Abstract
Objectives
The objective of this work is to describe the trends in antimicrobial resistance profiles of E. coli strains isolated from various clinical specimens at the main hospital in Dakar over a ten-year period.
Methodology
This was a retrospective, cross-sectional descriptive and analytical study over 10 years 2012–2021] of all E. coli isolated at the HPD laboratory. Data were collected from the INLOG laboratory information system.
The descriptive analysis of the data obtained was done with the software Excel (version 16.78.3, 23102801) and R (4.3.3).
Results
Of 23,311 bacterial species isolated, 7,797 E. coli (33.4%) were identified. The median age of patients was 52 (23–69), 1D; 100 years old] with a slight male predominance, sex ratio at 1.1.
The resistance rates of E. coli to antibiotics were generally high: 85% with ampicillin, 46% with amoxicillin + clavulanic acid, 27% with cephalosporins of 3rd generation and 43% with pefloxacin.
Between 2012 and 2021, a significant increase in E. coli resistance was observed (p < 0.005) for most antibiotics, except gentamicin, tobramycin, and cotrimoxazole, which showed a decreasing trend. Resistance rates increased from 28 to 41% for 3rd generation cephalosporins, 38 to 65% for amoxicillin + clavulanic acid and 51 to 56% for quinolones.
Multidrug-resistant bacteria accounted for 28.47% (n = 2220) with a predominance of extended spectrum beta lactamases ESBL 24.34% (n = 1898).
Conclusion
This study highlights a concerning resistance profile of Escherichia coli to commonly used antibiotics, particularly beta-lactams, fluoroquinolones, and aminoglycosides. Over time, a marked increase in multidrug-resistant (MDR) strains has also been observed, along with an alarming rise in carbapenem resistance. These findings underscore the urgent need to strengthen antibiotic stewardship policies, implement regular surveillance of resistance profiles, and reinforce infection prevention and control measures.Keywords: Escherichia coli, bacterial resistance, Dakar.
Keywords: Escherichia coli, Bacterial resistance, Dakar
Introduction
Escherichia coli (E. coli) is one of the most common pathogens responsible for a wide range of infections, including urinary tract infections, bloodstream infections, and intra-abdominal infections [1–3]. As a member of the Enterobacteria family, E. coli is also a key indicator organism for monitoring antimicrobial resistance (AMR) trends [4–6].
Over the past decades, the global rise in antibiotic resistance among E. coli strains has become a major public health concern, especially in healthcare settings. The widespread and often inappropriate use of antibiotics has contributed to the emergence of multidrug-resistant (MDR), extensively drug-resistant (XDR), and even pan-drug-resistant (PDR) strains, complicating the management of infections and increasing morbidity and mortality rates [7–9].
In low- and middle-income countries, including those in sub-Saharan Africa, surveillance data on antimicrobial resistance remain limited. However, available studies have reported alarming resistance rates, particularly to beta-lactams, fluoroquinolones, and aminoglycosides—antibiotics frequently used in empirical treatment [10–12].
In this context, understanding the evolution and distribution of resistance patterns is essential for guiding clinical decisions and shaping effective antibiotic stewardship programs. The present study aims to describe the trends in antimicrobial resistance profiles of E. coli strains isolated from various clinical specimens at the main hospital in Dakar over a ten-year period.
Materials and methods
Type and period of study
We conducted a retrospective, cross-sectional and descriptive study with an analytical purpose over a period of ten (10) years from 1 January, 2012 to 31 December, 2021.
Study population
It included all reports of the susceptibility tests carried out during the period of our study.
Inclusion criteria
The study included all antibiogram results obtained from isolatedE. colistrains of pathological products received in the laboratory for cytobacteriology.
Criteria for non-inclusion
Duplicates (same bacteria with the same resistance profile isolated in the same patient on the same type of disease product) and other bacterial species isolated were not included in the study.
Data collection
Data was collected from the laboratory information system (LIS) called Inlog server. The variables taken into account were age, sex, hospital service of patients concerned, year of isolation, nature of the sample and test results for strain sensitivity to tested antibiotics (betalactams, quinolones, aminoglycosides, cotrimoxazole…).
