Current Status of Food Poisoning & Foodborne Illness in sub-Saharan Africa & The Way Forward - A Review

Abstract

In sub-Saharan Africa, food contamination continues to wreak havoc. In this region, ready-to-eat foods are majorly sold by street food vendors where hygiene becomes a major challenge given the inadequate supply of portable water. Large numbers of unlicensed vendors operating their businesses in hard to reach areas, mostly after-work hours, thwart the efforts by the public health inspectors to ensure safe food for the public. Agrochemical use in food production is at an all-time high posing the risk of pesticide residues in foods. As health records indicate, food poisoning and foodborne illness cases are on the rise in the region. These food safety challenges will only worsen the global food crisis given the food supply deficit in most parts of the world. This is a cross-sectional desktop review of peer-reviewed journals, survey reports, and records from both government and private health facilities documenting food poisoning and foodborne illness outbreaks in sub-Sahara Africa. Books on microbial physiology and metabolism have been used to highlight how to deal with the causative microorganisms. Aetiological agents of food poisoning and foodborne illnesses can be broadly categorized as pathogenic and toxigenic bacteria, parasites and viruses. Incrementally, chemical contaminants and allergens that may find their way into food also play an important role. Unhygienic handling and deliberate contamination of food can be classified as human factors that also contribute to the problem. To address these issues, all the stakeholders in the food value chain should be involved. Food safety policies should promote surveillance and encourage players to adopt standards geared towards ensuring food safety. Training should be regularized to ensure players can monitor food safety and report outbreaks early for containment.  Multi-sectorial approach should be adopted to address challenges of policy implementation. Inter-departmental synergy is instrumental in addressing the current challenges.

Key wordsRisk factorsFood safety, Food contamination

ContributorsKevine Otieno; Imbahale Ruth; Stephen Odera & Cyrus Kihara

Introduction

Food, being a source of all the necessary nutrients for human sustenance, serves as the single greatest vehicle for foodborne infections. In the quest to fulfil the bodily requirements for nutrients, consumers find themselves grappling with many challenges to avoid intoxicating themselves in the process. Hygienic handling therefore remains the biggest key in ensuring that the source of nourishment does not serve as a death trap for the eager consumer.

In Africa, foodborne illnesses remain one of the biggest scares to human health and wellbeing. Given the level of poverty that is prevailing across the continent, the vulnerable groups such as children and the elderly as especially disadvantaged (CDC, 2018).

People with compromised immunity (HIV patients) find themselves in precarious situation, with their immunity unable to defend them against any minor attack. This increases the morbidity rates across the continent as a result of diarrhoeal diseases.

World Health Organization estimates that there are approximately 700,000 deaths in Sub Sahara Africa every year due to foodborne diseases. The proportion of children under five who succumb diarrhoeal foodborne illnesses is pegged at 15% by the same findings (WHO, 2008).

Foodborne Illnesses

Food borne illnesses are described by the world health organization as diseases of infectious or toxic nature caused by consumption of contaminated foods or water. Some chemicals that causes food borne illnesses are natural components of food, while other may be accidentally added during production and processing, either through carelessness or pollution.

The main causes of food borne illnesses are bacteria (66%), chemicals (26%), virus (4%) and parasites (4%) (Hoffmann, et al., 2017). Food borne illnesses comprise the various acute syndromes that result from ingestion of contaminated foods. They are classified as:

  • Food Intoxications caused by ingestion of foods containing either poisonous chemicals or toxins produced by microorganisms;
  • Toxin mediated infections caused by bacteria that produce enterotoxins (toxins that affect water, glucose, and electrolyte transfer) during their colonization and growth in the intestinal tract;
  • Food Infections caused when microorganisms invade and multiply in the intestinal mucosa or other tissues.

Manifestations of food illness

Manifestations range from slight discomfort to acute illness to severe reactions that may lead to death or chronic symptoms, depending on the nature of causative agent, the number of pathogenic microorganisms or concentration of poisonous substances ingested, and the host susceptibility and reaction.

Some microorganisms can use our food as a source of nutrients for their growth. By growing on the food, metabolizing them and producing by-products, they not only render the food inedible but also pose health problems upon consumption (Ibid).

Many of our foods will support the growth of pathogenic microorganisms or at least serve as vector for their transmission. Food can get contaminated from plant surfaces, animals, water, sewage, air, soil or from food handlers during handling and processing.

Typical symptoms of food borne illnesses include diarrhoea, vomiting, abdominal cramps, headaches, nausea, dry mouth, and difficulty swallowing and fluke-like symptoms (such as Fever, chills, backache).

Incidences of food illness

Despite repeated efforts to improve hygiene across many parts of Sub Sahara Africa, there are still several incidences of foodborne illnesses. Cases of cholera, aflatoxicosis, shigellosis, and konzo (paralysis due to consumption of cyanide in cassava) have been regularly observed.

Cases of contaminated foods are reported on a regular basis and multi drug resistant strains of pathogenic bacteria have been reported, and attributed to careless misuse of drugs in animal husbandry.

Ease of access due to rapidly increasing infrastructural developments across the continent has accelerated the transmission of foodborne and zoonotic illnesses. Lax enforcement of policies has been a big promoter of the increasing spread.

New challenges arise in places they never existed before as a result of globalization (Jay, 2000). The residents are found unprepared for the challenge and containment measures are either lacking or non-existent.

Effects of rural-urban migration on foodborne illness occurrence

The shifting population dynamics and rural-urban migration in most parts of the continent has popularized ready to eat foods. They target the low to mid income earners who have little time to prepare their own meals or cannot afford to eat from a decent food outlet.

These foods are mostly prepared under wanting hygienic conditions, which exposes the consumers to dangerous sources of food poisoning agents. In other instances, the food availability depends on the region from which such food is produced.

The process of handling and transformation of the food is a critical control point at which a pathogenic microorganism can gain entry into the food and wreak havoc to the public who eventually gets to consume the food (van-de-Venter, 2000).

This paper looks at the cases of foodborne illnesses in the Sub Sahara African region. It discusses the disease burden, major agents of disease, their aetiology, the risk factors and possible containment measures.

Foodborne Illness Outbreak Incidents in sub-Sahara Africa

One of the biggest challenges in addressing food safety issues in Africa is the inadequacy of conclusive surveillance and epidemiological data. Most outbreaks that occur in this region are not properly documented to give researchers a clear picture of the situation on the ground.

This leaves researchers with the option of relying on the available limited data, usually on infant morbidity. Even though insufficient, this serves as the baseline for many studies across the region.

In South Africa, there was an outbreak of bloody diarrhoea caused bEscherichia coli 0157. It was a serious case with up to 42% infection rate after the residents of the 157 townships consumed beef and untreated water. Strains of E, coli O157 were isolated by gel electrophoresis from the faecal matter as well as from the suspected sources. The high infection rate was attributed to heavy rains after a prolonged period of drought (Cowman, et al., 2017).

Kenya has been experiencing an upsurge of food borne disease cases. The first cholera outbreak reported in 2017 was in Tana River County. The outbreak started on 10 October 2016 and was controlled by April 2017. A second wave of cholera outbreaks started in Garissa County on 2 April 2017 and was reported later in nine other counties including Nairobi, Murang’a, Vihiga, Mombasa, Turkana, Kericho, Nakuru, Kiambu, and Narok.

Outbreaks in refugee camps and other parts of Kenya

The outbreak is being reported in the general population and in refugee camps. In Garissa County, the outbreak is affecting mainly Dadaab refugee camps and cases and deaths are being reported from Hagadera, Dagahaleh, and IFO2 camps. In Turkana County, the disease is also affecting Kakuma and Kalobeyei refugee camps (Cowman, et al., 2017).

In addition to the outbreak reported in the general population, there have been two-point source cholera outbreaks in Nairobi County. One occurred among participants attending a conference in a Nairobi hotel on 22 June 2017. A total of 146 patients associated with this outbreak have been treated in different hospitals in Nairobi. A second outbreak occurred at the China Trade Fair held at the KICC Tsavo Ball between 10 and 12 July 2017. A total of 136 cases were reported and one death (Ibid).

