Fisiopatología de la sepsis por gram positivos
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Las bacterias gram positivas vienen cobrando importancia como agentes etiológicos de la sepsis siendo algunos de principales representantes Staphylococcus aureus, las cepas de S.aureus meticilino resistentes (MRSA del inglés) y el Streptococcus pyogenes o también llamado Streptococcus del grupo A invasivo (GAS). Dado que en su estructura celular presentan diversas moléculas que pueden ser reconocidas como patrones moleculares asociados a patógenos (PAMPs) como son el peptidoglicano (PNG) el ácido teicoico (LTA), las lipoproteínas; y otras que activan directamente el sistema inmune adaptativo como son los Superantígenos; los pacientes infectados pueden exponerse de manera simultánea a una respuesta inmune amplifi cada de manera sinérgica entre todos estos tipos de antígenos, que a través de vías de señalización intracelular desencadenarán la transcripción de genes codifi cadores de citocinas pro infl amatorias como el TNFα, la IL-1β, la IL-6, el INFγ, IL-8, IL-18, IL-2, IL-12, IL-10 que darán lugar a muchas de las manifestaciones clínicas de la sepsis y se vienen asociando como predictores del pronóstico de esta junto a otros marcadores moleculares de la misma.
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Martin GS. Sepsis, severe sepsis and septic shock: changes in incidence, pathogens and outcomes. Expert Rev Anti Infect Ther. 2012;10(6):701-6.
Ramachandran G. Gram-positive and gram-negative bacterial toxins in sepsis: a brief review. Virulence. 2014;5(1):213-8.
Silveira-Lessa AL, Quinello C, Lima L, Redondo AC, Ceccon ME, Carneiro-Sampaio M, et al. TLR expression, phagocytosis and oxidative burst in healthy and septic newborns in response to Gram-negative and Gram-positive rods. Hum Immunol. 2016:S0198-8859(16)30383-4:1-9.
Reglinski M, Sriskandan S. The contribution of group A streptococcal virulence determinants to the pathogenesis of sepsis. Virulence.2014;5(1):127-36.
Powers ME1, Bubeck Wardenburg J. Igniting the fi re: Staphylococcus aureus virulence factors in the pathogenesis of sepsis. PLoS Pathog. 2014;10(2):1-1.
Kang SS, Sim JR, Yun CH, Han SH. Lipoteichoic acids as a major virulence factor causing inflammatory responses via Toll-like receptor 2. Arch Pharm Res [internet]. 2016:1-11 [consultado 2016 Agosto 20]. DOI:10.1007/s12272-016-0804-y
Henneke P1, Dramsi S, Mancuso G, Chraibi K, Pellegrini E, Theilacker C, et al. Lipoproteins are critical TLR2 activating toxins in group B streptococcal sepsis. J Immunol. 2008;180(9):6149-58.
Bern M, Beniston R, Mesnage S. Towards an automated analysis of bacterial peptidoglycan structure. Anal Bioanal Chem [internet]. 2016:1-10 [consulado 2016 Agosto 20]. DOI 10.1007/
s00216-016-9857-5
Malanovic N, Lohner K. Gram-positive bacterial cell envelopes: The impact on the activity of antimicrobial peptides. Biochim Biophys Acta. 2016;1858(5):936-46.
Gupta VK, Sekhar S, Dhanda V, Toor D, Kumar R, Chakraborti A. Immune response against M protein-conserved region peptides from prevalent group A Streptococcus in a North Indian population.J Microbiol Immunol Infect. 2016 ;49(3):352-8.
Young PG1, Moreland NJ2, Loh JM3, Bell A4, Atatoa Carr P5, Proft T, et al. Structural conservation, variability, and immunogenicity of the T6 backbone pilin of serotype M6 Streptococcus pyogenes. Infect Immun. 2014;82(7):2949-57.
