Properties of Foodborne Pathogens and Their Diseases

Abstract

Thousands of foodborne pathogens are causing a great number of diseases with significant effects on human health and economy. Foodborne pathogens can contaminate food items not only during production and processing, but also at the time of storage and transport before consuming. During their growth, these microorganisms are capable of secreting different type of toxins into the extracellular environment. Likewise, other harmful substances can be also released and can contaminate food after breakup of food pathogens. Many microbial toxins can withstand inactivation, and can endure harsh treatment during food processing. Many of these molecules are partaken in cellular processes and can display different mechanisms of pathogenesis of foodborne organisms. Thus studying the properties of foodborne pathogens can help in the understanding of their contamination and inactivation. In the present review, we discussed extensively on the properties of foodborne pathogens including bacteria, viruses and parasites. In addition, some of the diseases caused by foodborne pathogens and the mechanism of their pathogenesis were also discussed.

1. Introduction

Pathogenic microorganisms such as bacteria, virus, fungi and parasite caused foodborne diseases, however, bacteria are the most common cause of foodborne pathogen and exist in a variety of shapes, types and properties. Some are capable of spore formation and thus, highly heat-resistant (e.g. Clostridium botulinum, Clostridium perfringens, Bacillus subtilus, Bacillus cereus). Some are capable of producing heat-resistant toxins (e.g. Staphylococcus aureus, C. botulinum). Most are mesophilic with optimal growth temperature range from 20–45°C. Moreover, certain foodborne pathogens (i.e. psychrotrophs), such as Listeria monocytogenes, and Yersinia enterocolitica are capable of growing under refrigerated conditions or temperatures less than 10°C. Common disease associated with foodborne pathogens include botulism, cholera, typhoid, dysentery, listeriosis and many more. Foodborne illness is typically caused by micro-organisms or their toxins and most often manifests itself through gastrointestinal illness, which can vary markedly in severity and duration [1]. The zoonotic characteristics of foodborne pathogens and their capability to generate toxins causing diseases or even death are enough to consider the genuineness of the circumstances. Foodborne pathogens cause tremendous of cases of sporadic infections and chronic difficulties, as well as huge and terrible outbreaks in several countries and between countries. The degree of this problem is confirmed by the considerable number of the 1.5 billion annual diarrheal cases in children below 3 years of age that are caused by enteropathogenic microorganisms, which leads to more than 3 million deaths per year [2]. Report has indicated that in the United States alone, bacterial enteric pathogens cause 9.4 million cases of foodborne infection in humans, 55,961 hospitalizations, and 1,351 deaths each year [2]. The rapid increase of residents and urbanization, the level income per capita, the industrialization, the changes of the purchaser habits (eating more protein in the diet) have escalated the consumption of animal products [3]. Analysis proposed that consumption of these products will get higher to 376 million tons by 2030 [3]. This huge demand of animal products has triggered animal production and processing of products, with an increase of foods transportation worldwide. This condition could lead to substandard processing practices and enhance of the risk of contamination by foodborne pathogens at any place. Animal and animal products contamination is a major public health concern because it is hard to manage. Several factors could cause this contamination including water from different sources, frequent disposal of animal’s manure, and improper handling of animal during slaughtering and processing practices, and storage procedures [2]. Foodborne pathogens are capable of causing disease through consumption of the animal products polluted with microorganisms or their toxins. This chapter reviewed the properties and diseases of foodborne pathogens comprising bacteria, fungi viruses, and parasites. In addition, the mechanism through which these foodborne pathogens caused disease has also reviewed.

2. Common foodborne pathogens and their properties

2.1 Bacterial pathogens

Bacteria are the most widely foodborne pathogens causing numerous foodborne diseases either by ingestion of the microorganisms themselves or toxins produced by certain groups microorganisms. Common bacteria found in foods include but not limited to the following: V. cholera, C. botulinum, C. perfringens, E. coli, S. aureus, Salmonella species, Shigella species, Listeria monocytogens, Bacillus species, Yersinia species, Campylobacter species. They range from Gram-positive, Gram-negative, cocci to bacillus or rod shape. Some are aerobic, while others are anaerobic, some are psychrophiles, mesophiles while others are thermophiles, some bacteria form spores while others are non-spore forming. These foodborne bacteria are discussed in detail below.