Currently, the outbreak is active in two counties, namely Garissa and Nairobi. As of 17 July 2017, a total of 1216 suspected cases including 14 deaths (case fatality rate: 1.2%) have been reported since 1 January 2017. In the week ending 16 July 2017, a total of 38 cases with no deaths were reported ( Ibid; CDC, 2018).

A total of 124 cases tested positive for Vibrio cholerae in the reference laboratory. In the week ending 25 June 2017, 18 samples out of 25 tested positive for Vibrio cholerae Ogawa by culture at the National Public Health Laboratory in Nairobi (CDC, 2018).

The main causative factors of the current outbreak include the high population density that is conducive to the propagation and spread of the disease, mass gatherings (a wedding party held in Karen and in a hotel during an international conference), low access to safe water and proper sanitation and the massive population movements in country and with neighbouring countries (WHO, 2017).

Historical outbreaks and outbreak agents of interest

Between 1970 and 1993, 42 Kenyan districts were examined for food borne illnesses. Foodborne disease outbreak episodes due to Staphylococcus aureus, Clostridium perfringens, Clostridium botulinum, Bacillus cereus, Escherichia coli, Campylobacter jejuni, Yersinia enterocolitica, Listera monocytogenes, chemicals, aflatoxin, plant and animal poisons were of special interest during this study. Outcome parameters were the number of victims and aetiological causes of foodborne disease outbreaks reported in the study period showed.

Thirty-seven food poisoning outbreaks were reported to the Ministry of Health from various parts of the country in the study period 1970 to 1993, and only 13 of these involving a total of 926 people were confirmed to be due to particular aetiological agents.

Foods that were involved included milk and milk products, meat and meat products, maize flour, bread, scones and other wheat products, vegetables and lemon pie pudding. A high number of food poisoning cases were treated as outpatients in various health facilities.

Incidents of aflatoxin poisoning

An aflatoxicosis outbreak in Oloitokitok District of Kajiado County, happened. A total of twenty-seven suspected aflatoxicosis case patients were reported, ten of whom died, for a case fatality rate of 40%. Findings from this investigation indicated a high case-fatality rate similar to that observed in in the most extreme aflatoxicosis outbreak in Eastern Kenya in 2014.

Cases were also reported in Lenkisem Division; however, they were suggestive of a point source exposure as the affected cases reported having consumed maize which had been rained on during transportation from the market.

AETIOLOGICAL AGENTS AND RISK FACTORS OF FOODBORNE ILLNESSES

1.      Salmonellosis

Aetiology

The salmonella is small, gram negative, non-spore forming rod. They are widely distributed in nature with humans and animals being their primary reservoirs. Salmonella food poisonings result from indigestion of food containing appropriate strains of this genus in significant numbers.

The genus Salmonella are considered to have a two species named Salmonella enteric and Salmonella bongori. Serotyping differentiates the strains and they are referred as to by, for example S. eneterica serotype Typhimurium or as S. Typhimurium (Gracey & Collins, 1992).

Epidemiology

The primary habitat of Salmonella species is the intestinal tract of the animals such as farm animals, birds, humans, reptiles, and insects. The primary habitat is intestinal tract.

As an intestinal form, the organisms are excreted in faeces from which they may be transmitted by insects and other living creatures to large number of places (Kalpelmecher, 1993).

Salmonella can be grouped into Salmonella Typhi and S. Paratyphi which are agents of typhoid and paratyphoid fevers which are the most severe of diseases caused by Salmonella.

Pathogenesis

Salmonella often enter the host by ingestion, even with several systems to mediate acid resistance, few survive the stomach and move into the small intestines. Normal flora protects against colonization of administration of oral antibiotics facilitates establishment of infection.

Entry of salmonella usually occurs without mucosal damage in systemic infections but enteric infection is characterized by local damage without septicaemia-salmonella infection with M cells in payer’s patches is facilitated by fimbrial adhesions. This is followed by ruffling of the target cell membrane which results in internalization of the bacteria in membrane bound vacuoles (Brayan, 1994).

The ruffles facilitate uptake of bacteria in membrane bound vacuoles or vesicles which often coalesce. The organisms replicate in these vesicles and are eventually releases from the cells, which sustains only mild or transient damage. The complex invasion process is mediated by the product of a number of chromosomal genes, whereas growth within a cell depends on the presence of virulence plasmids (Walderhaug, 2007).

Symptoms

The incubation period of the salmonella is 12-36 hours. The clinical signs include diarrhoea, which may be watery, greenish and foul smelling. This may be preceded by headache and chills in most cases the symptoms resolve in 2-3 days without any complication (CDC, 2011).

The bacteria induce responses in the animal that is infecting which typically causes symptoms, rather than any direct toxin product. Symptoms are usually gastrointestinal, including nausea, vomiting, abdominal cramps and bloody diarrhoea with mucous, headache and fatigue.

Symptoms can be severe in young children and elderly. Symptoms last a week generally up to a week and can appear 12-72 hours after ingestion of the bacteria.

Detection of pathogens

It can be provided only by isolation of the agent from stool or vomit in human, feed samples in cases of animals, and samples concerned food items like milk and milk products samples. For culture and isolation, the use of selective enrichment media such as Salmonella-shigella agar, or deoxycholate agar after 24 hours is the usual procedure.

Selenite enrichment broth or tetrathionate broth can be used to isolate highly selective for salmonella, especially S. enterica serovar Typhi. Agar and plates are incubating at 37°C overnight and growth identified by biochemical tests and slide agglutination tests (Brayan, Mckiley, & Mixon, 1971; Brayan, 1994).

Prevention and control

The principal sources of infection are carrier animals and contaminated feeds containing food stuff of animal origin. There is a critical need to develop a method to control the spoilage or poisoning of food by Salmonella ordinary farms by instituting bio-containment practices in addition to enhanced food processing method, preparation and storage practices (Quinn, Markey, Carter, Demelly, & Leonard, 2001).

Effective heat processing of food of animal origin, which includes pasteurization of milk and eggs, irradiation of meat and poultry thermal processing, good hygiene practices during production of food, vaccination of food producing animals. Consumers, particularly vulnerable groups should avoid undercooked meat and poultry, raw milk, eggs and foods containing raw and uncleaned vegetables.

The control is also based on reducing the risk of exposure to infection. Intensively-reared, food producing animal are more likely to acquire infection and are also major source of human infection.

Occurrence is worldwide. Drastic increase in incidence of salmonellosis, particularly due to S. enteritidis, has occurred during the past two decades in Europe, North America and some other countries. In Europe and North America, contaminated eggs and poultry have been the major source of infection.

2.      Staphyloccocus aureus

Aetiology

Staphylococcus aureus is gram positive cocci that occur in singles, short chains and irregular grape like cluster. Only the strains that produce enterotoxin can cause food poisoning.

Epidemiology

The most important sources to foods are nasal carriers and individuals whose hands and arms are inflicted with boils and sores, who are permitted to handle foods (Quinn, Markey, Carter, Demelly, & Leonard, 2001).

Pathogenesis

If food is stored for some times in room temperature the organism may grow in the food and can produce toxin. The bacteria produce enterotoxin while multiplying in food. S. aureus is known to produce six serologically different types of enterotoxins (A, B, C1, C2, D and E) that differ in toxicity.

Most food poisoning is caused by enterotoxin A followed by type D. these enterotoxins are heat stable, with type B being most heat resistant. Enterotoxin stimulates the central Nervous Systems (CNS) vomiting and others, are classed as bacterial super antigens relative to in vivo antigen recognition in contrast to conventional antigens (Quinn, et al., 2008).

Symptoms

It is characterized by a short incubation period typically 2-4 hours. The onset is sudden and is characterized by vomiting and diarrhoea but no fever. The illness lasts less than 12 hours.

In severe cases dehydration, and collapse may require treatment through intravenously infusion. The short incubation periods are the characteristics of intoxication where illness in the results of ingestion of the preformed toxin in the food (Adams & Moss, 2008).

