ESPN 51th Annual Meeting

ESPN 2018


 
Shiga toxin-producing Escherichia Coli and Clostridium difficile coinfection in children with HUS.
FEDERICO GENTILE 1 LUISA SANTANGELO 2 DILETTA DOMENICA TORRES 2 VINCENZA CARBONE 2 SIMONA SIMONE 4 PAOLO GIORDANO 3 MARIO GIORDANO 2

1- PEDIATRIC CLINIC, UNIVERSITY OF BARI, ITALY
2- PEDIATRIC NEPHROLOGY AND DIALYSIS UNIT, PEDIATRIC HOSPITAL GIOVANNI XXIII, BARI, ITALY
3- PEDIATRIC CLINIC, UNIVERSITY OF GENOA, ITALY
4- DEPARTMENT OF EMERGENCY AND ORGAN TRANSPLANTATION - NEPHROLOGY, DIALYSIS AND TRANSPLANTATION UNIT, UNIVERSITY OF BARI ALDO MORO, BARI, ITALY
 
Introduction:

 Shiga toxin-producing Escherichia Coli (STEC) is a foodborne pathogen that may be responsible for severe human gastroenteric infections. Clostridium difficile can cause antibiotic-associated diarrhea in hospitalized patients. Asymptomatic colonization by C. difficile is common during the neonatal period and early infancy (ranging from 21% to 48%) and in childhood. In literature are reported few cases of isolated C. difficile infection associated HUS in an adults and children, but the role of the coinfection in the pathogenesis of HUS has never been investigated. We report three cases of STEC-HUS in children with C. Difficile coinfection.

Material and methods:

 

In the last summer we observed 12 cases of HUS. After early stools collection, microbiological tests were performed, consisting in ST free stool investigation, detection and STEC’s typing. Also were tested for Anti-lipopolysaccharide serum antibodies (anti LPS) against major STEC serotypes. 

 

Results:

All 12 cases were positive to STEC infection and three of them had also microbiological tests positive to C. Difficile. Two of these three children were 2 years old and the third was 9 years old with Sotos syndrome.  The first was positive to STEC O111 and was treated with oral vancomycin, plasmapheresis, hemodialysis and antihypertensive therapy; the second one was positive to STEC O121 and was treated only with plasmapheresis and antihypertensive therapy; the third one was positive to STEC O145 and was treated with oral metronidazole and vancomycin, plasmapheresis and hemodialysis. None had neurological complications. They have been discharged in good clinical condition after 10-12 days of hospitalization on average with other STEC-HUS.  Actually they are in a pediatric nephrological follow up.

 

Conclusions:

After stool test’s positivity for E. Coli and C. difficile, we confirmed STEC-HUS diagnosis in patients with C. difficile co-infection.  It is possible that the C. difficile’ discovery was completely random, but we could hypothesize, based on the pathophysiological knowledge, that C. difficile cytotoxins A and B bind to specific receptors on enterocytes membranes induced apoptosis leading to mucosal breach that consent access of other cytotoxins such as E. Coli’ Shiga Toxin promoting the onset of HUS.  Given the cases’ lack in literature, it might be interesting investigate the role of C. difficile on coinfection STEC-HUS through more dedicated studies.