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PubMed1999

Of mice, calves, and men. Comparison of the mouse typhoid model with other Salmonella infections.

Numerous Salmonella typhimurium virulence factors have been identified and characterized using experimental infection of mice. While the murine typhoid model has been used successfully for Salmonella typhi vaccine development and to infer virulence mechanisms important during typhoid fever, information derived from infection of mice has been of limited value in elucidating the mechanisms by which S. typhimurium causes enteritis in humans. Progress in our understanding of virulence mechanisms contributing to diarrheal disease comes from recent studies of bovine enteritis, a S. typhimurium infection, which manifests as acute gastroenteritis. This review compares virulence genes and mechanisms required during murine typhoid, typhoid fever, and bovine enteritis. Comparison of illnesses caused in different animal hosts identifies virulence mechanisms involved in species specific disease manifestations. The determination of the relative importance of virulence factors for disease manifestations in different host species provides an important link between the in vitro characterization of genes and their role during host pathogen interaction.

Animals↗
PubMed1997

Protective effects of dietary lactulose and calcium phosphate against Salmonella infection.

BACKGROUND: Protection against intestinal infections by lactulose fermentation might be enhanced by calcium phosphate, due to the increased buffering capacity and/or inhibition of the cytotoxicity of luminal contents. METHODS: SPF rats were fed a low-calcium control diet, a low-calcium/lactulose diet or a high-calcium/lactulose diet and orally infected with Salmonella enteritidis. Faeces and urine were sampled for microbiological and chemical analyses. RESULTS: The lactulose-fed rats had a better colonization resistance. Translocation was reduced by dietary calcium, whereas lactulose was ineffective. In addition, calcium supplementation stimulated lactulose fermentation, reversed the lactulose-induced increase in cytotoxicity of faecal water and normalized growth and faecal consistency. CONCLUSIONS: The combination of dietary lactulose and calcium phosphate is protective against Salmonella infection.

Animals↗
PubMedDate not supplied

[Clinical course and treatment regimes of Salmonella infection in children].

Salmonella infection in children caused by polyresistant S. typhimurium strains is characterized by a highly severe course with possible complications. In the treatment of young children with salmonellosis the use of the locally manufactured biologically active additive Bektit-M, possessing adsorption capacity, is recommended. The use of this preparation in complex treatment has made it possible to establish its clinical effect and positive influence on the biochemical characteristics of the blood.

Adolescent↗
PubMed1985

[Pleuropulmonary localizations of non-typhoid Salmonella infections].

Non-typhoid salmonella infections are extremely common, usually taking the form of a benign toxi-infection. In the context of the rare extra-digestive manifestations, the authors report 3 cases of pleuro-pulmonary involvement, in infections due to Salmonella Dublin. In 2 cases, the organism was identified from blood cultures, whilst in the 3rd case it was isolated from pleural fluid. As with other extra-digestive sites, pleuro-pulmonary involvement is favored by underlying pathology, accounting for the grave nature of the problem (amongst the 3 cases, gastrectomy and acute myeloblastic leukemia in one case and obliterative arterial disease in another case). Non-typhoid salmonella infections are sensitive to Sulfamethoxazole-trimethoprim which diffuses well in the respiratory system. They are also sensitive to Amoxicillin and to Chloramphenicol.

Aged↗
PubMed1990

[Clinical characteristics of the outbreak of Salmonella infection caused by Salmonella enteritidis].

The data are presented on an outbreak of salmonellosis induced by S. enteritidis. Gastrointestinal symptoms were recorded in 97.8% of 90 patients, 2.2% of them developed a generalized form. The disease ran a moderate course in 84.5% and a severe course in 2.2% of the patients majority of whom suffered from intoxication and dehydration. The therapeutic response was achieved upon rehydration treatment with crystalloid solutions.

Adult↗
PubMed1985

Ciprofloxacin treatment of systemic salmonella infection in sensitive and resistance mice.

Five days therapy with ciprofloxacin (10 mg/kg bd) starting on day 6 after infection with Salmonella typhimurium, significantly reduced mortality in A/J and CBA mice. In CBA mice ciprofloxacin therapy also resulted in significantly lower viable counts of Salm. typhimurium in the livers and spleens of surviving mice at day 36 than was found in untreated mice or those given chloramphenicol. Ciprofloxacin failed to prevent fatal Salm. typhimurium disease in the majority of Balb/C mice, a strain that has no natural immunity to salmonella infection. Death was delayed in ciprofloxacin-treated mice and ciprofloxacin did control the multiplication of salmonellae in liver and spleen within 3 days of commencement.

Animals↗
PubMed1997

Identification of a natural T cell epitope presented by Salmonella-infected macrophages and recognized by T cells from orally immunized mice.

