Antimicrobial Resistance in Diverse Escherichia coli Pathotypes from Nigeria

1. Introduction

Theodor von Escherich, a German-Austrian paediatrician was the first to isolate intestinal bacteria in neonates and infant faecal matter in 1857, which he termed ‘Bacterium coli commune’[1]. This bacterium was originally called Bacillus coli in 1895 and renamed Escherichia coli in 1919 in honour of Escherich. The nomenclature was then formally acknowledged in 1958, forming Escherichia as a genus, with E. coli as its first species [2]. E. coli is a Gram-negative, non-spore-forming, facultative anaerobic, rod-shaped bacteria belonging to the Family Enterobacteriaceae, Class Gammaproteobacteria, and Phylum Pseudomonadota. These are normal intestinal commensals of humans and warm-blooded animals and to date, thirteen species have been described of which E. adecarboxylata, E. albertii, E. blattae, E. coli, E. fergusonii, E. hermannii, E. marmotae, E. ruysiae, E. vulneris and E. whittamii are validly published under the International Code of Nomenclature of Prokaryotes (ICNP) whereas E. faecium, E. hominis and E. pseudocoscoroba are not validly published.

Escherichia coli is the most widely studied organism, a lactose fermenter with colonies on MacConkey agar, appearing bright pink with a typical diameter of 0.5 to 1 mm after overnight incubation at 37^oC/24 h. The colony appearance on blood agar plates can vary from grey to white, transparent to opaque, and raised convex to flat. On Eosin Methylene Blue (EMB) agar, E. coli produces a characteristic green metallic sheen. This bacterium can survive in water for 4 – 12 weeks and as a result, it is used as a faecal indicator organism for determining bacterial contamination in water, because of the availability of simple, and affordable techniques [3]. Some pathotypes of E. coli such as the O157: H7 strain are sorbitol non-fermenters, which is a feature that can help it to be distinguished from other strains of E. coli [4].

Most E. coli strains are harmless and essential to the human digestive system. E. coli can synthesise some essential vitamins for human health, such as vitamin K and some B vitamins, and aids in the breakdown of food and the absorption of nutrients. Additionally, they guard the gut by preventing the colonisation of harmful bacteria through colonisation resistance and resource limitation [5].

Most E. coli strains are harmless, but pathogenic types can adversely affect people and cause food poisoning, urinary tract infections, septic shock, or meningitis. E. coli can be divided into two broad categories: commensal and pathogenic [6]. Commensal E. coli is crucial for maintaining normal intestinal bacteria, supports innate and adaptive immunity, and is also important for the gastrointestinal tract because it produces vitamin K and vitamin B12 required by man [7]. Extra-intestinal pathogenic E. coli (ExPEC) can be divided into many main genetic subgroups such as A, B1, B2, C, D, E and I. Group A often includes isolates from the colon, ileum, and duodenum [8]. Phylogroup B1 contains both commensal and some strains belonging to the Enterohemorrhagic E. coli (EHEC) pathotype. B2, C, D1, D2, and E represent Intestinal Pathogenic E. coli (InPEC) which relates mainly to diarrheal diseases. Many ExPEC belong to group B2 and are primarily associated with adult urinary tract infections (UPEC) and neonatal meningitis (NMEC) [9].

The main source of pathogenic E. coli variations' capacity to cause intestinal or extraintestinal disease is their development of several specific virulence factors, including toxins, lipopolysaccharides, iron acquisition factors, adhesins, polysaccharide capsules, and invasins. These elements aid the organism's ability to get past the host's defences and infiltrate or colonize the organs.

E. coli is transmitted to humans primarily through the consumption of contaminated foods, such as raw or undercooked ground meat products and raw milk. An increasing number of outbreaks are associated with the consumption of fruits and vegetables (including sprouts, spinach, lettuce, coleslaw, and salad) whereby contamination may be due to contact with faeces from domestic or wild animals at some stage during cultivation or handling [10]. The reservoir of this pathogen includes cattle, sheep, goats, deer, pigs, horses, rabbits, dogs, cats, and birds including chicken and turkeys. Faecal contamination of water and other foods, as well as cross-contamination during food preparation (with beef and other meat products, contaminated surfaces and kitchen utensils), can also lead to infection [11].

