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Resumen El objetivo del estudio fue determinar la presencia de Acanthamoeba spp. en piscinas de uso recreacional, al aire libre, de la ciudad de Córdoba, Argentina. Se recolectaron 30 muestras de agua correspondientes a un total de 10 piscinas. Estas se sembraron en agar no nutritivo en presencia de Escherichia coli en solución de Page. Luego de 72 horas de incubación a 37 °C, la identificación genérica se realizó mediante criterios morfológicos. La prueba de transformación amebo-flagelar se realizó para diferenciar amebas de vida libre que desarrollan trofozoítos flagelados, como Naegleria. Se midieron parámetros fisicoquímicos en cada una de las piscinas. Se identificó Acanthamoeba spp. en el 20% del total de las muestras. Las piscinas en las que se aisló este parásito presentaron niveles no detectables de cloro residual, pH moderadamente alcalino y temperatura templada. Este estudio demuestra la presencia de Acanthamoeba spp. en piscinas recreativas de Córdoba, lo que puede representar un potencial riesgo para la salud pública.

Abstract The aim of the study was to determine the presence of Acanthamoeba spp. in outdoor recreational pools, in Córdoba city, Argentina. Thirty water samples corresponding to a total of 10 pools were collected. These samples were sown on a non-nutritive agar in the presence of Escherichia coli in Pages's solution. After 72 hours of incubation at 37 °C, the generic identification was done based on morphological criteria. The amoebo-flagellate transformation test was performed to differentiate from genera that develop flagellated trophozoites, such as Naegleria. Physicochemical parameters were measured in each of the pools. Acanthamoeba spp. was identified in 20% of the samples. The pools, where this parasite was isolated, presented undetectable levels of residual chlorine, moderately alkaline pH and warm temperature. This study demonstrates the presence of Acanthamoeba spp. in recreational pools in Córdoba, which may represent a potential risk to public health.

Resumo O objetivo do estudo foi determinar a presença de Acanthamoeba spp. em piscinas para uso recreativo, ao ar livre, na cidade de Córdoba, Argentina. Foram coletadas 30 amostras de água correspondentes a um total de 10 piscinas. Elas foram semeadas em ágar não nutritivo na presença de Escherichia coli em solução de Page. Após 72 horas de incubação a 37 °C, a identificação genérica foi realizada utilizando critérios morfológicos. O teste de transformação amebo-flagelar foi realizado para diferenciar amebas de vida livre que desenvolvem trofozoítos flagelados, como Naegleria. Parâmetros físico-químicos foram medidos em cada uma das piscinas. Acanthamoeba spp. foi identificada em 20% do total das amostras. As piscinas onde este parasita foi isolado apresentaram níveis indetectáveis de cloro residual, pH moderadamente alcalino e temperatura temperada. Esse estudo demonstra a presença de Acanthamoeba spp. em piscinas recreativas de Córdoba, o que pode representar um risco potencial para a saúde pública.

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La EGC es una patología de baja prevalencia incluida en el grupo de los defectos congénitos de los fagocitos. Existen dos formas de transmisión genética: ligada a X, la más frecuente y grave, y autosómica recesiva. Se debe a mutaciones de los genes que codifican para las proteínas que constituyen el complejo NADP oxidasa lo que induce incapacidad en fagocitos para realizar el estallido respiratorio. El diagnóstico se fundamenta en el fenotipo clínico y de laboratorio; la prueba de dihidrorodamina (DHR) con estímulo de PMA por citometría de flujo es el método diagnóstico de elección. El diagnóstico definitivo es la identificación de la mutación genética por secuenciación del ADN. La terapéutica curativa de esta patología es el trasplante de células madres hematopoyéticas (TCHP). (AU)

CGD is a low prevalence pathology included in the group of congenital phagocyte defects. There are two forms of genetic transmission: the X-linked, the most frequent and severe, and autosomal recessive. It is due to a mutation of the genes coding for proteins that constitute the NADP oxidase complex, which induces inability of phagocytes to perform respiratory burst. The initial diagnosis is based on the clinical and laboratory phenotype; the dihydrorhodamine (DHR) test with PMA stimulation by flow cytometry is a diagnostic method of choice. The demonstration of the genetic mutation by DNA sequencing is the definitive diagnosis. The haemopoietic stem-cell transplantation (HSCT) is the curative therapy of this pathology. (AU)

