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Category: Food Microbiology; Applied and Industrial Microbiology
Shigella Species, Page 1 of 2
< Previous page | Next page > /docserver/preview/fulltext/10.1128/9781555818463/9781555816261_Chap15-1.gif /docserver/preview/fulltext/10.1128/9781555818463/9781555816261_Chap15-2.gifAbstract:
Foodborne infections with Shigella species are an important source of illness in both economically developed and developing countries. This chapter presents to food microbiologists important features of Shigella spp., the disease they cause, and the impact that these pathogens have with respect to food safety. It discusses the diagnosis, epidemiology, ecology, modes of transmission, and examples of recent foodborne outbreaks, along with the current understanding of the genetics of Shigella pathogenesis, the genes involved in causing disease, and how they are regulated. Shigella can be transmitted by consumption of raw or processed food. Generally, poor personal hygiene practices by food workers at the point of final preparation and food service are the major factors for food contamination. The single most effective means of preventing secondary transmission of Shigella is hand washing with soap and chlorination of water. While foodborne infections due to members of the Shigella spp. may not be as frequently reported as those caused by other foodborne pathogens, they have the potential for explosive spread due to the low infectious dose that can cause overt clinical disease.
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Genetic steps that contribute to the formation of pathogenic Shigella species from an E. coli ancestor. These include the acquisition of the virulence plasmid, several pathogenicity islands (SHI-1 and SHI-2 are shown), and the loss of ancestral traits incompatible with virulence (e.g., cadA and avl; often referred to as antivirulence genes) ( 103 , 132 ). doi:10.1128/9781555818463.ch15f1
Genetic steps that contribute to the formation of pathogenic Shigella species from an E. coli ancestor. These include the acquisition of the virulence plasmid, several pathogenicity islands (SHI-1 and SHI-2 are shown), and the loss of ancestral traits incompatible with virulence (e.g., cadA and avl; often referred to as antivirulence genes) ( 103 , 132 ). doi:10.1128/9781555818463.ch15f1
S. flexneri 2a virulence plasmid map. A SalI restriction map of the 220-kb plasmid is shown in the center. Sections of SalI fragments B and P (upper map) and fragments P, H, and D (lower map) are expanded to illustrate the virulence loci carried in these regions. The expanded regions are contiguous and cover 32 kb. The open reading frame for icsB is separated from that of ipgD by 314 bp. doi:10.1128/9781555818463.ch15f2
S. flexneri 2a virulence plasmid map. A SalI restriction map of the 220-kb plasmid is shown in the center. Sections of SalI fragments B and P (upper map) and fragments P, H, and D (lower map) are expanded to illustrate the virulence loci carried in these regions. The expanded regions are contiguous and cover 32 kb. The open reading frame for icsB is separated from that of ipgD by 314 bp. doi:10.1128/9781555818463.ch15f2
Virulence-associated loci of Shigella
Virulence-associated loci of Shigella