Detection of the organism

The presence of a large number of S. aureus organism in a food indicate poor handling or sanitation. The dilution is placed on baird-parker agar or mannitol salt agar. The enterotoxin can be detected and identified by gel diffusion (Quinn, Markey, Carter, Demelly, & Leonard, 2001; Radostits, Gay, Hinchlif, & Constable, 2007).

Prevention and control

Can be prevented and control by proper cooking and preparing food as well as storing.

  • Control measures include education of those who prepare the food at home and other food handlers to take proper personal measures.
  • Prohibiting individuals with sores or other skin lesions from handling food is the second intervention.
  • Lastly, place food in cold place at 4°C or lower of all food in order to prevent bacterial multiplication and formation of toxin. Foods must be kept at room temperature for as little as possible (WHO, 2008).

The occurrence is worldwide but varies depending on conditions of food hygiene.

3.      Clostridium botulinum

Aetiology

It is gram positive anaerobic spore bearing bacilli that widely distributed in soil, sediments of lakes, ponds and decaying vegetation. Seven different strains of the organisms (A-G) are classified based on serologic specificity and another neurotoxin.

Most human outbreaks are associated with fish and sea food products. Botulism in animals is predominantly due to type C and D. All toxin producing strains have placed into 4 groups.

Group I contain the proteolytics, Group II the non-proteolytic and group IV serological type G. Group III consists of type C and D (Hall, McCroskey, Pincomb, & Hatheway, 1985).

Epidemiology

Sporadic outbreaks occur in most countries; it has no geographical limitations. The sources of exposure to the toxin and risk for the disease differ between regions because of difference in the food storage feeding and management practices.

In a study conducted in the USA, the type A was found in neutral and alkaline soil in the west while type B and C in damp or wet soil. Spores of   are present throughout the world, although most of recorded outbreaks of botulism have reported in North of the tropic of cancer with exception of Argentina.

The geographical prevalence of the disease necessitates some important observations such as home canning fruits and vegetables in most tropical countries (Jay, 2000; Radostits, Gay, Hinchlif, & Constable, 2007).

Pathogenesis

During their growth, C. botulinum produce a high potent neurotoxin that cause neuroparalytic disease known as botulism in humans and animals without the development of histological lesion. Botulism may lead to death due to respiratory muscle paralysis unless treated properly (Jay, 2000).

The toxin is released only after the death and lysis of cells. The toxin resists digestion and is absorbed by the upper part of the GI tract and then into the blood.

It then reaches the peripheral neuromuscular synapses where the toxin binds to the presynaptic stimulatory terminals and blocks the release of the neurotransmitter acetylcholine. This affects muscle of respiration, which leads to death due to respiratory failure. This results in flaccid paralysis.

Symptoms

Incubation period may be 12-36 hours. The most common features include vomiting, thirst, dryness of mouth, constipation, ocular paresis (blurred-vision), difficulty in speaking, breathing and swallowing. Death occurs due to respiratory paralysis within 7 days).

Detection of toxin

Diagnosis of botulism requires demonstration of toxin in plasma or tissue before death or from fresh carcass. Demonstration of the toxin in feedstuff, fresh stomach content or vomitus supports diagnosis of botulism.

The spoilage of food or swelling of cans or presence of bubbles inside the can indicate clostridial growth. Food is homogenized in broth and incubated in Robertson cooked meat medium and blood agar or egg yolk agar.

It is incubated anaerobically for 3-5 days at 37°C. The toxin can be demonstrated by injecting intra peritoneal the extract of food or culture into mice or guinea pig (Hirsh, Maclachian, & Walker, 2004).

Prevention and control

Preformed toxin in food can completely be destroyed by exposure to a temperature of 80°C for 30 minutes or boiling for 10 minutes. Therefore, all canned low acid foods should be boiled before tasting for consumption. Never taste a food if it has an odour and shows gas formation. 

Prevention of food borne botulism also depends on ensuring effective control of commercially and home canned foods are destroying all C. botulinum spores. This requires cooking at 121°C or higher.

Vegetables that are home canned should be boiled and stirred for at least 3 minutes prior to serving to destroy botulism toxins. Foods with apparent off odours or suspected odour should not be opened (Jay, 2000).

Its occurrence is worldwide particularly frequent among Alaskan populations. Case fatality ratio in industrialized countries is 5-10%.

4.      Clostridium perfringens

Aetiology

This is a gram-positive anaerobic spore bearing bacilli that is present abundantly in the environment, vegetation, sewage and animal faeces.

Perfringens food poisoning is most commonly caused by organisms producing type A enterotoxin. The other types of enterotoxin (B to G) do not normally cause food borne disease (Labbe & Nolan, 1981).

Epidemiology

Clostridium perfringens type A food poisoning remains one of the most prevalent food born disease in western countries. The food poisoning strains of C. perfringens exists in soils, water, food, dust, spices and intestinal tract of humans and other animals.

Pathogenesis

Spores in food may survive cooking and then germinate when they are improperly stored. When these vegetative cells form endospore in the intestine, they release enterotoxins. The bacterium is known to produce at least 12 different toxins.

Food poisoning is mainly caused by type A strains which produce alpha and theta toxins. The toxin results in excessive fluid accumulation in the intestinal lumen (CDC, 2011). The C. perfringens enterotoxin (CPE) is not a super antigen as are staphylococcal enterotoxins.

Enterotoxigenesis begins when C. perfringens enterotoxin bind to one or more protein receptors on epithelial cells in the gastro intestinal tract. It does not affect cyclic adenosine mono phosphate levels as do enterotoxigenic strains of E. coli.

It localizes in small plasma membrane complex and apparently associated with a membrane protein to form a larger complex This coincides with the onset of CPE-induced membrane permeability alterations that leads to cell death from lysis or metabolic disturbances (Radostits, Gay, Hinchlif, & Constable, 2007).

Symptoms

The incubation period is 8-24 hours. The illness is characterized by acute abdominal pain, diarrhoea and vomiting. The illness is self-limiting and the patient recovers within 8-24 hours.

The classic symptom of C. perfringens type A food poisoning is diarrhoea with lower abdominal cramps. Mortality is low and such cases have been associated with elderly patients (Robinson, Batt, & Patel, 2000).

Detection of the organism and enterotoxin

The criteria proposed for establishing an outbreak of C. perfringens type A food poisoning include;

·         More than 10spores/gram faeces from ill individuals;

·         More than 105 cells/gram incriminated food;

·         The presence of some serotypes of C. perfringens in an ill individual in an outbreak or detection of enterotoxin in faeces of individuals.

Homogenized food is diluted and plated on selective medium as well as Robertson cooked meat medium and incubated anaerobically. The isolated bacteria must be shown to produce enterotoxin.

Control and prevention

  • Cook meat until the internal temperature reaches at least 74°C, preferably higher;
  • Thoroughly wash and sanitation of all containers and equipment that previously had contact with raw meat/eggs
  • Wash hands and use disposable plastic gloves when handling raw or uncooked foods
  • Separate meat and other food stock before chilling;
  • Chill meat rapidly after cooking;
  • Use refrigeration for storage.

Since the organism is present in animals, it can be found in raw meat and poultry. The spores will also survive indefinitely in dust and in environmental niches. Cooking at temperatures not exceeding 100°C will allow the survival of the spores.

The cooking process drives off oxygen creating real anaerobic conditions in foods such as rolls of cooked meat, pies, and gravies and in poultry carcass. Therefore, prevention of vegetative cells in cooked foods is a practical way of preventing C. perfringens food borne illness (Ibid).

Occurrence is worldwide with varying incidences. Case fatality ratio in industrialized countries is 0.1%.

5.      Escherichia coli

Aetiology

It belongs to family Enterobacteriaceae. Are gram negative rods up to 3um in length, ferment glucose and wide range of sugars. Produce pink colonies on McConkey agar. Hemolytic activity on blood agar is a character of certain strains of E. coli.

