E-coli O157: H7 is first emerging microorganism that causes severe human diseases in the recent past. It has become a major foodborne infectious agent causing severe diseases like Hemolytic-Uremic Syndrome (HUS), hemorrhagic enteritis, dysentery, and diarrhea. Major reservoirs of this pathogen are healthy cattle, bovine food products, and other fresh products containing bovine waste. These products containing or polluted with bovine waste makes the major and primary sources of the outbreak of E-coli O157: H7 caused diseases in the U.S. Although it is thirty years from the time the discovery of Escherichia coli O157: H7 to be a dangerous pathogen (serotype) related to severe diseases, there is no current effective treatment. The treatment is difficult since the antibiotics cannot change enteritis course caused by Escherichia coli O157: H7. However, it could only increase incidences of HUS and Shiga-like toxins. Prevention strategies and a variety of treatment to deal with Escherichia coli O157: H7 are presently in developing process and include vaccine, toxin receptor analogs, and passive antibody therapy.
Keywords: hemolytic-uremic syndrome, E- coli O157: H7,
Theodor Escherichia first discovered and described this microbe in 1885. According to him, most of the Escherichia-coli strains inoffensively colonize the digestive tract of animals and human beings like normal human flora (Guan and Levin, 2002). Due to the use of antibiotics by farmers, some strains evolved into pathogenic like E. coli 0157: H7 by obtaining virulence factors via transposons, bacteriophages, pathogenicity islands, and plasmids. The various E-coli are categorized basing on pathogenicity mechanism, virulence factors, serogroups, or clinical systems. Enterohemorrhagic E. coli (EHEC is among them and is referred to as Shiga toxin-producing pathogenic E. coli strains (Guan and Levin, 2002). It causes hemorrhagic colitis (HC) as well as the life-threating sequelae Hemolytic Uremic Syndrome (HUS) in people. Many serotypes of EHEC are often associated with a human being infections like O157: NM. O111: H8, O26: H11, O157: H7, and O91: H21. According to Guan and Levin (2002), research E. coli O157: H7 is the most commonly isolated serotype of EHEC from ill persons in the U.S, U.K, Japan, and it is the main point of the interview.
E. coli O157: H7 which is EHEC serotype was first discovered in 1982 to be a human being pathogen associated with the outbreaks out of diarrhea with blood stains in Michigan and Oregon, U.S as well as 1983 sporadic cases of HUS. After the 1983 outbreaks, numerous cases of EHEC associated outbreaks become common in U.S with E. coli O157: H7 as the primary causative agent. E. coli O157: H7 becomes the most important foodborne pathogen (Guan and Levin, 2002).
Encounter of Escherichia coli
E- Coli is rod-shaped bacteria, which are gram-negative and usually negative. They are often used in laboratory experiments. E- Coli live in human digestive system or truck, and they are harmless forming the normal person flora. However, Escherichia coli 0157: H7- a strain of E-coli is pathogenic identified to cause diseases in U.S by 1982. The discovery of E-coli 0157: H7 to cause infections occurred during the investigation into the gastrointestinal infection outbreak in the United States. Enterohemorrhagic E. coli (EHEC) is another name of E-coli 0157: H7 since it causes intestinal upset with diarrhea containing bloodstain. The pathogen resides in the intestine of the healthy cattle but usually contaminates the beef during slaughter. According to Guan and Levin (2002), the extensive use of antibiotic by the U.S farmers has enhanced the horizontal transfer of pathogenicity islands and antibiotic resistance genes leading to the creation of dangerous strains of E. coli 0157: H7. Shiga toxin acquired from Shigella strains are the Vero-toxins that causes the disease. Research further shows that the industrialized countries like Japan, Canada, U.S, and other European countries. According to George, David, and Glen, (2002) research, the average occurrence ranges from three to thirty out of the one hundred thousand and the confirm cases keeps on increasing yearly. About 74,000 individuals get infected annually with about sixty people dying of the infection.
