Sistema de Gestión del Conocimiento ANLIS MALBRÁN
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Rodent-borne viruses survey in rural settlers from Central Brazil
No full textFil: Fernandes, Jorlan. Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Laboratório de Hantaviroses e Rickettsioses, Rio de Janeiro, RJ; Brasil.Fil: Oliveira, Renata Carvalho de. Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Laboratório de Hantaviroses e Rickettsioses, Rio de Janeiro, RJ; Brasil.Fil: Coelho, Thayssa Alves. Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Laboratório de Hantaviroses e Rickettsioses, Rio de Janeiro, RJ; Brasil.Fil: Martins, Regina Maria Bringel. Universidade Federal de Goiás, Instituto de Patologia Tropical e Saúde Pública, Goiânia, GO; Brasil.Fil: Caetano, Karlla Antonieta Amorim. Universidade Federal de Goiás, Faculdade de Enfermagem, Goiânia, GO; Brasil.Fil: Horta, Marco Aurélio Pereira. Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Rio de Janeiro, RJ; Brasil.Fil: Levis, Silvana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina.Fil: Carneiro, Megmar Aparecida Dos Santos. Universidade Federal de Goiás, Instituto de Patologia Tropical e Saúde Pública, Goiânia, GO; Brasil.Fil: Teles, Sheila A. Universidade Federal de Goiás, Faculdade de Enfermagem, Goiânia, GO; Brasil.Fil: Lemos, Elba Regina Sampaio de. Fundação Oswaldo Cruz-Fiocruz, Instituto Oswaldo Cruz, Laboratório de Hantaviroses e Rickettsioses, Rio de Janeiro, RJ; Brasil.Anthropogenic environmental changes arising from settlement and agriculture include deforestation and replacement of natural vegetation by crops providing opportunities for pathogen spillover from animals to humans. This study aimed to investigate the prevalence of rodent-borne virus infections in seven rural settlements from Midwestern Brazil. Of the 466 individuals tested 12 (2.57%) were reactive for orthohantavirus and 3 (0.64%) for mammarenavirus. These rural settlers lived under unfavorable infrastructure, socioeconomic disadvantages, and unsanitary conditions, representing a risk for rodent-borne infections. Development of public policies towards the improvement of health, sanitation and awareness of rodent-borne diseases in improvised camps and settlements is imperative, in order to reduce morbidity and mortality caused by these diseases
Chagas cardiomyopathy associated with serological cure after trypanocidal treatment during childhood
No full textFil: Fernández, Marisa Liliana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Clínica, Patología y Tratamiento; Argentina.Fil: Hernández, Yolanda. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Clínica, Patología y Tratamiento; Argentina.Fil: Scollo, Karenina. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Diagnóstico; Argentina.Fil: Esteva, Mónica Ines. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Investigación; Argentina.Fil: Riarte, Adelina Rosa. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Clínica, Patología y Tratamiento; Argentina.Fil: Prado, Graciela Nilda. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología. Departamento de Clínica, Patología y Tratamiento; Argentina.Chagas disease is a chronic parasitological disease, which could cause cardiac manifestations in approximately one-third of affected individuals. Benznidazole and nifurtimox are used to treat this parasitological infection caused by Trypanosoma cruzi. Conventionally, the criterion for cure is consistently negative serological tests after treatment. We report a case of a patient who was treated when she was 13 years old and achieved T. cruzi negative seroconversion but developed Chagas disease cardiomyopathy as an adult
A Functional Analysis of the Cyclophilin Repertoire in the Protozoan Parasite Trypanosoma Cruzi
