Mostrar el registro sencillo del documento

dc.rights.licenseReconocimiento 4.0 Internacional
dc.contributor.advisorSaavedra Trujillo, Carlos Humberto
dc.contributor.advisorEcheverry Gaitan, Maria Clara
dc.contributor.authorZapata Pinillos, Erik
dc.date.accessioned2021-08-27T22:52:33Z
dc.date.available2021-08-27T22:52:33Z
dc.date.issued2021-07-26
dc.identifier.urihttps://repositorio.unal.edu.co/handle/unal/80048
dc.descriptionCutaneous leishmaniasis is a neglected tropical disease, broadly distributed in the planet and with high incidence among socially vulnerable persons. It has been underestimated by healthcare systems and society, with a great burden of disease. Despite an available effective and well established treatment since the 50’s, it has been documented an increasing rate of resistance and treatment failure. Reports in Latin America, show resistance rates between 10-20% and 25% of subjects with treatment failure using first line drugs. Nevertheless, there is no clear association between reduced in vitro susceptibility from the parasite and treatment response. This case control study with 34 subjects in a reference center in Bogotá, aimed to establish an association between reduced in vitro susceptibility and response to treatment. The results showed an OR 0.71 (IC 95% 0.085 – 9.39), which possibly means that there is no relation among the mentioned variables. These results suggest that susceptibility testing would not impact clinical decision making as treatment failure predictors, therefore limiting its systematic use
dc.description.abstractLa leishmaniasis cutánea es considerada una enfermedad tropical desatendida, con una amplia distribución geográfica en el mundo e incidencia importante en población socialmente vulnerable. Tiene un impacto infravalorado por la sociedad y los sistemas de salud, con una carga de enfermedad no despreciable. A pesar de disponer de esquemas terapéuticos desde hace 70 años, en las ultimas décadas se ha venido documentando resistencia creciente por parte del parásito a las primeras líneas de tratamiento y altos índices de falla terapéutica. Trabajos realizados en América Latina reportan resistencia entre el 10-20% y tasas de falla terapéutica a la primera línea de tratamiento del 25%. Sin embargo, no es clara la correlación entre la disminución de la sensibilidad parasitaria in vitro y la respuesta terapéutica. Se realizó un estudio de casos y controles, con un total de 34 pacientes en un centro de referencia de Bogotá para determinar la asociación entre la sensibilidad in vitro disminuida y la respuesta clínica al tratamiento. Se obtuvo un OR 0.71 (IC 95% 0.085 – 9.39) con lo cual posiblemente no existe relación entre las variables. Estos resultados sugieren que las pruebas de sensibilidad disminuidas in vitro no impactan en la toma de decisiones en la practica clínica, como posibles predictores de falla al tratamiento por lo cual el papel en el uso sistemático de ellas es limitado.
dc.format.extent43 páginas
dc.format.mimetypeapplication/pdf
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subject.ddc610 - Medicina y salud::616 - Enfermedades
dc.titleAsociación entre disminución de la sensibilidad parasitaria in vitro y respuesta terapéutica en pacientes con Leishmaniasis cutánea tratados en el centro dermatológico Federico Lleras Acosta de la ciudad de Bogotá entre 2006 y 2012
dc.typeTrabajo de grado - Especialidad Médica
dc.type.driverinfo:eu-repo/semantics/masterThesis
dc.type.versioninfo:eu-repo/semantics/acceptedVersion
dc.publisher.programBogotá - Medicina - Especialidad en Medicina Interna
dc.description.degreelevelEspecialidades Médicas
dc.description.degreenameEspecialista en medicina interna
dc.description.researchareaDesarrollo de métodos diagnósticos en enfermedades de transmisión vectorial
dc.identifier.instnameUniversidad Nacional de Colombia
dc.identifier.reponameRepositorio Institucional Universidad Nacional de Colombia
dc.identifier.repourlhttps://repositorio.unal.edu.co/
dc.publisher.departmentDepartamento de Medicina Interna
dc.publisher.facultyFacultad de Medicina
dc.publisher.placeBogotá, Colombia
dc.publisher.branchUniversidad Nacional de Colombia - Sede Bogotá
dc.relation.references1. Bermudez H, Rojas E, Garcia L, et al. Efficacy and safety of a generic sodium stibogluconate for the treatment of tegumentary leishmaniasis in Isiboro Secure Park, Bolivia. Ann Trop Med Hyg.2006;100:591-600
dc.relation.references2. Oliveira-Neto MP, Schubach A, Mattos M,et al. A low dose antimony treatment in 159 patients with American cutaneous leishmaniasis: extensive follow up studies. Am J Trop Med Hyg.1997;57:651-655.
