Cuando la genética estaba oculta. Miocardiopatía hipertrófica por variante MYBPC3 c.1102A>T (p.Lys368*) refractaria a manejo médico. Reporte de un caso

La miocardiopatía hipertrófica es cada vez más diagnosticada. Es una condición genética que genera hipertrofia miocárdica, fibrosis, isquemia y apoptosis con obstrucción del tracto de salida del ventrículo izquierdo. Puede generar síncope, falla cardíaca y muerte súbita. El tratamiento es farmacológico y se requiere cirugía si hay refractariedad. Se presenta un caso de miocardiopatía hipertrófica asociada a variante genética patogénica en un paciente no respondedor a manejo médico óptimo. La importancia de este artículo radica en lo determinante que es la genética para el abordaje diagnóstico y el establecimiento del origen y pronóstico de esta enfermedad.

Summary: Hypertrophic cardiomyopathy is increasingly diagnosed. It is a genetic condition that leads to myocardial hypertrophy, fibrosis, ischemia, and apoptosis with obstruction of the left ventricular outflow tract. It can result in syncope, heart failure, and sudden death. Treatment is pharmacological, and surgery is required in cases of refractoriness. A case of hypertrophic cardiomyopathy associated with a pathogenic genetic variant is presented in a patient unresponsive to optimal medical management. The importance of this article lies in how crucial genetics is for the proper diagnostic approach and the establishment of the origin and prognosis of this disease.

A miocardiopatia hipertrófica está sendo diagnosticada cada vez mais. É uma condição genética que leva à hipertrofia miocárdica, fibrose, isquemia e apoptose com obstrução do trato de saída do ventrículo esquerdo. Pode resultar em síncope, insuficiência cardíaca e morte súbita. O tratamento é farmacológico e a cirurgia é necessária em casos de refratariedade. Apresenta-se um caso de miocardiopatia hipertrófica associada a uma variante genética patogênica em um paciente não responsivo ao manejo médico ótimo. A importância deste artigo reside na determinante genética para a abordagem diagnóstica adequada e para o estabelecimento da origem e prognóstico desta doença.

Adición de un probiótico de Lactobacillus plantarum microencapsulado en el alimento para pollos / Addition of a probiotic containing microenscapsulated Lactobacillus plantarum to chicken feed

Introducción: En producción avícola el uso de antibióticos promotores del crecimiento es limitado, debido al incremento de resistencia bacteriana. Una alternativa evalúa los probióticos microencapsulados y su efecto en la salud intestinal. Objetivo: Determinar el efecto de Lactobacillus plantarum microencapsulado sobre parámetros intestinales e inmunológicos en pollos de engorde. Materiales y métodos: A 240 pollos Ross-308-AP de un día de nacidos se suministró alimento con o sin adición de probiótico bajo el siguiente modelo: sin probiótico-(T0), con probiótico comercial-(T1), con L. plantarum microencapsulado-(T2) y sin microencapsular-(T3). L. plantarum ATCC-8014 se microencapsuló mediante secado por aspersión, determinando su viabilidad en (%). Se evaluaron parámetros intestinales, morfo-histopatológicos e inmunológicos por Azul de Alcian, microscopia de barrido e inmunohistoquímica y la abundancia microbial por UFC/mL. Resultados: El microencapsulado confirió una viabilidad in vivo de L. plantarum del 88,1%. El tratamiento T2 mejoró los parámetros inmunológicos y confirió beneficios intestinales con una abundancia de bacterias benéficas (Lactobacillus) de (9,13x105-UFC/mL), significativamente mayor a la encontrada en los tratamientos T1 (8,91x105) y T3 (8,23x105) y el control T0 (9,18x104), (p<0,05). Conclusiones: La adición de L. plantarum microencapsulado en alimento para pollos mejora parámetros inmunológicos y confiere mayor abundancia de bacterias benéficas presentes en la microbiota intestinal.

