PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “SALMONELLA INFECTIONS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Control of Salmonella infections in animals and prevention of human foodborne Salmonella infections. WHO Consultation.

In many countries the incidence of human salmonella infections has markedly increased in recent years. To discuss recent developments and current understanding on the control of salmonella infections in animals, WHO organized a Consultation on the Control of Salmonella Infections in Animals: Prevention of Foodborne Salmonella Infections in Humans, held in Jena, Germany, on 21-26 November 1993. The present article summarizes the recommendations made by the participants on the pathoimmunogenesis, diagnosis, epidemiology, and control of salmonella infections and contaminations in animal production.

Animals↗

Limited interleukin-18 response in Salmonella-infected murine macrophages and in Salmonella-infected mice.

Optimal immune responses against an intracellular bacterial pathogen, such as Salmonella, involve the production of gamma interferon (IFN-gamma), which activates macrophages. It has recently been suggested that, interleukin-18 (IL-18), in addition to IL-12, contributes to the induction of IFN-gamma following infection. Given this hypothesis, an optimal host immune response against intracellular bacterial pathogens would include the induction of IL-18 secretion by macrophages due to Salmonella infection. We questioned whether Salmonella could induce macrophages to upregulate their expression of IL-18 mRNA and secretion of IL-18. With cultures of murine macrophages, we were surprised to find that infection by wild-type Salmonella dublin resulted in decreased expression of IL-18 mRNA and IL-18 secretion rather than an increase. Reduction of macrophage-derived IL-18 expression by wild-type Salmonella occurred early in the response, suggesting a direct effect. Furthermore, mice orally inoculated with wild-type Salmonella were shown to have reduced IL-18 mRNA expression at mucosal sites within hours postinoculation. Together these studies demonstrate Salmonella-induced reductions in IL-18 expression, suggesting that this intracellular pathogen may be capable of limiting a potentially protective immune response.

Amino Acid Sequence↗

Salmonella infections in the mouse model: host resistance factors and in vivo dynamics of bacterial spread and distribution in the tissues.

The mouse model is widely used to study the mechanisms of the pathogenesis of, and immunity to, systemic salmonellosis. During infection, Salmonella grows in phagocytic cells that reside in well-defined pathological lesions, are activated by cytokines and control the growth of intracellular bacteria using oxygen and nitrogen derivatives. Salmonella growth in the tissues results in the spatial segregation of bacterial populations and in their continuous distribution to new phagocytes. High bacterial numbers within infected phagocytes are uncommon in vivo.

Animals↗

Pivotal advance: exposure to LPS suppresses CD4+ T cell cytokine production in Salmonella-infected mice and exacerbates murine typhoid.

A number of studies have documented suppression of lymphocyte activation in mice infected with Salmonella. Here, we describe incomplete activation of CD4+ T cells following intravenous injection of specific peptide and LPS into Salmonella-infected mice. Although antigen-specific CD4+ T cells were activated by peptide/LPS to increase surface CD69 expression, they did not produce IL-2 or TNF-alpha. Suppression of cytokine production did not require prolonged exposure of the T cells to the Salmonella-infected environment, was not antigen specific, but was dependent upon the presence of LPS during stimulation. These data suggest that Salmonella-infected mice are exquisitely sensitive to the generation of a suppressive environment following innate immune stimulation with LPS. In agreement with this interpretation, repeated low-dose administration of LPS caused uncontrolled replication of attenuated Salmonella in vivo.

Adoptive Transfer↗

[Clinical importance of infective agent persistence in Salmonella infection in children].

The persistence properties of 70 S. enteriditis cultures and 12 S. typhimurium cultures isolated from the feces of children of the earliest age groups with the gastrointestinal form of Salmonellosis infection were studied. The study revealed that the low level of persistence properties occurred in most cases of mild forms of the disease. Salmonellae with a high level of anticomplement and antilysozyme activity were more often isolated in cases of moderate and severe forms of salmonellosis. The presence of correlation between the expression of the factors under study and the severity of the symptoms of intoxication in combination with the duration of the diarrhea syndrome in moderate and severe forms of Salmonella infection in children of the earliest age groups was established. The suggestion was made that the evaluation of the persistence properties of bacteria may be used for the prognosis of the course of the infectious process.

