(1) Background: Although published recommendations are available, the use of antibiotics in non-typhoidal Salmonella (NTS) infections in children is still controversially debated in clinical practice. Patients might even be put at risk, with necessary antibiotic therapy being withheld due to the widespread concern of prolonged post-convalescent shedding. The authors conducted a systematic review to assess whether antibiotic treatment influences fecal excretion or the clinical course in children with NTS infection. (2) Methods: The review was carried out following the PRISMA guidelines. In a Medline database search, studies assessing the influence of antibiotic therapy on excretion and/or the clinical course of NTS infections were selected. Studies reporting on adults only were not considered. Out of 532 publications which were identified during the systematic literature search, 14 publications were finally included (3273 patients in total). Quality and bias assessment was performed using the Newcastle-Ottawa scale (NOS) or the Cochrane risk-of bias tool (ROB-2). (3) Results: Four early studies from decades ago demonstrated a prolongation of intestinal NTS excretion in children after antibiotic treatment, whereas most studies published more recently observed no significant influence, which might be due to having used more “modern” antibiotic regimes (n = 7 studies). Most studies did not describe significant differences regarding the severity and duration of symptoms between untreated patients and those treated with antibiotics. Quality and bias were mainly moderate (NOS) or variable (ROB-2), respectively. (4) Conclusions: There is no substantial evidence of prolonged excretion of NTS in pediatric patients after treatment with newer antimicrobials. Consequently, clinicians should not withhold antibiotics in NTS infection for children at risk, such as for very young children, children with comorbidities, and those with suspected invasive disease due to concerns about prolonged post-convalescent bacterial excretion. In the majority of cases with uncomplicated NTS diarrhea, clinicians should refrain from applying antibiotics.

Mycoplasma pneumoniae (M. pneumoniae) is a common causative pathogen of community-acquired pneumonia. Here, we report the development of macrolide resistance during a school outbreak of severe M. pneumoniae infections in southwest Germany. We conducted a case series to assess the clinical and laboratory characteristics of hospitalized children with M. pneumonia infection and the prevalence of macrolide-resistant M. pneumoniae (MRMP) in this patient group. We retrospectively analyzed 23 children with serologically (19 patients) and/or PCR (eight patients) confirmed M. pneumoniae infection between October 2019 and December 2019. Most of the 15 hospitalized patients had lower respiratory tract infection (n = 10) and required oxygen therapy (83%). The median length of hospitalization was 7 days (range 3–10 days). In 8/15 patients (53.3%) azithromycin and in 4/15 (26.6%) clarithromycin treatment was applied. However, among the five patients for which extended molecular characterization was performed, sequencing of 23S rRNA revealed no mutation only in the first case, but development of macrolide resistance A2058G in four subsequent cases. Hence, we identified a cluster of hospitalized patients with emerging MRMP. Further studies are warranted to confirm a potential link between macrolide resistance and disease severity.

The human choroid plexus (CP) is the location of the blood–cerebrospinal fluid (CSF) barrier (BCSFB). Whereas the epithelial cells of the CP mainly contribute to the formation of the BCSFB, the vessels of the CP are built by fenestrated endothelial cells. Still, the CP endothelium can contribute to barrier function. By ectopic expression of human telomerase reverse transcriptase (hTERT) in primary human CP endothelial cells (HCPEnCs), we recently generated and characterized immortalized HCPEnCs (iHCPEnCs). Here, we compared primary cells of the sixth passage (HCPEnCs p6) with a lower (p20) and a higher passage (p50) of iHCPEnCs by transcriptome analysis. A high concordance of HCPEnCs and both passages of iHCPEnCs was observed, as only small proportions of the transcripts examined were significantly altered. Differentially expressed genes (DEGs) were identified and assigned to potentially affected biological processes by gene set enrichment analysis (GSEA). Various components of the endothelial barrier-relevant Wnt signaling were detected in HCPEnCs and iHCPEnCs. Functional analysis of HCPEnCs and iHCPEnCs showed equal marginal activation of Wnt signaling, supporting the downregulation of β-catenin (CTNNB) signaling in CP endothelial cells, and a contribution to the barrier function by the CP endothelium was retained until passage 100 (p100) of iHCPEnCs. Overall, our data support the suitability of iHCPEnCs as an in vitro model of the CP endothelium over extended passages.