2.1.1 Vibrio cholerae

V. cholerae is a Gram negative rod (comma) or curved shaped facultative anaerobe bacterium that ranges from 0.7–1.0 by 1.5–3.0 μm in size. It thrives well on thiosulfate citrate bile salts sucrose (TCBS) agar, upon growing on TCBS, the pathogen produces pale-yellow, shining (translucent) colonies 3 mm in diameter V. choleraeis one of the most abundant species of Vibros that causes infections to humans apart from Vibrio parahaemolyticus and Vibrio vulnificus. The pathogen undergoes two (2) lifestyles; as a free-living when it inside aquatic environment or pathogenic when in the gastrointestinal tract. It has the ability to remain virulent without multiplying in fresh water and sea water for a long time. They are numerous in temperate waters and can be isolated in seafood and fish. The most notable species are V. choleraeO1 and O139, causative serogroups of cholera. Non-O1 strains and the rest of about 9 species cause cholera-like diarrheal syndromes, but they are not as severe, even though they frequently produce extra intestinal infections. The CTX toxin (Cholera toxin) is the main virulence factor of V. choleraeO1 [4]. V. cholerae has a single polar flagellum located at the extreme side of the bacterium which enables it to move (motility) from one place to another and colonization across the intestinal mucosa. However, there are other virulent factors that helps the organism survive or damage the host cell, these include; lipopolysaccharide (LPS), biotin, flagellin, iron-regulated outer membrane proteins [5].

2.1.2 C. perfringens

C. perfringens is a Gram-positive, spore forming, anaerobic bacillus about 3.0–8.0 by 0.4–1.2 μm in size. They are mesophiles that is they can grow well at some moderate temperatures between 20–45°C. C perfringens is a fastidious non-motile bacterium that shows hemolysis when growing on blood agar. Because they are too demanding and requires much vitamins and amino acids for growth and multiplication, hence, they thrive well in meat products because meat product contains high amount of vitamins and amino acids especially beef meat [6]. It’s virulence factors are incorporated within the plasmids, these include but not limited to alpha toxin (phospholipase C), kappa toxin (Collagenase), beta epsilon, iota toxins, delta toxins (hemolysins), theta toxins (streptolysin O) [7].

2.1.3 C. botulinum

C. botulinum are Gram-positive, catalase negative, motile, spore-forming, obligate anaerobic rod bacterium about 4.0–6.0 μm in size. They are Psychrophiles which grow at a temperature ranges between 3 and 15°C, however, proteolytic strains thrive well at an optimum temperature of 35–37°C, however, non-proteolytic strains grow well at a temperature ranges between 26 and 28°C respectively. Its virulent factors include toxin: botulinum neurotoxin (BoNT) which specifically damage the neurons, C2 and C3 toxins which causes cell damage and helps in spreading botulinum toxin in the tissue, flagella [8]. C. botulinum are motile by means of peritrichous flagella. There are seven types of botulinum neurotoxin; A through G, based on the antigenic specificity of the toxin produced by each strain [9].

2.1.4 L. monocytogenes

L. monocytogenes are Gram-positive rods, non-spore forming bacterium that contained peritrichous flagellation with tumbling motility. They range from 1 to 2 μm in size, which exist as either single or double cells. They are psychrophiles which grow well at a temperature range from 1 to 45°C [10]. The organism is cultured under aerobic conditions on blood agar which formed small gray colonies surrounded by discreet hemolytic zone, caused by listeriolysin O. [11]. They occur ubiquitously in nature and they are present in many food products, mainly in soft cheeses, dairy products, and many cheeses made with unpasteurized milk, celery, cabbage, ice cream, hot dogs, and processed meats [12].

2.1.5 B. cereus

B. cereus are Gram-positive, motile rods, spore-forming bacterium which is about 0.5 × 1.2–2.5 × 10 μm in diameter in size. Most Bacillus spp. Are predominantly found as free-living in nature, they are present in soils, fresh and marine water environments. B. cereus produced spores which are hydrophobic in nature with many attachments (appendages) and/or pili. The spores are the virulent factor of B. cereus which enable the bacterium to adsorbed firmly to different types of surfaces and do repel removal during disinfection. Vegetative cells of B. cereus grow at temperatures ranging from 4 to 15 to 35–55°C [13].

2.1.6 Campylobacter jejuni

C. jejuniare members of the family Campylobacteriaceae and is one of the most common cause of diarrheal illness. C. jejuniis responsible for approximately 850,000 illnesses, 8,500 hospitalizations, and 76 deaths in the US each year. Based on staining characteristics, the pathogen is biochemically, C. jejuniis a Gram- negative consisting of thin layer of peptidoglycan in their cell wall, catalase positive, oxidase positive, urease negative. Morphologically, they exist in spiral or helical rods (S-shape), they do not form spore (non-spore-forming organism) and occur mostly from 0.5–5.0 μm in length. C. jejunipossessed a polar flagellation with one at both end and undergoes twisting-like locomotion. Culturally, C. jejuniis a fastidious and most successful foodborne microbe that has a rigorous growth conditions, in terms of oxygen concentration, C. jejuni is microaerophilic organism which require oxygen concentration as low as 3–5% and carbon dioxide concentration range from 3 to 10% respectively. Unlike other gram negative organism, C. jejuni are thermophiles that grow well at 42°C, they consume amino acids instead of carbohydrates for growth, hence, require complex media for growth artificially [14].