E. coli 0157: H7 Prevalence and Economic Cost
According to the research carried out by Centers for Disease Control and Prevention (CDC), 734000 are E. coli 0157: H7 caused illnesses in the United States, 23000 of these illnesses are hospitalized, and 65 people succumb as a result of these diseases annually. DCD surveillance data on E. coli 0157: H7 outbreak shows that 1999 marked the peak of the epidemic, however, E. coli 0157: H7 prevalence has decreased continually with sporadic outbreaks reported occasionally (Kouchakkhani et al., 2016).
Annual economic effect of E. coli 0157: H7 is threateningly high, and is estimated at 406 million U.S dollars. This cost estimate incorporated medical care, premature deaths, and lost productivity among other things. According to Kouchakkhani et al., (2016).The high cost of illness demands an extra additional effort towards the control of E. coli O157: H7.
Identification and Isolation E. coli O157: H7
The microbe expresses flagella (H) antigen 7, somatic (O), and antigen 157 hence the E. coli O157: H7. It has distinctive characteristics of postponed D-sorbitol fermentation (>24 h) and the lack of ability to produce β-glucuronidase to hydrolyze a synthetic molecule, 4-methyle-umbellifery-D-glucuronide (MUG). The detection of E-coli O157: H7 is carried out using Sorbitol MacConkey (SMAC) agar supplemented with MUG. To increase the discrimination for cefixime, Escherichia coli 0157: H7, potassium, vancomycin, and tellurite is added to SMAC agar plates to inhibit other Gram-negative flora. The serotypes H7 and O157 are additional confirmed using chemically accessible latex agglutination assay (George, David, and Glen, 2002).
Spread, transmission, Entry, and Multiplication
When E. coli 0157: H7 contaminated food is consumed and digested, it travels through the digestive system and finally get attached to mucosal epithelial cells of the large intestine forming a pedestals hence leading to the destruction of the microvilli. The pathogenic bacterium multiplies producing toxins. The generated toxic condition additionally causes vomiting other than diarrhea ring (George, David, and Glen, 2002). According to research, 50% of the vomiting cases, as well as 30% of the fever cases, are associated with the infection. Averagely, the incubation period of the E. coli 0157: H7 is three to four days. Surprisingly as few as fifty E. coli 0157: H7 cells are enough to cause illness since the pathogen is acid resistance and friendly high temperature in the stomach hence quickly pass through the stomach. The microbe can also grow from 10-50C with an ideal temperature of thirty-seven degree Celsius. Up to ten percent of individual diagnosed with this infection develop the hemolytic uremic disorder, which is the main complication of E. coli 0157: H7. This hemolytic uremic disease is mostly relating to acute renal failure and exclusively affects the elderly, the children, and is deadly to many leading to over 5% of cases needing intensive care. According to the research, 90% of HUS cases are as a result of E. coli 0157: H7. The same research indicates that the E. coli 0157: H7 is the leading root cause of kidney failure in children, which comes about due to the spread of the microorganisms and the toxins throughout the bloodstream. The disease affects any human organ. However, certain renal organs are more vulnerable as Guan and Levin (2002) indicates.
Another research shows that E. coli 0157: H7 is passed by consumption of contaminated food, uncooked meat, water, and other contaminated products. It is indicated that most of the foodborne diseases outbreaks are related to EHEC, and some of them are life threatening. However, it important to note that not all E-coli strains are harmful and causes diseases like serotype O157: H7, which is a public importance as they are main, causes of public diseases outbreak related to food born disease (Guan and Levin, 2002). It known to cause bloody diarrhea or hemorrhagic colitis, that is, it affects large intestine and then passes to the stomach where it causes abdominal pains and bloody diarrhea. Transmission is majorly through oral-fecal. There are also a lot of asymptomatic transporters who shed bacterium in their feces and infect others but do not show any sign and symptoms of the disease on themselves.
