Guidelines on

Urological Infections
M. Grabe (chairman), T.E. Bjerklund-Johansen, H. Botto, B. Wullt, M. Çek, K.G. Naber, R.S. Pickard, P. Tenke, F. Wagenlehner

© European Association of Urology 2011

TABLE OF CONTENTS
1. INTRODUCTION 1.1 Aim of the guidelines 1.2 Pathogenesis of UTIs 1.3 Microbiological and other laboratory findings 1.4 Methods 1.5 Level of evidence and grade of guideline recommendations 1.6 References CLASSIFICATION OF UTIs 2.1 Introduction 2.2 Level of infection 2.3 Grade of severity 2.4 Pathogens 2.5 Classification of UTI 2.6 Reference

pAgE
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UNCOMPLICATED UTIs IN ADULTS 3.1 Summary and recommendations 3.2 Definition 3.2.1 Aetiological spectrum 3.3 Acute uncomplicated cystitis in premenopausal, non-pregnant women 3.3.1 Diagnosis 3.3.1.1 Clinical diagnosis 3.3.1.2 Laboratory diagnosis 3.3.2 Therapy 3.3.3 Follow-up 3.4 Acute uncomplicated pyelonephritis in premenopausal, non-pregnant women 3.4.1 Diagnosis 3.4.1.1 Clinical diagnosis 3.4.1.2 Laboratory diagnosis 3.4.1.3 Imaging diagnosis 3.4.2 Therapy 3.4.2.1 Mild and moderate cases of acute uncomplicated pyelonephritis 3.4.2.2 Severe cases of acute uncomplicated pyelonephritis (Table 3.2) 3.4.3 Follow-up 3.5 Recurrent (uncomplicated) UTIs in women 3.5.1 Diagnosis 3.5.2 Prevention 3.5.2.1. Antimicrobial prophylaxis 3.5.2.2 Immunoactive prophylaxis 3.5.2.3 Prophylaxis with probiotics 3.5.2.4 Prophylaxis with cranberry 3.6 UTIs in pregnancy 3.6.1 Definition of significant bacteriuria 3.6.2 Screening 3.6.3 Treatment of asymptomatic bacteriuria 3.6.4 Duration of therapy 3.6.5 Follow-up 3.6.6 Prophylaxis 3.6.7 Treatment of pyelonephritis 3.6.8 Complicated UTI 3.7 UTIs in postmenopausal women 3.7.1 Risk factors 3.7.2 Diagnosis 3.7.3 Treatment 3.8 Acute uncomplicated UTIs in young men 3.8.1 Men with acute uncomplicated UTI 3.8.2 Men with UTI and concomitant prostate infection

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Asymptomatic bacteriuria 3.9.1 Diagnosis 3.9.2 Screening References

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COMPLICATED UTIs DUE TO UROLOGICAL DISORDERS 4.1 Summary and recommendations 4.2 Definitions and classification 4.2.1 Clinical presentation 4.2.2 Urine cultures 4.3 Microbiology 4.3.1 Spectrum and antibiotic resistance 4.3.2 Complicated UTIs associated with urinary stones 4.3.3 Complicated UTIs associated with urinary catheters 4.4 Treatment 4.4.1 General principles 4.4.2 Choice of antibiotics 4.4.3 Duration of antibiotic therapy 4.4.4 Complicated UTIs associated with urinary stones 4.4.5 Complicated UTIs associated with indwelling catheters 4.4.6 Complicated UTIs in patients with spinal cord injury 4.4.7 Follow-up after treatment 4.5 References SEPSIS SYNDROME IN UROLOGY (UROSEPSIS) 5.1 Summary and recommendations 5.2 Background 5.3 Definition and clinical manifestation of sepsis in urology 5.4 Physiology and biochemical markers 5.4.1 Cytokines as markers of the septic response 5.4.2 Procalcitonin is a potential marker of sepsis 5.5 Prevention 5.5.1 Preventive measures of proven or probable efficacy 5.5.2 Appropriate perioperative antimicrobial prophylaxis 5.5.3 Preventive measures of debatable efficacy 5.5.4 Ineffective or counterproductive measures 5.6 Algorithm for the management of urosepsis 5.7 Treatment 5.7.1 Clinical algorithm for management of urosepsis 5.7.2 Relief of obstruction 5.7.3 Antimicrobial therapy 5.7.4 Adjunctive measures 5.8 Conclusion 5.9 Acknowledgements 5.10 References CATHETER-ASSOCIATED UTIs 6.1 Abstract 6.2 Summary of recommendations 6.3 Reference UTIs IN CHILDREN 7.1 Summary and recommendations 7.2 Background 7.3 Aetiology 7.4 Pathogenesis and risk factors 7.5 Signs and symptoms 7.6 Classification 7.6.1 Severe UTI 7.6.2 Simple UTI

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3 Other biochemical markers 7.4 Urinary N-acetyl-ß-glucosaminidase 7.2.3 Imaging of the urinary tract 7.2 Bladder catheterisation 7.3.1.1 Treatment of UTI in renal transplant recipients 52 52 52 52 52 53 53 53 53 53 53 53 53 54 54 54 55 55 56 56 56 56 56 57 57 57 57 58 4 UPDATE MARCH 2011 .7.1.3.5 Urodynamic evaluation Schedule of investigation Treatment 7.3 Plastic bag attached to the genitalia 7.5.1 Adult dominant polycystic kidney disease (ADPKD) 8.6 Antibiotic therapy in renal failure and transplant recipients 8.7.4 Additional imaging 7.3 Cystourethrography 7.3 Prophylaxis Acknowledgement References 43 43 43 43 43 43 43 43 44 44 44 44 44 44 45 45 45 45 45 45 45 45 46 46 46 46 47 47 47 48 UTIs IN RENAL INSUFFICIENCY.7.7.3.2.2 Chronic renal disease and UTI 8.3.1.1 Diabetes mellitus 8.7.1 Collection of the urine 7.1 VUR and intrarenal reflux 8.3.8 7.5 UTI in renal transplantation 8.2 Simple UTIs 7.3. Diagnosis 7.2 Tuberculosis 8.3 UTI in renal transplantation and immunosuppression 8.1.2 Radionuclide studies 7.3.2.3.3.1.3.1 Conventional voiding cystourethrography 7.2 Graft failure 8.7.3.4.3 Obstruction of the urinary tract and UTI 8.7.7 7.2 Background 8.1 Donor organ infection 8.2.1.5.1 Ultrasonography 7.6.2.1 Physical examination 7.1 Summary and recommendations 8.7.3.3 C-reactive protein 7.6.7.7.2.1 Acute effects of UTI on the kidney 8.2.3.3.5.10 7. TRANSPLANT RECIPIENTS.4 Chronic renal disease and UTI 8.2 Laboratory tests 7.3 Acute effects of UTI on the kidney 8.7.3.7.6 Specific conditions in which an acute UTI causes renal damage 8.9 7.2.1.3.1 Suprapubic bladder aspiration 7.7.9.3 Renal effects of severe UTI 8.7.9.3.2.2 Quantification of bacteriuria 7.1.2 Obstructive neuropathy 8.2.2.4 Acute effects of UTI on the normal kidney 8.1.7.3.7.1 APCKD 8.3 Cystosonography 7.3.1.2.4 Antibiotic treatment for UTI in renal insufficiency and after renal transplantation 8.7.5 Renal scarring 8.2 Leukocyte esterase 7.7.1 Severe UTIs 7.2.2 Calculi and UTI 8.3.7.3.3.1 Nitrite 7.9.4.3 Kidney and whole-organ pancreas transplantation 8.7.2 Radionuclide cystography (indirect) 7.7.7.7.6.2.5 IL-6 7.2 Renal calculi 8.11 8.3.3. DIABETES MELLITUS AND IMMUNOSUPPRESSION 8.

3.3.7 Treatment 11.3.3.7 Follow-up and prevention 9.2 Clinical findings 10.7.2 Definition and classification 11.6 Diagnosis 11.2 Introduction and definition 10. UPDATE MARCH 2011 5 .1.3 Other oral medication 10.3.7 8.2 Fungal infections 8.3.8 References PROSTATITIS AND CHRONIC PELVIC PAIN SYNDROME 10. URETHRITIS 9.7.1.3 Urine cultures and expressed prostatic secretion 10.1 Further reading 59 59 59 59 59 59 63 63 63 63 63 63 63 63 63 64 64 64 65 65 65 66 66 66 66 66 67 67 68 68 68 69 69 69 70 70 70 71 71 73 73 74 74 74 74 74 75 75 75 76 76 76 76 76 76 9.3 Schistosomiasis Immunosuppression 8.3 Incidence and prevalence 11.1 Epidemiology 9.3 Diagnosis 10. Treatment of non-gonorrhoeal urethritis 9.5 Surgery 10.3.1 Differential diagnosis 11.4 Treatment 10.4.2 Viral and fungal infections References 8.6.6.5 References EPIDIDYMITIS AND ORCHITIS 11.1 History and symptoms 10. 12.8 Additional investigations 10.1 Summary and recommendations 11.2 Antibiotics and β-blockers in combination therapy 10.1 Symptom questionnaires 10. 11.1 References FOURNIER’S GANGRENE 13.1 HIV infection 8.2.4.2 Background 13.6 Therapy 9.4.2 Pathogens 9.5 Pathogenesis and pathology 11.4. 13.4.8.3.7 Diagnostic evaluation 10.8 References SEXUALLY TRANSMITTED INFECTIONS 12.1 Summary of recommendations 13.4.8.1 Antibiotics 10.8 8.1 Summary and recommendations 10.4 Perineal biopsy 10.4 Intraprostatic injection of antibiotics 10.6.6. Treatment of gonorrhoeal urethritis 9.6 Other treatment forms 10.6.5 Diagnosis 9.3 Route of infection and pathogenesis 9.5 Other tests 10.4 Morbidity 11.3 Clinical presentation 10.4 Clinical course 9.3.6 Classification systems 10.