Murine infection with Salmonella typhimurium provides models for typhoid fever and long-lasting protective immunity conferred by oral vaccination with viable attenuated bacteria. To further understand the role of T cells in these systems, we identified a bacterial Ag recognized by murine T cells responding to a Salmonella infection. From orally infected mice, we derived a CD4+ Ak-restricted T cell clone (7.4.8) the stimulatory Ag of which was provided by S. typhimurium or its flagella, but not by other salmonellae or S. typhimurium mutants unable to synthesize the flagellar filament protein FliC. We mapped antigenic activity to FliC hypervariable region VI using a generally applicable method of sequential C-terminal truncation of recombinant MalE-FliC fusion proteins. Residues 339-350 are the minimal FliC structure capable of stimulating 7.4.8 and represent the first reported Salmonella-specific epitope recognized by T cells from infected mice. T cells with this specificity are generated by oral immunization, reactivity can be recovered for at least 5 mo afterwards, and FliC is the dominant recall Ag for CD4+ T cells from protectively immunized C3H/HeJ mice. FliC 339-350 is presented by macrophages infected with viable S. typhimurium, and presentation, but not bacterial uptake, is greatly enhanced by pretreatment of macrophages with IFN-gamma. These data point to the importance of IFN-gamma-activated macrophages in the stimulation of T cells responding to facultative intracellular pathogens like S. typhimurium and provide a model system for studying Ag-specific T cell responses in murine salmonellosis.

Administration, Oral↗
PubMed1983

Hemopoietic responses of LPS-unresponsive C3H/HeJ mice to salmonella infection.

Effects of Salmonella enteritidis infection on hemopoietic stem cells were examined in LPS-unresponsive C3H/HeJ mice. The salmonella infection increased pluripotent stem cells (CFUs) and granulocyte-macrophage progenitor cells (CFUc) in the spleen and decreased these hemopoietic stem cells in the bone marrow. These responses seemed to be specific to salmonella infection and not due to biological activities of LPS.

Animals↗
PubMed1993

Tumor necrosis factor-alpha mediates the early pathology in Salmonella infection of the gastrointestinal tract.

Salmonella infection of the intestinal tract results in damage to the gut epithelium. While it is generally believed that bacteria and/or bacterial products account for this pathology, the role of host factors has not been explored. Using a ligated intestinal loop model, we investigated whether tumor necrosis factor-alpha (TNF-alpha) could contribute to the tissue pathology associated with Salmonella infection. Intestinal segments infected with Salmonella typhimurium had high levels of fluid secretion as early as 6 h post-bacterial infection. At this time point, low levels of TNF activity were also present in the fluid obtained from infected segments. At 20 h post-infection, high levels of TNF activity were present in fluids obtained from infected intestinal segments and was characterized as TNF-alpha by neutralization experiments using rabbit antisera to TNF-alpha. TNF-alpha production was further verified by Northern blot analysis using RNA obtained from cells eluted from the infected intestinal segments. In contrast, no TNF activity was found in fluid obtained from intestinal segments challenged with cholera toxin, which induces fluid secretion with little to no inflammatory response. Double labeling by in situ hybridization and immunocytochemistry revealed that macrophages in the lamina propria were producing the TNF-alpha mRNA. To investigate what role TNF-alpha might play in Salmonella-induced inflammation, intestinal segments were injected with recombinant mouse TNF-alpha (rTNF-alpha) or mice were pretreated with antibody to TNF-alpha or a control antibody prior to Salmonella infection. The histological profile of intestinal segments injected with rTNF-alpha appeared identical to segments infected with S. typhimurium. Further, pathology was completely eliminated in infected mice pretreated with antibody to TNF-alpha. These results document the production of TNF-alpha in the intestinal tract following S. typhimurium infection and show that the early pathology induced by Salmonella infection of the gastrointestinal tract is mediated by immune mechanisms.

Animals↗
PubMed2004

Hospitalizations and deaths due to Salmonella infections, FoodNet, 1996-1999.

Nontyphoidal Salmonella causes a higher proportion of food-related deaths annually than any other bacterial pathogen in the United States. We reviewed 4 years (1996-1999) of population-based active surveillance data on laboratory-confirmed Salmonella infections from the Emerging Infections Program's Foodborne Diseases Active Surveillance Network (FoodNet), to determine the rates of hospitalization and death associated with Salmonella infection. Overall, 22% of infected persons were hospitalized, with the highest rate (47%) among persons aged >60 years. Fifty-eight deaths occurred, for an estimated annual incidence of 0.08 deaths/100,000 population. These deaths accounted for 38% of all deaths reported through FoodNet from 1996 through 1999, and they occurred primarily among adults with serious underlying disease. Although Salmonella infection was seldom listed as a cause of death on hospital charts and death certificates, our chart review suggests that Salmonella infection contributed to these deaths.