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PROBLEM: IgG is the only antibody class, that is, actively transferred from the mother to the fetus across the placenta by an active, neonatal Fc receptor (FcRn) mediated process during pregnancy, conferring passive immunity and protection against infections to the newborn during the first months of life. Preterm infants may not receive sufficient titers of protective antibodies, as most of them are transferred only after the 34th week of gestation. Because of the great importance of this process, we investigated in a clinical setting the placental transmission of IgG antibodies in term and preterm newborns. METHOD OF STUDY: This work was conducted in 85 woman and their newborns, divided into four groups according to their clinical gestational age (≤37 weeks were considered as preterm). Blood samples were collected from the mothers and their newborns' umbilical cords to analyze total serum IgG concentrations, and a subgroup of 32 placentas was analyzed by immunohistochemistry to quantify the expression of the FcRn receptor. RESULTS: Total IgG levels in both mothers and neonates increased significantly through the third trimester of gestation. Regarding the newborns, in all groups, IgG levels exceeded their mother's values by a ~2.4%. A higher expression of FcRn was detected in placentas from newborns at week 36 of gestation onwards. CONCLUSION: Our results obtained from clinical samples, were in line with previous descriptions in model systems and confirmed that the IgG transfer from maternal serum to the fetus is positively correlated with FcRn expression in placental tissue throughout gestation.

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Dogs play a major role in the domestic cycle of Trypanosoma cruzi, acting as reservoirs. In a previous work we have developed a model of vaccination of dogs in captivity with nonpathogenic Trypanosoma rangeli epimastigotes, resulting in the production of protective antibodies against T. cruzi, with dramatic decrease of parasitaemia upon challenge with 100,000 virulent forms of this parasite. The aim of this work was to evaluate the immunogenicity of this vaccine in dogs living in a rural area. Domestic dogs, free from T. cruzi infection, received three immunisations with fixed T. rangeli epimastigotes. Dogs were not challenged with T. cruzi, but they were left in their environment. This immunisation induced antibodies against T. cruzi for more than three years in dogs in their natural habitat, while control dogs remained serologically negative.

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In America, there are two species of Trypanosoma that can infect humans: Trypanosoma cruzi, which is responsible for Chagas disease and Trypanosoma rangeli, which is not pathogenic. We have developed a model of vaccination in mice with T. rangeli epimastigotes that protects against T. cruzi infection. The goal of this work was to study the pattern of specific immunoglobulins in the peritoneum (the site of infection) and in the sera of mice immunized with T. rangeli before and after challenge with T. cruzi. Additionally, we studied the effects triggered by antigen-antibodies binding and the levels of key cytokines involved in the humoral response, such as IL-4, IL-5 and IL-6. The immunization triggered the production of antibodies reactive with T. cruzi in peritoneal fluid (PF) and in serum, mainly IgG1 and, to a lesser magnitude, IgG2. Only immunized mice developed specific IgG3 antibodies in their peritoneal cavities. Antibodies were able to bind to the surface of the parasites and agglutinate them. Among the cytokines studied, IL-6 was elevated in PF during early infection, with higher levels in non-immunized-infected mice. The results indicate that T. rangeli vaccination against T. cruzi infection triggers a high production of specific IgG isotypes in PF and sera before infection and modulates the levels of IL-6 in PF in the early periods of infection.

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In America, there are two species of Trypanosoma that can infect humans: Trypanosoma cruzi, which is responsible for Chagas disease and Trypanosoma rangeli, which is not pathogenic. We have developed a model of vaccination in mice with T. rangeli epimastigotes that protects against T. cruzi infection. The goal of this work was to study the pattern of specific immunoglobulins in the peritoneum (the site of infection) and in the sera of mice immunized with T. rangeli before and after challenge with T. cruzi. Additionally, we studied the effects triggered by antigen-antibodies binding and the levels of key cytokines involved in the humoral response, such as IL-4, IL-5 and IL-6. The immunization triggered the production of antibodies reactive with T. cruzi in peritoneal fluid (PF) and in serum, mainly IgG1 and, to a lesser magnitude, IgG2. Only immunized mice developed specific IgG3 antibodies in their peritoneal cavities. Antibodies were able to bind to the surface of the parasites and agglutinate them. Among the cytokines studied, IL-6 was elevated in PF during early infection, with higher levels in non-immunized-infected mice. The results indicate that T. rangeli vaccination against T. cruzi infection triggers a high production of specific IgG isotypes in PF and sera before infection and modulates the levels of IL-6 in PF in the early periods of infection.

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