Salmonellosis and Systemic Lupus Erythematosus. Report of Ten Cases

Abstract

A retrospective study of Salmonella infection was carried out in 109 SLE patients followed over the last 15 yr at a rheumatology unit. Ten cases of non-typhoid salmonellosis were identified. All patients had bacteraemia and two focal pyogenic complications. No cases of salmonellosis limited to the gastrointestinal tract were found. Death occurred in three cases and was significantly associated with renal failure. A comparative analysis of the patients with and without salmonellosis failed to detect risk factors for infection other than an older age at SLE onset in patient with salmonellosis. We suggest that a heterogeneous group of SLE patients can be at risk for Salmonella bacteraemia. Renal failure or severe pharmacologic immunosuppression might lend an additional risk of complications to infection. It can be speculated that the increased susceptibility to both severe Salmonella infection and SLE might be related to the same immunogenetic background.

Undiagnosed systemic lupus erythematosus presenting with salmonella bacteremia: a case report and mini-review

“…Salmonella bacteremia has usually occurred in patients with an established diagnosis of SLE who have received immunosuppressive drug therapy. However, in addition to our case, four previous reports [4,7–9] indicate that salmonella bacteremia may also occur concurrently with the first presentation of SLE in patients who have not received immunosuppressive therapy. First, one of the three cases with SLE and Salmonella typhimurium bacteriuria reported by Frayha et al.…”

“…Pablos et al. [4] and De Luis et al. [5] reported 10 and four cases of non‐typhoid salmonellosis in 109 and 96 cases of SLE, respectively.…”

Amyloid-DNA Composites of Bacterial Biofilms Stimulate Autoimmunity

“…A working hypothesis is that in non-lupus-prone individuals, or murine strains, natural infections do not normally result in the systemic release of curli-DNA composites in amount equivalent to those we injected in this study; while in susceptible individuals, genetically determined dysfunctions may increase the systemic exposure to curli-DNA composites during chronic infections. The more frequent outcome of Salmonella infection in bacteremia and complications in soft tissues in SLE patients (Lim et al, 2001; Pablos et al, 1994; Tsao et al, 2002) and the recent identification of increased levels of circulating endotoxin in SLE patients (Shi et al, 2014), support this hypothesis. In addition, since inflammatory cytokines can decrease intestinal mucosal barrier function (Turner, 2009), the high levels of cytokines present in pre-disease stages of lupus (Connolly and Hakonarson, 2012; Sriram et al, 2012), might compromise mucosal barrier function and allow the biofilm material produced by microbiota at mucosal sites to access the immune system, act as danger signals and trigger lupus onset.…”

“…Frequent Salmonella infections have been reported, especially those caused by Salmonella enterica serovar Typhimurium and serovar Enteritidis (Gerona and Navarra, 2009). Moreover, Salmonella behave more aggressively in SLE patients: instead of causing localized gastroenteritis, infection may result in bacteremia or complications in soft tissues with high mortality rates (Costa-Reis et al, 2013; Lim et al, 2001; Pablos et al, 1994; Tsao et al, 2002). Although bacterial infections are thought to contribute to SLE pathogenesis by inducing cell death and inflammation, the exact mechanisms by which bacteria contribute to SLE pathogenesis remain unknown.…”

Clinical problem‐solving: ‘persistent knee arthritis and prolonged fever in a lupus patient’

“…Several cases of salmonellosis have been reported among SLE patients. [2][3][4] In fact, SLE was cited as the most frequent underlying disease for salmonella bacteremia among hospitalized patients. 5 In addition to steroids and cytotoxic drugs, other factors which enhance this susceptibility include abnormal functioning of mononuclear phagocytic systems due to previous occupation of Fc receptors by circulating immune complexes, or complement consumption resulting in decreased serum opsonizing activity, functional hyposplenism and haemolysis.…”