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jueves, 7 de mayo de 2026
jueves, 16 de abril de 2026
lunes, 2 de marzo de 2026
martes, 7 de octubre de 2025
Artículo de Daniel Garzón
Abstract
The global rise of antimicrobial resistance (AMR), exacerbated by the COVID-19 pandemic, has led to a surge in infections caused by multidrug-resistant (MDR) bacteria. A key driver of this phenomenon is co-selection, where exposure to one antimicrobial promotes resistance to others via horizontal gene transfer (HGT) mediated by mobile genetic elements (MGEs). Carbapenem-resistant Enterobacteriaceae, known for their genomic plasticity, are particularly worrisome; yet genomic data from Latin America—especially Ecuador—remain scarce. This study investigated four carbapenem-resistant clinical isolates (two Klebsiella pneumoniae ST1440 and two Serratia marcescens) from tracheal aspirates of three ICU patients during a COVID-19 outbreak at Hospital IESS Quito Sur, Ecuador. Phenotypic profiling and whole-genome sequencing were performed, followed by bioinformatic reconstruction of plasmid content. Nineteen plasmids were identified, carrying 70 resistance-related genes, including antimicrobial resistance genes (ARGs), metal resistance genes (MRGs), integrons, transposons, and insertion sequences. Hierarchical clustering revealed six distinct gene clusters, with several co-localizing ARGs and genes for resistance to disinfectants and heavy metals—suggesting strong co-selective pressure. Conjugative plasmids harboring high-risk elements such as blaKPC-2, qacE, and Tn4401 were found in multiple isolates, indicating potential interspecies dissemination. These findings emphasize the importance of plasmid-mediated resistance during the pandemic and highlight the urgent need to enhance genomic surveillance and infection control, particularly in resource-limited healthcare settings.
Keywords: Klebsiella pneumoniae; ST1440; Serratia marcenses; plasmids; co-selective pressure; clusters
1. Introduction
Antimicrobial resistance (AMR) has become an increasingly complex global health threat, driven by limited therapeutic options and widespread misuse of antibiotics and disinfectants—issues that have intensified during the COVID-19 pandemic [1,2]. These selective pressures have contributed to a global rise in hospital-acquired infections caused by multidrug-resistant (MDR) bacteria [3].
In Enterobacterales, β-lactam resistance is mainly mediated by β-lactamases, which are classified into four molecular classes (A–D) according to Ambler’s system [4]. Class A includes extended-spectrum β-lactamases (ESBLs) such as CTX-M, TEM, and SHV, as well as carbapenemases such as KPC-2, capable of hydrolyzing penicillins, cephalosporins, and carbapenems [5]. Class B comprises metallo-β-lactamases (MBLs), including NDM, VIM, and IMP, which require zinc and efficiently degrade carbapenems [6]. Class C encompasses AmpC enzymes, usually chromosomally encoded, that confer resistance to cephalosporins. Finally, Class D consists of OXA-type carbapenemases with variable activity [7]. In addition to β-lactam resistance, Enterobacterales often carry determinants for fluoroquinolone resistance. These include plasmid-mediated quinolone resistance (PMQR) genes—such as qnrA, qnrB, qnrS, and aac (6′)-Ib-cr—as well as chromosomal mutations in DNA gyrase (gyrA, gyrB) and topoisomerase IV (parC, pare) [8]. Resistance to aminoglycosides typically involves enzymatic modification via acetyltransferases (aac), nucleotidyltransferases (ant), and phosphotransferases (aph), with these genes often co-located on plasmids alongside other resistance determinants [9].
Klebsiella pneumoniae is one of the most worrisome MDR pathogens, responsible for a wide range of healthcare-associated infections, including pneumonia, bloodstream infections, urinary tract infections, and surgical site infections—especially in immunocompromised patients and those admitted to intensive care units [10]. Its clinical success is attributed to a diverse set of virulence factors, such as capsular polysaccharides, siderophores (e.g., enterobactin and yersiniabactin), adhesins (e.g., fimbriae and mannose-resistant Klebsiella-like hemagglutinins), and serum resistance proteins [11]. Globally, high-risk clones such as ST258, ST11, ST147, and ST307 have contributed to the dissemination of carbapenem resistance genes, particularly blaKPC-2 and blaNDM, via epidemic plasmids [12]. These clones display exceptional genomic plasticity, enabling rapid adaptation to selective pressures and efficient horizontal transfer of resistance determinants [13]. Serratia marcescens has become an increasingly relevant nosocomial pathogen, especially in intensive care units, where it is associated with ventilator-associated pneumonia, catheter-related bloodstream infections, and urinary tract infections [14]. This opportunistic bacterium displays intrinsic resistance to ampicillin, first-generation cephalosporins, and polymyxins, mainly due to chromosomal AmpC β-lactamase production and lipopolysaccharide modifications [15]. Additionally, S. marcescens can acquire resistance mechanisms such as carbapenemases (e.g., KPC-2, NDM, and OXA-48-like), extended-spectrum β-lactamases (ESBLs), and 16S rRNA methylases that confer high-level aminoglycoside resistance [16]. Genomic studies have revealed distinct S. marcescens lineages with diverse resistance profiles, including clones harboring multiple β-lactamases and extensive plasmid content [17].
These bacteria efficiently exchange mobile genetic elements (MGEs) through horizontal gene transfer (HGT), allowing rapid adaptation to stress conditions and promoting the spread of antibiotic resistance genes (ARGs) [18,19]. During the COVID-19 pandemic, studies reported a marked increase in ARG abundance and HGT activity, likely triggered by intensified co-selective pressures [20].
Co-selection occurs when exposure to a single selective agent—such as an antibiotic—also promotes resistance to unrelated agents. This can happen through (i) co-resistance, where multiple resistance genes coexist on the same MGE; (ii) cross-resistance, when a single mechanism confers resistance to different agents; and (iii) co-regulation, involving coordinated expression of resistance genes in response to common stimuli [21].
Despite global concern, research on carbapenem-resistant Enterobacterales in Latin America—particularly in Ecuador—remains scarce. Most studies in Ecuador focus solely on phenotypic resistance profiles, lacking detailed molecular characterization to elucidate the underlying genetic mechanisms [22]. Although carbapenem-resistant strains have been reported in clinical and food-related settings, information on clonal lineages, mobile genetic elements, and transmission dynamics is still limited [23,24]. This gap hampers the development of effective surveillance and containment strategies, emphasizing the urgent need for genomic studies at the local level.