2.1.7 Escherichia coli

E. coli is a Gram-negative, catalase positive, oxidase negative, VP negative, indole positive, urease and citrate negative, non-spore forming rod about 1.0–2.0 μm in size. Some are motile with the means of flagella while others are non-motile. They are facultative anaerobe, because they utilize carbohydrate during growth on artificial media, hence, they convert glucose to lactic, acetic, and formic acids as byproducts; however, in terms pH concentrations, E. coli grow at an optimum pH of 6.0 to 8.0 (i.e., they grow well in alkaline as well as in acidic environment). E. coli comprise a large and diverse group of bacteria with majority harmless strains; other strains are pathogenic and are harmful, thus, have acquired characteristics, such toxins production, which make them pathogenic to humans [15]. Based on the pathogenicity and mechanism of pathogenicity, E. coli have been categorized into six groups: (1) EnteropathogenicE. coli (EPEC); (2) EnterohemorrhagicE. coli (EHEC, also known as Shiga toxin-producing E. coli [STEC] and formerly referred to as verotoxin-producing E. coli [VTEC]); (3) EnterotoxigenicE. coli (ETEC); (4) EnteroaggregativeE. coli (EAggEC); (5) EnteroinvasiveE. coli (EIEC) are non-motile, lactose negative, lysin dicarboxylic negative. EIEC are biochemically, genetically and pathogenetically associated to Shigellaspp, like Shigellaspp, EIEC causes watery diarrhea and dysentry; and (6) Attaching and Effacing E. coli (A/EEC) also known diffusely adhering E. coli (DAEC) [16].

2.1.8 S. aureus

S. aureus are Gram-positive cocci bacterium which exists as single (monococcus), pairs as in (diplococci), tetrads or short chains (Streptococci) or grape-like clusters (Staphylococci) and gliacoccus based on cellular arrangements. S. aureus is one of the abundant normal flora of animals including humans which are predominantly found on the skin, blood, mammary glands, intestine, genitals, respiratory tracts and mouth. They are non-motile, non-spore forming bacterium of about. 0.5–1.5 μm in size which are able to proliferate rapidly in aerobic environments [9]. Under normal condition, and when grown in immunocompetent individual S. aureus is non-pathogenic and form a communalistic relationship (Commensalism), however, when they change environment apart from where they are naturally found or when the host immunity is weakened or become compromised, they become opportunistic and caused what is called opportunistic infections (OIs). S. aureus can remain dormant outside human body for a long period of time in air, sewage, water and dust, apart from environmental sources, S. aureus can be found in foods such as beef, turkey, pork sausage, oysters, milk, salads, cream pies. Depending on the strain, S. aureus grow at a temperatures ranging from 7 to 48C [9]. Biochemically, S. aureus is catalase positive, coagulase positive and ferment mannitol. S. aureus produces a family of virulence factors such as adhesion proteins such as fibronectin, fibrinogen, teichoic acid, enolase, biofilm-associated proteins, enterotoxins such as staphylococcal enterotoxins, super antigens such as Toxic Shock Syndrome Toxin (TST), exfoliative toxins (A, B), hemolysins such as alpha, beta, gamma and delta hemolysins, ADP-ribosylating toxins such as leucocidin, pyrogenic exotoxin, and enzymes (proteases) such as collagenase, Hyaluronidase, Endopeptidase, Elastase [17].

2.1.9 Salmonella spp.

The genus Salmonella belongs to the family Enterobacteriaciae mostly coliform which are indicators. The present of such organisms in water indicated that the water is contaminated with fecal material. Morphologically, Salmonella possess peritrichous flagella which enable the organism to locomote or move from one place to another in the living host, they are non-spore-forming, Gram-negative rods bacterium [18]. These Salmonella were named after the scientist Dr. Daniel Salmon who isolated the first organism, Salmonella choleraesuis, from the intestine of a pig. The genus Salmonella is divided into two species that can cause illness in humans: Salmonella enterica and Salmonella bongori. Salmonella is further subdivided into serotypes, based on the Kaufmann-White typing scheme first published in 1934, which differentiates Salmonella strains by their surface and flagellar antigenic properties [19].

2.1.10 Shigella spp.

The genus Shigellais a member of the family Enterobacteriaceaeand possesses four serogroupsthat have been traditionally treated as species: serogroup A as Shigelladysenteriae, serogroup B as Shigellaflexneri, serogroup C as Shigellaboydii, and, serogroup D as Shigellasonnei. Whereas serogroups A, B, and C consist of 38 serotypes, serogroup D possesses only one [20]. They are Gram-negative, non-motile, non-spore forming rod and facultative anaerobic bacterium. Based on staining and biochemical characteristics, Shigellaspp are catalase-positive, but oxidase and lactose negative respectively. They are good fermenters of sugars and grow well at an optimum temperature 37°C, however, other strains grow at less or greater temperature. Their virulence factors are encoded within their extra chromosomal material called plasmid [21]. Plasmid is located in the chromosome of the bacterium; it contains genes that aid the organism during reproduction.