It is motile with peritrichous flagella and often fimbriate (Jay, 2000). E. coli 0157:H7 is an important serotype and seems to be predominate in most areas. The strains producing verotoxin are shiga-like toxin (SLT) which produces diarrhoea in humans and animals.

Source of infection is contamination of food by human and animal faeces. The organism can persist in manure, water trough and other farm location. The association of E. coli 0157:H7 with raw meat, under cooked ground beef and raw milk lead to investigation of the role of cattle as a reservoir of the pathogens (Buchanan & Doyle, 1997).

Pathogenesis

Enterohemorrhagic E. coli (EHEC) strain may produce one or more types of cytotoxins which are collectively referred as shiga-like toxins (SLTs) since they are antigenically and functionally similar to shiga toxin produced by Shigella dysenterica.

However, new terminology has been applied, and what was SLT is now Stx. All Stxs consists of a single enzymatically active A subunits and multiple B subunits.  Stx-sensitive cells possess the toxin receptor, globotriaosyceramide (Gb3), and sodium butyrate appears to play a role in sensitizing cells to Stxs.

Once toxins bind toGb3, internalization follows with transport to the trans-Golgi network. Inside the host cells, the A subunits binds to and releases and adenine residue that inhibits protein synthesis. The B subunits form pentamers in association with a single A subunit and thus are responsible for the binding of the toxin to the neutral glycolipid receptors (Ibid).

Symptoms

The incubation period is 72-120 hours. The clinical signs initially may be diarrhoea in a few days. However, there is no fever. The symptoms of E. coli septicaemia are mainly referable to bacteraemia, end toxaemia and the effect of bacteria localization in a variety of tissue spaces throughout the body (Quinlan, 2013).

Detection of toxin

Laboratory diagnoses involve culturing the food on McConkey agar or sorbitol. Strains can be identified by serotyping using specific antisera. Stxs can be detected by ELISA and gene coding can be detected by DNA hybridization techniques. Sorbitol McConkey agar is recommended for isolation of E. coli 0157:H7 from food and faeces samples.

Control and Prevention

The prevention of food borne illnesses caused by E. coli can be prevented by the same method as prevention of other food borne illness caused by bacteria. Food should be properly cooked since the organism is heat sensitive.

Occurrence is worldwide with most incidences in developing countries. Case fatality ratio for EPEC, ETEC, EIEC infections in industrialized countries <0.1%, for EHEC infection about 2%.

Case fatality ratio of E. coli infections in infants and children much higher in developing countries. Children and the elderly are particularly vulnerable and may suffer more severely. Most cases of EHEC infections are reported in summer.

6.      Shigellosis

Aetiology

Shigella is a species of enteric bacteria that causes disease in humans and other primates. Shigella is gram-negative rods that are non-motile and non-spore forming.

The bacteria are primarily a human disease, but has been found in some primates. Shigella are facultative anaerobes, similar to enterics such as E. coli (Brayan, Mckiley, & Mixon, 1971).

Epidemiology

Shigella transmission can occur through direct person-to-person spread or from contaminated food and water. The minimal infectious dose can be transmitted directly from contaminated fingers, since intermediate bacterial replication is not required to achieve the low infectious dose.

In developed countries, most cases are transmitted by faecal-oral spread from people with symptomatic infection. In developing countries, both faecal-oral spread and contamination of common food and water supplies are important mechanisms of transmission symptom.

Pathogenesis

Shigella attaches to and penetrate intestinal cell walls of the small intestines by producing toxins that may promote the diarrhoea characteristic of the disease. The Shiga toxin enables the bacteria to penetrate the epithelial lining of the intestines, leading to a breakdown of the lining and haemorrhage.

Shigella also have adhesins that promote binding to epithelial cell surfaces and invasion plasmid antigens that allow the bacteria to enter target cells, thus increasing its virulence (CDC, 2011).

Symptoms

They include abdominal pain, cramps, diarrhoea, fever, vomiting, blood, pus or mucus in stools. Mild infections cause low-grade fever (38 - 38.9°C) and watery diarrhoea 1 to 2 days after people ingest the bacteria.

Abdominal cramps and a frequent urge to defecate are common with more severe infections. Children, particularly young children, are most likely to have severe complications of high fever (41oC) sometimes with delirium. Severe dehydration with weigh loss is also a symptom.

Detection of toxin

Shigella infection is diagnosed through testing of a stool sample. First a stool sample must be obtained from the potentially infected person, and then the sample is placed on a medium to encourage the growth of bacteria.

If and when there is growth, the bacteria are identified, usually by looking at the growth under a microscope (Ibid).

Control and prevention

Shigella is heat-sensitive and will be killed by thorough heating (over 70oC). Raw or undercooked foods and cross-contamination, when cooked material comes into contact with raw produce or contaminated materials (cutting boards), are the main causes of infection.

Proper cooking and hygienic food handling thus can prevent Shigella infections to a large extend. There is currently no vaccine for Shigellosis prevention, but there is current research that appears promising.

The most effective method for prevention is frequent and vigorous hand washing with warm, soapy water and ensuring clean drinking water sources and proper sewage disposal in developing nations (Malangu, 2016).

Occurrence is worldwide and has higher prevalence in developing countries. Shigellosis is a major cause of diarrhoea in infants and children under the age of 5 years and accounts for 5-15% of diarrhoeal diseases cases seen at treatment centres.

7.      Campylobacteria

Aetiology

Campylobacteriosis is an infection caused by bacteria of the genus Campylobacter. There are approximately sixteen species associated with Campylobacter, but the most commonly isolated are C.jejuni, C. coli, and C. upsaliensis.

The most prevalent species associated with human illness is C. jejuni. Campylobacter is also responsible for 15% of foodborne illness-related hospitalizations, and 6% of foodborne illness-related deaths (Hoffmann, et al., 2017).

Epidemiology

Campylobacter is one of the most common causes of human bacterial gastroenteritis. A large animal reservoir is present as well, with up to 100% of poultry, including chickens, turkeys, and waterfowl, having asymptomatic infections in their intestinal tracts.

Infected chicken feces may contain up to 109 bacteria per 25 grams, and due to the installations, the bacteria are rapidly spread to other chickens. Tis vastly exceeds the infectious dose of 1000-10,000 bacteria for human (Ibid).

Pathogenesis

Bacterial motility, mucus colonization, toxin production, attachment, internalization, and translocation are among the processes associated with C. jejuni virulence. Infection begins with ingestion of the C. jejuni in contaminated foods or water.

Gastric acid provides a barrier, and the bacteria must reach the small and large intestines to multiply; C. jejuni invades both epithelial cells and cells within the lamina propria (Ibid).

Symptoms

The symptoms associated with this disease are usually flu-like: fever, nausea, abdominal cramping, vomiting, enteritis, diarrhoea, and malaise. Symptoms begin within 2-5 days after ingestion of the bacteria, and the illness typically lasts 7-10 days.

Recurrence of this disease can occur up to three months after pathogen ingestion (Shonhiwa, Ntshoe, Essel, Thomas, & McCarthy, 2018). Other complications can include meningitis, urinary tract infections and short-term reactive arthritis.

Detection of Toxin

Because of the unique growth characteristics of Campylobacter, isolation of these organisms from field samples requires the use of special media and culture conditions. Campylobacter jejuni and Campylobacter coli can be isolated from the intestines of healthy farm animals, poultry, pets, zoo animals, and wild birds.

Diagnosis of C. jejuni is based on isolation of the organism on selective media under micro aerophilic conditions. PCR-based methods are effective in identifying infection especially if cultivation is difficult or if the sample has been somewhat mishandled.

However, a positive test is not sufficient evidence to determine causation and must be considered in conjunction with clinical signs (van-de-Venter, 2000).

Control and Prevention

Control depends on sanitation and hygiene in livestock barns to reduce the bacterial populations in the environment of the animals. The number of organisms can be reduced and controlled in meat processing plants by using HACCP protocols including the washing, handling and freezing of carcasses.