dc.relation.references3. Llanos Cuentas A, Tulliano G, Araujo Castillo R. Clinical and parasite species risk factors for pentavalent antimonil treatment failure in cutaneous Leishmaniasis in Peru.2008;46(2):223-231.
dc.relation.references4. Palacios R, Osorio LE, Grajalew LF, et al. Treatment failure in children in a randomized clinical trial with 10 and 20 days of meglumine antimonate for cutaneous leishmaniasis due to Leishmania Viannia species. Am J Trop Med Hyg.2001;64:187-193.
dc.relation.references5. Rojas R, Valderrama L, Valderrama M, et al. Resistance to antimony and treatment failure in human Leishmania (Viannia) infection. J Infect Dis. 2006;193(10):1375-1383.
dc.relation.references6. Obonaga R, Fernandez OL, Valderrama L. Treatment failure and miltefosine susceptibility in dermal leishmaniasis caused by Leishmania subgenus Viannia species. Antimicrob Agents Chemother.2014;58(1):144-152.
dc.relation.references7. Castro MM, Cossio A, Velasco C, Osorio L. Risk factors for therapeutic failure to meglumine antimoniate and miltefosine in adults and children with cutaneous leishmaniasis in Colombia: a cohort study. Plos Negl Trop Dis.2017;11(4):e005515 DOI: https://doi.org/10.1371/journal. pntd.0005515
dc.relation.references8. Robledo SM, Puerta JA, Muñoz DL, Guardo M, Velez ID. Eficacia y tolerancia de la pentamidina en el tratamiento de la leishmaniasis cutánea producida por L. panamensis en Colombia. Biomédica.2006;26(1):188-193.
dc.relation.references9. Fernandez OL, Diaz Toro Y, Ovalle C, et al. Miltefosine and antimonial drug susceptibility of Leishmania Viannia species and populations in regions of high transmission in Colombia. Plos Negl Trop Dis.2014;8(5):e2871 DOI: 10.1371/journal.pntd.0002871
dc.relation.references10. Arevalo J, Ramirez L, Adaui V, et al. Influence of Leishmania (Viannia) species on the response to antimonial treatment in patients with american tegumentary leishmaniasis. The journal of infectious diseases. 2007;195:1846-1851.
dc.relation.references11. Llanos Cuentas A, Tulliano G, Araujo Castillo R, et al. Clinical and parasite species risk factors for pentavalent antimonial treatment failure in cutaneous leishmaniasis in Peru. Clinical infectious diseases.2008;46:223-231.
dc.relation.references12. Coelho A, Trinconi C, Costa C, Uliana S. In vitro and in vivo miltefosine susceptibility of a leishmania amazonensis isolate from a patient with diffuse cutaneous leishmaniasis. Plos Negl Trop Dis. 2014;8(7):e2999 DOI: 10.1371/journal.pntd.0002999
dc.relation.references13. Espada C, Ribeiro Dias F, Dorta M, et al. Susceptibility to miltefosine in Brazilian clinical isolates of Leishmania braziliensis. AM J Trop Med Hyg.2017;96(3):656-659.
dc.relation.references14. Berman JD, Chulay JD, Hendricks LD, Oster CN. Susceptibility of clinically sensitive and resistant Leishmania to pentavalent antimony in vitro. Am J Trop Med Hyg. 1982; 31(3 parte 1):459-465.
dc.relation.references15. Grogl M, Thomason TN, Franke ED. Drug resistance in leishmaniasis: its implication in systemic chemotherapy of cutaneous and mucocutaneous disease. Am J Trop Med Hyg. 1992; 47(1):117-126.
dc.relation.references16. Robledo SM, Valencia AZ, Saravia NG. Sensitivity to glucantime of leishmania viannia isolated from patients prior treatment. J Parasitol. 1999; 85(2):360-366.
dc.relation.references17. Jackson JE, Tally JD, Ellis WY, et al. Quantitative in vitro drug potency and drug susceptibility evaluation of Leishmania spp from patients unresponsive to pentavalent antimony therapy. Am J Trop Med Hyg. 1990;43:464-480
dc.relation.references18. Azeredo Coutinho RB, Mendoza SC, Callahan H, et al. Sensitivity of Leishmania braziliensis promastigotes to meglumine antimoniate is higher tan that of other Leishmania species and correlates with response to therapy in American tegumentary leishmaniasis. J Parasitol. 2007;93(3):688-693.