5 14.1 Penicillins 16.1 Urogenital tuberculosis 14.7. 6 UPDATE MARCH 2011 .4 Choice of antibiotics 15.6 Meares & Stamey localisation technique 16.5.5 Recommendations for perioperative antibiotic prophylaxis in urology 15.2 Introduction 15.1 References 16.3 Group 3 oral cephalosporins 16.6.7 Postoperative drainage of the urinary tract 15.2 Group 2 cephalosporins 16.2.6.3 Laparoscopic surgery 15.7.4 13.1.13.6 Prophylactic regimens in defined procedures 15.2 Endourological treatment procedures (urinary tract entered) 15.8 Implantation of prosthetic devices 15.2.3.7.3 Group 3a cephalosporins 16.6.1 Summary and recommendations 15.2 Recommendations for antimicrobial therapy in urology 16.3.1 Timing 15.1 Reference PERIOPERATIVE ANTIBACTERIAL PROPHYLAXIS IN UROLOGY 15. as modified according to IDSA/European Society of Clinical Microbiology and Infectious Diseases guidelines 16.4 Recommendations for perioperative antibiotic prophylaxis in urology 16.2.7.4 Monobactams 15.5 CPSI 16.2.5 Group 4 cephalosporins 16.1.1 Criteria for the diagnosis of UTI.6.7.7 Antibacterial agents 16.7.4 Group 3b cephalosporins 16.5.7.1.1 Aminopenicillins 16.6 Open urological operations with bowel segment (clean-contaminated or contaminated procedures) 15.6.3.1 Diagnostic procedures 15.7.5.2 Route of administration 15.7.3 Isoxazolylpenicillins 16.5 Principles of antibiotic prophylaxis 15.7.6.1 Group 1 oral cephalosporins 16.7.3 Oral cephalosporins 16.2.4 Open or laparoscopic urological operations without opening of the urinary tract (clean procedures) 15. 16.6 Group 5 cephalosporins 16.5 Open or laparoscopic urological operations with open urinary tract (cleancontaminated procedures) 15.7.4 Risk factors 15.2.7.2 Acylaminopenicillins 16.7 References APPENDICES 16.1 Group 1 cephalosporins 16.2.7.2 Urogenital schistosomiasis 14.6.3 Duration of the regimen 15.2 Group 2 oral cephalosporins 16.7.6.1 Reference 14.7.5.1.3 Goals of perioperative antibacterial prophylaxis 15.3 Recommendations for antimicrobial prescription in renal failure 16.1.2 Parenteral cephalosporins 16. Microbiology Management 76 77 78 78 78 78 78 78 78 80 80 81 82 82 82 82 82 82 84 84 84 85 85 85 85 85 85 88 94 94 94 95 96 99 101 102 102 103 103 104 104 104 104 104 104 104 104 104 105 105 106 106 106 SPECIFIC INFECTIONS 14.

8 Fosfomycin 16.15 References Relevant bacteria for urological infections 106 106 107 107 107 107 107 108 108 108 108 108 108 108 110 111 ABBREVIATIONS USED IN THE TEXT UPDATE MARCH 2011 7 .7.13 Glycopeptides 16. Carbapenems Fluoroquinolones 16.3 Group 3 fluoroquinolones 16.7.7.8 17.2 Group 2 fluoroquinolones 16.6.9 Nitrofurantoin 16.6.7.7.16.5 16.7.7.7.7 Co-trimoxazole 16.7.7.10 Macrolides 16.7.14 Oxazolidinones 16.6.12 Aminoglycosides 16.11 Tetracyclines 16.7.7.6 16.1 Group 1 fluoroquinolones 16.7.

They also account for at least 40% of all hospital-acquired infections and are. The concept of bacterial virulence or pathogenicity in the urinary tract infers that not all bacterial species are equally capable of inducing infection. especially organisms of enteric origin (e. introitus vaginae or periurethral area up the urethra into the bladder. or less frequently. coli and other Enterobacteriaceae).1. with a substantial financial burden on society. such data are urgently needed. UTIs are responsible for over 7 million physician visits annually. in the majority of cases. This provides a logical explanation for the greater frequency of UTIs in women than in men.6 billion (1). the USA. or following antibiotic therapy. In addition. The guidelines cover male and female UTIs. Furthermore. nor are there good data regarding the impact of UTIs on economics in general and that of the health care system in particular.2 pathogenesis of UTIs Microorganisms can reach the urinary tract by haematogenous or lymphatic spread. immunosuppression. which cause primary infections elsewhere in the body. This is supported by the well-documented in vitro observation that bacteria isolated from patients with a complicated UTI frequently fail to express virulence factors. or bladder catheterisation). A single insertion of a catheter into the urinary bladder in ambulatory patients results in urinary infection in 1-2% of cases. including more than 2 million visits for cystitis (1). Bacteriuria develops in up to 25% of patients who require a urinary catheter for > 7 days. Much attention is given to antibiotic prophylaxis. but is also an infrequent cause of an ascending infection if an indwelling catheter is present. The virulence concept also suggests that certain bacterial strains within a species are uniquely equipped with specialised virulence factors. and for the increased risk of infection following bladder catheterisation or instrumentation. but ultimately does not prevent it. It has been estimated that an episode of healthcare-associated (nosocomial) bacteriuria adds significantly to the direct cost of acute-care hospitalisation (6). there are no good data regarding the prevalence of various types of UTIs and their impact on the quality of life of the affected population. The use of a closed-drainage system. with the aim of reducing the misuse of antibiotics in conjunction with surgery. E. Candida sp. UTIs account for more than 100. such as Staphylococcus aureus. The more compromised the natural defence mechanisms (e. the pathogens are fully exposed to the nosocomial environment.g. and Mycobacterium tuberculosis. including selective pressure by antibiotic or antiseptic substances. Candida albicans readily causes a clinical UTI via the haematogenous route. the fewer the virulence requirements of any bacterial strain to induce infection. It is the ambition of the present guidelines to provide both the urologist and the physician from other medical specialties with advices in their daily practice. obstruction. It is thought that bacteria migrate within the mucopurulent space between the urethra and catheter.000 hospital admissions annually. e.. in Europe. it has become imperative to limit the use of antibiotics. with a daily risk of 5% (5). and that this leads to the development of bacteriuria in almost all patients within about 4 weeks. Nosocomial UTIs therefore comprise perhaps the largest institutional reservoir of nosocomial antibioticresistant pathogens (5). Indwelling catheters with open-drainage systems result in bacteriuria in almost 100% of cases within 3-4 days. renal insufficiency and kidney transplant recipients. 1. the direct and indirect costs associated with community-acquired UTIs in the USA alone exceed an estimated US $1. 8 UPDATE MARCH 2011 . Approximately 15% of all community-prescribed antibiotics in the USA are dispensed for UTI. In the USA. which facilitate the ascent of bacteria from the faecal flora. including a valve to prevent retrograde flow. Haematogenous infection of the urinary tract is restricted to a few relatively uncommon microbes. male genital infections. INTRODUCTION Urinary tract infections (UTIs) are among the most prevalent infectious diseases. and special fields such as UTIs in paediatric urology. Data obtained from other countries and societies.1 Aim of the guidelines Due to the increasing threat of resistant pathogens worldwide. and consequently. delays the onset of infection. allow the organisms to reach the kidneys to induce systemic inflammation. High quality clinical research is strongly encouraged.g. can only be applied with caution to the European situation. at an estimated annual cost of over US $1 billion (2). catheterassociated (2-4).g. e. different types of pili. Salmonella sp.g. but there is abundant clinical and experimental evidence to show that the ascent of microorganisms from the urethra is the most common pathway that leads to a UTI. For a well-functioning public health system. 1. most often for pyelonephritis (1). to monitor established treatment strategies closely. Unfortunately.

must be recognised. histological findings usually contribute very little to the treatment decisions. T. One example is the breakpoints for classification of pathogen susceptibility. or > 104 cfu/mL uropathogens in an MSU in men. it has recently become clear that there is no fixed bacterial count that is indicative of significant bacteriuria. urine or expressed prostatic secretion (EPS)].C. PubMed was searched for published meta-analyses. show bacteriuria of > 105 cfu/mL of uropathogens. • results of selected laboratory tests [blood. > 104 cfu/mL of uropathogens in an MSU in acute uncomplicated pyelonephritis in women. however. A basic standard level is necessary for routine assessment.E. The problem of counting low numbers. then in this setting.g. Bergman. including a reference link. fever of unknown origin in immunocompromised patients.E. but also which methods and standards were applied. • or in straight catheter urine in women. Palou. B. A second Working Group composed of M. as well as the quality of laboratory investigations.g. that microbiological methods and definitions applied must follow accepted standards with regard to specimen transport. one of which deals with catheter-associated UTIs (Chapter 6). Naber.g. Chapters 12 and 14 of the present guidelines present short summaries. any count of bacteria is relevant. including: • clinical symptoms. Botto. and P. T. B. e. in a complicated UTI. taken > 24 h apart. F. In a suprapubic bladder puncture specimen. and F. and several updates have been made. histology can be diagnostic. • most of these investigations can today be performed in any laboratory. or the National Committee for Clinical Laboratory Standards (NCCLS) (11). Otherwise. In 1960. such as the time that urine is kept in the bladder. have been published elsewhere. UPDATE MARCH 2011 9 . however. can be problematic and requires careful interpretation. which can be applied to all kinds of UTIs and in all circumstances. A chapter on Fournier’s gangrene has been added (Chapter 13).B. Histological investigation sometimes shows the presence of non-specific inflammation. such findings [e. rates of bacterial resistance. It is obvious that methods of urine collection and culture. H. there was a non-structured literature review process by the group members. Selvaggi. such as the European Committee for Antimicrobial Susceptibility Testing (EUCAST) (8-10). In research. Botto. Lobel.1. • > 105 cfu/mL of uropathogens in an MSU in women. the need for a precise definition of sampling methods. a number of basic criteria must be looked at before a diagnosis can be established. and antimicrobial susceptibility testing. Jiminez Cruz. 1.C. such as tuberculosis and actinomycosis. These methods and microbiological definitions may vary between countries and institutions. Asymptomatic bacteriuria is diagnosed if two cultures of the same bacterial strain (in most cases the species only is available). In clinical routine assessment.1 mL of urine is used and 10 identical colonies are necessary for statistical reasons of confidence. Kass developed the concept of significant bacteriuria (> 105 cfu/mL) in the context of pyelonephritis in pregnancy (7). Naber (chairman). The present version of Chapter 3 on uncomplicated UTIs has been rewritten in view of the International Consultation on Urological Diseases (ICUD) publication on UTI. urogenital tuberculosis (15) and urogenital schistosomiasis (16). M. • evidence of the presence of microorganisms by culturing or other specific tests. For a literature review. As described in Appendix 16. Çek. however. such as sexually transmitted infections (14).4 Methods A first UTI Working Group composed of K. and is therefore still of general importance. and these parameters carefully recorded. It is important to report not only the results. which were used as far as available. may vary. J. pathogen identification. Bishop. In general. Although this concept introduced quantitative microbiology into the diagnosis of infectious diseases. Tenke updated the guidelines and added several chapters. K. If an inoculum of 0. M. the lowest number that can be counted is 100 cfu/mL of uropathogens. M. Only in some cases. established the first version of these guidelines in several consensus conferences. H. prostatitis in patients who have elevated levels of prostate-specific antigen (PSA)] might help determine the appropriate treatment. e.G. It has to be considered.P.3 Microbiological and other laboratory findings The number of bacteria is considered relevant for the diagnosis of a UTI. Two levels of standard must therefore be used for the management of patients. has to be considered. the following bacterial counts are clinically relevant: > 103 cfu/mL of uropathogens in a mid-stream sample of urine (MSU) in acute uncomplicated cystitis • in women. Bishop. Lobel.G. Bjerklund-Johansen. EAU guidelines on special forms of urogenital infections.1. whereas a higher standard level is required for scientific assessment and in special clinical circumstances. Mixing results obtained by different methods. The initial edition was published in 2001 in Geneva by the EAU (12) and a modified version was published for the first time in 2001 (13). whereas in more specific inflammation. BjerklundJohansen. Grabe (chairman).