Antimicrobial susceptibility testing was performed using the disc diffusion method on Mueller-Hinton agar, according to CASFM-EUCAST guidelines [13]. The antibiotic discs and their respective concentrations were as follows: ampicillin (10 µg), amoxicillin–clavulanic acid (20/10 µg), cefotaxime (30 µg), ceftazidime (30 µg), cefepime (30 µg), imipenem (10 µg), pefloxacin (5 µg), nalidixic acid (30 µg), gentamicin (10 µg), amikacin (30 µg), tobramycin (10 µg), cotrimoxazole (1.25/23.75 µg).
Data analysis
Descriptive analysis of data was performed with Excel version 16.78.3 (23102801) and the R software version (4.3.3). The quantitative data were expressed as an average more or less standard deviation or median and IIQ according to their distribution. The absolute and percentage proportions and the comparison of the proportions concerning the evolution of the resistance rate between 2012 and 2021 was carried out using the Pearson Chi square test or the Fisher test according to their applicability condition (the data are selected randomly, and for each category, the expected frequency is greater than or equal to 5 otherwise the Fisher test is used). The significance threshold was set at 5% (p-value
Results
Epidemiological data
Between 2012 and 2021, a total of 7,797 Escherichia coli strains were identified among 23,311 bacterial isolates, corresponding to an isolation frequency of 33.4%. The median age of patients from whom E. coli was isolated was 52 years (interquartile range: 23–69), with extremes ranging from 1 day to 100 years. The study population showed a slight male predominance, with a sex ratio of 1.1.
Among the E. coli isolates, 34.38% (n = 2,681) originated from outpatients, while 65.62% (n = 5,116) were recovered from hospitalized patients. The hospitalized isolates were distributed across the following departments: medicine (20.41%, n = 1,592), surgery (17.84%, n = 1,391), pediatrics (17.77%, n = 1,386), and emergency-resuscitation (9.6%, n = 747).
Regarding the specimen types, E. coli was primarily isolated from urine samples (61%, n = 4,755), followed by suppurations (18.3%, n = 1,425), blood cultures (10.2%, n = 797), and gastric samples (8.2%, n = 637) (see Table 1).
Table 1.
Distribution of E. coli isolated at HPD from 2012 to 2021 by sample
| Samples | Number of isolated E. coli | |
|---|---|---|
| n | Percentage (%) | |
| Urine | 4755 | 61 |
| Blood | 797 | 10,2 |
| Suppuration | 1425 | 18,3 |
| Gastric sample | 637 | 8,2 |
| Bronchial secretions | 54 | 0,7 |
| Vaginal sample | 53 | 0,7 |
| Cerebrospinal fluid | 9 | 0,1 |
| Broncho-alvéolar wash | 19 | 0,2 |
| Stool | 19 | 0,24 |
| Broncho-aspiration | 10 | 0,13 |
| Urethral sample | 15 | 0,2 |
| Pleural fluid | 3 | 0,04 |
| Joint fluid | 1 | 0,01 |
E. coli resistance profile
The resistance rate of E. coli to beta-lactams was 85% (n = 6,603) for both ampicillin and ticarcillin, 46% (n = 3,590) for amoxicillin/clavulanic acid, 42% (n = 3,304) for cephalothin, 27% (n = 2,122) for third-generation cephalosporins (C3G), 24% (n = 1,852) for cefepime, 8% (n = 648) for cefoxitin, and only 1% (n = 49) for imipenem.
With respect to aminoglycosides, resistance rates were 28% (n = 2,170) for gentamicin, 25% (n = 1,928) for tobramycin, and 3% (n = 216) for amikacin.
Regarding quinolones, E. coli showed resistance rates of 57% (n = 4,446) to nalidixic acid and 43% (n = 3,381) to pefloxacin. Additionally, cotrimoxazole was ineffective against 68% of the E. coli isolates.
The full resistance profiles of E. coli to the tested antibiotics are presented in Table 2.
Table 2.
