Typhoid fever: pathogenesis and disease

House, Deborah; Bishop, Anne L.; Parry, Christopher M.; Dougan, Gordon; Wain, John

doi:10.1097/00001432-200110000-00011

Cited by 165 publications

(106 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…For examples, Shigella flexneri, the causative agent of human dysentery, modifies PI metabolism in host cells to favor its internalization through the PI-4-phosphatase activity of the virulent factor IpgD (14). Salmonella typhimurium, which is responsible for most food-borne gastroenteritis (15), delivers the PI phosphatase SigD/SopB into the host. By hydrolyzing PI(3,4,5)P 3 , SopB contributes to the localized membrane ruffling that leads to bacterial internalization in nonphagocytic cells (16,17).…”

mentioning

confidence: 99%

Structural basis for substrate recognition by a unique Legionella phosphoinositide phosphatase

Hsu

Zhu

Brennan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

104

113

View full text Add to dashboard Cite

Legionella pneumophila is an opportunistic intracellular pathogen that causes sporadic and epidemic cases of Legionnaires' disease. Emerging data suggest that Legionella infection involves the subversion of host phosphoinositide (PI) metabolism. However, how this bacterium actively manipulates PI lipids to benefit its infection is still an enigma. Here, we report that the L. pneumophila virulence factor SidF is a phosphatidylinositol polyphosphate 3-phosphatase that specifically hydrolyzes the D3 phosphate of PI(3,4)P 2 and PI(3,4,5)P 3 . This activity is necessary for anchoring of PI(4)Pbinding effectors to bacterial phagosomes. Crystal structures of SidF and its complex with its substrate PI(3,4)P 2 reveal striking conformational rearrangement of residues at the catalytic site to form a cationic pocket that specifically accommodates the D4 phosphate group of the substrate. Thus, our findings unveil a unique Legionella PI phosphatase essential for the establishment of lipid identity of bacterial phagosomes.phosphoinositide signaling | phagocytosis | membrane trafficking | type IV secretion system | virulence factor

show abstract

mentioning

confidence: 99%

Structural basis for substrate recognition by a unique Legionella phosphoinositide phosphatase

Hsu

Zhu

Brennan

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

104

113

View full text Add to dashboard Cite

show abstract

“…Instead, Salmonella resides within intestinal epithelial cells or resident macrophages, typically not in the bloodstream, and escapes immense attack from the immune system (29)(30)(31). Although Salmonella is exposed to the host immune system while in the intestine through mucosal surveillance, including potential sampling by dendritic cells resulting in IgA release into the intestinal lumen (32), it is not bombarded by the strong host immune pressure experienced by H. influenza and N. meningitidis during an infection.…”

mentioning

confidence: 99%

Protozoan predation, diversifying selection, and the evolution of antigenic diversity in Salmonella

Wildschutte

Wolfe

Tamewitz

et al. 2004

Proc. Natl. Acad. Sci. U.S.A.