The aim of grading recommendations is to provide transparency between the underlying evidence and the recommendation given. But whenever this data is available. Epidemiology of urinary tract infections: incidence. and economic costs. values and preferences and cost when a grade is assigned (17-20). The EAU Guidelines Office. but without randomised clinical trials. Table 2: grade of recommendation* grade A B C Nature of recommendations Based on clinical studies of good quality and consistency addressing the specific recommendations and including at least one randomised trial. if there is overwhelming clinical experience and consensus. (17) 1. Availability of RCTs may not necessarily translate into a grade A recommendation where there are methodological limitations or disparity in published results.ncbi. The formal agreement to each updated chapter was achieved by the EAU working group in a series of meetings. http://www. there may be exceptional situations where corroborating studies cannot be performed. Alternatively.113 Suppl 1A:5S-13S. References Foxman B.Each member was responsible for one chapter (reporter).nih.5 Level of evidence and grade of guideline recommendations References used in the text have been assessed according to their level of scientific evidence (Table 1). discussed and incorporated accordingly. Based on well-conducted clinical studies. the link between the level of evidence and grade of recommendation is not directly linear. do not perform cost assessments.nih. Am J Med 2002 Jul.has to be balanced against benefits and burdens.nlm.nlm. such as comparative studies. http://www. nor can they address local/national preferences in a systematic fashion.6 1. The quality of the underlying scientific evidence although a very important factor .ncbi. which were then considered.168(4 Pt 2):1720-2. Made despite the absence of directly applicable clinical studies of good quality. correlation studies and case reports Evidence obtained from expert committee reports or opinions or clinical experience of respected authorities *Modified from Sackett et al. Resistance trends in urinary tract pathogens and impact on management.gov/pubmed/12352343 2. J Urol 2002 Oct.gov/pubmed/12113866 Mazzulli T. absence of high level evidence does not necessarily preclude a grade A recommendation. the expert panels will include the information. *Modified from Sackett et al. 10 UPDATE MARCH 2011 . morbidity. The first draft of each chapter was sent to the committee members asking for comments. perhaps for ethical or other reasons and in this case unequivocal recommendations are considered helpful for the reader. Table 1: Level of evidence* Level 1a 1b 2a 2b 3 4 Type of evidence Evidence obtained from meta-analysis of randomised trials Evidence obtained from at least one randomised trial Evidence obtained from one well-designed controlled study without randomisation Evidence obtained from at least one other type of well-designed quasi-experimental study Evidence obtained from well-designed non-experimental studies. In addition. (17) It should be noted that when recommendations are graded. 1. and guideline recommendations have been graded (Table 2) according to the Oxford Centre for Evidence-based Medicine Levels of Evidence (17).

Members of the Urinary Tract Infection (UTI) Working Group of the European Association of Urology (EAU) Guidelines Office. Naber KG. June 2000: Determination of minimum inhibitory concentrations (MICs) of antibacterial agents by agar dilution.ncbi. Sexually transmitted diseases (STDs) . 16. Emerg Infect Dis 2001 Mar-Apr.ncbi. Infection 1997 JulAug.nlm.nlm.nih.25(4):199-202. Gordon KA. August 2000: Determination of antimicrobial susceptibility test breakpoints.gov/pubmed/11752870 Schneede P. et al. Brian Haynes.40(5):576-88.ncbi.nlm. Tambyah PA.ncbi.2.6(10):570-2.nih.ncbi. Arch Intern Med 1960 Feb.cebm. Chris Ball.ncbi.gov/pubmed/11168187 European Committee for Antimicrobial Susceptibility Testing (EUCAST) of the European Society of Clinical Microbiology and Infectious Dieases (ESCMID). 2004. http://www. Cek M. Eur Urol 2001 Nov. http://www. Def 1.nlm.3. 4.nlm.49(6):998-1003.75(2):495-513.DEF 3. 11. Bishop MC. http://www. 10. EUCAST Definitive Document E. http://www. Methods for dilution antimicrobial susceptibility tests for bacteria that grow aerobically. Bergman B. Gales AC. Clin Microbiol Infect 2000 Sep. Jones RN. Naber KG. Gastmeier P. Nash DB. May 2000: Terminology relating to methods for the determination of susceptibility of bacteria to antimicrobial agents. Edition presented at the 16th EAU Congress. Redorta JP. PA.gov/pubmed/1996046 Kass EH. Botto H. http://www.48(3):353-62.44(1):1-7. 5. Cek M. Naber KG.105:194-8. Bischop MC. 8. Wayne. Activity and spectrum of 22 antimicrobial agents tested against urinary tract infection pathogens in hospitalized patients in Latin America: report from the second year of the SENTRY antimicrobial surveillance program (1998). 7. http://www. http://www. http://www.ncbi. ISBN 90-806179-3-9. Hofstetter AG. In: EAU Guidelines.ncbi.ncbi. et al. 17.nih.gov/pubmed/10702547 Rüden H.nih. Eur Urol 2005 Sep. 14. BjerklundJohansen TE. EAU guidelines for the management of genitourinary tuberculosis.nih.nih.net/index. Abrutyn E.nih. Clin Microbiol Infect 2000 Oct.nlm. Martin Dawes since November 1998. Naber KG.gov/pubmed/9266256 Maki DG.nih.gov/pubmed/12814668. Lenk S.DEF 2. Bjerklund-Johansen TE.nih.gov/pubmed/14404662 European Committee for Antimicrobial Susceptibility Testing (EUCAST) of the European Society of Clinical Microbiology and Infectious Dieases (ESCMID). EUCAST Definitive Document E. 9.nlm. the Members of the Urinary Tract Infection (UTI) Working Group of the Guidelines Office of the European Association of Urology (EAU):.aspx?o=1025 UPDATE MARCH 2011 11 . Doug Badenoch.a synoptic overview for urologists.gov/pubmed/11168058 National Committee for Clinical Laboratory Standards (NCCLS). http://www.ncbi. http://www.nlm. Approved Standard 4th Edition M7-A5 (2002) and M100-S12.nih. http://www.gov/pubmed/11168186 European Committee for Antimicrobial Susceptibility Testing (EUCAST) of the European Society of Clinical Microbiology and Infectious Diseases (ESCMID). Eur Urol 2003 Jul. Dave Sackett.6(9):509-15. Produced by Bob Phillips. Urinary Tract Infection (UTI) Working Group of the Health Care Office (HCO) of the European Association of Urology (EAU).1. Savatovsky I.gov/pubmed/16519990 Oxford Centre for Evidence-based Medicine Levels of Evidence (May 2001). Bacteriuria and pyelonephritis of pregnancy.6(9):503-8. 2001.nih. et al.7(2):342-7. http://www.nlm.gov/pubmed/15982799 Bichler KH.ncbi.gov/pubmed/11294737 Patton JP. EAU guidelines for the management of urogenital schistosomiasis.ncbi. Switzerland. Sharon Straus. EAU guidelines for the management of urinary and male genital tract infections. Grabe M. 15. Nosocomial and community-acquired infections in Germany. Engineering out the risk for infection with urinary catheters. J Antimicrob Chemother 2000 Mar. 13. et al. Bergman B. Tenke P.1. Daschner FD. 6. Eur Urol 2006 Jun.nlm. Urinary tract infection: economic considerations. Lobel B. Clin Microbiol Infect 2000 Sep. Med Clin North Am 1991 Mar. Summary of the results of the First National Prevalence Study (NIDEP).nlm. Urinary Tract Infection Working Group of the Health Care Office of the European Association of Urology. Geneva.nlm. Tenke P. [access date January 2011] http://www.nih.45(3):295-303. Guidelines on urinary and male genital tract infections. EUCAST Definitive Document E. 12. et al.

20.ncbi. BMJ 2008. signs and laboratory finding focus on the anatomical level and the degree of severity of the infection. Best D.3 grade of severity The grade of severity is set on a scale of 1-6 that is related to the risk of fatal outcome (Figure 2.gov/pubmed/15205295 Guyatt GH. http://www.2 Level of infection The symptoms.nlm.328(7454):1490. et al. 19. Grading quality of evidence and strength of recommendations. It is a working instrument. Briss PA. defined as: • urethritis (UR) • cystitis (CY) • pyelonephritis (PN) • sepsis (US).1.nih. BMJ 2008 May 10. The overall aim is to provide the clinician and researcher with a standardised tool and nomenclature for UTI. BMJ 2004 Jun 19. Oxman AD. The male genital infections prostatitis and epididymitis are also not included.e. drainage). 2. Asymptomatic bacteriuria (ABU) needs to be considered a special entity because it can have its source in both the lower and upper urinary tracts.nlm. GRADE Working Group. Atkins D.1) 12 UPDATE MARCH 2011 . The symptoms. Oxman AD. GRADE: an emerging consensus on rating quality of evidence and strength of recommendations. Urethritis being poorly understood is for the time being not included in the algorithm and treatment strategy of pure UTI. focus on the level of infection. and sepsis. UTIs have been divided in uncomplicated and complicated UTIs. http://www.nih. Kunz R. UTIs are classified based on clinical symptoms. GRADE Working Group.long 2.ncbi. 2. et al. It is important to underline that the following proposed classification is still not validated or recognised.bmj.gov/pubmed/18436948 Guyatt GH. as presented in the Appendix 16.1 CLASSIFICATION OF UTIs Introduction Traditionally. The risk factor analysis contributes to define any additional therapeutic measure required (i. Vist GE. and requires no treatment unless the patient is subjected to urological surgery. The present guidelines give a short summary of a tentative improved system of classification of UTI based on: • Anatomical level of infection • Grade of severity of infection • Underlying risk factors • Microbiological findings. http://www. laboratory data and microbiological findings.1. 2. Going from evidence to recommendations. A critical review of present classifications was undertaken for the EAU/ICUD Urogenital Infections initiative (1) in chapter 16. Practically.18.336(7650):924-6. et al.com/content/336/7652/1049.336(7652):1049-51.

stone.Asymptomatic Bacteriuria** .Connective tissue diseases* .V. organ failure Investigation Dipstick (MSU Culture + S) Dipstick MSU Culture + S Renal US or I. circulatory failure Systemic response SIRS + Organ dysfunction.Sexual behaviour and contraceptive devices .Figure 2. Traditional and improved classification of UTI as proposed by the EAU European Section of Infection in Urology (ESIU) (1) gradient of severity Symptoms Local symptoms Dysuria. with risk or more severe outcome.Secretory type of certain blood groups . with risk of more severe outcome Urological RF. shivering.Male gender .Controlled diabetes mellitus .Controlled neurogenic bladder dysfunction .Urological surgery UPDATE MARCH 2011 13 . with risk or more severe outcome N U Nephropathic disease. pain. Pyelogram/ renal CT Dipstick MSU Culture + S Renal US and/or Renal and abdominal CT Complicated UTI Type of UTI Complication level Uncomplicated UTI Anatomical* ABU CY-1 pN-2 pN-3 Febrile UTI US-4 US-5 US-6 Risk factor assessment* ORENUC assessment Treatment NO Empirical 3-5 days Empirical + directed 7-14 days Surgical as required Empirical + directed Consider 2 antibiotics 7-14 days Surgical as required Empirical + directed Consider 2 antibiotics 10-14 days Surgical as required Table 2.Polycystic nephropathy E Extra-urogenital RF.Healthy premenopausal women . but no risk of severe outcome Examples of risk factors .Pregnancy .Transient short-term urinary tract catheter . + nausea.1.Prematurity.1. stricture) which can be resolved during therapy .Hormonal deficiency in post menopause . vomiting Systemic response SIRS + Fever. bladder tenderness general symptoms Fever.Relevant immunosuppression* .Badly controlled diabets mellitus .Ureteral obstruction (i. . Host risk factors in UTI Type O R Category of risk factor No known/associated RF RF of recurrent UTI. flank pain. new-born .Relevant renal insufficiency* .e.