Improvement of food-handling skills in restaurants and in the home, kitchen will reduce transmission of the organism and adequate cooking of raw meat such as poultry to an internal temperature of 82oC will eliminate the organism (Walderhaug, 2007).

Occurrence is worldwide. It is one of the most frequently reported foodborne diseases in industrialized countries; a major cause of infant and travellers’ diarrhoea in developing countries. Campylobacter spp cause 10-15% of cases of diarrhoeal diseases in children seen at treatment centres.

8.      Listeria

Aetiology

Listeria monocytogenes is the bacterium that causes the infection listeriosis. It is a facultative anaerobic bacterium, capable of surviving in the presence of oxygen.

It can grow and reproduce inside the host’s cells and is one of the most virulent food-borne pathogens, with 20 to 30 percent of clinical infections resulting in death (van-de-Venter, 2000).

Epidemiology

Listeria species are widely distributed in the environment and can be isolated from soil, plants, decaying vegetation and silage (pH 5.5) in which the bacteria can multiply. Asymptomatic faecal carrier occurs in man and animal species (Ibid).

Pathogenesis

Listeria originally evolved to invade membranes of the intestines, as an intracellular infection, and developed a chemical mechanism to do so. This involves a bacterial protein “internalin” which attaches to a protein on the intestinal cell membrane “cadherin”.

L. monocytogenes has also D-Galactose residues on its surface that can attach to D-Galactose receptors on the host cell walls. These host cells are generally M cells and Payer’s patches of the intestinal mucosa.

Once attached to these cells, L. monocytogenes can translocate past the intestinal membrane and into the body. L. monocytogenes may invade the gastrointestinal epithelium. Once the bacterium enters the host’s monocytes, macrophages, or polymorphonuclear leukocytes, it becomes blood-borne (septicaemic) and can grow.

Its presence intracellularly in phagocytic cells also permits access to the brain and probably trans-placental migration to the foetus in pregnant women (CDC, 2011).

Symptoms

The symptoms of listeriosis usually last 7-10 days, with the most common symptoms being fever, muscle aches, and vomiting. Diarrhoea is another, but less common symptom. If the infection spreads to the nervous system it can cause meningitis, an infection of the covering of the brain and spinal cord (Bean & Griffins, 1990; Adams & Moss, 2008).

Detection of toxin

Enrichment procedures are required for this organism. This involves inoculation of selective or non-selective broths that are incubated at 4°C for up to 8 weeks.

An ELISA, using monoclonal antibodies, has been developed to identify listeria in food, and also DNA probe for detection of bacterium in dairy products (Niehaus, Apalata, Coovadia, Smith, & Moodley, 2011).

Control and prevention

The main means of prevention is through the promotion of safe handling, cooking and consumption of food. This includes washing raw vegetables and cooking raw food thoroughly as well as reheating leftover or ready-to-eat foods like hot dogs until steaming hot (CDC, 2011).

Preventing listeriosis as a food illness requires effective sanitation of food contact surfaces. Alcohol and Quaternary ammonium are an effective topical sanitizer against Listeria.

Refrigerated foods in the home should be kept below 4°C (39.2°F) to discourage bacterial growth. Preventing listeriosis also can be done by carrying out an effective sanitation of food contact surfaces.

Occurrence is worldwide. Most cases have been reported from Europe, North America and the Pacific islands.

9.      Cholera

Aetiological agent

Vibrio cholerae 01 and 0139 are the bacterial agents for the disease. V. cholarae 01 includes two biotypes- classical and E1 Tor- each of which includes organisms of Ogawa, Inaba and rarely Hikojima serotypes.

Epidemiology

Are Gram-negative, facultative anaerobic, motile, non-spore forming rods that grow at 18-42oC (optimum 37oC), pH 6-11 (optimum 7.6) water activity of 0.97.

Growth is stimulated by salinity levels of around 3% but prevented by levels of 6%. Organism is resistant to freezing but sensitive to heat and acid (National Disease Surveillance Centre, 2004).

Pathogenesis

May survive for some days on fruit and vegetables. It is often found in aquatic environments and is part of the normal flora in brackish water and estuaries. V. cholera is non-invasive and diarrhoea is mediated by cholera toxin formed in the gut (toxico-infection).

Symptoms

Incubation period 1-3 days. Profuse watery diarrhoea, which can lead to severe dehydration, collapse and death within a few hours unless lost fluid and salt are replaced; abdominal pain and vomiting. Duration is up to 7 days.

Mode of transmission

Food and water contaminated through contact with faecal matter or infected food handlers, Contamination of vegetables may occur through sewage or waste water used for irrigation.

Person to person transmission through the fecal-oral route is also an important mode of transmission. Foods involved include seafood, vegetables, cooked rice and ice.

Control and Prevention

Safe disposal of sewage and waste water, treatment of drinking water e.g. chlorination or irradiation, heat treatment of foods e.g. canning; high pressure treatment; good hygiene practices during production and processing.

In food service establishment/household, personal hygiene (hand washing with soap and water); thorough cooking of food and careful washing of fruit and vegetables; boiling drinking-water when safe water is not available. Consumers should avoid eating raw seafood.

Occurrences: Africa, Asia, parts of Europe and Latin America. In most industrialized countries, reported cholera cases are imported by travellers or occurs as a result of imported food.

10.  Brucellosis (Undulant Fever)

Aetiological agent

Bacteria: Brucella abortus, Brucella melitensis and Brucella suis

Epidemiology

Are Gram-negative, aerobic, non-spore forming, short, oval, non-motile rods that grow optimally at 37oC and pH 6.6-7.4; heat-labile.

Symptoms

Incubation period varies and can take several weeks or months. Continuous, intermittent or irregular fever, sweat, headache, chills, constipation, generalized aching, weight loss, and anorexia.

Mode of Transmission

Brucella abortus is found in cows, Brucella melintensis in sheep and goats while Brucella suis are found in pigs.

The disease is contracted principally from close association with infected animals and therefore an occupational disease of farmers, herdsmen, veterinarians and slaughterhouse workers.

Can also be contracted by consumption of milk and products made from unpasteurized milk such as fresh goat’s cheese (Quinn, Markey, Carter, Demelly, & Leonard, 2001).

Control and prevention

Heat treatment of milk (Pasteurization or sterilization); use of pasteurized milk for cheese production, ageing cheese for at least 90 days; thermal processing’ good hygiene practices during production and processing.

Other measures include: Vaccination of animals, eradication of diseased animals (testing and slaughtering). Consumers should avoid consumption of raw milk and cheese made with raw milk.

The occurrence of Brucellosis is worldwide with the exceptions of northern Europe where it occurs rarely. Prevalent in eastern Mediterranean areas, southern Europe, North and east Africa, central and southern Asia, Mexico, Central and South America.

The disease is often unrecognized and unreported. Case-fatality ratio is up to 2% if the disease is untreated.

11.  Bacillus cereus (Gastroenteritis)

Aetiology

Aetiological agent is Bacillus cereus bacteria toxin. B. cereus can cause two different types of foodborne illnesses: the diarrhoeal type and the emetic type. Diarrhoeal toxin causing toxico-infection due to production of heat-labile toxins either in the gut or in food.

The enterotoxins are produced during vegetative growth of B. cereus in the small intestines. Emetic toxin causing intoxication due to heat stable toxin produced in food. For both types of foodborne types of food borne illness is caused by a toxin that is performed by B. cereus while growing in the food.

Epidemiology

The bacteria are Gram-positive, facultative anaerobic, motile rod that produces heat-resistant spores; generally mesophilic, grows at 10-50oC (optimum temperature 28-37oC), pH 4.3-9.3 and water activity (aw)>0.92.

Spores are moderately heat-resistant and survive freezing and drying. Some strains require heat activation for spores to germinate and outgrow. It is found abundantly in environment and vegetables.

Symptoms

Symptoms for diarrhoeal syndrome are acute diarrhoea, nausea and abdominal pain. Symptoms for emetic syndrome acute nausea, vomiting and abdominal pain and sometimes diarrhoea.