Antibiotic resistance profile of E. coli isolated in HPD from 2012 to 2021
| Antibiotic tested | E. coli resistance rate | |
|---|---|---|
| n (N = 7797) | % | |
| Ampicillin | 6503 | 85 |
| Ticarcillin | 6503 | 85 |
| Amoxicillin + clavulanic acid | 3590 | 46 |
| Cefalothin | 3304 | 42 |
| Cefoxitin | 648 | 8 |
| Cefotaxime | 2122 | 27 |
| Ceftazidime | 2122 | 27 |
| Aztreonam | 2122 | 27 |
| Cefepime | 1852 | 24 |
| Imipenem | 49 | 1 |
| Nalidixic acid | 4446 | 57 |
| Pefloxacin | 3381 | 43 |
| Gentamicin | 2170 | 28 |
| Tobramycin | 1928 | 25 |
| Amikacin | 216 | 3 |
| Netilmicin | 312 | 4 |
| Co-trimoxazole | 5302 | 68 |
This table presents the percentage and absolute number (n) of E. coli strains resistant to each antibiotic. Antibiotics are grouped by family: beta-lactams, aminoglycosides, quinolones, and others. The highest resistance rates were observed for ampicillin, ticarcillin, and nalidixic acid, while imipenem and amikacin remained the most active agents against the isolates.
Among the resistance phenotypes to beta-lactams, low-level penicillinase producers (PBN) were the most prevalent, accounting for 36.47% (n = 2,844) of E. coli isolates. These were followed by extended-spectrum beta-lactamase (ESBL) producers at 24.34% (n = 1,898), high-level penicillinase producers (PHN) at 19.57% (n = 1,526), and wild-type phenotypes (susceptible to all beta-lactams) at 15.17% (n = 1,183). The least frequent phenotypes were depressed cephalosporinase producers (CASED) at 3.69% (n = 288), and probable carbapenemase producers at 0.43% (n = 34).
Figure 1 presents the distribution of these beta-lactam resistance phenotypes among the E. coli isolates.
Fig. 1.
Distribution of resistance phenotypes of E. coli isolated at HPD from 2012 to 2021
Prevalence of multi-drug-resistant E. coli (antibiotics)
Out of all E. coli isolates, 2,220 strains (28.47%) were resistant to at least three different classes of antibiotics, indicating a high prevalence of multidrug-resistant (MDR) E. coli. Among these MDR strains, 24.34% (n = 1,898) were ESBL-producing E. coli, 3.69% (n = 288) were E. coli with acquired AmpC beta-lactamase (CASED), and 0.44% (n = 34) were carbapenemase-producing E. coli.
Progression of antibiotic resistance in E. coli isolated at HPD from 2012 to 2021.
Table 3 represents the overall evolution of antibiotic resistance rates in isolated E. coli from 2012 to 2021.
Table 3.
Progression of antibiotic resistance in Escherichia coli isolates at HPD from 2012 to 2021
| ABX | n | 2012 (%) |
2013 (%) |
2014 (%) |
2015 (%) |
2016(%) | 2017 (%) |
2018 (%) |
2019 (%) |
2020 (%) |
2021 (%) |
P-value |
|---|---|---|---|---|---|---|---|---|---|---|---|---|
| 3GC | 2120 | 28 | 24,3 | 22,5 | 23,8 | 21,2 | 20,1 | 27,4 | 36,6 | 39,4 | 41 | |
| AMC | 3590 | 38 | 39,8 | 46,5 | 44,1 | 39,4 | 40,5 | 45,8 | 55,1 | 61,8 | 65 | |
| IPM | 49 | 0,1 | 0,2 | - | 0,5 | 0,1 | 0,3 | 0,8 | 0,7 | 1,9 | 3,2 | 0,002 |
| NAL | 4446 | 56,2 | 53,5 | 55,9 | 59,5 | 48,2 | 57 | 57,5 | 62 | 62,5 | 64,4 | |
| PEF | 3381 | 50,6 | 45,7 | 44 | 43,9 | 35,4 | 38,2 | 37,4 | 40,3 | 50,4 | 56,1 | |
| GEN | 2170 | 32 | 29,9 | 24,4 | 33,9 | 30 | 31,5 | 20,4 | 21,2 | 28 | 25 | |
| TOB | 1928 | 30 | 27,5 | 9,9 | 31,8 | 28,4 | 30 | 18,8 | 21,5 | 22,1 | 25 | |
| AKN | 216 | 2,7 | 3 | 1,6 | 2,9 | 2,2 | 4,5 | 0,6 | 3,8 | 2,4 | 4,9 | 0,02 |
| STX | 5298 | 75 | 72 | 67,7 | 76,6 | 72,8 | 50,1 | 59,9 | 63,8 | 75,3 | 71 | |
| AMP | 6603 | 85 | 82 | 86 | 87 | 84 | 80 | 84 | 82 | 90 | 90 |
Between 2012 and 2021, the resistance of E. coli to beta-lactam antibiotics increased significantly. Resistance rates rose from 85% to 90% for ampicillin (p = 0.006), from 38% to 65% for amoxicillin-clavulanic acid (p < 0.001), from 28% to 41% for third-generation cephalosporins such as cefotaxime and ceftazidime (p < 0.001), from 25% to 36% for cefepime (p < 0.001), and from 0.1% to 3.2% for imipenem (p < 0.001). These trends indicate a significant escalation in beta-lactam resistance over the decade (Figure2).
