Last data update: May 06, 2024. (Total: 46732 publications since 2009)
Records 1-3 (of 3 Records) |
Query Trace: Reynolds JL[original query] |
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Extensively drug-resistant typhoid fever in the United States
Hughes MJ , Birhane MG , Dorough L , Reynolds JL , Caidi H , Tagg KA , Snyder CM , Yu AT , Altman SM , Boyle MM , Thomas D , Robbins AE , Waechter HA , Cody I , Mintz ED , Gutelius B , Langley G , Francois Watkins LK . Open Forum Infect Dis 2021 8 (12) ofab572 Cases of extensively drug-resistant (XDR) typhoid fever have been reported in the United States among patients who did not travel internationally. Clinicians should consider if and where the patient traveled when selecting empiric treatment for typhoid fever. XDR typhoid fever should be treated with a carbapenem, azithromycin, or both. |
Prophage induction is enhanced and required for renal disease and lethality in an EHEC mouse model
Tyler JS , Beeri K , Reynolds JL , Alteri CJ , Skinner KG , Friedman JH , Eaton KA , Friedman DI . PLoS Pathog 2013 9 (3) e1003236 Enterohemorrhagic Escherichia coli (EHEC), particularly serotype O157:H7, causes hemorrhagic colitis, hemolytic uremic syndrome, and even death. In vitro studies showed that Shiga toxin 2 (Stx2), the primary virulence factor expressed by EDL933 (an O157:H7 strain), is encoded by the 933W prophage. And the bacterial subpopulation in which the 933W prophage is induced is the producer of Stx2. Using the germ-free mouse, we show the essential role 933W induction plays in the virulence of EDL933 infection. An EDL933 derivative with a single mutation in its 933W prophage, resulting specifically in that phage being uninducible, colonizes the intestines, but fails to cause any of the pathological changes seen with the parent strain. Hence, induction of the 933W prophage is the primary event leading to disease from EDL933 infection. We constructed a derivative of EDL933, SIVET, with a biosensor that specifically measures induction of the 933W prophage. Using this biosensor to measure 933W induction in germ-free mice, we found an increase three logs greater than was expected from in vitro results. Since the induced population produces and releases Stx2, this result indicates that an activity in the intestine increases Stx2 production. |
Activation of a prophage-encoded tyrosine kinase by a heterologous infecting phage results in a self-inflicted abortive infection
Friedman DI , Mozola CC , Beeri K , Ko CC , Reynolds JL . Mol Microbiol 2011 82 (3) 567-77 Bacteria in their struggle for survival have evolved or acquired defences against attacking phage. However, phage often contribute to this defence through mechanisms in which a prophage protects the bacterial population from attack by another, often unrelated, phage. The 933W prophage, which carries Shiga toxin genes that enhance pathogenicity of enterohaemorrhagic Escherichia coli strain O157:H7, also carries the stk gene encoding a eukaryotic-like tyrosine kinase that excludes (aborts) infection by phage HK97. This exclusion requires the kinase activity of Stk. Little, if any, protein tyrosine phosphorylation can be detected in a 933W lysogen prior to infection with HK97, while extensive Stk-mediated tyrosine phosphorylation is evident following infection. This includes autophosphorylation that stabilizes Stk protein from degradation. Although increased levels of Stk are found following HK97 infection, these higher levels are not necessary or sufficient for exclusion or protein phosphorylation. An HK97 open reading frame, orf41, is necessary for exclusion and Stk kinase activity. We hypothesize that interaction with gp41 stimulates Stk kinase activity. Exclusion of HK97 appears to be specific since other phages tested, lambda, phi80, H-19B, lambda-P22dis and T4rII, were not excluded. Infection of the 933W lysogen with a non-excluded phage fails to induce Stk-determined phosphorylation. |
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