Hospital Muniz

Buenos Aires, Argentina

Hospital Muniz

Buenos Aires, Argentina
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Alfonso C.,Hospital Santojanni | Lopez M.,Hospital Ramos Mejia | Arechavala A.,Hospital Muniz | Perrone M.D.C.,Hospital Penna | And 2 more authors.
Revista Iberoamericana de Micologia | Year: 2010

Fungal infections caused by yeasts have increased during the last decades and invasive forms represent a serious problem for human health. Candida albicans is the species most frequently isolated from clinical samples. However, other emerging yeast pathogens are increasingly responsible for mycotic infections, and some of them are resistant to some antifungal drugs. Consequently, it is necessary to have methods that can provide a rapid presumptive identification at species level.Numerous chromogenic agar media have been shown to be of value as diagnostic tools. We have compared a chromogenic medium, Brilliance Candida Agar, with CHROMagar Candida, the chromogenic medium most used in our country. A multicentre study was conducted in 16 Hospitals belonging to the Mycology Net of Buenos Aires City Government. A total of 240 yeast isolates were included in this research.The new chromogenic agar showed results very similar to those obtained with CHROMagar Candida. © 2009 Revista Iberoamericana de Micología.


PubMed | Pan American Health Organization, University of Buenos Aires, Hospital Muniz, Laboratorio Central Of Cordoba and Direccion de Sida
Type: | Journal: The Journal of antimicrobial chemotherapy | Year: 2016

In Argentina, current national guidelines recommend starting with NNRTI-based regimens. Recently, there have been some local reports regarding concerning levels of NNRTI-transmitted resistance, but surveillance has never been carried out at a national level.To determine the prevalence of HIV drug resistance in people starting ART in Argentina using a WHO-proposed methodology.This was a cross-sectional, nationally representative study. Twenty-five antiretroviral-dispensing sites throughout the country were randomly chosen to enrol at least 330 persons starting ART, to generate a point prevalence estimate of resistance-associated mutations (RAMs) with a 5% CI (for the total population and for those without antiretroviral exposure). All consecutive patients older than 18 years starting or restarting ART in the chosen clinics were eligible. Samples were processed with Trugene and analysed using the Stanford algorithm.Between August 2014 and March 2015, we obtained 330 samples from people starting ART. The meanSD age was 3511 years, 63.4% were male, 16.6% had prior antiretroviral exposure and the median (IQR) CD4 count was 275 cells/mmThis surveillance study showed concerning levels of HIV drug resistance in Argentina, especially to NNRTIs. Due to this finding, Argentinas Ministry of Health guidelines will change, recommending performing a resistance test for everyone before starting ART. If this is taken up properly, it also might function as a continuing surveillance tool.


Balboa L.,Institute Investigaciones Hematologicas | Romero M.M.,Institute Investigaciones Hematologicas | Yokobori N.,Institute Investigaciones Hematologicas | Schierloh P.,Institute Investigaciones Hematologicas | And 7 more authors.
Immunology and Cell Biology | Year: 2010

During a chronic infection such as tuberculosis, the pool of tissue dendritic cells (DC) must be renewed by recruitment of both circulating DC progenitors and monocytes (Mo). However, the microenvironment of the inflammatory site affects Mo differentiation. As DC are critical for initiating a Mycobacterium tuberculosis-specific T-cell response, we argue that interference of M. tuberculosis with a correct DC generation would signify a mechanism of immune evasion. In this study, we showed that early interaction of γ-irradiated M. tuberculosis with Mo subverts DC differentiation in vitro. We found that irradiated M. tuberculosis effect involves (1) the loss of a significant fraction of monocyte population and (2) an altered differentiation process of the surviving monocyte subpopulation. Moreover, in the absence of irradiated M. tuberculosis, DC consist in a major DC-specific intercellular adhesion molecule 3-grabbing non-integrin receptor (DC-SIGNhigh)/ CD86low and minor DC-SIGNlow/CD86high subpopulations, whereas in the presence of bacteria, there is an enrichment of DC-SIGNlow/CD86high population. Besides, this population enlarged by irradiated M. tuberculosis, which is characterized by a reduced CD1b expression, correlates with a reduced induction of specific T-lymphocyte proliferation. The loss of CD1molecules partially involves toll-like receptors (TLR-2)/p38 MAPK activation. Finally, several features of Mo, which have been differentiated into DC in the presence of irradiated M. tuberculosis, resemble the features of DC obtained from patients with active tuberculosis. In conclusion, we suggest that M. tuberculosis escapes from acquired immune response in tuberculosis may be caused by an altered differentiation into DC leading to a poor M. tuberculosis-specific T-cell response. © 2010 Australasian Society for Immunology Inc. All rights reserved.


