Extended-spectrum Beta-lactamase and AmpC beta-lactamases producing gram negative bacilli isolated from clinical specimens at International Clinical Laboratories, Addis Ababa, Ethiopia

Abstract

Background Extended spectrum Beta-lactamases (ESBLs) and AmpC beta-lactamases (AmpC) are the common enzymes produced by gram negative bacilli, which are their main mechanisms of resistance to all generations of cephalosporins. Hence, this study aimed to determine the magnitude of ESBLs and AmpC producing gram negative bacilli (GNB) isolated from clinical specimens at International clinical Laboratories in Addis Ababa, Ethiopia. Methods A cross sectional study was conducted from January to May 2018. From different clinical specimens, 338 GNB were isolated and characterized. Bacterial species identification, antimicrobial susceptibility testing and screening for ESBLs and AmpC production were performed using Phoenix automated system (BD phoenix100). ESBLs production was confirmed using a combination disc method. All Cefoxitin resistant and confirmed ESBLs producing GNB were confirmed for AmpC beta-lactamases production by AmpC confirmatory Neo-Sensitabs discs (ROSCO tablet). Data were analyzed using SPSS version 20 software. Results E. coli 66.0% (224/338) followed by K. pneumoniae 12.1% (41/338) were GNB most frequently isolated. The overall magnitude of ESBLs producing GNB was 38.8% (131/338) and the extent of AmpC beta-lactamase producing GNB was 2.4% (8/338). Majority of ESBLs and AmpC beta-lactamases producing GNB were isolated from urine specimens 47.5% (116/338). Ampicillin (75.4%), amoxicillin with clavulanic acid (64.0%) and sulfamethoxazole-trimethoprim (55.6%) were most the antibiotics to which resistance was most commonly found. The multidrug resistance (MDR) level of GNB was 74.0% (250/338). Of ESBLs and AmpC beta-lactamases producing GNB, 99.3% were MDR (p < 0.05). Conclusion The high magnitude of ESBLs and AmpC beta-lactamases producing GNB calls the needs of strong intervention to minimize further occurrence and spread of such GNB. More importantly, the MDR level was high which suggests continuous monitoring & reviewing of antimicrobial policy in hospitals and the country at large.

Antimicrobial Activity of Selected Medicinal Plants from a Sub-Saharan African Country against Bacterial Pathogens from Post-Operative Wound Infections

“…The antimicrobial investigations from this study showed E. coli clinical isolates to have the highest resistance to cefepime, followed by amikacin and piperacillin/tazobactam, but was highly susceptible to trimethoprim/sulfamethoxazole and meropenem. This observation is in contrast to what was recently observed in Ethiopia by Tekele et al [35] where E. coli (from various clinical specimens such as urine, pus, body fluids, sputum, stool, ear and eye discharges) showed the highest resistance to ampicillin followed by amoxicillin with clavulanic acid. Also, although E. coli isolates from this study showed the highest resistance to cefepime, followed by amikacin, a study by Yılmaz et al [36] showed to E. coli (from urinary tract infections) as having the highest resistance to ampicillin.…”

Prevalence of plasmid-mediated AmpC β-lactamases among uropathogenic Escherichia coli isolates in southwestern Iran

“…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 ].…”

Predisposition of Blood group Non-secretors to Urinary tract infection with Escherichia coli Anti-microbial Resistance and Acute Kidney Injury

“…ESBL has the ability to confer bacterial resistance to penicillin; first-, second-and thirdgeneration cephalosporins; and aztreonam (but not the cephamycins or carbapenems) by hydrolysis of these antimicrobials, and which are inhibited by β-lactamase inhibitors such as clavulanic acid. [7][8][9][10] ESBL was first identified in 1983. Within a short span of time ESBL has evolved drastically with over 300 variants being detected in different members of the family Enterobacteriaceae and other nonenteric organisms.…”

“…ESBL was differentiated from Amp C-type β-lactamases, when the isolates were resistant to cephalosporins but sensitive to clavulanic acid in combination with cephalosporins and are resistant to carbapenem. [7][8][9]…”