Fig. 2.
Progression of Escherichia coli resistance to beta-lactam antibiotics from 2012 to 2021
Similarly, a significant increase in E. coli resistance to quinolones was observed between 2012 and 2021, rising from 56% to 64% for nalidixic acid (p < 0.001) and from 51% to 56% for pefloxacin (p = 0.02). In contrast, the resistance rate to cotrimoxazole showed a slight, non-significant decrease, from 75% in 2012 to 71% in 2021 (p = 0.069) (Figure 3).
Fig. 3.
Progression of Escherichia coli resistance to quinolones and co-trimoxazole from 2012 to 2021
Regarding aminoglycosides, we observed a statistically significant decrease in E. coli resistance to gentamicin, from 32% in 2012 to 25% in 2021 (p = 0.003), and to tobramycin, from 30% to 25% (p = 0.047). Conversely, resistance to amikacin increased significantly over the same period, from 2.75% to 5.05% (p = 0.031) (Figure 4).
Fig. 4.
Progression of Escherichia coli resistance to aminoglycosides from 2012 to 2021
Figure 5 illustrates the evolution of various E. coli resistance phenotypes between 2012 and 2021. A significant increase was observed in multidrug-resistant phenotypes, including ESBL-producing strains, CASED, carbapenemase-producing strains, and the low-level penicillinase profile (p< 0.001). In contrast, the proportion of E. coli strains with a wild-type phenotype and low-level penicillinase decreased over the same period.
Fig. 5.
Evolution of resistance phenotypes of Escherichia coli isolates at HPD from 2012 to 2021
Discussion
Epidemiological characteristics
A total of 7,797 E. coli strains were isolated from 23,311 bacterial isolates collected during the study period, representing an isolation frequency of 33.4%. E. coli showed high resistance rates to most of the antibiotics tested, with the exception of imipenem, which remained effective against 95% of the strains. Furthermore, a significant increase in E. coli resistance was observed for nearly all tested antibiotics between 2012 and 2021. The large size of our study population represents a major strength. However, the unavailability of certain antibiotic discs during specific periods limited our ability to assess the evolution of E. coli resistance to those agents, representing the main limitation of this study.
As a major component of the aerobic commensal flora of the human digestive tract, E. coli is also the most frequent Gram-negative bacillus responsible for both community-acquired and nosocomial infections. This may explain the relatively high isolation frequency observed in our study (33.4%), which is consistent with findings from other studies, such as those by Foka in Cameroon [14] and Fortune in Togo [15], who reported isolation frequencies of 29.5% (n = 444, N = 1,502) and 63.93% (n = 3,778, N = 11,263), respectively.
E. coli strains were predominantly isolated from urine samples (61%). This relatively high frequency has also been reported by several authors, including Oualeguem et al. [16], Longala et al. [17], and Foka et al. [14], who observed urinary isolation rates of 62.4%, 70%, and 57.5%, respectively.
The recurrent isolation of E. coli from urine can be attributed to its ability to colonize the urinary tract. This colonization is facilitated by the expression of surface adhesion proteins known as adhesins, particularly fimbriae. Among these, P-fimbriae play a central role in the pathogenesis of uropathogenic E. coli, enabling specific adhesion to uroepithelial cells [18].
