Advances in Microbial Food Safety (eBook)

Volume 2

J Sofos (Herausgeber)

eBook Download: PDF | EPUB

2014 | 1. Auflage
444 Seiten
Elsevier Science (Verlag)
978-1-78242-115-3 (ISBN)

Infos

Research and legislation in food microbiology continue to evolve, and outbreaks of foodborne disease place further pressure on the industry to provide microbiologically safe products. This second volume in the series Advances in Microbial Food Safety summarises major recent advances in this field, and complements volume 1 to provide an essential overview of developments in food microbiology. Part one opens the book with an interview with a food safety expert. Part two provides updates on single pathogens, and part three looks at pathogen detection, identification and surveillance. Part four covers pathogen control and food preservation. Finally, part five focuses on pathogen control management. - Extends the breadth and coverage of the first volume in the series - Includes updates on specific pathogens and safety for specific foods - Reviews both detection and management of foodborne pathogens

Textauszug

1

Update on non-O157 Shiga toxin-producing E. coli as a foodborne pathogen: analysis and control*

J.L. Smith; P.M. Fratamico; N.R. Launchi    United States Department of Agriculture, USA

Abstract

Although Shiga toxin-producing Escherichia coli (STEC) O157:H7 is a leading cause of foodborne illness worldwide, non-O157 STEC serogroups may cause more illnesses than O157:H7, and information on transmission and outbreaks is presented. The role of ruminants as a major reservoir for both O157 and non-O157 STEC is explored, and how ingestion of contaminated animal products or produce contaminated by animal feces can lead to illness is discussed. Intervention strategies that control STEC O157:H7 and also inactivate non-O157 STEC are identified. Methods for detection of highly virulent non-O157 STEC are described and the need for additional research to understand the prevalence, epidemiology, and virulence of these pathogens is emphasized for their effective control.

Key words

non-O157 Shiga toxin-producing Escherichia coli

foodborne pathogens

Shiga toxin

virulence genes

animal reservoirs

1.1 Introduction

Shiga toxin-producing Escherichia coli (STEC) are diarrheic foodborne pathogens that are the major causative agents of hemorrhagic colitis (HC) and postdiarrheal hemolytic uremic syndrome (HUS) leading to severe kidney disease and even death. E. coli O157:H7 has, for many years, been the major STEC strain causing HUS. Use of improved methods for the detection and identification of non-O157 STEC have revealed that the number of non-O157 STEC infections is overtaking O157:H7 as the main cause of STEC-associated illness (Gould et al., 2013; Scallan et al., 2011). In general, the non-O157 STEC do not cause as severe disease as the O157 STEC but some non-O157 STEC strains have caused HUS (Gould et al., 2013).

The intestinal tracts of animals used as a food source, particularly cattle and other ruminants, are reservoirs of both O157 and non-O157 STEC; therefore, during slaughtering operations, the carcass may become contaminated, leading to meat products containing the pathogens. Surveys of cattle (feces, hides, and pre- and post-intervention carcasses) showed similar levels of E. coli O157:H7 and non-O157 STEC. Produce and vegetables may be contaminated with STEC strains because fecal excretion by animals can contaminate soil and water sources (Kaspar et al., 2010). Other animal reservoirs for STEC include goats, sheep, guanaco, deer, and elk. There was an outbreak associated with deer meat contaminated with STEC O103:H2 in high school students in Minnesota in 2010 (Rounds et al., 2012). Non-ruminants, including cats, dogs, pigs, horses, rabbits, and poultry, as well as transport hosts, including birds, rodents, flies, and beetles can also carry STEC.

An awareness of the importance of the non-O157 STEC as foodborne pathogens is critical for food microbiologists, food processors, food regulators, and clinicians; however, there is, overall, less known about this heterogeneous group of pathogens than about STEC O157:H7. This chapter provides information on transmission and outbreaks caused by non-O157 STEC, virulence factors, reservoirs, ecology, control strategies, and detection.

1.2 Virulence of non-O157 Shiga toxin-producing E. coli (STEC)

1.2.1 Non-O157 STEC serogroups and serotypes associated with human disease

Based on data from US FoodNet sites for the period of 2000 to 2010, Gould et al. (2013) found that the non-O157 STEC serogroups caused a total of 2006 infections, and serogroup O157 was responsible for 5688 infections. Over 70% of the total non-O157 infections were caused by serogroup O26, O45, O103, O111, O121, and O145. Overall, 7.5% of non-O157 STEC infections were linked to outbreaks, whereas 19.5% of O157 STEC infections were outbreak-associated. Infections caused by non-O157 STEC were more commonly associated with international travel (16.2%) than O157 (2.7%). In addition to the six non-O157 serogroups listed above, Gould et al. (2013) list 66 other non-O157 serogroups responsible for illness in the United States. For the period 2007 to 2010, the European Union (EU) reported 2140 cases of STEC-induced illness. STEC O157:H7/H − was responsible for 1047/2140 (49.0%) cases, and 1093/2140 (51%) cases were attributable to non-O157 STEC (EFSA, 2013). Serogroups O26, O63, O91, O103, O111, O117, O121, O128, O145, and O146 accounted for 48.5% (530/1093) of non-O157 STEC cases in the EU. Non-O157 STEC serotypes associated with confirmed HUS cases in the EU during 2007 to 2010 include: O1:H42, O7:H6, O26:H11, O76:H19, O80:H2, O86:H27, O91:H10, O104:H21, O105:H18, O111:H −/H8, O121:H19/H2, O123:H2, O128:H2, O145:H −/H28, and O174:H2/H21 (EFSA, 2013 [their table 13]). Although there are some STEC serotypes such as O26:H11, O111:H −, O121:H19, and O145:H − that are important causes of serious illness both in the USA and in Europe, there are other serotypes that are more common in Europe than in the USA and vice versa.