Non resolvable urinary obstruction . pregnancy.4 pathogens Urine culture will usually identify the causative pathogen (> 104 cfu/mL) and its susceptibility pattern.2: Additive parameters of UTI classification and severity assessment Clinical presentation Grade of severity UR: Urethritis CY: Cystitis PN: Pyelonephritis US: Urosepsis MA: Male genital glands Risk factors ORENUC 1: Low. The degree of susceptibility is defined as grade a (susceptible) to c (resistant). 2. with underlying urological disease (e. coli (a): simple cystitis but recurrent with susceptibility to standard antibiotics. PN-3U: K pneumonia (b): severe pyelonephritis (with high fever and vomiting). moderate 3: PN.6 1.g. Cek M. severe. ** = usually in combination with other RF (i.2 shows a summary of the additive parameters that make up an individual class of UTI. 14 UPDATE MARCH 2011 . Both characteristics can be introduced in the final classification of the clinical stage of infection. a UTI can be classified as follows (1): CY-1R: E. with a moderate antibiotic resistance profile. Critical review of current definitions of urinary tract infections and proposal of an EAU/ESIU classification system. cystitis 2: PN. urological internvention) 2. In Naber et al. * = not well defined.5 Classification of UTI Figure 2..1:980-991.Badly controlled neurogenic bladder RF = Risk Factor. et al.C Permanent urinary Catheter and non resolvable urological RF. Figure 2. Urogenital infections. established 4: US: SIRS 5: US: Organ dysfunction 6: US: Organ failure O: No RF R: Recurrent UTI RF E: Extra urogenital RF N: Nephropathic RF U: Urological RF C: Catheter RF Pathogens Species Susceptibility grade • Susceptible • Reduced susceptibility • Multi-resistant By cumulating the different parameters.Long-term urinary tract catheter treatment . Botto H. EAU/ICUD 2010. with risk of more severe outcome . Reference Bjerklund Johansen TE. in a patient with an indwelling catheter. US-5C: Enterococcus sp (a): severe urosepsis with an antibiotic-sensitive Enterococcus sp. 2.16. stones or obstruction) due to Klebsiella sp.e.

as opposed to urinary microscopy. frequency and urgency) and the absence of vaginal discharge or irritation. GR: A). Women who present with atypical symptoms of either acute uncomplicated cystitis or acute uncomplicated pyelonephritis. 3.2 Laboratory diagnosis Urine dipstick testing.3. with E.6) (LE: 2a. chapter 3 on uncomplicated UTI (1). fosfomycin trometamol 3 g single dose. The choice of an antibiotic for therapy should be guided by: • spectrum and susceptibility patterns of the aetiological uropathogens • efficacy for the particular indication in clinical studies • tolerability • adverse effects • cost • availability. uncomplicated UTIs in adults include episodes of acute cystitis and acute pyelonephritis in otherwise healthy individuals. or comorbidity that could lead to more serious outcomes and therefore require additional attention (2). such as Proteus mirabilis and Klebsiella sp. GR: B). norfloxacin 400 mg bid. is a reasonable alternative to urinalysis for diagnosis of acute uncomplicated cystitis (5. and ofloxacin 200 mg bid.1 Clinical diagnosis: The diagnosis of acute uncomplicated cystitis can be made with a high probability based on a focused history of urinary irritative symptomatology (dysuria.1 Diagnosis 3. pivmecillinam 400 mg for 3 days. Alternative antibiotics are ciprofloxacin 250 mg bid. GR: A). other Enterobacteriaceae. GR: B).1. ciprofloxacin extended release 500 mg qd.1 UNCOMpLICATED UTIs IN ADULTS Summary and recommendations This chapter is by itself the summary of the EAU/ICUD initiative on urogenital infections.2 Therapy Antibiotic therapy is recommended because clinical success is significantly more likely in women treated with antibiotics compared with placebo (10) (LE: 1a. adverse effects have to be considered (Table 3. GR: B). 3.2 Definition Acute. coli of < 20% (14.1 Aetiological spectrum The spectrum of aetiological agents is similar in uncomplicated upper and lower UTIs. According to these principles and the available susceptibility patterns in Europe. in those women who have no other risk factors for complicated UTIs (4) (LE: 2a. non-pregnant women 3. GR: B).1.3. levofloxacin 250 mg qd.3. UPDATE MARCH 2011 15 .3. are isolated (3) (LE: 2a).1). Cotrimoxazole 160/800 mg bid for 3 days or trimethoprim 200 mg for 5 days should only be considered as drugs of first choice in areas with known resistance rates for E.8) (LE: 4. are considered as drugs of first choice in many countries. each as a 3-day course (16) (LE: 1b. These UTIs are seen mostly in women without structural and functional abnormalities within the urinary tract. Urine cultures are recommended for those with: (i) suspected acute pyelonephritis. as well as those who fail to respond to appropriate antimicrobial therapy should be considered for additional diagnostic studies (LE:4.3.15) (LE: 1b. 3. coli the causative pathogen in 70-95% of cases and Staphylococcus saprophyticus in 5-10%. Occasionally. 3. when available (11-13) (LE: 1a. GR: B). GR: B). However. and (iii) those women who present with atypical symptoms (7. 3.3 Acute uncomplicated cystitis in premenopausal.2. (ii) symptoms that do not resolve or recur within 2-4 weeks after the completion of treatment. GR: B). A colony count of > 103 cfu/mL of uropathogens is microbiologically diagnostic in women who present with symptoms of acute uncomplicated cystitis (9) (LE: 3. 3.. kidney diseases. and nitrofurantoin macrocrystal 100 mg bid for 5 days.

GR: C). Austria. GR: C). is recommended for routine diagnosis (19) (LE: 4. For therapy in this situation. should be considered if the patients remain febrile after 72 h of treatment (LE: 4. Colony counts > 104 cfu/mL of uropathogens are considered to be indicative of clinically relevant bacteriuria (20) (LE: 2b. including the assessment of white and red blood cells and nitrites.4. the Netherlands. and Canada.4. 3. 3. In women whose symptoms do not resolve by the end of treatment. fever (> 38°C).g. urine culture and antimicrobial susceptibility tests should be performed (LE: 4.1 Diagnosis 3.2 Laboratory diagnosis Urinalysis (e. GR: B). one should assume that the infecting organism is not susceptible to the agent originally used. GR: B). GR: B). or costovertebral angle tenderness.1: Recommended antimicrobial therapy in acute uncomplicated cystitis in otherwise healthy premenopausal women Antibiotics Fosfomycin trometamol° Nitrofurantoin Nitrofurantoin macrocrystal Pivmecillinam* Pivmecillinam* Alternatives Ciprofloxacin Levofloxacin Norfloxacin Ofloxacin Cefpodoxime proxetil Trimethoprim-sulphamethoxazole Trimethoprim 250 mg bid 250 mg qd 400 mg bid 200 mg bid 100 mg bid 160/800mg bid 200 mg bid 3 days 3 days 3 days 3 days 3 days 3 days 5 days Daily dose 3 g SD 50 mg q6h 100 mg bid 400 mg bid 200 mg bid Duration of therapy 1 day 7 days 5-7 days 3 days 7 days If local resistance pattern is known (E. non-pregnant women 3. saprophyticus is less frequent in acute pyelonephritis as compared to acute cystitis (LE: 4.1 Clinical diagnosis Acute pyelonephritis is suggested by flank pain. S. nausea and vomiting.3 Imaging diagnosis Evaluation of the upper urinary tract with ultrasound should be performed to rule out urinary obstruction or renal stone disease (LE: 4. coli resistance < 20%): °not available in all countries. GR: C).3 Follow-up Routine post-treatment urinalysis or urine cultures in asymptomatic patients are not indicated (17) (LE: 2b.3.Table 3. GR: C). Additional investigations.1. the spectrum and susceptibility patterns of uropathogens that cause uncomplicated cystitis can be used as a guide for empirical therapy (3) (LE: 4.4.4 Acute uncomplicated pyelonephritis in premenopausal. and it can occur in the absence of symptoms of cystitis (18).4. However.2 Therapy As a result of the lack of suitable surveillance studies.4. *available only in Scandinavia.1. Retreatment with a 7-day regimen using another agent should be considered (LE: 4. 3. excretory urography. such as an unenhanced helical computed tomography (CT). 3. and in those whose symptoms resolve but recur within 2 weeks. GR: B). 16 UPDATE MARCH 2011 .1. GR: C). or dimercaptosuccinic acid (DMSA) scanning. using a dipstick method). 3.

