Urinary tract infections (UTIs) represent one of the most common bacterial infections worldwide, accounting for significant morbidity and healthcare burden in both community and hospital settings [1]. Diabetic individuals are at a particularly increased risk of developing UTIs due to a combination of factors including immune dysfunction, impaired neutrophil function, poor glycemic control, autonomic neuropathy, and glucosuria, which collectively create an ideal environment for microbial growth and colonization in the urinary tract [2–4]. The incidence of UTIs among patients with diabetes mellitus is estimated to be 2–4 times higher than in the non-diabetic population [5]. Moreover, these infections tend to be more severe, recurrent, and complicated, leading to a greater risk of progression to upper urinary tract infections, emphysematous pyelonephritis, renal abscesses, and even urosepsis [6]. Women with diabetes are especially vulnerable due to anatomical predisposition and hormonal factors, with postmenopausal changes further exacerbating the risk [7]. Pathophysiologically, hyperglycemia impairs several host defense mechanisms, including chemotaxis, phagocytosis, and intracellular killing by neutrophils. Additionally, diabetic cystopathy—characterized by incomplete bladder emptying—promotes urinary stasis, thereby facilitating bacterial proliferation [8]. Glycosuria serves as a nutrient source for uropathogens such as Escherichia coli, Klebsiella spp., and Enterococcus spp., which are frequently implicated in diabetic UTIs [9]. Antimicrobial resistance among uropathogens, particularly in diabetic patients, has become a growing concern. Overuse and misuse of antibiotics, coupled with repeated empirical treatments, contribute to the emergence of multidrug-resistant (MDR) organisms [10]. Studies have shown increasing resistance of E. coli and Klebsiella spp. to commonly prescribed antibiotics like fluoroquinolones, beta-lactams, and sulfonamides, thereby complicating the management of UTIs in this vulnerable group [11–13]. Furthermore, infections caused by extended-spectrum beta-lactamase (ESBL)-producing organisms are notably more common in diabetic patients [14]. While empirical treatment remains common in resource-limited settings, the high prevalence of antimicrobial resistance emphasizes the necessity for local epidemiological data to guide effective therapy. Periodic surveillance of the etiological spectrum and antimicrobial sensitivity profiles of uropathogens in diabetic individuals is vital for informed decision-making and rational antibiotic use [15].

The present study was undertaken to assess the etiology and antibiotic sensitivity patterns of uropathogens isolated from diabetic patients diagnosed with UTIs in selected hospitals over a one-year period. By understanding local trends, this research aims to contribute to better management strategies and antibiotic stewardship in diabetic care.

This was a prospective, cross-sectional, hospital-based observational study conducted over a period of one year, from June 2024 to May 2025. The study population included adult patients (aged 18 years and above) with a confirmed diagnosis of diabetes mellitus who presented with clinical symptoms suggestive of urinary tract infection, such as dysuria, increased frequency or urgency of urination, suprapubic discomfort, hematuria, or fever. Patients who had received antibiotics within the preceding 72 hours, those with indwelling urinary catheters, or those who declined to provide informed consent were excluded from the study.

Midstream clean-catch urine samples were collected from all enrolled participants using sterile, wide-mouthed, leak-proof containers following standard aseptic precautions. The samples were transported to the microbiology laboratory within two hours of collection and were subjected to routine macroscopic and microscopic examination followed by culture and sensitivity testing. Urine cultures were performed using cysteine lactose electrolyte-deficient (CLED) agar and blood agar. The samples were inoculated using a calibrated 0.001 mL loop and incubated aerobically at 37°C for 24–48 hours. A colony count of ≥10⁵ colony-forming units (CFU)/mL was considered significant bacteriuria.

Identification of bacterial isolates was carried out using conventional biochemical tests, Gram staining, and when necessary, automated identification systems. Antimicrobial susceptibility testing was performed using the Kirby-Bauer disk diffusion method on Mueller-Hinton agar, and results were interpreted according to the guidelines of the Clinical and Laboratory Standards Institute (CLSI), 2023 edition. The panel of antibiotics tested included ampicillin, amoxicillin-clavulanate, ciprofloxacin, norfloxacin, nitrofurantoin, ceftriaxone, gentamicin, amikacin, piperacillin-tazobactam, imipenem, vancomycin, and linezolid, depending on the isolate's Gram stain reaction.

All data were compiled and analyzed using Microsoft Excel and SPSS software version 25. Descriptive statistics were used to summarize demographic characteristics, isolate frequency, and antibiotic sensitivity patterns. Ethical clearance for the study was obtained from the institutional ethics committee, and informed consent was taken from all study participants prior to sample collection.

A total of 320 diabetic patients with clinical suspicion of urinary tract infection were included in the study over a one-year period. Among them, 196 (61.3%) showed significant growth on urine culture and were considered culture-positive for UTI.

