Salmonellosis pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The pathogenesis of [[salmonellosis]] varies between different ''[[Salmonella]]'' [[serovar|serovars]] and depends on the interaction of multiple [[virulence]] programs with host defense mechanisms. These interactions occur in different tissues and at various stages of infection leading to variable host [[morbidity]] and [[mortality]].<ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref> [[salmonella enterica|''Salmonella enterica'' serovar Typhi]] ([[S. Typhi|''S''. Typhi]]) and [[salmonella enterica|Salmonella Paratyphi A]] both cause [[bacteremia]]. [[Non-typhoidal Salmonella]] ([[NTS]]) usually cause self-limiting [[diarrhea]] although NTS may lead to secondary [[bacteremia]]. [[Immunocompromised]] individuals and infants in sub-Saharan Africa may develop primary NTS bacteremia.<ref name="pmid23055923">{{cite journal| author=de Jong HK, Parry CM, van der Poll T, Wiersinga WJ| title=Host-pathogen interaction in invasive Salmonellosis. | journal=PLoS Pathog | year= 2012 | volume= 8 | issue= 10 | pages= e1002933 | pmid=23055923 | doi=10.1371/journal.ppat.1002933 | pmc=PMC3464234 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23055923 }} </ref> | The pathogenesis of [[salmonellosis]] varies between different ''[[Salmonella]]'' [[serovar|serovars]] and depends on the interaction of multiple [[virulence]] programs with host defense mechanisms. These interactions occur in different tissues and at various stages of infection leading to variable host [[morbidity]] and [[mortality]].<ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref> [[salmonella enterica|''Salmonella enterica'' serovar Typhi]] ([[S. Typhi|''S''. Typhi]]) and [[salmonella enterica|''Salmonella'' Paratyphi A]] both cause [[bacteremia]]. [[Non-typhoidal Salmonella]] ([[NTS]]) usually cause self-limiting [[diarrhea]] although NTS may lead to secondary [[bacteremia]]. [[Immunocompromised]] individuals and infants in sub-Saharan Africa may develop primary NTS bacteremia.<ref name="pmid23055923">{{cite journal| author=de Jong HK, Parry CM, van der Poll T, Wiersinga WJ| title=Host-pathogen interaction in invasive Salmonellosis. | journal=PLoS Pathog | year= 2012 | volume= 8 | issue= 10 | pages= e1002933 | pmid=23055923 | doi=10.1371/journal.ppat.1002933 | pmc=PMC3464234 | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=23055923 }} </ref> | ||
Typhoidal and [[salmonella|nontyphoidal Salmonella]] (NTS) serovars elicit different [[immune responses]] in humans.<ref name="pmid25136336">{{cite journal| author=Gal-Mor O, Boyle EC, Grassl GA| title=Same species, different diseases: how and why typhoidal and non-typhoidal Salmonella enterica serovars differ. | journal=Front Microbiol | year= 2014 | volume= 5 | issue= | pages= 391 | pmid=25136336 | doi=10.3389/fmicb.2014.00391 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25136336 }} </ref> In [[typhoid]] infection, [[S. Typhi]] bacteria is first ingested, usually through contaminated water or animal products. The bacteria is able to withstand the highly acidic environment of the stomach and proceeds to colonize the ileum and cecum. Upon colonization, the bacteria can gain entry into host circulation by either invading phagocytic M-cells or through dendritic cell uptake. Dissemination via the reticuloendothelial system (RES)occurs once extraintestinal infection is achieved. The bacteria can then take up residence in splenocytes, mostly within macrophages, dendritic cells, and polymorphonuclear leukocytes. Hepatocytes and other hepatic non-professional phagocytes may also serve as targets for infection and replication. Once Salmonella is internalized in the host cells, it resides in the Salmonella containing vacuole(SCV). In phagocytes, this specific vacuole formation evades fusion with the phagocyte oxidase complex. The ability of Salmonella to survive phagocytic killing is a central component of the bacteria's virulence. <ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref> | Typhoidal and [[salmonella|nontyphoidal ''Salmonella'']] (NTS) serovars elicit different [[immune responses]] in humans.