147

142

View full text Add to dashboard Cite

Extensive population-level genetic variability at the Salmonella rfb locus, which encodes enzymes responsible for synthesis of the O-antigen polysaccharide, is thought to have arisen through frequency-dependent selection (FDS) by means of exposure of this pathogen to host immune systems. The FDS hypothesis works well for pathogens such as Haemophilus influenzae and Neisseria meningitis, which alter the composition of their O-antigens during the course of bloodborne infections. In contrast, Salmonella remains resident in epithelial cells or macrophages during infection and does not have phase variability in its O-antigen. More importantly, Salmonella shows host-serovar specificity, whereby strains bearing certain O-antigens cause disease primarily in specific hosts; this behavior is inconsistent with FDS providing selection for the origin or maintenance of extensive polymorphism at the rfb locus. Alternatively, selective pressure may originate from the host intestinal environment itself, wherein diversifying selection mediated by protozoan predation allows for the continued existence of Salmonella able to avoid consumption by host-specific protozoa. This selective pressure would result in high population-level diversity at the Salmonella rfb locus without phase variation. We show here that intestinal protozoa recognize antigenically diverse Salmonella with different efficiencies and demonstrate that differences solely in the O-antigen are sufficient to allow for prey discrimination. Combined with observations of the differential distributions of both serotypes of bacterial species and their protozoan predators among environments, our data provides a framework for the evolution of high genetic diversity at the rfb locus and host-specific pathogenicity in Salmonella.T he enteric pathogen Salmonella enterica presents at least 70 different O-antigens [the outermost structure of the Gramnegative lipopolysaccharide (LPS)] to mammalian immune systems (1); this polysaccharide decorates the outer surface of the cell. Historically, extensive genetic diversity at the rfb locus, which encodes enzymes directing O-antigen synthesis (2-6), has been attributed to frequency-dependent selection (FDS) (7,8) imposed by the host immune system (5, 9, 10). Novel rfb loci would have an advantage because their cognate O-antigens would be unrecognized by immune systems (Fig. 1A); strains carrying rare loci would have higher fitness and would avoid rapid stochastic loss, rising to higher frequency. Yet selective advantages decrease with abundance; as a result, strains with common rfb loci cannot dominate the population or elicit a selective sweep (7) because their fitnesses become lower as they become more abundant. In concert, FDS prevents the loss of rare alleles or the dominance of common alleles, thus maintaining diversity (8).According to the FDS model, expression of different LPS molecules through gene regulation allows invading bacteria to escape host immunity, survive, and proceed throughout its life cycle; this hypothesis explains...

show abstract

“…After that there is an interaction between host immunologic mediators and bacterial factors leading ultimately to the necrosis of Peyer's patches. 53,56,57 Interestingly, in Africa the disease is often due to nontyphoidal salmonellae such as Typhimurium. In contrast to the Asian situation; however, the two are clinically indistinguishable.…”

Section: Pathogenesismentioning

confidence: 99%

Typhoid fever: a review

Paul¹,

Bandyopadhyay²

2017

Int J Adv Med

View full text Add to dashboard Cite

Typhoid fever is still a deadly disease in developing countries, particularly in India. Although, the paediatric population is mostly affected by this disease, yet the disease is an important cause of morbidity and mortality in adult populations also. In India, most of the cases of typhoid fever are diagnosed clinically, or at the most by the Widal test which is not fool proof. The disease typhoid fever is an orally transmitted communicable infectious disease caused by the bacteria Salmonella typhi. It is usually caused by consuming impure water and contaminated food. Salmonella typhi is serologically positive for lipopolysaccharide antigens O9 and O12, protein ﬂagellar antigen Hd, and polysaccharide capsular antigen Vi. S. typhi Vi-positive strains are more infectious and virulent than Vi-negative strains. Following the incubation period of 7 to 14 days, there is onset of fever and malaise. The fever is then accompanied by chills, headache, malaise, anorexia, nausea, vague abdominal discomfort, dry cough and myalgia. These are followed by coated tongue, tender abdomen, hepatomegaly, and splenomegaly. Azithromycin (10mg/kg) given once daily for seven days has proven eﬀective in the treatment of typhoid fever in some adults and children. A dose of 1g per day for ﬁve days was also found to be more effective in most adults. Of the third generation cephalosporins, oral Ceﬁxime (15-20mg per kg per day, for adults, 100-200mg twice daily) has been widely used. Intravenous third generation cephalosporins (ceftriaxone, cefotaxime) are eﬀective. Aztreonam and imipenem are potential third line drugs.

show abstract

Typhoid fever: pathogenesis and disease

Cited by 165 publications

References 50 publications

Structural basis for substrate recognition by a unique Legionella phosphoinositide phosphatase

Structural basis for substrate recognition by a unique Legionella phosphoinositide phosphatase

Protozoan predation, diversifying selection, and the evolution of antigenic diversity in Salmonella

Typhoid fever: a review

Contact Info

Product

Resources

About