The COVID-19 pandemic profoundly disrupted the management of nosocomial infections and contributed to the spread of plasmids in healthcare environments. Emergency responses—such as increased antimicrobial use, healthcare system overload, and intensified disinfection practices—altered infection dynamics and heightened the selective pressures that favor MDR bacterial dissemination [25,26].
In this context, the present study aimed to characterize the genomic features of four carbapenem-resistant clinical isolates—two K. pneumoniae ST1440 and two S. marcescens—obtained during a localized outbreak in a tertiary hospital in Ecuador. Special emphasis was placed on plasmid-mediated resistance and co-selection dynamics under pandemic conditions.
2. Methodology
2.1. Sample Collection
This study included four carbapenem-resistant bacterial strains. Inclusion criteria were (1) isolates recovered from adult ICU patients presenting clinical signs of bacterial infection during the COVID-19 pandemic, (2) growth on selective culture media, and (3) confirmed carbapenem resistance through initial phenotypic screening. The strains were obtained from tracheal aspirates collected during routine diagnostics at Hospital IESS Quito Sur (Quito, Ecuador) between August and September 2021, coinciding with the second wave of the pandemic in the country. The isolates were obtained from three patients: two K. pneumoniae strains (from patients 1 and 2) and two S. marcescens strains (from patients 2 and 3). All patients presented with severe respiratory symptoms, including dyspnea, fever, leukocytosis, changes in tracheal secretions, and the need for invasive mechanical ventilation.
2.2. Microbiology Techniques
Bacterial identification and antimicrobial susceptibility testing were performed using standard microbiological techniques. Pure colonies from each isolate were cultured on MacConkey agar and adjusted to a 0.5 McFarland standard for fitness assays, conducted in triplicate. An automated blood culture system (BD BACTEC, BD Diagnostics, Franklin Lakes, NJ, USA) with a fluorescent CO2 sensor was used to monitor growth at 10-min intervals, with positive detection set at a threshold of 10 CFU/mL. Genotypic identification was confirmed through whole-genome sequencing and multilocus sequence typing (MLST). Species identity was validated using Average Nucleotide Identity (ANI) analysis.
2.3. DNA Extraction and Sequencing
Genomic DNA was extracted using the DNeasy UltraClean Microbial Kit (Qiagen, Hilden, Germany), following the manufacturer’s instructions. DNA concentration and purity were assessed using both a NanoDrop One (Thermo Fisher Scientific, Waltham, MA, USA) and a Qubit 3.0 Fluorometer (Invitrogen, Carlsbad, CA, USA), ensuring A260/A280 ratios between 1.8 and 2.0 and concentrations above 20 ng/μL. DNA integrity was verified by agarose gel electrophoresis. Library preparation was carried out with the NEBNext Ultra II DNA Library Prep Kit (New England Biolabs, Ipswich, MA, USA). Sequencing was performed on the Illumina HiSeq 4000 platform, producing 101 bp paired-end reads with a minimum genome coverage of 100×.
2.4. Data Availability and Bioinformatic Analysis
Whole-genome sequencing (WGS) was performed, and raw reads were deposited in the Sequence Reads Archive (SRA) under BioProject PRJNA1051122, with BioSample IDs: SAMN38765470 (27026352), SAMN38765469 (2729958), SAMN38765468 (27026351), and SAMN38765467 (2684096). Additional bioinformatics data and analysis files are available at: https://www.bv-brc.org/workspace/sebas007@patricbrc.org/PROJECT_PLASMIDS. (accessed on 30 July 2024).
A multi-stage bioinformatic pipeline was used to ensure quality control, accurate annotation, and reproducibility. Raw reads were assessed with FastQC v0.12.0 and trimmed using Trimmomatic v0.39. Assemblies were generated with Unicycler v0.5.0 and evaluated using QUAST v5.2.0. Plasmid-associated contigs were identified using MOB-suite v3.1.9. To detect mobile genetic elements (MGEs) and horizontal gene transfer (HGT) events, we used mobileOG-db v1.1.3, BacAnt, Alien Hunter v1.1.0, Phigaro v1.0.1, and PHASTEST. Functional annotation and prophage prediction were included in this analysis. CRISPRCasFinder v1.1.0 was employed to identify CRISPR arrays and associated Cas genes. Resistance genes were annotated using ResFinder v4.5.0, CARD v3.2.9, and staramr v0.10.0, applying thresholds of ≥90% identity and ≥60% coverage. The complete list of detected resistance genes is provided in Supplementary File S1. Genome annotations were completed with Bakta, and additional plasmid-like elements were searched using PLSDB (version 2023_11_03_v2). Data analysis and visualization were conducted using Python v3.12.3 with libraries such as pandas, seaborn, and matplotlib.
3. Results
3.1. General Features
Patient 2 was found to harbor both carbapenem-resistant K. pneumoniae (CrKp) and S. marcescens (CrSm), corresponding to isolates 27026351 and 27026352, respectively. In contrast, patient 1 carried only CrKp (isolate 2684096), while patient 3 was colonized by CrSm (isolate 2,729,958). All CrKp strains were identified as sequence type ST1440. Species identity and genomic similarity were confirmed using ANI through the TYGS platform. CrKp and CrSm isolates from patient 2 showed high genomic similarity to those from patients 1 and 3, respectively. However, the CrSm strains differed notably in plasmid content. Growth kinetics assays revealed variability between strains and species, although the differences were not statistically significant. Interestingly, CrSm isolate 27,026,352 exhibited the longest growth time among all isolates, possibly due to the metabolic burden imposed by an atypical plasmid.
3.2. Chromosomal Features
We observed that the draft chromosomes of the isolates exhibited both consistent and distinctive characteristics corresponding to their respective species, as shown in Table 1. Our analysis identified 32 genes and point mutations of interest on CrKp chromosomes and 13 on CrSm chromosomes, which were classified into five groups: (i) associated with antibiotic resistance, (ii) expression regulators, (iii) components of membranes, efflux pumps, and permeability, (iv) virulence and adhesion factors, and (v) insertion sequences (IS). Each group displayed unique compositions across the two species. In the first group, predominantly associated with AMR, we identified a diverse array in CrKp, including fosA5, parC, gyrA, gyrB, emrR, emrD, ArnT, eptB, and rpsL. In contrast, CrSm displayed a more limited set, featuring only aac (6′)-Ic and multiple copies of blaSRT-1. In the second group, focused on expression regulators, CrKp showed a richer genetic landscape, with UhpT, acrR, ramR, marA, baeR, H-NS, and CRP, while CrSm contained only CRP. This disparity suggests potential differences in regulatory mechanisms between the two species. In the third group, encompassing components of membranes, efflux pumps, and permeability, CrKp possessed a wide range, including OmpA, ompK35, ompK36, ompK37, msbA, fieF, kdeA, KpnF, KpnG, KpnE, KpnH, and LptD. In contrast, CrSm exhibited a distinct set: smfY, ssmE, sdeY, and sdeB. In the fourth group, focused on virulence and adhesion factors, we observed distinct genetic profiles for each species. CrKp contained iutA, fimH, and mrkA, while CrSm harbored smdA, fyua, irp2, sdeA, and ybtQ. These differences contribute to the unique virulent characteristics of each species. In the fifth group, concerning insertion sequences (IS), we found ISKpn1 and ISKpn2 in CrKp, with ISRaq1 and ISRaq2 present in CrSm. These groups may play crucial roles in genetic mobility and adaptability within each species.
