CASE REPORT
Group A Escherichia coli-Related Purpura Fulminans: an Unusual Manifestation Due to an Unusual Strain? Marlène Amara,a Stéphane Bonacorsi,b,c,d Jérôme Bedel,e Jean-Paul Mira,f Virginie Laurent,e Koryna Socha,g Fabrice Bruneel,e Béatrice Pangon,a Jean-Pierre Bédos,e David Grimaldie
We describe an exceptional case of life-threatening group A Escherichia coli-induced purpura fulminans. Genotyping of common polymorphisms in genes involved in innate immunity or coagulation did not reveal known susceptibility to such a manifestation. Genetic analysis of the strain revealed an unusual conserved virulence plasmidic region, pointing out its potential virulence. CASE REPORT
A
53-year-old woman had a medical history of penicillin allergy and morbid obesity (body mass index [BMI], 46 kg/m2), treated by a banding gastroplasty in 2007. In 2009, she suffered from gastric necrosis complicated by peritonitis associated with a first episode of Escherichia coli bacteremia. At that time, she presented with septic shock without disseminated intravascular coagulation (DIC). She underwent a total gastrectomy with esojejunal anastomosis. Following gastrectomy, her BMI decreased dramatically, to 16 kg/m2. In May 2013, she presented at the emergency department with weakness. Her central body temperature was 38.6°C, with a heart rate of 144 beats/min and blood pressure of 85/52 mm Hg. A physical exam did not point to a particular site of infection. A thoracoabdominal computed tomography (CT) scan did not show an infectious process. Laboratory results showed evidence of severe sepsis: a C-reactive protein level of 113 mg/liter, leukocyte count of 1.8 ⫻ 109/liter, prothrombin ratio of 59%, and arterial lactate level of 7.3 mmol/liter. The other results were normal: creatininemia at 80 mol/liter, platelet count of 201 ⫻ 109/liter, factor V level of 81%, and creatine phosphokinase (CPK) level of 111 IU/liter. Administration of vancomycin, aztreonam, and gentamicin was initiated, along with fluid loading of 3 liters crystalloids and continuous noradrenalin infusion up to 2.4 g/kg of body weight/min. The patient was referred to the intensive care unit (ICU), and 6 h after admission, she suddenly developed diffuse map-like purple skin lesions that were particularly prominent in the lower limbs (Fig. 1A and B). The legs became cold and mottled. Simultaneously, she developed multiorgan failure and severe DIC (platelet count, 36 ⫻ 109/liter; prothrombin rate, 32%; factor V, 31%; D dimers, 1,830 ng/ml). Arterial Doppler examination of the legs ruled out arterial thrombosis. The diagnosis of purpura fulminans was made. Fresh frozen plasma and platelet concentrate were transfused. The patient’s status slowly improved; the coagulation tests normalized at day 3, and the patient was weaned off norepinephrine at day 7. By day 20, the patient underwent surgical debridement of cutaneous and subcutaneous tissues. After 12 weeks in the ICU, she was discharged in the hospital ward for renutrition. A skin graft was performed after 5 months. The
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two blood cultures drawn at ICU admission, as well as a cutaneous biopsy specimen of a necrotic lesion, grew with a penicillinaseproducing E. coli strain identified using a Microflex matrix-assisted laser desorption ionization–time-of-flight (MALDI-TOF) mass spectrometer (Bruker, Germany). Histopathological exam of the skin was in accordance with the diagnosis of purpura fulminans (Fig. 1C). The cytobacteriological examination of urine was negative. Following written consent, 32 well-characterized human genetic polymorphisms associated with severe sepsis susceptibility were searched for (1). The patient’s genotyping did not reveal any variant of the genes associated with Gram-negative detection (Toll-like receptor 2 [TLR2], TLR4, and CD14 genes) (2), severity of sepsis (tumor necrosis factor alpha [TNF-␣], interleukin 6 [IL-6], and IL-10 genes) (3), and coagulation disorders (coagulation factor V, tissue factor, protein C receptor endothelial, thrombin, and PAI-1 genes) (4). The 2009 and 2013 E. coli strains were further characterized by multilocus sequence typing (MLST). Both the 2009 and 2013 strains belonged to phylogenetic group A, and they harbored sequence types ST398 and ST10, respectively. The search for 14 virulence factors (VFs) was performed by PCR as previously described (5, 6). The 2013 strain did not carry any of the adhesin/invasin (Pap, Sfa, and IbeA) nor any of the toxin (Hly, Cnf-1, Sat, Vat, and colibactin) genes sought. Interestingly, it harbored two iron acquisition systems, yersiniabactin and salmochelin, and the sit system; plasmidic ompT (ompTp), encoding a putative outer membrane protease (omptin), and cva, encoding colicin V, hlyF, encoding ␣-hemolysin, a pore-forming toxin, the ets operon, encoding a type I secretion system, and iss, the increased serum survival gene. This combination of genes, together with the aerobactin gene, lacking in this
