (1) foodborne infections, (2) intoxications, (3) toxicoinfections.[11],[27] Previously, the food safety according to the legislative bodies was reported showing the factors associated with foodborne microbiological hazards.

Foodborne infections

Advances in the next-generation sequencing technology for whole-genome sequencing of foodborne pathogens have provided radical recuperation in food pathogen outbreak scrutiny.[28] In case of “foodborne infections” (Salmonella spp., Campylobacter spp., E. coli O157:H7, etc.), the bacterial cells are usually noticed to keep themselves alive, gradually colonize within the host cells, and can even release toxin [Figure 1]. In this case, microorganisms are ingested through the food items in a relatively dose of the recommended levels. The intestinal epithelial cell lining is mostly occupied by the invading microorganisms which further spread to the lower intestinal tract or even to the lever. It is to be noted that campylobacteriosis has also been allied to Guillain–Barré syndrome, irritable and inflammatory bowel syndrome, and, sporadically, reactive arthritis.[29]
Figure 1: General model of foodborne infections caused by foodborne microbial pathogens. Microorganisms ingested through the contaminated foods in sufficient numbers (equal to or above the defined infectious dose) are likely to adhere to the intestinal epithelial cells with subsequent dissemination into the liver and the lower intestinal tract, resulting in the weakened immune system or the diarrheal syndromes

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Most E. coli strains are known to be the commensal along the intestinal tract of which a group produces virulence factors.[12] This group includes enteropathogenic E. coli, STEC, enteroinvasive E. coli, enteroaggregative E. coli, diffusely adherent E. coli, and enterotoxigenic E. coli, and a new pathotype, the adherent invasive E. coli. However, these are very well known to the food microbiologists although the pathogenic mechanisms are yet to be chalked out.

Recently, the livestock-associated methicillin-resistant Staphylococcus aureus has been reported to be a novel pathogen responsible for emerging infections.[26]S. aureus, with the combined traits of toxin-mediated virulence, invasiveness, and antibiotic resistance is known to trigger wide spectrum of infections together with invasiveness and fatality. Both nosocomial and community-acquired infections from this microorganism have been reported. Another interesting report has been published on angiostrongyliasis which is a foodborne parasitic disease, i.e., eosinophilic meningitis (EM) caused by the nematode Angiostrongylus cantonensis.[30]

S. aureus is measured as one of the foremost causes of foodborne chronic and persistent infections, and this very species is known to produce a variety of toxins including the staphylococcal enterotoxins (SEs), hemolysins, Panton–Valentine leukocidin, toxic shock syndrome toxin-1, and invasive enzymes such as plasma coagulase and deoxyribonuclease.[31] Interestingly, as has been known for long time, the capacity of this species to form biofilms may go a long way to achieve the survival traits in hostile environments within the host.[31] Later, the biofilm-related adhesion genes (ica D, ica A, fnb A, bap, clf A, and cna), the enterotoxin genes (sea, seb, sec, sed, and see), and tst-1 gene were detected.[32]

Foodborne intoxications

Bacterial toxin-mediated foodborne outbreaks have been frequently reported principally with the pathogenic species including C. perfringens, S. aureus, and B. cereus. Preformed toxins (formed in the food and are responsible for gastroenteritis) are produced by S. aureus and B. cereus, while thein vivo toxins are known to be produced by C. perfringens and B. cereus.[33] The toxin cereulide (a small dodeca depsipeptide toxin that evokes emesis a short time after ingestion of contaminated food) produced by a genetically closely related subgroup of B. cereus is of special attention.[34] Botulism, an apparently rare but fatal sickness, is caused by the neurotoxin produced by C. botulinum.[35]

