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[PMID]: 29487233
[Au] Autor:Robertson CD; Hazen TH; Kaper JB; Rasko DA; Hansen AM
[Ad] Address:Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
[Ti] Title:Phosphotyrosine-Mediated Regulation of Enterohemorrhagic Virulence.
[So] Source:MBio;9(1), 2018 Feb 27.
[Is] ISSN:2150-7511
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Enteric pathogens with low infectious doses rely on the ability to orchestrate the expression of virulence and metabolism-associated genes in response to environmental cues for successful infection. Accordingly, the human pathogen enterohemorrhagic (EHEC) employs a complex multifaceted regulatory network to link the expression of type III secretion system (T3SS) components to nutrient availability. While phosphorylation of histidine and aspartate residues on two-component system response regulators is recognized as an integral part of bacterial signaling, the involvement of phosphotyrosine-mediated control is minimally explored in Gram-negative pathogens. Our recent phosphotyrosine profiling study of identified 342 phosphorylated proteins, indicating that phosphotyrosine modifications in bacteria are more prevalent than previously anticipated. The present study demonstrates that tyrosine phosphorylation of a metabolite-responsive LacI/GalR family regulator, Cra, negatively affects T3SS expression under glycolytic conditions that are typical for the colonic lumen environment where production of the T3SS is unnecessary. Our data suggest that Cra phosphorylation affects T3SS expression by modulating the expression of , which encodes the major activator of EHEC virulence gene expression. Phosphorylation of the Cra Y47 residue diminishes DNA binding to fine-tune the expression of virulence-associated genes, including those of the locus of enterocyte effacement pathogenicity island that encode the T3SS, and thereby negatively affects the formation of attaching and effacing lesions. Our data indicate that tyrosine phosphorylation provides an additional mechanism to control the DNA binding of Cra and other LacI/GalR family regulators, including LacI and PurR. This study describes an initial effort to unravel the role of global phosphotyrosine signaling in the control of EHEC virulence potential. Enterohemorrhagic (EHEC) causes outbreaks of hemorrhagic colitis and the potentially fatal hemolytic-uremic syndrome. Successful host colonization by EHEC relies on the ability to coordinate the expression of virulence factors in response to environmental cues. A complex network that integrates environmental signals at multiple regulatory levels tightly controls virulence gene expression. We demonstrate that EHEC utilizes a previously uncharacterized phosphotyrosine signaling pathway through Cra to fine-tune the expression of virulence-associated genes to effectively control T3SS production. This study demonstrates that tyrosine phosphorylation negatively affects the DNA-binding capacity of Cra, which affects the expression of genes related to virulence and metabolism. We demonstrate for the first time that phosphotyrosine-mediated control affects global transcription in EHEC. Our data provide insight into a hitherto unexplored regulatory level of the global network controlling EHEC virulence gene expression.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review

  2 / 5773 MEDLINE  
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[PMID]: 28461395
[Au] Autor:Merrill SA; Brittingham ZD; Yuan X; Moliterno AR; Sperati CJ; Brodsky RA
[Ad] Address:Division of Hematology and.
[Ti] Title:Eculizumab cessation in atypical hemolytic uremic syndrome.
[So] Source:Blood;130(3):368-372, 2017 07 20.
[Is] ISSN:1528-0020
[Cp] Country of publication:United States
[La] Language:eng
[Mh] MeSH terms primary: Antibodies, Monoclonal, Humanized/therapeutic use
Atypical Hemolytic Uremic Syndrome/drug therapy
[Mh] MeSH terms secundary: Antibodies, Monoclonal, Humanized/administration & dosage
Antibodies, Monoclonal, Humanized/economics
Atypical Hemolytic Uremic Syndrome/economics
Atypical Hemolytic Uremic Syndrome/therapy
Drug Administration Schedule
Drug Costs
Female
Follow-Up Studies
Humans
Male
Middle Aged
Recurrence
Renal Dialysis/statistics & numerical data
Retrospective Studies
[Pt] Publication type:LETTER; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Name of substance:0 (Antibodies, Monoclonal, Humanized); A3ULP0F556 (eculizumab)
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:170503
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-02-770214

  3 / 5773 MEDLINE  
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[PMID]: 29216383
[Au] Autor:Kallianpur AR; Bradford Y; Mody RK; Garman KN; Comstock N; Lathrop SL; Lyons C; Saupe A; Wymore K; Canter JA; Olson LM; Palmer A; Jones TF
[Ad] Address:Genomic Medicine Institute, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, Ohio.