2.1.11 Y. enterocolitica

The genus Yersinia belongs to the family Enterobacteriaceaeand includes ten (10) established species. They are Gram-negative usually short rod bacterium; non-spore-forming, facultative anaerobes which grow at the temperature ranges between 0 and 44°C however, require optimum temperature range between 24.5–28.5°C. Some species are motile with the aid of flagella while others are non-flagellated, hence, they are non-motile. The swimming and/or swarming motility is dependent upon the temperature of the surrounding environment. At 25°C the organism is able to grow peritrichous flagella, while at 37°C, they are non-motile because they do not possess flagella. Based on cultural characteristics, Y. enterocoliticagrows slowly on MacConkey agar, blood agar, they are good fermenters of sugars (sucrose) but not lactose or xylose. Yersinia can grow in both environment/food and in human bodies, thus, they undergo two types of lifecycles (diphasic). Yersinia pestisis the causative agent of plague, Yersinia pseudotuberculosis is primarily an animal pathogen but may infect humans after the ingestion of contaminated food or water, and Y. enterocolitica has surfaced as a cause of foodborne gastroenteritis in humans [22]. Based on the degree of infectivity, ecologic and geographic distributions, Y. enterocoliticaare classified into five (5) groups and 60 serotypes namely: 1(A and B), 2, 3, 4 and 5 respectively. It is not all Yersinia strains that are virulent, some virulent Yersinia stains have their virulent factors encoded within their plasmid, these virulence plasmids are called pVY. They aid in adhesion, invasion and colonization of intestinal epithelial cells and lymph nodes [23].

2.2 Viral pathogen

Viruses are inert, obligate ultramicroscopic parasites. They possess either RNA or DNA but not both. They may be enveloped or non-envelope, symmetrical or asymmetrical, segmented or unsegmented, helical, or icosahedral in shape. Unlike bacteria, and other microorganisms, virus are non-cellular and as such they cannot be cultured on artificial culture media. Some viruses that causes foodborne are discuss in details below.

2.2.1 Hepatitis a virus (HAV)

Hepatitis A virus particle belong to the family Picornaviridae and genus Heparnavirus also called enterovirus 72. This pathogen, genetically, it is a non-enveloped single stranded positive sense polarity RNA, icosahedral virus with about 7.5 kb and 27 nm in diameter in size. Despite genetic heterogeneity, HAV has only one serotype group but multiple genotypes. However, genotypes I and III are most prevalent affecting humans. Because of it morphological characteristics, HAV can remain viable on the environmental surfaces for a long period of time under favorable environmental conditions such as temperature, pressure and humidity. However, when on human hands, it can remain viable for many hours to few days. HAV can also remain viable in sewage and water bodies for several weeks despite freezing. Serologically, the present of immunoglobulin M (IgM) is indicative of the virus hepatitis A [24]. Recently, outbreaks of viral gastroenteritis and Hepatitis A have been associated with eating usually uncooked shellfish. A clam-associated outbreak of Hepatitis A in Shanghai may have been the largest recorded outbreak of foodborne disease in history, with 292,301 cases [25].

2.2.2 Noroviruses

Norovirus is a non-enveloped single-stranded positive sense RNA which belongs to the family Caliciviridae, genus Lagovirus, or Vesivirus [26]. Most Novoviruses are classified into five (5) genogroups, and in some textbooks six (6) from GI-VI, however, most human infections resulting from genogroups GI and GII. The genome is about 7.5 kb in length and encodes for about three open reading frames (ORFs): ORF1,2 and 3. ORF1 encodes a large polyprotein that is post-translationally cleaved into six nonstructural proteins which include the RNA-dependent RNA polymerase (RdRp), while ORF2 and ORF3 codes for major (Viral protein, VP1) and minor (VP2) capsid proteins respectively [27]. Majority of acute viral gastroenteritis cases worldwide, including an estimated 5.4 million episodes of foodborne illnesses in the US annually are usually caused by norovirus, it is also the leading cause of pediatric acute gastroenteritis particularly among children under the age of 5 [28]. The virus’s abilities to withstand a wide range of temperatures (from freezing to 60°C) and to persist on environmental surfaces and food items contribute to rapid dissemination, particularly via secondary spread (via food handlers or to family members) [29].