The incubation period is 8-16 hours for diarrhoeal syndrome while the incubation period for emetic syndrome is 1-5 hours. The diarrhoeal syndrome lasts 24-36 hours while emetic syndrome lasts 24-36 hours (Hirsh, Maclachian, & Walker, 2004).

Mode of transmission

Ingestion of food that has been stored at ambient temperatures after cooking, permitting the growth of bacterial spores and toxin production. Many outbreaks (particularly those of the emetic syndrome) are associated with cooked or fried rice that has been kept at ambient temperature.

Foods involved include starchy products such as boiled or fried rice, spices, dried foods, milk, dairy products, vegetable dishes and sauces.

Control and prevention

Food service establishment or household require effective temperature control to prevent spore germination and growth. Food storage at >70oC or <10oC until use unless other factors such as pH or water activity prevent growth.

When refrigeration facilities are not available, cook only quantities required for immediate consumption. Toxins associated with emetic syndrome are heat resistant and reheating, including stir-frying, will not destroy them. Good hygiene practices during production and processing.

Incidences are occurring worldwide.

12.  Amoebiasis (Amoebic Dysentery)

Aetiology

Aetiological agent is Protozoa: Entamoeba histolytica

Epidemiology

The organisms are amoeboid, aero-tolerant anaerobe that survives in the environment in an encysted form. Cysts remain viable and infective in faeces for several days, in soil for at least 8 days at 24-34oC. They are relatively resistant to chlorine (Mensah, Mwamakamba, Mohamed, & Nsue-Milang, 2012).

Symptoms

The incubation period is 2-4 weeks (range several days to several months). Severe bloody diarrhoea, stomach pains, fever and vomiting. Most infections remain symptomless.

Mode of Transmission

Transmission occurs mainly through the ingestion of faecal contaminated food and water containing cysts. Cysts are excreted in large numbers by an infected individual. Illness is spread by faecal-oral route, person-to-person contact or faecal contaminated food and water.

Foods involved include fruits and vegetables and drinking water. The main reservoirs are humans, but also dogs and rats, the organism is also found in sewage used for irrigation.

Occurrence is worldwide particularly in young adults.

Control and Prevention

Filtration and disinfection of water supply; hygiene disposal of sewage water; treatment of irrigation water; thermal processing; good hygiene practices during production and processing.

In food service establishment or household, boiling of water when safe water is not available; thorough washing of fruits and vegetables; thorough cooking of food; thorough hand-washing.

13.  Ascariasis

Aetiology

Aetiological agent is Helminth, nematode: Ascaris lumbricoiedes.

Epidemiology

The agent is a large nematode (roundworm) infecting the small intestine. Adult males measure 15-31cm*2-4mm, females 20-40cm*3-6mm. Eggs undergo embryonation in the soil; after 2-3 weeks they become infective and may remain viable for several months or even years in favourable soils.

The larvae emerge from the egg in the duodenum, penetrate the intestinal wall and reach heart and lungs via the blood. Larvae grow and develop in the lungs. Nine to ten days after infection they break out of the pulmonary capillaries into the alveoli and migrate through the bronchial tubes and tracheae of the pharynx where they are swallowed.

They reach the intestine 14-20 days after infection. In the intestine they develop into adults and begin laying eggs 40-60 days after ingestion of the embryonated eggs. The life cycle is complete after 8 weeks.

Symptoms

Incubation period: First appearance of eggs in stools 60-70 days following ingestion of the eggs. Symptoms of larval ascariasis appear occur 4-16 days after infection.

It is generally asymptomatic. Gastrointestinal discomfort, colic and vomiting; fever; observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during mitigation of the larvae (van-de-Venter, 2000).

Adult worms can live 12 months or more. The source/reservoir includes humans; soil and vegetation on which faecal matter containing eggs have been deposited.

Mode of transmission

Ingestion of infective eggs from soil contaminated with faeces or of contaminated vegetables and water.

Control and prevention

Use of toilet facilities; safe excreta disposal; protection of food from dirt and soil; thorough washing of produce.

Food dropped on the floor should not be eaten without washing or cooking, particularly in endemic areas. Thermal processing, good hygiene practices during production and processing.

The occurrence is worldwide.

14.  Clonorchiasis

Aetiology

Helminth, trematode (flatworm): Clonorchis sinensis i.e. the Chinese liver fluke.

It is a flattened worm, 10-25 mm long, 3-5mm wide, usually spatula-shaped, yellow-brown in colour (Owing to bile staining); has an oral and a ventral sucker and is a hermaphrodite.

Eggs measure 20-30*15-17 micrometres, are operculate and are among the smallest trematode eggs to occur in man.

Symptoms

The incubation period varies with the number of warms present. Symptoms begin with the entry of immature flukes into the biliary system one month after encysted larvae (metacercaria) are ingested.

Most patients are asymptomatic but may have eosinophilia. Gradual onset of discomfort in the right upper quadrant, anorexia, indigestion, abdominal pain or distension and irregular bowel movement.

Patients with heavy infection experience weakness, weight loss, epigastric discomfort, abdominal fullness, diarrhoea, anaemia, and oedema. In later stages, jaundice, portal hypertension, ascites and upper gastrointestinal bleeding occur (Bean & Griffins, 1990).

An acute illness occasionally develops 2-3 weeks after initial exposure. Adult worms can live many years.

Source

Snails are the first intermediate host. Some 40 species of river fish serve as the second intermediate host. Humans, dogs, cast, and many other species of fish-eating mammals are definitive hosts.

Mode of transmission

People are infected by eating raw or under-processed freshwater fish contain encysted larvae (metacercaria). During digestion, the larvae are freed from the cysts and migrate via the common bile duct to biliary radicles.

Eggs in faeces contain fully developed miracidia; when ingested by a susceptible operculate snail, they hatch in its intestine, penetrate the tissues and asexually generate larvae (cercariae) that migrate into the water.

On contact with a second intermediate host, the cercariae penetrate the host and encyst, usually in muscle, occasionally on the undesirable of scales. The complete life cycle from person to snail to fish to person requires at least 3 months.

Control and Prevention

Safe disposal of sewage or wastewater to prevent contamination of rivers; treatment of wastewater used for aquaculture; irradiation of freshwater fish; freezing; heat treatment (canning); good hygiene practices during production and processing.

Thorough cooking of freshwater fish. Consumers should avoid consumption of raw or undercooked freshwater fish. Other measures include control of snails with molluscicides where feasible; drug treatment of the population to reduce the reservoir of infection; elimination of stray dogs and cats.

Occurrence is common in endemic part of western Pacific (China, Japan, Korean peninsula, Malaysia, Vietnam). In Europe (eastern part of Russian Federation).

15.  Cryptosporidiosis

Aetiology

The agent is a protozoon; Cryptosporidium parvum

The organism has a complex life cycle that can take in a single animal host. It produces oocysts (diameter 4-6 micrometres) which are very resistant to chlorination but killed by conventional cooking procedures.

Symptoms

The incubation period is 2-4 days.

Persistent diarrhoea, nausea, vomiting and abdominal pain, sometimes accompanied by an influenza-like illness with fever. 

The reservoir or source is humans, wild and domestic animals e.g. cattle. Children under the age 5 years are at a higher risk of infection. Immuno-compromised individuals may suffer from longer and more severe infection; may be fatal in AIDS patients.

The mode of transmission

It is spread through the faecal-oral route, person-to-person contact or consumption of faecal contaminated food and water, bathing in contaminated pools. Foods involved include raw milk, drinking-water and apple cider.

Control and Prevention

Pasteurization/sterilization of milk; filtration and disinfection of water; sanitary disposal of excreta, sewage and wastewater; thermal processing; good hygiene practices during production and processing.

In food service establishment boiling of water when safe water is not available; boiling of milk; thorough cooking of food; thorough hand-washing.

Occurrence is worldwide.

MAJOR SOURCES OF FOODBORNE PATHOGENS

a)      Ingredients and agricultural produce

Due to their proximity to contaminants such as soil, water and air, agricultural produce can harbour a host of foodborne pathogens. Faecal coliforms form a bulk of these pathogens.