Table 1. Overall characteristics of WGS assemblies, chromosomes, and plasmids.
Furthermore, our results revealed significant enrichment at both metabolic and functional levels in five key pathways: amino acids and derivatives, cofactors and vitamins, energy generation, xenobiotic degradation and stress response, and membrane transport. This pattern indicated the enrichment of three major families of protein CDS: transporters and permeases for diverse substrates, transcriptional regulators of multiple families, and a wide range of enzymes, including hydrolases, transferases, and oxidoreductases.
Considering the average number of copies per genome, the principal CDS products in the four chromosome drafts were a DNA-binding transcriptional regulator (LysR family) and a putative AraJ arabinose efflux permease (MFS family). The distribution of other products was equitable between species and samples, except for those associated with phage, hypothetical proteins, and diverse transcriptional regulators, as shown in Figure 1. These findings suggest substantial metabolic and functional adaptation.
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Figure 1. Distribution of predicted protein products in chromosomal (a) and plasmid (b) contigs. The left-side bar plots show the top 30 predicted protein products for each contig based on the average copy number per genome. The stacked bar plots on the right represent the distribution of these products across species (middle) and specific samples (right). In (a), dominant products include DNA-binding transcriptional regulators, lipoproteins, and ABC transporters, while (b) highlights plasmid-related proteins such as transposases, transcriptional regulators, and conjugation proteins. The color legend indicates the specific isolates analyzed.
Moreover, we identified putative HGT regions and prophages. CrKp exhibited more HGT regions (123/121) compared to CrSm (93/87), while CrSm contained more prophage regions (5/6) than CrKp (3). Based on the annotations of mobile orthologue groups, which encompass protein families involved in integration/excision (IE), replication/recombination/repair (RRR), and stability/transfer/defense (STD) and phages, our analysis revealed that CKp possessed more RRR genes (242) than CrSm (188), whereas CrSm harbored more phage-related genes (219) than CrKp (146). Intraspecies comparisons showed no significant differences (Figure 2). Notably, CRISPR/Cas system-associated genes were absent in both species. These findings elucidate the distribution of MGEs in CrKp and CrSm, providing insights into their genomic plasticity.
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Figure 2. Distribution of mobile genetic element (MGE)-related genes in chromosomal (a) and plasmid (b) contigs. The left-side bar plots show the total number of MGE-related genes for each contig, while the stacked bar plots on the right represent the distribution of these genes across major and minor mobileOG categories. Major categories include functions such as transfer, replication/recombination/repair, phage, and integration/excision, while minor categories provide more detailed functional classifications, including regulation, conjugation, and plasmid replication control.
3.3. Plasmid Features
We assembled nineteen plasmids, including fourteen from CrKp isolates and five from CrSm isolates, and designated them as AA275 (2 copies), AA002 (4 copies), AB595 (3 copies), AA119 (2 copies), AA531 (4 copies), AB042 (3 copies), and AD092 (2 copies). We categorized the plasmids into conjugative (AA275, AA002), non-mobilizable (AB595, AA119), and mobilizable (AA531, AB042, AD092) types. We obtained only one AA002 plasmid from the CrSm isolate ID 27026352 from the MDB patient. The AA002 plasmid appeared in all four isolates, while AB595, AB042, and AA531 appeared in three isolates. We detected AA119, AA275, and AD092 exclusively in CrKp isolates. Although the AD092 plasmid carried the dfrA8 gene, it exhibited a unique configuration unrelated to other plasmids, so we excluded it from certain analyses. The largest plasmids observed were the conjugative plasmids AA275 and AA002, averaging 184,931 bp (n = 2) and 90,122 bp (n = 4), respectively. AB595 averaged 14,991 bp (n = 3), while the remaining plasmids had a mean size of 3264 bp (n = 7). Conjugative plasmids exhibited a GC content of 53.8 ± 0.2%, non-mobilizable plasmids 51.0 ± 5.4%, and mobilizable plasmids 51.7 ± 4.9%. AB042 and AA119 displayed the lowest GC content at 47.2 ± 0.1% and 46.4 ± 0.0%, respectively. Replicons detected included IncF in AA275, IncM1 in AA002, and both Col (pHAD28) and Col440I in the remaining plasmids. We predicted a circular topology for all recovered plasmids (Table 2).
Table 2. Comparative analysis of conjugative, nonmobilizable, and mobilizable plasmids in CrKp and CrSm isolates.
The main coding sequences (CDS) products were hypothetical proteins distributed equally among species and samples. On the other hand, we observed a marked difference in transposases that were almost exclusively in CrKp plasmids, as opposed to a wealth of transcriptional regulators in CrSm plasmids (Figure 1). AA275 and AA002 exhibited regions indicative of putative HGT events and prophage regions, as well as a higher number of CDS compared to the other plasmids. A higher proportion of elements in the mobile orthologue groups were associated with integration/excision (IE), comprising 163 (44.7%), followed by transfer elements, which included 105 (28.8%). Elements from various groups were evenly distributed in AA002, AA275, and AB595, whereas AA531 contained exclusively transfer elements, and AA119 featured elements related to stability/transfer/defense (STD) and replication/recombination/repair (RRR) (Table 2 and Figure 2).
3.4. Clusters
Clustering analysis excluded AA119 and AA531 due to the absence of genes of interest. Among the examined plasmids, we identified seventy genes, including ARGs, metal resistance genes (MRGs), and MGEs such as transposons, insertion sequences (IS), and integrons. To cluster the identified genes, we conducted an occurrence analysis using the average linkage method and Jaccard dissimilarity distance, with a cut-off value of 0.4. The resulting clustering demonstrated high quality, as evidenced by a Silhouette coefficient of 0.89, total inertia of 246.6, and a Davies-Bouldin index of 0.31 (Figure 3).