Resistance profile
Under the selective pressure induced by the irrational use of antibiotics, E. coli can acquire plasmids that confer resistance to antibiotics that are normally effective [1]. Accordingly, our study revealed high resistance rates to nearly all antibiotics tested, in line with findings reported in other studies [11, 12, 19–22].
These elevated resistance levels support the fact that certain molecules—such as aminopenicillins and quinolones—which were once effective against E. coli, are no longer recommended for empirical treatment, particularly of urinary tract infections [23]. Notably, imipenem has retained its activity against the majority of E. coli strains isolated in our study. This finding highlights the importance of preserving carbapenems through prudent use, in order to prevent the emergence of resistance mechanisms against this critical class of antibiotics.
Progression of resistance
With regard to resistance trends, our results revealed a significant increase in E. coli resistance rates to nearly all antibiotics tested over the study period, as demonstrated by the associated p-values. Exceptions to this trend were gentamicin, tobramycin, and cotrimoxazole, for which resistance rates remained lower or showed a slight decrease. Between 2012 and 2021, E. coli resistance increased from 85% to 90% for ampicillin, 38% to 65% for amoxicillin–clavulanic acid, 28% to 41% for third-generation cephalosporins, 50% to 56% for pefloxacin, and 2.7% to 4.9% for amikacin.
This upward trend is consistent with findings from other regions. In Cameroon, Ebongue et al. [19] reported an increase in E. coli resistance between 2005 and 2012 from 30% to 50% for third-generation cephalosporins, 37% to 49% for aminoglycosides, and 57.1% to 71.2% for quinolones. In Togo, Fortune Djimabi Salah et al. [15] observed similar trends between 2010 and 2017, with resistance rising from 18.6% to 39.26% for third-generation cephalosporins and from 42.3% to 63.23% for quinolones.
In Senegal, a study by Diop-Ndiaye et al. [11] on E. coli isolated from urine also reported a significant increase in resistance to ampicillin, from 71.8% in 2003 to 81.2% in 2013. However, the increase in resistance to third-generation cephalosporins reported in that study (from 8.96% in 2003 to 16.9% in 2013) was lower than the trends observed in our data. In 2014, the Swiss Centre for Antimicrobial Resistance reported that E. coli resistance to fluoroquinolones had doubled, while resistance to third- and fourth-generation cephalosporins had increased fivefold [23].
The rise in E. coli antibiotic resistance rates can largely be attributed to the irrational and widespread use of antibiotics, which exerts selective pressure that promotes the emergence and dissemination of resistant strains.
However, a decrease in E. coli resistance rates was observed for certain antibiotics, such as gentamicin, tobramycin, and cotrimoxazole. This may be attributed to the fact that these antibiotics are less frequently prescribed in the treatment of E. coli infections [24]. Over the past decade, several high-risk multidrug-resistant clones, such as ESBL-producing E. coli (ESBL-E. coli), have emerged [3]. In our study, the prevalence of ESBL-producing E. coli was 24.34%, which is comparable to findings reported in other studies, including those by Akouétévi Gérard Toudji et al. [2] (39.89%) and Kiiru J. et al. [25] (27%). The high prevalence of ESBL-E. coli isolates may be explained by several factors: the irrational use of broad-spectrum antibiotics, which promotes the selection of resistant mutants; the commensal nature of E. coli and its ease of transmission through contact; and, most importantly, the fact that resistance genes—particularly those encoding ESBLs—are often carried on plasmids, which play a central role in the horizontal transfer of resistance among bacterial populations [26].
Conclusion
Our study highlighted the relatively high frequency of E. coli isolation in our laboratory, as well as the significant increase in its resistance to commonly used antibiotics. These findings underscore the urgent need to:
Intensify efforts to combat the rise of antimicrobial resistance by promoting the rational use of antibiotics and reinforcing adherence to infection prevention and control measures in healthcare settings;
Encourage further research on clinically important bacteria such as E. coli, in order to better understand the underlying drivers of resistance and to inform evidence-based public health policies aimed at controlling this global threat
Acknowledgements
We would like to thank the staff of the Microbiology Laboratory at the University Hospital Center of Dakar for their assistance with data collection and record maintenance. We are also grateful to the clinical teams for their collaboration throughout the study. Finally, we acknowledge all individuals who contributed directly or indirectly to the completion of this work.