Escherichia coli 0157: H7 chromosomal size is about 5.5 Mb according to research. This size has included the backbone sequence of 4. 1 Mb preserved in all E. coli strains. The genomes tha remains of about 1.4 Mb are particular to Escherichia coli 0157: H7. Furthermore, E. coli O157: H7 genome comparison with nonpathogenic E. coli K12 shows that 0.53 Mb of E. coli O157: H7 DNA is missing which suggest that genomic reduction also played a part in E. coli O157: H7 development (Kouchakkhani et al., 2016). The majority of E. coli O157: H7-specific DNA sequences of 1.4 Mb are horizontally transmitted different DNAs such as prophage and prophage-like elements. All the researchers and laboratory tests have indicated that E. coli O157: H7 contains 463 phage-related genes as compared to only 29 in E. coli K-12. It is also faithful to note that a change in G+C content is among others one of the indicators that horizontal transmission has acquired a deferent genomic region and that the Jabbar’s research of (2016) was estimating at least 53 diverse species have donated to the distinctive sequences in the E. coli O157: H7. It is vital to note, those virulence-related genes amongst the two sequenced of the E. coli O157: H7 strains are almost identical to about 99% similarity. Therefore, it is very clearly that both the loss of DNA and acquisition of DNA have played a vital role in the pathogenesis progression of the E. coli O157: H7.
E. coli O157: H7 Evolution
Evolution of the E. coli O157: H7 forms the backbone on how best the disease can be handled and therefore it is important that we dwell on this concept. Several epidemiological and comparative studies carried out by many scholars indicate that E. coli O157: H7 is likely to have developed from the less virulent strain E. coli O55: H7 and non-toxigenic E. coli O55: H7 (Kouchakkhani et al., 2016). The researchers suggest that E. coli O15:H7 has arisen through four consecutive events; one, the acquisition of a stx2-having bacteriophage, two, the acquisition of the rfb region and the pO157, third, the acquisition of the stx1-having bacteriophage, and finally, the loss of the ability to ferment D-sorbitol and the loss of beta-glucuronidase (GUD) activity. These factors contributed and led to the rise of the E. coli O157: H7 (Kouchakkhani et al., 2016).
Animals as the Main Reservoir of E. coli O157: H7
The early and the current studies have indicated that cattle are the main reservoir of E. coli O157: H7. It is noted that cattle as the reservoir host is usually asymptomatic when harboring this microbe. Studies have indicated that there are rare cases of young calves suffering from a diarrheal disease caused by the E. coli O157: H7 serotype (George, David, and Glen, 2002). The at which cattle shed when the E. coli O157: H7 attacked differs at any one time. Furthermore, it is not only cattle that shed; the test runs on other animals like goats, Sheep, goats, turkeys, and pigs, show that they also shed E. coli O157: H7 in their excretion. Further study indicates that soil and water as well harbor these deadly microbes.
E. coli O157: H7 Acid Resistance
Survival of the E. coli O157: H7 in the stomach has raised questions given the fact that the stomach has a very low pH. The ability of the bacterium to offer self-protection against extreme low pH of below pH 3.0 is referred to as Acid resistance (AR). The stomach pH, which is as low as 1.5 to 3.0, is a mechanism the stomach uses to fight against the enteric pathogens causing foodborne diseases. Since the bacteria can survive in the acidic condition of the stomach, the chances of attacking and colonizing the intestine, leading to infection are very high. Acid resistance is related to lowering of the communicable amount of enteric pathogens. However, it unfortunate that the low contagious dose is one major characteristic of the E. coli O157: H7, which makes this pathogen very highly infectious (Kouchakkhani et al., 2016).