Apart from the virulence profile of E. coli, antibiotic resistance mechanisms of this bacterium are one of the most significant issues in recent research. Antibiotic resistance happens when bacteria evade the effect of antibiotics either by mutations in functional genes or by acquiring genes that can hydrolyse antibiotics and can also be transferred via plasmids between different strains [12]. One of the most clinically and epidemiologically significant mechanisms of antibiotic resistance in Enterobacteriaceae is the synthesis of carbapenemases, AmpC-type β-lactamases, and extended-spectrum β-lactamases (ESBLs) [13]. In this study, we review the prevalence of different E. coli pathotypes and their underlying mechanisms of antibiotic resistance in Nigeria.

1.1. Diarrheagenic E. coli Pathotypes

According to the WHO Global Burden of Foodborne Diseases report, diarrheagenic E. coli (DEC) causes around 200,000 deaths and over 300 million illnesses worldwide each year [10]. Approximately 40% of bouts of acute diarrhoea in children in underdeveloped countries are caused by diarrheagenic E. coli [14]. Additionally, they significantly contribute to both adult and paediatric diarrhoea in Nigeria [14]. Enterotoxigenic (ETEC), enterohaemorrhagic (EHEC), enteroinvasive (EIEC), enteropathogenic (EPEC), enteroaggregative (EAEC), diffusely adherent (DAEC), cytolethal distending toxin-producing (CDTPEC), and cell-detaching E. coli (CDEC) are the eight pathotypes of DEC strains that are currently known [14,15]. Each pathotype of DEC has a unique set of virulence factors encoded either on the plasmids or on the chromosomes. E. coli pathotypes cause substantial diarrheal illnesses in Nigeria. These infections are especially serious for children under five, as they increase morbidity and mortality and exacerbate public health issues in an environment where access to clean water and quality healthcare is frequently restricted.

1.2. Enterohaemorrhagic E. coli (EHEC)

One of the major foodborne infections, enterohaemorrhagic E. coli O157:H7, frequently results in a high death rate among humans [16]. Common infections brought on by this bacterium have the potential to be fatal. Haemorrhagic colitis and other problems including hemolytic uremic syndrome and thrombotic thrombocytopenic purpura are among the symptoms that susceptible people may experience [17,18]. Toxin tests and stool cultures are used for diagnosis. E. coli O157 was found to be one of the main causes of foodborne disability-adjusted life years, placing Nigeria in a sub-region with the greatest prevalence of foodborne disease worldwide. According to Gambushe et al [19], this infection is also common in South Africa and Ethiopia. Wells, water troughs, and bodies of water (such as ponds and streams) have all been shown to contain EHEC which could be due to the contamination of water with ruminant faeces which are common carriers of this pathogen. Nigeria is among the nations where 90 million people lack access to potable water, and 130,000 children under the age of five pass away every year from preventable waterborne illnesses as a result of government agencies' disorganised efforts, lack of funding, and basic public education about hygienic practices, public health policies, and engaging with various stakeholders. The majority of people, especially those living in rural and suburban areas, use untreated water from wells and streams for domestic use, which puts them at risk of E. coli infection through the faecal-oral route [20,21]. Waterborne transmission where 88.9% of E. coli isolates were of EHEC pathotype has been reported in Nigeria, both from contaminated drinking water and recreational waters [22].

Although it has also been found to survive for months in manure, beef and mutton used in steaks; however, in Nigeria, meats are cooked thoroughly and therefore STEC outbreaks linked with undercooked meat are rare. Interpersonal contact is a crucial means of transmission via the faecal-oral pathway. There have been reports of an asymptomatic carrier condition, in which a person can infect others yet exhibit no clinical symptoms of the illness. Another known risk factor for STEC infection is going to farms and other places where the general public may have direct contact with farm animals. Ruminants such as cattle, sheep and goats are largely reared by pastoralists & agro-pastoralists and common practice in the Fulani tribe can also be exposed to strains such as E. coli O157 [23].

