Itziar Chapartegui-González

Dr. Itziar Chapartegui-González

Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden
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Research Focus & Metrics

Academic Career Length

11Years (2016-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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22 August 2018 in PLOS ONE
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Journal Article
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Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
MLMaria Lazaro-Diez
Maria Lazaro-Diez
ZBZaloa Bravo
Zaloa Bravo
JNJesús Navas
Jesús Navas
JIJosé M Icardo
José M Icardo
Jose Ramos-VivasJose Ramos-Vivas
Jose Ramos-Vivas
Acinetobacter baumannii is a cause of healthcare-associated infections. Although A. baumannii is an opportunistic pathogen, its infections are notoriously difficult to treat due to intrinsic and acquired antimicrobial resistance, often limiting effective therapeutic options. A. baumannii can survive for long periods in the hospital environment, particularly on inanimate surfaces. Such environments may act as a reservoir for cross-colonization and infection outbreaks and should be considered a substantial factor in infection control practices. Moreover, clothing of healthcare personnel and gadgets may play a role in the spread of nosocomial bacteria. A link between contamination of hospital surfaces and A. baumannii infections or between its persistence in the environment and its virulence has not yet been established. Bacteria under stress (i.e., long-term desiccation in hospital setting) could conserve factors that favor infection. To investigate whether desiccation and/or starvation may be involved in the ability of certain strains of A. baumannii to retain virulence factors, we have studied five well-characterized clinical isolates of A. baumannii for which survival times were determined under simulated hospital conditions. Despite a considerable reduction in the culturability over time (up to 88% depending on strain and the condition tested), some A. baumannii strains were able to maintain their ability to form biofilms after rehydration, addition of nutrients, and changing temperature. Also, after long-term desiccation, several clinical strains were able to grow in the presence of non-immune human serum as fine as their non-stressed homologs. Furthermore, we also show that the ability of bacterial strains to kill Galleria mellonella larvae does not change although A. baumannii cells were stressed by long-term starvation (up to 60 days). This means that A. baumannii can undergo a rapid adaptation to both the temperature shift and nutrients availability, conditions that can be easily found by bacteria in a new patient in the hospital setting.

20 June 2019 in Scientific Reports
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Jose Ramos-VivasJose Ramos-Vivas
Jose Ramos-Vivas
Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
MFMarta Fernández-Martínez
Marta Fernández-Martínez
CGClaudia González-Rico
Claudia González-Rico
JFJesús Fortún
Jesús Fortún
JCJulián de la Torre Cisneros
Julián de la Torre Cisneros
Solid organ transplant (SOT) recipients are especially at risk of developing infections by multidrug resistant bacteria (MDR). In this study, the biofilm-forming capability of 209 MDR strains (Escherichia coli n = 106, Klebsiella pneumoniae n = 78, and Enterobacter spp. n = 25) isolated from rectal swabs in the first 48 hours before or after kidney (93 patients), liver (60 patients) or kidney/pancreas transplants (5 patients) were evaluated by using a microplate assay. Thirty-nine strains were isolated before transplant and 170 strains were isolated post-transplant. Overall, 16% of E. coli strains, 73% of K. pneumoniae strains and 4% Enterobacter strains showed moderate or strong biofilm production. Nine strains isolated from infection sites after transplantation were responsible of infections in the first month. Of these, 4 K. pneumoniae, 1 E. coli and 1 Enterobacter spp. strains isolated pre-transplant or post-transplant as colonizers caused infections in the post-transplant period. Our results suggest that in vitro biofilm formation could be an important factor for adhesion to intestine and colonization in MDR K. pneumoniae strains in SOT recipients, but this factor appears to be less important for MDR E. coli and Enterobacter spp.

4 July 2017 in Scientific Reports
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MLMaria Lazaro-Diez
Maria Lazaro-Diez
Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
SRSantiago Redondo-Salvo
Santiago Redondo-Salvo
CLChike Leigh
Chike Leigh
DMDavid Merino
David Merino
Jose Ramos-VivasJose Ramos-Vivas
Jose Ramos-Vivas
Acinetobacter baumannii is a common cause of health care associated infections worldwide. A. pittii is an opportunistic pathogen also frequently isolated from Acinetobacter infections other than those from A. baumannii. Knowledge of Acinetobacter virulence factors and their role in pathogenesis is scarce. Also, there are no detailed published reports on the interactions between A. pittii and human phagocytic cells. Using confocal laser and scanning electron microscopy, immunofluorescence, and live-cell imaging, our study shows that immediately after bacteria-cell contact, neutrophils rapidly and continuously engulf and kill bacteria during at least 4 hours of infection in vitro. After 3 h of infection, neutrophils start to release neutrophil extracellular traps (NETs) against Acinetobacter. DNA in NETs colocalizes well with human histone H3 and with the specific neutrophil elastase. We have observed that human neutrophils use large filopodia as cellular tentacles to sense local environment but also to detect and retain bacteria during phagocytosis. Furthermore, co-cultivation of neutrophils with human differentiated macrophages before infections shows that human neutrophils, but not macrophages, are key immune cells to control Acinetobacter. Although macrophages were largely activated by both bacterial species, they lack the phagocytic activity demonstrated by neutrophils.

2 July 2020 in Expert Review of Vaccines
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NKNittaya Khakhum
Nittaya Khakhum
Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
ATAlfredo Torres
Alfredo Torres
Is an environmental intracellular Gram-negative bacterium that causes melioidosis, a severe infectious disease affecting humans and animals. An increase in melioidosis cases worldwide and the high ...

13 July 2020 in Antibiotics
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Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
MFMarta Fernández-Martínez
Marta Fernández-Martínez
ARAna Rodríguez-Fernández
Ana Rodríguez-Fernández
DRDANILO J P G ROCHA
DANILO J P G ROCHA
Eric AguiarEric Aguiar
Eric Aguiar
Jesús NavasJesús Navas
Jesús Navas
Corynebacterium urealyticum is a non-diphtherial urease-producing clinically relevant corynebacterial, most frequently involved in urinary tract infections. Most of the C. urealyticum clinical isolates are frequently resistant to several antibiotics. We investigated the susceptibility of 40 C. urealyticum isolated in our institution during the period 2005–2017 to eight compounds representative of the main clinically relevant classes of antimicrobial agents. Antimicrobial susceptibility was determined by the Epsilometer test. Resistance genes were searched by PCR. All strains were susceptible to vancomycin whereas linezolid and rifampicin also showed good activity (MICs90 = 1 and 0.4 mg/L, respectively). Almost all isolates (39/40, 97.5%) were multidrug resistant. The highest resistance rate was observed for ampicillin (100%), followed by erythromycin (95%) and levofloxacin (95%). Ampicillin resistance was associated with the presence of the blaA gene, encoding a class A β-lactamase. The two rifampicin-resistant strains showed point mutations driving amino acid replacements in conserved residues of RNA polymerase subunit β (RpoB). Tetracycline resistance was due to an efflux-mediated mechanism. Thirty-nine PFGE patterns were identified among the 40 C. urealyticum, indicating that they were not clonally related, but producing sporadic infections. These findings raise the need of maintaining surveillance strategies among this multidrug resistant pathogen.

29 July 2017 in Journal of Hospital Infection
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ZBZ. Bravo
Z. Bravo
Itziar Chapartegui-GonzálezItziar Chapartegui-González
Itziar Chapartegui-González
MLMaria Lazaro-Diez
Maria Lazaro-Diez
JRJ. Ramos-Vivas
J. Ramos-Vivas