[Ti] Title:Genetic Susceptibility to Postdiarrheal Hemolytic-Uremic Syndrome After Shiga Toxin-Producing Escherichia coli Infection: A Centers for Disease Control and Prevention FoodNet Study.
[So] Source:J Infect Dis;217(6):1000-1010, 2018 Mar 05.
[Is] ISSN:1537-6613
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Background: Postdiarrheal hemolytic-uremic syndrome (D+HUS) following Shiga toxin-producing Escherichia coli (STEC) infection is a serious condition lacking specific treatment. Host immune dysregulation and genetic susceptibility to complement hyperactivation are implicated in non-STEC-related HUS. However, genetic susceptibility to D+HUS remains largely uncharacterized. Methods: Patients with culture-confirmed STEC diarrhea, identified through the Centers for Disease Control and Prevention FoodNet surveillance system (2007-2012), were serotyped and classified by laboratory and/or clinical criteria as having suspected, probable, or confirmed D+HUS or as controls and underwent genotyping at 200 loci linked to nondiarrheal HUS or similar pathologies. Genetic associations with D+HUS were explored by multivariable regression, with adjustment for known risk factors. Results: Of 641 enrollees with STEC O157:H7, 80 had suspected D+HUS (41 with probable and 32 with confirmed D+HUS). Twelve genes related to cytokine signaling, complement pathways, platelet function, pathogen recognition, iron transport, and endothelial function were associated with D+HUS in multivariable-adjusted analyses (P ≤ .05). Of 12 significant single-nucleotide polymorphisms (SNPs), 5 were associated with all levels of D+HUS (intergenic SNP rs10874639, TFRC rs3804141, EDN1 rs5370, GP1BA rs121908064, and B2M rs16966334), and 7 SNPs (6 non-complement related) were associated with confirmed D+HUS (all P < .05). Conclusions: Polymorphisms in many non-complement-related genes may contribute to D+HUS susceptibility. These results require replication, but they suggest novel therapeutic targets in patients with D+HUS.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180308
[Lr] Last revision date:180308
[St] Status:In-Data-Review
[do] DOI:10.1093/infdis/jix633

  4 / 5773 MEDLINE  
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[PMID]: 29485195
[Au] Autor:Gurjar BS; Sriharsha TM; Bhasym A; Prabhu S; Puraswani M; Khandelwal P; Saini H; Saini S; Verma AK; Chatterjee P; Gucchait P; Bal V; George A; Rath S; Sahu A; Sharma A; Hari P; Sinha A; Bagga A
[Ad] Address:National Institute of Immunology, Aruna Asaf Ali Road, New Delhi, 110067, India.
[Ti] Title:Characterization of genetic predisposition and autoantibody profile in atypical hemolytic uremic syndrome.
[So] Source:Immunology;, 2018 Feb 27.