Hynes W, Sloan M. Secreted Extracellular Virulence Factors. En: Ferretti JJ, Stevens DL, Fischetti VA. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [internet]. Oklahoma: University of Oklahoma Health Sciences Center; 2016 [Consultado 2016 febrero 22]. Disponible en: https://www.ncbi.nlm.nih. gov/books/NBK333411/
Immacuada Margarit y Ros. Streptococcus pyogenes Pili. En: Ferretti JJ, Stevens DL, Fischetti VA. Streptococcus pyogenes:Basic Biology to Clinical Manifestations [internet]. Oklahoma:University of Oklahoma Health Sciences Center; 2016 [Consultado 2016 febrero 22]. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK333423/
Ryan PA, Juncosa B. Group A Streptococcal Adherence. En: Ferretti20 JJ, Stevens DL, Fischetti VA. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [internet]. Oklahoma: University of Oklahoma Health Sciences Center; 2016 [Consultado 2016 febrero 22]. Disponible en: https://www.ncbi.nlm.nih.gov/ books/NBK333427/
Fischetti VA. M Protein and Other Surface Proteins on Streptococci. En: Ferretti JJ, Stevens DL, Fischetti VA. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [internet]. Oklahoma: University of Oklahoma Health Sciences Center; 2016 [Consultado 2016 febrero 22]. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK333431/
Cole JN, Barnett TC, Nizet V, Walker MJ. Molecular insight into invasive group A streptococcal disease. Nat Rev Microbiol. 2011;9(10):724-36.64 Revista Cuarzo - Fundación Universitaria Juan N. Corpas Vol. 22 No. 1
Golińska E, Van der Linden M, Więcek G, Mikołajczyk D, Machul A, Samet A, et al. Virulence factors of Streptococcus pyogenes strains from women in peri-labor with invasive infections. Eur J Clin Microbiol Infect Dis. 2016;35(5):747-54.
Kim HK, Thammavongsa V, Schneewind O, Missiakas D. Recurrent infections and immune evasion strategies of Staphylococcus aureus. Curr Opin Microbiol. 2012 Feb;15(1):92-9. doi: 10.1016/j.mib.2011.10.012. Epub 2011 Nov 14.
Spaulding AR, Salgado-Pabón W, Kohler PL, Horswill AR, Leung DY, Schlievert PM. Staphylococcal and streptococcal superantigen exotoxins. Clin Microbiol Rev. 2013;26(3):422-47.
Krakauer T. Therapeutic down-modulators of staphylococcal superantigen-induced infl ammation and toxic shock. Toxins (Basel).2010;2(8):1963-83.
Proft T, Fraser JD. Streptococcal Superantigens: Biological propierties and potential role in disease. En: Ferretti JJ, Stevens DL, Fischetti VA. Streptococcus pyogenes: Basic Biology to Clinical Manifestations [internet]. Oklahoma: University of Oklahoma Health Sciences Center; 2016 [Consultado 2016 febrero 22]. Disponible en: https://www.ncbi.nlm.nih.gov/books/NBK333435/
Aman MJ. Superantigens of a superbug: Major culprits of Staphylococcus aureus disease?. Virulence. 2016; 2:1-4.
Liu Q, Yeo WS, Bae T. The SaeRS Two-Component System of Staphylococcus aureus. Genes (Basel). 2016;7(10):1-20.
Corredor Arias LF1, Luligo Espinal JS2, Moncayo Ortiz JI2, Santacruz Ibarra JJ3, Álvarez Aldana A. Relationship between super antigenicity, antimicrobial resistance and origin of Staphylococcus aureus isolated. Colomb Med (Cali). 2016;47(1):15-20.
Salgado-Pabón W1, Breshears L, Spaulding AR, Merriman JA, Stach CS, Horswill AR, et al. Superantigens are critical for Staphylococcus aureus Infective endocarditis, sepsis, and acute kidney injury. MBio. 2013;4(4):1-9.
Deodhar D, Varghese G, Balaji V, John J, Rebekah G, Janardhanan J, et al. Prevalence of Toxin Genes among the Clinical Isolates of Staphylococcus aureus and its Clinical Impact. J Glob Infect Dis. 2015;7(3):97-102. doi: 10.4103/0974-777X.162234.
Imani Fooladi AA, Ashrafi E, Tazandareh SG, Koosha RZ, Rad HS, Amin M, et al. The distribution of pathogenic and toxigenic genes among MRSA and MSSA clinical isolates. Microb Pathog. 2015;81:60-66.
McAdow M, Kim HK, Dedent AC, Hendrickx AP, Schneewind O, Missiakas DM. Preventing Staphylococcus aureus sepsis through the inhibition of its agglutination in blood. PLoS Pathog. 2011;7(10):e1002307.
Aslam R, Laventie BJ, Marban C, Prévost G, Keller D, Strub JM, Dorsselaer Av, Haikel Y, Taddei C, Metz-Boutigue MH. Activation of neutrophils by the two-component leukotoxin LukE/D from Staphylococcus aureus: proteomic analysis of the secretions J Proteome Res. 2013;12(8):3667-3678.
Yoong P, Torres VJ. The effects of Staphylococcus aureus leukotoxins on the host: cell lysis and beyond. Curr Opin Microbiol. 2013;16(1):63-69.
Yoong P, Torres VJ. Counter inhibition between leukotoxins attenuates Staphylococcus aureus virulence. Nat Commun.2015;6(8125.):1-10.