Antibiotic therapy is generally not recommended for EHEC infections [24] because it is of no benefit [25], or even harm, in particular, but an increased risk of hemolytic uremic syndrome (HUS) development in patients treated with antibiotics during the initial period of diarrhoea [26]. Shiga toxin (Stx), the primary virulence component of EHEC implicated in the pathogenesis of HUS, is produced and/or released more frequently when antibiotics are used, which is one conceivable mechanism by which they raise the chance of developing HUS [27]. The goal of treating STEC is to remove the bacteria from the intestine without causing it to start producing toxins. Recently, STEC has been treated with different methods such as antisera or monoclonal antibodies [28].

1.3. Enterotoxigenic E. coli (ETEC)

ETEC is a primary enteric pathogen that is responsible for annual millions of diarrheal diseases, globally [29]. In the laboratory, ETEC is diagnosed when the microbe is cultured from faecal samples and tested for the presence of toxins (LT, STh, and STp) using phenotypic assays like dot blotting or through the use of conventional PCR [30]. Children less than 5 years old are vulnerable to ETEC, especially in developing countries like Nigeria where the disease is endemic. ETEC accounts for about 100 million diarrhoea episodes and 60,000 mortalities in 2015 [29]. ETEC is also the major cause of traveller’s diarrhoea affecting travellers visiting developing countries of the world [31]. In underdeveloped nations, where there is no infrastructure for the collection of human waste and the supply of clean drinking water, ETEC infections are caused by consuming contaminated food and water. Previous research has shown that ETEC may live in faeces for up to six months and that it often grows in water as biofilms, which gives it a better chance of surviving [32].

1.4. Enteroinvasive E. coli (EIEC)

EIEC appear to be a less frequent cause of diarrheal sickness than other E. coli infections, however, this may be due to the methods employed to identify these organisms [33]. It is diagnosed in the laboratory by culturing stool samples and by the detection of EIEC pathogenicity genes by DNA hybridization or PCR. EIEC produce a diarrheal illness that is indistinguishable from shigellosis. The majority of diarrheal illness cases that are caused by EIEC seem to be sporadic. Shigella spp. are closely linked to the EIEC which uses Shigella-like genetic material to encode virulence components including the type III secretion system (TTSS). The EIEC enters the intestinal cell, multiplies intracellularly, and extends into neighbouring intestinal cells via virulence proteins known as "invasins." Cell death and occasionally bloody diarrhoea result from this process [33]. The majority of EIEC illness manifests clinically as watery diarrhoea and is difficult to recognize at the bedside from the many other causes of diarrhoea [33].

1.5. Enteropathogenic E. coli (EPEC)

According to Lanata and Walter [34], enteropathogenic Escherichia coli (EPEC) is a common strain of E. coli that causes persistent diarrhoea and is one of the main causes of pediatric E. coli infections worldwide [35]. Over the past few decades, the importance of EPEC as a pathogen has generally decreased in the published [36,37]. In contrast to more recent studies that relied on molecular techniques and/or adherence assays to identify EPEC, it is unclear whether the decrease in EPEC infections is the result of interventions, particularly breastfeeding promotion, or if earlier studies that overestimated the relative contribution of these organisms in diagnosis based on O- or O: H-typing [38].

1.6. Enteroaggregative E. coli (EAEC)

Enteroaggregative E. coli (EAEC) has gained increased attention in the last ten years as a potential cause of persistent, watery diarrhoea. According to Kaur et al. [39], EAEC is a rather diverse category of an emerging enteric pathogen connected to episodes of acute or chronic diarrhoea in children and adults worldwide. In both developing and wealthy nations, EAEC infection is a significant contributor to diarrhoea in both outbreak and non-outbreak situations. Irritable bowel syndrome has recently been linked to EAEC, albeit this has not yet been proven [39].