Balboa L.,CONICET | Romero M.M.,CONICET | Laborde E.,CONICET | Sabio y Garcia C.A.,CONICET | And 8 more authors.
European Journal of Immunology | Year: 2013

Tuberculosis (TB) is one of the world's most pernicious diseases mainly due to immune evasion strategies displayed by its causative agent Mycobacterium tuberculosis (Mtb). Blood monocytes (Mos) represent an important source of DCs during chronic infections; consequently, the alteration of their differentiation constitutes an escape mechanism leading to mycobacterial persistence. We evaluated whether the CD16+/CD16- Mo ratio could be associated with the impaired Mo differentiation into DCs found in TB patients. The phenotype and ability to stimulate Mtb-specific memory clones DCs from isolated Mo subsets were assessed. We found that CD16- Mos differentiated into CD1a+DC-SIGNhigh cells achieving an efficient recall response, while CD16+ Mos differentiated into a CD1a-DC-SIGNlow population characterized by a poor mycobacterial Ag-presenting capacity. The high and sustained phosphorylated p38 expression observed in CD16+ Mos was involved in the altered DC profile given that its blockage restored DC phenotype and its activation impaired CD16- Mo differentiation. Furthermore, depletion of CD16+ Mos indeed improved the differentiation of Mos from TB patients toward CD1a+DC-SIGNhigh DCs. Therefore, Mos from TB patients are less prone to differentiate into DCs due to their increased proportion of CD16+ Mos, suggesting that during Mtb infection Mo subsets may have different fates after entering the lungs. © 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.


Di Benedetto N.,Hospital Muniz | Peralta M.,Hospital Muniz | Alvarez E.,Hospital Posadas | Teresa Schroder M.,Hospital Muniz | And 3 more authors.
Annals of Hepatology | Year: 2014

Introduction. High activity antiretroviral therapy (HAART) has allowed people infected with human immunodeficiency virus (HIV) to live longer. In the course of time, hepatocellular carcinoma (HCC) began to be found in these patients. Investigations have suggested that, as it has been described for other tumors, HIV infection raises the risk of developing HCC. However, convincing evidence is still required. Our aim was to quantify the incidence of HCC in hepatitis C cirrhotic patients with and without human immunodeficiency virus infection in the HAART era. Material and methods. This prospective cohort study was conducted in hepatitis C cirrhotic patients with and without HIV co-infection, between june 1, 1999 and May 21, 2010. Ultrasound screening for HCC was performed every 6 to 12 months to all the patients until January 15, 2011. Incidence rate and cumulative incidence (Kaplan-Meier) were calculated. Results. One hundred and forty eight patients (69 hepatitis C virus mono-infected and 79 HIV/hepatitis C virus co-infected) were followed for a median time of 43 months, with a total follow-up of 555 person-years (324 for co-infected and 231 for mono-infected patients). Twelve patients developed HCC (5 co-infected and 7 mono-infected). The incidence of HCC in co-infected patients and mono-infected patients was 1.54 (95% confidence interval = 0.5 to 3.6) and 3.03 (95% confidence interval = 1.22 to 6.23) cases per 100 person-year respectively (log-rank p = 0.3225). Conclusion. In the HAART era, HIV co-infection is not associated with a higher incidence of HCC in hepatitis C cirrhotic patients.


Eldholm V.,Norwegian Institute of Public Health | Rieux A.,University College London | Monteserin J.,Instituto Nacional Of Enfermedades Infecciosas | Monteserin J.,CONICET | And 8 more authors.
eLife | Year: 2016

The tuberculosis (TB) epidemic is fueled by a parallel Human Immunodeficiency Virus (HIV) epidemic, but it remains unclear to what extent the HIV epidemic has been a driver for drug resistance in Mycobacterium tuberculosis (Mtb). Here we assess the impact of HIV co-infection on the emergence of resistance and transmission of Mtb in the largest outbreak of multidrug-resistant TB in South America to date. By combining Bayesian evolutionary analyses and the reconstruction of transmission networks utilizing a new model optimized for TB, we find that HIV co-infection does not significantly affect the transmissibility or the mutation rate of Mtb within patients and was not associated with increased emergence of resistance within patients. Our results indicate that the HIV epidemic serves as an amplifier of TB outbreaks by providing a reservoir of susceptible hosts, but that HIV co-infection is not a direct driver for the emergence and transmission of resistant strains. © Eldholm et al.


