The growing frequency of antibiotic resistance as a primary public health concern in developing and undeveloped countries has resulted in the failure to treat various infections, higher handling costs, limited therapeutic choices, and increased mortality and morbidity [
13]. pAmpC β-lactamases have become increasingly significant from a therapeutic standpoint, and their identification will be useful for both monitoring and epidemiological and infection control strategies [
5]. In this study, the level of antibiotic resistance of
E. coli isolates ranged from 7.4% to 90.5%. Antimicrobial susceptibility testing revealed that the bacterial isolates studied had relatively high resistance to β-lactam antibiotics (amoxicillin, cephalothin, cefoxitin, ceftriaxone, cefpodoxime, and ceftizoxime). Meanwhile, they had the highest susceptibility to colistin, piperacillin/tazobactam, and amikacin. Comparable results were reported by some previous studies from Nepal [
13], India [
14], and Iran [
15]. As shown in
Figure 1, AmpC producers exhibited significantly higher resistance rates than AmpC-negative strains. This observation extensively corroborated the findings of previous authors, associating AmpC production with increasing resistance to diverse antimicrobial classes [
16−
18]. Antimicrobial resistance is linked to the increasing spread of MDR strains, and since infections caused by these organisms are extremely difficult to treat, recognition and awareness of their prevalence in the community are crucial [
19]. In the present study, almost half of the
E. coli isolates (49, 51.6%) were found to be MDR, which is in line with the results of other studies carried in Iran [
20] and Gabon [
1] and contrary to that of Bala et al. [
14]. There are several reasons for the reduction in sensitivity towards newer generations of antibiotics, including bacterial production of β-lactam ring hydrolyzing enzymes such as extended-spectrum β-lactamases, AmpC β-lactamases, and metallo-β-lactamases [
21]. Although various screening and confirmatory phenotypic methods for AmpC β-lactamase have been introduced, most of them are not suitable for routine use in diagnostic laboratories. However, the inhibitor-based method, which serves as a reliable confirmatory marker with acceptable negative predictive values, has been employed by many researchers to detect AmpC production [
17]. As expected, in the present study, screening and confirmatory phenotypic tests yielded different results, and the production of AmpC β-lactamase was confirmed in only 14.7% (14/95) of cefoxitin-resistant isolates. Studies conducted in Spain (14.2%) [
22], Nigeria (15.2%) [
23], and Iran (15.1%) [
5] have reported equivalent frequencies. However, the frequency rate of AmpC production in the present study was lower than those found in other studies conducted in India [
14], Bahrain [
24], Iran [
25], and Egypt [
6], which reported rates of 47.1%, 87%, 54.4%, and 73.4%, respectively. There are several reasons for this discrepancy in the findings, including differences in the diagnostic methods employed, geographical location, study participants, and the study period. Various studies have been conducted on the prevalence of the pAmpC genes at different time points and in different countries, which can provide valuable information about AmpC-type resistance over time and its course. According to the multiplex PCR assay results of this study, 3 types of pAmpC cluster genes (
blaCIT,
blaDHA, and
blaDHA) were detected in 15 isolates (15.8%). The prevalence of the
blaDHA,
blaCIT, and
blaEBC genes in
E. coli isolates was also found to be 8.4%, 4.2%, and 3.2%, respectively. These results were in accordance with a previous study reported by Kazemian et al. [
26], from Iran. Although some studies have reported the coexistence of
blaDHA,
blaEBC, and
blaCIT in
E. coli isolates [
15,
25,
27], only 1 pAmpC gene family was detected in the strains of our study. Some limitations of this study included the lack of data on the molecular typing of the strains and the sequencing of pAmpC cluster genes. In addition, due to a lack of funding, only the presence of pAmpC genes was targeted, and other potential associates of cefoxitin resistance, such as chromosomal hyperproduction or purine loss mutations, were not investigated.