Introduction: Usage of growth-promoting antibiotics in poultry production is limited due to the increase in bacterial resistance. An alternative to assess microencapsulated probiotics and their effect on gut health is presented in this study. Objective: To determine the effect of microencapsulated L. plantarum on intestinal and immunological parameters in broilers. Materials and methods: 240 Ross-308-AP chickens (one day old) were fed with or without the addition of a probiotic, under the following model: without probiotic (T0); with commercial probiotic (T1); with probiotic containing either microencapsulated (T2) or non-microencapsulated (T3) L. plantarum. ATCC-8014 was microencapsulated by spray drying, assessing its viability in (%). Alcian blue, scanning microscopy, and immunohistochemistry were used to evaluate intestinal, morpho-histopathological, and immunological parameters. Microbial abundance was quantified by UFC/ml. Results: Microencapsulation of L. plantarum induced an 88.1% in vivo viability. T2 treatment improved both immunological parameters and the intestinal population of beneficial bacteria (Lactobacillus) (9.13x105 UFC/ml), which was significantly higher than that found in T1 (8.91x105), T3 (8.23x105), and control T0 (9.18x104), (p<0.05). Conclusion: Adding microencapsulated L. plantarum to chicken feed improves immunological parameters and increases the population of beneficial bacteria in the intestinal microbiota.

Polimorfismos IL1B-511 y TNF-A-308 en una población infectada con Helicobacter pylori de una zona de bajo riesgo de cáncer gástrico en Nariño-Colombia / IL1B-511 and TNF-A-308 polymorphisms in a population infected with Helicobacter pylori from a low-risk area of gastric cancer in Nariño-Colombia

Objetivo: Estudiar los polimorfismos IL1B-511 y TNF-A-308 asociaciados a lesiones precursoras de cáncer gástrico (CG) en una población infectada con Helicobacter pylori (H. pylori) de bajo riesgo de CG de Nariño. Material y método: De 105 pacientes con síntomas de dispepsia se incluyeron 81 infectados por H. pylori, (n=63) con gastritis no atrófica y (n=18) con lesiones precursoras de CG de Tumaco: población de bajo riesgo de CG. Las lesiones gástricas se clasificaron por el sistema de Sydney y H. pylori por tinción de Giemsa. Los polimorfismos de IL1B-511 y TNF-A-308 se genotipificaron por PCR-RFLP's. Los polimorfismos y su asociación con lesiones gastricas se evaluaron por análisis bivariado y regresión logística binomial. Resultados: Los pacientes portadores del alelo mutante T (IL-1B-511) no se encontraron a riesgo de lesiones precursoras de malignidad (OR=0,7). No se calculó el OR para TNF-A-308, por fijación del alelo normal G. Ser hombre y estar infectado por H. pylori incrementa 4,3 veces el riesgo de presentar lesiones precursoras de CG y no estar vinculado al régimen de salud aumenta 6,7 veces el riesgo de atrofia gástrica, (OR=4,27 y OR=6,72), respectivamente. Conclusión: El alelo mutante T (IL-1B-511) es un biomarcador de resistencia de los pobladores de Tumaco, de bajo riesgo de CG e infectados con H. pylori a padecer lesiones precursoras de CG.

Aim: To study the IL1B-511 and TNF-A-308 polymorphisms and their possible association with gastric cancer (GC) precursor lesions in a population infected with Helicobacter pylori (H. pylori) of low risk area of GC of Nariño. Material/method: 105 patients with symptoms of dyspepsia were included, 81 infected with H. pylori, (n=63) with non-atrophic gastritis and (n=18) with precursor lesions of GC of Tumaco: population of low risk of GC. Gastric lesions were classified by the Sydney System an H. pylori by Giemsa staining. The IL1B-511 and TNFA-308 polymorphisms were genotyped by PCR-RFLPs. Polymorphisms and their association with gastric lesions were evaluated by bivariate analysis and binomial logistic regression. Results: Patients carryng the mutant T allele (IL-1B-511) were not at risk of precursor lesions of malignancy (OR=0,7). The OR was not calculated for TNF-A-308, by fixing the normal allele G. Being a man and being infected with H. pylori increases 4,3 times the risk of presenting precursor lesions of GC and not being linked to the health regimen increases 6,7 times the risk of gastric atrophy, (OR=4,27 and OR=6,72), respectively. Conclusion: The mutant T allele (IL-1B-511) is a resistance biomarker of Tumaco residents, low risk of GC and infected with H. pylori to suffer precursor lesions of GC.