In case of “foodborne intoxication,” the toxins instead of the bacterial or fungal cells are ingested into the consumer body as is widely noticed for Staphylococcus gastroenteritis and C. botulinum [Figure 2]. Fungal toxins such as fumonisins, aflatoxin B, and ochratoxin A and bacterial toxins such as botulinum neurotoxin, cholera toxins, Shiga toxin, and Staphylococcus enterotoxin are widely known to be the etiological agents for the foodborne illnesses.[25] In Korea, a study revealed the probabilities for growth of S. aureus and the enterotoxin production by the strain in pork meat-based foods.[35] The correlation between the level of toxin production and the cell number was estimated. The least toxin dose was adopted to assess the possible staphylococcal intoxication. The data detected an increased possibility of staphylococcal intoxication dependent on the increased levels of initial contamination in the raw meats.[36]
Figure 2: Proposed model of foodborne microbial intoxication and toxicoinfection within host cells. Pathogenic bacteria (such as Vibrio cholerae, Bacillus spp., Clostridium spp., and Staphylococcus spp.) which may come into contact of the food items in various ways are frequently associated with foodborne intoxication and toxicoinfection through imparting toxins (besides causing the food borne infection as shown in Figure 1). This schema presents the route of transmission and mode of action of toxins produced by Vibrio cholerae and Clostridium botulinum in causing cholera (intoxication) and botulism (toxicoinfection), respectively

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Foodborne toxicoinfection

Biological toxins are known to affect the nervous systems of mammals, blockage of main cellular metabolism, causing cellular death. The most dreadful toxins are the botulinum toxin, SEs, C. perfringens toxins, ricin, abrin, and T-2 toxin.[37] In case of “toxicoinfection,” vegetative or dormant cells (spores) of C. perfringens, B. cereus, Bacillus anthracis, etc., are ingested which, after death, release toxins [Figure 2]. Earlier research on microbial toxicology revealed that S. aureus produces an array of toxins including the SEs consisting of a family of nine major serological types of heat stable enterotoxins.[38] Furthermore, Vibrio cholerae, Bacillus spp., Clostridium spp., Staphylococcus spp., etc., gain access into the food items in various ways and thereafter release toxins.[25]

Besides toxin production, V. cholerae is also found the nonpathogenic biofilms; and during its propagation to human hosts, it is greatly orchestrated by the significant changes in gene expression patterns accompanied with the expression of virulence factors. Such a signal transduction phenomenon is principally coordinated by the bacterial phosphoenolpyruvate phosphotransferase system that is involved in the quorum sensing and biofilm formation.[39]C. perfringens has recently been found to excrete alpha (α), beta (β), beta2 (β2), epsilon (ε), and iota (ι) toxins.[40] Eighteen species of B. cereus have been isolated so far, with nine being dominant in different food samples.[41] E. coli O157:H7, another foodborne bacterium, causes the hemorrhagic diarrhea and hemolytic uremic syndrome in humans.[42]

Because of increasing demand for rapid and accurate detection of microbial pathogens within the food samples tested, molecular techniques are now being applied in the enriched laboratory settings especially in the developed countries for the detection of microorganisms in foodstuffs.[43],[44],[45],[46],[47],[48],[49],[50],[51],[52],[53],[54] For example, S. aureus enterotoxin can be detected on the basis of bioassays, molecular techniques (including polymerase chain reaction (PCR), reverse transcription PCR, and RT-quantitative PCR), enzyme immunoassay and enzyme-linked fluorescent assay, and/or immunological techniques.[55] Such techniques would aid to improve the proposed models of foodborne illnesses.

  Conclusion Top

A clear understanding of the mechanism of food-spoiling pathogenesis may contribute to the more extensive research on the molecular level to identify and resolve the foodborne complications, may generate advanced technology to detect not only the spoiling microorganisms but also the toxins produced by them, and finally may construct a database for different food-spoilage microorganisms on the basis of their mode of pathogenesis. Besides maintaining the nutritional quality and food safety, such measures would scientifically heighten the knowledge on food microbiology and can be considered in risk assessment as well as to conduct the appropriate public health interventions.

Financial support and sponsorship


Conflicts of interest

There are no conflicts of interest.

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