Received 15 May 2014 Returned for modification 13 June 2014 Accepted 8 September 2014 Published ahead of print 17 September 2014 Editor: W. M. Dunne, Jr. Address correspondence to David Grimaldi, [email protected]. Copyright © 2014, American Society for Microbiology. All Rights Reserved. doi:10.1128/JCM.01362-14
p. 4404 – 4406
December 2014 Volume 52 Number 12
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
Service de Biologie, Unité de Microbiologie, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Francea; IAME, UMR 1137, INSERM, Paris, Franceb; IAME, UMR 1137, Université Paris Diderot, Sorbonne Paris Cité, Paris, Francec; Service de Microbiologie, Hôpital Robert-Debré, AP-HP, Centre National de Référence Associé Escherichia coli, Paris, Franced; Service de Réanimation, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Francee; Service de Réanimation, Centre Hospitalier Universitaire Cochin Saint Vincent de Paul, AP-HP, Paris, Francef; Service d’Anatomo-Pathologie, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Franceg
Case Report
around the vessels, extravasated erythrocytes, and edema of the dermis.
observation, is considered to be the signature of the conserved virulence plasmidic (CVP) region, which contains eight operons or genes amplified by multiplex PCR, as previously described (7). A complete or almost-complete CVP region has been identified in sequenced plasmids of human, avian, and environmental origins (7–11). The 2009 strain carried neither the CVP region genes nor any of the VFs sought.
Purpura fulminans is a life-threatening condition caused by a sudden and severe DIC, typically caused by meningococcemia and sometimes pneumococcemia, but Escherichia coli-related purpura fulminans remains exceptional (12, 13). Extraintestinal pathogenic Escherichia coli (ExPEC) infections represent a growing public health concern (14, 15). Strains commonly belong to phylogenic groups B2 and D (16) and lead to various clinical features, such as urinary tract infections, meningitis, and occasionally severe skin infections (17), (18). Phylogenic group A is, along with the B1 group, the group to which almost all commensal strains belong (19). However, some of these strains may be responsible for severe invasive infections, and we recently showed that the CVP region contributes to the extraintestinal virulence of E. coli isolates belonging to these phylogroups (7). We describe herein an unusual case of commensal group A E. coli-related purpura fulminans in a patient that had previously exhibited an episode of E. coli bacteremia without such presentation. At the time of the second bacteremia, the patient had experienced a total gastrectomy and severe weight loss. The alteration of the gastrointestinal tract anatomy may predispose to bacterial translocation, and malnutrition could increase the severity of the infection; however, neither of these two factors is involved in DIC. The absence of DIC during the first episode of bacteremia, together with the fact that known genetic markers for increased susceptibility to DIC were lacking in the host, suggest that the
December 2014 Volume 52 Number 12
unusual presentation was related to the pathogen’s genotype and possibly to the presence of the CVP region, since the strain does not carry other particular VFs. In conclusion, this observation points out the potential virulence associated with the CVP region, which could be involved in the emergence of “unconventional” ExPEC belonging to human commensal phylogroups A/B1 (7) and should be explored in further studies. The role of bacterial genetic determinants such as the CVP region in this life-threatening syndrome remains to be elucidated. ACKNOWLEDGMENTS We thank Christophe Rousseau for his technical help with genotyping and Maher Anous for his help in the redaction of the manuscript.
