Escherichia coli: most strains are spaniels – but a few are pit bulls will tear you to pieces given half a chance
There are many strains of E. coli and almost all are completely harmless. It is one of the most common of the gut flora – but the pathogenic strains can be very nasty and potentially fatal. E. coli was behind the South Wales outbreak that resulted in the Pennington Report and wholesale changes to food hygiene law in the UK. Strains like O157 and the other non-O157 Shiga Toxin-Producing (STEC) can cause nausea, diarrhoea (often bloody), severe abdominal cramps and can lead to haemolytic uraemic syndrome (HUS) and death – with 5 – 10% mortality in children under 5 years of age. These organisms are part of a diverse group of Escherichia coli that are capable of producing Shigatoxin(s), as is E. coli O157:H7. However, they are of widely differing pathogenic potential, varying from those that can cause disease similar to that produced by E. coli O157:H7 to those that have never been associated with disease.
Between 10 and 100 organisms of E. coli O157 are sufficient to cause infection – compared to over 1,000,000 required for other pathogenic E. coli stains.
And this is the strain most commonly associated with play farms and petting zoos…
Growth and Control Survival Inactivation (CCPs and Hurdles) Clinical Notes Reservoirs / Sources
Optimum 37°C, minimum 7-8, maximum 46°C. Doubling time approx. 0.4h at 37°C.
Optimum 6-7, range 4.4 to 9.0 or 10.0. The limit at the low pH end depends on the acidulant used. Mineral acids such as HCl are less inhibitory than organic acids (e.g. acetic, lactic) at the same pH. Growth was inhibited in the presence of 0.1% acetic acid (pH 5.1).
Can grow in the presence or absence of oxygen. E. coli can grow at 8 and 9°C on beef under vacuum-packaged conditions, but not under 100% CO2.
Optimum growth is at aw =0.995 minimum aw = 0.950 (about 8% NaCl).
Survives well in chilled and frozen foods.
Dies at pH values outside the range allowing growth. However, when exposed to low pH at low temperature, cells may survive for some time.
Rapidly inactivated by heating at 71°C. D time at 54.4°C = 40 min D time at 60°C = 0.5–0.75 min D time at 64.3°C = 0.16 min Freeze thawing can lead to a reduction in numbers but the effect is strain dependent. D times may increase if the organism is heat shocked prior to heat treatment.
Inactivated at pH values outside the range allowing growth at rates dependent on the conditions encountered. Inactivation is generally more rapid at warmer temperatures at low pH.
Don’t forget to read the disclaimer! Depending on the strain, haemorrhagic colitis (HC), Haemolytic Uraemic Syndrome (HUS) and thrombocytopaenic purpura (TTP) are all associated with certain E. coli strains. By definition all STEC must produce one of two toxins (denoted Stx1 and Stx2), but other factors are also involved in pathogenicity and it is the possession of these that seems to determine the virulence of any one serotype. Other factors known to be involved include the ability to adhere to intestinal cells, and the ability to produce a haemolysin. An isolate possessing the ability to produce either Stx in the absence of other virulence determinants is unlikely to be a major pathogen. Individual members are denoted by their O and H serotypes.
Some serotypes appear to be restricted to man, e.g. O1, O55:H7 and H:10 and O148:H21.
Ruminant animals, notably bovines, seem to be a natural reservoir of many of the non-O157 STEC that cause disease in humans. Food, environment, transmission routes: Little is known about the distribution of these organisms in food and the environment. However, it seems likely that the situation will be similar to that for serotype O157:H7. Non-O157 STEC are likely to be much more common than serotype O157:H7 in foods, but only a small proportion of the isolates appear to be pathogenic to humans. Non-O157 STEC has been detected in beef, pork and lamb mince, and unpasteurised milk. It has been estimated that 85% of cases are foodborne.
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