Child, Preschool↗

Effects of mu, kappa or delta opioids administered by pellet or pump on oral Salmonella infection and gastrointestinal transit.

Our laboratory has shown previously that subcutaneously implanted, slow-release morphine pellets markedly enhanced susceptibility to oral infection with Salmonella typhimurium. Further, morphine, kappa and delta opioid receptor agonists infused via osmotic minipumps were immunosuppressive. The present study compared morphine pellets to morphine pumps and also examined the differential effects of morphine versus U50,488H (kappa agonist), deltorphin II (delta2 agonist), and (D-Pen2, D-Pen5)-enkephalin (DPDPE, delta1 agonist), administered via Alzet minipumps, on oral Salmonella infection and on gastrointestinal transit. The results show that all morphine-pelleted mice (26/26) had a marked increase in Salmonella burden in the Peyer's Patches, mesenteric lymph nodes and spleen. In comparison, only 8/20 mice receiving morphine by minipump at doses ranging from 1 to 25 mg/kg/day had any culturable Salmonella in their organs and the number of bacteria was very low. The level of Salmonella colonization correlated with blood morphine levels and gut transit measured using an intragastric charcoal meal. Morphine pellets inhibited gut transit by 38%, while mice receiving morphine by minipump at doses of 1 to 25 mg/kg/day showed only a dose-dependent 7% to 17% inhibition. Mice receiving various doses of U50,488H or DPDPE had no culturable Salmonella in the three sites. Deltorphin II given by minipump resulted in a moderate level of Salmonella in the spleen. Deltorphin II and U50,488H (0.1 to 10 mg/kg/day) did not suppress gut transit. The present studies indicate that a predominantly mu opioid receptor agonist, morphine, given by slow-release pellet, potentiated Salmonella infection and inhibited gastrointestinal transit. In contrast, morphine in pumps slightly inhibited intestinal transit, but did not sensitize to Salmonella infection. A delta1 opioid receptor agonist did not sensitize to infection, and a delta2 and a kappa opioid receptor agonist had minimal effects on either parameter.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Predominant appearance of NK1.1+ T cells producing IL-4 may be involved in the increased susceptibility of mice with the beige mutation during Salmonella infection.

C57BL/6 mice with the beige mutation (beige mice) showed a high susceptibility to infection with Salmonella choleraesuis compared with C57BL/6 (B6) control mice, as assessed by bacterial number in the peritoneal cavity and the liver. The appearance of NK1.1+ CD3- NK cells was significantly suppressed, while NK1.1+ T cells were increased in the peritoneal cavity of beige mice after Salmonella infection. The expression level of IL-4 mRNA was much higher in freshly isolated NK1.1+ T cells of the infected beige mice, but the expression level of IFN-gamma mRNA was lower than that in the infected control mice. The NK1.1+ T cells produced more IL-4 in response to TCR alphabeta cross-linking, whereas IFN-gamma production upon TCR triggering was significantly impaired in the beige mice compared to that in the control mice. Furthermore, the generation of Salmonella-specific Th1 cells producing IFN-gamma was significantly inhibited in the peritoneal cavity of beige mice after Salmonella infection. However, administration of anti-IL-4 neutralizing mAb to beige mice during salmonellosis restored the generation of Salmonella-specific Th1 cells and decreased the susceptibility to Salmonella. These results suggested that the predominant activation of NK1.1+ T cells producing IL-4 over those producing IFN-gamma may be at least partly involved in the poor generation of Salmonella-specific protective Th1 cells, resulting in the increased susceptibility of beige mice to Salmonella infection.