Demographic Profile
Of the 196 culture-positive cases, 118 (60.2%) were females and 78 (39.8%) were males, with a female-to-male ratio of 1.5:1. The age distribution revealed that the majority of patients (52.6%) were in the 51–70 years age group, followed by 71–80 years (24.5%), 31–50 years (18.4%), and ≤30 years (4.5%).

Table 1: Age and Sex Distribution of Culture-Positive Patients

Bacteriological Profile
The most commonly isolated uropathogen was Escherichia coli, accounting for 95 (48.5%) cases, followed by Klebsiella pneumoniae (20.9%), Enterococcus spp. (13.8%), Pseudomonas aeruginosa (9.1%), and Proteus mirabilis (4.6%). Less frequent isolates included Staphylococcus saprophyticus and Citrobacter spp.

Table 2: Distribution of Bacterial Isolates in Culture-Positive Diabetic Patients

Antibiotic Sensitivity Pattern.
Antibiotic susceptibility testing showed that Gram-negative organisms (E. coli, Klebsiella, Pseudomonas, Proteus) were highly sensitive to imipenem (89.2%), amikacin (82.1%), and nitrofurantoin (74.3%). A high resistance rate was observed for ciprofloxacin (64.8%) and ampicillin (71.6%).

Among the Gram-positive isolates (Enterococcus spp., Staphylococcus spp.), maximum sensitivity was noted to linezolid (100%) and vancomycin (96.3%).

Table 3: Antibiotic Sensitivity Pattern of Gram-Negative Uropathogens

        (Note: — Indicates intrinsic resistance or not tested for that species.)

Table 4: Antibiotic Sensitivity Pattern of Gram-Positive Uropathogens (n = 31)

These findings indicate that Gram-negative bacteria, particularly E. coli, remain the leading cause of UTIs in diabetic patients, and are increasingly resistant to commonly used oral antibiotics. Nitrofurantoin and amikacin showed favorable sensitivity patterns, whereas carbapenems remained the most effective for multidrug-resistant isolates. Among Gram-positive organisms, linezolid and vancomycin were the most effective options.

Urinary tract infections (UTIs) are a frequent complication in individuals with diabetes mellitus, a finding reaffirmed by our study, where 61.3% of diabetic patients with UTI symptoms were culture-positive. This aligns with previous reports indicating that diabetic patients are predisposed to UTIs due to multiple factors such as impaired immune responses, glycosuria, and autonomic neuropathy leading to bladder dysfunction and urinary stasis [1,2].

Our results demonstrated a marked female predominance (60.2%) among culture-positive cases, consistent with the well-established fact that anatomical and hormonal factors make females more susceptible to UTIs [3]. The peak incidence was observed in the 51–70-year age group, which coincides with the age when diabetes-related complications and immune dysfunction are typically more pronounced. These findings are in agreement with studies conducted by Geerlings et al. and Boyko et al., who reported increased UTI prevalence in older diabetic women [4,5].

The most commonly isolated pathogen in our study was Escherichia coli (48.5%), followed by Klebsiella pneumoniae (20.9%), Enterococcus spp. (13.8%), and Pseudomonas aeruginosa (9.1%). This pattern mirrors global data, where E. coli remains the predominant uropathogen in both diabetic and non-diabetic populations [6,7]. However, the relatively high proportion of non-E. coli Gram-negative pathogens such as Klebsiella and Pseudomonas, and Gram-positive Enterococcus, suggests a more complex and diverse microbiological spectrum in diabetic patients, likely influenced by prior antibiotic exposure, hospitalization, or subclinical urinary retention [8].

Antibiotic resistance was a significant concern in our findings. High resistance rates were observed against commonly used oral antibiotics such as ciprofloxacin (64.8%) and ampicillin (71.6%), similar to the resistance patterns reported by Bonadio et al. and Sahin et al. in diabetic cohorts [9,10]. These results raise serious concerns regarding the empirical use of fluoroquinolones and penicillins for UTI management in diabetic patients, particularly in regions with high resistance burden.

In contrast, nitrofurantoin showed a promising sensitivity rate (74.3%) among Gram-negative isolates, particularly E. coli, indicating its continued relevance as a first-line oral agent for uncomplicated lower UTIs in diabetics. Similar observations have been reported by Gupta et al. and Mazzulli, who emphasized the retained efficacy of nitrofurantoin in uncomplicated cases despite rising multidrug resistance [11,12]. However, nitrofurantoin is not effective for upper tract or complicated infections and is contraindicated in patients with renal insufficiency—frequently encountered in diabetics—highlighting the need for judicious selection of patients.

Imipenem and amikacin were the most effective agents against multidrug-resistant (MDR) strains, with overall sensitivities of 89.2% and 82.1%, respectively. Carbapenems remain the cornerstone of therapy for severe or resistant UTIs, but their use should be restricted to proven cases to preserve their efficacy and reduce the selection pressure for carbapenem-resistant Enterobacteriaceae (CRE), a rapidly emerging global threat [13]. The relatively high susceptibility to piperacillin-tazobactam (73.6%) makes it a suitable alternative for parenteral therapy in hospitalized patients with moderate-severity infections.