Zurbriggen R.,Centro Asistencial Metalurgico | Zurbriggen R.,National University of Rosario | Capone L.,Hospital Muniz
Medicina (Argentina) | Year: 2013

Asbestos-related diseases are caused by the inhalation of asbestos fibers in their variety chrysotile or white asbestos. Although the ban in Argentina dates from 2003, there are numerous industries where work continues with this mineral, including iron and steel industries. It is currently known the high pathogenicity of this material, so that in many countries there are programs to monitoring the exposed workers. Here we describe the general characteristics and pulmonary manifestations in 27 patients who had worked in a very huge steel factory in South America. The diagnosis of asbestos-related diseases was made by a medical-occupational record, history of asbestos exposure, additional studies of lung function and chest images. Then the sources of exposure (occupational, domestic and environmental), exposure time and latency period were analyzed, in those patients in whom a related disease was detected. Smoking history was also taken into account. Twenty-two patients had benigns pathologies (81.4%), sixteen of them with lesions localyzed in pleura, and other six pulmonary asbestosis. The malignant pathologies occurred in five patients (18.5%), in four of them mesothelioma and in other one lung cancer. The problem of asbestos exposure has contemporary relevance. Hence the need for a surveillance program in workers exposed to asbestos in the past or currently, to detect, report, record and investigate the characteristics of these pathologies.


PubMed | CONICET, Instituto Nacional Of Enfermedades Infecciosas and Hospital Muniz
Type: Journal Article | Journal: Clinical and experimental immunology | Year: 2016

We have reported previously that T cells from patients with multi-drug-resistant tuberculosis (MDR-TB) express high levels of interleukin (IL)-17 in response to the MDR strain M (Haarlem family) of Mycobacterium tuberculosis (M. tuberculosis). Herein, we explore the pathways involved in the induction of Th17 cells in MDR-TB patients and healthy tuberculin reactors [purified protein derivative healthy donors (PPD


PubMed | Imperial College London, Instituto Nacional Of Enfermedades Infecciosas, Hospital Muniz, University College London and Norwegian Institute of Public Health
Type: | Journal: eLife | Year: 2016

The tuberculosis (TB) epidemic is fueled by a parallel Human Immunodeficiency Virus (HIV) epidemic, but it remains unclear to what extent the HIV epidemic has been a driver for drug resistance in Mycobacterium tuberculosis (Mtb). Here we assess the impact of HIV co-infection on the emergence of resistance and transmission of Mtb in the largest outbreak of multidrug-resistant TB in South America to date. By combining Bayesian evolutionary analyses and the reconstruction of transmission networks utilizing a new model optimized for TB, we find that HIV co-infection does not significantly affect the transmissibility or the mutation rate of Mtb within patients and was not associated with increased emergence of resistance within patients. Our results indicate that the HIV epidemic serves as an amplifier of TB outbreaks by providing a reservoir of susceptible hosts, but that HIV co-infection is not a direct driver for the emergence and transmission of resistant strains.


PubMed | Hospital Muniz and Hospital Posadas
Type: Journal Article | Journal: Annals of hepatology | Year: 2013

INTRODUCTION. High activity antiretroviral therapy (HAART) has allowed people infected with human immunodeficiency virus (HIV) to live longer. In the course of time, hepatocellular carcinoma (HCC) began to be found in these patients. Investigations have suggested that, as it has been described for other tumors, HIV infection raises the risk of developing HCC. However, convincing evidence is still required. Our aim was to quantify the incidence of HCC in hepatitis C cirrhotic patients with and without human immunodeficiency virus infection in the HAART era. MATERIAL AND METHOds. This prospective cohort study was conducted in hepatitis C cirrhotic patients with and without HIV co-infection, between june 1, 1999 and May 21, 2010. Ultrasound screening for HCC was performed every 6 to 12 months to all the patients until January 15, 2011. Incidence rate and cumulative incidence (Kaplan-Meier) were calculated. RESULTS. One hundred and forty eight patients (69 hepatitis C virus mono-infected and 79 HIV/hepatitis C virus co-infected) were followed for a median time of 43 months, with a total follow-up of 555 person-years (324 for co-infected and 231 for mono-infected patients). Twelve patients developed HCC (5 co-infected and 7 mono-infected). The incidence of HCC in co-infected patients and mono-infected patients was 1.54 (95% confidence interval = 0.5 to 3.6) and 3.03 (95% confidence interval = 1.22 to 6.23) cases per 100 person-year respectively (log-rank p = 0.3225). CONCLUSION. In the HAART era, HIV co-infection is not associated with a higher incidence of HCC in hepatitis C cirrhotic patients.

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