Purpose Bloodstream infections (BSIs) cause morbidity and mortality in postpartum patients, resulting in poor prognosis for both mother and neonate. Gram-negative bacteremia is a public health threat, with high mortality among vulnerable populations and significant global economic costs. Gram-negative bacteremia and antimicrobial resistance are increasing. This study retrospectively analyzed the pathogen distribution and drug sensitivity among postpartum patients with BSIs to identify appropriate antibacterial agents for perioperative therapy. Material and Methods All bacteremia cases between January 2015 and December 2020 from three Health Centers for Women and Children in Chongqing, China, were retrospectively reviewed. Clinical data were collected from medical records and charts. Blood samples were cultured by BD BACTEC FX200. Bacterial and fungal species and bacterial susceptibility were identified by a BD Phoenix TM M50 automatic detection machine. Results In total, 274 pathogenic strains were isolated from 272 blood samples. Excluding 25 suspected contamination strains, 248 blood samples yielded 249 microorganisms, including 214 gram-negative bacteria (85.9%), 34 gram-positive bacteria (13.6%), and 1 fungus (0.5%). Escherichia coli ( E. coli ) was the most frequently isolated pathogen, both overall and among gram-negative bacilli (73.5%). Streptococcus agalactiae represented 3.6% of gram-positive cocci (n = 9). Laboratory-confirmed anaerobic infections comprised 9.2% of cases (n = 23). Additionally, 47.4% of postpartum patients with BSIs suffered premature rupture of membranes (PROM), a suspected infection risk factor. Drug sensitivity levels remained unchanged for less commonly used drugs, but resistance increased against commonly used drugs. Specifically, E. coli resistance against fourth-generation cephalosporins increased during this study period. Conclusion E. coli is the most common gram-negative bacillus in postpartum patients with BSIs, and increased anaerobic bacterial detections suggest genital tract inflammation control before delivery is necessary. Effective drug resistance monitoring remains necessary to alleviate bacterial resistance, such as preventing inappropriate antibiotic applications.

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Monogenic autoinflammatory diseases (mAIDs) are a heterogeneous group of diseases affecting primarily innate immunity, with various specific genetic causes.Genetic diagnosis of mAIDs can assist in the patient's management and therapy.However, a large number of sporadic and familial cases remain genetically . CC-BY-ND 4.0 International license It is made available under a is the author/funder, who has granted medRxiv a license to display the preprint in perpetuity.

Chronic granulomatous disease (CGD) is a rare inborn error of immunity (IEI) characterized by a defective respiratory burst by phagocytes and defective clearance of phagocytosed microorganisms; these phenomena, caused by a defect in NADPH oxidase, result in severe and life-threatening infections in affected children. The genetically heterogeneous X-linked recessive (XL-CGD) form of GCD is caused by mutations in the CYBB gene, whereas the autosomal recessive (AR-CGD) form is caused by mutations in the CYBA, NCF1, NCF2, NCF4, or CYBC1 genes. Mutations in the CYBA gene account for a small number of CGD cases; the vast majority of these patients become symptomatic in childhood, but rarely within the first weeks of life. Here, we report a 19-day-old neonate who developed pustular rashes and invasive pulmonary aspergillosis, which was identified by a galactomannan (GM) assay of both bronchoalveolar lavage fluid (BALF) and peripheral blood samples, and by metagenomic next-generation sequencing (mNGS) of BALF. A diagnosis of CGD was based on the respiratory burst test. Detailed assessment of neutrophil activity revealed that production of reactive oxygen species (ROS) was entirely absent. Whole-exome sequencing (WES) detected a nonsense mutation (c.7G>T). In addition, copy number variation (CNV) analysis detected a novel de novomicrodeletion of 200 kb at 16q24.2-q24.3. Thus, we have identified novel compound heterozygous CYBA mutations that cause neonatal AR-CGD, thereby expanding the clinical spectrum of CYBA deficiency.

The dedicator of cytokinesis 2(DOCK2) protein, an atypical guanine nucleotide exchange factor (GEFs), is a member of the DOCKA protein subfamily. DOCK2 protein deficiency is characterized by early-onset lymphopenia, recurrent infections, and lymphocyte dysfunction, which was classified as combined immune deficiency with neutrophil abnormalities as well. The only cure is hematopoietic stem cell transplantation. Here, we report two patients harboring four novel DOCK2 mutations associated with recurrent infections including live attenuated vaccine-related infections. The patient’s condition was partially alleviated by symptomatic treatment or intravenous immunoglobulin. We also confirmed defects in thymic T cell output and T cell proliferation, as well as aberrant skewing of T/B cell subset TCR-Vβ repertoires. In addition, we noted neutrophil defects, the weakening of actin polymerization, and BCR internalization under TCR/BCR activation. Finally, we found that the DOCK2 protein affected antibody affinity although with normal total serum immunoglobulin. The results reported herein expand the clinical phenotype, the pathogenic DOCK2 mutation database, and the immune characteristics of DOCK2-deficient patients. Supplementary Information The online version contains supplementary material available at 10.1007/s10875-023-01466-y.