REFERENCES 1. Descheemaeker P-N, Mira J-P, Bruneel F, Houzé S, Tanguy M, Gangneux J-P, Flecher E, Rousseau C, Le Bras J, Mallédant Y. 2009. Nearfatal multiple organ dysfunction syndrome induced by Plasmodium malariae. Emerg. Infect. Dis. 15:832– 834. http://dx.doi.org/10.3201/eid1505 .081091. 2. Bochud P-Y, Bochud M, Telenti A, Calandra T. 2007. Innate immunogenetics: a tool for exploring new frontiers of host defence. Lancet Infect. Dis. 7:531–542. http://dx.doi.org/10.1016/S1473-3099(07)70185-8. 3. Sutherland AM, Walley KR. 2009. Bench-to-bedside review: association of genetic variation with sepsis. Crit. Care (Lond. Engl.) 13:210. http://dx .doi.org/10.1186/cc7702. 4. Texereau J, Pene F, Chiche J-D, Rousseau C, Mira J-P. 2004. Importance of hemostatic gene polymorphisms for susceptibility to and outcome of severe sepsis. Crit. Care Med. 32:S313–S319. http://dx.doi.org/10 .1097/01.CCM.0000126363.46191.DC. 5. Mahjoub-Messai F, Bidet P, Caro V, Diancourt L, Biran V, Aujard Y, Bingen E, Bonacorsi S. 2011. Escherichia coli isolates causing bacteremia via gut translocation and urinary tract infection in young infants exhibit different virulence genotypes. J. Infect. Dis. 203:1844 –1849. http://dx.doi .org/10.1093/infdis/jir189. 6. Bidet P, Mahjoub-Messai F, Blanco J, Blanco J, Dehem M, Aujard Y, Bingen E, Bonacorsi S. 2007. Combined multilocus sequence typing and
jcm.asm.org 4405
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
FIG 1 (A and B) Bilateral necrotic leg lesions of purpura fulminans. (C) Histopathological exam of the skin revealed a sparse infiltrate of often altered neutrophils
Case Report
7.
8.
9.
11.
12.
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13.
14.
15.
16.
17.
18.
19.
coli septicemia. Wien. Klin. Wochenschr. 116:82. http://dx.doi.org/10 .1007/BF03040700. Helviz Y, Hersch M, Shmuelevitz L, Atrash J, Einav S. 2011. Bad to worse. Am. J. Med. 124:215–217. http://dx.doi.org/10.1016/j.amjmed .2010.11.007. Russo TA, Johnson JR. 2003. Medical and economic impact of extraintestinal infections due to Escherichia coli: focus on an increasingly important endemic problem. Microbes Infect. 5:449 – 456. http://dx.doi.org/10 .1016/S1286-4579(03)00049-2. de Kraker MEA, Jarlier V, Monen JCM, Heuer OE, van de Sande N, Grundmann H. 2013. The changing epidemiology of bacteraemias in Europe: trends from the European Antimicrobial Resistance Surveillance System. Clin. Microbiol. Infect. 19:860 – 868. http://dx.doi.org/10.1111 /1469-0691.12028. Johnson JR, Russo TA. 2002. Extraintestinal pathogenic Escherichia coli: “the other bad E coli.” J. Lab. Clin. Med. 139:155–162. http://dx.doi.org /10.1067/mlc.2002.121550. Grimaldi D, Bonacorsi S, Roussel H, Zuber B, Poupet H, Chiche J-D, Poyart C, Mira JP. 2010. Unusual “flesh-eating” strain of Escherichia coli. J. Clin. Microbiol. 48:3794 –3796. http://dx.doi.org/10.1128/JCM.00491-10. Petkovsek Z, Elersic K, Gubina M, Zgur-Bertok D, Starcic Erjavec M. 2009. Virulence potential of Escherichia coli isolates from skin and soft tissue infections. J. Clin. Microbiol. 47:1811–1817. http://dx.doi.org/10 .1128/JCM.01421-08. Escobar-Páramo P, Clermont O, Blanc-Potard A-B, Bui H, Le Bouguénec C, Denamur E. 2004. A specific genetic background is required for acquisition and expression of virulence factors in Escherichia coli. Mol. Biol. Evol. 21:1085–1094. http://dx.doi.org/10.1093/molbev/msh118.
Journal of Clinical Microbiology
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
10.