Among Gram-positive isolates, Enterococcus spp. showed excellent susceptibility to linezolid (100%) and vancomycin (96.3%), corroborating findings from earlier studies by Nicolle and Rowe et al., which emphasized the increasing incidence of resistant Gram-positive cocci in diabetic UTIs, particularly in recurrent or hospital-acquired settings [14,15].

The high prevalence of multidrug-resistant organisms (MDROs) in our study further underscores the importance of culture-based antibiotic selection. Overreliance on empirical therapy not only risks treatment failure but also accelerates the emergence of resistance. Routine urine culture and antimicrobial sensitivity testing, especially in diabetic individuals with recurrent or complicated infections, should be standard practice, as recommended by international guidelines [16].

An important implication of our study is the need for regular regional antibiogram development to inform empiric therapy. Moreover, patient education on hygiene, glycemic control, adequate hydration, and early reporting of urinary symptoms is crucial to prevent recurrent infections and reduce antibiotic misuse. Clinicians should also be vigilant about screening for asymptomatic bacteriuria in specific populations, such as pregnant diabetic women, as per IDSA guidelines [17].

Our study was limited to a hospital-based population, which may not reflect the microbial trends in the general diabetic community. Molecular characterization of resistance mechanisms (ESBL or Carbapenemase genes) was not performed, which could have provided deeper insights into the resistance epidemiology. A follow-up to assess clinical outcomes of culture-directed versus empirical therapy was also beyond the scope of this study but is recommended for future research.

In conclusion, diabetic patients exhibit a high prevalence of UTIs, with E. coli being the most common causative organism, followed by other Gram-negative and Gram-positive bacteria. Rising antibiotic resistance, particularly against fluoroquinolones and penicillins, highlights the need for culture-guided therapy and local surveillance. Nitrofurantoin and amikacin remain useful options for empirical treatment, while carbapenems should be reserved for MDR infections. Tailored antibiotic policies, effective glycemic control, and rational prescribing practices are critical in managing UTIs in diabetic patients and preventing the development of antimicrobial resistance.

1. Geerlings SE. Urinary tract infections in patients with diabetes mellitus: epidemiology, pathogenesis and treatment. Int J Antimicrob Agents. 2008;31(Suppl 1):S54–S57.
2. Shah BR, Hux JE. Quantifying the risk of infectious diseases for people with diabetes. Diabetes Care. 2003;26(2):510–513.
3. Foxman B. Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. Am J Med. 2002;113 Suppl 1A:5S–13S.
4. Geerlings SE et al. Asymptomatic bacteriuria may be considered a risk factor for symptomatic UTIs in diabetic women. Diabetes Care. 2000;23(6):744–749.
5. Boyko EJ, et al. Risk of urinary tract infection among diabetic and non-diabetic women. Am J Epidemiol. 2005;161(6):557–564.
6. Nicolle LE. Urinary tract infection in diabetes. Curr Opin Infect Dis. 2005;18(1):49–53.
7. Flores-Mireles AL et al. Urinary tract infections: mechanisms of infection and treatment options. Nat Rev Microbiol. 2015;13(5):269–284.
8. Harding GK, Zhanel GG, Nicolle LE, Cheang M. Antimicrobial treatment in diabetic women with asymptomatic bacteriuria. N Engl J Med. 2002;347(20):1576–1583.
9. Bonadio M et al. Uropathogens and antimicrobial resistance in diabetic patients. BMC Infect Dis. 2006;6:54.
10. Sahin K et al. Antimicrobial resistance in diabetic and non-diabetic patients with community-acquired UTIs. J Infect Dev Ctries. 2019;13(4):308–314.
11. Gupta K et al. International clinical practice guidelines for the treatment of acute uncomplicated cystitis and pyelonephritis in women. Clin Infect Dis. 2011;52(5):e103–e120.
12. Mazzulli T. Resistance trends in urinary tract pathogens. J Urol. 2002;168(4 Pt 2):1720–1722.
13. Paterson DL. Resistance in Gram-negative bacteria: Enterobacteriaceae. Am J Med. 2006;119(6 Suppl 1):S20–S28.
14. Nicolle LE. Managing complicated UTIs in diabetic patients. Drugs Aging. 2005;22(8):627–639.
15. Rowe TA, Juthani-Mehta M. Urinary tract infection in older adults. Aging Health. 2013;9(5):519–528.
16. Antibiotic resistance threats in the United States. Atlanta: U.S. Department of Health and Human Services; 2019.
17. Nicolle LE, Bradley S, Colgan R, et al. IDSA guidelines for the diagnosis and treatment of asymptomatic bacteriuria. Clin Infect Dis. 2005;40(5):643–654.