Febrile infection-related epilepsy syndrome (fires), a possible cause of super-refractory status epilepticus. case report

ABSTRACT Introduction: Super-refractory status epilepticus (SRSE) is a pathology that affects the neuronal environment depending on the types of seizure and their duration. Case presentation. This paper presents the case of a 7-year old child presenting with super-refractory status epilepticus and multifocal seizures. Metabolic, structural, infectious, toxicological and autoimmune causes were discarded, while different anticonvulsive agents were administered without any clinical improvement; seizures were controlled 6 weeks after admission to ICU. A 12-year follow-up was performed, during which time the patient presented recurrent status epilepticus with autonomic seizures and progressive cognitive decline. Discussion: This type of status epilepticus is part of the syndrome known as Febrile Infection-Related Epilepsy Syndrome (FIRES), a possibly autoimmune form of epileptic encephalopathy that is refractory to acute and chronic management. There is no report in the literature that includes long term follow-up, therefore, there is no actual consensus about the appropriate management of the chronic phase of the disease. Conclusion: FIRES must be considered as one of the possible etiologies of super-refractory status epilepticus, so early management strategies (like ketogenic diet) can be used in order to achieve control of the critically ill patient, control long term seizures and improve cognitive outcomes, having as the final result a positive impact on the quality of life of the patient.

RESUMEN Introducción: El estado epiléptico superrefractario (EES) es una patología con importante morbimortalidad que afecta el ambiente neuronal según el tipo y duración de las crisis. Presentación del caso: Se presenta el caso de un escolar con estado epiléptico superrefractario y crisis multifocales. Se descartaron causas metabólicas, estructurales, infecciosas, toxicológicas y autoinmunes y se utilizaron diferentes manejos anticonvulsivantes sin respuesta, lográndose control de las crisis 6 semanas después del ingreso a UCI. Se realizó un seguimiento de 12 años, periodo en el que el paciente presentó múltiples recaídas del estado epiléptico asociadas a la presencia de epilepsia refractaria con múltiples tipos de crisis, en su mayoría vegetativas; además se dio involución cognitiva. Discusión: Esta forma de estado epiléptico corresponde al síndrome de estado epiléptico facilitado por fiebre (FIRES), entidad de posible origen inmunológico conocida por ser refractaria al tratamiento agudo y al manejo crónico de la epilepsia y que se presenta como secuela. Su evolución no se ha descrito a largo plazo y por tanto no hay consenso sobre el manejo en la fase crónica. Conclusión: Es importante considerar esta etiología en estado epiléptico superrefractario para utilizar de forma temprana diferentes estrategias terapéuticas, como la dieta cetogénica, que permitan, por un lado, controlar su condición crítica y las crisis epilépticas a largo plazo y, por el otro, mejorar el pronóstico cognitivo, logrando así un impacto en la calidad de vida.

Ética y progreso de la ciencia: [Editorial] / Ethics and Scientific Progress: [Editorial]

En este número de la Revista se publica un artículo sobre "La Comisión Reed y el origen del Consentimiento Informado" que es una completa revisión histórica sobre los experimentos en voluntarios realizados para dilucidar el modo de transmisión de la Fiebre Amarilla, una de las enfermedades epidémicas que asolaban los puertos del continente americano y del Caribe en el Siglo XIX. El documento que firmaban los voluntarios que se sometían a las experimentaciones es el origen del consentimiento informado que aún hoy en día es la piedra angular de la ética en la experimeción clinica y epidemiologica

This issue of the Journal contains an article on "The Reed Commission and the origin of Informed Consent", which is a complete historical review of the experiments on volunteers carried out to elucidate the mode of transmission of Yellow Fever, one of the epidemic diseases that ravaged the ports of the American continent and the Caribbean in the 19th century. The document signed by the volunteers who underwent the experiments is the origin of the informed consent that is still today the cornerstone of ethics in experimentation.

Carlos Chagas: biographical sketch.