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Figure 3. Correlation analysis and hierarchical clustering of plasmid-borne antimicrobial resistance (AMR) gene profiles. (a) Heatmap displaying pairwise correlations between AMR genes across different genomes, with correlation values ranging from white (no correlation) to black (high correlation), accompanied by dendrograms representing hierarchical clustering based on gene similarity. (b) Presence/absence matrix of AMR genes shown before and after applying hierarchical clustering using the average linkage method, with distinct clusters highlighted in red boxes revealing coherent groups of AMR genes shared across genomes. (c) Dendrogram generated from the clustering process, grouping AMR genes into clusters that reflect their genomic similarities, with each cluster clearly labeled and enclosed in red boxes. This comprehensive visualization aids in understanding the organization and relationships of AMR genes across multiple genomes.
Clustering analysis identified six robust clusters, each containing at least three genes. Three of these were smaller clusters: Cluster 1 (Tn4401, blaKPC-2, qacE, and sul1), Cluster 2 (ISVsa3, blaTEM-1A, rmtG, sul2, and tetD), and Cluster 3 (ISKpn11, ISKpn12, and aac (3)-Iia). The larger clusters included Cluster 4 (twelve members of diverse gene types), Cluster 5 (twenty-six members, primarily MRGs with IS and transposons, including the heat resistance-associated clpK1), and Cluster 6 (nine members, featuring several blaTEM gene family variants and associated Tn801). Additionally, we observed three frequently associated gene pairs: silC and silF, v and blaCTX-M-12, and IS5075 and merT. Five genes (blaSHV-1, aadA1, qnrB19, dfrA8, and Integron1) showed no significant associations with others. For more details, refer to Figure 3 and Figure 4.
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Figure 4. Schematic representation of plasmid and antimicrobial resistance (AMR) gene distribution in clinical isolates obtained from tracheal aspirates of three patients [(1), (2), (3)]. The plasmids recovered from K. pneumoniae (blue) and S. marcescens (orange) isolates are displayed on the left, with annotated key resistance genes. The middle section illustrates the experimental workflow, starting with bacterial isolate recovery from tracheal aspirates, followed by shotgun sequencing using HiSeq Illumina 4000, and subsequent plasmid reconstruction using bioinformatics tools. AMR gene identification was performed using databases such as PLSDB, ResFinder, CARD, and MobileElementFinder. The right panels detail the six AMR gene clusters and integrons (1 and 2), showing genes related to resistance mechanisms, including blaKPC-2, aac (3)-lia, Tn4401, and various transposons and integron cassettes, revealing the genetic architecture of resistance across the isolates.
4. Discussion
The COVID-19 pandemic has significantly impacted the management of nosocomial infections and plasmid dissemination in healthcare settings, particularly in developing countries. Emergency measures to control SARS-CoV-2, including increased antimicrobial usage, healthcare system overload, and enhanced infection control protocols, have disrupted the typical dynamics of nosocomial infections. These changes have intensified the selective pressures that promote the selection and spread of MDR bacteria, promoting HGT, especially of plasmid-borne genes, and exacerbating cross- resistance problems. Understanding these evolutionary dynamics is crucial for developing effective control strategies in resource-limited settings during future pandemics.
In Ecuador, epidemiological studies have focused on isolates of K. pneumoniae belonging to the high- risk clonal complex CG258, which includes globally widespread sequence types (STs) such as ST258, ST25, ST348, and ST512 (23,27). Additionally, isolates with unique sequence types, including ST42, ST111, ST147, ST859, ST1088, ST1199, ST1758, and ST1850 [27], have been identified in more localized nosocomial outbreaks. In this study, we describe two ST1440 isolates, a lineage for which limited information is available. This data scarcity is reflected in the specialized database (https://bigsdb.pasteur.fr/klebsiella/) (accessed on 14 October 2024), where only seventeen isolates have been reported, with just three originating from Latin America.
In recent years, S. marcescens isolates have harvested significant attention due to their increasing AMR in nosocomial environments and the diversification of their resistance mechanisms, particularly those mediated by plasmids [28]. Matteoli et al., through a comprehensive pangenome analysis, identified twelve distinct lineages, with Sm7 and Sm9 exhibiting the most worrying resistome profiles [17]. Sm7 lineage demonstrated widespread distribution of blaKPC-2-harboring plasmids with lower plasmid diversity (one per genome), while Sm9 showed the highest plasmid diversity (averaging three per genome) and multiple beta-lactamases. These findings align with numerous studies indicating that carbapenem resistance in nosocomial isolates is attributed to the presence of plasmid-borne blaKPC genes, with a secondary contribution from beta-lactamase overexpression and porin loss [16,29].
Studies have reported varying rates of bacterial superinfection in patients with SARS-CoV-2 infection. Initial reports documented a 16% prevalence [30], while subsequent meta-analyses found superinfections in 24% of COVID-19 patients, correlating with increased mortality risk [31]. Other investigations revealed coinfection rates ranging from 3.5% to 14% [32,33]. An intensive care unit (ICU) study found even higher rates, with respiratory coinfections at 33.3% and superinfections at 43.9%. In this ICU population, the most frequently isolated bacteria were Pseudomonas aeruginosa, Enterococcus faecium, K. pneumoniae, and Acinetobacter baumannii [34]. Despite the variable rates of confirmed bacterial infections, Rawson et al. reported widespread use of broad-spectrum antibacterials, with 72% of COVID-19 patients receiving antimicrobial therapy. However, these analyses lacked crucial data on antimicrobial susceptibility patterns and prescribing practices [25]. Collectively, these findings highlight not only the significant variability in respiratory coinfection and superinfection rates among COVID-19 patients across different clinical settings but also raise concerns about potentially excessive antibiotic use.
The pandemic period saw a concerning rise in multidrug-resistant organisms (MDROs), including both bacteria and fungi [35]. i et al. documented particularly high bacterial resistance rates, with K. pneumoniae showing 75.5% carbapenem resistance and A. baumannii reaching 91.2% resistance [36]. This increase in resistant organisms likely stemmed from multiple factors during the COVID-19 pandemic: hospital units faced overwhelming patient admissions, experienced shortages in personal protective equipment, and increased broad-spectrum antimicrobial usage. These challenges collectively may have contributed to enhanced transmission of MDROs within hospital settings.
