The taxonomy of the genus Neisseria remains confusing, particularly regarding Neisseria mucosa and Neisseria sicca. In 2012, ribosomal multi-locus sequence typing reclassified both as N. mucosa, but data concerning 17 N. sicca strains remain available in GenBank. The continuous progress of high-throughput sequencing has facilitated ready accessibility of whole-genome data, promoting vigorous development of average nucleotide identity (ANI) and high-resolution phylogenetic analysis. Here, we report that a Neisseria isolate, which caused native-valve endocarditis and multiple embolic brain infarcts in a patient with congenital heart disease, was misidentified as N. sicca by VITEK MS. This isolate was reclassified as N. mucosa by ANI blast (ANIb) and by phylogenetic analysis using whole-genome data yielded by the PacBio Sequel and Illumina NovaSeq PE150 platforms. The confusion evident in the GenBank and matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF MS) databases suggests that N. mucosa (n = 13) and N. sicca (n = 16) in GenBank should be reclassified using ANIb and high-resolution phylogenetic analysis. The whole-genome data of 30 strains (including the clinical isolate) were compared with the data of 27 type Neisseria strains (including one N. sicca and two N. mucosa type strains) as a genomic index. In total, 25 (8 originally identified as N. mucosa and 17 originally identified as N. sicca) and 7 (1 originally identified as N. sicca and 6 originally identified as N. mucosa) strains were reclassified into the N. mucosa and Neisseria subflava groups, respectively; 1 residual N. mucosa strain was reclassified as Neisseria meningitidis. In conclusion, a combination of ANIb and robust phylogenetic analysis reclassified strains originally identified as N. mucosa and N. sicca into (principally) the N. mucosa group and the N. subflava group. The misclassified N. sicca and N. mucosa strains in the GenBank and MALDI-TOF MS databases were supposed to be corrected. Updated genomic classification strategy for originally identified N. mucosa and N. sicca strains was recommended to be adopted in GenBank.

Thrombotic thrombocytopenic purpura (TTP) is one of the two classic thrombotic microangiopathy (TMA) diseases which could be induced by infections. To the best of our knowledge, this is the first report of an acquired immunodeficiency syndrome (AIDS) patient with acquired TTP induced by infection with Salmonella enterica serovar Typhimurium (hereafter, S. Typhimurium) isolate, S. Typhimurium_zhang, which was confirmed by serology and genetic taxonomy. The literature review identified 17 TMA-related genes encoding the candidate triggers, which were searched in the annotated genome sequence of S. Typhimurium_zhang. Anaerobic nitric oxide reductase flavorubredoxin (FlRd), encoded by norV which is related to another TMA, haemolytic uraemic syndrome (HUS), was found in S. Typhimurium_zhang. Basic local alignment search tool (BLAST) analysis revealed that norV and FlRd in S. Typhimurium_zhang, as well as eight S. Typhimurium type strains, have high identity with HUS-related Escherichia coli O157:H7 strain TW14359. Similar results were obtained from the BLAST analysis of 73 S. enterica isolates for congenital TTP which was also previously reported to be triggered by S. enterica. Phylogenetic analysis and amino acid sequence alignment revealed that FlRd was functional and highly conservative on 69 Enterobacteriaceae, including S. Typimurium_zhang and TW14359. In brief, we found norV in the genome of a S. Typhimurium clinical isolate that induced TTP in an AIDS patient. FlRd, the protein encoded by norV, probably triggered the TTP and was highly conservative, functional, and widespread in S. enterica and Enterobacteriaceae. More in vitro and in vivo studies are required to confirm our findings and determine the underlying mechanism.