Animals↗

Antimicrobial drug resistance in salmonella-infected aortic aneurysms.

BACKGROUND: Salmonella infection of the aorta and adjacent arteries is rare, but life-threatening. There is an increasing number of infections caused by antimicrobial drug resistant Salmonella. This study sought to assess the association between antimicrobial drug resistance and clinical outcomes of patients with Salmonella-infected aortic aneurysm. METHODS: Data were collected by retrospective chart review. Between October 1995 and October 2004, 34 patients with Salmonella-infected aortic aneurysm were included. Aneurysm-related deaths were defined as hospital deaths and late deaths due to prosthetic graft infection. Analysis was performed using the chi2 test, Fisher's exact test, and Mann-Whitney test. RESULTS: Nineteen patients had a suprarenal and 15 patients had an infrarenal aortic infection. The most common responsible pathogen was group C Salmonella (47%). Ciprofloxacin-resistant Salmonella infection occurred since March 2001 and the rate increased from 0 per 15 in the years before March 2001 to 5 per 19 in the years after March 2001 (p = 0.005 by Fisher's exact test). Among the 26 patients who had combined medical and surgical therapy, 4 died in the hospital and 4 died of late prosthetic graft infection 3 to 6 months after operation, whereas 4 of the 8 who had medical therapy alone died of aneurysm rupture during hospitalization. The actuarial survival rates by the Kaplan-Meier method were 64% at 6 months, 61% at 1 year, and 56% at 5 years. The risk factors for aneurysm-related death were old age (78.5 +/- 9.7 years vs 63.5 +/- 11.4 years; p < 0.001) and ciprofloxacin-resistant Salmonella infection (4 of 5 vs 8 of 29; p = 0.042). CONCLUSIONS: There was an increased mortality associated with ciprofloxacin resistance in infected aortic aneurysms with Salmonella. With an increasing incidence of ciprofloxacin resistant Salmonella, third generation cephalosporin is the antibiotic of choice for Salmonella-infected aneurysm.

Adult↗

Two-staged revision total hip arthroplasty due to Salmonella infection: case report.

Salmonella infection of a hip prosthesis has rarely been reported, and only a few cases have been documented. It is painful, disabling, costly, and may be associated with life-threatening sepsis even in a healthy individual. Removal of the implant is often required to eradicate the infection. Several early studies reported procedures to control the salmonella infection, but none described reconstruction of the destroyed hip joint. We present a case of salmonella sepsis 4 years after a total hip arthroplasty (THA). After prosthesis removal, radical debridement of the infected tissues, and administration of Imipenum (500 mg, 4 times daily), the systemic sepsis and hip infection were ameliorated. Four months later, a 2-stage revision THA was done for reconstruction of the hip joint. The clinical results 51 months following the THA procedure were satisfactory without an infectious reaction.

Arthroplasty, Replacement, Hip↗

MHC class II-dependent NK1.1+ gammadelta T cells are induced in mice by Salmonella infection.

We observed the emergence of a novel population of gammadelta T cells expressing NK1.1 Ag in the peritoneal cavity of mice infected with Salmonella choleraesuis. The NK1.1+gammadelta T cells accounted for approximately 20% of all gammadelta T cells emerging in the peritoneal cavity of C57BL/6 mice and expressed preferentially rearranged Vgamma4-Jgamma1 and Vdelta6.3-Ddelta1-Ddelta2-Jdelta1 genes with N diversity. The gammadelta T cells proliferated vigorously in response to PHA-treated spleen cells and produced IFN-gamma in the culture supernatant. However, spleen cells from Abetab-deficient mice were unable to stimulate the gammadelta T cells. Furthermore, the NK1.1+gammadelta T cells were stimulated not only by Chinese hamster ovary (CHO) cells expressing wild-type IAb but also by those expressing IAb/Ealpha52-68 or IAb/pigeon cytochrome c-derived analogue peptide complex. These proliferation activities were inhibited by mAb specific for IAb chain. Consistent with these findings, the emergence of NK1.1+gammadelta T cells was reduced in the peritoneal cavity of Abetab-deficient mice after Salmonella infection, whereas NK1.1+gammadelta T cells were rather abundant in the peritoneal cavity of Salmonella-infected beta2m-deficient mice. Moreover, the NK1.1+gammadelta T cells were easily identified in the thymus of beta2m-deficient but not Abetab-deficient mice. Our results indicated that MHC class II expression is essential for development and activation of NK1. 1+gammadelta T cells in the thymus and the periphery.