[Is] ISSN:1365-2567
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:We previously reported that Indian pediatric patients of atypical hemolytic-uremic syndrome (aHUS) showed high frequencies of anti-complement factor H (FH) autoantibodies that are correlated with homozygous deletion of the genes for FH-related proteins 1 and 3 (FHR1 and FHR3) (FHR1/3-/-). We now report that Indian pediatric aHUS patients without anti-FH autoantibodies also showed modestly higher frequencies of the FHR1/3-/- genotype. Further, when we characterized epitope specificities and binding avidities of anti-FH autoantibodies in aHUS patients, most anti-FH autoantibodies were directed towards the FH cell-surface anchoring polyanionic binding site-containing C-terminal short conservative regions (SCRs) 17-20 with higher binding avidities than for native FH. FH SCR17-20-binding anti-FH autoantibodies also bound the other cell-surface anchoring polyanionic binding site-containing region FH SCR5-8, at lower binding avidities. Anti-FH autoantibody avidities correlated with antibody titres. These anti-FH autoantibody characteristics did not differ between aHUS patients with or without the FHR1/3-/- genotype. Our data suggest a complex matrix of interactions between FHR1-FHR3 deletion, immunomodulation and anti-FH autoantibodies in the etiopathogenesis of aHUS. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180227
[Lr] Last revision date:180227
[St] Status:Publisher
[do] DOI:10.1111/imm.12916

  5 / 5773 MEDLINE  
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[PMID]: 29443761
[Au] Autor:Birlutiu V; Birlutiu RM
[Ad] Address:Lucian Blaga University of Sibiu, Faculty of Medicine Sibiu.
[Ti] Title:Haemolytic-uremic syndrome due to infection with adenovirus: A case report and literature review.
[So] Source:Medicine (Baltimore);97(7):e9895, 2018 Feb.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:RATIONALE: Haemolytic-uremic syndrome is a rare but serious complication of bacterial and viral infections, which is characterized by the triad of: acute renal failure, microangiopathic haemolytic anemia and thrombocytopenia, sometimes severe, requiring peritoneal dialysis. In Europe, hemolytic-uremic syndrome (HUS) in paediatric pathology is primarily caused by Shiga toxin-producing Escherichia coli (STEC) O157, followed by O26. Beside these etiologies, there are other bacterial and viral infections, and also noninfectious ones that have been associated to lead to HUS as well: in the progression of neoplasia, medication-related, post-transplantation, during pregnancy or associated with the antiphospholipid syndrome, systemic lupus erythematosus or family causes with autosomal dominant or recessive inheritance. In terms of pathogenesis, HUS is the result of endothelial injury, most commonly being a result of the action of Shiga toxin. The unfavorable prognosis factors being represented by the age of more than 5 years old, different etiologies from STEC, persistent oligoanuria, central nervous system and glomerular impairment, the association of fever with leukocytosis. HUS is responsible for 7% of cases of hypertension in infants, and an important cause of significant kidney damage in adults. PATIENT CONCERNS: We present one case of HUS caused by adenovirus in a boy of 1 year and 7 months old with severe evolution, which required peritoneal dialysis. DIAGNOSE: Stool sample repeated examination for adenovirus antigen was positive in 2 samples. INTERVENTION: During hospitalization, the patient required 8 peritoneal dialysis sessions. OUTCOME: The renal function was corrected on discharge, the patient required cardiovascular monitoring 1 month after discharge. LESSON: Although the most common cause that leads to HUS remains STEC, other etiologies like viral ones that may be responsible for severe enteric infection with progression into HUS should not be neglected.
[Mh] MeSH terms primary: Acute Kidney Injury
Adenoviridae
Hemolytic-Uremic Syndrome
Peritoneal Dialysis/methods
[Mh] MeSH terms secundary: Acute Kidney Injury/diagnosis
Acute Kidney Injury/etiology
Acute Kidney Injury/therapy
Adenoviridae/immunology
Adenoviridae/isolation & purification
Diagnosis, Differential
Hemolytic-Uremic Syndrome/physiopathology
Hemolytic-Uremic Syndrome/therapy
Hemolytic-Uremic Syndrome/virology
Humans
Infant
Kidney Function Tests/methods
Male
Treatment Outcome
[Pt] Publication type:CASE REPORTS; JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180222
[Lr] Last revision date:180222
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180215
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009895

  6 / 5773 MEDLINE  
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[PMID]: 29208248
[Au] Autor:Sanghera P; Ghanta M; Ozay F; Ariyamuthu VK; Tanriover B
[Ad] Address:Division of Nephrology, University of Texas Southwestern Medical Center, Dallas, Texas.