Carlos Chagas was born on 9 July 1878 in the farm "Bon Retiro" located close to the City of Oliveira in the interior of the State of Minas Gerais, Brazil. He started his medical studies in 1897 at the School of Medicine of Rio de Janeiro. In the late XIX century, the works by Louis Pasteur and Robert Koch induced a change in the medical paradigm with emphasis in experimental demonstrations of the causal link between microbes and disease. During the same years in Germany appeared the pathological concept of disease, linking organic lesions with symptoms. All these innovations were adopted by the reforms of the medical schools in Brazil and influenced the scientific formation of Chagas. Chagas completed his medical studies between 1897 and 1903 and his examinations during these years were always ranked with high grades. Oswaldo Cruz accepted Chagas as a doctoral candidate and directed his thesis on "Hematological studies of Malaria" which was received with honors by the examiners. In 1903 the director appointed Chagas as research assistant at the Institute. In those years, the Institute of Manguinhos, under the direction of Oswaldo Cruz, initiated a process of institutional growth and gathered a distinguished group of Brazilian and foreign scientists. In 1907, he was requested to investigate and control a malaria outbreak in Lassance, Minas Gerais. In this moment Chagas could not have imagined that this field research was the beginning of one of the most notable medical discoveries. Chagas was, at the age of 28, a Research Assistant at the Institute of Manguinhos and was studying a new flagellate parasite isolated from triatomine insects captured in the State of Minas Gerais. Chagas made his discoveries in this order: first the causal agent, then the vector and finally the human cases. These notable discoveries were carried out by Chagas in twenty months. At the age of 33 Chagas had completed his discoveries and published the scientific articles that gave him world recognition and a deserved high place in medical history. After the publication of his classic article the world paid homage to Chagas who was elected member of the National Academy of Medicine of Brazil on 26 October 1910, and at the age of 31, of other National Academies of the continent. The Committee of Hygiene of the Society of Nations, precursor of the World Health Organization, was created in 1929. Chagas was elected member of this Committee from its inception until 1933. The example of Chagas' life can be summarized in his interest that medical research should be translated into concrete benefits for human beings because he was convinced that disease had not only biological but social determinants as well. Carlos Chagas was a laboratory researcher, a clinician and a health administrator. For all these accomplishments he deserves our respect and admiration.

Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy.

Chagas disease, named after Carlos Chagas, who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, which is transmitted to humans by blood-sucking triatomine bugs and via blood transfusion. Chagas disease has two successive phases: acute and chronic. The acute phase lasts six-eight weeks. Several years after entering the chronic phase, 20-35% of infected individuals, depending on the geographical area, will develop irreversible lesions of the autonomous nervous system in the heart, oesophagus and colon, and of the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980s as a result of the demographically representative cross-sectional studies in countries where accurate information was not previously available. A group of experts met in Brasilia in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country programme in the Southern Cone countries, the transmission of Chagas disease by vectors and via blood transfusion was interrupted in Uruguay in 1997, in Chile in 1999 and in Brazil in 2006; thus, the incidence of new infections by T. cruzi across the South American continent has decreased by 70%. Similar multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been reported towards the goal of interrupting the transmission of Chagas disease, as requested by a 1998 Resolution of the World Health Assembly. The cost-benefit analysis of investment in the vector control programme in Brazil indicates that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the programme is a health investment with very high return. Many well-known research institutions in Latin America were key elements of a worldwide network of laboratories that carried out basic and applied research supporting the planning and evaluation of national Chagas disease control programmes. The present article reviews the current epidemiological trends for Chagas disease in Latin America and the future challenges in terms of epidemiology, surveillance and health policy.

Current epidemiological trends for Chagas disease in Latin America and future challenges in epidemiology, surveillance and health policy

Chagas disease, named after Carlos Chagas, who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, which is transmitted to humans by blood-sucking triatomine bugs and via blood transfusion. Chagas disease has two successive phases: acute and chronic. The acute phase lasts six-eight weeks. Several years after entering the chronic phase, 20-35% of infected individuals, depending on the geographical area, will develop irreversible lesions of the autonomous nervous system in the heart, oesophagus and colon, and of the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980s as a result of the demographically representative cross-sectional studies in countries where accurate information was not previously available. A group of experts met in Brasilia in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country programme in the Southern Cone countries, the transmission of Chagas disease by vectors and via blood transfusion was interrupted in Uruguay in 1997, in Chile in 1999 and in Brazil in 2006; thus, the incidence of new infections by T. cruzi across the South American continent has decreased by 70 percent. Similar multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been reported towards the goal of interrupting the transmission of Chagas disease, as requested by a 1998 Resolution of the World Health Assembly. The cost-benefit analysis of investment in the vector control programme in Brazil indicates that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the programme is a health investment with very high return. Many well-known research institutions in Latin America...

[Diagnosis, management and treatment of chronic Chagas' heart disease in areas where Trypanosoma cruzi infection is not endemic]. / Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica.

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment.

Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica / Diagnosis, Management and Treatment of Chronic Chagas' Heart Disease in Areas Where Trypanosoma cruzi Infection Is Not Endemic

La enfermedad de Chagas o tripanosomiasis americana es una parasitosis originaria del continente americano. En la naturaleza, Trypanosoma cruzi se transmite vectorialmente a través de diversas especies de chinches triatominos. No obstante, se han descrito otros mecanismos de transmisión no vectorial, como la transmisión a través de productos sanguíneos o mediante el trasplante de órganos infectados, y la transmisión vertical. Actualmente, la enfermedad de Chagas afecta a unos 10-12 millones de personas en el mundo y el proceso de urbanización en América Latina y los movimientos migratorios desde los países endémicos han posibilitado que la enfermedad de Chagas sea diagnosticada en zonas donde la infección no es endémica. Se considera que un 20-30% de las personas infectadas por T. cruzi desarrollarán a lo largo de su vida alteraciones cardíacas. Las características diferenciales de la cardiopatía chagásica, el escaso conocimiento que se tiene de ella en nuestro medio y la elevada frecuencia de arritmias y muerte súbita como primeras manifestaciones potenciales de esta enfermedad hacen prioritarias la elaboración y divulgación de protocolos diagnósticos y terapéuticos para la atención de estos pacientes a fin de mejorar el conocimiento de esta patología por los profesionales sanitarios potencialmente implicados en su detección y manejo (AU)

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment (AU)

[Diagnosis, management and treatment of chronic Chagas' heart disease in areas where Trypanosoma cruzi infection is not endemic]. / Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica.

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment.

Diagnóstico, manejo y tratamiento de la cardiopatía chagásica crónica en áreas donde la infección por Trypanosoma cruzi no es endémica / Diagnosis, management and treatment of chronic Chagas' heart disease in areas where Trypanosoma cruzi infection is not endemic

La enfermedad de Chagas o tripanosomiasis americana es una parasitosis originaria del continente americano. En la naturaleza, Trypanosoma cruzi se transmite vectorialmente a través de diversas especies de chinches triatominos. No obstante, se han descrito otros mecanismos de transmisión no vectorial, como la transmisión a través de productos sanguíneos o mediante el trasplante de órganos infectados, y la transmisión vertical. Actualmente, la enfermedad de Chagas afecta a unos 10-12 millones de personas en el mundo y el proceso de urbanización en América Latina y los movimientos migratorios desde los países endémicos han posibilitado que la enfermedad de Chagas sea diagnosticada en zonas donde la infección no es endémica. Se considera que un 20-30% de las personas infectadas por T. cruzi desarrollarán a lo largo de su vida alteraciones cardiacas. Las características diferenciales de la cardiopatía chagásica, el escaso conocimiento que se tiene de ella en nuestro medio y la elevada frecuencia de arritmias y muerte súbita como primeras manifestaciones potenciales de esta enfermedad hacen prioritarias la elaboración y divulgación de protocolos diagnósticos y terapéuticos para la atención de estos pacientes a fin de mejorar el conocimiento de esta patología por los profesionales sanitarios potencialmente implicados en su detección y manejo

Chagas' disease, or American trypanosomiasis, is a parasitic zoonosis found only in the Americas. Under natural conditions, Trypanosoma cruzi is transmitted by insects belonging to different species of Triatoma. However, several routes of transmission that do not involve insect vectors have also been described, such as transmission via blood products or transplantation of infected organs, and vertical transmission. At present, the number of people infected with Chagas' disease worldwide is estimated to be about 10-12 million. The process of urbanization in Latin America and migratory population movements from endemic countries have led to the disease being diagnosed in non-endemic areas. It is estimated that 20-30% of individuals infected with T. cruzi will develop symptomatic heart disease at some point during their lives. The specific differential characteristics of chronic chagasic cardiopathy, lack of knowledge of the disease among many healthcare workers, and the fact that arrhythmia or sudden death is frequently the first manifestation of disease all make it essential that diagnostic and therapeutic protocols for the disease are developed and disseminated. The aim should be to improve patient care by increasing understanding of the condition by physicians and other healthcare professionals who may be involved in its detection and treatment

Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries.