Abbreviations
- ABX
Antibiotics
- 3GC
Third-generation Cephalosporins
- AMC
Amoxicillin-clavulanic Acid
- IPM
Imipenem
- GEN
Gentamicin
- NAL
Nalidixic Acid
- PEF
Pefloxacin
- AKN
Amikacin
- TOB
Tobramycin
- SXT
Trimethoprim-sulfamethoxazole (co-trimoxazole)
- AMP
Ampicillin
Authors’ contributions
All authors reviewed the manuscript.
Funding
No funding was granted for the study, we worked on the laboratory data that were obtained from the pathological products received for diagnostic purposes.
Data availability
The data that support the findings of this study are available from corresponding author but restrictions apply to the availability of these data, which were used under license for the current study, and so are not publicly available. Data are however available from the authors upon reasonable request and with permission of Maguette Ndoye.
Declarations
Ethics approval and consent to participate
Our study does not necessarily involve any invasive act and was limited only to the exploitation of laboratory data without direct individual interview, so no consent to participate was requested
Consent for publication
Not applicable.
Competing interests
The authors declare no competing interests.
Footnotes
Publisher’s Note
Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.
References
- 1.AQLavigne J-P, Sotto A, Merle C. Escherichia coli enzyme resistance to beta-lactam and clinical prevalence. Pathol Biol. 2002;50(6):388–93. [DOI] [PubMed] [Google Scholar]
- 2.Akouétévi Gérard TOUDJI, Bouraïma DJERI, Simplice Damintoti KAROU. Prevalence of beta-lactamase-producing broad-spectrum enterobacterial strains isolated in Togo and their susceptibility to antibiotics int. J Biol Chem Sci. 2017;11(3):1165–77. [Google Scholar]
- 3.Paitan Y. Current trends in antimicrobial resistance of Escherichia coli. Curr Top Microbiol Immunol. 2018;416:181–211. [DOI] [PubMed] [Google Scholar]
- 4.World Health Organization. Global antimicrobial resistance and use surveillance system (GLASS) report: 2022. Geneva: WHO. 2022. Available from: https://www.who.int/publications/i/item/9789240062705
- 5.Collignon P, Jarlier V, Richet H, Skov R, Møller JK, Espinal MA. Monitoring resistance trends: the WHO global antimicrobial resistance surveillance system (GLASS). Lancet Infect Dis. 2018;18(4):e99–106. 10.1016/S1473-3099(18)30003-2.29102325 [Google Scholar]
- 6.European Centre for Disease Prevention and Control (ECDC). Antimicrobial resistance surveillance in Europe 2022–2020 data. Stockholm: ECDC. 2022. Available from: https://www.ecdc.europa.eu/en/publications-data
- 7.World Health Organization. Antibacterial agents in clinical development: an analysis of the antibacterial clinical development pipeline. Geneva: World Health Organization. 2021. Available from: https://www.who.int/publications/i/item/9789240062705
- 8.Tacconelli E, Carrara E, Savoldi A, Harbarth S, Mendelson M, Monnet DL, et al. Discovery, research, and development of new antibiotics: the WHO priority list of antibiotic-resistant bacteria and tuberculosis. Lancet Infect Dis. 2018;18(3):318–27. 10.1016/S1473-3099(17)30753-3. [DOI] [PubMed] [Google Scholar]
- 9.Tamma PD, Aitken SL, Bonomo RA, Mathers AJ, van Duin D, Clancy CJ. Antibiotic resistance among gram-negative bacteria: a clinical perspective. Clin Microbiol Rev. 2021;34(2):e00038–19. 10.1128/CMR.00038-19. [Google Scholar]
- 10.Tadesse BT, Ashley EA, Ongarello S, Havumaki J, Wijegoonewardena M, González IJ, et al. Antimicrobial resistance in Africa: a systematic review. BMC Infect Dis. 2017;17(1):616. 10.1186/s12879-017-2713-1. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 11.Diop-Ndiaye H, Macondo E, Camara M. Antibiotics resistance evolution of communitary uropathogens Escherichia coli (2003–2013). Uro’Andro. 2014;1(2):71–8. [Google Scholar]