[Ti] Title:Kidney Diseases Associated With Alternative Complement Pathway Dysregulation and Potential Treatment Options.
[So] Source:Am J Med Sci;354(6):533-538, 2017 12.
[Is] ISSN:1538-2990
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Atypical hemolytic uremic syndrome and C3 glomerulopathy (dense deposit disease and C3 glomerulonephritis) are characterized as inappropriate activation of the alternative complement pathway. Genetic mutations affecting the alternative complement pathway regulating proteins (complement factor H, I, membrane cofactor protein and complement factor H-related proteins) and triggers (such as infection, surgery, pregnancy and autoimmune disease flares) result in the clinical manifestation of these diseases. A decade ago, prognosis of these disease states was quite poor, with most patients developing end-stage renal disease. Furthermore, renal transplantation in these conditions was associated with poor outcomes due to graft loss to recurrent disease. Recent advances in targeted complement inhibitor therapy resulted in significant improvement in disease remission, renal recovery, health-related quality of life and allograft survival.
[Mh] MeSH terms primary: Complement Pathway, Alternative/physiology
Kidney Diseases/etiology
[Mh] MeSH terms secundary: Atypical Hemolytic Uremic Syndrome/drug therapy
Atypical Hemolytic Uremic Syndrome/etiology
Complement Inactivating Agents/therapeutic use
Complement Pathway, Alternative/drug effects
Glomerulonephritis/drug therapy
Glomerulonephritis/etiology
Glomerulonephritis, Membranoproliferative/drug therapy
Glomerulonephritis, Membranoproliferative/etiology
Humans
[Pt] Publication type:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Name of substance:0 (Complement Inactivating Agents)
[Em] Entry month:1712
[Cu] Class update date: 180223
[Lr] Last revision date:180223
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:171207
[St] Status:MEDLINE

  7 / 5773 MEDLINE  
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[PMID]: 29308852
[Au] Autor:Demyanova KA; Kozlovskaya NL; Bobrova LA; Kozlov LV; Andina SS; Yurova VA; Kuchieva AM; Roshchupkina SV; Shilov EM
[Ti] Title:Complement System Abnormalities in Patients with Atypical Hemolytic Uremic Syndrome and Catastrophic Antiphospholipid Syndrome.
[So] Source:Vestn Ross Akad Med Nauk;72(1):42-52, 2017.
[Is] ISSN:0869-6047
[Cp] Country of publication:Russia (Federation)
[La] Language:eng
[Ab] Abstract:Background: The role of the alternative complement pathway (AP) abnormalities in the pathogenesis of aHUS is well studied. Clinical and morphological manifestations of atypical HUS and catastrophic APS are often similar. However, studies on the state of AP in patients with CAPS are virtually absent. Aims: The aim of our study was to assess the state of AP in patients with CAPS and aHUS. Patients and methods: The study enrolled 67 patients (pts) with a diagnosis of CAPS (28 pts) and aHUS (39 pts). Studies of the complement system are made of 10 pts with CAPS and 20 aHUS. Factor H, I, B, D content, functional activity of factor H, and complement components C3, C4 was determined in serum by ELISA kit. Results: Patients with CAPS and aHUS showed similar changes in complement biomarkers. The factor H level in the serum was significantly higher than the standard value. However, the specific activity of factor H reduced, mean rate 59% for aHUS and 26% for CAPS. The median value of factor D was twice higher than the normal range in both groups, indicating the activation of the AP. Conclusions: There are indications of an AP activation not only in pts with aHUS but in CAPS pts too. We suppose that the activity of factor H is a more sensitive indicator of complement system changes than factor H level. Patients with CAPS and aHUS have similar clinical and laboratory characteristics. However, CAPS is more severe, with the involvement of a larger number of vascular beds. Perhaps this is due to the double damaging effects on the endothelium ­ of antiphospholipid antibodies (aPL) and activated complement. So we hypothesize that CAPS can be called aPL-mediated TMA in pts with a complement system defect.