dc.relation.references19. Desjeux P. Leishmaniasis: current situation and new perspectives. Comp Immunol Microbiol Infect Dis. 2004;27:305-318.
dc.relation.references20. Kolaczinski JH, Hope A, Ruiz JA, et al. Kala-azar epidemiology and control, southern Sudan. Emerg Infect Dis. 2008;14:664- 666
dc.relation.references21. Magill AJ. Cutaneous leishmaniasis in the returning traveler. Infect Dis Clin North Am. 2005;19:241-266
dc.relation.references22. Organización Panamericana de la Salud. Manual de procedimientos para vigilancia y control de las leishmaniasis en las Américas. Washington, D.C.: OPS; 2019.
dc.relation.references23. Instituto Nacional de Salud. Informe de evento leishmaniasis cutánea, mucosa y visceral,Colombia,2018. Bogotá;2018. https://www.ins.gov.co/buscador-eventos/Informesdeevento/LEISHMANIASIS_2018.pdf (ultimo acceso 29 de Junio de 2019)
dc.relation.references24. Bailey F, Mondragon Shem K,Hotez P, et al. A new perspective on cutaneous Leishmaniasis implications for global prevalence and burden of disease estimates. Plos Negl Trop Dis.2017;11(8):e0005739 DOI: 10.1371/journal.pntd.0005739
dc.relation.references25. Hotez PJ, Alvarado M, Basañez MG, et al. The global burden of disease study 2010: Interpretation and implications for neglected tropical diseases. Plos Negl Trop Dis.2014;8(7):e2865 DOI: https://doi.org/10.1371/journal.pntd.0002865 P
dc.relation.references26. Okwa OO. Tropical parasitic diseases and women. Ann Afr Med. 2007; 6: 157–163
dc.relation.references27. Homsi Y, Makdisi G. Leishmaniasis: a forgotten disease among neglected people. Int J Health. 2010; 11: 2
dc.relation.references28. Magill Alan. Leishmania species: visceral (Kala-Azar), cutaneous, and mucosal leishmaniasis. En: Principles and practice of infectious disease. Seventh edition. Philadelphia: Churchil Livingstone Elsevier; 2010. 3463-3480.
dc.relation.references29. Akhoundi M, Downing T, Votypka J, et al. Leishmania infections: molecular targets and diagnosis. Molecular aspects of medicine.2017;57:1-29.
dc.relation.references30. Peacock CS, Seeger K, Harris D, et al. Comparative genomic analysis of three Leishmania species that cause diverse human disease. Nat Genet. 2007;39:839-847.
dc.relation.references31. Reithinger R, Dujardin JC, Louzir H, et al. Cutaneous leishmaniasis. Lancet Infect Dis 2007;7:581-596.
dc.relation.references32. Medical parasitology. En: Medical microbiology. 27th edition. New York: Mc Graw Hill;2013. 705-739.
dc.relation.references33. Ghersetich J, Menchini G, Teofoli P, et al. Immune response to Leishmania infection in human skin. Clin Dermatol.1999;17:333-338.
dc.relation.references34. Weina PJ, Neafle RC, Wortmamm G, Polhemus M, Aronson NE. Old World leishmaniasis: an emerging infection among deployed US military and civilian workers. Clin Infect Dis. 2004; 39: 1674-1680
dc.relation.references35. Ramirez JR, Adugelo S, Muskus C. Diagnosis of cutaneous leishmaniasis in Colombia: the sampling site within lesions influences the sensitivity of parasitological diagnosis. J Clin Microbiol. 2000; 38: 3768-3773.
dc.relation.references36. Vega-López F. Review: Diagnosis of cutaneous leishmaniasis. Curr Opin Infect. 2003; Dis 16: 97-101.
dc.relation.references37. Blum J, Desjeux P, Schwartz E, Beck B, Hazt C. Treatment of cutaneous leishmaniasis among travellers. J Antimicrob Chemother.2004; 53: 158-166.
dc.relation.references38. Srivastava P, Dayama A, Mehrotra S, Sundar S. Diagnosis of visceral leishmaniasis. Trans R Soc Trop Med Hyg.2011; 105: 1-6
dc.relation.references39. Vilaplana C, Blanco S, Domínguez J, Giménez M, Ausina V, Tural C, Muñoz C. Noninvasive method for diagnosis of visceral leishmaniasis by a latex agglutination test for detection of antigens in urine samples. J Clin Microbiol.2004; 42: 1853-1854.