but it can be used after sensitivity has been confirmed through susceptibility testing (26) (LE: 1b. coli resistance rates >10%. coli in the community have already been found in some parts of the world.2. cotrimoxazole is not suitable for empirical therapy in most areas. It is recommended when susceptibility testing shows a susceptible Gram-positive organism (LE: 4. have to be treated initially with one of the following parenteral antibiotics: LE a parenteral fluoroquinolone. A third-generation oral cephalosporin.2. GR: B).23) (25) (24) Alternatives (clinical but not microbiological equivalent efficacy compared with fluoroquinolones): Only if the pathogen is known to be susceptible (not for initial empirical therapy): UPDATE MARCH 2011 17 . the treatment can probably be reduced to 5 days (22. LE = level of evidence.3.1 Mild and moderate cases of acute uncomplicated pyelonephritis (Table 3. increasing numbers of fluoroquinolone-resistant E.4. coli resistance rates 1b < 10% an aminopenicillin plus a β-lactamase-inhibitor in cases of known susceptible Gram-positive pathogens an aminoglycoside or carbapenem in communities with fluoroquinolone and/or ESBLproducing E. thus restricting the empirical use of fluoroquinolones. GR: A). GR: C). coli resistance rates > 10%.2: Recommended initial empirical antimicrobial therapy in acute uncomplicated pyelonephritis in otherwise healthy premenopausal women I. could be an alternative (24. Table 3. 3. available studies have demonstrated only equivalent clinical. Co-amoxiclav is not recommended as a drug of first choice for empirical oral therapy of acute pyelonephritis (LE: 4.23) (LE: 1b. GR = grade of recommendation 4 1b Hospital admission should be considered if complicating factors cannot be ruled out by available diagnostic procedures and/or the patient has clinical signs and symptoms of sepsis (LE: 4. A fluoroquinolone for 7-10 days can be recommended as first-line therapy if the resistance rate of E. coli (> 10%). GR: B). coli is still < 10% (21) (LE: 1b. GR: B). GR: B). If the fluoroquinolone dose is increased. but not microbiological. coli fluoroquinolone-resistance rates < 10% 1b gR B B B B a third-generation cephalosporin. in communities with ESBL-producing E. Oral therapy in mild and moderate cases Antibiotics Ciprofloxacin1 Levofloxacin1 Levofloxacin Cefpodoxime proxetil Ceftibuten Daily dose 500-750 mg bid 250-500 mg qd 750 mg qd 200 mg bid 400 mg qd Duration of therapy 7-10 days 7-10 days 5 days 10 days 10 days Reference (21) (27) (22. After improvement. GR: B). oral therapy of 10-14 days is usually sufficient (LE: 1b. As a result of increasing E.) In mild and moderate cases of acute uncomplicated pyelonephritis. GR: B). GR: B). initial empirical therapy with an aminoglycoside or carbapenem has to be considered until susceptibility testing demonstrates that oral drugs can also be used (LE: 4. if active against the infecting organism. In communities with high rates of fluoroquinolone-resistant and extended-spectrum β-lactamase (ESBL)-producing E.2) Patients with severe pyelonephritis who cannot take oral medication because of systemic symptoms such as nausea and vomiting.4. in communities with E.2. to complete the 1-2-week course of therapy (LE: 1b.25) (LE: 1b. the patient can be switched to an oral regimen using one of the above-mentioned antibacterials. such as cefpodoxime proxetil or ceftibuten. However. However.2 Severe cases of acute uncomplicated pyelonephritis (Table 3. efficacy compared with ciprofloxacin. GR: B).

3. Appropriate diagnostic steps are necessary to rule out any complicating factors (LE: 4. In patients with no urological abnormality. the diagnosis of uncomplicated pyelonephritis should be reconsidered.4 Ceftazidime2 Cefepime1. GR: C). 3mainly for Gram-positive pathogens.5 g tid Reference (21) (27) (22) (28) (29) (30) (31) (28) (31) (29) (32) dose studied. 18 UPDATE MARCH 2011 .5 g tid 1 g tid 0.5/0. Antibiotics Ciprofloxacin Levofloxacin1 Levofloxacin Alternatives: Cefotaxime2 Ceftriaxone1.125 g tid 14 days 14 days (21) dose studied. but higher dose recommended by experts. it should be assumed that the infecting organism is not susceptible to the agent originally used. 2not studied as monotherapy in acute uncomplicated pyelonephritis. Therefore. For patients who relapse with the same pathogen.5 g tid 5 mg/kg qd 15 mg/kg qd 1 g qd 0.5/0. GR: C). CT or renal scintigraphy.4 Gentamicin2 Amikacin2 Ertapenem4 Imipenem/cilastatin4 Meropenem4 Doripenem4 1lower Daily dose 400 mg bid 250-500 mg qd 750 mg qd 2 g tid 1-2 g qd 1-2 g tid 1-2 g bid 1. but higher dose recommended by experts. 3mainly for Gram-positive pathogens.5-4. An algorithm of the clinical management of acute pyelonephritis is shown in Figure 3.3 Piperacillin/tazobactam1.4. studied as monotherapy for acute uncomplicated pyelonephritis. and an alternative tailored treatment should be considered based on culture results (LE: 4. such as renal ultrasound. II. repeated urine culture and antimicrobial susceptibility tests and an appropriate investigation. should be performed (LE: 4.Trimethoprim-sulphamethoxazole Co-amoxiclav2. 4same protocol for acute uncomplicated pyelonephritis and complicated UTI (stratification not always possible).3 1lower 2not 160/800 mg bid 0.4 Co-amoxiclav2. only daily dose and no duration of therapy are indicated. GR: B).3 Follow-up Routine post-treatment urinalysis and urine cultures in an asymptomatic patient might not be indicated (LE: 4. or resolve and then recur within 2 weeks. the patient can be switched to an oral regimen using one of the above-mentioned antibacterials (if active against the infecting organism) to complete the 1-2-week course of therapy. Initial parenteral therapy in severe cases After improvement. GR: B).1.5 g tid 2. In women whose pyelonephritis symptoms do not improve within 3 days.

or piperacillin plus BLI ➢ group 3 cephalosporin ➢ aminoglycosid clinical improvement within 72 h oral therapy continued (test conform) total duration of therapy 1-2 Weeks no clinical improvement or even detoriation switch to parenteral Therapy (test conform) hospitalisation clinical improvement within 72 h switch to oral therapy (test conform) Outpatient therapy total duration of therapy 1-2 Weeks no clinical improvement or even detoriation parenteral therapy continued (test conform) hospitalisation continued urine culture at day 4 of therapy (optional) urine culture at 5-10 days additional urine and blood cultures urological investigation for complicating factors drainage. UPDATE MARCH 2011 19 . flank pain nausea vomiting NO YES urinalysis und urine culture sonography (if anomaly suspected) outpatient therapy initial oral therapy urinalysis und urine culture sonography (in all patients) hospitalisation initial parenteral therapy for 1-3 days ➢ ciprofloxacin or levofloxacin ➢ aminopenicillin plus BLI ➢ group 3 cephalosporin (e. only if susceptibility of pathogen is known (not for empirical therapy) ➢ ciprofloxacin or levofloxacin ➢ aminopenicillin. in case of obstruction or abscess total duration of therapy 2-3 Weeks urine culture at day 4 of therapy (optional) urine culture at 5-10 days additional urine and blood cultures urological investigation for complicating factors drainage. TMP = trimethoprim.1 Clinical management of acute pyelonephritis. in case of obstruction or abscess total duration of therapy 2-3 Weeks BLI = ß-lactamase inhibitor.Figure 3. cefpodoxime proxetil) ➢ TMP-SMX. SMX = sulphamethoxazole.g. symptoms /signs of pyelonephritis fever.

3: Continuous antimicrobial prophylaxis regimens for women with recurrent UTIs (33) Regimens TMP-SMX* 40/200 mg once daily TMP-SMX 40/200 mg thrice weekly Trimethoprim 100 mg once daily Nitrofurantoin 50 mg once daily Nitrofurantoin 100 mg once daily Cefaclor 250 mg once daily Cephalexin 125 mg once daily Cephalexin 250 mg once daily Norfloxacin 200 mg once daily Ciprofloxacin 125 mg once daily Fosfomycin 3 g every 10 days Expected UTIs per year 0-0. Table 3.1. Before any prophylaxis regimen is initiated. even though they generally have anatomically and physiologically normal urinary tracts (33) (LE: 2a). GR: A). Continuous or postcoital antimicrobial prophylaxis should be considered to prevent recurrent uncomplicated cystitis in women in whom non-antimicrobial measures have been unsuccessful (35) (LE: 1a.03 0.5.00 0. cystography and cystoscopy are not routinely recommended for evaluation of women with recurrent UTIs (34) (LE: 1b.1 Diagnosis Recurrent UTIs are common among young.10 0.5. The choice of antibiotics should be based upon the identification and susceptibility pattern of the organism that causes the UTI and the patient’s history of drug allergies. eradication of a previous UTI should be confirmed by a negative urine culture 1-2 weeks after treatment (LE: 4. GR: A).2 0. Drug regimens are shown in Tables 3.2 Prevention Different therapeutic options can be recommended to the patient.0 0.00 0.14 *Trimethoprim-sulfamethoxazole **high recurrence rates observed with trimethoprim use associated with trimethoprim resistance Table 3.3.7 0. Expected UTIs per year 0.5** 0-0. 3.2 0. Excretory urography.6 0-0.5.30 0. Antimicrobial prophylaxis Antimicrobial prophylaxis for prevention of recurrent UTI should be considered only after counselling and behavioural modification has been attempted (LE: 4. GR: B).5 Recurrent (uncomplicated) UTIs in women 3.00 0. healthy women.4: postcoital antimicrobial prophylaxis regimens for women with recurrent UTIs (33) Regimens TMP-SMX* 40/200 mg TMP-SMX 80/400 mg Nitrofurantoin 50 or 100 mg Cephalexin 250 mg Ciprofloxacin 125 mg Norfloxacin 200 mg Ofloxacin 100 mg *Trimethoprim-sulfamethoxazole In appropriate women with recurrent uncomplicated cystitis.3 and 3. GR: A).4.0 0.0 0. GR: A). self-diagnosis and self-treatment with a shortcourse regimen of an antimicrobial agent should be considered (36) (LE: 2b. Recurrent UTIs need to be diagnosed by urine culture (LE: 4.06 20 UPDATE MARCH 2011 .1 0-1.2.1 0. 3. GR: A).