O serogrouping distinguishes Escherichia coli subtypes associated with infant urosepsis and/or meningitis. J. Infect. Dis. 196:297–303. http://dx .doi.org/10.1086/518897. Lemaître C, Mahjoub-Messai F, Dupont D, Caro V, Diancourt L, Bingen E, Bidet P, Bonacorsi S. 2013. A conserved virulence plasmidic region contributes to the virulence of the multiresistant Escherichia coli meningitis strain S286 belonging to phylogenetic group C. PLoS One 8:e74423. http://dx.doi.org/10.1371/journal.pone.0074423. Johnson TJ, Siek KE, Johnson SJ, Nolan LK. 2006. DNA sequence of a ColV plasmid and prevalence of selected plasmid-encoded virulence genes among avian Escherichia coli strains. J. Bacteriol. 188:745–758. http://dx .doi.org/10.1128/JB.188.2.745-758.2006. Peigne C, Bidet P, Mahjoub-Messai F, Plainvert C, Barbe V, Médigue C, Frapy E, Nassif X, Denamur E, Bingen E, Bonacorsi S. 2009. The plasmid of Escherichia coli strain S88 (O45:K1:H7) that causes neonatal meningitis is closely related to avian pathogenic E. coli plasmids and is associated with high-level bacteremia in a neonatal rat meningitis model. Infect. Immun. 77:2272–2284. http://dx.doi.org/10.1128/IAI.01333-08. Johnson TJ, Jordan D, Kariyawasam S, Stell AL, Bell NP, Wannemuehler YM, Alarcón CF, Li G, Tivendale KA, Logue CM, Nolan LK. 2010. Sequence analysis and characterization of a transferable hybrid plasmid encoding multidrug resistance and enabling zoonotic potential for extraintestinal Escherichia coli. Infect. Immun. 78:1931–1942. http://dx .doi.org/10.1128/IAI.01174-09. Tivendale KA, Noormohammadi AH, Allen JL, Browning GF. 2009. The conserved portion of the putative virulence region contributes to virulence of avian pathogenic Escherichia coli. Microbiology (Reading, Engl.) 155:450 – 460. http://dx.doi.org/10.1099/mic.0.023143-0. Huemer GM, Bonatti H, Dunst KM. 2004. Purpura fulminans due to E.
Group A Escherichia coli-Related Purpura Fulminans: an Unusual Manifestation Due to an Unusual Strain? Marlène Amara,a Stéphane Bonacorsi,b,c,d Jérôme Bedel,e Jean-Paul Mira,f Virginie Laurent,e Koryna Socha,g Fabrice Bruneel,e Béatrice Pangon,a Jean-Pierre Bédos,e David Grimaldie
We describe an exceptional case of life-threatening group A Escherichia coli-induced purpura fulminans. Genotyping of common polymorphisms in genes involved in innate immunity or coagulation did not reveal known susceptibility to such a manifestation. Genetic analysis of the strain revealed an unusual conserved virulence plasmidic region, pointing out its potential virulence. CASE REPORT
A
53-year-old woman had a medical history of penicillin allergy and morbid obesity (body mass index [BMI], 46 kg/m2), treated by a banding gastroplasty in 2007. In 2009, she suffered from gastric necrosis complicated by peritonitis associated with a first episode of Escherichia coli bacteremia. At that time, she presented with septic shock without disseminated intravascular coagulation (DIC). She underwent a total gastrectomy with esojejunal anastomosis. Following gastrectomy, her BMI decreased dramatically, to 16 kg/m2. In May 2013, she presented at the emergency department with weakness. Her central body temperature was 38.6°C, with a heart rate of 144 beats/min and blood pressure of 85/52 mm Hg. A physical exam did not point to a particular site of infection. A thoracoabdominal computed tomography (CT) scan did not show an infectious process. Laboratory results showed evidence of severe sepsis: a C-reactive protein level of 113 mg/liter, leukocyte count of 1.8 ⫻ 109/liter, prothrombin ratio of 59%, and arterial lactate level of 7.3 mmol/liter. The other results were normal: creatininemia at 80 mol/liter, platelet count of 201 ⫻ 109/liter, factor V level of 81%, and creatine phosphokinase (CPK) level of 111 IU/liter. Administration of vancomycin, aztreonam, and gentamicin was initiated, along with fluid loading of 3 liters crystalloids and continuous noradrenalin infusion up to 2.4 g/kg of body weight/min. The patient was referred to the intensive care unit (ICU), and 6 h after admission, she suddenly developed diffuse map-like purple skin lesions that were particularly prominent in the lower limbs (Fig. 1A and B). The legs became cold and mottled. Simultaneously, she