2.2.3 Bird-flu virus

Bird-Flu Virus also called avian influenza virus or influenza virus belongs to family Orthomyxoviridae, genus influenza virus. The virus is classified into three: Influenza virus A, B and C, however, type A influenza virus is the most important of the three types. Because of the changes or alterations in antigenic structure due to point mutation within narrower range and recombination within broader range which occur less frequently than the latter, influenza type A virus is the major pathogen responsible for epidemics and pandemics. However, type B tends to be endemics more than type C. influenza virus is the pathogen responsible for flu, whereby, the clinical picture or manifestations is associated with bacterial co-infection such as pneumonia. Genetically, influenza virus contains single-stranded RNA, while morphologically, it is segmented, nucleocapsid, and spike proteins which are encapsulated within a structure called envelope. It also contains other proteins such as hemagglutinin, neuraminidase which help in viral pathogenicity and pathogenesis. As earlier said, the genome of influenza virus has about eight separate antisense RNA strands and mostly segmented which encodes for separate and specific proteins each [11].

2.3 Parasites

Parasites are eukaryotic protozoans which exists in various shapes and forms. They have true nucleus which is enclosed within a nuclear membrane. Some parasites have mitochondria while absent in others. Others organelles present in their cytoplasm include but not limited to endoplasmic reticulum, ribosomes, flagella, pseudopods, cilia. Parasitic organisms that causes foodborne illness are discussed below.

2.3.1 Toxoplasma gondii

Toxoplasma gondiiis an obligate intracellular microscopic protozoan which belong to the phylum Apicomplexa, itcauses toxoplasmosis in humans. Its life cycle consists of two phases: intestinal (enteroepithelial) phase and extra intestinal phase. The intestinal phase is taking place mostly in the primary host such as cats; while the extra intestinal phase is mostly seen in all animals including humans. However, humans and other mammals are the intermediate hosts. The pathogen has three (3) stages in its lifecycle; Tachyzoites, bradyzoites and sporozoites, however, tachyzoites (endozoites) and bradyzoites (cystozoites) takes place in the tissues, whereas tachyzoites multiply and damage infected host cells by means endodyogeny (the formation of two daughter cells from mother cells by means of budding, while the bradyzoites proliferate inside the tissue cysts [4].

2.3.2 Giadia lamblia

Giardia duodenalisalso known as Giardia lamblia or Gasterophilus intestinalis is responsible for giardiasis. The pathogen consists of two stages oflife cycle: trophozoite (a jewel shape, non-infective stage, about 9–21 m long and 5–15 μm wide, and contain nuclei with four flagella) and cyst (ovoid; 9–12 m long, resistant and highly infective and matured stage). Infective dose is 10–100 cysts and the incubation period is 1–2 weeks. Reproduction is by asexual means through binary fission. Because it is flagellated organism, Giadialimbliaundergoes tumbling motility [4].

2.3.3 Entamoeba histolytica

E. histolyticais a pathogenic and the most invasive member of the genus and is responsible for amebic dysentery. It exists in two forms morphologically, as a cyst and as a trophozoite. The cyst of E. coli is about 0–15 μm in diameter, and are highly infective in nature, while the trophozoites are usually 10–60 μmin diameter, non-motile and do adhere and invade intestinal epithelial cells. Their virulence factors include Gal/GalNAc-inhibitable lectin which a pivotal role in adhesion and tissue demolition, these virulence factors also help the pathogen to interact with host glycoprotein to adhere (adsorb), to block complement activation, as well as to promote cytotoxicity of neutrophils and macrophages. E. coli also produced a structure called amoebapore which cannels ions in to the host cell membrane causing cytolysis. The genus Entamoeba comprises of a number of species: E. histolytica, E. dispar, E. moshkovski, E. coli, Entamoeba hartmanni, and Entamoeba polecki. Others exist as commensals in human intestine. E. histolyticaproduces amoebapore that forms ion channels in the host cell membrane causing cytolysis. Each trophozoite carries single nucleus and can convert into precyst and matures into tetra nucleated cysts which are released with feces. Cysts can survive outside the body for several weeks to months if the temperature is favorable (−5°C or over 40°C) [4].

2.3.4 Ascaris lumbricoids

Ascarislumbricoids, A nematode that parasitize in the small intestine of humans, The adult worm (giant round worm) is about 15–40 cm in length, yellowish pin in color and thick as pencil. The sexually matured female Ascaris produce about 200 000 eggs per day usually in unembrayonated state which are then released in feces. The eggs of A. limbricoides which exist in spherical or oval in shape are about 60 x 45 um in size, with thick brownish shell and uneven shape. It takes almost three to 6 weeks for an egg to develop into larval stage at optimum temperature from 20–25°C, sufficient water (moisture) and oxygen [11]. They are associated with food when prepared under poor sanitary conditions [4].