Animals↗

The role of intrahepatic gammadelta-T cells for liver injury induced by Salmonella infection in mouse.

Liver injury was induced after infection with Salmonella choleraesuis 31N-1. In T-cell receptor-delta knockout mice, serum alanine transferase level was significantly decreased in comparison with normal control mice after Salmonella infection. On the contrary, in vivo administration of anti-gammadelta T-cell receptor monoclonal antibody (UC7-13D5) to stimulate gammadelta-T cells in infected mice significantly increased serum alanine transferase level but decreased bacterial growth compared with infected mice given control antibody (UC8; hamster IgG). These data suggest that gammadelta-T cells have effector activities not only for protection but also for liver injury during Salmonella infection.

Alanine Transaminase↗

Mesenteric cyst infected with non-typhoidal salmonella infection.

Although extra-intestinal non-typhoidal Salmonella infections are common in developing countries, infection of the mesenteric cyst with Salmonella enteritidis is an extremely rare occurrence. Review of the English literature has revealed one report up to this date. The case of a 4-year-old boy with a mesenteric cyst infected with Salmonella enteritidis is presented.

Child, Preschool↗

Immunological and gene expression responses to a Salmonella infection in the chicken intestine.

Besides infection in humans, Salmonella enteritidis can also cause serious illness in young chickens. However, the genetic and immunological parameters important for the disease in chickens are not well characterized. In this study, processes in the chicken intestine in response to a Salmonella infection were investigated in two different chicken lines. One-day-old chickens were orally infected with Salmonella. T-cell subpopulations, phagocytic properties of intestinal mononuclear cells and RNA expression levels of the jejunum were investigated. The two chicken lines differed in the amount of cfu in the liver and growth retardation after the infection. Differences in phagocytic activity of intestinal mononuclear cells were found between control and Salmonella infected chickens. The number of CD4+ T-cells of the intestine decreased after the Salmonella infection in one chicken line, while the number of CD8+ T-cells increased in both chicken lines, but the time post infection of this increase differed between the lines. In one chicken line the expression levels of the genes carboxypeptidase M and similar to ORF2 decreased after the Salmonella infection, which might be related to a decrease in the amount of macrophages. With the microarray, ten genes were found that were regulated in only one of the chicken lines, while we found six genes regulated in response to the infection in both chicken lines. So differences in genetic background of the chickens influence the intestinal host response of the Salmonella infection as observed by phagocytic activity, gene expression and changes in the number of T-cell subpopulations and macrophages.

Animals↗

Ciprofloxacin versus chloramphenicol in the treatment of salmonella infection.

Strains of Salmonella typhi resistant to chloramphenicol and ampicillin have been isolated in several countries. This study compares treatment of Salmonella infection using ciprofloxacin (500 mg twice daily) for 10 days with chloramphenicol (50 mg/kg per day divided into four doses) for 14 days. The pathogen eradication rates for patients receiving ciprofloxacin was 18/20 (90%), compared with 25/28 (89%) for those who received chloramphenicol. Signs and symptoms in patients receiving chloramphenicol lasted longer and sometimes twice as long as patients treated with ciprofloxacin. In this study, ciprofloxacin was superior to cloramphenicol in the treatment of S. typhi infection and also had fewer side-effects and the convenience of a twice-a-day dosing

Adult↗