1.7. Diffusely Adherent E. coli (DAEC)

DAEC strains are a varied group of isolates that all exhibit diffuse adherence (DA) to epithelial cells in the conventional laboratory assay of adherence to HEp-2 or HeLa cells [40]. The production of adhesins encoded by a family of operons connected to afa/dra/daa is often the cause of the DA pattern of DAEC isolates.

1.8. Cytolethal-Distending Toxin-Producing E. coli (CDTEC)

Escherichia coli strains obtained from patients with diarrhoea were shown to have the cytolethal distending toxin (CDT) in 1987 [41]. Since then, several pathogenic Gram-negative bacteria have been found to express CDT, including Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans, Campylobacter spp., Escherichia spp., Haemophilus ducreyi, Helicobacter spp., Providencia alcalifaciens, and Shigella sp. In vitro studies, it has been shown to stop the proliferation of various cell lines [42].

1.9. Cell-Detaching E. coli (CDEC)

When CDEC was initially identified, it was discovered to relate to diarrhoea in Australian aboriginal children [43]. Although no conclusive evidence links it to diarrhoea, it has also been discovered in Brazil [44]. Notably, the majority of the CDEC isolates found in this investigation (87.0%) did not ferment lactose and were like a group of non-lactose-fermenting haemolytic strains that had been previously isolated from stool specimens in Somalia [45]. Lactose-negative CDEC strains may be significant pathogens in Africa [46]. Unfortunately, as is the case with most E. coli strains, their slow rate of lactose fermentation means that they are likely to be disregarded (or mistaken for Shigella or other non-lactose fermenters) in a lot of investigations. Additionally, diarrhoea may potentially be linked to diffusely adherent E. coli (DAEC). However, rates of infection vary by region in Africa [47].

The clonal classification of pathogenic strains of E. coli is listed in Table 1 highlighting the symptom, pathogenic mechanism, reservoirs and epidemiological aspects for each of those groups.

2. Molecular Mechanisms of Antibiotic-Resistant E. coli

Globally, there is a growing issue with resistance to broad-spectrum β-lactams, which is caused by enzymes such as AmpC β-lactamases (AmpC), Metallo β-lactamases (MBL), and extended-spectrum β-lactamases (ESBL) [48]. The most common mechanism for β-lactam resistance in clinical isolates from the Enterobacteriaceae family is the synthesis of β-lactamases [49]. These groups of resistant E. coli have more diarrheagenic pathotypes than uropathogenic E. coli but could increase the risk for the latter [50].

2.1. Community-Acquired Antibiotic-Resistant E. coli

The rise of community-acquired antibiotic-resistant E. coli is primarily attributed to several factors. One key factor is the overuse and misuse of antibiotics in both human medicine and livestock production. It is noteworthy to mention that there are either no or little regulations of the use of antibiotics in Africa [51]. Widespread and irrational use of antibiotics creates an environment where bacteria can develop resistance mechanisms, rendering antibiotics ineffective at killing them. The implications of community-acquired antibiotic-resistant E. coli infections are significant. These infections are often more difficult to treat, as the bacteria are resistant to commonly used antibiotics which can result in prolonged illness, increased healthcare costs, and in some severe cases, life-threatening complications. Furthermore, treating these infections requires the use of more potent and costly antibiotics, which can further contribute to the emergence of antibiotic resistance. Globally, there is currently significant concern over the advent of strains of E. coli that produce extended-spectrum beta-lactamases (ESBLs) and community-acquired resistance to fluoroquinolones. A higher frequency of E. coli with elevated resistance to antibiotics is identified in patients suffering from complex UTIs [52]. This is a result of the organisms acquired after being exposed to hospital settings, as well as the fact that many individuals with persistent abnormalities who suffer from recurring infections have taken numerous courses of antibiotics in the past [53].

