Angiostrongylus cantonensis, the rat lungworm, is the most common infectious cause of eosinophilic meningoencephalitis worldwide. This parasite is endemic to Southeast Asia and the Pacific Islands, and its global distribution is increasing. We report A. cantonensis meningoencephalitis in a 12-month-old boy in Tennessee, USA, who had not traveled outside of southwestern Tennessee or northwestern Mississippi.
Background
Genes conferring carbapenem resistance have disseminated worldwide among Gram-negative bacteria. Here we present longitudinal changes in clinically obtained Escherichia coli isolates from 1 immunocompromised pediatric patient. This report demonstrates potential for antibiotic resistance genes and plasmids to emerge over time in clinical isolates from patients receiving intensive anticancer chemotherapy and broad-spectrum antibiotics.
Methods
Thirty-three isolates obtained over 7 months from 1 patient were included. Clinical data were abstracted from the medical record. For each isolate, studies included phenotypic antibacterial resistance patterns, sequence typing, bacterial isolate sequencing, plasmid identification, and antibiotic resistance gene identification.
Results
Sites of isolation included blood, wound culture, and culture for surveillance purposes from the perianal area. Isolates were of 5 sequence types (STs). All were resistant to multiple classes of antibiotics; 23 (69.6%) were phenotypically resistant to all carbapenems. The blaNDM-5 gene was identified in 22 (67%) isolates, all of ST-167 and ST-940, and appeared to coincide with the presence of the IncFII and IncX3 plasmid.
Conclusions
We present unique microbiologic data from 33 multidrug-resistant E. coli isolates obtained over the course of 7 months from an individual patient in the United States. Two E. coli sequence types causing invasive infection in the same patient and harboring the blaNDM-5 gene, encoded on the IncX3 plasmid and the IncFII plasmid, were identified. This study highlights the emergence of multidrug-resistant bacteria on antibiotic therapy and the necessity of adequate neutrophil number and function in the clearance of bacteremia.
Acute respiratory distress syndrome (ARDS), termed pediatric ARDS (pARDS) in children, is a severe form of acute respiratory failure (ARF) that is associated with significant morbidity and mortality. Pathologic immune responses have been implicated in the development of pARDS. Here, we present a unique description of microbial sequencing and single cell gene expression in tracheal aspirates (TAs) obtained longitudinally from infants admitted to the pediatric intensive care unit (PICU) with ARF. Important alterations in TA epithelial cell, mononuclear phagocyte (MNP), and neutrophil transcription were associated with subjects’ illness severity, etiology (of ARF), and sampling time point. Specifically, in patients with moderate to severe pARDS compared to those with no to mild pARDS we identified reduced interferon stimulated gene (ISG) and cytokine expression in epithelial cells, reduced development over time of a regulatory IL-10 expressing macrophage population, and progressive airway neutrophilia associated with a unique transcriptional profile in aged neutrophils. In addition, we incorporated viral capture sequencing (ViroCap) with single cell transcriptomic analysis to explore interactions between respiratory syncytial virus (RSV) and host cells in infected and bystander epithelia. Our findings indicate that pARDS is defined by distinct inflammatory cell profiles that are etiology- and severity-dependent and implicate inadequate induction of ISGs, cytokines/chemokines, and repair-associated macrophage transcriptional programs in the pathogenesis of moderate to severe pARDS.
Acute respiratory distress syndrome (ARDS), termed pediatric ARDS (pARDS) in children, is a severe form of acute respiratory failure (ARF). Pathologic immune responses are implicated in pARDS pathogenesis. Here, we present a description of microbial sequencing and single cell gene expression in tracheal aspirates (TAs) obtained longitudinally from infants with ARF. We show reduced interferon stimulated gene (ISG) expression, altered mononuclear phagocyte (MNP) transcriptional programs, and progressive airway neutrophilia associated with unique transcriptional profiles in patients with moderate to severe pARDS compared to those with no or mild pARDS. We additionally show that an innate immune cell product, Folate Receptor 3 (FOLR3), is enriched in moderate or severe pARDS. Our findings demonstrate distinct inflammatory responses in pARDS that are dependent upon etiology and severity and specifically implicate reduced ISG expression, altered macrophage repair-associated transcriptional programs, and accumulation of aged neutrophils in the pathogenesis of moderate to severe pARDS caused by RSV.
A 6-week-old infant presented to the emergency department with decreased oral intake, listlessness, diarrhea, and emaciation. The initial laboratory values revealed hypoglycemia, lactic acidosis, hyperammonemia, and azotemia. A diagnostic evaluation was initiated for inborn errors of metabolism. She developed bacteremia and disseminated intravascular coagulation. Hypoalbuminemia, conjugated hyperbilirubinemia, hypotriglyceridemia, and persistent hyperammonemia were noted. Doppler ultrasonography discovered multiple high-flow congenital intrahepatic portosystemic shunts (IHPSS, Figure).
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