2.4 Fungal pathogens

Fungal are eukaryotic organisms unlike bacteria which are prokaryotic. Depending on the temperature upon which the fungal cells are growing, fungal pathogens exists in two forms: (as a molds, and as a yeasts). The phenomenon of which they are grown is called dimorphism. Dimorphism is the phenomenon whereby fungal cells exists in two forms based on the temperature, at 2⁰5 C, the fungi exists as molds e.g.; Aspergillus species, while at 37°C they exist as a yeast e.g. Candida albicans. Unlike bacteria in which their cell wall consist of peptidoglycan, fungal cell wall constitute primarily of chitin (which is a polysaccharide composed of long chains of N-acetylglucoseamine). They reproduced both sexually and asexually, some fungal hyphae are segmented hence, they are called septate while others are unsegmented, thus, they are aseptate. Most fungal cell walls consist of ergosterol. Details explanation on fungal pathogens that are associated with foodborne diseases are discussed below.

2.4.1 Aspergillus flavus

A. flavusare multicellular microorganisms and a typical mold possesses hyphae, conidiophore—consisting of stalk, vesicle, sterigmata, and conidia. They produced mycotoxin called Aflatoxin, which exist in different chemical forms; B1, B2, G1, G2, and M1. The B and G stand for blue fluorescence and green fluorescence, respectively. Aflatoxins are found in nuts, spices, and figs and produced during storage under hot and humid conditions. The allowable toxin limits are 20 ppb in nuts (example, Brazil-nuts, peanuts, pistachio). Aflatoxin contaminated feed causes high mortality in farm animals. These aflatoxins cause harm in human body in three ways: mutagenic- they caused mutation either in the form of substitution, frame-shift, deletion and/or addition mutation which cause infection of the liver (hepatotoxic), Teratogenic action leads to birth defects and the carcinogenic effect cause irreversible defects in cell physiology resulting in abnormal cell growth and metastasis (called cancer or tumor) [4].

2.4.2 Aspergillus ochraceus

These are microscopic molds fungi consist of hyphae, conidiophore and conidia. They produced mycotoxin called ochratoxin. It is found in a large variety of foods including wheat, corn, soybeans, oats, barley, coffee beans, meats and cheese however, barley is thought to be the predominant source. Ochratoxin is hepatotoxic and nephrotoxic and a potent teratogen and carcinogen. Nephropathy and renal problem are predominant consequences of ochratoxin poisoning. It inhibits cellular function by inhibiting the synthesis of phenylalanine–tRNA complex, and ATP production. It also stimulates lipid peroxidation. The LD50 value in rats is between 20 and 22 mg kg⁻¹ [30].

2.4.3 Fussarium spp

These microscopic saprophytic, filamentous fungi that belong to the hyphomycetes. The genus Fussarium has over 300species. They reproduce asexually by spore production. Fusarium species produced three kinds of asexual spores; microconidia, macroconidia and chlamydospores respectively. However, the spore formation defends on the type of specie, some species produces three while others produce only one. Microconidia are developed in conidiophores, these microconidia are produced in the aerial mycelium with different shapes and sizes. They caused variety of plant and animal disease including humans. Their ability to cause disease is based on the ability to produce mycotoxins. Some mycotoxins produced by some species of Fussarium include; fumonosins, zearalenone (Fussariumgraminearum). Fumonosins are water soluble compound which are produced by the condensation of amino acid alanine into acetate. It is abundant as fumonosin B1. They cause variety of disease in humans such as leukoencephalomalacia, pulmonary edema, hydrothorax and esophageal cancers [4]. Zearalenone is a mycoestrogen produced by Fussariumgraminearumin the human ovary which result to infertility in humans [30].

2.4.4 Penicilliumpatulum

Penicillium is a saprophytic microscopic fungus, commonly known as blue or green mold. Their vegetative thallus or body called mycelium is copiously branched with septate (cross-wall) hyphae range from unicellular to multicellular in nature that reproduces by sexual, asexual and vegetative means. They produced a conidiospores during asexual reproduction which are non-motile and are developed inside a conidiophore as well as an ascospores. They produced secondary metabolites called patulin. Bread, sausage, fruits (apricots, grapes, peaches, pears, and apples), and apple juice are the major source of this toxin. Patulin is a carcinogen and is reported to be responsible for subcutaneous sarcoma, it must be present in high quantity for as much as 15–25 mg kg − 1 (LD50 value) for infection to occur [30].

2.4.5 Penicilliumcitrinum

Penicilliumcitrinumis a saprophytic microscopic fungus, commonly known as blue or green mold. Their vegetative thallus or body called mycelium is copiously branched with septate (cross-wall) hyphae range from unicellular to multicellular in nature that reproduces by sexual, asexual and vegetative means. They produced a conidiospores during asexual reproduction which are non-motile and are developed inside a conidiophore as well as an ascospores. These fungal pathogens produced a mycotoxin called citrinin. The major source of this toxin is rice, moldy bread, ham, wheat, oats, rye and barley. Citrinin is a nephrotoxin and causes nephropathy in animals. It is reported that the LD50 value for citrinin in chicken is 95 mg kg − 1; in rabbits, 134 mg kg − 1 and its significance in human health is unknown [4].