developed multiorgan failure and severe DIC (platelet count, 36 ⫻ 109/liter; prothrombin rate, 32%; factor V, 31%; D dimers, 1,830 ng/ml). Arterial Doppler examination of the legs ruled out arterial thrombosis. The diagnosis of purpura fulminans was made. Fresh frozen plasma and platelet concentrate were transfused. The patient’s status slowly improved; the coagulation tests normalized at day 3, and the patient was weaned off norepinephrine at day 7. By day 20, the patient underwent surgical debridement of cutaneous and subcutaneous tissues. After 12 weeks in the ICU, she was discharged in the hospital ward for renutrition. A skin graft was performed after 5 months. The
4404
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Journal of Clinical Microbiology
two blood cultures drawn at ICU admission, as well as a cutaneous biopsy specimen of a necrotic lesion, grew with a penicillinaseproducing E. coli strain identified using a Microflex matrix-assisted laser desorption ionization–time-of-flight (MALDI-TOF) mass spectrometer (Bruker, Germany). Histopathological exam of the skin was in accordance with the diagnosis of purpura fulminans (Fig. 1C). The cytobacteriological examination of urine was negative. Following written consent, 32 well-characterized human genetic polymorphisms associated with severe sepsis susceptibility were searched for (1). The patient’s genotyping did not reveal any variant of the genes associated with Gram-negative detection (Toll-like receptor 2 [TLR2], TLR4, and CD14 genes) (2), severity of sepsis (tumor necrosis factor alpha [TNF-␣], interleukin 6 [IL-6], and IL-10 genes) (3), and coagulation disorders (coagulation factor V, tissue factor, protein C receptor endothelial, thrombin, and PAI-1 genes) (4). The 2009 and 2013 E. coli strains were further characterized by multilocus sequence typing (MLST). Both the 2009 and 2013 strains belonged to phylogenetic group A, and they harbored sequence types ST398 and ST10, respectively. The search for 14 virulence factors (VFs) was performed by PCR as previously described (5, 6). The 2013 strain did not carry any of the adhesin/invasin (Pap, Sfa, and IbeA) nor any of the toxin (Hly, Cnf-1, Sat, Vat, and colibactin) genes sought. Interestingly, it harbored two iron acquisition systems, yersiniabactin and salmochelin, and the sit system; plasmidic ompT (ompTp), encoding a putative outer membrane protease (omptin), and cva, encoding colicin V, hlyF, encoding ␣-hemolysin, a pore-forming toxin, the ets operon, encoding a type I secretion system, and iss, the increased serum survival gene. This combination of genes, together with the aerobactin gene, lacking in this
Received 15 May 2014 Returned for modification 13 June 2014 Accepted 8 September 2014 Published ahead of print 17 September 2014 Editor: W. M. Dunne, Jr. Address correspondence to David Grimaldi, [email protected]. Copyright © 2014, American Society for Microbiology. All Rights Reserved. doi:10.1128/JCM.01362-14
p. 4404 – 4406
December 2014 Volume 52 Number 12
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
Service de Biologie, Unité de Microbiologie, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Francea; IAME, UMR 1137, INSERM, Paris, Franceb; IAME, UMR 1137, Université Paris Diderot, Sorbonne Paris Cité, Paris, Francec; Service de Microbiologie, Hôpital Robert-Debré, AP-HP, Centre National de Référence Associé Escherichia coli, Paris, Franced; Service de Réanimation, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Francee; Service de Réanimation, Centre Hospitalier Universitaire Cochin Saint Vincent de Paul, AP-HP, Paris, Francef; Service d’Anatomo-Pathologie, Centre Hospitalier de Versailles—Site André Mignot, Le Chesnay, Franceg
Case Report
around the vessels, extravasated erythrocytes, and edema of the dermis.
observation, is considered to be the signature of the conserved virulence plasmidic (CVP) region, which contains eight operons or genes amplified by multiplex PCR, as previously described (7). A complete or almost-complete CVP region has been identified in sequenced plasmids of human, avian, and environmental origins (7–11). The 2009 strain carried neither the CVP region genes nor any of the VFs sought.