The available literature in Ecuador is very scarce [22]. This combined scenario underlines the urgent local need to intensify the study and reporting of these nosocomial strains. During the first stage of the analysis of the draft chromosomes, we identified multiple genes involved in the degradation of xenobiotics such as 1,4-dichlorobenzene, tetrachloroethylene, 2,4-dichlorobenzoate, and others. These are surprising and worrisome. This finding is consistent with several studies that indicate oxidative stress caused by using cleaning products, disinfectants, and solvents as significant drivers of AMR. This oxidative stress can increase HGT by up to 8-fold, resulting in a 20-fold increase in ARGs abundance [20,37]. Moreover, exposure to these chemicals can induce the Viable-But-Non-Culturable (VBNC) state in nosocomial strains [38].
These findings suggest that these strains have adapted their genomes to these pressures to tolerate and metabolize, to some extent, common disinfectants and solvents used in healthcare environments. This phenomenon is probably intensified by the high dynamics of their membranes, which makes them highly selective, either by point mutations in antimicrobial targets or by the expression of multiple efflux pumps. For example, two CRISPR arrays were identified on each chromosome of K. pneumoniae, although these sequences serve as Level 1 evidence and may potentially yield false positives [39]. This finding is consistent with several studies collectively indicating an inverse relationship between the presence of CRISPR/Cas systems and other restriction-modification systems and the capacity to acquire MGEs, thereby facilitating their dissemination, such as epidemic IncF plasmids. This phenomenon has been observed in strains ST258, ST307, ESBL-producing strains, strains resistant to carbapenems, and various clinical isolates [40]. Furthermore, sequences associated with type I cas3 were detected on the AA275 plasmids. It has been reported that the presence of Cas3 on ColE1 plasmids can induce uncontrolled replication into concatemers at 37 °C, solely driven by the helicase activity of the enzyme without requiring other CRISPR-Cas components [41].
However, complete CRISPR/Cas systems have been observed in much larger plasmids [42] (>200 kb) with multiple ARGs, associated with replicons such as IncFIB and IncHI1B [42]. Our study reports the presence of Cas3 on non-ColE1 plasmids and the absence of CRISPR arrays in ST1440 strains, potentially indicating an optimal scenario for the plasmid-borne ARGs in nosocomial environments. However, experimental validation is required. Additionally, sequences associated with type I Cas3 were detected in the AA275 plasmids. It has been documented that the presence of Cas3 in ColE1 plasmids can lead to uncontrolled replication in concatemers at 37 °C, driven solely by the helicase activity of the enzyme without the need for other CRISPR-Cas components. This study identifies the presence of Cas3 in plasmids other than ColE1 and the absence of CRISPR arrays in ST1440 strains, suggesting an optimal scenario for the transmission of plasmid-mediated AMR in hospital settings. Our bacterial fitness assay shows a potential high growth rate related to ColE1 plasmids, which could bring an advantage to bacteria that have it; however, metabolic-related pathways with these findings still need to be labeled.
In conclusion, this dual outbreak affecting three patients from the same ward, infected with CrKp and CrSm, underscores the complexity of nosocomial infections caused by enteropathogens. The occurrence of two patients infected with CrSm, two with CrKp, and one case of co-infection by both pathogens presents a concerning scenario. HGT via plasmids shared among different pathogenic Enterobacteriaceae species represents a significant threat, particularly when co-selective pressures exist, which could exacerbate AMR in alignment with WHO predictions for 2050. Continuous monitoring of this dynamic is not only crucial for analyzing the efficacy of control measures but also for mitigating the alarming projections detailed in the O’Neill report [43]. This case serves as a valuable model for developing cost-effective strategies to address the growing threat of antimicrobial resistance. Furthermore, it highlights the urgent need for comprehensive surveillance and innovative approaches to combat the spread of MDR organisms in healthcare settings.
Supplementary Materials
The following supporting information can be downloaded at: https://www.mdpi.com/article/10.3390/microorganisms13102286/s1. Supplementary File S1: contains the staramr results.
Author Contributions
D.G.-C., M.G. and J.R.-C. were responsible for the conception and design of the study. Data acquisition was performed by V.P., F.E. and E.L. The screening process and quality assessment were completed by D.G.-C., A.C.A. and F.C.-M. Eligibility criteria were set by D.G.-C. and F.C.-M. Data analysis and statistical methodologies were developed by F.C.-M., E.T.-G., Á.A.P.-M. and D.G.-C. The writing manuscript was elaborated by D.G.-C., J.R.-C. and F.C.-M. Reviewing the manuscript was realized by D.G.-C., A.C.A. and J.R.-C. Research project supervision was conducted by A.C.A. and M.G. at the Medicine research laboratory at USFQ. All authors have read and agreed to the published version of the manuscript.
Funding
This study was financed by the Medicine School of the USFQ University, Hubi project code: 17118.
Institutional Review Board Statement
This study was approved by the Human ethics committee of the University of San Francisco of Quito, with code number: 2024-055IN and approval date 18 July 2024.
Informed Consent Statement
The requirement for an informed consent statement was waived, as anonymized patient information was obtained from external health facilities, in accordance with ethical approval No. 2024-055IN.
Data Availability Statement
The data presented in this study are openly available in NCBI at https://www.ncbi.nlm.nih.gov/search/all/?term=PRJNA1051122, reference number PRJNA1051122 (accessed on 14 August 2024).
Acknowledgments
Special recognition is deserved by all colleagues of Hospital IESS Quito Sur, the Medicine Laboratory of USFQ and COCSA, and the Research Office of Universidad San Francisco de Quito.
Conflicts of Interest
The authors declare no conflict of interest.