dc.relation.references40. Ryan JR, Smithyman AM, Rajasekariah GH, Hochberg L, Stiteler JM, Martin SK. Enzyme-linked immunosorbent assay based on soluble promastigote antigen detects immunoglobulin M (IgM) & IgG antibodies in sera from cases of visceral and cutaneous leishmaniasis. J Clin Microbiol.2002; 40: 1037-1043.
dc.relation.references41. Rajasekariah GH, Ryan JR, Hillier SR, Yi LP, Stiteler JM, Cui L, Smithyman AM, Martin SK. Optimisation of an ELISA for the serodiagnosis of visceral leishmaniasis using in vitro derived promastigote antigens. J Immunol Methods.2001; 252: 105-119.
dc.relation.references42. Kumar R, Pai K, Pathak K, Sundar S.Enzyme-linked immunosorbent assay for recombinant K39 antigen in diagnosis, prognosis of Indian visceral leishmaniasis. Clin Diagn Lab Immunol.2001; 8: 1220-1224.
dc.relation.references43. Elmahallawy EK, Martínez AS, Rodríguez Graner J, et al. Diagnosis of leishmaniasis. J Infect Dev Ctries.2014;8(8):961-972.
dc.relation.references44. Maurya R, Mehrotra S, Prajapati VK, Nylén S, Sacks D, Sundar S. Evaluation of blood agar microtiter plates for culturing leishmania parasites to titrate parasite burden in spleen and peripheral blood of patients with visceral leishmaniasis. J Clin Microbiol.2010; 48: 1932-1934.
dc.relation.references45. Vinayak VK, Mahaja D, Sobt RC, Singl N, Sunda S. Anti-66 kDa anti-leishmanial antibodies as specific immunodiagnostic probe for visceral leishmaniasis. Indian J Med Res.1994; 99: 109-114.
dc.relation.references46. Pattabhi S, Whittle J, Mohamath R, El-Safi S, et al. A Design development and evaluation of rK28-based point-of-care tests for improving rapid diagnosis of visceral leishmaniasis. PLoS Negl Trop Dis.2010; 4: e822.
dc.relation.references47. Croft S, Sundar S, Fairlamb AH. Drug resistance in Leishmaniasis. Clinical Microbiology Reviews.2006;19(1):111-126.
dc.relation.references48. Denton H, McGregor JC, Coombs GH. Reduction of antileishmanial pentavalent antimonial drugs by a parasite specific thiol dependent reductase, TDR1. Biochem J. 2004;381:405-412
dc.relation.references49. Zhou Y, Messier N, Ouellette M, Rosen BP, Mukhopadhyway R. Leishmania major LmACR2 is a pentavalent antimony reductase that confers sensitivity to the drug Pentostam. J Biol Chem. 2004;279:37445-37451.
dc.relation.references50. Haldar AK, Sen P, Roy S. Use of antimony in the treatment of Leishmaniasis: current status and future directions. Molecular biology international.2011:PMID 571242
dc.relation.references51. Walker J, Saravia NG. Inhibition of Leishmania donovani promastigote DNA topoisomerase I and human monocyte DNA topoisomerase I and II by antimonial drugs and classical antitopoisomerase agents. Journal of parasitology. 2004;90(5):1155-1162.
dc.relation.references52. Ferreira CDS, Castro Pimienta AM, Demicheli C, Frezard F. Characterization of reactions of antimoniate and meglumine antimoniate with a guanine ribonucleoside at different pH. 2006;19(5):573-581.
dc.relation.references53. Basu JM, Mookerjee A, Sen P, et al. Sodium antimony gluconate induces generation of reactive oxygen species and nitric oxide via phosphoinositide 3 kinase and mitogen activated protein kinase activation in Leishmania donovani infected macrophages. Antimicrobial agents and chemotherapy.2006;50(5):1788-1797.
dc.relation.references54. Bray P, Barrett MP, Ward SA, Konning HP. Pentamidine uptake and resistance in pathogenic protozoa: past, present and future. Trends Parasitol. 2003;19:232-239.
dc.relation.references55. Barratt G, Saint Pierre Chazalet M, Loiseau PM. Cellular transport and lipid interactions of miltefosine. Curr Drug Metab.2009;10(3):247-255.