Purpura fulminans is a life-threatening condition caused by a sudden and severe DIC, typically caused by meningococcemia and sometimes pneumococcemia, but Escherichia coli-related purpura fulminans remains exceptional (12, 13). Extraintestinal pathogenic Escherichia coli (ExPEC) infections represent a growing public health concern (14, 15). Strains commonly belong to phylogenic groups B2 and D (16) and lead to various clinical features, such as urinary tract infections, meningitis, and occasionally severe skin infections (17), (18). Phylogenic group A is, along with the B1 group, the group to which almost all commensal strains belong (19). However, some of these strains may be responsible for severe invasive infections, and we recently showed that the CVP region contributes to the extraintestinal virulence of E. coli isolates belonging to these phylogroups (7). We describe herein an unusual case of commensal group A E. coli-related purpura fulminans in a patient that had previously exhibited an episode of E. coli bacteremia without such presentation. At the time of the second bacteremia, the patient had experienced a total gastrectomy and severe weight loss. The alteration of the gastrointestinal tract anatomy may predispose to bacterial translocation, and malnutrition could increase the severity of the infection; however, neither of these two factors is involved in DIC. The absence of DIC during the first episode of bacteremia, together with the fact that known genetic markers for increased susceptibility to DIC were lacking in the host, suggest that the
December 2014 Volume 52 Number 12
unusual presentation was related to the pathogen’s genotype and possibly to the presence of the CVP region, since the strain does not carry other particular VFs. In conclusion, this observation points out the potential virulence associated with the CVP region, which could be involved in the emergence of “unconventional” ExPEC belonging to human commensal phylogroups A/B1 (7) and should be explored in further studies. The role of bacterial genetic determinants such as the CVP region in this life-threatening syndrome remains to be elucidated. ACKNOWLEDGMENTS We thank Christophe Rousseau for his technical help with genotyping and Maher Anous for his help in the redaction of the manuscript.
REFERENCES 1. Descheemaeker P-N, Mira J-P, Bruneel F, Houzé S, Tanguy M, Gangneux J-P, Flecher E, Rousseau C, Le Bras J, Mallédant Y. 2009. Nearfatal multiple organ dysfunction syndrome induced by Plasmodium malariae. Emerg. Infect. Dis. 15:832– 834. http://dx.doi.org/10.3201/eid1505 .081091. 2. Bochud P-Y, Bochud M, Telenti A, Calandra T. 2007. Innate immunogenetics: a tool for exploring new frontiers of host defence. Lancet Infect. Dis. 7:531–542. http://dx.doi.org/10.1016/S1473-3099(07)70185-8. 3. Sutherland AM, Walley KR. 2009. Bench-to-bedside review: association of genetic variation with sepsis. Crit. Care (Lond. Engl.) 13:210. http://dx .doi.org/10.1186/cc7702. 4. Texereau J, Pene F, Chiche J-D, Rousseau C, Mira J-P. 2004. Importance of hemostatic gene polymorphisms for susceptibility to and outcome of severe sepsis. Crit. Care Med. 32:S313–S319. http://dx.doi.org/10 .1097/01.CCM.0000126363.46191.DC. 5. Mahjoub-Messai F, Bidet P, Caro V, Diancourt L, Biran V, Aujard Y, Bingen E, Bonacorsi S. 2011. Escherichia coli isolates causing bacteremia via gut translocation and urinary tract infection in young infants exhibit different virulence genotypes. J. Infect. Dis. 203:1844 –1849. http://dx.doi .org/10.1093/infdis/jir189. 6. Bidet P, Mahjoub-Messai F, Blanco J, Blanco J, Dehem M, Aujard Y, Bingen E, Bonacorsi S. 2007. Combined multilocus sequence typing and
jcm.asm.org 4405
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
FIG 1 (A and B) Bilateral necrotic leg lesions of purpura fulminans. (C) Histopathological exam of the skin revealed a sparse infiltrate of often altered neutrophils
Case Report
7.
8.
9.
11.
12.
4406
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13.
14.
15.
16.
17.
18.
