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Table of Contents
REVIEW ARTICLE
Year : 2020  |  Volume : 17  |  Issue : 1  |  Page : 26-30

Pervasiveness of urinary tract infection in diabetic patients and their causative organisms with antibiotic sensitivity pattern


Division of Microbiology, ICMR-National Institute of Occupational Health, Ahmedabad, Gujarat, India

Date of Submission14-Jan-2020
Date of Decision25-Jan-2020
Date of Acceptance05-Feb-2020
Date of Web Publication17-Mar-2020

Correspondence Address:
Mahesh Chandra Sahu
Division of Toxicology, ICMR-National Institute of Occupational Health, Meghani Nagar, Ahmedabad - 380 016, Gujarat
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/am.am_2_20

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  Abstract 


Diabetes mellitus (DM) being polygenic disorder, affects several other organs. One of the major coinfection in DM is urinary tract infection (UTI). Due to increased blood glucose levels, a favorable environment is offered to bacteria for their growth leading to infection. DM also hampers immunologic functions such as phagocytosis, decrease in antibody production, failure of T cells and B cells to fight against pathogens which ameliorate bacterial growth. Not only bacteria but even several fungi can lead to UTI. Several factors such as duration of diabetes, age, gender, route of drug administration, type of drugs used in diabetes, poor glycemic control, obesity, unhygienic conditions, sexual intercourse, and type of DM are enhancing factors for causing UTI in diabetic patients. Day-to-day use of antibiotics has made several pathogenic bacteria resistant to the effects of antibiotics. In long terms, if UTI remains untreated in diabetic patients, then it may have severe complications. Furthermore, the resistance pattern of antibiotics differs according to the geographical locations. Hence, the use of susceptible antibiotics to cure UTI in diabetic patients is now crucial.

Keywords: Antibiotics, bacteria, diabetes mellitus, fungi, resistant, risk factors, susceptible, urinary tract infection, virulence factors


How to cite this article:
Bhagat ZP, Sahu MC. Pervasiveness of urinary tract infection in diabetic patients and their causative organisms with antibiotic sensitivity pattern. Apollo Med 2020;17:26-30

How to cite this URL:
Bhagat ZP, Sahu MC. Pervasiveness of urinary tract infection in diabetic patients and their causative organisms with antibiotic sensitivity pattern. Apollo Med [serial online] 2020 [cited 2020 Jul 4];17:26-30. Available from: http://www.apollomedicine.org/text.asp?2020/17/1/26/280909




  Introduction Top


Diabetes mellitus (DM) is polygenic disorder which can cause several other health problems worldwide. One of the complications due to DM is urinary tract infection (UTI). Due to DM, there are defects in immune host response which leads to bacterial infection. Increased glucose levels also provide favorable environment for the bacterial growth thus even the normal microbial flora of the body turns into pathogens leading to infection. Thus, diabetic patients become more prone to UTI. Not only bacteria but also several fungi were also responsible for causing UTI in Diabetic patients. Due to increasing use of antibiotics, several UTI causing pathogens are becoming resistant to routinely used antibiotics used as medication. Diabetic females were at the highest risk of UTI. Several other factors causing diabetic UTI were obesity, BMI, duration of diabetes, age, gender, socioeconomic status, unhygienic conditions, and intercourse.

Diabetes mellitus

Kaveeshwar and Cornwall studied in 2000 that India (31.7 million) topped the world with the highest number of people with DM followed by China (20.8 million) and the United States (17.7 million) in second and third place, respectively. According to Wild et al., the prevalence of diabetes is predicted to be double globally from 171 million in 2000 to 366 million in 2030 with a maximum increase in India.[1],[2]

A study by Eisenbarth explained about the IIDM.