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Tisalema-Guanopatín, E.; Cabezas-Mera, F.; Pérez-Meza, Á.A.; Palacios, V.; Espinosa, F.; Ligña, E.; Cristina Aguilar, A.; Reyes-Chacón, J.; Grunauer, M.; Garzón-Chavez, D. Genomic Characterization of Carbapenem-Resistant Klebsiella pneumoniae ST1440 and Serratia marcescens Isolates from a COVID-19 ICU Outbreak in Ecuador. Microorganisms 2025, 13, 2286. https://doi.org/10.3390/microorganisms13102286
AMA Style
Tisalema-Guanopatín E, Cabezas-Mera F, Pérez-Meza ÁA, Palacios V, Espinosa F, Ligña E, Cristina Aguilar A, Reyes-Chacón J, Grunauer M, Garzón-Chavez D. Genomic Characterization of Carbapenem-Resistant Klebsiella pneumoniae ST1440 and Serratia marcescens Isolates from a COVID-19 ICU Outbreak in Ecuador. Microorganisms. 2025; 13(10):2286. https://doi.org/10.3390/microorganisms13102286
Chicago/Turabian Style
Tisalema-Guanopatín, Estefanía, Fausto Cabezas-Mera, Álvaro A. Pérez-Meza, Veronica Palacios, Franklin Espinosa, Edison Ligña, Ana Cristina Aguilar, Jorge Reyes-Chacón, Michelle Grunauer, and Daniel Garzón-Chavez. 2025. "Genomic Characterization of Carbapenem-Resistant Klebsiella pneumoniae ST1440 and Serratia marcescens Isolates from a COVID-19 ICU Outbreak in Ecuador" Microorganisms 13, no. 10: 2286. https://doi.org/10.3390/microorganisms13102286
APA Style
Tisalema-Guanopatín, E., Cabezas-Mera, F., Pérez-Meza, Á. A., Palacios, V., Espinosa, F., Ligña, E., Cristina Aguilar, A., Reyes-Chacón, J., Grunauer, M., & Garzón-Chavez, D. (2025). Genomic Characterization of Carbapenem-Resistant Klebsiella pneumoniae ST1440 and Serratia marcescens Isolates from a COVID-19 ICU Outbreak in Ecuador. Microorganisms, 13(10), 2286. https://doi.org/10.3390/microorganisms13102286
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https://www.mediafire.com/file/1xhdy07rr3ip56e/Garzón+Daniel_microorganisms-13-02286.pdf/file
Artículo de las toxinas de escorpión
lunes, 25 de agosto de 2025
sábado, 16 de noviembre de 2024
jueves, 14 de septiembre de 2023
A 31 años de la desaparición de Gustavo Garzón Guzmán, por Gustavo Salazar. Casapalabras 52
Gustavo Salazar, 27 de julio de 2021
A doña Clorinda Guzmán, madre del escritor
Nos presentó el entusiasta hacedor de revistas Ramiro Pérez, animador del grupo de la revista La Mosca Zumba. De naturaleza tímida y reservada, su rostro y su trato denotaban generosidad y tolerancia. No desaprovechábamos oportunidades para hablar de la vida o de literatura, pues él perteneció, con su grupo, a los fervorosos lectores de autores «contemporáneos»: estaban con Cortázar, Böll, Frisch, Borges o Vargas Llosa, mientras yo me había quedado —y, treinta años después, sigo— con Gógol, Moravia, Wilde, Eça de Queiroz, Rabelais, Quevedo y Céline, aunque coincidimos en uno u otro autor.
En alguna de mis visitas a la librería de la Casa de la Cultura Ecuatoriana, lugar en el que trabajaba Gustavo —habrá sido en el año 1984—, al comprar algunos títulos de la Colección Básica de Escritores Ecuatorianos, que costaban 12 sucres cada uno, me vendió el último muñeco articulado que había tallado y armado con sus propias manos. Pese a haber transcurrido siete lustros, lo conservo entre mis bienes entrañables; mi hija jugaba con él cuando era niña.
En un par de ocasiones fui con mi buen amigo Iván Rodrigo, hermano suyo, a visitarlo en la cárcel —en la que estaba recluido a la espera de juicio por razones políticas— y le llevé algunos libros, ya que seguía empeñado en realizar su tesis doctoral sobre la narrativa de Humberto Salvador aplicando la lingüística de Noam Chomsky, metodología que, lo confieso, jamás he entendido; él estaba interesado en la obra vanguardista del narrador ecuatoriano, mientras que yo superponía su obra paródica y humorística a la militante. A su salida del Panóptico solicitamos a un amigo común, el librero Édgar Freire, que nos ayudase a conseguir las raras ediciones de las obras del autor de Noviembre, empeño que quedó inconcluso ya que poco después «desapareció» nuestro querido Gustavo.
Recuerdo la última vez que nos encontramos: habrá sido la tarde del jueves 8 de noviembre de 1990. De casualidad coincidimos en la
Han pasado más de treinta años y ningún Gobierno en todo este lapso ha respondido qué sucedió con el escritor, clamorosa y continuada dejación de funciones por la que, en los próximos meses, será la Corte Interamericana de Derechos Humanos la que se vea obligada a pronunciarse.
librería Cima, regentada por Édgar, con quien conversamos un rato, y luego, tras despedirnos, Gustavo y yo fuimos a tomar unas cervezas, pues yo disponía de tiempo para recoger a mi pasión de aquel entonces, la que al año siguiente sería la madre de mi hija Sofía, que salía de su trabajo a las 7:30 de la noche; con mi tocayo tuvimos un grato y entrañable diálogo, no puedo decir al calor, sino al frío de unas cervezas. Minutos antes de ir a recoger a mi pareja sentimental le consulté si quería esperarme y asintió, no sin antes llamar por teléfono a su madre desde la cantina en la que estábamos, bajo el «teatro» Capitol, pues habían acordado que se reportaría cada hora para preservar su bienestar y la tranquilidad familiar: ya se veía venir su infausta «desaparición».
Nuestra bella acompañante se avino a la «reunión», y pasamos un rato agradable entre risas, libros y cervezas, de las que agotamos varias botellas. Hacia las 9:00 p.m., llegada la hora de partir, lo acompañamos hasta donde se bifurcaban nuestros caminos, el edificio del Banco Central del Ecuador, frente al monumento a Bolívar: él iba hacia San Juan y nosotros hacia La Ronda; antes del efusivo abrazo y la correspondiente recomendación de que se cuidara, me comentó que el día siguiente, viernes, iría a la salsoteca Son Candela, pidiéndome que, si yo podía, nos viésemos. Tengo entendido que tras salir de allí no se supo más de él.
Gustavo había sido miembro activo del grupo subversivo Montoneras Patria Libre, y deseo resaltar que «desapareció» en el período de gobierno democrático de Rodrigo Borja; había sido constantemente vigilado por los cuerpos de seguridad del Estado desde su salida, libre de cargos, de la cárcel. Han pasado más de treinta años y ningún Gobierno, en todo este lapso, ha respondido qué sucedió con el escritor, clamorosa y continuada dejación de funciones por la que, en los próximos meses, será la Corte Interamericana de Derechos Humanos la que se vea obligada a pronunciarse.
