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Chapter 9 :

Authors: April M. Lewis1, Melanie C. Melendrez2, Ryan C. Fink3
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Affiliations: 1: Prestage Department of Poultry Science, North Carolina State University, Raleigh, North Carolina; 2: Department of Biology, St. Cloud State University, St. Cloud, Minnesota; 3: Department of Biology, St. Cloud State University, St. Cloud, Minnesota
Content Type: Reference
Publication Year: 2019

Category: Food Microbiology

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Abstract:

is a ubiquitous rod-shaped member of the family . Thanks to the ability to swiftly adapt to diverse environments, this human pathogen can infect a multitude of hosts, animals, plants, and protozoa and can colonize diverse environments. This characteristic makes this pathogen a major public health threat that cannot be eradicated, only identified and contained. In developed and industrialized countries, spp. contaminate mainly animal products and produce, whereas in developing countries, waterborne transmission and person-to-person transmission play a more important role. There are as many as 130 million cases of nontyphoidal salmonellosis worldwide each year, and of those, about 80 million are foodborne. In the United States alone, nontyphoidal is responsible for approximately 1.2 million illnesses and more than 450 deaths each year. These estimates make nontyphoidal serovars the leading cause of bacterial foodborne illness. This chapter provides a detailed historical perspective on the discovery, nomenclature, and characterization of this microorganism. The discussion covers the classification of this complex taxon based on the recent concepts of core genomes and pangenomes and the most prevalent isolation and identification methods currently used. The most recent understandings of virulence mechanisms and antibiotic resistance prevalence are also covered to present a complete overview of this important human pathogen.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
/content/10.1128/9781555819972.ch9.ch9fig1
Figure 9.1
Schematic representation of persistent infection with Typhi in humans. Bacteria invade the M cells of the Peyer's patches of the intestinal tract mucosal surface. This induces the inflammatory response, including recruitment of neutrophils and macrophages, phagocytosis of bacteria, and deployment of T and B cells. In systemic infections, such as typhoid fever, the pathogen targets host cells, such as dendritic cells and/or macrophages, which allow systemic spread through the lymphatic and blood circulatory systems to the lymph nodes present in the mesenteries. This then leads to transport to the spleen, bone marrow, liver, and gallbladder. Bacteria can colonize all these tissues and organs and periodically can restart shedding from the mucosal surface. IFN-γ, which can be secreted by T cells, has a role in maintaining persistence by controlling intracellular replication. Interleukin 12, which can increase IFN-γ production, and the proinflammatory cytokine tumor necrosis factor alpha also contribute to the control of persistent (not shown).
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Figure 9.1

Schematic representation of persistent infection with Typhi in humans. Bacteria invade the M cells of the Peyer's patches of the intestinal tract mucosal surface. This induces the inflammatory response, including recruitment of neutrophils and macrophages, phagocytosis of bacteria, and deployment of T and B cells. In systemic infections, such as typhoid fever, the pathogen targets host cells, such as dendritic cells and/or macrophages, which allow systemic spread through the lymphatic and blood circulatory systems to the lymph nodes present in the mesenteries. This then leads to transport to the spleen, bone marrow, liver, and gallbladder. Bacteria can colonize all these tissues and organs and periodically can restart shedding from the mucosal surface. IFN-γ, which can be secreted by T cells, has a role in maintaining persistence by controlling intracellular replication. Interleukin 12, which can increase IFN-γ production, and the proinflammatory cytokine tumor necrosis factor alpha also contribute to the control of persistent (not shown).

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.2
Schematic representation of the genes carried within the five SPIs and their putative virulence-related functions.
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Figure 9.2

Schematic representation of the genes carried within the five SPIs and their putative virulence-related functions.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.3
Diagram showing how Typhi moves through the body during systemic infection.
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Image of Figure 9.3
Figure 9.3

Diagram showing how Typhi moves through the body during systemic infection.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.4
Diagrams and micrographs showing how uses the trigger (A and B) and zipper (C and D) mechanisms to enter cells. (A) Diagram of the trigger mechanism. Using a TTSS, effector proteins (SipA, SipC, SopB, SopE, and SopE2) are injected into the cell. SopE, SopE2, and SopB activate the Rho GTPases Rac, Cdc42, and RhoG to allow rearrangement of the actin cytoskeleton using the cellular proteins WASP, Scar, WAVE, and WASH, which activate the Arp2/3 complex. SipA and SipC bind to the actin. SipC and SopE, in concert with the Ras-related protein RalA, mediate formation of membrane ruffles and the recruitment of the exocyst complex. (B and D) Scanning electron microscopy images of entering cells using the trigger and zipper mechanisms. Large membrane ruffles can be seen at the entry site. (C) Diagram of the zipper mechanism. Phosphorylation of tyrosine kinase is mediated by the Rck invasin protein expressed on the outer membrane when it interacts with its receptor on the host cell membrane. The class I phosphatidylinositol 3-kinase is activated and induces phosphatidylinositol(3,4,5)-trisphosphate formation, using Akt activation. GTPase Rac1 and GTPase Cdc42 trigger actin polymerization via the Arp2/3 nucleator complex. The mechanism controlling Cdc42 during Rck-induced signaling is still unknown. Dotted arrows represent possible signaling events and/or interactions.
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Image of Figure 9.4
Figure 9.4