  Insulin Independent Diabetes Mellitus Top


There are six stages of DM as given below:

  • Stage I: (Genetic susceptibility) genes of MHC become susceptible to Type I DM. When individuals express both the high-risk HLA alleles DR3 and DR4 have the highest risk of type I DM. Thus, for Type I DM to occur at least 2 genes of HLA region (1 recessive gene and 1 DR3 and DR4 associated) are necessary but not sufficient for diabetes
  • Stage II: (Triggering) due to several infections by virus and use of drugs, there is triggering of the development of autoimmunity. This leads to the abnormality of the T cell which eventually disrupts the normal immunoregulation (e.g. destruction of various tissues that can include islets and thyroid)
  • Stage III: (Active immunity) in many nondiabetic individuals, it was found that there was the presence of islet cell antibodies. This antibody reacts with the surface of islet cell and thus inhibiting insulin secretion
  • Stage IV: (Progressive loss of glucose-stimulated insulin secretion) when glucose was given to individuals intravenously, there was loss of response to intravenous glucose due to the reduction of beta-cell mass
  • Stage V: (Overt diabetes) at this stage, hyperglycemia develops and the destruction of beta cells has occurred. In this stage, islets have cells containing glucagon, somatostatin, and pancreatic polypeptide but no beta cells. Still there remains some residual insulin secretion
  • Stage VI: (Destruction of beta cells) here in this stage there is complete destruction of beta cells. Thus, no secretion of insulin leading to Type I DM.[3]


A study by Sacks and McDonald explained the NIDDM.


  Noninsulin Dependent Diabetes Mellitus Top


In general, glucose homeostasis is maintained by the balance between glucose produced by the liver and uptake of glucose by peripheral tissues. This is mainly achieved by hormones which are secreted by pancreas: Glucagon from α cell and insulin from β cell. Glucose disposal depends on the following: (i) ability of pancreas to secrete insulin, (ii) insulin capacity to suppress hepatic glucose production, and (iii) capability of insulin to enhance uptake of glucose in peripheral tissues (insulin sensitivity). However, DM insulin is enable to act on peripheral tissues (insulin resistance). The other defect seen is the dysfunctional beta cell, due to which pancreas are not able to produce enough of insulin to compensate for the insulin resistance. This fundamental defect is a combination of the both environmental and genetic factors. Environmental factors include diet and exercise. Genetic factors may be bifurcated into two types (i) primary diabetogenes and (ii) diabetes-related genes. Gene expressed in adipose tissue (ob) was cloned and its product, leptin, was considered a significant factor for regulating body weight homeostasis and energy balance. This suggested that insulin can be a mediator of the effects of food intake on ob expression. This provided link between obesity and NIDDM.[4]

Urinary tract infection

Due to different types of defense mechanisms, human urinary tract is well protected against several microbial infections. However, some bacterial strains have distinctive properties which make them capable of invading the human urinary tract. Usually, bacteria can invade urinary tract by repeated copulation, defect in immune system, delay in host immune response, duration of diseases such as diabetes which provides favorable environment for their growth. After invading the urinary tract, the bacterial strains release virulence factors leading to infection. The most common bacterial strain is the  Escherichia More Details coli. It is the predominant organism found in UTI. Virulence factors are adhesins, siderophores, toxins, polysaccharide coatings, other serum resistance mechanisms, invasins, and proteases.

Adhesins

FimH, an adhesion molecule, contributes to the bacterial colonization. In the urinary tract, adherence of FimH molecule to the uroepithelium makes the bacteria resistant to flushing action of urine flow and bladder emptying. In the bladder, Type 1 fimbriae (FimH) bind to uroplakins (mannosylated glycoproteins on the bladder surface epithelium). This binding can be inhibited by urinary Tamm–Horsfall protein. This leads to apoptosis of the epithelial cells.

Siderophores

Extra intestinal pathogenic E. coli (UPEC, ExPEC) has a property of extracting iron from host and also heme uptake. This is needed for bacterial growth.