rhamnosus GR-1 and L. Recommended antibiotic regimens are shown in Table 3. bacteriuria is considered significant if a voided or catheterised urine specimen grows > 103 cfu/mL of a uropathogen (LE: 4.2. When commercially available. Its efficacy in other groups of patients.2 Screening Pregnant women should be screened for bacteriuria during the first trimester (42) (LE: 1a. GR: B). it is reasonable to consider the use of intravaginal probiotics that contain L. giving a minimum of 36 mg/day proanthocyanindin A (the active compound). 3.5. 3. The best approach is to use those compounds that have demonstrated clear bioactivity in urine.5.2. and these products can be used once or twice weekly (LE: 4. no controlled studies are available. Therefore. For other immunotherapeutic products. StroVac® and Solco-Urovac® have been shown to be effective when administered with a booster cycle of the same agents (LE: 1a. GR: C). For everyday practice. is recommended (LE: 1b. Most women acquire bacteriuria before pregnancy. GR: A). the daily consumption of cranberry products.6 UTIs in pregnancy UTIs are common during pregnancy. such as Urostim® and Urvakol®. Daily use of the oral product with strains GR-1 and RC-14 is worth testing given that it can restore the vaginal lactobacilli. 3. compete with urogenital pathogens. 3-5 days q12 h.2 Immunoactive prophylaxis OM-89 (Uro-Vaxomâ) is sufficiently well-documented and has been shown to be more effective than placebo in several randomised trials.6.5: Treatment regimens for asymptomatic bacteriuria and cystitis in pregnancy (44) Antibiotics Nitrofurantoin (Macrobid®) 100 mg Amoxicillin 500 mg Co-amoxicillin/clavulanate 500 mg Cephalexin (Keflex®) 500 mg Fosfomycin 3 g Trimethoprim-sulfamethoxazole Duration of therapy q12 h. 3. 3.3. 3-5 days Avoid trimethoprim in first trimester/term and sulfamethoxazole in third trimester/term Increasing resistance Comments Avoid in G6PD deficiency Increasing resistance G6PD = glucose-6-phosphate dehydrogenase UPDATE MARCH 2011 21 . and prevent bacterial vaginosis. GR: C). reuteri RC-14 for the prevention of recurrent UTI (39). bacteriuria is considered significant if two consecutive voided urine specimens grow > 105 cfu/mL of the same bacterial species on quantitative culture.6. Table 3.4 Prophylaxis with cranberry Despite the lack of pharmacological data and the small number of weak clinical studies. In smaller phase II studies. there is evidence to suggest that cranberry (Vaccinium macrocarpon) is useful in reducing the rate of lower UTIs in women (40.5. GR: A). For other immunotherapeutic products on the market. in a pregnant woman with symptoms compatible with UTI. • 3. GR: C).1 • Definition of significant bacteriuria in an asymptomatic pregnant woman. a condition that increases the risk of UTI (39) (LE: 1b.3 Prophylaxis with probiotics Accessibility of clinically proven probiotics for UTI prophylaxis is currently not universal.3 Treatment of asymptomatic bacteriuria Asymptomatic bacteriuria detected in pregnancy should be eradicated with antimicrobial therapy (42) (LE: 1a. no recommendations are possible.2. or a single catheterised specimen grows > 105 cfu/mL of a uropathogen (17) (LE: 2a. larger phase III studies are still missing. 3-5 days q8 h.41) (LE: 1b. GR: B). it can be recommended for immunoprophylaxis in female patients with recurrent uncomplicated UTI (37. GR: C). Therefore. 3-5 days q8 h. and its efficacy relative to antimicrobial prophylaxis remain to be established. Only the specifically in studies tested Lactobacillus strains should be used for prophylaxis. 3-5 days Single dose q12 h. GR: C). GR: A). and 20-40% of women with asymptomatic bacteriuria develop pyelonephritis during pregnancy.5.6.38) (LE: 1a.

3. GR: B).7. When indicated.3.7 Treatment of pyelonephritis Outpatient management with appropriate antibiotics should be considered in women with pyelonephritis in pregnancy.6. 3. GR: A).6 (46).4 Duration of therapy Short courses of antimicrobial therapy (3 days) should be considered for the treatment of asymptomatic bacteriuria and cystitis in pregnancy (43) (LE: 1a.6: Treatment regimens for pyelonephritis in pregnancy Antibiotics Ceftriaxone Aztreonam Piperacillin-tazobactam Cefepime Imipenem-cilastatin Ampicillin + Gentamicin Dose 1-2 g IV or IM q24 h 1 g IV q8-12 h 3. Genitourinary symptoms are not necessarily related to UTI and an indication for antimicrobial treatment.6. Table 3.375-4.5 Follow-up Urine cultures should be obtained soon after completion of therapy for asymptomatic bacteriuria and symptomatic UTI in pregnancy (LE: 4.6. physical examination and urinalysis.6.5 g IV q6 h 1 g IV q12 h 500 mg IV q6 h 2 g IV q6 h 3-5 mg/kg/day IV in 3 divided doses 3. urine catheterisation and functional status deterioration appear to be the most important risk factors associated with UTI. UTI before menopause. ultrasonography or magnetic resonance imaging (MRI) should be used preferentially to avoid radiation risk to the foetus (LE: 4. Non-secretor status of blood group antigens. cystocele and post-voiding residual urine. Incontinence. including culture.6 Prophylaxis Postcoital prophylaxis should be considered in pregnant women with a history of frequent UTIs before onset of pregnancy.8 Complicated UTI Prolonged antibiotic therapy (7-10 days) should be considered in this patient population (LE: 4.7. 3.1 UTIs in postmenopausal women Risk factors Reference LE 2a 2a 2a 2a 2a In older institutionalised women. 3. 48 LE 4 1b gR B B 22 UPDATE MARCH 2011 .6. Recommended antibiotic regimens are shown in Table 3. provided symptoms are mild and close follow-up is feasible (45) (LE: 1b. GR: A). Atrophic vaginitis. GR: B).2 Diagnosis Diagnosis of UTI in postmenopausal women should always consider the following: 47 47 47 47 47 Reference History. GR: B). 3. GR: A).7 3. to reduce their risk of UTI (44) (LE: 2b.

7. a count of > 105 cfu/mL is diagnostic of bacteriuria. Asymptomatic bacteriuria in elderly women should not be treated with antibiotics. or whenever a complicating factor is suspected. antimicrobial prophylaxis should be carried out as recommended for premenopausal women. a count of > 105 cfu/mL of a microorganism in a voided urine specimen is diagnostic of bacteriuria. For men with specimens collected using an external condom catheter.1 Asymptomatic bacteriuria Diagnosis Reference LE 2b 2a 2a 2b 2a 2b gR B B B B B B For women. as minimum therapy. 49 4 17 2b 4 50 51 1b 1b 4 C A C C C C 3. preferably with a fluoroquinolone since prostatic involvement is frequent. as measured by transient increases in serum PSA and prostate volume. For men. For patients with indwelling urethral catheters.8. a count of > 100 cfu/mL is consistent with bacteriuria.8 3. a count of > 103 cfu/mL of a microorganism in a voided urine specimen is diagnostic of bacteriuria. Optimal antimicrobials. but results are contradictory. a 7-day antibiotic regimen. > 105 cfu/ mL is an appropriate quantitative diagnostic criterion. If complicating factors. Such men should receive. Treatment of pyelonephritis in postmenopausal women is similar to that in premenopausal women.9.8. 3. A minimum treatment duration of 2 weeks is recommended. 54 53 LE 2a 4 gR A 2a B 3. short-term therapy is not so well-established as in premenopausal women. 17 55 56 17 17 17 UPDATE MARCH 2011 23 . Alternative methods.3 Treatment Reference LE 1b gR C Treatment of acute cystitis in postmenopausal women is similar to that in premenopausal women. however. Urological evaluation should be carried out routinely in adolescents and men with febrile UTI.2 Men with UTI and concomitant prostate infection 52 Reference Most men with febrile UTI have a concomitant infection of the prostate. pyelonephritis. Oestrogen (especially vaginal) can be administered for prevention of UTI. doses and duration of treatment in elderly women appear to be similar to those recommended for younger postmenopausal women. Pyuria in the absence of signs or symptoms in a person with bacteriuria should not be interpreted as symptomatic infection or as an indication for antimicrobial therapy. can contribute but they are not sufficient to prevent recurrent UTI. such as cranberry and probiotic lactobacilli. or recurrent infection.3. are ruled out. such as urinary obstruction and neurogenic bladder.1 Acute uncomplicated UTIs in young men Men with acute uncomplicated UTI Reference LE 4 gR B Only a small number of 15-50-year-old men suffer from acute uncomplicated UTI. For a urine specimen collected by in and out catheter.9 3.

349(3):259-66. Epidemiology of urinary tract infections: transmission and risk factors.nlm.nih.gov/pubmed/10979067 Foxman B.ncbi.ncbi. Diagnosis and treatment of uncomplicated urinary tract infection. 3. http://www. References Naber KG (chair). et al (Eds) (2010). Infect Dis Clin North Am 2003 Jun. European Association of Urology. 329(18):1328-34.gov/pubmed/18511178 Stamm WE. 5. Screening for or treatment of asymptomatic bacteriuria is not recommended for: Reference Premenopausal. 6.ncbi. Eur Urol 2008 Nov. Kramer L.160(16):2537-40. Surveillance study in Europe and Brazil on clinical aspects and Antimicrobial Resistance Epidemiology in Females with Cystitis (ARESC): implications for empiric therapy. 2. http://www.nih. http://www. The Netherlands.nlm. Schito G. N Engl J Med 2003 Jul 17. 4. http://www.ncbi.nih. Hooton TM.gov/pubmed/9378923 Naber KG. 24 UPDATE MARCH 2011 .ncbi.ncbi. and costs.gov/pubmed/3256648 Lifshitz E.3. http://www.nlm. 7. Acute uncomplicated urinary tract infection in women.9.11:(3)551-81.nlm. Botto H. EAU/International Consultation on Urological Infections. Hynes CF. Schaeffer AJ.2 Screening Screening for and treatment of asymptomatic bacteriuria is recommended: Reference For pregnant women Before an invasive genitourinary procedure for which there is a risk of mucosal bleeding.10 1. Outpatient urine culture: does collection technique matter? Arch Intern Med 2000 Sep 11.nlm.nih. Hooton TM.ncbi. http://www.gov/pubmed/12848468 Fihn SD. GR: B). Collection of urine specimens in general practice: to clean or not to clean? J R Coll Gen Pract 1988 Aug. Clinical practice. No recommendation can be made with respect to screening for or treatment of bacteriuria in patients with neutropenia (LE: 4). Brown P.nlm.nih.nlm. 54(5):1164-75.17(2):227-41.gov/pubmed/8413414 Bradbury SM. http://www. Infect Dis Clin North Am 1997 Sep.gov/pubmed/12867610 3. Management of urinary tract infections in adults. N Engl J Med 1993 Oct 28. Stamm WE. non-pregnant women Postmenopausal women Women with diabetes Healthy men Residents of long-term care facilities Patients with an indwelling urethral catheter Patients with nephrostomy tubes or ureteric stents Patients with spinal cord injury Patients with candiduria 59 60 17 17 57 58 17 17 LE 1a 1b 1b 2b 1a 1b 4 2a 1b C B A gR A A A B A 42 17 LE 1a 1b gR A A Screening for or treatment of asymptomatic bacteriuria in renal transplant patients beyond the first 6 months is not recommended (62) (LE: 2b. incidence.nih. et al.nih. 38(313): 363-5. 8.