Diagrams and micrographs showing how uses the trigger (A and B) and zipper (C and D) mechanisms to enter cells. (A) Diagram of the trigger mechanism. Using a TTSS, effector proteins (SipA, SipC, SopB, SopE, and SopE2) are injected into the cell. SopE, SopE2, and SopB activate the Rho GTPases Rac, Cdc42, and RhoG to allow rearrangement of the actin cytoskeleton using the cellular proteins WASP, Scar, WAVE, and WASH, which activate the Arp2/3 complex. SipA and SipC bind to the actin. SipC and SopE, in concert with the Ras-related protein RalA, mediate formation of membrane ruffles and the recruitment of the exocyst complex. (B and D) Scanning electron microscopy images of entering cells using the trigger and zipper mechanisms. Large membrane ruffles can be seen at the entry site. (C) Diagram of the zipper mechanism. Phosphorylation of tyrosine kinase is mediated by the Rck invasin protein expressed on the outer membrane when it interacts with its receptor on the host cell membrane. The class I phosphatidylinositol 3-kinase is activated and induces phosphatidylinositol(3,4,5)-trisphosphate formation, using Akt activation. GTPase Rac1 and GTPase Cdc42 trigger actin polymerization via the Arp2/3 nucleator complex. The mechanism controlling Cdc42 during Rck-induced signaling is still unknown. Dotted arrows represent possible signaling events and/or interactions.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.5
Diagram of proposed cellular responses to transition to a low-moisture environment. Responses include K uptake by the Kdp transporter, osmoprotectant transport (ProU, ProP, and OsmU), glutamate synthesis, trehalose biosynthesis, upregulation of fatty acid catabolism and RpoE and RpoS regulators, Fe-S cluster formation and filament formation, and an increase in the number of OmpC porins. There may also be a role for cellulose and curli fimbriae in survival in low-moisture environments.
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Image of Figure 9.5
Figure 9.5

Diagram of proposed cellular responses to transition to a low-moisture environment. Responses include K uptake by the Kdp transporter, osmoprotectant transport (ProU, ProP, and OsmU), glutamate synthesis, trehalose biosynthesis, upregulation of fatty acid catabolism and RpoE and RpoS regulators, Fe-S cluster formation and filament formation, and an increase in the number of OmpC porins. There may also be a role for cellulose and curli fimbriae in survival in low-moisture environments.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.6
Global distribution of antimicrobial drug resistance in Typhi. MDR, multi-drug resistant; ESBL, extended-spectrum β-lactamase. Reprinted from reference .
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Image of Figure 9.6
Figure 9.6

Global distribution of antimicrobial drug resistance in Typhi. MDR, multi-drug resistant; ESBL, extended-spectrum β-lactamase. Reprinted from reference .

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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Figure 9.7
Diagram of the core sequence of IncC plasmids and SGI-1. The positions and orientations of open reading frames are indicated by arrowed boxes. Function was determined by BLAST comparisons and is indicated by colors. AcaCD binding sites are indicated by green flags. SGI-1 is flanked by the and attachment sites for integration into the 3′ end of the gene in the chromosome of Typhimurium DT104.
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Image of Figure 9.7
Figure 9.7

Diagram of the core sequence of IncC plasmids and SGI-1. The positions and orientations of open reading frames are indicated by arrowed boxes. Function was determined by BLAST comparisons and is indicated by colors. AcaCD binding sites are indicated by green flags. SGI-1 is flanked by the and attachment sites for integration into the 3′ end of the gene in the chromosome of Typhimurium DT104.

Citation: Lewis A, Melendrez M, Fink R. 2019. , p 225-262. In Doyle M, Diez-Gonzalez F, Hill C (ed), Food Microbiology: Fundamentals and Frontiers, 5th Edition. ASM Press, Washington, DC. doi: 10.1128/9781555819972.ch9
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