Toxins

Known toxins of ExPEC are alpha hemolysin, cytotoxic necrotizing factor-I, cytolethal distending toxin, and secreted autotransporter toxins causes abnormality in the host cell functioning or morphology, cell cycle arrest, or frank cellular lysis.

Protectins

ExPEC strains have property of exhibiting a variety of defense mechanism against host antibacterial system. ExPEC has extra coating of richly glycosylated lipopolysaccharide and group 2 or 3 polysaccharide capsule which interfere with the process of phagocytosis and provides protection against complement-mediated opsonization or lysis. It also has outer membrane proteins called TraT and Iss, which enhances serum resistance. Another is OmpT which is virulence-associated protease can cleave immunoglobulins or other host defense proteins.[5]

The prevalence of diabetic urinary tract infection in India and world

As per a study carried out by Saleem and Daniel, 2011, in Bengaluru, India, the prevalence of diabetic UTI was more in patients with lower socioeconomic status than patients with higher socioeconomic status. The prevalence of UTI among diabetic patients with lower socioeconomic status was 56.4% and among nondiabetic individuals, it was 43.6%. The prevalence of UTI among diabetic patients with higher socioeconomic status was 51.6% and among nondiabetic individuals, it was 48.4%.[6]

As per the study carried out by Chiţă et al., 2013, in Romania Emergency Clinical Country Hospital, Timisoara, Romania, among 1470 hospitalized diabetic patients (847W, 623M) with both Type I and Type II diabetes, 12.8% of Type I and 10.5% of Type II diabetic patients had UTI.[7]


  Diabetic Urinary Tract Infection Top


A study was carried out by Forland et al. in 1977 which had determined the prevalence of UTI in diabetic patients and also revealed that UTI causing bacteria were coated with antibody. The presence of antibody-coated bacteria was done by direct immunofluorescence with the use of fluorescein-conjugated horse antiserum to human globulin. In 1-year follow-up study, among 333 patients, 19% of women and 2% men had UTI. Renal parenchymal infection was indicated by the presence of antibody-coated bacteria. Parenchymal infection was observed in 43% patients which increased to 79% within a mean pretreatment of 7 weeks. Patients who had recurrent infection followed by treatment, were having reinfections than relapses including kidney infection (67%) and bladder infection (57%).[8]

A study was carried out by Geerlings et al. which consisted diabetic population of 589 females and the results revealed that 241 women (40.9%) were suffered with Type 1 diabetes. Among them, 34 women (14%) were suffered with UTI. According to him, risk factor of UTI related with these females was sexual intercourse and use of oral contraceptive pills. Rest 348 females (65.19%) among 589 studied populations were revealed with type 2 diabetes. From all type 2 diabetic female patients, 81 (23%) were suffered with UTI. The risk factor associated with these females was the presence of ASB. He concluded that Diabetes was not only the major factor for causing UTI but also said that increased glucose levels in urine due to diabetes serves favorable environment for bacterial growth.[9]

Goswami et al. conducted a study to detect the prevalence of UTI and renal scars in patients with DM. In his study, 155 (76 F, 79 M) diabetic patients and 128 healthy controls were included. The frequency of UTI in diabetic patients was higher as compared to control and diabetic females were more prone to UTI then diabetic males. In addition, the prevalence of renal scars was higher in diabetic patients with UTI as compared to patients without UTI.[10]

As per prospective cohort study conducted by the Second Dutch National Survey of General practice, a total of 390,000 patients were included. Among these 705 patients with DM1, 6712 with DM2, and 18,911 patients with hypertension were present. According to these studies, diabetic patients were more prone to several infections such as respiratory tract infection, UTI, and skin and mucus membrane infection as compared to patients without diabetes. Simultaneously, it was noted that females were more prone to infection as compared to males. Even patients with hypertension were prone to infection.[11]