2.4.6 Clavicepspurpurea

Clavicepspurpurea is some microscopic saprophytic fungi with septate hyphae. It produces a toxic cocktail of alkaloid, which is not considered a typical mycotoxin. Ergots grow on the heads of grasses such as wheat and ryes and the disease is known as St Anthony’s Fire because of severe burning sensations in the limbs and extremities of the victim. Two forms of egotism are reported: gangrenous and convulsive. In the gangrenous form, the blood supply is affected causing tissue damage. In the convulsive form, the toxin affects the central nervous system. The egotism is a serious problem in animals including cattle, sheep, pigs and chicken resulting in gangrene, convulsions, abortion, hypersensitivity and ataxia. In cattle, ergotism spreads around the hooves and animal may lose hooves and are unable to walk and die by starvation [30]

3. Common disease associated with food

The Table 1 describes some common foodborne diseases caused by bacteria, viruses, parasites and fungal pathogens respectively including the mode of transmission/food associated and clinical manifestation.

Diseases	Pathogen	Mode of transmission and associated food	Clinical Manifestations	Reference
Cholera	Vibrocholerae	Fecal-oral route via vegetables, seafood, rice and beans	Vomiting, watery diarrhea, dehydration, loss of appetite, fever, weakness of the body, headache, malaise.	[31]
Enteritis	Clostridium perfringens	Ingestion of beef and poultry meat	Vomiting, abdominal pains, fever, dizziness, putrefactive diarrhea.	[32]
Botulism	Clostridium botulinum	Ingestion of toxin-preformed food such as vegetables, pepper, meat, fish and baked potatoes	Diarrhea, fever, vomiting, eyes disturbance, weakness of the muscles, dizziness, constipation, fatigue, dry mouth, respiratory track failure, heart attack, paralysis, vertigo.	[33]
Listeriosis	Listeria monocytogens	Ingestion of food such as raw milk, soft cheese, meat based paste, jellied pork tongue, raw vegetables and coleslaw	Gastrointestinal discomfort, fever, headache, athalgia, malady, chills, swollen nymph nodes.	[34]
Gastroenteritis	Bacillus cereus	Ingestion of contaminated food such raw milk and raw or undercooked poultry is the mode of transmission	Diarrhea, nausea, abdominal pain, vomiting.	[35]
Escherichia coli infection	E. coli	Consumption of food and water contaminated with fecal matter. Food involved include; vegetables, raw milk, ground meat,	Vomiting, diarrhea (bloody, mucus), nausea, fever, abdominal cramps.	[36]
Intoxication	Staphylococcus aureus	Consumption of foods containing the toxin. Example of food include meat, rice, raw milk, stew.	Nausea, vomiting, diarrhea, adoration (prostration), constipation, heaving, abdominal discomfort.	[9]
Typhoid; and paratyphoid fever	Salmonella typhiand paratyphi	Transmission is via ingestion of food and water contaminated with fecal matter such as raw milk, meat, selfish, salad.	Excessive fever, vomiting, headache, abdominal pains, constipation, diarrhea, psychosis in some cases, chills, rose spot, cough.	[37]
Yersiniosis	Yersinia enterocolitica.	is transmitted through consumption of pork products (tongue, tonsils, gut), cured or uncured, as well as milk and milk products	Diarrhea, vomiting, fever, abdominal cramp.	[22]
Shigellosis (bacillary dysentery)	Shigelladysentriae	Ingestion of food and water contaminated with fecal matter such as salads and vegetables; water, raw milk	Diarrhea containing blood, pus and mucus, abdominal discomfort, fever, vomiting.	[38]
Hepatitis A	Hepatitis A Virus	Transmitted fecal-orally in food and drinking water such as shellfish, raw fruit and vegetables, bakery products	Nausea, loss of appetite, fever, vomiting, inflammation of the liver, jaundice, dark urine.	[39]
Viral gastroenteritis	Norovirus(Norwalk virus)	Fecal-orally in drinking water and food. E.g. shellfish or drinking water contaminated with sewage	Diarrhea, fever, vomiting, abdominal pain, dehydration.	[39]
Bird flu or avian influenza	Bird flu virus or influenza virus or avian influenza virus	Fecal-orally in food and drinking water	Fever, headache, coughing, flu, vomiting, diarrhea.	[11]
Viral gastroenteritis	Rotavirus or Adenovirus	Transmitted fecal-orally via contaminated food and water.	Watery diarrhea, vomiting, fever, stomach cramp.	[40]
Amoebiasis (amoebic dysentery)	Entamoeba hystolitica	Ingestion of faecally contaminated food and water containing amoebic cysts. Food involved include fruits, vegetables and drinking water.	Diarrhea, vomiting, dehydration, fever, headache, dizziness, insomnia, ulcer, drowsiness, weight loss, gastroenteritis.	[11]
Txoplsmosis	Toxoplasma gondii	Transmitted by taking vegetables containing the parasite.	Fever, headache, myalgia, rash	[41]
Taeniasis	Taeniasaginata, Taeniasolium	Transmitted vi eating fruits, vegetables, pork meat, beef meat that is contaminated with the pathogen.	Vomiting, diarrhea, insomnia, anorexia, weight loss, nervousness, gastroenteritis	[11]
Ascariasis	Ascarislimbriocoids	ingestion of infective eggs from soil contaminated with feces or of contaminated vegetables and water	Vomiting, excretion of lived worms in the stool, indigestion, gastrointestinal discomfort.	[11]
Acute aflatoxicosis	Aspergillusflavus	Ingestion of aflatoxin in contaminated food such as milk, various cereals, oilseeds, spices, and nuts.	Nausea, vomiting, abdominal pain, convulsions, hepatotoxicity, immunotoxicity, and teratogenicity	[42]
Ochratoxicosis	Aspergillus ochraceus	Ingestion of food and water contaminated with ochratoxin A (OTA). Common food associated with OTA include but not limited to wine, beer, coffee, dried vine fruit, grape juices, pork, poultry, diary, spices, and chocolate	Loss of consciousness, fever, convulsion, inflammation of the liver, diarrhea.	[43]
Ergotism	Clavisepspurpurea	Transmitted via eating contaminated rye grass or by ergotamine orally.	Pains in the calf of the leg, swollen foot, mild diarrhea.	[30]