No full textFil: Perrone, Alina E. ANLIS Dr. C. G. Malbrán. Instituto Nacional de Parasitología “Dr. Mario Fatala Chaben”; Argentina.Fil: Milduberger, Natalia. ANLIS Dr. C. G. Malbrán. Instituto Nacional de Parasitología “Dr. Mario Fatala Chaben”; Argentina.Fil: Fuchs, Alicia G. ANLIS Dr. C. G. Malbrán. Instituto Nacional de Parasitología “Dr. Mario Fatala Chaben”; Argentina.Fil: Bustos, Patricia L. ANLIS Dr. C. G. Malbrán. Instituto Nacional de Parasitología “Dr. Mario Fatala Chaben”; Argentina.Fil: Bua, Jacqueline. ANLIS Dr. C. G. Malbrán. Instituto Nacional de Parasitología “Dr. Mario Fatala Chaben”; Argentina.Trypanosoma cruzi is the etiological agent of Chagas disease. It affects eight million people worldwide and can be spread by several routes, such as vectorborne transmission in endemic areas and congenitally, and is also important in non-endemic regions such as the United States and Europe due to migration from Latin America. Cyclophilins (CyPs) are proteins with enzymatic peptidyl-prolyl isomerase activity (PPIase), essential for protein folding in vivo. Cyclosporin A (CsA) has a high binding affinity for CyPs and inhibits their PPIase activity. CsA has proved to be a parasiticidal drug on some protozoa, including T. cruzi. In this review, we describe the T. cruzi cyclophilin gene family, that comprises 15 paralogues. Among the proteins isolated by CsA-affinity chromatography, we found orthologues of mammalian CyPs. TcCyP19, as the human CyPA, is secreted to the extracellular environment by all parasite stages and could be part of a complex interplay involving the parasite and the host cell. TcCyP22, an orthologue of mitochondrial CyPD, is involved in the regulation of parasite cell death. Our findings on T. cruzi cyclophilins will allow further characterization of these processes, leading to new insights into the biology, the evolution of metabolic pathways, and novel targets for anti-T. cruzi control
Some Limitations for Early Diagnosis of Congenital Chagas Infection by PCR
No full textFil: Volta, Bibiana Julieta. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Perrone, Alina E. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Rivero, Rocio. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Scollo, Karenina . ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Bustos, Patricia L. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Fil: Bua, Jacqueline. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Parasitología; Argentina.Trypanosoma cruzi, the causing agent of Chagas disease, can be transmitted to the offspring of infected pregnant women, thus being an epidemiologically important way of parasite transmission in humans. In addition, the migration of infected women from endemic areas to nonendemic countries may export this parasite infection. The diagnosis of congenital Chagas disease relies on the detection of the parasite because maternal antibodies are passively transferred to infants during pregnancy. The diagnosis of congenital infection can also be confirmed by detection of infant-specific anti-T cruzi antibodies at 10 months after delivery. Because early detection of T cruzi infection in newborns allows an efficient trypanocidal treatment and cure, more sensitive molecular techniques such as DNA amplification are being used for a prompt parasitological diagnosis of children born to seropositive mothers. In this report, we describe a diagnosis case of a child congenitally infected with T cruzi who tested negative for parasite detection both by microscopic observation and DNA amplification at 20 days and 6 months after delivery. However, at 7 months of age, a hemoculture was made from the infant's blood, and the infective parasite was finally isolated and classified as T cruzi discrete typing unit I. In a retrospective study, real-time polymerase chain reaction also allowed detecting the parasite but failed to detect any parasite load in earlier control samples. This case report stresses that even when molecular techniques are negative, a long-term follow-up is necessary for the diagnosis of infants congenitally infected with T cruzi
Effective population size differences in Calomys musculinus, the host of Junín Virus: their relationship with the epidemiological history of Argentine Hemorrhagic fever
No full textFil: Chiappero, Marina B. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Diversidad y Ecología Animal; Argentina.Fil: Piacenza, María Florencia. Universidad Nacional de Río Cuarto. Departamento de Ciencias Naturales; Argentina.Fil: Provensal, María Cecilia. Universidad Nacional de Río Cuarto. Departamento de Ciencias Naturales; Argentina.Fil: Calderón, Gladys E. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas; Argentina.Fil: Gardenal, Cristina N. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Diversidad y Ecología Animal; Argentina.Fil: Polop, Jaime J. Universidad Nacional de Río Cuarto. Departamento de Ciencias Naturales; Argentina.Argentine hemorrhagic fever (AHF) is a serious endemic disease in Argentina, produced by Junín virus, whose host is the Sigmodontinae rodent Calomys musculinus. Within the endemic area, human incidence and proportion of infected rodents remains high for 5-10 years after the first appearance of the disease (epidemic [E] zone) and then gradually declines to sporadic cases (historic [H] zone). We tested the hypothesis that host populations within the E zone are large and well connected by gene flow, facilitating the transmission and maintenance of the virus, whereas those in the H and nonendemic (NE) zones are small and isolated, with the opposite effect. We estimated parameters affected by levels of gene flow and population size in 14 populations of C. musculinus: population effective size (Ne), genetic variability, and mean relatedness. Our hypothesis was not supported: the lowest levels of variability and of Ne and the highest genetic relatedness among individuals were found in the H zone. Populations from the NE zone displayed opposite results, whereas those in the E zone showed intermediate values. If we consider that populations are first NE, then E, and finally H, a correlative decrease in Ne was observed. Chronically infected females have a low reproductive success. We propose that this would lower Ne because each cohort would originate from a fraction of females of the previous generation, and affect other factors such as proportion of individuals that develop acute infection, probability of viral transmission, and evolution of virulence, which would explain, at least partly, the changing incidence of AHF
Epidemiología de las dermatofitosis en 31 municipios de la provincia de Buenos Aires, Argentina: estudio de 6 años
No full textFil: Mazza, Mariana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Refojo, Nicolás. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Davel, Graciela Odelsia. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Micología; Argentina.Fil: Lima, Nelson. Universidade do Minho. Campus de Gualtar. Centre for Biological Engineering; Portugal.Fil: Dias, Nicolina. Universidade do Minho. Campus de Gualtar. Centre for Biological Engineering; Portugal.Fil: Passos da Silva, Cosme Marcelo Furtado. Oswaldo Cruz Foundation. National School of Public Health. Department of Epidemiology and Quantitative Methods in Health; Brasil.Fil: Canteros, Cristina Elena. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Background: No reliable data are available in the province of Buenos Aires regarding the frequency of dermatophytoses and other fungal diseases. The distribution of the clinical forms and the species involved are also unknown.
Aims: To present the data collected by the laboratories participating in the Mycology Network of the province of Buenos Aires (MNPBA) from a retrospective epidemiological survey on dermatophytoses.
Methods: A descriptive and exploratory analysis was performed on the cases of dermatophytoses gathered between 2002 and 2007 by the Mycology Network of the province of Buenos Aires.
Results: Of the 3966 dermatophytosis cases reported by 41 laboratories in 31 municipalities, more than a half occurred in three highly populated urban municipalities. The male:female ratio was 1:1.5. The most frequent clinical form was tinea unguium, diagnosed in 904 cases (51.83%), followed by tinea capitis (19.32%), tinea corporis (15.19%), tinea pedis (6.77%), tinea cruris (3.73%), and tinea manuum (2.18%). The species involved was identified in 1368 (33.49%) cases. Trichophyton rubrum was the most common species, with a frequency of 42.03%. An association was found between urban municipalities and T. rubrum or the Trichophyton mentagrophytes complex.
Conclusions: Results from the MNPBA survey provide valuable information that should enable further interventions to be designed in order to prevent and control the disease
Fatal canine encephalitozoonosis in Latin America, first report