Malachowa N, Kobayashi SD, Braughton KR, Whitney AR, Parnell MJ, Gardner DJ, Deleo FR. Staphylococcus aureus leukotoxin GH promotes infl ammation. J Infect Dis. 2012;206(8):1185- 1193.
Tilahun AY, Karau M, Ballard A, Gunaratna MP, Thapa A, David CS, Patel R, Rajagopalan G. The impact of Staphylococcus aureus-associated molecular patterns on staphylococcal superantigen-induced toxic shock syndrome and pneumonia. Mediators Infl amm. 2014; 2014:468285.
Tilahun AY, Chowdhary VR, David CS, Rajagopalan G. Systemic infl ammatory response elicited by superantigen destabilizes T regulatory cells, rendering them ineffective during toxic shock syndrome. J Immunol. 2014;193(6):2919-30.
Kulhankova K, King J, Salgado-Pabón W. Staphylococcal toxic shock syndrome: superantigen-mediated enhancement of endotoxin shock and adaptive immune suppression. Immunol Res. 2014;59(1-3):182-7.
Xu SX, McCormick JK. Staphylococcal superantigens in colonization and disease. Front Cell Infect Microbiol. 2012;2(52):1-11.
Kak V. Mediators of systemic infl ammatory response syndrome and the role of recombinant activated protein C in sepsis syndrome. Infect Dis Clin North Am. 2011;25(4):835-50.
Schmidt RR, Pedersen CM, Qiao Y, Zähringer U. Chemical synthesis of bacterial lipoteichoic acids: an insight on its biological signifi cance. Org Biomol Chem. 2011;9(7):2040-52.
Ray A, Cot M, Puzo G, Gilleron M, Nigou J. Bacterial cell wall macroamphiphiles: pathogen-/microbe-associated molecular patterns detected by mammalian innate immune system. Biochimie. 2013;95(1):33-42.
Zapata JP. Sepsis: la otra cara de la respuesta inmune. Iatreia. 2011;24(2):179-190.
Wu T, Xing J, Birukova AA Cell-type-specifi c crosstalk between p38 MAPK and Rho signaling in lung micro- and macrovascular barrier dysfunction induced by Staphylococcus aureus-derivedpathogens. Transl Res. 2013;162(1):45-55.
Surbatovic M, Popovic N, Vojvodic D, Milosevic I, Acimovic G, Stojicic M, et al. Cytokine profi le in severe Gram-positive and Gram-negative abdominal sepsis. Sci Rep. 2015;5(11355):1-12.
Xu XJ, Tang YM, Liao C, Song H, Yang SL, Xu WQ, Shi SW, Zhao N. Infl ammatory cytokine measurement quickly discriminates gram-negative from gram-positive bacteremia in pediatric hematology/oncology patients with septic shock. Intensive Care Med. 2013;39(2):319-26.
Abe R, Oda S, Sadahiro T, Nakamura M, Hirayama Y, Tateishi Y, et al. Gram-negative bacteremia induces greater magnitude of infl ammatory response than Gram-positive bacteremia. Critical Care 2010;14:1-7. Fisiopatología de la sepsis por gram positivos Méndez Y. y Barrera MC. 65
Arai T1, Ohta S2, Tsurukiri J2, Kumasaka K2, Nagata K2, Okita T, et al. Procalcitonin levels predict to identify bacterial strains in blood cultures of septic patients. Am J Emerg Med. 2016;34(11):2150-2153.
Feezor RJ, Oberholzer C, Baker HV, Novick D, Rubinstein M, Moldawer LL, et al. Molecular characterization of the acute inflammatory response to infections with gram-negative versus gram-positive bacteria. Infect Immun. 2003;71(10):5803-5813.
Foster TJ. The remarkably multifunctional fi bronectin binding proteins of Staphylococcus aureus. Eur J Clin Microbiol Infect Dis. 2016. [Epub ahead of print]. Disponible en: https://www. ncbi.nlm.nih.gov/pubmed/27604831
Carrillo R.C, Tapia J, Peña C.A, Kim Kohd M.J, Jaime A.R, Montalvo E. Bases moleculares de la sepsis. Revista de la Facultad de Medicina de la UNAM. 2014;57(3):1-13.
Brosnahan AJ, Schlievert PM. Gram-positive bacterial superantigen outside-in signaling causes toxic shock syndrome. FEBS J. 2011;278(23):4649-67.
Briceño I. Sepsis: Etiología, Manifestaciones Clínicas y Diagnóstico. Medicrit 2005; 2(9):203-213.
Latini R, Caironi P, Masson S. Cardiac dysfunction and circulating cardiac markers during sepsis. Minerva Anestesiol. 2016;82(6):697-710.
