ABSTRACT
This case aims to remind all providers to scrutinise for atypical presentations of multisystem inflammatory syndrome in children (MIS-C) which may mimic a more routine diagnosis. In the absence of mucocutaneous symptoms, the diagnosis of MIS-C can be missed. Given the potential for rapid deterioration of patients with MIS-C, early treatment and inpatient interventions are necessary.
Subject(s)
Abdominal Pain/immunology , COVID-19/diagnosis , Fever/immunology , SARS-CoV-2/isolation & purification , Systemic Inflammatory Response Syndrome/diagnosis , Tachycardia/immunology , Abdominal Pain/blood , Abdominal Pain/therapy , Abdominal Pain/virology , Adenosine Monophosphate/analogs & derivatives , Adenosine Monophosphate/therapeutic use , Alanine/analogs & derivatives , Alanine/therapeutic use , C-Reactive Protein/analysis , COVID-19/blood , COVID-19/immunology , COVID-19/therapy , COVID-19 Nucleic Acid Testing , COVID-19 Serological Testing , Child , Diagnosis, Differential , Fever/blood , Fever/therapy , Fever/virology , Humans , Interleukin 1 Receptor Antagonist Protein/therapeutic use , Intubation, Intratracheal , Male , Mucocutaneous Lymph Node Syndrome/diagnosis , Myocarditis/diagnosis , Nasopharynx/virology , Natriuretic Peptide, Brain/blood , SARS-CoV-2/immunology , Systemic Inflammatory Response Syndrome/blood , Systemic Inflammatory Response Syndrome/immunology , Systemic Inflammatory Response Syndrome/therapy , Tachycardia/blood , Tachycardia/therapy , Tachycardia/virology , Treatment Outcome , COVID-19 Drug TreatmentABSTRACT
Escherichia coli encodes two DNA ligases, ligase A, which is essential under normal laboratory growth conditions, and ligase B, which is not. Here we report potential functions of ligase B. We found that across the entire Enterobacteriaceae family, ligase B is highly conserved in both amino acid identity and synteny with genes associated with oxidative stress. Deletion of ligB sensitized E. coli to specific DNA damaging agents and antibiotics resulted in a weak mutator phenotype, and decreased biofilm formation. Overexpression of ligB caused a dramatic extension of lag phase that eventually resumed normal growth. The ligase function of ligase B was not required to mediate the extended lag phase, as overexpression of a ligase-deficient ligB mutant also blocked growth. Overexpression of ligB during logarithmic growth caused an immediate block of cell growth and DNA replication, and death of about half of cells. These data support a potential role for ligase B in the base excision repair pathway or the mismatch repair pathway.