1.2.2 Diseases caused by non-O157 STEC

In general, non-O157 STEC infections are not as severe as O157 infections. The median hospital stay is 3 days with both types of STEC infections; however, during the period of 2000 to 2010 in the USA, only 13.7% of patients infected with non-O157 STEC were hospitalized compared with 43.4% for O157 cases (Gould et al., 2013). During that period, 33 deaths were reported for O157 STEC but only two were due to non-O157 STEC. Data from cases reported in 2008 to 2009 indicated that diarrhea was common with both types of STEC but 85.5% of O157 STEC cases presented with bloody diarrhea compared with 54.8% of non-O157 STEC cases. Only 1.3% (4/301) of non-O157 cases developed HUS whereas 10.7% (83/773) of O157 cases contracted HUS. The four cases of HUS associated with non-O157 infection were attributable to serogroups O111 (two cases) and one case each by O103 and O121 (Gould et al., 2013). In 2012, STEC O157 accounted for 531 foodborne infections whereas non-O157 accounted for 551 infections. Reports indicated that O157 and non-O157 STEC caused 187 and 88 hospitalizations, respectively (CDC, 2013). Long-term consequences may occur in some patients with diarrhea-associated HUS. HUS occurs more often in children and the elderly, and it is the most common cause of acute renal failure in children. Shiga toxin causes glomerular damage with development of anemia, thrombocytopenia, and renal failure. Extrarenal lesions may involve the gastrointestinal tract, pancreas, liver, cardiovascular system, and central nervous system (Gallo and Gianantonio, 1995). Extrarenal lesions are rarer today because of early intervention by dialysis of the affected patient.

1.2.3 Non-O157 STEC virulence genes

Some genes that may be necessary for virulence in O157:H7 and non-O157 STEC are presented in Table 1.1. The production of Shiga toxin (Stx) by STEC strains is the most critical virulence factor responsible for HC and HUS. There are two types of Stx: Stx1 and Stx2; and several variants of both are known. Stx2 is ca. 1000 times more toxic than Stx1 toward renal micro-vascular endothelial cells (Gyles, 2007). The toxins are encoded by genes carried on lysogenic phages located in the STEC chromosome. Both toxins have an A1B5 structure; the B moiety binds to globotriaosylceramide (Gb3) present on host microvascular endothelial cell surfaces (kidney, intestine, and brain) followed by endocytosis of the toxin (Ivarsson et al., 2012). The A subunit is released from the B moiety and enters the cytosol via chaper-one-mediated transfer. The A subunit acts as a 28S RNA N-glycosidase, blocking protein synthesis and inducing apoptosis of endothelial cells, particularly those of the kidneys (Ivarsson et al., 2012; Khan and Naim, 2011). The renal glomerular endothelial cells swell and detach from the basement membrane, fibrin thrombi form, and there is narrowing of the capillary lumen leading to a reduced blood supply to the glomeruli causing a loss of kidney function (Gyles, 2007).

Table 1.1

Virulence genes present in O157 and non-O157 STEC. Values are number of isolates positive by PCR with percentages given in parentheses

Shiga toxins

stx1

18 (34.6)

5 (26.3)

137 (70.6)

stx2

52 (100)

17 (89.5)

81 (41.7)

LEE genes

eae

52 (100)

17 (89.5)

118 (60.8)

Plasmid-associated genes

ehxA

51 (98.1)

18 (94.7)

133 (68.6)

saa

0 (0.0)

1 (5.3)

12 (6.2)

subA

0 (0.0)

1 (5.3)

7...

Produkt-Details

• Erscheint lt. Verlag: 25.11.2014
• Sprache: englisch
• Themenwelt: Medizin / Pharmazie ► Gesundheitsfachberufe
• Themenwelt: Medizin / Pharmazie ► Medizinische Fachgebiete ► Mikrobiologie / Infektologie / Reisemedizin
• Themenwelt: Studium ► 2. Studienabschnitt (Klinik) ► Pharmakologie / Toxikologie
• Themenwelt: Naturwissenschaften ► Biologie ► Mikrobiologie / Immunologie
• Themenwelt: Technik ► Lebensmitteltechnologie
• ISBN-10: 1-78242-115-7 / 1782421157
• ISBN-13: 978-1-78242-115-3 / 9781782421153