<ref name="pmid25136336">{{cite journal| author=Gal-Mor O, Boyle EC, Grassl GA| title=Same species, different diseases: how and why typhoidal and non-typhoidal Salmonella enterica serovars differ. | journal=Front Microbiol | year= 2014 | volume= 5 | issue= | pages= 391 | pmid=25136336 | doi=10.3389/fmicb.2014.00391 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=25136336 }} </ref> In [[typhoid]] infection, [[''S''. Typhi]] bacteria is first ingested, usually through contaminated water or animal products. The bacteria is able to withstand the highly acidic environment of the stomach and proceeds to colonize the ileum and cecum. Upon colonization, the bacteria can gain entry into host circulation by either invading phagocytic M-cells or through dendritic cell uptake. Dissemination via the reticuloendothelial system (RES)occurs once extraintestinal infection is achieved. The bacteria can then take up residence in splenocytes, mostly within macrophages, dendritic cells, and polymorphonuclear leukocytes. Hepatocytes and other hepatic non-professional phagocytes may also serve as targets for infection and replication. Once ''Salmonella'' is internalized in the host cells, it resides in the ''Salmonella'' containing vacuole(SCV). In phagocytes, this specific vacuole formation evades fusion with the phagocyte oxidase complex. The ability of ''Salmonella'' to survive phagocytic killing is a central component of the bacteria's virulence. <ref name="pmid17146467">{{cite journal| author=Coburn B, Grassl GA, Finlay BB| title=Salmonella, the host and disease: a brief review. | journal=Immunol Cell Biol | year= 2007 | volume= 85 | issue= 2 | pages= 112-8 | pmid=17146467 | doi=10.1038/sj.icb.7100007 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17146467 }} </ref> | ||
==Transmission== | ==Transmission== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Pathophysiology
The pathogenesis of salmonellosis varies between different Salmonella serovars and depends on the interaction of multiple virulence programs with host defense mechanisms. These interactions occur in different tissues and at various stages of infection leading to variable host morbidity and mortality.[1] Salmonella enterica serovar Typhi (S. Typhi) and Salmonella Paratyphi A both cause bacteremia. Non-typhoidal Salmonella (NTS) usually cause self-limiting diarrhea although NTS may lead to secondary bacteremia. Immunocompromised individuals and infants in sub-Saharan Africa may develop primary NTS bacteremia.[2]
Typhoidal and nontyphoidal Salmonella (NTS) serovars elicit different immune responses in humans.[3] In typhoid infection, ''S''. Typhi bacteria is first ingested, usually through contaminated water or animal products. The bacteria is able to withstand the highly acidic environment of the stomach and proceeds to colonize the ileum and cecum. Upon colonization, the bacteria can gain entry into host circulation by either invading phagocytic M-cells or through dendritic cell uptake. Dissemination via the reticuloendothelial system (RES)occurs once extraintestinal infection is achieved. The bacteria can then take up residence in splenocytes, mostly within macrophages, dendritic cells, and polymorphonuclear leukocytes. Hepatocytes and other hepatic non-professional phagocytes may also serve as targets for infection and replication. Once Salmonella is internalized in the host cells, it resides in the Salmonella containing vacuole(SCV). In phagocytes, this specific vacuole formation evades fusion with the phagocyte oxidase complex. The ability of Salmonella to survive phagocytic killing is a central component of the bacteria's virulence. [1]
Transmission
Salmonella bacteria are widely distributed in domestic and wild animals. They are prevalent in food animals such as poultry, pigs, cattle; and in pets, including cats and dogs, birds and reptiles such as turtles. Salmonella can pass through the entire food chain from animal feed, primary production, and all the way to households or food-service establishments and institutions. Salmonellosis in humans is generally contracted through the consumption of contaminated food of animal origin (mainly eggs, meat, poultry and milk), although other foods, including green vegetables contaminated by manure, have been implicated in its transmission. Person-to-person transmission through the faecal-oral route can also occur. Human cases also occur where individuals have contact with infected animals, including pets. These infected animals often do not show signs of disease.[4]
Human typhoid usually occurs after ingesting water or animal products contaminated with S. Typhi. Close contact with carriers or infected individuals may also cause typhoid.
References
- ↑ 1.0 1.1 Coburn B, Grassl GA, Finlay BB (2007). "Salmonella, the host and disease: a brief review". Immunol Cell Biol. 85 (2): 112–8. doi:10.1038/sj.icb.7100007. PMID 17146467.
- ↑ de Jong HK, Parry CM, van der Poll T, Wiersinga WJ (2012). "Host-pathogen interaction in invasive Salmonellosis". PLoS Pathog. 8 (10): e1002933. doi:10.1371/journal.ppat.1002933. PMC 3464234. PMID 23055923.
- ↑ Gal-Mor O, Boyle EC, Grassl GA (2014). "Same species, different diseases: how and why typhoidal and non-typhoidal Salmonella enterica serovars differ". Front Microbiol. 5: 391. doi:10.3389/fmicb.2014.00391. PMID 25136336.
- ↑ "Salmonella(non-typhoidal)".