Table 1.

Common foodborne disease.

Common foodborne disease includes: botulism, cholera, gastroenteritis, intoxication, enteritis, listeriosis, shigellosis, typhoid, salmonellosis, dysentery, yersiniosis, amoebiasis, hepatitis A, viral gastroenteritis, bird flu, taxoplasmosis, taeniasis, ascariasis, aflatoxicosis, ergotism which are discussed in Table 1.

4. Mechanism of pathogenesis of foodborne pathogens

Microbial pathogenesis is a complex task that involves both the pathogens and the host, in this relationship, microbes are trying to gain into the host cell using their virulence factors such as flagella, pili, fimbriae, adhesins (adhesion proteins) e.g. fibronectin, collagen, laminin, integrin, internalin, and biofilm formation e.g. phospholipids, teichoic acids, nucleic acids, polysaccharides, proteins, capsules, enzymes, toxins, spikes, super antigens such as O, H, F, A, B antigens respectively [44]. on the other hand, host is trying to fight the effect of the pathogens using their immune cells such as gastric acids, mucus, bile salts, antimicrobial inhibitors, complement systems and phagocytic cells. At the end of the day, if the microbes succeeded, then the resultant effect is infection, while if the host immunity is strong the pathogens will be neutralized and they will eventually be killed [45].

Generally, foodborne microbes (virus, bacteria, fungi and/or parasites) get into the intestine through the mouth (oral route). Foodborne microbes cause variety of infections range from localized infection to general infection which can spread to almost all part of the body to caused systemic or generalized infection. Because the process is complex, for foodborne infection to be achieved, several factors must come together within the host. The process begins when the human ingests the pathogen in food or water that is contaminated with the pathogen, it will then eventually penetrate into the host cell in large quantity that can damage the host cell. As soon as it gains into the host cell, it then survives in the changing environment, multiply and propagate rapidly. After then, the pathogen colonizes the intestine using adhesive and invasive factors and chemotaxis respectively [46]. Several factors such as capsules, biofilm formation do protect the microbes to survive harsh environment, bacterial enzyme and toxins also safeguard the cells from eradication by the host immunity, certain commensals can also help the pathogen invade to find a suitable habitat for their growth and multiplication [47]. It is important to understand that most foodborne diseases attacked intestine, liver as a target size, thus resulting to liver damage and cancer in some cases can result to death. The pattern of pathogenesis by foodborne microbes is the same be it bacteria, virus, parasite, or fungi as it all started when the host ingest the pathogen in the faecally contaminated food or water, however, they mostly have the same target site; the intestine and the liver, that is why most of the resultant effect of the pathogenesis is gastroenteritis, liver damage and abdominal pain.

5. Conclusion

Foodborne microbial diseases are a significant public health threat. They occur in both developed and developing countries with different food industry expansion, food safety regulations, food hygiene and consumption habits, and climate and environmental situations should be considered as a preventive measure. The subsequent economic burden associated to them is also different. Most foodborne diseases are sporadic and often not reported, but sometimes foodborne outbreaks may affect a large number of individuals and compromise economic sectors and sanitary resources.

Acknowledgments

We would like to thank the authors and reviewers for their wonderful contributions and constructive criticisms to this special issue. We sincerely hope that this collection of papers will prompt further research and contribute to novel or improved strategies of foodborne pathogens- recent advances in control and detection to be able to further reduce the incidence of foodborne microbial diseases.