2.2. Hospital-Acquired Antibiotic-Resistant E. coli

Worldwide, urinary tract infections (UTIs), are the most prevalent type of hospital-acquired illnesses. E. coli is the most frequent bacterium associated with UTIs. Different E. coli strains obtained from community and hospital sources may have different levels of antibiotic resistance and can often display multi-drug resistant phenotypes. Studies show that ESBL-producing E. coli is becoming increasingly prevalent in hospitals [54,55].

2.3. Extraintestinal Pathogenic E. coli (ExPEC)

According to Nicolas-Chanoine et al.[56], ST131 is currently the most prevalent E. coli lineage discovered in extraintestinal pathogenic E. coli (ExPEC) isolates worldwide. Based on population genetics, ST131 is composed of several clades, including A, B, and C. Of these, clade C is the most widely distributed worldwide [57]. Compared to other traditional group B2 ExPEC isolates, almost all of the ST131 isolates are fluoroquinolone-resistant and are often reported to produce extended-spectrum β-lactamases, like CTX-M-15 [56]. Furthermore, ST131 E. coli isolates are thought to be extremely dangerous due to the range of infections they can cause in both community and hospital settings, as well as the quantity of virulence-associated genes they carry [56].

2.4. Antibiotic-Resistant E. coli of Origins in Animals and the Environment

E. coli of animal origin exhibits resistance against a range of antibiotics due to overuse and abuse, including tetracyclines, aminoglycosides, β-lactams, fluoroquinolones, and third-generation cephalosporins [58]. A recent report revealed that the extended-spectrum beta-lactamase Escherichia coli (ESBL-EC) strains from the human, chicken, and chicken market environments had the same sequence type (ST-155), indicating that there may have been a transmission between these hosts and the environment [59]. This finding also shows that co-colonization of antimicrobial-resistant E. coli from a shared source is a possibility. The ESBL-positive E. coli ST-155 represents a significant zoonotic strain that is responsible for the transmission to humans [60,61].

It is also important to note that ST-155 has been detected in E. coli isolates from water samples [61] and was detected in isolates from environmental samples [62]. Antibiotic-resistant E. coli concentrations in some wastewater treatment facilities and aquatic ecosystems reached 10⁴-10⁵ CFU/mL, which is more than what is needed for irrigation water usage presenting a severe risk to public health [62].

3. Distribution of E. coli with Sources in Nigeria

3.1. Prevalence of Urinary Tract Infections Caused by E. coli

Among other studies, Olorunshola et al., [63] reported a 6% prevalence of E. coli in Nigeria (Table 2). This study which was in a city of more than 13.4 million in 2000 was the least while Mofolorunsho et al showed a higher prevalence of 70.3% in Anyigba town in Kogi State which has less than 500,000 people in 2021.

3.2. E. coli in Food and Environment

Table 3 describes the prevalence of E. coli in food and environment. Besides human samples, E. coli can also be found in animals, animal products, plants, and environmental samples including water and soil. Adesiji et al., [72]showed a very high prevalence of the organism in fresh meat on sale which could be due to faecal contamination. The prevalence of the organism from other animals and animal products has public health implications. Wastewater and dumpsite have a high prevalence which is expected. Ruminant milk samples were seen to be contaminated by E. coli with prevalence rates of 44.8%, 43.1% and 39.2% in cows, goats and ewes respectively [73,74]. Anueyiagu et al., [75] also isolated 22.73% of E. coli from domestic birds and 6.67% of E. coli from wild birds found in the same vicinity.

Fresh fruits and vegetables sold in Nigerian flea markets have been reported to be laden with microorganisms such as E. coli. Maikai and Akubo [76] recorded a 21.3% prevalence while Reuben and Makut [77] recorded a 17.5% prevalence.

Environmental sources of E coli were reported by Edward et al., (2020) [78], Garba et al (2009) and Ijabani et al. (2022) [80] among many other authors.

Table 3. E. coli isolated from humans in Nigeria.

