[Salmonella infections in upper volta (author's transl)].
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Eight strains of Salmonellae were incubated in TSB culture medium at 37 degrees C for 24 h. Volatile compounds derived from the bacteria were collected using solid-phase microextraction fibers and then applied to gas chromatography (GC). Similarity analysis of the GC patterns thus obtained could separate these strains on principal component similarity (PCS) scattergrams. Five major food-related pathogenic bacteria and 10 other bacteria (including one Salmonella strain) were also classified by growing in the same medium. It is then proposed to utilize this approach to improve the GC/PCS method of Nakai et al. [Nakai, S.; Wang, Z. H.; Dou, J.; Nakamura, S.; Ogawa, M.; Nakai, E.; Vangerstoep, J. J. Agric. Food Chem. 1999, 47, 576-583] that has been developed for screening safe foods by detecting bacteria contaminated foods. Inoculating food samples pre-enriched through preliminary incubation into a culture medium and then subjecting to the GC/PCS method after secondary incubation enhances the detectability of pathogenic bacteria.
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The role of TNF in immunity to Salmonella in mice was studied. Antiserum specific for murine TNF was raised and used to neutralize TNF activity in vivo. Injection of this serum into mice infected with the moderately mouse virulent Salmonella typhimurium strain M525 caused exacerbation of disease. Such treatment had no effect on the course of an infection with an attenuated S. typhimurium aroA (strain SL3261) mutant. However, the protection afforded by immunisation with live SL3261 against challenge with the virulent parent strain (SL1344) was abolished by anti-TNF antiserum. Interestingly both early (3 wk) immunity and late (10 wk) immunity was neutralized by such treatment. Inasmuch as early immunity is considered to be nonspecific and macrophage-mediated while late immunity is considered to be serotype-specific and T cell mediated, this suggests that TNF plays a role in protection from Salmonellosis in both cases.
Many pathogens can establish a lethal infection from relatively small inocula, yet the effect of infectious dose upon CD4 T cell activation is not clearly understood. This issue was examined by tracking Salmonella flagellin-specific SM1 T cells in vivo, after i.v. and oral challenge of mice with virulent Salmonella typhimurium. SM1 T cells rapidly expressed activation markers and expanded in response to high-dose infection but remained completely unresponsive in mice challenged with low doses of Salmonella. SM1 T cells, in these mice, remained unresponsive, despite massive bacterial replication in vivo. Naive SM1 T cells in low-dose Salmonella-infected mice were activated rapidly after the injection of flagellin peptide, demonstrating that these T cells were fully capable of responding, ruling out the possibility of a bacterial-induced suppressive environment. The inability of flagellin-specific SM1 T cells to respond to low-dose infection was not due to Ag down-regulation, because flagellin expression was detected using a functional assay. Together, these data suggest that low-dose Salmonella infection can evade flagellin-specific CD4 T cell activation in vivo.
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BACKGROUND: The relative paucity of information about systemic nontyphoidal Salmonella (NTS) infection in infants without an underlying disease prompted this study. METHODS: Infants without an underlying disease, who had positive cultures for NTS from their normally sterile sites during 1978 through 1998, were included. Their medical records were reviewed. RESULTS: The study included 75 eligible infants; 68 (91%) had positive blood cultures. The spectrum of disease included transient bacteremia (5), bacteremia without localized infection (37), bone and joint infection (5) and meningitis (28); 53 and 88% of infants were < or =3 and < or =6 months old, respectively. All infants with localized infection were < or =7 months old, and infants with meningitis were 3.35+/-1.87 (mean +/- SD) months old. In bacteremic infants risks for localized infection and meningitis were 30 and 24%, respectively. Abnormal neurologic findings were the only predictor for meningitis. Relapse of meningitis occurred in two infants despite treatment with cefotaxime for 4 and 6 weeks. Severe neurologic deficit occurred in 21% of infants with meningitis. Of 11 infants with meningitis who received early treatment at this tertiary care center, 1 died but none had severe neurologic deficits; whereas of 17 referred cases, 2 died and 6 had severe neurologic abnormalities. No death occurred in infants without meningitis. CONCLUSION: Systemic NTS infection in normal infants has a variable disease spectrum. Infants 0 to 6 months of age are at high risk for localized infection, especially meningitis.
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We examined the immunogenicity of a Salmonella enterica complex vaccine (CV), consisting of flagellin and polysome purified from serotype Typhimurium LT2. CV plus cholera toxin (CT), in three oral doses given at 7-day intervals, conferred complete protection on C57BL/6 mice against lethal oral infection with a wild-type strain. It elicited mucosal IgA > IgG2a > IgG1 and systemic IgG2a > IgG1 > IgA antibodies to flagellin and polysome, and delayed footpad response (DFR) to both antigens. In Peyer's patches (PPs) and lamina propria (LP), IgA was produced under a Th1-dominant environment; CD4+T cells from produced interleukin (IL)-2, interferon (IFN)-gamma, and IL-10 by stimulation with salmonella extract. On the same protocol, flagellin plus CT induced flagellin-specific mucosal and systemic IgA and IgG1 antibodies, CD4+T cells producing IL-10 and IFN-gamma in PPs and LP, and only minimal levels of flagellin-specific DFR. Polysome plus CT induced polysome-specific mucosal and systemic IgG2a in addition to IgG1 and IgA antibodies, CD4+T cells producing IFN-gamma and IL-2 in PPs and LP, and polysome-specific DFR. These two vaccines, however, conferred at most 50-60% survival rates. Our results suggest that polysomes in CV provide effective adjuvant activity for the induction of both mucosal and systemic Th1-biased responses toward flagellin.
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