According to study carried out at Dasman Diabetes Institute, urine samples of 722 diabetic patients were collected. Three hundred and twenty-three (45%) were showing sterile urine samples, while 147 (20%) showed mixed growth of bacteria possibly due to improper collection of the sample. The remaining 252 (35%) samples were positive for uropathogens with colony count higher than 104 CFU/mL of urine. E. coli was predominant organism among 6 positive Extended spectrum beta-lactamases (ESBL) cases according to study. In addition, one ESBL positive case of strain Klebsiella pneumoniae was found. Adult women were more prone to UTI as compared to men.[12]

A study by Hirji et al., in 2012, revealed that patients with Type II diabetes were more prone to UTI. In a 1-year follow-up, 5967 cases of UTI were observed within diabetic patients and 3708 UTI cases in nondiabetic individuals. Overall incidence rate (IR) of UTI among diabetic patients was 46.9/1000 patients/year and among nondiabetic individuals was 29.9/1000 patients/year. Among newly diagnosed diabetic patients the overall IR was 45.5/1000 patients/year and with patients with previous history of diabetes, the IR was 58.8/1000 patients/year. When classified by gender, the IR of UTI in females was 72.8/1000 patients/year and 25.5/1000 patients/year for males. The IR of UTI in nondiabetic females was 45.7/1000 patients/year, and for male, it was 16.5/1000 patients/year. Classification on the basis of route of drug, the IR of UTI in patients treated with oral antidiabetic drugs was 49.7/1000 patients/year and for patients treated with insulin was 66.8/1000 patients/year. IR of UTI was higher in poorly controlled diabetic patients than patients with controlled diabetes. Thus, this study concluded that IR of UTI in diabetic patients differ with respect to route of drug, gender, glycemic control, and newly diagnosed patients.[13]

Cross-sectional study was carried out to detect the presence of organisms causing UTI in Diabetic patients. Furthermore, the antibiotic sensitivity was noted. Among 100 patients, 57 were female and 43 were male. In total, 21% of them had culture positive UTI. UTI was more common in females than in males. It was noted that postmenopausal females were prone to UTI and even patients taking insulin. There was difference in infection pattern according to sex, age, weight, newly diagnosed diabetic patients, and patients having diabetes more than 5 years. It was noted that E. coli was common organism found in UTI followed by Klebsiella, proteus, and Pseudomonas.[14]


  Organisms of Diabetic Urinary Tract Infection Top


As per se veral studies carried out in India, E. coli was found to be predominant organism causing UTI in diabetic patients.[15],[16],[17],[18],[19],[20],[21] Apart, from E. coli other species such as coagulase negative Staphylococcus and ESBL positive E. coli were also found to be predominant organism.[22],[23] In one of the studies carried out by Sabharwal, 2010, fungi such as Trichosporon asahii was found to be dominant in diabetic UTI patients.[24]

Worldwide studies had also revealed that E. coli is the predominant organism found in Diabetic UTI.[25],[26],[27],[28] Apart from E. coli, other organisms such as Streptococcus, S. aureus and coagulase negative S. aureus were also predominant organisms.[26],[29],[30]Candida spp. were also found to be predominant organisms of diabetic UTI.[31]


  Risk Factors Associated With Diabetic Urinary Tract Infection Top


High levels of C-reactive protein, microalbumiuria, and glycosylated hemoglobin level more than 7% increases the risk of UTI in diabetic patients.[32] Poor glycemic control and defects in polymorphonuclear leukocyte activity increases the risk of UTI.[33] One of the major risks of diabetic UTI is the duration of diabetes.[34] The use of sodium glucose cotransporter 2 inhibitors increases slightly the risk of UTI in diabetes.[35] A study by Al-Rubeaan et al., in 2103, revealed that even hypertension and insulin therapy were the risk factors.[36] Wang et al., in 2103, documented that the presence of more virulent E. coli isolates leads to urosepsis in diabetic patients.[37] Hirji et al., in 2012, stated that people with Type 2 diabetes were more prone to infection.[13]


