Escherichia coli, known shortly as E. coli, is a rod-shaped, facultative, Gram-negative bacterium. The present bacterium harbors the potential to thrive in environments that lack oxygen. Different strains of this bacterium naturally colonize animal and human gastrointestinal tracts without causing possible harm to their hosts. Over time, however, particular strains of these bacteria have managed to develop virulence due in part to the interplay of widespread factors, including transposons, pathogenicity islands, plasmids, and phages. Pathogenic variants of E. coli fall within diverse categories as determined based on an interplay of widespread factors ranging from pathogenicity mechanisms to virulence factors, serogroups, and clinical symptoms. A rigorous examination of Escherichia coli offers profound insights into its historical background, evolution, genetic changes, resistance mechanisms, and drugs used to counter such resistance.
History of the Biology of bacterium
Recognized in 1982, the serotype 0157:H7 of enterohemorrhagic E. coli became fully affiliated with human pathogenesis drawing on its virulence to cause a massive diarrhea outbreak in Michigan and Oregon in the US. In the following year, this particular strain became further associated with direct causal links to the hemolytic uremic syndrome in humans (Blount e05826). Going forward, the said strain has led to the development of countless cases of foodborne pathogenesis. According to the Centers for Disease Control and Prevention, EHEC has contributed toward the development of 60 fatalities, 2,200 cases of clinical hospitalizations, and 73,000 cases of acute illnesses within the US alone. The greatest peak of this particular disease was last reported in 1999. Thereafter the prevalence of the disease greatly waned. The prevalence of E. coli 0157:H7 amongst individuals across the US amounted to $405 million, including medical care, premature deaths, and lost productivity.
Evolution of Escherichia coli
Different strains of Escherichia coli have undergone successful mutation over the years from the interplay of diverse factors, including pathogenicity islands, exposure to phages, plasmids, and transposons (Otter 752). Such exposure subsequently paved the way to developing new strains of these bacteria with more virulence, unlike the harmless colonies that occur naturally in the gastrointestinal tracts of animals and humans.
Pathogenic strains of E. coli 0157:H7 arise from a family of complex and clonal genotypic bacteria that occur worldwide. In particular, the present enteropathogenic serotype E. coli 0157:H7 evolved from a closely related genotype of the strain called E. coli 055:H7 by undergoing an alteration of serotype and subsequent adoption of pathogenic traits (Otter 756). Drawing on this proposed evolutionary pathway, it is believed that E. coli 0157:H7 stemmed from lysogenization by syntaxin 2 protein-coding gene and serotypic change from 055 to0157 (Otter 762). The latter serotypic change drew from the subsequent adoption of 0157 gnd-rfb locus. To that end, pathogenic EHEC bacteria apparently lost their capacity to initiate Sorbitol fermentation, thereby paving the way to the manifestation of virulence amongst E. coli 0157:H7 over time.
Genetic changes in Escherichia coli
Much of the genetic changes that subsequently culminated in developing a new strain of Escherichia coli, particularly the E. coli 0157:H7 strain, directly drew from the interplay of diverse factors. Ideally, most EHEC strains developed a complex clonal genomic variation from the acquisition of Syntaxin 1 and 2 phages (Mageiros et al. 3). Phages, in particular, denote viruses with the potential to attack and replicate in bacteria, thereby paving the way to subsequent mutation of bacterial genes into complex and pathogenic genomic variants (Mageiros et al. 6). For this reason, EHEC strains developed pathogenicity, thereby rendering them lethal to their hosts, such as animals and humans.
Considerable changes to the genetic structures of these bacteria resultantly led to the development of two distinct lineages of EHEC, namely EHEC I and EHEC II. Findings from reputable studies seemingly pinpoint the former EHEC lineage as directly responsible for instigating illnesses in humans, unlike the latter lineage, which seems to trigger the manifestation of illnesses in cattle (Singh et al. 23). As such, this goes to show that the two strains of EHEC (I and II) exhibit disparities in their modes of transmission and virulence.
Mechanisms of the bacteria’s resistance
The different strains of pathogenic E. coli 055:H7 have developed widespread resistance mechanisms over time. In particular, pathogenic E. coli 055:H7 strains have mastered acidic resistance and the ability to cope in diverse environments (Akhtar et al. 332). Ideally, E. coli 055:H7 strains harbor a unique capability to survive in an acidic environment, particularly the low pHs (i.e., <3). This makes them potentially dangerous as they can survive in the acidic environment mostly found within the stomach, thereby enabling these bacteria to attack and cause more damage in the gastrointestinal tracts of their hosts (Akhtar et al. 334). Research has shown that E. coli 055:H7 strains exhibit multiple acid resistance systems, which they deploy in a bid to survive in wide-ranging acidic environments. In the same vein, these bacteria possess the capability to reside in wide-ranging places, including cattle reservoirs, water, food, and soil (Akhtar et al. 335). The E. coli 055:H7 strain can survive in treated and raw manure for longer periods. Additionally, these pathogenic bacteria similarly survive in cold water and fecal animal matter, which mostly acts as their reservoir for over 8 months (Akhtar et al. 336). To that end, individuals must become wary of such factors mentioned herein, lest one succumbs to a debilitating fit of diarrhea caused by E. coli 055:H7 pathogenic strain.
Suffice to say, a recap of E. coli reviews its historical background, evolution, genetic variation, and resistance mechanisms developed over time. E. coli 0157:H7 denotes the pathogenic strain of E. coli and commonly affects the human gastrointestinal tract. The other EHEC of lineage II attack animals. E. coli 0157:H7 ideally evolved from its ancestral variant E. coli 055:H7 after acquiring Stx-1 and Stx-2 conversion phages and alteration of serotypes from ancestral to the present one.
Akhtar, Mastura, et al. “Does antibiotic resistance influence shiga-toxigenic Escherichia coli O26 and O103 survival to stress environments?” Food Control 68 (2016): 330-336.
Blount, Zachary D. “The natural history of model organisms: The unexhausted potential of E. coli.” Elife 4 (2015): e05826.
Mageiros, Leonardos, et al. “Genome evolution and the emergence of pathogenicity in avian Escherichia coli.” Nature communications 12.1 (2021): 1-13.
Otter, Chris. “Toxic Foodways: Agro-Food Systems, Emerging Foodborne Pathogens, and Evolutionary History.” environmental HISTORY (2015): 751-764.
Singh, Shilpi, et al. “Prevalence and characterization of waterborne multi drug resistant E. coli O157: H7.” Journal of Innovation in Applied Research 1.1 (2017): 23.