Con este escueto testimonio me sumo con un saludo cordial a su homenaje.
sábado, 23 de noviembre de 2019
viernes, 22 de noviembre de 2019
martes, 5 de noviembre de 2019
miércoles, 14 de agosto de 2019
El mejor homenaje a Miguel Donoso: mantener sus talleres con su metodología
https://www.culturaypatrimonio.gob.ec/el-mejor-homenaje-a-miguel-donoso-mantener-sus-talleres-con-su-metodologia/
El mejor homenaje a Miguel Donoso: mantener sus talleres con su metodología
Desde noviembre de 2014 hasta el último viernes 13 de marzo, el Ministerio de Cultura y Patrimonio estaba trabajando de la mano del escritor guayaquileño Miguel Donoso para abrir en varias provincias del país talleres de corte literario. Pese a la muerte del maestro Donoso –el día de ayer (16 de marzo), debido a una afección pulmonar- esta Cartera de Estado ratificó el compromiso –como una manera de homenajear su memoria- de continuar con el proyecto.
La idea que se trabajaba con Donoso era emplear en los talleres su metodología, que, entre otros aspectos, propone analizar los textos de manera impersonal, ajena, para que en la crítica no interfieran afectos personales. Es decir, analizar directamente el cuerpo del texto sin pensar en quién lo escribió.
No iba a ser Donoso quien dictaría las clínicas literarias –por su estado de salud no podía- sino otros facilitadores capacitados por él mismo. El proyecto, actualmente en estado piloto, continúa. Este año se pretende arrancar los talleres en tres provincias del país.
En la década de los setenta, Donoso dirigió talleres literarios en México. Entre sus alumnos consta el ahora reconocido escritor mexicano Juan Villoro, quien para entonces –según contó en su reciente visita a la Feria Internacional del Libro de Quito 2014- tan sólo había escrito un cuento. Sus clínicas también abarcaron Ecuador. Desde los años 80, cuando retornó al país, formó a narradores de al menos dos generaciones. Entre esos, Huilo Ruales, Alfredo Noriega, Jorge Martillo, Fernando Balseca, Jenny Carrasco, Gustavo Garzón, Gilda Holst, Byron Rodríguez V., Jorge Velasco McKenzie y Raúl Vallejo.
jueves, 25 de julio de 2019
Tortura: un delito sin castigo, La Hora, 2 de septiembre de 1991
"Tortura: un delito sin castigo". La Hora. Enfoque (Quito), 2 de septiembre de 1991. 3
lunes, 22 de julio de 2019
Kathmann, Atención San Miguel, 11 de febrero de 1994
Kathmann, Lucina. "¿Dónde está Gustavo Garzón?". Atención San Miguel. Published by Biblioteca Pública de San Miguel de Allende. vol.XX, No.5, 11 de febrero de 1994. 48.
sábado, 20 de julio de 2019
Paredes, Gustavo Garzón, su palabra y la ciudad que lo devoró, 2010-11-13
Gustavo Garzón, su palabra y la ciudad que lo devoró
Ampliar TIEMPO DE LECTURA: 6' 23'' NO. DE PALABRAS: 1047
Flavio Paredes Cruz. 00:00 Sábado 13/11/2010
La avenida De la Prensa, una tarde gris. Un largo bus amarillo transita sobre el asfalto y arrastra un ruido de bocinas y motores. Hace más de una veintena de años, esta vía se abría como una herida en la ciudad, una llaga que supuraba hacia los nuevos barrios del norte de Quito, asentamientos de concreto y metal. Aquí, ahora, y con los cuentos de ‘Vivo en medio de tantos muertos’, de Gustavo Garzón bajo el brazo, rehago, más de veinte años después, el recorrido del narrador de ‘Tu rostro en la multitud’, el último relato de ese libro presentado el miércoles por la Casa de la Cultura.El narrador lo hace persiguiendo una silueta femenina, yo lo hago en solitario. Gustavo Garzón tenía una camioneta Datsun 1200 verde, pero también prefería la caminata, con paso lento y las manos en los bolsillos. Así encontraba el universo de su literatura, de esos textos que se gestaron en los talleres que el escritor Miguel Donoso Pareja dictaba en los años 80. La apariencia de la avenida ha cambiado. En la Y, ya no está la panadería, desde donde el narrador descubrió a su perseguida, talvez Leonor. En los cuentos de Garzón se respiran amores imposibles, perfiles de mujeres: de Susana, de J, de Fabiola, de Madonna, de Liliana' o de esa mujer de los zapatos azules que le despertó la esperanza, de quien el autor habla en la dedicatoria de su ‘Brutal como el rasgar de un fósforo’. Siempre por la vereda, pero toreando automóviles, acompaño al narrador hasta el cruce de la 10 de agosto y la Naciones Unidas. Ahora el paso deprimido facilita el tránsito; pero en el cuento, la intersección se describe difícil, pues el movimiento de los autos se rige por semáforos en cada esquina. En una de ellas, la mujer enciende un cigarrillo. Garzón fumaba Lark, leía a Cortázar, escuchaba jazz y rock. Desde la Mañosca hasta la Eloy Alfaro el narrador no encuentra una tienda, yo sí: una tienda, un local de autos usados, una ferretería y el Trole, con una melodía como bocina. Él en cambio se topó con una picantería y, en la Mariana de Jesús, con los trabajadores de la Empresa Eléctrica jugando volley. Garzón trabajó en Ecuatoriana, pues era técnico de aviación, así viajó a EE.UU. e Israel, país que le gustaba y donde tuvo una novia, como las demás más alta que él. Era también matemático y estadístico, y dominaba el inglés. Leonor avanza hasta la Colón y el narrador mide las posibilidades de entrar al bar Patricia, de desviarse al café Royal; en el Peñón pide una cerveza. Los lugares y los nombres me resultan extraños y ya no los veo. Garzón sí visitó eso sitios – dicen quienes lo conocieron y también los visitaron. Sus conversaciones sobre literatura se hacían con Pilsener y Ron Caney. Luego, el autor salía a aullarle a esa ciudad que le fascinó y que, el 10 de noviembre de 1990, lo devoró. Esa noche, tras cobrar un cheque en la editorial El Conejo, por la publicación de ‘Las coplas populares del Azuay’, se fue con amigos al Son Candela. Ahora las esquinas de la Carrión y Reina Victoria, ya no muestran la fachada del bar. De ahí salió Garzón, solo, con la madrugada y un posible desengaño amoroso. La más cruel de las versiones y el Informe de la Comisión de la verdad hablan de una desaparición forzosa. En 1985, el escritor dijo a sus amigos de La mosca zumba que se alejaba temporalmente de las letras y de la revista que el colectivo editaba, por una convicción ideológica. En sus relatos también hay desaparecidos y guerrilleros enfrentados a poderosos dinosaurios. Garzón fue investigado por presuntos vínculos con Alfaro Vive Carajo y Montoneras Patria Libre. El 7 de agosto de 1989 fue detenido y permaneció en prisión sin pruebas, hasta el 7 de septiembre de 1990, tres meses antes de su desaparición. ‘Tu rostro en la multitud’ termina cuando mujer y narrador caminan por San Juan. La cuesta de la Matovelle me lleva a ese barrio y a su murmullo. El barrio donde Garzón vivía, y donde hasta hoy vive su madre Clorinda Guzmán, con un retrato de su hijo en blanco y negro, que siempre portó en las manifestaciones por los derechos humanos. Dicen - quienes lo conocieron - que era un hombre bueno y tranquilo. Ellos lo sueñan, con sus chalecos de lana y camisas de manga corta, en bosques alejados, o lo recuerdan en sabrosas tertulias. 