Abstract
This study was carried out to assess the survival of Shiga toxin-producing E. coli (STEC) and atypical enteropathogenic Escherichia coli (aEPEC) during the traditional manufacturing and ripening of Spanish hard cheese from raw cow’s milk. Milk samples were spiked with up to 3.1–3.5 log cfu/mL of one strain of STEC (O140:H32 serotype) and one of aEPEC (serotype O25:H2). The first steps of cheesemaking allow for a STEC and aEPEC increase of more than 1 log cfu/mL (up to 4.74 log cfu/g and 4.55 log cfu/g, respectively). After cheese pressing, a steady reduction of both populations was observed, with the STEC strain being more sensitive. The studied pathogenic E. coli populations decreased by 1.32 log cfu/g in STEC and 0.59 log cfu/g in aEPEC in cheese ripened during a minimum period of 60 d. Therefore, a moderate contamination by these diarrhoeagenic E. coli pathotypes, in particular, with aEPEC, on cheese manufactured from raw milk may not be totally controlled through the cheesemaking process and during a maturation of 90 d. These findings remark the importance of improvement in bacteriological quality of raw milk and cross-contamination prevention with diarrhoeagenic E. coli in the dairy industry.
Highlights
Shiga toxin/verocytotoxin-producing Escherichia coli (STEC) represent one of the most common causes of foodborne illness in the world
Infections was O157, the proportion of non-O157 serogroups has been increasing over the years and non-O157 serogroups have been involved in many haemolytic uremic syndrome (HUS) cases, suggesting an increased risk of acute infections by this group of bacteria [4]
Our results show that the first steps of cheesemaking allow for an increment in Shiga toxin-producing E. coli (STEC) and atypical enteropathogenic Escherichia coli (aEPEC) counts and that STEC is more sensitive to the ripening than aEPEC
Summary
Shiga toxin/verocytotoxin-producing Escherichia coli (STEC) represent one of the most common causes of foodborne illness in the world. The most commonly reported STEC serogroup in confirmed cases of human STEC infections was O157, the proportion of non-O157 serogroups has been increasing over the years and non-O157 serogroups have been involved in many haemolytic uremic syndrome (HUS) cases, suggesting an increased risk of acute infections by this group of bacteria [4]. These non-O157 serogroups were responsible for 68.1% of STEC infections in the EU [5]. A similar increment of the non-O157 serogroups was observed in the USA, where the Centers for Disease Control and Prevention reported a total of 1272 cases of STEC infections, 60.2% caused in 2015 by non-O157 strains [6]
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