Streptococcus pneumoniae, or pneumococcus, is a normal inhabitant of nasopharynx, but also causes infections such as otitis, bacteremia, pneumonia and meningitis. It’s one of the main bacterial pathogens involved in human health and causes 1.5 million of deaths annually. The pneumococcus is a typical extracellular pathogen, however, an intracellular transient life has been recently reported in host cells.
In our lab, we have described different signaling transduction systems that pneumococcus use to sense and adapt to acidic and oxidative conditions that bacteria must overcome into host cells, and it is performed by controlling expression of stress response genes. For this purpose, we use molecular biology methods to construct mutants of genes that encode these systems, as well as to analyze expression of these genes.
In addition, we have also established an S. pneumoniae infection model in pneumocytes, macrophages and neutrophils to elucidate the survival mechanism of this pathogen at intracellular level. We also use cellular biology methods, as fusion to fluorescent proteins, to localize to pneumococcus with different cellular markers to identify the type of intracellular vesicles where this pathogen survives on host cells.
He did his postdoctoral work between 1997 and 2001 at the Universite Paul Sabatier, Toulouse, France with a grant from the Rhone-Poulenc Rorer laboratory (now Sanofi). During this period he identified signal transduction systems of S. pneumoniae involved in virulence.
In university management, he held the position of Director of the Bacteriology Specialty Course (2008-2011) and Secretary of International Relations of the UNC (2011-2013).
Since 2002 he has been a member of the CONICET Research Career, where he is currently an Independent Researcher at CIBICI.
He teaches in the Department of Clinical Biochemistry FCQ-UNC, currently occupying the position of Associate Professor in charge of the subject Bacteriology and Virology. In addition, he is currently Vice-Director of CIBICICI.
He also teaches in the Department of Clinical Biochemistry FCQ-UNC, occupying the position of Assistant Professor DSE by competition.
She is a CONICET doctoral fellow under the direction of Dr. José Echenique. She is working on her PhD thesis in Chemical Sciences at the FCQ-UNC, addressing the topic: «Cell division of Streptococcus pneumonie».
She is also a lecturer in the Department of Clinical Biochemistry FCQ-UNC, holding the position of Assistant Professor.
She is a CONICET Doctoral Fellow under the direction of Dr. José Echenique. She is doing her PhD thesis in Chemical Sciences at FCQ-UNC, addressing the topic: «Contribution of the response to oxidative stress in the intracellular survival mechanism of Streptococcus pneumoniae in eukaryotic cells».
She is also a lecturer in the Department of Clinical Biochemistry FCQ-UNC, holding the position of Assistant Professor.
She is a FONCyT Doctoral Fellow, under the direction of Dr. José Echenique. She is doing her PhD thesis in Chemical Sciences at FCQ-UNC, addressing the topic: «Study of the mechanisms of resistance to oxidative stress in Streptococcus Pneumoniae».
She is also a lecturer in the Department of Clinical Biochemistry FCQ-UNC, holding the position of Assistant Professor (DS).

Collaborators and Partners
Dr. Luis Martinez Sobrido (Texas Biomedical Research Institute, San Antonio, USA)
Dr. German Piñas (School of Biological Sciences, University of Utah, Salt Lake City, USA)
Dr. Nicolás Reinoso Vizcaíno (Molecular Genetics and Microbiology, Duke University, Duham, USA)
Dr. Jan Willen Veening (Faculty of Biology and Medicine, University of Lausanne, Switzerland)
Selected Publications
1) Hernandez-Morfa M, Reinoso-Vizcaíno NM., Olivero, NB., Victoria E. Zappia, VE., Cortes PR, Jaime, A. and J. Echenique. Host cell oxidative stress promotes intracellular fluoroquinolone persisters of Streptococcus pneumoniae. Microbiology Spectrum, 29:e0436422 (2022) [JIF:9.04].
2) Olivero N. B.; A.S. Gonzalez-Reiche, V.E., G.M. Castro, M.B. Pisano, P. Sicilia, M.G. Barbas, Z. Khan, A. van de Guchte, J. Dutta, P.R. Cortes, M. Hernandez-Morfa, V.E. Zappia, L. Ortiz, G. Geiger, D. Rajao, D.R. Perez, H. van Bakel, J. Echenique. Phylogenetic analysis and comparative genomics of SARS-CoV-2 from survivor and non-survivor COVID-19 patients in Cordoba, Argentina. BMC Genomics, 23(1):510 (2022) [JIF:4.26].
3) Reinoso-Vizcaíno N., Cian, M.B. Cortes, P.R. Olivero, N.B. Hernandez-Morfa, M. Piñas, G.E, Badapanda, C. Rathore, A. Perez, D.R. and J. Echenique. The pneumococcal two-component system SirRH is linked to enhanced intracellular survival of Streptococcus pneumoniae in influenza-infected pulmonary cells. PLOS Pathog. Aug 13;16(8):e1008761 (2020) [JIF:6.21].
4) Serradell MC., LL. Rupil, RA. Martino, CG. Prucca, PG. Carranza, A Saura, EA. Fernández, PR. Gargantini, RR. Tonelli, N Reinoso-Vizcaino, J. Echenique, L. Berod, E. Piaggio, B. Bellier, T. Sparwasser, D. Klatzmann, HD. Luján. Efficient oral vaccination by bioengineering virus-like particles with protozoan surface protein. Nature Communications 10:361. (2019) [JIF:12.2].
5) Piñas GE, Reinoso-Vizcaino NM, Yandar-Barahona NY, Cortes PR, Rosario Duran R, Badapanda C, Rathore A, Bichara DR, Cian MB, Olivero NB, Perez DR and J Echenique. Crosstalk between the serine/threonine kinase StkP and the response regulator ComE controls the stress response and intracellular survival of Streptococcus pneumoniae. PLOS Pathogens, 14(6):e1007118 (2018) [JIF:7.64].
6) Cortes PR, Chiapello LS, Dib D, Herrero MV, Nuncira CT, CDe Petris C and J Echenique. 7.21 Cortes PR., GE. Piñas, MB Cian, N. Yandar-Barahona and José Echenique. Stress-Triggered Signaling Affecting Survival or Suicide of Streptococcus pneumoniae. International Journal of Medical Microbiology 305(1):157-69. (2015). [IF 4.12].
7) Albarracín Orio AG, GE. Piñas; PR. Cortes and J. Echenique. Compensatory evolution of pbp mutations ameliorates fitness costs of β-lactam resistance in Streptococcus pneumoniae. PLOS Pathogens, 7(2): e1002000 (2011). [JIF: 8.81].
8) Cortes PR., GE. Piñas, AG Albarracín Orio and J. Echenique. Subinhibitory concentrations of penicillin increase the mutation rate to optochin resistance in Streptococcus pneumoniae. Journal of Antimicrobial Chemotherapy, 62(5):973-7 (2008). [JIF: 5.02].