The most common strains that are usually associated with these contaminations include, Salmonella spp., Shigella spp., and Escherichia coli.

Meats are particularly contaminated. Fish vegetables, fruits and salads are not spared either. The pathogens can survive for long periods in the sewage water and infest the crops when such water is used to irrigate crop fields.

Sewage water also has high loads of heavy metals, which bio-accumulate in the crops and pass on to humans at the point of consumptions (CDC, 2018). Toxicity often arise when these elements exceed safe levels in the crops and eventually, in the consumers.

Rampant and careless use of antibiotics has led to an increased (unsafe even) levels of trace drugs in foods. The antibiotics applied for therapeutic purposes in poultry, fish, and beef are visible in meat and milk derived from these animals (Hoffmann, et al., 2017).

As a consequence, there has been multiple drug resistance, which jeopardizes the fight against food borne pathogens because the pathogens will eventually mutate into drug resistant strains and cause deaths in human consumers because they cannot be contained using any available antibiotic.

b)     Prepared foods

The popularity of ready-to-eat foods has shifted the preference from homemade foods to street prepared foods. The latter is characterized by inadequate hygiene since running clean water is lacking, there are limited toilet facilities, and the foods are not protected from flies.

From studies, there is a direct link between diarrhoea cases and street foods. Cholera outbreaks in Kenya has been, on several occasions, been linked to street vended pork, poultry, and nyama choma (roasted meat).

The common factor in all these outbreaks has always been concerns over hygiene (Cowman, et al., 2017; Hoffmann, et al., 2017). This means that food preparation is a critical control point for foodborne illnesses and food poisoning.

Cooking should be done at adequate temperatures that will ensure the pathogenic microorganisms do not survive. The foods and the food handling equipment need to be washed properly.

The patrons need to wash their hands properly with soap before and after eating. There should be screens to protect the eating area from dust, flies and insects.

c)      Food vendors

Food vendors play a crucial role in the food value chain. They are usually at the last mile of the chain, ensuring the food reaches the final consumer in a wholesome manner.

Due to their close contact with the food items they vend, they are a potential hazard for foodborne pathogens. This is especially the case if the vendor in question has very little regard for hygiene (Shonhiwa, Ntshoe, Essel, Thomas, & McCarthy, 2018).

Food vendors need to be trained on food handling aspects that will ensure safe food delivery to the final consumer. They need to be regularly trained and certified to streamline food safety policies at the last mile of the food value chain.

They need to renew their food handlers’ certificate every six months to ensure they are not harbouring any potential pathogen, which they can transfer to the consumer unintentionally through food handling.

ECONOMIC CONSEQUENCES OF FOODBORNE ILLNESS

Foodborne pathogens in any given food supplchain affects the health of the consumers of that particular food, whether local or abroad. The burden of the disease on health and economy is great due to the lost man hours and investment in health systems to manage the conditions and treat the sick.

The families of the victims are affected directly due to the lost opportunity to make an income and they are forced to use their little resources to treat the sick, further deteriorating their quality of life.

The compounded cost of illness arising Campylobacter jejuni, Clostridium perfringens, E coli 0157:H7, Listeria monocytogenesSalmonellaStaphylococcus aureus and Toxoplasma gondii is estimated to range between US$ 6 – 35 million annually with 3.3 – 12.3 million caseand up to 39,00 deaths annually (CDC, 2011). The figure has since gone up and the global economic growth cannot keep up with the escalation.

Victim countries also lose out on trade opportunities as the importing countries put trade embargoes on them. They cancel food imports due to food safety concerns, which further robs these countries of development opportunities.

Fish imports from Tanzania into the UK was cancelled, beef from Kenya is no longer accepted into Europe. Aflatoxin contaminated maize have been intercepted in Kenya, Nigeria and other countries within the Sub-Sahara Africa (Yard, et al., 2013).

IMPLEMENTATING THE FOOD SAFETSTRATEGY IN SSA

There is need to adopt a holistic approach to the implementation of the food safety strategy in Sub-Sahara Africa. Through initiatives like the African Centres of Excellence, human resources will be trained to adopt a unified strategy to problem solving. This can be implemented across the board since the region faces fairly similar challenges.

The information needs to be communicated in simple language that every actor in the food value chain can understand and implement without the need for sophisticated equipment or advanced schooling.

Surveillance of foodborne diseases needs to be heightened to ensure outbreaks are reported in time and containment measures adopted immediately to arrest the spread of foodborne illnesses.

HACCP systems need to be adopted across the food value chain to eliminate opportunistic pathogens that cause foodborne diseases. Regulators need to improve on inspection of food outlets to ensure there is a strict adherence to the food safety regulations and policy provisions.

Funding for the food safety programs need to cater for implementation costs as well. There is need to adopt unified standards, which should be set by consenting regional partners, to ensure that every player will follow through with the program.

Codex Alimentarius Commission, through the Codex Trust Fund, needs to come in and help the developing countries with standards development and implementation to ensure that no single country is discriminated against using punitive and impractical standards that have been set up in a secluded boardroom.

HUMAN RESOURCE AND TRAINING REQUIREMENTS TO COMBAT FOODBORNE ILLNESSES IN SSA

In the implementation of food safety policies, human resources remain a key ingredient, Due to the dynamism of the process, there is need for continuous capacity development to meet the ever-present needs. Sub-Sahara African countries need to allocate funds for this purpose.

The African Centres of Excellence (ACEs) are setting the pace in human capacity development by training high level human resources that will be handy in addressing the challenges of food safety. Through research and development, these centres are committed to producing applicable science to address the unique challenges of the region.

The data produced from these centres of excellence will need to be shared across the region to help in reducing associated costs while driving development through high quality research and development programs.

Given that the personnel hail from the local regions, they will be conducting research that directly affects them and they will be the most important people in dissemination of the research findings to the community for adoption.

This means that the communities will easily adopt the research findings as their own. This is an ongoing process in the quest to improve quality. As a result, different institutions of learning are constantly realigning their courses to address the current problems of food safety.

FOODBORNE ILLNESSES IN SSA - CHALLENGES AND OPPORTUNITIES

Inadequate human resources and funding for the food safety programmes remains to be the key challenge in addressing food safety issues in Sub-Sahara Africa. Governments have competing development priorities which divert attention from the pressing need to address food safety.

Unsafe food is a major contributor to hunger because it wastes the limited food resources by making them unsafe for both human and animal consumption.

Most participant countries in standard setting committees have little scientific outputs to present in the conferences. This has led to adoption of foreign scientific inputs that have little consideration of the local challenges. A majority of the Sub-Sahara African countries do not have prescribed standards for microbial safety and chemical adulterants in foods.

Despite these challenges, there is increased participation in the food safety network. This has provided a headway for increasing awareness to the challenges and the pressing need to adopt standards that will ensure a unified way of looking at food safety in the region.

Funding for food safety programmes have also been increasing gradually. This trend ought to continue at an accelerated pace so that countries that are still lagging behind can catch up and implement strategies that will ensure the citizens access safe and nutritious food.

CONCLUSION AND WAY FORWARD ON FOODBORNE ILLNESSES IN SSA

Even though countries are rushing to increase the awareness on food safety and implementing policies to ensure the population remains safe, there remains the challenges in capacity development.