Adult↗
PubMed2006

Isolation and characterization of bacteriophages infecting Salmonella spp.

Bacteriophages infecting Salmonella spp. were isolated from sewage using soft agar overlays containing three Salmonella serovars and assessed with regard to their potential to control food-borne salmonellae. Two distinct phages, as defined by plaque morphology, structure and host range, were obtained from a single sample of screened sewage. Phage FGCSSa1 had the broadest host range infecting six of eight Salmonella isolates and neither of two Escherichia coli isolates. Under optimal growth conditions for S. Enteritidis PT160, phage infection resulted in a burst size of 139 PFU but was apparently inactive at a temperature typical of stored foods (5 degrees C), even at multiplicity of infection values in excess of 10 000. While neither isolate had characteristics that would make them candidates for biocontrol of Salmonella spp. in foods, phage FGCSSa1 behaved unusually when grown on two Salmonella serotypes at 37 degrees C in that the addition of phages appeared to retard growth of the host, presumably by the lysis of a fraction of the host cell population.

Cold Temperature↗
PubMed1999

Regulatory role of peritoneal NK1.1+ alpha beta T cells in IL-12 production during Salmonella infection.

NK1.1+ alpha beta T cells emerge in the peritoneal cavity after an i.p. infection with Salmonella choleraesuis in mice. To elucidate the role of the NK1.1+ alpha beta T cells during murine salmonellosis, mice lacking NK1.1+ alpha beta T cells by disruption of TCR beta (TCR beta-/-), beta 2m (beta 2m-/-), or J alpha 281 (J alpha 281-/-) gene were i.p. inoculated with S. choleraesuis. The peritoneal exudate T cells in wild type (wt) mice on day 3 after infection produced IL-4 upon TCR alpha beta stimulation, whereas those in TCR beta-/-, beta 2m-/-, or J alpha 281-/- mice showed no IL-4 production upon the stimulation, indicating that NK1.1+ alpha beta T cells are the main source of IL-4 production at the early phase of Salmonella infection. Neutralization of endogenous IL-4 by administration of anti-IL-4 mAb to wt mice reduced the number of Salmonella accompanied by increased IL-12 production by macrophages after Salmonella infection. The IL-12 production by the peritoneal macrophages was significantly augmented in mice lacking NK1.1+ alpha beta T cells after Salmonella infection accompanied by increased serum IFN-gamma level. The aberrantly increased IL-12 production in infected TCR beta-/- or J alpha 281-/- mice was suppressed by adoptive transfer of T cells containing NK1.1+ alpha beta T cells but not by the transfer of T cells depleted of NK1.1+ alpha beta T cells or T cells from J alpha 281-/- mice. Taken together, it is suggested that NK1. 1+ alpha beta T cells eliciting IL-4 have a regulatory function in the IL-12 production by macrophages at the early phase of Salmonella infection.

Adoptive Transfer↗
PubMed1975

Interaction of T-2 toxin with Salmonella infections of chickens.

A significant (P less than 0.05) interaction resulting in increased mortality occurred in chickens fed T-2 toxin (16 mug./g. of diet) and infected with either Salmonella worthington, S. thompson, S. derby, or S. typhimurium var. copenhagen, all species that cause paratyphoid. No interaction on growth rate or relative size of the bursa of Fabricus occurred, although T-2 toxin alone caused a significant (P less than 0.05) regression of that organ. The spleen size relative to the body weight was decreased (P less than 0.05) by T-2 toxin and increased (P less than 0.05) by the Salmonella infections. Interactions were observed on spleen size between the toxin and S. thompson (P less than 0.05) and S. derby (P less than 0.10). Total serum proteins were not affected by T-2 toxin or Salmonella infections. Agglutinins were formed in response to the infections, but the titers were unaltered by T-2 toxin.

Animals↗
PubMedDate not supplied

Intrahepatic hematoma with secondary Salmonella infection via biliary fistula.

Usually liver hematoma after blunt trauma is treated conservatively as long as clinically possible, in order to avoid infection via drainage. We report a patient who developed a huge liver abscess after a minor blunt trauma caused by a piece of wood that hit his hepatic region during work with a circular saw. Neither conservative treatment nor percutaneous drainage was successful and intraoperatively a biliary fistula was identified as the route of infection by salmonella. Cholecystectomy (here meaning removal of the salmonella reservoir) and consequent drainage of the gall flow via T-drain were the crucial therapeutic steps and the fistula finally closed after three months. Therapeutic possibilities in the management of blunt liver trauma, and biliary and septic complications are discussed.

Biliary Fistula↗