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BackgroundPathways coordinated by innate pattern recognition receptors like mannose-binding lectin (MBL) and nucleotide-binding oligomerization domain 2 (NOD2) are among the first immune responses to Staphylococcus aureus (S. aureus) bloodstream infections (BSI) in animal models, but human data are limited. Here, we investigated the role of MBL deficiency and NOD2 mutations in the predisposition to and severity of S. aureus BSI.Patients and MethodsA matched case-control study was undertaken involving 70 patients with S. aureus BSI and 70 age- and sex-matched hospitalized controls. MBL levels, MBL2 and NOD2 polymorphisms were analyzed.ResultsAfter adjusting for potential confounders, MBL deficiency (<0.5 µg/ml) was found less frequently in cases than controls (26 vs. 41%, OR 0.4, 95% confidence interval (CI) 0.20-0.95, p=0.04) as were low producing MBL genotypes (11 vs. 23%, OR 0.2, 95% CI 0.08-0.75, p=0.01), whereas NOD2 polymorphisms were similarly distributed. Cases with NOD2 polymorphisms had less organ dysfunction as shown by a lower SOFA score (median 2.5 vs. 4.5, p=0.02), whereas only severe MBL deficiency (<0.1 µg/ml) was associated with life-threatening S. aureus BSI (OR 5.6, 95% CI 1.25-24.85, p=0.02).ConclusionsContrary to animal model data, our study suggests MBL deficiency may confer protection against acquiring S. aureus BSI. NOD2 mutations were less frequently associated with multi-organ dysfunction. Further human studies of the innate immune response in S. aureus BSI are needed to identify suitable host targets in sepsis treatment.

titres. Our patient meets the 2015 Consensus Diagnostic Criteria for NMOSD. 1 Treatment with high dose corticosteroids and rituximab lead to clinical and radiological improvement, but she had a clinical relapse 10 months later with new LETM (T3-T7), necessitating increased immunosuppression with more rigorous rituximab dosing of 1000mg every 6 months. Conclusions Double positivity for both Aquaporin-4 and MOG antibodies in NMOSD is rare. We describe a case of doublepositive NMOSD occurring following an infective illness. This case demonstrates that NMOSD may occasionally masquerade as post-infectious Acute Disseminated Encephalomyelitis and highlights the importance of checking antibodies in these patients, given the treatment strategies and risk of relapse differs considerably.