[Mh] MeSH terms primary: Antiphospholipid Syndrome
Atypical Hemolytic Uremic Syndrome
Complement Factor H
Complement System Proteins
Thrombotic Microangiopathies/metabolism
[Mh] MeSH terms secundary: Adult
Antibodies, Antiphospholipid/blood
Antiphospholipid Syndrome/diagnosis
Antiphospholipid Syndrome/metabolism
Antiphospholipid Syndrome/physiopathology
Atypical Hemolytic Uremic Syndrome/diagnosis
Atypical Hemolytic Uremic Syndrome/metabolism
Atypical Hemolytic Uremic Syndrome/physiopathology
Complement Factor H/analysis
Complement Factor H/metabolism
Complement Pathway, Alternative
Complement System Proteins/analysis
Complement System Proteins/metabolism
Endothelium, Vascular/metabolism
Endothelium, Vascular/physiopathology
Female
Humans
Male
Statistics as Topic
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Name of substance:0 (Antibodies, Antiphospholipid); 80295-65-4 (Complement Factor H); 9007-36-7 (Complement System Proteins)
[Em] Entry month:1802
[Cu] Class update date: 180220
[Lr] Last revision date:180220
[Js] Journal subset:IM
[Da] Date of entry for processing:180109
[St] Status:MEDLINE
[do] DOI:10.15690/vramn769

  8 / 5773 MEDLINE  
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[PMID]: 29390523
[Au] Autor:Freist M; Garrouste C; Szlavik N; Coppo P; Lautrette A; Heng AE
[Ad] Address:Service de Néphrologie, Pôle REUNNIRH, CHU Clermont-Ferrand, Clermont-Ferrand.
[Ti] Title:Efficacy of eculizumab in an adult patient with HIV-associated hemolytic uremic syndrome: A case report.
[So] Source:Medicine (Baltimore);96(51):e9358, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:INTRODUCTION: Hemolytic uremic syndrome (HUS) in Human Immunodeficiency Virus (HIV)-positive patients has become a rare cause of kidney injury since the era of highly active antiretroviral therapy (HAART). Plasma exchange and antiretroviral therapy were previously recommended but often failed to achieve remission. We report a case of HUS in a HIV-positive patient treated successfully with eculizumab. CASE SUMMARY: A 52-year-old woman presented to hospital with acute renal failure, thrombocytopenia, anemia, and hypoxemia. She had been diagnosed with HIV infection in 1997. Kidney biopsy showed several fibrinous microthrombi in the glomerular capillaries, formation of thrombi in arterioles, moderate parietal and mesangial deposits of C3 and Immunoglobulin M, and intense glomerular and arterial deposits of Complement component 5b9 complement component. Serum HIV viral load was 227,848 copies/mL, and CD4 lymphocyte count was 120 cells/µL. A diagnosis of HIV-associated HUS was made. The patient had no confounding cause of HUS. Initiation of eculizumab and HAART resulted in complete hematological remission on day 32 and dialysis withdrawal on day 110. The patient has not relapsed during long-term follow-up (M17). CONCLUSION: This observation suggests that eculizumab can achieve remission in HIV patients with HUS.
[Mh] MeSH terms primary: Antibodies, Monoclonal, Humanized/therapeutic use
Antibodies, Monoclonal/therapeutic use
HIV Infections/complications
Hemolytic-Uremic Syndrome/complications
Hemolytic-Uremic Syndrome/therapy
[Mh] MeSH terms secundary: Acute Kidney Injury/diagnosis
Acute Kidney Injury/etiology
Antiretroviral Therapy, Highly Active/methods
Biopsy, Needle
Female
Follow-Up Studies
HIV Infections/diagnosis
HIV Infections/drug therapy
Hemolytic-Uremic Syndrome/diagnosis
Humans
Immunohistochemistry
Kidney Function Tests
Middle Aged
Plasma Exchange/methods
Renal Dialysis/methods
Risk Assessment
Treatment Outcome
[Pt] Publication type:JOURNAL ARTICLE
[Nm] Name of substance:0 (Antibodies, Monoclonal); 0 (Antibodies, Monoclonal, Humanized); A3ULP0F556 (eculizumab)
[Em] Entry month:1802
[Cu] Class update date: 180219
[Lr] Last revision date:180219
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180203
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009358

  9 / 5773 MEDLINE  
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[PMID]: 29447477
[Au] Autor:Li CH; Bai YL; Chen YC
[Ad] Address:a Department of Applied Chemistry , National Chiao Tung University , Hsinchu , Taiwan.