23. 10. Vouloumanou EK.nlm.gov/pubmed/19454521 Lecomte F.gov/pubmed/15630106 Shoff WH.1997. Clin Infect Dis 2005 Mar. 17.nlm. http://www.nlm.ncbi. Hooton TM. Bradley S. Urology 2008 Jan.ncbi. 16. Roberts PL. http://www. 15. 12. Single-dose treatment of cystitis with fosfomycin trometamol (Monuril): analysis of 15 comparative trials on 2. et al. http://www. Peterson J. McKevitt M.10:29-34.46 Suppl 1:35-9. randomized comparison of levofloxacin 750 mg once-daily for five days with ciprofloxacin 400/500 mg twice-daily for 10 days for the treatment of complicated urinary tract infections and acute pyelonephritis. Colgan R.nih.nlm.23(11):2637-45.gov/pubmed/11440218 Naber KG.40(5):643-54. discussion 63-5. Scholes D. Levofloxacin versus ciprofloxacin versus lomefloxacin in acute pyelonephritis. et al. 11. Talan DA.ncbi.19(6):554-6.52(1):51-5. Comparison of ciprofloxacin (7 days) and trimethoprimsulfamethoxazole (14 days) for acute uncomplicated pyelonephritis pyelonephritis in women: a randomized trial. American Society of Nephrology.nih. et al.nlm.gov/pubmed/11051622 Gupta. Karageorgopoulos DE.nih. Fewer bacterial relapses after oral treatment with norfloxacin than with ceftibuten in acute pyelonephritis initially treated with intravenous cefuroxime.nih.nih. 26. Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women.nih.gov/pubmed/12135847 Rafalsky V. Quinolones for uncomplicated acute cystitis in women. et al. 25.3:CD003597. Scand J Infect Dis 2001.9.19:399-404. Edwards C.64(1):16-24. et al.nlm. Infectious Diseases Society of America. 21. Urology 1998 Jul. Acute Pyelonephritis.ncbi.167(20):2207-12. 27.] Chemotherapie Journal 2001. Roberts PL. Clin Infect Dis 1999 Oct. Giorn It Ost Gin 1997.nlm. Infectious Diseases Society of America (IDSA). A randomized trial. http://www.com/article/245559-overview Rubin US.nlm. Andriole VT. http://www.ncbi. Urinary tract infections.gov/pubmed/16856014 Nicolle LE. http://www.nih. et al. http://www.gov/pubmed/10735395 Klausner HA. Evaluation of new anti-infective drugs for the treatment of UTI. prevention and management. A trial of levofloxacin 750 mg once daily for 5 days versus ciprofloxacin 400 mg and/or 500 mg twice daily for 10 days in the treatment of acute pyelonephritis. http://www. et al. International. 13. Counts GW. Banke S. Ann Intern Med 1987 Mar. Fowler CL. Ann Intern Med 2005 Jan.gov/pubmed/17880755 Peterson J.nih.nih. Brown P.nlm. et al. 2009 http://emedicine. Kaul S.ncbi. [article in German] Stamm WE. Outcomes associated with trimethoprim/sulphamethoxazole (TMP/SMX) therapy in TMP/SMX resistant community-acquired UTI. Davis RJ. A double-blind.nlm. Pivmecillinam in the treatment of urinary tract infections. [Cefpodoxime proxetil in patients with acute uncomplicated pyelonephritis. Stamm WE. Clin Infect Di. Acute renal infection in women: treatment with trimethoprimsulfamethoxazole or ampicillin for two or six weeks.29(4):745-58. Green-McKenzie J. 1992. Risk factors associated with acute pyelonephritis in healthy women.ncbi. Kunin C. Infectious Diseases Society of America guidelines for the diagnosis and treatment of asymptomatic bacteriuria in adults.ncbi. American Geriatric Society.ncbi. 14.ncbi.048 patients. 5th edition.ncbi. et al.142(1):20-7. Hooton TM.283(12):1583-90. Allaert FA.nih. J Antimicrob Chemother 2000 Sep. Bergman B. In: Detection. Nicolle LE.gov/pubmed/18242357 Cronberg S. 20. Khashab M. Abrutyn E. J Infect 2009 Jul. 22. et al.nlm. Philadelphia: Lea & Febiger. Hooton TM. Rjabkova E. Int J Antimicrob Agents 2002 Jun.gov/pubmed/3492950 Richard GA. 19.nih. http://www.nih.gov/pubmed/9671870 UPDATE MARCH 2011 25 . Hauke W. Hebel JR.gov/pubmed/17998493 Warren JW. K.nlm. Kazantzi MS. et al. http://www.medscape. Short-course nitrofurantoin for the treatment of acute uncomplicated cystitis in women.ncbi. Klimberg IN.33(5):339-43.gov/pubmed/10589881 Gupta K. randomized comparative study versus ciprofloxacin in general practice. Schoenwald S.15:216.ncbi.71(1):17-22. Curr Med Res Opin 2007 Nov. JAMA 2000 Mar. prospective. http://www.nih. Cochrane Database Syst Rev 2006 Jul 19. 18. Arch Intern Med 2007 Nov. Antibiotics versus placebo in the treatment of women with uncomplicated cystitis: a meta-analysis of randomized controlled trials. Stamm WE. http://www. et al.nlm. Andreeva I. http://www.106(3):341-5. 24.

nih.gov/pubmed/11850161 Naber KG. 32. Woods GL.gov/pubmed/10037399 Bauer HW.gov/pubmed/17443502 Vazquez JC.(2):CD000490. http://www.nlm. http://www.5 g is as effective as imipenem 0.ncbi. BA Stuppy. Can J Urol 2002 Jun.gov/pubmed/11431298 Stothers L. Jiang Q.ncbi.gov/pubmed/8543490 Giamarellou H. Antibiotics for preventing recurrent urinary tract infection in nonpregnant women. Cochrane Database Syst Rev 2004(3):CD001209.nih. Hooton. N Engl J Med 1981 Feb.ncbi. Wells WG. Cochrane Database Syst Rev 2007 Apr 18.nlm.322(7302):1571.32 Suppl B:123-32. 44. Sundqvist K.ncbi. http://www.nih. 34.nih.nlm. http://www. Clinical study comparing probiotic Lactobacillus GR-1 and RC-14 with metronidazole vaginal gel to treat symptomatic bacterial vaginosis. Savov O. J Urol 1999 Jan.nih.gov/pubmed/7453771 Albert X.gov/pubmed/12121581 Smaill F. et al. http://www. Immunoactive prophylaxis of recurrent urinary tract infections: a meta-analysis. and cystoscopy in the evaluation of women with urinary-tract infection: a prospective study. cystography. Int J Antimicrob Agents 2009 Feb.ncbi.19(2):95-103.nlm. 40. Cho YH. 43.nlm. BMJ 2001 Jun. http://www. Excretory urography.gov/pubmed/18963856 Anukam KC. Llorens L. multicentre trials comparing ertapenem and ceftriaxone followed by an appropriate oral therapy. http://www. 33.gov/pubmed/17045832 Kontiokari T. 36.161(1):207-11. 29. Rahlfs VW. submitted. Osemene GI.ncbi. http://www. Clin Infect Dis. Beuscart C.ncbi. http://www.5 g for the treatment of acute uncomplicated pyelonephritis and complicated urinary tract infections. Sacks TG.gov/pubmed/15150185 Mouton YJ. Recurrent urinary tract infection in women. Cochrane Database Syst Rev 2000. Intravenous therapy with doripenem versus levofloxacin with an option to switch to oral therapy for the treatment of complicated lower urinary tract infection and pyelonephritis.ncbi. double-blind. Treatment of complicated urinary tract infection in adults: combined analysis of two randomized.(3):CD002256. http://www.gov/pubmed/11295405 Fowler JE Jr.nih. Efficacy and safety of self-start therapy in women with recurrent urinary tract infections. http://www. Prevention of recurrent urinary tract infections with immuno-active E.ncbi. Meropenem Study Group.nlm. 41. Antimicr Agents Chemotherapy. J Antimicrob Chemother 2004 Jun. et al.nlm. Low-dosage cefepime as treatment for serious bacterial infections.ncbi. A randomized trial to evaluate effectiveness and cost effectiveness of naturopathic cranberry products as prophylaxis against urinary tract infection in women.53 Suppl 2:ii67-74.nih.19(6):451-6. et al. Salmen HC. Empirical monotherapy with meropenem in serious bacterial infections. Vazquez JC.gov/pubmed/12135831 Naber KG.ncbi. 1992 Apr 14.gov/pubmed/10908537 Pfau A. TM.ncbi. http://www. Effective prophylaxis for recurrent urinary tract infections during pregnancy.nlm.nih. coli fractions: a meta-analysis of five placebo-controlled double-blind studies.33(2):111-9.nih.nih.nih.28. Pulaski ET. Osazuwa E.9(3):1558-62. 42. Int J Antimicrob Agents 2002 Feb. 37. Int J Antimicrob Agents 2002 Jun.304(8):462-5.nlm.ncbi. Microbes Infect 2006 Oct.ncbi.nih.nlm. et al.8(12-13):2772-6.nih. http://www. et al. Nuutinen M. Matsumoto T.nih. Kaniga K. 39.17(4): 259-68.ncbi. http://www.gov/pubmed/8150755 Naber KG. Villar J.nlm.nih. 38. et al. 35.(4): 810-4. et al. Huertas I.5 g/ cilastatin 0.gov/pubmed/15266443 Schaeffer AJ. Pereiró II. Treatments for symptomatic urinary tract infections during pregnancy. Piperacillin 2 g/tazobactam 0.nlm. J Antimicrob Chemother 1995 Jul. Randomised trial of cranberrylingonberry juice and Lactobacillus GG drink for the prevention of urinary tract infections in women. 30.nlm. 31.36 Suppl A:145-56.ncbi. http://www. http://www. Antibiotics for asymptomatic bacteriuria in pregnancy.gov/pubmed/1576275 26 UPDATE MARCH 2011 .nlm.nih. Int J Antimicrob Agents 2001 Apr.nlm. J Antimicrob Chemother 1993 Nov. Lauener PA.nlm.