Chagas disease, named after Carlos Chagas who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, transmitted to humans by blood-sucking triatomine bugs and by blood transfusion. Chagas disease has two successive phases, acute and chronic. The acute phase lasts 6 to 8 weeks. After several years of starting the chronic phase, 20% to 35% of the infected individuals, depending on the geographical area will develop irreversible lesions of the autonomous nervous system in the heart, esophagus, colon and the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980's as a result of the demographically representative cross-sectional studies carried out in countries where accurate information was not available. A group of experts met in Bras lia in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country program in the Southern Cone countries the transmission of Chagas disease by vectors and by blood transfusion has been interrupted in Uruguay in1997, in Chile in 1999, and in 8 of the 12 endemic states of Brazil in 2000 and so the incidence of new infections by T. cruzi in the whole continent has decreased by 70%. Similar control multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been recorded to ensure the interruption of the transmission of Chagas disease by 2005 as requested by a Resolution of the World Health Assembly approved in 1998. The cost-benefit analysis of the investments of the vector control program in Brazil indicate that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the program is a health investment with good return. Since the inception in 1979 of the Steering Committee on Chagas Disease of the Special Program for Research and Training in Tropical Diseases of the World Health Organization (TDR), the objective was set to promote and finance research aimed at the development of new methods and tools to control this disease. The well known research institutions in Latin America were the key elements of a world wide network of laboratories that received - on a competitive basis - financial support for projects in line with the priorities established. It is presented the time line of the different milestones that were answering successively and logically the outstanding scientific questions identified by the Scientific Working Group in 1978 and that influenced the development and industrial production of practical solutions for diagnosis of the infection and disease control.

Chagas disease: current epidemiological trends after the interruption of vectorial and transfusional transmission in the Southern Cone countries

Chagas disease, named after Carlos Chagas who first described it in 1909, exists only on the American Continent. It is caused by a parasite, Trypanosoma cruzi, transmitted to humans by blood-sucking triatomine bugs and by blood transfusion. Chagas disease has two successive phases, acute and chronic. The acute phase lasts 6 to 8 weeks. After several years of starting the chronic phase, 20 percent to 35 percent of the infected individuals, depending on the geographical area will develop irreversible lesions of the autonomous nervous system in the heart, esophagus, colon and the peripheral nervous system. Data on the prevalence and distribution of Chagas disease improved in quality during the 1980's as a result of the demographically representative cross-sectional studies carried out in countries where accurate information was not available. A group of experts met in Brasília in 1979 and devised standard protocols to carry out countrywide prevalence studies on human T. cruzi infection and triatomine house infestation. Thanks to a coordinated multi-country program in the Southern Cone countries the transmission of Chagas disease by vectors and by blood transfusion has been interrupted in Uruguay in1997, in Chile in 1999, and in 8 of the 12 endemic states of Brazil in 2000 and so the incidence of new infections by T. cruzi in the whole continent has decreased by 70 percent. Similar control multi-country initiatives have been launched in the Andean countries and in Central America and rapid progress has been recorded to ensure the interruption of the transmission of Chagas disease by 2005 as requested by a Resolution of the World Health Assembly approved in 1998. The cost-benefit analysis of the investments of the vector control program in Brazil indicate that there are savings of US$17 in medical care and disabilities for each dollar spent on prevention, showing that the program is a health investment with good return. Since the inception in 1979 of the Steering Committee on Chagas Disease of the Special Program for Research and Training in Tropical Diseases of the World Health Organization (TDR), the objective was set to promote and finance research aimed at the development of new methods and tools to control this disease. The well known research institutions in Latin America were the key elements of a world wide network of laboratories that received - on a competitive basis - financial support for projects in line with the priorities established...

Progreso en la interrupción de la transmisión de la enfermedad de Chagas en América Latina / Progress in the prevention of Chagas disease transmission in Latin America

Alrededor de 18 millones de personas estaban infectadas en América Latina con el parásito Trypanosoma cruzi, causante de la epidemia de Chagas. Estudios de prevalencia hechos en la década de los 80, mostraron además que un 25/100 de estas personas desarrollaron lesiones caerdíacas crónicas y digestivas irreversibles. La Organización Mundial de la Salud y el Banco Mundial vienen adelantando investigaciones por cerca de un cuarto de siglo, conducentes al control y eventual eliminación de esta patología en el sub-continente. Este artículo enumera las actividades referentes a la enfermedad de Chagas y que se denominan iniciativas del Cono Sur, de los países andinos y de los países centroamericanos.