dc.relation.references56. Lux H, Heise N, Klenner T, et al. Ether lipid (alkyl phospholipid) metabolism and the mechanism of action of ether lipid analogues in Leishmania. Mol Biochem Parasitol.2000;111:1-14.
dc.relation.references57. Paris C, Loiseau PM, Bories C, Breard J. Miltefosine induces apoptosis like death in Leishmania donovani promastigotes. Antimicrob Agents Chemother.2004;48:852-859.
dc.relation.references58. Dorlo TP, Balasegaram M, Beijnen JH, de Vries PJ. Miltefosine: a review of its pharmacology and therapeutic efficacy in the treatment of Leishmaniasis. J Antimicrob Chemother.2012;67(11):2576-2597.
dc.relation.references59. Perez Victoria FJ, Gamarro F, Ouellette M, Castanys S. Functional cloning of the miltefosine transporter. A novel P type phospholipid translocase from Leishmania involved in drug resistance. J Biol Chem. 2003;278:49965-49971.
dc.relation.references60. Sundar S, Olliaro PL. Miltefosine in the treatment of Leishmaniasis: clinical evidence of informed clinical risk management. Ther Clin Risk Manag.2007;3(5):733-740.
dc.relation.references61. Ramos H, Valdivieso E, Gamargo M, Dagger F, Cohen BE. Amphotericin B kills unicelular leishmanias by forming aqueous pores permeable to small cations and anions. J Membr Biol. 1996;152(1):65-75
dc.relation.references62. Anderson TM, Clay MC, Cioffi AG, Diaz KA,Hisao GS, Turttle MD, et al. Amphotericin forms an extra-membranous and fungicidal sterol sponge. Nat Chem Biol. 2014;10(5):400-406.
dc.relation.references63. Ministerio de salud y protección social. Lineamientos para la atención clínica integral de leishmaniasis en Colombia. Bogotá; 2018. https://www.minsalud.gov.co/sites/rid/Lists/BibliotecaDigital/RIDE/VS/PP/PAI/Lineamientos-leishmaniasis.pdf (ultimo acceso 15 de Mayo de 2019).
dc.relation.references64. Maltezou H. Drug resistance in visceral Leishmaniasis. Journal of Biomedicine and Biotechnology.2010;2010:PMID:19888437
dc.relation.references65. Singh N. Drug resistance mechanism in clinical isolates of Leishmania donovani. Indian J Med Res. 2006;123(3):411-422.
dc.relation.references66. El Fadili K, Messier N, Leprohon P, Roy G, Guimond C, Trudel N, et al. Role of the ABC transporter MRPA in antimony resistance in Leishmania infantum axenic and intracelular amastigotes. Antimicrob Agents Chemother. 2005;49(5):1988-93.
dc.relation.references67. Manzano JI, Garcia Hernandez R, Castanys S, Gamarro F. A new ABC half transporter in Leishmania major is involved in resistance to antimony. Antimicrob Agents Chemother. 2013;57():3719-30.
dc.relation.references68. Perea A, Manzano JI, Castanys S, Gamarro F. The LABCG2 Transporter from the Protozoan Parasite Leishmania is involved in antimony resistance. Antimicrob Agents Chemother. 2016;60(6):3489-96
dc.relation.references69. Wyllie S, Vickers TJ, Fairlamb AH. Roles of trypanothione S tranferase and tryparedoxin peroxidase in resistance to antimonials. Antimicrob Agents Chemother. 2008;52(4):1359-65
dc.relation.references70. Mandal G, Wyllie S, Singh N, Sundar S, Fairlamb AH, Chatterjee M. Increased levels of thiols protect antimony unresponsive Leishmania donovani field isolates against reactive oxygen species generated by trivalent antimony. Parasitology. 2007;134(Pt 12):1679-87
dc.relation.references71. Basselin M, Denise H, Coombs GH, Barrett MO. Resistance to pentamidine in Leishmania mexicana involves exclusión of the drug from the mithocondrion. Antimicrob Agents Chemother.2002;46:3731-3738.
dc.relation.references72. Sundar S, Olliaro PL. Miltefosine in the treatment of Leishmaniasis: clinical evidence for informed clinical risk management. Ther Clin Risk Manag.2007;3(5):733-740.
dc.relation.references73. Castanys Muñoz E, Perez Victoria JM, Gamarro F, Castanys S. Characterization of an ABCG like transporter from the protozoan parasite Leishmania with a role in drug resistance and transbilayer lipid movement. Antimicrob Agents Chemother.2008;52:3573-3579.