  Antibiotic Sensitivity Pattern Top


A total of 288 diabetics (196 females and 92 males) and 63 nondiabetic individuals with symptomatic UTI were included in a study. Among that, 43.8% diabetic patients and 42.9% nondiabetic individuals have a positive growth from urine. E. coli isolated from diabetic patient was significantly (P< 0.05) less sensitive to ceftriaxone, ceftazidime, cefuroxime, netilmicin, gentamicin, ciprofloxacin, and nitrofurantoin than that of nondiabetic individuals.[38]

A study was carried out by Sibi et al., 2011 which focused on the frequency of uropathogens and their antibiotic susceptibility in different gender of diabetic patients. It was noted that among all the antibiotics tested, trimethoprim was found to be effective for treatment followed by nalidixic acid, chloramphenicol, and kanamycin. The most frequently prescribed antibiotic oxytetracycline was resistant to most of the isolates and indicates that increased consumption of a particular antibiotic increases resistance of uropathogens.[39]

A study by Yismaw et al. had shown that increased resistance of E. coli to amoxicillin-clavulanic acid is the result of hyper production of TEM-BETA lactamase, production of penicillinase resistant to inhibitors, and production of cephalosporinase. Klebsiella species showed high level of resistance to most of antimicrobials except ciprofloxacin. It is known fact that Klebsiella species is inherently resistant to ampicillin, cephalosporin, and aminoglycosides due to increasing acquisition of R-plasmids and also producing SHV, chromosomally mediated penicillinase which can hydrolyze ampicillin and first-generation cephalosporin. S. aureus was resistant to penicillin (100%) because it produces penicillinase and alternative penicillin binding proteins-2A which helps organisms to become resistant to most beta-lactam antibiotics.[40]

Gutema et al. carried out study in Metu Karl Heinz Referral Hospital Southwest Ethiopia from January 2018 to March 2018. E. coli was highly sensitive to ceftriaxone (80%), ciprofloxacin (70%) and gentamycin (70%), whereas resistance to tetracycline (75%). Sensitivity of Proteus Spp. to amoxicillin-clavulanic acid (100%) and ceftriaxone (100%) whereas resistance to ciprofloxacin (66.7%), tetracycline (66.7%), gentamycin (66.7%), and norfloxacin (66.7%). Pseudomonas aeruginosa were 100% resistant to amoxicillin-clavulanic acid, ciprofloxacin, tetracycline, nitrofurantoin, and norfloxacin. Gram-positive bacteria such as S. aureus was sensitive to amoxicillin-clavulanic acid (85.7%) and gentamycin (57.1%) and resistance to tetracycline (85.7%), nitrofurantoin (85.7%), and ampicillin (71.4%).[41]

As documented by Tandogdu and Wagenlehner, 2016, E. coli was susceptible to fosfomycin, nitrofurantoin, and mecillinam. They also stated that antibiotic resistance pattern varies according to the geographical locations.[42]


  Conclusion Top


With this review, we have concluded that UTI is a major coinfection in diabetic patients. All the studies carried out worldwide and India found E. coli to be predominant organism causing UTI in diabetic patients. In addition, apart from E. coli several other studies showed Staphylococcus Spp. to be predominant organism. Factors such as age, gender, duration of diabetes, type of diabetes, route of drug administration, drugs used in diabetes, defects in immune system, and poor glycemic control proved to risk factors for causing UTI in diabetic patients. Most of the pathogenic UTI causing organisms found to be susceptible to broad range of antibiotics.

Acknowledgments

Authors are grateful to Dr. K. Sarkar, Director, ICMR-National Institute of Occupational Health, Ahmedabad, Gujarat, India, for encouraging and exceeding facilities in research.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
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Abstract
Introduction
Insulin Independ...
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Diabetic Urinary...
Organisms of Dia...
Risk Factors Ass...
Antibiotic Sensi...
Conclusion
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