S/No	Source	Prevalence (n)	Author
1.	Raw milk from cows	44.8% (640)	Anueyiagu et al., [74]
2.	Raw milk from does	43.1% (206)	Anueyiagu et al., [74]
3.	Raw milk from ewes	39.2% (206)	Anueyiagu et al., [74]
4.	Fresh meat on sale	26% (300)	Adesiji et al [72]
5.	Fresh/Roasted beef	52.5% (300)/ 25.3% (150)	Dahiru et al., [81]
6.	Poultry	31.8% (111)	Aworh et al., [59]
7.	Wild birds	48.1% (160)	Oludairo et al., [82]
8.	Vegetables	17.5% (40)	Reuben and Makut, [77]
9.	Fresh fruits	21.3% (108)	Maikai and Akubo, [76]
10.	Wastewater	62.4% (700)	Edward et al., [78]
11.	Municipal water	45.5% (300)	Garba et al., [79]
12.	Soil	20% (75)	Ijabani et al., [80]

Table 3. E. coli isolated from humans in Nigeria.

S/No	Source	Prevalence (n)	Author
1.	Raw milk from cows	44.8% (640)	Anueyiagu et al., [74]
2.	Raw milk from does	43.1% (206)	Anueyiagu et al., [74]
3.	Raw milk from ewes	39.2% (206)	Anueyiagu et al., [74]
4.	Fresh meat on sale	26% (300)	Adesiji et al [72]
5.	Fresh/Roasted beef	52.5% (300)/ 25.3% (150)	Dahiru et al., [81]
6.	Poultry	31.8% (111)	Aworh et al., [59]
7.	Wild birds	48.1% (160)	Oludairo et al., [82]
8.	Vegetables	17.5% (40)	Reuben and Makut, [77]
9.	Fresh fruits	21.3% (108)	Maikai and Akubo, [76]
10.	Wastewater	62.4% (700)	Edward et al., [78]
11.	Municipal water	45.5% (300)	Garba et al., [79]
12.	Soil	20% (75)	Ijabani et al., [80]

4. Genotypes of E. coli in Nigeria and Other African Countries

The prevalence of Shiga toxigenic E. coli (STEC) differs by country. Most regions of the world, including several African nations, have reported cases of Shiga toxigenic E. coli infections [83]. One or more Shiga-toxin (stx) strains are produced by human pathogenic STEC. These strains are classified into two groups: stx1 (which includes the three variants stx1a, stx1c, and stx1d) and stx2 (which includes seven unique variants stx2a, stx2b, Stx2c, Stx2d, Stx2e, Stx2f, and Stx2g). Among these variations, stx2b and stx2e are connected to minor clinical symptoms or asymptomatic faecal carriage, while stx2a, stx2c, and stx2d are linked to severe disease [84,85,86]. The main STEC serogroups include E. coli O26, O45, O91, O103, O111, O113, O121, O128, O145, and O157, and they are all capable of producing Shiga toxins. In addition to stx1 and stx2, certain isolates also have eaeA and/or hlyA [87]. The hlyA genes encode for cytolysin while eae gene encodes for intimin which plays a vital role in the attaching and effacing (A/E) lesions on epithelial surfaces [88].

In 1990, in the South African city of Johannesburg, the first E. coli O157:H7 infection in humans was identified and recorded [89,90]. Nonetheless, in the Central African Republic in 1996, deadly pathogenic bacteria were discovered in patients suffering from hemorrhagic colitis. Following the emergence of bloody diarrhoea in Cameroon in 1998, STEC O157:H7 isolation in humans was reported [91]. There have been reports of pathogen isolation in Tanzania, Kenya, and Ethiopia in East Africa. In terms of the zoonotic disease epidemic on the African continent, Ethiopia is ranked second only to Nigeria [89]. In Nigeria, pathogenic STEC such as stx1, stx2, eaeA and hylA are common according to the literature. Stx1, stx2, eaeA and hylA were isolated from beef & beef products, faeces and meat of food-animal and beef abattoirs according to Fayemi et al., [92], Ojo et al., [93], and Ayoade et al., [94] respectively. The same E. coli variants were isolated from diarrheic patients from southwestern Nigeria [95]. In general, the evidence of STEC O157:H7 infection among the environment, animals, and humans, is obvious in Africa. In the laboratory, Sorbitol MacConkey agar is used to isolate STEC in Nigeria.