19.
coli septicemia. Wien. Klin. Wochenschr. 116:82. http://dx.doi.org/10 .1007/BF03040700. Helviz Y, Hersch M, Shmuelevitz L, Atrash J, Einav S. 2011. Bad to worse. Am. J. Med. 124:215–217. http://dx.doi.org/10.1016/j.amjmed .2010.11.007. Russo TA, Johnson JR. 2003. Medical and economic impact of extraintestinal infections due to Escherichia coli: focus on an increasingly important endemic problem. Microbes Infect. 5:449 – 456. http://dx.doi.org/10 .1016/S1286-4579(03)00049-2. de Kraker MEA, Jarlier V, Monen JCM, Heuer OE, van de Sande N, Grundmann H. 2013. The changing epidemiology of bacteraemias in Europe: trends from the European Antimicrobial Resistance Surveillance System. Clin. Microbiol. Infect. 19:860 – 868. http://dx.doi.org/10.1111 /1469-0691.12028. Johnson JR, Russo TA. 2002. Extraintestinal pathogenic Escherichia coli: “the other bad E coli.” J. Lab. Clin. Med. 139:155–162. http://dx.doi.org /10.1067/mlc.2002.121550. Grimaldi D, Bonacorsi S, Roussel H, Zuber B, Poupet H, Chiche J-D, Poyart C, Mira JP. 2010. Unusual “flesh-eating” strain of Escherichia coli. J. Clin. Microbiol. 48:3794 –3796. http://dx.doi.org/10.1128/JCM.00491-10. Petkovsek Z, Elersic K, Gubina M, Zgur-Bertok D, Starcic Erjavec M. 2009. Virulence potential of Escherichia coli isolates from skin and soft tissue infections. J. Clin. Microbiol. 47:1811–1817. http://dx.doi.org/10 .1128/JCM.01421-08. Escobar-Páramo P, Clermont O, Blanc-Potard A-B, Bui H, Le Bouguénec C, Denamur E. 2004. A specific genetic background is required for acquisition and expression of virulence factors in Escherichia coli. Mol. Biol. Evol. 21:1085–1094. http://dx.doi.org/10.1093/molbev/msh118.
Journal of Clinical Microbiology
Downloaded from http://jcm.asm.org/ on April 29, 2015 by ST ANDREWS UNIV
10.
O serogrouping distinguishes Escherichia coli subtypes associated with infant urosepsis and/or meningitis. J. Infect. Dis. 196:297–303. http://dx .doi.org/10.1086/518897. Lemaître C, Mahjoub-Messai F, Dupont D, Caro V, Diancourt L, Bingen E, Bidet P, Bonacorsi S. 2013. A conserved virulence plasmidic region contributes to the virulence of the multiresistant Escherichia coli meningitis strain S286 belonging to phylogenetic group C. PLoS One 8:e74423. http://dx.doi.org/10.1371/journal.pone.0074423. Johnson TJ, Siek KE, Johnson SJ, Nolan LK. 2006. DNA sequence of a ColV plasmid and prevalence of selected plasmid-encoded virulence genes among avian Escherichia coli strains. J. Bacteriol. 188:745–758. http://dx .doi.org/10.1128/JB.188.2.745-758.2006. Peigne C, Bidet P, Mahjoub-Messai F, Plainvert C, Barbe V, Médigue C, Frapy E, Nassif X, Denamur E, Bingen E, Bonacorsi S. 2009. The plasmid of Escherichia coli strain S88 (O45:K1:H7) that causes neonatal meningitis is closely related to avian pathogenic E. coli plasmids and is associated with high-level bacteremia in a neonatal rat meningitis model. Infect. Immun. 77:2272–2284. http://dx.doi.org/10.1128/IAI.01333-08. Johnson TJ, Jordan D, Kariyawasam S, Stell AL, Bell NP, Wannemuehler YM, Alarcón CF, Li G, Tivendale KA, Logue CM, Nolan LK. 2010. Sequence analysis and characterization of a transferable hybrid plasmid encoding multidrug resistance and enabling zoonotic potential for extraintestinal Escherichia coli. Infect. Immun. 78:1931–1942. http://dx .doi.org/10.1128/IAI.01174-09. Tivendale KA, Noormohammadi AH, Allen JL, Browning GF. 2009. The conserved portion of the putative virulence region contributes to virulence of avian pathogenic Escherichia coli. Microbiology (Reading, Engl.) 155:450 – 460. http://dx.doi.org/10.1099/mic.0.023143-0. Huemer GM, Bonatti H, Dunst KM. 2004. Purpura fulminans due to E.