Some studies have reported that the acid resistance characteristics of the E. coli O157: H7 strains are high and this makes it thrive well. According to their research, they have determined three efficient Acid Resistance systems. The first, Acid Resistance system needs the different factor of Sigma RpoS and suppression glucose. The rpoS of the E. coli O157: H7 mutant was shed in less quantity in experimentally ill calves and mice. The second Acid Resistance system needs the addition of arginine at the time of the exposure to acidic the condition. The regulator of Adia (cysB) and the arginine decarboxylase (Adia) were described in the second Acid Resistance system. The third Acid Resistance system needs glutamate for defense at low pH state (George, David, and Glen, 2002). The vital components of the Acid Resistance system comprise of the two isozymes of glutamate decarboxylase (gadA or gadB), and a putative glutamate, γ-amino butyric acid antiporter (gadC). Further studies have indicated that even though only one of the required two glutamate decarboxylases is vitally required to protect the microbe at pH 2.5, it is noted that at pH 2.0, both glutamate decarboxylase isozymes is a primary requirement for protection. The primary outcome shows that glutamate-reliant on AR is a major effect to protect the microbe at pH 2.0 in a medium, which is complex. The E. coli O157: H7 contains the three overlapping Acid Resistance systems. However, the control and necessities for Acid Resistance activities are varying in every AR system.
Many scholars have indicated that other than the three Acid Resistance systems, some proteins entailed in the Acid Resistance of the E. coli O157: H7 are known. According to Shadi et al., (2015), the proteins must involve DNA-binding protein Dps, RNA of the polymerase-related protein SspA, and chaperone HdeA. Besides, the research has shown that the alteration that occurs at the colonic acid production or the cell membrane are related to the successful Acid Resistance. Therefore, the E-coli O157: H7 uses various Acid Resistance systems depending on the acid environment type encountered naturally.
Great scholars concerning the effect of these diseases on human beings have put many types of research forward. In the recent past, the E. coli O157: H7 disorder has become a major public health problem in the European countries like the U.S.A, North America, and other major developed countries of the world. Even though many research outcome indicates that some cases of the E. coli O157: H7 disorders are lower as compared to other diseases caused by enteric pathogens like the Campylobacter spp or Salmonella, the infections arising from the E. coli O157: H7 are high (Shadi et al., 2015). The numbers are regarding hospitalization as well as regarding higher number of fatality rate in the developed countries. The E. coli O157: H7 caused human infection caused has in the recent past, presented a broader clinical spectrum that ranges from the asymptomatic as well as leading to death. According to numerous researches that have been conducted medically, most of the cases that are associated with non-bloody diarrhea are naturally cured or self-resolve with no further complication in future. Nevertheless, in severe cases, victims take one to three days to get to a stage of HC or bloody diarrhea. Out of the total number of the HC diagnosed patients, five to ten percent cases of the disease becomes life-threatening consequence in a few days. The study further indicates that thrombocytopenic purpura also called TTP or HUS is the most common infections. In the United States of America E. coli O157:H7 commonly the main cause of the HUS. Both the elderly and the children increasingly at risk of severe medical symptoms like HUS.
Medical practitioners have researched out several strategical therapies including even the vaccines and antibiotics use to control and treat the disease. Unfortunately, none of the remedies can be certified to specifically treat the E. coli O157: H7 disorder, furthermore, the use of the antibiotics is likely to be contraindicated (Shadi et al., 2015). This means that all of the treatment are only to suppress the disease and supportive mainly to reduce the symptoms duration as well as reduce systemic problems. Owing to the fact that no permanent and specific treatment can be administered to E. coli O157: H7 infected patients, the U.S government, have taken effective measures to ensure that control and prevention of the disease are carried out at the onset. And these measures are mandatory to every citizen (Shadi et al., 2015).
In conclusion, this paper is a review that has majored on the E. coli O157: H7 serotype. We have seen that E-coli O157: H7 is a major cause of fatal human infections across the whole world. The pathogen has Shiga toxin, the F-like products of the plasmid pO157, and the pathogenicity island products known as the locus of enterocyte effacement as the major virulence factors. The microbes survive very comfortably in acidic conditions environment, which explains their reason of dominant in the stomach. The body of healthy cattle forms the primary reservoir for the diseases causing microorganism. A lot of research are needed to be carried out to get more break through on the treatment of the diseases associated with E-coli O157: H7. As it stands now, the disease is quite expensive to manage and control. It affects so many people as well as the government economically.