Clinical aspects of a nationwide epidemic of severe haemolytic uremic syndrome (HUS) in children

<p>Abstract</p> <p>Background</p> <p>Report a nationwide epidemic of Shiga toxin-producing E. coli (STEC) O103:H25 causing hemolytic uremic syndrome (D+HUS) in children.</p> <p>Methods</p> <p>Description of clinical presentation, complications and outcome in a nationwide outbreak.</p> <p>Results</p> <p>Ten children (median age 4.3 years) developed HUS during the outbreak. One of these was presumed to be a part of the outbreak without microbiological proof. Eight of the patients were oligoanuric and in need of dialysis. Median need for dialysis was 15 days; one girl did not regain renal function and received a kidney transplant. Four patients had seizures and/or reduced consciousness. Cerebral oedema and herniation caused the death of a 4-year-old boy. Two patients developed necrosis of colon with perforation and one of them developed non-autoimmune diabetes.</p> <p>Conclusion</p> <p>This outbreak of STEC was characterized by a high incidence of HUS among the infected children, and many developed severe renal disease and extrarenal complications. A likely explanation is that the O103:H25 (<it>eae </it>and <it>stx₂</it>-positive) strain was highly pathogen, and we suggest that this serotype should be looked for in patients with HUS caused by STEC, especially in severe forms or outbreaks.</p

Sudden emergence of a Neisseria gonorrhoeae clade with reduced susceptibility to extended-spectrum cephalosporins, Norway

Neisseria gonorrhoeae multilocus sequence type (ST)-7827 emerged in a dramatic fashion in Norway in the period 2016–2018. Here, we aim to shed light on the provenance and expansion of this ST. ST-7827 was found to be polyphyletic, but the majority of members belonged to a monophyletic clade we termed PopPUNK cluster 7827 (PC-7827). In Norway, both PC-7827 and ST-7827 isolates were almost exclusively isolated from men. Phylogeographical analyses demonstrated an Asian origin of the genogroup, with multiple inferred exports to Europe and the USA. The genogroup was uniformly resistant to fluoroquinolones, and associated with reduced susceptibility to both azithromycin and the extended-spectrum cephalosporins (ESCs) cefixime and ceftriaxone. From a genetic background including the penA allele 13.001, associated with reduced ESC susceptibility, we identified repeated events of acquisition of porB alleles associated with further reduction in ceftriaxone susceptibility. Transmission of the strain was significantly reduced in Norway in 2019, but our results indicate the existence of a recently established global reservoir. The worrisome drug-resistance profile and rapid emergence of PC-7827 calls for close monitoring of the situation

Clinical aspects of a nationwide epidemic of severe haemolytic uremic syndrome (HUS) in children

Background: Report a nationwide epidemic of Shiga toxin-producing E. coli (STEC) O103:H25 causing hemolytic uremic syndrome (D+HUS) in children. Methods: Description of clinical presentation, complications and outcome in a nationwide outbreak. Results: Ten children (median age 4.3 years) developed HUS during the outbreak. One of these was presumed to be a part of the outbreak without microbiological proof. Eight of the patients were oligoanuric and in need of dialysis. Median need for dialysis was 15 days; one girl did not regain renal function and received a kidney transplant. Four patients had seizures and/or reduced consciousness. Cerebral oedema and herniation caused the death of a 4-year-old boy. Two patients developed necrosis of colon with perforation and one of them developed non-autoimmune diabetes. Conclusion: This outbreak of STEC was characterized by a high incidence of HUS among the infected children, and many developed severe renal disease and extrarenal complications. A likely explanation is that the O103:H25 (eae and stx2-positive) strain was highly pathogen, and we suggest that this serotype should be looked for in patients with HUS caused by STEC, especially in severe forms or outbreaks