20 años después de la noche del Son Candela, la palabra de Garzón regresa... Un narrador en un laberinto Gustavo Garzón Guzmán, gran amigo y lúcido escritor, nunca se ha ido. Una prueba es el libro de cuentos ‘Vivo en medio de tantos muertos’, una obra intensa y poética que acaba de editar la Casa de la Cultura. Garzón fue un narrador urbano que supo recrear con sensibilidad y talento los vericuetos de su Quito: sus calles largas y estrechas, su barrio San Juan, los parques, las plazas, los bares, los templos añejos. Y en medio de esta ciudad laberíntica, a ratos asfixiante y cruel, dio vida a sus criaturas: burócratas robotizados, parejas siempre contrariadas y ocultas; un dinosaurio como símbolo del poder ciego. En su escritura ágil y plena de imágenes se percibe la huella de sus autores favoritos: Borges, Sábato, Cortázar, Whitman; el rock experimental y demoledor de Pink Floyd. Lo evocamos con sus chalecos de lana y sus camisas de manga corta. Siempre con el látigo exigente de Truman Capote y asumiendo la literatura como un destino inexorable. En ‘Brutal como el rasgar de un fósforo’, el primer libro que publicó, extraño y alucinante, Quito late y perdura. BRV.
Donoso, III. Brutal como el rasgar, Matapalo, 1 de marzo de 1992
El Texto como Prueba.
III. Brutal como el rasgar de un fósforo: La Desaparición.
(Miguel Donoso Pareja, 1 de marzo de 1992, Matapalo, p.5)
Gustavo Garzón desapareció (¿lo desaparecieron?) el 9 de noviembre de 1990, después de salir de un discoteca. Militante de Montonera Patria Libre, había sido apresado antes por una supuesta tenencia de armas. Fue sobreseído de esta imputación en forma definitiva.
Libre y limpio de toda culpa, Gustavo manifestó a sus amigos, en diferentes oportunidades, que había dejado la militancia y que lo que ahora le interesaba era obtener su doctorado en Literatura por la Universidad Católica. En ese centro de estudios hizo las gestiones pertinentes para lograrlo, con lo que sus ilusiones anteriores – Técnico en aviónica y Licenciado en Estadística y Banca por la Universidad Central – aumentaría un tercero, Gustavo era, pues, ¿lo es?, un hombre de estudio, autor por ejemplo, de una investigación titulada “Coplas Populares del Azuay” (El Conejo PUCE – 1987) y coeditor de la revista “La Mosca Zumba” (1984 – 87), en Quito. Sin embrago, desapareció o “lo desaparecieron”.
Se ha dicho que sus compañeros del taller no han hecho nada después de su desaparición. Y eso no es verdad. Así el “Frente por la vida de Gustavo Garzón” presidido por el escritor Marco Antonio Rodríguez, tiene entre sus integrantes a ex – talleristas; Byron Rodríguez, Vicente Robalino y Pablo Salgado, por ejemplo, junto a dos valientes mujeres Liliana Vásconez y Martha Palacios. Y siempre colaboran con el Frente personas como: Rubén Darío Buitrón (ex – tallerista), Luís Saavedra, Simón Zabala, Patricio Icaza y Elsie Monge.
La respuesta de los medios y de los intelectuales, en general, ha sido débil en el primer caso y en el segundo no ha repercutido. Cuatro o cinco notas han aparecido en diarios de Quito (una de ellas de Raúl Vallejo); dejé sentada una protesta tres o cuatro días después de la desaparición de Gustavo en el IV Encuentro de Literatura Ecuatoriana “Alfonso Carrasco Vintimilla” de Cuenca, encuentro auspiciado por el programa nacional “Ecuador Estudia”, algo dije al respecto en una entrevista que me hicieron (Semana, Expreso, 6 de enero de 1991); en el “Telégrafo” apareció un artículo desinformador y tardío en lo esencial de Leonardo Valencia Azogan. Fernando Villavicencio, en Radio Tarqui (Quito) ha hablado casi a diario sobre la desaparición de Gustavo. Lo mismo lo ha hecho en forma tarada (perdonen el galicismo) y hasta vituperiosa Carlos Calderón Chico en el dominical de Expreso. El “Frente por la vida de Gustavo Garzón” consiguió cuatro o cinco comparecencias en diversos canales de televisión quiteños. Con Decreto Ejecutivo Nº 2694 (está publicado en el Registro Oficial) el presidente constitucional de la República prorrogó el mandato de la Comisión Especial Internacional integrada para investigar la desaparición de los hermanos Restrepo, “a fin de dar el mismo tratamiento…(…) a otros casos denunciados, tales como, la desaparición del señor Gustavo Garzón Guzmán”. El Decreto data del 2 de septiembre de 1991.
Pero el caso de Gustavo, no es igual del de los hermanos Restrepo. La familia del escritor desaparecido es pobre, la madre – sumamente valiente, llena de entereza según me han dicho – apenas sobrevive. Sin embargo, la opinión pública no se ha conmovido por la desaparición del escritor; además ¿A quien le importa en este país un escritor? Y nadie ha dado pistas cuando se ha acercado la Comisión, dice su Presidente Juan de Dios Parra.
Mientras tanto, como cuenta Otto Raúl González gran poeta y narrador guatemalteco, refiriéndose a Chema López (José María López Valdizón), escritor a quien desaparecieron hace muchos años “las autoridades de Xibalbá le permiten” (lo extendemos a Gustavo, si es que está muerto) “corporizarse solamente una vez al año (…). Come y chupa tal como se disponía a hacerlo el día de su desaparición” (Gustavo lo hizo) “Y se le ha conferido el cargo de abrir anualmente las válvulas de la alegría en el corazón de todos los rabibalenses.
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