5. Antibiotic Resistance

The O157:H7 strain's high resistance is recognized as one of the key elements that contributes to the possibility of the bacterium becoming more harmful. E. coli O157:H7 is found in food samples obtained from animals, particularly meat. It is extremely resistant to a class of widely used antibiotics, including quinolones, aminoglycosides, macrolides, cephalosporins, sulfonamides, fluoroquinolones, and tetracyclines. Antimicrobial resistance genes, such as those that confer resistance to cephalosporins (bla_CTX-M), broad-spectrum penicillins/beta-lactams (bla_SHV), gentamicin (aac(3)-IV), sulphonamide (sul1), tetracycline (tetA and tetB), and trimethoprim (dfrA1), are among those that enable resistance. However, it has been shown that the antimicrobial resistance of STEC strains is caused by aminoglycoside resistance genes (aadA1) [96,97,98]. Investigating the distribution and prevalence of antimicrobial-resistance variables and antimicrobial resistance patterns of E. coli O157:H7 strains acquired from raw beef, goat, chicken, and turkey meats is crucial given the ambiguity surrounding the dissemination of E. coli O157:H7 in raw meat samples.

Numerous studies conducted across the African continent have identified and documented resistance of E. coli O157:H7 to a range of antimicrobial drugs. For instance, multidrug-resistant E. coli O157:H7 was isolated from humans, animals, and the environment in Egypt and its detection and documentation have been reported [91]. A multidrug-resistant E. coli O157:H7 was found and claimed to have been isolated from a cow in South Africa. In Nigeria, similar outcomes have been documented. Antimicrobial drugs' severe overuse in treating E. coli O157:H7 infections is one of the main causes of concern. This leads to multidrug resistance, which is not only concerning because it doesn't seem to be given much attention, but it also aids in the selection of resistance genes [91].

Given the advent of CTX-M-type extended-spectrum β-lactamases (ESBLs), recent reports in the literature indicated that E. coli is emerging as the Enterobacteriaceae species most impacted by ESBLs. It has been discovered that bla_CTX-M bacteria can have virulence genes in addition to resistance genes. Out of 9 UTI samples collected from patients in Southwest Nigeria, 6 were positive for bla_CTX-M [95], and in Minna Metropolis of Nigeria, 60% of 10% E. coli isolated from urine harboured bla_CTX-M [99]. In ruminant mastitis, the genetic characterization revealed a higher prevalence of bla_CTX-M (24.39 %) than bla_TEM (12.19 .0%) in the bovine milk samples analysed [75].

Additionally, it has been noted that the majority of blaCTX-M from E. coli strains implicated in outbreaks across various nations also demonstrated the presence of additional antibiotic resistance genes, including bla_OXA-1, bla_TEM-1, tetA, aac(6)-Ib, and aac(3)-II, as well as occasionally a class 1 integron [100].

6. Conclusions

Nigeria and Africa face serious public health issues because of the spread of E. coli-resistant strains. Due to a lack of access to good healthcare, overused and misused of antibiotics, and use of antibiotics without a prescription, AMR can spread quickly throughout Nigerian communities. In addition to its enhanced virulence, highly pathogenic and antibiotic-resistant E. coli poses a severe hazard to food systems. These infections have been linked to one or more genetic factors of pathogenicity and pose a risk to human health. As a result of this research, policymakers should create a more proactive strategy to reduce the rise in E. coli infections in Nigeria. Therefore, to reduce the spread of potentially harmful or resistant E. coli strains, surveillance, low-cost diagnosis, and stringent hygiene practices of food (of animal and plant origin) should be continuously monitored. In general, individuals should prepare and consume food with greater hygiene standards. This assessment encourages Nigeria and other African nations to write and adopt new legislative measures for infectious diseases.