Get PDFFil: Postma, Gabriela Cintia. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias; Argentina.Fil: Pardini, Lais. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Laboratorio de Inmunoparasitología; Argentina.Fil: Carnevale, Silvana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas. Departamento de Parasitología; Argentina.Fil: Gregnoli, Elena. Actividad privada; Argentina.Fil: Quiroga, María Alejandra. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Laboratorio de Patología Especial Veterinaria; Argentina.Fil: Venturini, María Cecilia. Universidad Nacional de La Plata. Facultad de Ciencias Veterinarias. Laboratorio de Inmunoparasitología; Argentina.Fil: Minatel, Leonardo. Universidad de Buenos Aires. Facultad de Ciencias Veterinarias; Argentina.Encephalitozoon cuniculi is an obligate, intracellular microsporidian organism capable of establish infection in a wide variety of animals. In carnivores it may cause a sporadic, severe disease in the first few months of life, which usually culminates with the death of the animal. The objective of this study was to report a natural fatal case of encephalitozoonosis in a puppy from Argentina. Clinical signs included reduced appetite, depression, vocalizing, weight loss, weakness, convulsions and recumbency. No significant gross lesions were noticed at necropsy. Microscopically, severe, diffuse, lymphocytic encephalitis was seen. Large cytoplasmic vacuoles containing spores, morphologically compatible with E. cuniculi, were present within endothelial cells of brain and kidney, in renal tubular epithelium and hepatocytes. Encephalitozoon cuniculi DNA was detected by PCR in the kidney. Antibody titers to E. cuniculi in serum from the surviving puppies and the dam were ≥1:200. This report contributes to our understanding of neurologic disease in puppies. Encephalitozoonosis should be considered as a differential diagnosis in cases of fatal encephalitis in puppies
Further delineation of Malan syndrome
Get PDFFil: Priolo, Manuela. Grande Ospedale Metropolitano Bianchi-Melacrino-Morelli. Unità Operativa di Genetica Medica; Italia.Fil: Schanze, Denny. University Hospital Magdeburg. Institute of Human Genetics; Alemania.Fil: Tatton-Brown, Katrin. St. George's University Hospitals NHS Foundation Trust. London and South West Thames Regional Genetics Service. Institute of Cancer Research. Division of Genetics and Epidemiology; Reino Unido.Fil: Mulder, Paul A. Lentis Psychiatric Institute. Jonx Department of Youth Mental Health. Autism Team Northern-Netherlands; Países Bajos.Fil: Tenorio, Jair. Institute of Medical and Molecular Genetics; España.Fil: Kooblall, Kreepa. University of Oxford. Radcliffe Department of Medicine. Academic Endocrine Unit; Reino Unido.Fil: Hernández Acero, Inés. Hospital Universitario Central de Asturias. Genetics Unit; España.Fil: Alkuraya, Fowzan S. King Faisal Specialist Hospital and Research Center. King Abdulaziz City for Science and Technology. Saudi Human Genome Project. Department of Genetics; Arabia Saudita.Fil: Arias, Pedro. Institute of Medical and Molecular Genetics; España.Fil: Bernardini, Laura. Casa Sollievo della Sofferenza Foundation. Cytogenetics Unit; Italia.Fil: Bijlsma, Emilia K. Leiden University Medical Centre. Department of Clinical Genetics; Países Bajos.Fil: Cole, Trevor. Birmingham Women's and Children's NHS Foundation Trust. Department of Clinical Genetics; Reino Unido.Fil: Coubes, Christine. Hôpital Arnaud de Villeneuve. Hospital Center University De Montpellier. Département de Génétique Médicale; Francia.Fil: Dapia, Irene. Institute of Medical and Molecular Genetics; España.Fil: Davies, Sally. University Hospital of Wales. Institute of Medical Genetics; Reino Unido.Fil: Di Donato, Nataliya. Technical University Dresden. Institute for Clinical Genetics; Alemania.Fil: Elcioglu, Nursel H. Marmara University Medical School. Department of Pediatric Genetics; Turquía.Fil: Fahrner, Jill A. Johns Hopkins University School of Medicine. McKusick-Nathans Institute of Genetic Medicine. Department of Pediatrics; Estados Unidos.Fil: Foster, Alison. University of Birmingham. College of Medical and Dental Sciences. Institute of Cancer and Genomic Sciences; Reino Unido.Fil: García González, Noelia. Unit Hospital Universitario Central de Asturias; España.Fil: Huber, Ilka. Sørland Hospital; Noruega.Fil: Iascone, Maria. Azienda Socio Sanitaria Territoriale Papa Giovanni XXIII. Laboratorio di Genetica Medica; Italia.Fil: Kaiser, Ann-Sophie. Heidelberg University. Institute of Human Genetics; Alemania.Fil: Kamath, Arveen. University Hospital of Wales. Institute of Medical Genetics; Reino Unido.Fil: Liebelt, Jan. SA Pathology. South Australian Clinical Genetics Services; Australia.Fil: Lynch, Sally Ann. University College Dublin. School of Medicine and Medical Sciences. Academic Centre on