The deadly E. coli outbreak

The mention of E. coli O157:H7 sends a chill through the spine of every food processor. This deadly pathogen has been implicated in disease outbreaks all over the world and only a small load can cause illness. But in the latest outbreak in Germany and France, a new serotype is proving even more deadly.

Escherichia coli (E. coli) bacteria are commonly found in the gut of humans and animals and most strains do not cause harm in the bowels, although they can cause infections if they spread to urine or blood.

However, a few strains have acquired characteristics that allow them to attach to cells in the gut, invade the lining of the gut and/or produce toxins that cause damage or secretory malfunctions of gut cells. One such toxin, the ‘Shiga’ toxin, is capable of causing diarrhoea that may be watery or bloody. Strains that produce Shiga toxin are also called ‘STEC’ strains. If an STEC strain also has acquired the ability to adhere to cells in the gut, it is referred to as an ‘enterohaemorrhagic E. coli’ or EHEC. The most common EHEC is E. coli O157:H7, but other variants exist, including the one that caused the 2011 E. coli outbreak that originated in Germany.

The STEC strain that caused the outbreak in Germany is in fact not a typical virulent STEC strain, but instead is a much rarer hybrid pathotype that harbours the phage-mediated Shiga toxin determinant with an enteroaggregative E. coli (EAggEC) background, more precisely described as enteroaggregative, Shiga toxin/verotoxin-producing E. coli (EAggEC STEC/VTEC).

Even a small number of organisms can cause disease, so EHEC can spread easily and widely.

Most people with EHEC infection recover completely and usually fewer than 10% develop complications. However, with the recent E. coli O104:H4 outbreak in Germany and France, the risk was about 30%.

The deadly E. coli O104:H4 strain that has killed dozens and hospitalised thousands across Europe was genetically sequenced using 454 Life Sciences’ benchtop GS Junior sequencing system to generate the “most accurate and detailed genetic analysis to date” of this particularly virulent strain. The sequencing was performed by scientists at the UK’s Health Protection Agency and the data has been uploaded onto the National Centre for Biotechnology Information (NCBI) website for use by the scientific community.

The results suggest that the strain has a unique combination of features containing genes from two different types of E. coli as well as its own genes. The sequencing assembly shows that the strain contains two extrachromosomal elements or plasmids which may factor into its pathogenicity. In essence, this strain of E. coli may have ‘picked up’ some extra genetic material along the way.

What most predominantly differentiates O104 from O157 is its adoption of numerous traits not typically found congregated in one strain: not only does it produce the noxious Shiga toxin of the virulent enterohaemorrhagic strains, it also possesses defensive enteroaggregative traits - a combined mouthful of properties much more difficult to tolerate physically than verbally.

The term ‘enteroaggregative’ refers to sticky strains of the bacteria that group together - aggregate - into a ‘stacked-brick pattern’ and cling to intestinal tracts. Once there, they induce heavy mucus production in their host’s intestines, which they then use for both protection and sustenance.

Enteroaggregative E. coli are known to cause persistent diarrhoea, but are historically unrelated to haemorrhaging and haemolytic-uremic syndrome (HUS), the acute kidney disease caused by Shiga toxin-producing enterohaemorrhagic E. coli.

O157 is enterohaemorrhagic, but not enteroaggregative. The bacteria do not aggregate together, but they possess cell structures that help them adhere to intestines, where they produce the Shiga toxin known for inflicting HUS and making E. coli a household name among pathogens.

By comparison, O104 clumps together and spurs mucus production for protection while also releasing Shiga toxin into the bloodstream, an adaptation that has resulted in well over 800 cases of HUS in this outbreak.

Physicians now know not to prescribe antibiotics for O157 infections because the sudden killing of the bacteria can release HUS-inducing and potentially deadly amounts of Shiga toxin. In the early days of the latest outbreak it is likely that German hospitals were only screening patients for O157 and not O104, which no one would have suspected before news of the outbreak spread. Not finding O157, they may have prescribed antibiotics without knowing that O104 would produce the Shiga toxin.

This potential misunderstanding over antibiotics might at least partially explain the high rate of HUS among the ill.

In regard to its environmental origins, O104 takes after the more prevalent enteroaggregative E. coli in that only humans are its host, not cattle or other ruminants. It can spread through contact with objects in the environment, water, food or human faecal matter.

The ease with which a virulent new strain of E. coli entered the food supply of a first-world country and sickened and killed thousands is a call to vigilance for all involved in the food industry.