Dr. Alpuche graduated as Medical Doctor at the Autonomous University of Yucatán State, Mexico, then she specialized as a Pediatrician at the O´Horan Teaching Hospital, Autonomous University of Yucatan and Infectious Diseases at Federico Gomez Children’s Hospital of Mexico. She also received a master´s degree in 1990 and a doctoral degree in 1995 both in Medical Science- Microbiology from the National Autonomous University of Mexico. From 1990 to 1994, Dr. Alpuche was postdoctoral fellow at Infectious Diseases Unit-Massachusetts General Hospital and at Harvard University School of Medicine. She was a visitor scientist at Infectious Diseases Unit-Massachusetts General Hospital in 1995 and 1996 and at Health Science Building at Dr. Samuel I Miller´s Laboratory in Seattle Washington in 1997 and 1998. Back in México from 1998 to 2006 Dr. Alpuche developed a research Laboratory at Experimental Medicine Department, Medical School, and National University of México. She was deputy-director of Research at Mexico Children´s Hospital from 2005 and 2006 and from 2007-2012 she was directing the National Institute of Diagnostic and Referral for Epidemiological surveillance at Secretary of Health, Mexico. Currently she is Director of Research Center for Infectious Diseases at the National Institute of Public Health in México. Along all these years she has participated in several technical advisory groups at PAHO and WHO in different aspects of infectious diseases. Dr. Alpuche Research focus has been bacterial pathogenesis, epidemiological and molecular mechanisms of antimicrobial resistance and more recently laboratory-based surveillance of influenza, dengue among other transmissible diseases. She has also been an associate professor at a number of educational institutions.
July 21, 2016
In collaboration with colleagues from Mexico, University of Texas Medical Branch at Galveston researchers were the first to directly connect the Aedes aegypti mosquito with Zika transmission in the Americas, during an outbreak in southern Mexico. The findings are available in the Journal of Infectious Diseases.
April 06, 2015
En 2050, los patógenos multirresistentes causarán más muertes que el cáncer y los accidentes viales juntos, por lo que autoridades de salud de México y el mundo urgen a tomar medidas, como en su momento las aplicaron ante la malaria o el sida.
February 23, 2010
A new study suggests that the bacteria that cause typhoid fever collect in tiny but persistent communities on gallstones, making the infection particularly hard to fight in so-called "carriers" -- people who have the disease but show no symptoms.
2016Different Arboviruses Reflecting the Same Spreading Routes and Poor Vector-Control Policies.
Risk factors for extended-spectrum β-lactamases-producing Escherichia coli urinary tract infections in a tertiary hospitalSalud Publica de Mexico
2015Objective: To assess the risks factors for urinary tract infections (UTIs) caused by Extended-Spectrum Beta-Lactamases (ESBLs)-producing E. coli and the molecular characterization of ESBLs. Materials and methods: A case-control study was performed to identify risk factors in consecutively recruited patients with UTIs caused by ESBLs or non-ESBLs-producing E. coli in a tertiary hospital in Mexico. Results: ESBLs-producing E. coli were isolated from 22/70 (31%) patients with E. coli UTIs over a three month period. All isolates were resistant to cephalosporins and quinolones but susceptible to carbapenems, amikacin and nitrofurantoin. Prior antibiotic treatment with more than two antibiotic families (OR=6.86; 95%CI 1.06-157.70; p=0.028), recurrent symptomatic UTIs (OR=5.60; 95%CI 1.88-17.87; p=0.001) and previous hospitalization (OR=5.06; 95%CI 1.64-17.69; p=0.002) were significant risk factors. Sixteen isolates harbored the beta-lactamase (bla)CTX-M-15 gene and five the blaTEM-1 gene. Conclusions: One of every three patients presented UTIs with ESBLs-producing beta-lactams and fluoroquinolone resistant E. coli. Risk factors and resistance patterns must be taken into account for developing antibiotic use policies in these settings.
2015This book addresses the major neglected tropical diseases (NTDs) – based on their prevalence and the years of healthy life lost to disability – in Latin American and Caribbean countries. These include Chagas disease, leishmaniasis, hookworm infection, and other soil-transmitted helminth infections, followed by dengue, schistosomiasis, leishmaniasis, leprosy, cysticercosis, bartonellosis, Plasmodium vivax malaria, and onchocerciasis. Topics like disease burden, major manifestations and approaches to the control and elimination of NTDs in Latin America and the Caribbean are discussed in detail. As such, the book will be of general interest to basic researchers and clinicians engaged in infectious disease, tropical medicine, and parasitology, and a must-have for scientists specialized in the characteristics of this region of the world.
Salmonella Downregulates Nod-like Receptor Family CARD Domain Containing Protein 4 Expression To Promote Its Survival in B Cells by Preventing Inflammasome Activation and Cell DeathThe Journal of Immunology
2013Salmonella infects and survives within B cells, but the mechanism used by the bacterium to promote its survival in these cells is unknown. In macrophages, flagellin secreted by Salmonella activates the Nod-like receptor (NLR) family CARD domain containing protein 4 (NLRC4) inflammasome, leading to the production of IL-1β and pyroptosis of infected cells. In this study, we demonstrated that the NLRC4 inflammasome is functional in B cells; however, in Salmonella-infected B cells, IL-1β secretion is prevented through the downregulation of NLRC4 expression. A functional Salmonella pathogenicity island 1 type III secretion system appears to be required for this process. Furthermore, infection induces Yap phosphorylation and promotes the interaction of Yap with Hck, thus preventing the transcriptional activation of NLRC4. The ability of Salmonella to inhibit IL-1β production also prevents B cell death; thus, B cells represent an ideal niche in which Salmonella resides, thereby promoting its persistence and dissemination.
Salmonella infects B cells by macropinocytosis and formation of spacious phagosomes but does not induce pyroptosis in favor of its survivalMicrobial Pathogenesis
2012We have previously reported that Salmonella infects B cells and survives within endosomal-lysosomal compartments. However, the mechanisms used by Salmonella to enter B cells remain unknown. In this study, we have shown that Salmonella induces its own entry by the induction of localized ruffling, macropinocytosis, and spacious phagosome formation. These events were associated with the rearrangement of actin and microtubule networks. The Salmonella pathogenesis island 1 (SPI-1) was necessary to invade B cells. In contrast to macrophages, B cells were highly resistant to cell death induced by Salmonella. These data demonstrate the ability of Salmonella to infect these non-professional phagocytic cells, where the bacterium can find an ideal intracellular niche to support persistence and the possible dissemination of infection.
Area of Expertise
Epidemiological and Molecular Mechanisms
Health and Wellness
Health Care - Providers
Autonomous University of Yucatán State :
National Autonomous University of Mexico : Medical Science-Biology
National Autonomous University of Mexico : Medical Science-Biology