Of the infection could be demonstrated, however, stool frequency was reduced [45]. Antibody to E. coli lipopolysaccharide (LPS) also has the potential of therapeutic use through its blocking effect on adherence of STEC to the human 3-Nitro-6-(trifluoromethyl)pyridin-2(1H)-one intestinal epithelial (Henle 407) cell line [46]. Likewise, human trials would be needed to show clinical effectiveness.Other toxin binders/neutralizersMost of these agents bind to toxin directly and inhibit the binding to its receptor present on the target cellsGoldwater and Bettelheim BMC Medicine 2012, 10:12 http://www.biomedcentral.com/1741-7015/10/Page 4 ofTable 1 Approach to management: summarizing trialed and experimental treatments.Problem Fluid and electrolyte imbalance Treatment Intravenous fluids Detail and comments Fluid balance and attention to the volume and sodium content of intravenous fluids administered early in the disease have been shown to reduce the risk of developing oligoanuric HUS after Escherichia coli O157:H7 infections Intravenous fluids within first 4 days of onset of diarrhea (isotonic preferable). The overall oligoanuric rate of the 50 participants was 68 , but was 84 among those not given intravenous fluids in the first 4 days of illness. The relative risk of oligoanuria when fluids were not given in this interval was 1.6 (95 CI, 1.1 to PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/8086425 2.4; P = 0.02). Children with oligoanuric HUS were given less total intravenous fluid (r = -0.32; P = 0.02) and sodium (r = -0.27; P = 0.05) in the first 4 days of illness than those without oligoanuria. Acute renal failure Acute renal replacement therapy Peritoneal dialysis (safe with thrombocytopenia) Hemodialysis Plasma infusion and plasma exchange Uncertain benefit Where indicated Transfusion (packed red cells) Platelet transfusion (usually avoided) Antibiotics Generally to be avoided because of VT/Stx/endotoxin release from dying/ dead bacteria. b-lactams to be avoided. Subinhibitory levels may increase toxin production/release The quinolone ciprofloxacin but not fosfomycin causes Shiga toxinencoding bacteriophage induction and enhanced Stx production from E. coli O157:H7 in vitro and in vivo in a mouse model. Fosfomycin showed evidence of better outcomes in a mouse-model of STEC infection and was recommended for human studies. Similar results were observed in a gnotobiotic piglet model. Pooled prospective data showed no benefit of antibiotics There is only a single study purportedly connecting fosfomycin with a reduced risk of HUS Fosfomycin benefit in humans remains in doubt. The validity of the study has been questioned on the basis that the meta-analysis mischaracterized fosfomycin as being superior to no PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/17591728 antibiotics. Lumenal toxin neutralisers: Synthetic ligand mimics Modified bacteria decorated with Gb3 or Gb4 Super Twig (Gb3 polymer) Antibodies: 1H Monoclonal against A subunit Oral bovine colostrum LPS antibodies Receptor 3-(2,4-Dichlorophenoxy)azetidine blockers and toxin intracellular transport inhibitors Synsorb K; trial showed no benefit Not yet trialed Clinical trials awaited Protective in lethally-challenged animals refs [25][24][26] [27] [28] [29] [13,30] [13] [13,30] [13] [39] [32] [33,34]Apheresis Antihypertensives Hematological: hemolytic anemia Hematological: thrombocytopenia Preventing further effects of toxin[35][36][37] [40][41]No effect on complications; decreases stool frequency but not STEC carriage [42] Reduces in vitro adherence. No human data. Experimental only. Ac-PPP-tet blocks intracellular transport of Stx2 from Golgi to endoplasmic reticulum.