[Ti] Title:Inhibition of the lethality of Shiga-like toxin-1 by functional gold nanoparticles.
[So] Source:Artif Cells Nanomed Biotechnol;:1-11, 2018 Feb 15.
[Is] ISSN:2169-141X
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Escherichia coli O157:H7 is a pathogen, which can generate Shiga-like toxins (SLTs) and cause hemolytic-uremic syndrome. Foodborne illness outbreaks caused by E. coli O157:H7 have become a global issue. Since SLTs are quite toxic, effective medicines that can reduce the damage caused by SLTs should be explored. SLTs consist of a single A and five B subunits, which can inhibit ribosome activity for protein synthesis and bind with the cell membrane of host cells, respectively. Pigeon ovalbumin (POA), i.e. a glycoprotein, is abundant in pigeon egg white (PEW) proteins. The structure of POA contains Gal-α(1→4)-Gal-ß(1→4)-GlcNAc ligands, which have binding affinity toward the B subunit in SLT type-1 (SLT-1B). POA immobilized gold nanoparticles (POA-Au NPs) can be generated by reacting PEW proteins with aqueous tetrachloroauric acid in one-pot. The generated POA-Au NPs have been demonstrated to have selective trapping-capacity toward SLT-1B previously. Herein, we explore that POA-Au NPs can be used as protective agents to neutralize the toxicity of SLT-1 in SLT-1-infected model cells. The results show that the cells can be completely rescued when a sufficient amount of POA-Au NPs is used to treat the SLT-1-infected cells within 1 h.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180215
[Lr] Last revision date:180215
[St] Status:Publisher
[do] DOI:10.1080/21691401.2018.1438449

  10 / 5773 MEDLINE  
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[PMID]: 29429664
[Au] Autor:Sarc A; Kosel J; Stopar D; Oder M; Dular M
[Ad] Address:University of Ljubljana, Faculty of Mechanical Engineering, Askerceva 6, 1000 Ljubljana, Slovenia.
[Ti] Title:Removal of bacteria Legionella pneumophila, Escherichia coli, and Bacillus subtilis by (super)cavitation.
[So] Source:Ultrason Sonochem;42:228-236, 2018 Apr.
[Is] ISSN:1873-2828
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:In sufficient concentrations, the pathogenic bacteria L. pneumophila can cause a respiratory illness that is known as the "Legionnaires" disease. Moreover, toxic Shiga strains of bacteria E. coli can cause life-threatening hemolytic-uremic syndrome. Because of the recent restrictions imposed on the usage of chlorine, outbreaks of these two bacterial species have become more common. In this study we have developed a novel rotation generator and its effectiveness against bacteria Legionella pneumophila and Escherichia coli was tested for various types of hydrodynamic cavitation (attached steady cavitation, developed unsteady cavitation and supercavitation). The results show that the supercavitation was the only effective form of cavitation. It enabled more than 3 logs reductions for both bacterial species and was also effective against a more persistent Gram positive bacteria, B. subtilis. The deactivation mechanism is at present unknown. It is proposed that when bacterial cells enter a supercavitation cavity, an immediate pressure drop occurs and this results in bursting of the cellular membrane. The new rotation generator that induced supercavitation proved to be economically and microbiologically far more effective than the classical Venturi section (super)cavitation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180212
[Lr] Last revision date:180212
[St] Status:In-Process


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