- 12.El bouamri MC, Arsalane L, Kamouni Y, Yahyaoui H, Bennouar N. Current profile of antibiotic resistance of Escherichia coli uropathogenic strains and consequences therapeutic. Progress Urol. 2014;24(16):1058–62. [DOI] [PubMed] [Google Scholar]
- 13.European Committee on Antimicrobial Susceptibility Testing (EUCAST). Breakpoint tables for interpretation of MICs and zone diameters. Versions 2011 to 2021. Available from: https://www.eucast.org/clinical_breakpoints/
- 14.Foka Fonkam RG, Noubom Michel. Chafa anicette evolution of Escherichia coli antibiotic resistance profile at the Yaounde university teaching hospital from 2012 to 2021. Health Sci Dis. 2023;24(9):16–24. [Google Scholar]
- 15.Salah FD, Sadji AY, Akolly K. Increase in antibiotic resistance of Enterobacteria isolated at the National Institute of hygiene in Lomé from 2010 to 2017. J Interventional Epidemiol Public Health. 2021;4(3):3. [Google Scholar]
- 16.Ouologuem BJ. Susceptibility and evolution of the resistance of Escherichia coli to antibiotics from 2004 to 2008 at the G point CHU. PhD thesis, 2012, Bamako Mali, University of Bamako, 87p. https://www.bibliosante.ml/handle/123456789/1885
- 17.Longla ME, Lyonga-Mbamyah EE, Kalla CGM, Baiye WA, Chafa BA, Gonsu HK. Evolution profile of Escherichia coli resistance from January 2009– April 2013 to antibiotics at the Yaounde university teaching hospital, Cameroon. Br Microbiol Res J. 2016;17(5):1–9. [Google Scholar]
- 18.Johnson JR. Virulence factors in Escherichia coli urinary tract infection. Clin Microbiol Rev. 1991;4:80–128. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 19.Ebongue CO, Tsiazok MD, Mefo o JPN. Evolution of antibiotic resistance of Enterobacteriaceae isolated at the Douala general hospital from 2005 to 2012. Pan Afr Med J. 2015;12:20:227. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 20.Goro AA. Study of the antibiotic resistance of enterobacteria isolated in Bamako from January 2020 to June 2020, 2021. Doctoral thesis, Bamako Mali, University of Bamako 2021 https://www.bibliosante.ml/handle/123456789/4658
- 21.Dia ML, Chabouny H. R Diagne Antibiotypical profile of uropathogenic bacteria isolated at the University Hospital of Dakar Uro’Andro. 2015;1(4):212–7.
- 22.Sy A, Diop O, Mbodji M, Faye M, Faye., FA, NdiayeF., et al. Resistance profile to beta-lactams of uropathogenic Enterobacteria isolated in the medical biology laboratory of the regional hospital center of Thies. Afr J Intern Med. 2021;8(1):39–47. [Google Scholar]
- 23.Federal Office of Public Health and Federal Food Safety and Veterinary Office. Swiss Antibiotic Resistance Report 2022. Usage of Antibiotics and Occurrence of Antibiotic Resistance in Switzerland. November 2022. P74.
- 24.French agency for health product safety. Practical recommendations: diagnosis and antibiotic treatment of community-based bacterial urinary tract infections in adults. Med Infect Dis. 2008;38S:203–52. [Google Scholar]
- 25.Kiiru J, Kariuki S, Goddeeris BM, Butaye P. Analysis of β-lactamase phenotypes and carriage of selected β-lactamase genes among Escherichia coli strains obtained from Kenyan patients during an 18-year period. BMC Microbiol. 2012;12(28):155. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 26.Martinez-Martinez L, Pascual A, Jacoby GA, Jacoby GA, Hooper DC. Quinolone resistance from a transferable plasmid. Lancet. 1998;351:797–9. [DOI] [PubMed] [Google Scholar]
Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The data that support the findings of this study are available from corresponding author but restrictions apply to the availability of these data, which were used under license for the current study, and so are not publicly available. Data are however available from the authors upon reasonable request and with permission of Maguette Ndoye.