dc.relation.references74. Rakotomanga M, Sain Pierre Chazalet M, Loiseau PM. Alteration of fatty acid sterol metabolism in miltefosine resistant Leishmania donovani promastigotes and consequences for drug membrane interactions. Antimicrob Agents Chemother.2005;49:2677-2686.
dc.relation.references75. Gamarro F, Sanchez Caete MP, Castanys S. Mechanisms of miltefosine resistance in Leishmania. En: Drug resistance in Leishmania parasites. First Edition. Springer Verlag.2013.
dc.relation.references76. Purkait B, Kumar A, Nandi N, et al. Mechanism of amphotericin B resistance in clinical isolates of Leishmania donovani. Antimicrob Agents Chemother. 2012;56(2):1031-1041.
dc.relation.references77. Pourshafie M, Morand S, Virion A, Rakotomanga M, et al. Cloning of S-adenosyl-L-methionine:C-24-Delta-sterol-methyltransferase (ERG6) from Leishmania donovani and characterization of mRNAs in wild type and amphotericin B resistant promastigotes. Antimicrob Agents Chemother.2004;48(7):2409-2414.
dc.relation.references78. Mwenechanya R, Kovarova J, Dickens NJ, et al. Sterol 14 alpha demethylase mutation leads to amphotericin B resistance in Leishmania mexicana. PLos Negl Trop Dis.2017;11(6):e0005649 PMID: 28622334.
dc.relation.references79. Fernandez Prada C, Vincent IM, Brotherton MC, Roberts M, Roy G, et al. Different mutations in a P-type ATPase transporter in Leishmania parasites are associated with cross resistance to two leading drugs by distinct mechanism. Plos Negl Trop Dis.2016;10(12):e0005171. PMID:27911896
dc.relation.references80. Salgado Almario J, Hernandez CA, Ovalle CE. Geographical distribution of Leishmania species in Colombia, 1985-2017. Biomedica. 2019 Jun 15;39(2):278-290
dc.relation.references81. Ramirez JD, Hernandez C, León CM, et al. Taxonomy, diversity, temporal and geographical distribution of cutaneous Leishmaniasis in Colombia: A retrospective study. Sci Rep. 2016 Jun 22;6:28266
dc.relation.references82. Rojas R, Valderrama L, Valderrama M, et al. Resistance to antimony and treatment failure in human Leishmania (Viannia) infection. J Infect Dis. 2006 May 15;193(10):1375-83.
dc.relation.references83. Azeredo Coutinho RBG, Mendoca SCF, Callahan H, et al. Sensitivity of Leishmania braziliensis promastigotes to meglumine antimoniate (glucantime) is higher than that of other Leishmania species and correlates with response to therapy in American tegumentary leishmaniasis. J Parasitol. 2007 Jun;93(3):688-693
dc.rights.accessrightsinfo:eu-repo/semantics/openAccess
dc.subject.proposalLeishmaniasis
dc.subject.proposalMiltefosine
dc.subject.proposalResistencia a drogas
dc.subject.proposalAntimoniato de meglumina
dc.subject.proposalPentamidina
dc.subject.proposalLeishmaniasis cutánea
dc.subject.proposalLeishmaniasis
dc.subject.proposalMiltefosine
dc.subject.proposalDrug resistance
dc.subject.proposalMeglumine antimoniate
dc.subject.proposalPentamidine
dc.subject.proposalCutaneous leishmaniasis
dc.subject.proposalMiltefosine
dc.subject.proposalresistencia a drogas
dc.title.translatedAssociation between reduced in vitro susceptibility and response to treatment in cutaneous leishmaniasis patients treated in the dermatologic centre Federico Lleras Acosta in Bogota between 2006 and 2012
dc.type.coarhttp://purl.org/coar/resource_type/c_bdcc
dc.type.coarversionhttp://purl.org/coar/version/c_ab4af688f83e57aa
dc.type.contentText
dc.type.redcolhttp://purl.org/redcol/resource_type/TM
oaire.accessrightshttp://purl.org/coar/access_right/c_abf2


Archivos en el documento

Thumbnail
Thumbnail

Este documento aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del documento

Reconocimiento 4.0 InternacionalEsta obra está bajo licencia internacional Creative Commons Reconocimiento-NoComercial 4.0.Este documento ha sido depositado por parte de el(los) autor(es) bajo la siguiente constancia de depósito