Rare Diseases; Irlanda.Fil: Maas, Saskia M. Academic Medical Center. Department of Clinical Genetics; Países Bajos.Fil: Mammì, Corrado. Grande Ospedale Metropolitano Bianchi-Melacrino-Morelli. Unità Operativa di Genetica Medica; Italia.Fil: Mathijssen, Inge B. Academic Medical Center. Department of Clinical Genetics; Países Bajos.Fil: McKee, Shane. Belfast Health and Social Care Trust. Northern Ireland Regional Genetics Service; Irlanda del Norte.Fil: Menke, Leonie A. University of Amsterdam. Academic Medical Center. Department of Pediatrics; Países Bajos.Fil: Mirzaa, Ghayda M. Seattle Children's Research Institute. Center for Integrative Brain Research; Estados Unidos.Fil: Montgomery, Tara. Newcastle upon Tyne National Health Service Foundation Trust; Reino Unido.Fil: Neubauer, Dorothee. University Hospital Magdeburg. Institute of Human Genetics; Alemania.Fil: Neumann, Thomas E. Mitteldeutscher Praxisverbund Humangenetik; Alemania.Fil: Pintomalli, Letizia. Grande Ospedale Metropolitano Bianchi-Melacrino-Morelli. Unità Operativa di Genetica Medica; Italia.Fil: Pisanti, Maria Antonietta. Antonio Cardarelli Hospital. Medical Genetic and Laboratory Unit; Italia.Fil: Plomp, Astrid S. Academic Medical Center. Department of Clinical Genetics; Países Bajos.Fil: Price, Sue. Northampton General Hospital National Health Service Trust. Department of Clinical Genetics; Reino Unido.Fil: Salter, Claire. Princess Ann Hospital. Wessex Clinical Genetics Service; Reino Unido.Fil: Santos-Simarro, Fernando. Institute of Medical and Molecular Genetics; España.Fil: Sarda, Pierre. Hôpital Arnaud de Villeneuve. Hospital Center University De Montpellier. Département de Génétique Médicale; Francia.Fil: Segovia, Mabel. ANLIS Dr.C.G.Malbrán. Centro Nacional de Genética Médica; Argentina.Fil: Shaw-Smith, Charles. Royal Devon and Exeter National Health Service Foundation Trust; Reino Unido.Fil: Smithson, Sarah. University Hospitals Bristol National Health Service Trust; Reino Unido.Fil: Suri, Mohnish. Nottingham University Hospitals National Health Service Trust. Nottingham Clinical Genetics Service; Reino Unido.Fil: Valdez, Rita Maria. Hospital Militar Central Cirujano Mayor Dr. Cosme Argerich. Genetics Unit; Argentina.Fil: Van Haeringen, Arie. Leiden University Medical Centre. Department of Clinical Genetics; Países Bajos.Fil: Van Hagen, Johanna M. Vrije Universiteit Medical Centre. Department of Clinical Genetics; Países Bajos.Fil: Zollino, Marcela. Catholic University. Institute of Medical Genetics. Department of Laboratory Medicine; Italia.Fil: Lapunzina, Pablo. Institute of Medical and Molecular Genetics; España.Fil: Thakker, Rajesh V. University of Oxford. Radcliffe Department of Medicine. Academic Endocrine Unit; Reino Unido.Fil: Zenker, Martin. University Hospital Magdeburg. Institute of Human Genetics; Alemania.Fil: Hennekam, Raoul C. University of Amsterdam. Academic Medical Center. Department of Pediatrics; Países Bajos.Malan syndrome is an overgrowth disorder described in a limited number of individuals. We aim to delineate the entity by studying a large group of affected individuals. We gathered data on 45 affected individuals with a molecularly confirmed diagnosis through an international collaboration and compared data to the 35 previously reported individuals. Results indicate that height is > 2 SDS in infancy and childhood but in only half of affected adults. Cardinal facial characteristics include long, triangular face, macrocephaly, prominent forehead, everted lower lip, and prominent chin. Intellectual disability is universally present, behaviorally anxiety is characteristic. Malan syndrome is caused by deletions or point mutations of NFIX clustered mostly in exon 2. There is no genotype-phenotype correlation except for an increased risk for epilepsy with 19p13.2 microdeletions. Variants arose de novo, except in one family in which mother was mosaic. Variants causing Malan and Marshall-Smith syndrome can be discerned by differences in the site of stop codon formation. We conclude that Malan syndrome has a well recognizable phenotype that usually can be discerned easily from Marshall-Smith syndrome but rarely there is some overlap. Differentiation from Sotos and Weaver syndrome can be made by clinical evaluation only
Autochthonous case of spotted fever caused by Rickettsia parkeri in Ensenada, Buenos Aires
