The prevalence of UTI in the present study was 16.7% (95% CI 12.7-20.4, N=50). It is in line with the study done in Addis Ababa 15.8% [18]. However, it is lower than the findings of the studies in Gondar, 26.45% [19], and Hawassa, 27.5% [8]. This difference might be a female predominance to Gondar University Hospital, 60.94% in contrast to our study 44.8%. The majority of male study participants, 71.7% in the Hawassa University Hospital were not circumcised. Therefore, a tight foreskin may interfere with the normal passage of urine and can prevent the full emptying of the bladder [25, 26].
Though UTI can be caused by both Gram-negative and Gram-positive bacteria, Gram-negative bacteria are the most common cause of the infection, because the agents are the normal constituent of the normal intestinal microbiota [27]. Acquisition of UTI starts with periurethral contamination by uropathogens inhabiting in the gut, followed by colonization of the urethra and successive migration of the pathogen to the bladder [28]. Among these, E. coli is the predominant one [14, 29, 30]. Similarly, the present study reveals that 88% (44/50, 95% CI 80-96%) of the isolate are Gram-negative bacteria. Of these, E. coli accounted for about 63.63% of Gram-negatives followed by Klebsiella species (15.9%), and Citrobacter species (13.63%). This predominance might be due to their unique structures such as flagella and pili, which help for their attachment to the uroepithelium and increases risks for infection [31]. Similar percentage of Citrobacter species, E. coli species, and Klebsiella species was documented in Nigeria, 10.7% [32], in Iran, 57.4% [33], and in Scotland, 19% [3] respectively. A study in Bangladesh reported the same prevalence of E. coli, 63.3% of the total Gram-negative bacterial isolates [34]. About 30/50 (60%) of the isolate and 20/28 (72%) of E. coli and Klebsiella species were isolated from females. This might be due to poor hygienic conditions, the proximity of anal and urethral openings, and relatively wide urethra [14].
All Gram-negative bacterial isolates 44/44(100%) were resistant to ampicillin followed by augmentin 39/44(88.6%) and tetracycline 36/44 (81.8%). Similar findings were seen in Scotland, 93% [35] and in Pakistan, 100% [36]. The reason may be due to the continuous use of these drugs for many years, easily availability, self-prescription, the tendency of patients using relatively cheaper antibiotics for all types of infection, and misuse. About 43/44(97.3%) of isolates were sensitive to Meropenem. This might be due to the unavailability of this drug in the area. As table 2 shows, ciprofloxacin, cefoxitin, and ceftazidime showed the best performance against E. coli. This finding was almost similar with the findings reported at Gondar Hospital and Yekatit 12 hospital [18]. According to the findings in Gondar Hospital, the sensitivity of gentamicin and cotrimoxazole to E. coli was 80% and 73% [19] respectively. However, in the present study, the susceptibility to the above-listed drugs were 15/28(53.4%) and 16/28(57.1%) respectively. This might be due to the gradual increase of drug resistance/selective pressure of bacteria to the drug /mutation, or the difference in antibiotic practices in the study area. Similar research from Iraq also revealed 75% sensitivity to chloramphenicol [2].
All Gram-positive isolates showed 6/6(100%) sensitivity to nitrofurantoin. A similar result was reported at Yekatit 12 hospital 100% [18].The reason for the effectiveness of this drug might be, due to the nature of having multiple mechanisms and site of actions of the drug with a non-specific blockage of protein synthesis limited access to the drug, and narrow-spectrum nature of the drug. However, about 71.4% resistance rate was documented in Hawasa [8]. Higher resistance to this antibiotic is perhaps due to its wrongly usage as an empirical therapy.
Furthermore, the overall MDR prevalence in this study was (66%) (95% CI 52-78, N=33). Specifically, Gram-negative bacterial isolates showed significant level of MDR 31/44(70.5%) compared to Gram-positive bacteria 2/6(33.33%). This was comparable to the findings reported in Gondar 58.53% [30] and Addis Ababa, 73.7% [18]. Although antimicrobial resistance comes primarily as a result of selective pressure on susceptible microbes by the use of therapeutic agents, there are also further multiple factors for the spread of resistance. Using broad-spectrum agents, easy availability of antimicrobials in non-controlled pharmacy, sub-standard/poor drug quality, treatment termination, and over-prescription due to a poor diagnostic set-up or fear of loss of follow-up are among common factors enhancing antimicrobial resistance [37].
The emergence of resistant strains among uropathogens are alarmingly increasing with different resistance patterns [38]. Acquisition of resistance might be either mutational (changing the target site of a bacteria within its genetic material) or acquisition of new genetic material from other bacteria. This problem is also magnified by an irrational use and poor administration of drugs. Once a patient acquires resistant strain bacteria, then it transfers antibiotic resistance genes to other bacteria [39].
The present study also demonstrated the prevalence of ESBL producing strains which was 13.6% (95% CI 6.5-32.3%, N=6). The prevalence is dynamically rising just due to multiple factors; lack of early treatment of the case, fast transmission ESBL strains to the community and healthcare institutions, and environmental stress. Inappropriate use of carbapenems, increased use of third-generation cephalosporin and quinolones in the community, stool-mediated infections, and the existence of the ESBL gene in the plasmid are other possible factors [40]. Having plasmids and other mobile genetic materials can help ESBL producing bacterial strains to be resistant for other multiple antimicrobial agents. This may let physicians to have narrow treatment options and increase the mortality and morbidity of patients infected with ESBL producing bacteria [41].
In this study, associated factors were also determined. Among assessed factors, the history of previous UTI and male uncircumcision was the independent risk factors for the acquisition of UTI. A recurrent urinary tract infections can be attributed to two common enhancing factors: ascending of identical urethral microbiota, particularly uropathogenic E. coli to the bladder and/or untreated chronic/persistent bladder infection resulted from either ascending or bloodstream infections [42]. This fact is supported by a study done in Denmark, and it depicted that 77% of recurrent UTIs have resulted from infection with identical uropathogenic E. coli strains [43]. Adhesion structures like P and type 1 pili may help E. coli for progression to the bladder [44].
Having facultative intracellular multiplication in uroepithelial cells helps E. coli to escape from being killed by humoral immunity and antimicrobial agents. This multiplication takes place to a certain extent and forms loose colonies and escapes out to the lumen of the bladder. However, some of the bacterial colonies remain intracellularly and can be a reservoir for persistent infection [45]. This study, however, couldn’t assess the molecular characteristics of bacterial isolates.