  • Limitation in human resources and financing is a major challenge to most of the food safety policy regulators around the world. This is attributed to the unique nature of the cases as well as the emerging trends that makes it difficult to say with certainty that a particular pathogen should be controlled using a given strategy.
  • The agents are living organisms and mutate from time to time. This means that a dynamic approach needs to be adopted and continuous surveillance needs to be put in place to address the challenges.
  • Even with the development challenges, governments In Sub-Sahara Africa need to adopt strategies that prioritize food safety to ensure that no produced food goes to waste as a result of food contamination.
  • Keeping the citizens from illnesses and infection will ensure a more productive population hence the government will gain more from the increased labour hours. Food safety affects all sectors hence the need to shift away from the traditional fragmented approach to food safety.
  • A multi-sectorial approach needs to be adopted so that all the departments contribute their effort in addressing the problem that is food safety.
  • Through the African Centres of Excellence (ACEs), Sub-Sahara Africa can address food safety challenges by concentrating its resources on a few effective centres that are mandated to train high quality human resources and conduct research on these emerging trends. The output of these centres should be implemented with a direct impact on the ground where their effects are felt most.
  • In the food value chain, no player should be left out. The street food vendors need to be encouraged to adopt a holistic approach to food safety so that no loophole remains for the opportunistic agents. Consumers need to be enlightened on food safety as well so that they can make informed choices regarding their food.
  • Both government and non-governmental agencies need to collaborate in the quest to address food safety issues. Data collected by these agencies should be shared and the information used to enlighten the public on the best ways to ensure food safety. There should be continuous allocation of resources for capacity building and enhancement to ensure a perpetual culture is propagated within the value chain.
  • Since food is a basic human right, it is only right to ensure every human being is accessible to safe and nutritious food. Same standards should be used for both local consumption and foods meant for export. Every person everywhere should be able to access safe and nutritious food, whether produced locally or imported. The holistic approach to food safety management is the only hope for countries in Sub-Sahara Africa to catch up with the developed nations in the quest to implement a lasting food safety strategy.

REFERENCES

Adams, M., & Moss, M. (2008). Food Microbiology. London, UK: RSC Press.

Anderson, K., & Pritchard, D. (2008). An Update on Staphyloccocus sureus Mastitis (4th ed.). Cummings Publishing Company.

Bean, N., & Griffins, P. (1990). Foodborne Diseases Outbreaks in the United States, 1973-1987: Pathogens, Vehicles and Trends. Journal of Food Microbiology, 53, 804-817.

Brayan, F. (1994). Microbiological Food Hazards Based on Epidemiological Information. Food Technology, 28, 52-59.

Brayan, F., Mckiley, T., & Mixon, B. (1971). Use of Time Temperature in Detecting the Responsible Vehicles and Contributing Factors of Foodborne Disease Outbreaks. Journal of Milk Food Technology, 34, 576-582.

Buchanan, R., & Doyle, M. (1997). Food Borne Disease: Significance oof E. coli O157:H7 and other Enterohaemorrhagic E. coli. Food Technology, 5, 69-76.

CDC. (2011). Estimates of Foodborne Illnesses in the United States. New York: Centers of Disease Control.

CDC. (2018). Centers for Disease Control and Prevention: Kenya Annual Report 2017. Nairobi, Kenya: Centers for Disease Control and Prevention.

Cowman, G., Otipo, S., Njeru, I., Achia, T., Thirumurthy, H., Bartram, J., & Kioko, J. (2017). Factors associated with cholera in Kenya, 2008-2013. Pan African Medical Journal, 28, 101.

Gracey, L., & Collins, D. (1992). Food Poisoning: Salmonella Surveillance in Meat Hygiene (9th ed.). London, UK: Bailliere Tindal.

Hall, J., McCroskey, L., Pincomb, B., & Hatheway, C. (1985). Isolation of an Organism Resembling Clostridium barati which Produces Type F Botulinal Toxin from an Infant with Botulism. Journal of Clinical Microbiology, 21, 654-655.

Hirsh, D., Maclachian, J., & Walker, R. (2004). Botulism in Veterinary Microbiology (2nd ed.). Washington, DC: Blackwell Publishing.

Hoffmann, S., Devleesschauwer, B., Aspinall, W., Cooke, R., Corrigan, T., Havelaar, A., . . . Hald, T. (2017). Attribution of Global Foodborne Diseases to Specific Foods: Findings from World Health Organization Structured Expert Elicitation. Plos One, 12, 9.

Jay, J. (2000). Modern Food Microbiology (6th ed.). Gaithersburg, Maryland: Aspen Publications.

Kalpelmecher, K. (1993). The Role of Salmonella in Foodborne Diseases: In Microbiological Quality of Foods. New York: Academic Press.

Labbe, R., & Nolan, L. (1981). Stimulation of Clostridium perfringens Enterotoxin Formation by Caffeine and Theobromine. Infectious Immunology, 34, 50-54.

Malangu, N. (2016). Risk Factors and Outcomes of Food Poisoning in Africa. Intech Open.

Mensah, P., Mwamakamba, L., Mohamed, C., & Nsue-Milang, D. (2012). Public Health and Food Safety in the WHO African Region. African Journal of Food, Agriculture, Nutrition and Development, 12, 3617-35.

Ministry of Health and Sanitation, Republic of Kenya. (2012). Accelerating Access to Rural Sanitation in Kenya. Nairobi: The Government Press.

Mutonga, D., Langat, D., Mwangi, D., Tonui, J., Njeru, M., Abade, A., . . . Dahlke, M. (2013). National Surveillance Data on the Epidemiology of Cholera in Kenya, 1997-2010. Journal of Infectious Diseases, 208, 55-61.

National Disease Surveillance Centre. (2004). Preventing Foodborne Disease: A Focus on the Infected Food Handler. Dublin, Ireland: National Disease Surveillance Centre.

Niehaus, A., Apalata, T., Coovadia, Y., Smith, A., & Moodley, P. (2011). An Outbreak of Foodborne Salmonellosis in Rural KwaZulu-Natal, South Africa. Foodborne Pathogens and Disease, 8, 693-7.

Ntshiqa, T., Mpangane, H., Mpambane, D., & Moshime, M. (2016). Staphylococcal Foodborne Illness Outbreak, Tshwane District, Gauteng Province - South Africa, June 2015. Journal of Infectious Diseases, 45, 235.

Ombui, J., Kagiko, M., & Arimi, S. (2001). Foodborne Diseases in Kenya. East African Medical Journal, 78, 40-44.

Quinlan, J. J. (2013). Foodborne Illness Incidence Rates and Food Safety Risks for Populations of Low Socioeconomic Status and Minority Race/Ethnicity: A Review of the Literature. International Journal of Environmental Research and Public Health, 10, 3634-52.

Quinn, P., Markey, B., Carter, M., Demelly, W., & Leonard, F. (2001). Veterinary Microbiology and Microbial Disease (8th ed.). Oxford, UK: Blackwell Publishing.

Radostits, O., Gay, C., Hinchlif, K., & Constable, P. (2007). Veterinary Medicine Text Book of Diseases of Cattle, Horses, Sheep, Pigs and Goats (10th ed.). Philadelphia: Saunders.

Robinson, R., Batt, C., & Patel, P. (2000). Encyclopedia of Food Microbiology (5th ed.). San Diego: Academic Press.

Shonhiwa, A. M., Ntshoe, G., Essel, V., Thomas, J., & McCarthy, K. (2018). A Review of Foodborne Disease Outbreaks Reported to the Outbreak Response Unit, National Institute of Communicable Diseases, South Africa: 2013-2017. National Institute for Communicable Diseases, 16, 3-8.

van-de-Venter, T. (2000). Emerging food-borne diseases: A Global Responsibility. Durban: Department of Health, Republic of South Africa.

Walderhaug, M. (2007). Foodborne Pathogenic Microorganisms and Natural Toxins. Food and Drug Administration, Center for Food Safety and Applied Nutrition, 28, 48-65.

WHO. (2008). Foodborne Disease Outbreaks: Guidelines for Investigation and Control. Geneva, Switzerland: World Health Organization.

Yard, E. E., Daniel, J. H., Lewis, L. S., Rybak, M. E., Paliakov, E. M., Kim, A. A., . . . Shahnaaz, K. S. (2013). Human Aflatoxin Exposure in Kenya, 2007: A Cross-sectional Study. Food Additives and Contaminants: Part A, Chemistry, Analysis, Control, Exposure and Risk Assessmentt, 30, 1322-31.

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Food Scientist | Interested in Data Science for Quality Management | Learning python | Agribusiness consultant with special interest in food processing and quality assurance. | Solve this if you can - if a ship had 26 goats and 10 sheep onboard, how old is the ship's captain?