No full textFil: Villalba, Pedro. Hospital Escuela de Agudos "Dr. Ramón Madariaga". Servicio de Infectología; Misiones, Argentina.Fil: Nava, Santiago. Estación Experimental Agropecuaria Rafaela. Instituto Nacional de Tecnología Agropecuaria. Laboratorio de Parasitología e Inmunología; Santa Fe, Argentina.Fil: Brignone, Julia. ANLIS. Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas. Departamento Diagnóstico Laboratorial y Referencial; Argentina.Fil: Sen, Carina. ANLIS. Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Virales Humanas. Departamento Diagnóstico Laboratorial y Referencial; Argentina.Fil: Esposto, Amadeo. Hospital Interzonal General de Agudos General San Martin. Servicio de Infectologia; Buenos Aires, Argentina.Fil: Angeletti, Virginia. Hospital Interzonal General de Agudos General San Martin. Servicio de Infectologia; Buenos Aires, Argentina.Se comunica un caso autóctono de fiebre manchada por Rickettsia parkeri en un adulto residente en Ensenada, Provincia de Buenos Aires ocurrido en el verano de 2016. El cuadro, secundario a una mordedura de garrapata en la pierna izquierda, se presentó como un síndrome febril agudo con deterioro del estado general, cefalea, mialgias, artralgias y exantema maculopapular. El sitio de la mordedura presentaba una úlcera con escara necrótica. El diagnóstico se confirmó por conversión serológica IgG anti-antígenos del género Rikettsia. La secuencia de un fragmento del gen gltA amplificado a partir de la lesión de piel presentó 100% identidad nucleotídica con las secuencias de cepas de R. parkeri aisladas en Argentina y en varios países de América. El paciente evolucionó favorablemente al tratamiento con doxiciclina
Genotypic diversity of Mycobacterium tuberculosis in Buenos Aires, Argentina
No full textFil: Monteserin, Johana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Paul, Roxana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Gravina, Elida. Hospital Interzonal General de Agudos Dr. Diego Paroissien; Argentina.Fil: Reniero, Ana. Hospital Central de San Isidro; Argentina.Fil: Hernández, Teresa. Centro de Zooantroponosis de La Matanza; Argentina.Fil: Mazzeo, Eduardo. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Togneri, Ana. Hospital Interzonal de Agudos Evita; Argentina.Fil: Simboli, Norberto. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: López, Beatriz. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Fil: Couvin, David. Institut Pasteur de la Guadeloupe. WHO Supranational TB Reference Laboratory; Francia.Fil: Rastogi, Nalin. Institut Pasteur de la Guadeloupe. WHO Supranational TB Reference Laboratory; Francia.Fil: Ritacco, Viviana. ANLIS Dr.C.G.Malbrán. Instituto Nacional de Enfermedades Infecciosas; Argentina.Buenos Aires is an overpopulated port city historically inhabited by people of European descent. Together with its broader metropolitan area, the city exhibits medium tuberculosis rates, and receives migrants, mainly from tuberculosis highly endemic areas of Argentina and neighboring countries. This work was aimed to gain insight into the Mycobacterium tuberculosis population structure in two suburban districts of Buenos Aires which are illustrative of the overall situation of tuberculosis in Argentina. The Lineage 4 Euro-American accounted for >99% of the 816 isolates analyzed (one per patient). Frequencies of spoligotype families were T 35.9%, LAM 33.2%, Haarlem 19.5%, S 3.2%, X 1.5%, Ural 0.7%, BOV 0.2%, Beijing 0.2%, and Cameroon 0.2%. Unknown signatures accounted for 5.3% isolates. Of 55 spoligotypes not matching any extant shared international type (SIT) in SITVIT database, 22 fitted into 15 newly-issued SITs. Certain autochthonous South American genotypes were found to be actively evolving. LAM3, which is wild type for RDrio, was the predominant LAM subfamily in both districts and the RDrio signature was rare among autochthonous, newly created, SITs and orphan patterns. Two genotypes that are rarely observed in neighboring countries ̶ SIT2/H2 and SIT159/T1 Tuscany ̶ were conspicuously represented in Argentina. The infrequent Beijing patterns belonged to Peruvian patients. We conclude that the genotype diversity observed reflects the influence of the Hispanic colonization and more recent immigration waves from Mediterranean and neighboring countries. Unlike in Brazil, the RDrio type does not play a major role in the tuberculosis epidemic in Buenos Aires