ncbi.gov/pubmed/10619727 Takai K.nih. 51. et al.gov/pubmed/8350884 Avorn J.pp.ncbi. Clinically inapparent (asymptomatic) bacteriuria in ambulatory elderly men: epidemiological.transplantation-proceedings. 58. http://www.9(5):596-7. A controlled trial of intravaginal estriol in postmenopausal women with recurrent urinary tract infections.170(4):469-73. http://www. et al. et al. Paul RH. Scand J Infect Dis 2003.nih.nlm. Hendershott CM.nih.26(6):1115-9. double-blind study of treatment with fluconazole and placebo. http://www. Urinary tract infections.nlm. 53.nlm. The National Institute of Allergy and Infectious Diseases (NIAID) Mycoses Study Group.92(2):249-53. et al. et al. http://www.nih.nlm.ncbi. Asymptomatic bacteriuria in the elderly. Reliability of a single urine culture in establishing diagnosis of asymptomatic bacteriuria in adult males. Clin Infect Dis 2000 Jan. http://www. http://www. et al. Millar LK.22 Suppl 2:89-93. clinical. A randomized trial of three antibiotic regimens for the treatment of pyelonephritis in pregnancy. 60. Basel. Antimicrobial treatment in diabetic women with asymptomatic bacteriuria. Int J Antimicrob Agents 2003 Oct. et al. 59. Suga A. Significance of asymptomatic bacteriuria in neurogenic bladder disease. 49.nih. et al.45.gov/pubmed/7675380 Wing DA.ncbi. et al. http://www. 86(4 Pt 1):560-4.ncbi.11(3):647-62. Obstet Gynecol 1995 Oct.nih.ncbi.nih. In: Bergan T (ed).gov/pubmed/9378928 Foxman B.nlm.nlm. Sandberg T. Debuque L. J Clin Microbiol 1979 May.gov/pubmed/8093138 Stamm WE. Stamm WE.gov/pubmed/2246458 Lewis RI.ncbi.nlm.nih.329(11):753-6. Harding GK. http://www. 47. Lockhart JL. 61. Monane M.nlm. Gurwitz JH. 52. 54. and microbiological findings. N Engl J Med 1993 Sep.ncbi. et al. http://www. Yamamura RH.com/ProdukteDB/produkte. Urinary tract infections in young men.nlm.54(7):710-8.nih. Crowley M.nlm.org/article/S0041-1345(98)00968-3/abstract UPDATE MARCH 2011 27 . http://www.gov/pubmed/14527778 Ulleryd P.gov/pubmed/11438412 Vogel T. Aoki A.gov/pubmed/6369712 Sobel JD. Kennedy J. N Engl J Med 2002 Nov 14. J Clin Epidemiol 2001 Jul. CMAJ 2004 Feb. Wing DA.gov/pubmed/9699761 Nicolle LE.karger.gov/pubmed/383746 Nicolle LE. Urology 1984 Apr.gov/pubmed/12432044 Mims AD. http://www. et al.ncbi. Urinary tract infections following renal transplantation. Esposito A.271(10):751-4.asp?Doi=61396 Ulleryd P.nih. Urine specimen collection with external devices for diagnosis of bacteriuria in elderly incontinent men. Optimal duration of antibiotic therapy for uncomplicated urinary tract infection in older women: a double-blind randomized controlled trial. http://content. Zhanel GG. Reduction of bacteriuria and pyuria after ingestion of cranberry juice. Somsel P. http://www. Outpatient treatment of pyelonephritis in pregnancy: a randomized controlled trial. http://www. Candiduria: a randomized. 55. Carrion HM. Obstet Gynecol 1998 Aug. http://www.nih.nih. 50.nih. 57. Kauffman CA.nlm.347(20):1576-83.12(1):19-23. Ciprofloxacin for 2 or 4 weeks in the treatment of febrile urinary tract infection in men: a randomized trial with a 1 year follow-up.nlm. J Am Geriatr Soc 1990 Nov.35(1):34-9.38(11):1209-14.nlm. Norman DC. 1997 vol 1. Gourdeau M. Manitoba Diabetes Urinary Tract Infection Study Group.nlm. et al.gov/pmc/articles/PMC332712/ Raz R. Verreault R.nih.ncbi. McKinsey D. Switzerland: Karger. 48.ncbi. http://www. Nicolle LE.ncbi.23(4):343-7. 46.ncbi.gov/pubmed/12685882 Gleckman R.ncbi.gov/pubmed/3384923 Harding GK.nlm. 46-7. JAMA 1994 Mar.nih. http://www.30(1):19-24. 56. Febrile urinary tract infection in men. Urinary tract infection among women aged 40 to 65: behavioral and sexual risk factors. J Clin Microbiol 1988 Jun. Tallman P. Clin Transplant 1998 Nov. Infect Dis Clin North Am 1997 Sep.ncbi.

stent or splint (urethral. an aminopenicillin plus a ß-lactamase inhibitor (BLI). Until predisposing factors are completely removed. With regard to prognosis and clinical studies. a Group 2 or 3a cephalosporin or.g. therapy should be guided by urine culture whenever possible. A broad range of bacteria can cause a complicated UTI. a broader-spectrum antibiotic should be chosen that is also active against Pseudomonas (LE: 1b. are recommended alternatives (LE: 1b.1: Factors that suggest a potential complicated UTI The presence of an indwelling catheter. GR: A).g. true cure without recurrent infection is usually not possible. permanent indwelling catheter. 4. Patients in whom the complicating factors could be eliminated by therapy.g.g. or a carbapenem. such as a structural or functional abnormality of the genitourinary tract.and postoperative UTI Renal insufficiency and transplantation. Treatment strategy depends on the severity of the illness. removal of an indwelling catheter. Two criteria are mandatory to define a complicated UTI: a positive urine culture and one or more of the factors listed in Table 4. a urine culture should be carried out 5-9 days after completion of therapy and also 4-6 weeks later (GR: B). To avoid the emergence of resistant strains. which increases the risks of acquiring an infection or of failing therapy (1-3). with or without combination with an aminoglycoside (LE: 1b. depending on the underlying conditions. and supportive care when needed. diabetes mellitus and immunodeficiency Complicated UTI can arise in a heterogeneous group of patients. antimicrobial therapy. Table 4. renal) or the use of intermittent bladder catheterisation Post-void residual urine of > 100 mL An obstructive uropathy of any aetiology. GR: B). a Group 3b cephalosporin. A fluoroquinolone with mainly renal excretion. neither patient age nor sex per se are part of the definition of a complicated UTI. However.1 COMpLICATED UTIs DUE TO UROLOgICAL DISORDERS Summary and recommendations A complicated UTI is an infection associated with a condition. especially in a treatmentrelated complicated UTI. In case of failure of initial therapy. or in case of clinically severe infection. GR: B). an aminoglycoside. 2. such as an ileal loop or pouch Chemical or radiation injuries of the uroepithelium Peri. an acylaminopenicillin (piperacillin) plus a BLI. e. Therefore.1. it is advisable to stratify complicated UTIs due to urological disorders into at least two groups (4): 1. stone residues after treatment or neurogenic bladder.4. such as structural or functional abnormalities of the genitourinary tract or the presence of an underlying disease. 28 UPDATE MARCH 2011 . The duration of therapy is usually 7-14 days (LE: 1b. Patients in whom the complicating factor could not be or is not removed satisfactorily during therapy. However. or the presence of an underlying disease that interferes with host defence mechanisms. 4. GR: B). Treatment encompasses three goals: management of the urological abnormality. GR: A). ureteral. a fluoroquinolone (if not used for initial therapy). but sometimes has to be prolonged for up to 21 days (LE: 1b. stone extraction. e. and bacteria are more likely to be resistant to antimicrobials. with E. Pseudomonas aeruginosa) and Gram-positive cocci (e. The spectrum is much larger than in uncomplicated UTIs. e.2 Definitions and classification A complicated UTI is an infection associated with a condition. e. If empirical therapy is necessary. in the case of parenteral therapy. staphylococci and enterococci) may also play an important role. stones and tumour Vesicoureteric reflux or other functional abnormalities Urinary tract modifications.g. coli being the most common pathogen. Enterobacteriaceae are the predominant pathogens. non-fermenters (e. Hospitalisation is often required. bladder outlet obstruction (including neurogenic urinary bladder).g. which increase the risks of acquiring infection or of failing therapy. the antibacterial spectrum of the antibiotic agent should include the most relevant pathogens (GR: A).

g. 4. diabetes mellitus and immunosuppression. especially lower urinary tract symptoms (LUTSs). coli as the most common pathogen.4 Treatment 4. Klebsiella.14). The spectrum is much larger than with an uncomplicated UTI and the bacteria are more likely to be antibiotic-resistant (especially in a treatment-related complicated UTI) than those isolated in an uncomplicated UTI. urease. 4. both community and hospital-acquired. with E.2. The pathogenic potential of coagulase-negative staphylococci and non-group D streptococci is controversial (13.1 Spectrum and antibiotic resistance Patients with a complicated UTI. Under certain circumstances.4 on UTIs in renal insufficiency. staphylococci can be relevant pathogens. Of the urease-producing organisms. the frequency of E. Proteus. Pseudomonas and Serratia sp. Otherwise. and staphylococci are also urease producers to a certain extent. according to published reports (6. which can be related to urological abnormalities (5). and Corynebacterium urealyticum are predominant.4.3 Complicated UTIs associated with urinary catheters In catheter-associated UTIs.4. 4. frequency.2 Urine cultures Significant bacteriuria in a complicated UTI is defined by counts of > 105 cfu/mL and > 104 cfu/mL. A dipstick method can also be used for routine assessment. such as benign prostatic hyperplasia (BPH). splits urea into carbon dioxide and ammonia. The enzyme.3. a greater portion of Proteus and Pseudomonas sp.3. Enterobacteriaceae predominate (6075%) (6-8).2 Complicated UTIs associated with urinary stones In the subset of complicated UTIs related to urinary stones. are not only caused by UTIs but also by other urological disorders. two consecutive urine cultures (at least 24 h apart) yielding > 105 cfu/mL of the same microorganism are required.3 Microbiology 4. Antimicrobial therapy may only be effective in the early stages of the infection (15). Appropriate antimicrobial therapy and the UPDATE MARCH 2011 29 . such as the presence of a stone or foreign bodies. E. The requirement for pyuria is > 10 white blood cells (WBC) per high-power field (x400) in the resuspended sediment of a centrifuged aliquot of urine or per mm3 in unspun urine. staphylococci are not so common in complicated UTIs (0-11%). Apart from urological abnormalities. In contrast. Pseudomonas and Serratia sp. > 104 cfu/mL can be considered relevant.2).1. 4. coli. 88% were found to have a UTI at the time of diagnosis. particularly if the UTI is a first infection. such as diabetes mellitus (10%) and renal failure. and biofilm has to be considered. coli and enterococci infection seems less important pathogens. transurethral resection of the prostate (TURP). For an asymptomatic patient. the bacterial spectrum may vary over time and from one hospital to another. These aggregate to form renal stones and incrustations on urinary catheters (12). haemoglobin and probably a nitrite reaction. Providencia and Morganella sp.2.3.3 and 8. the presence of a resistant strain on its own is not enough to define a complicated UTI. which might disappear spontaneously as soon as the catheter is removed. (9) is found. Clinical presentation can vary from severe obstructive acute pyelonephritis with imminent urosepsis to a catheter-associated postoperative UTI. dysuria. and enterococci are the usual strains found in cultures. Otherwise. including a leukocyte esterase test. These are discussed in more details in Sections 8..1 Clinical presentation A complicated UTI may or may not be associated with clinical symptoms (e. If a straight catheter urine sample is taken. urgency. A broad range of bacteria can cause a complicated UTI. and higher rates of treatment failure if the underlying abnormality cannot be corrected. transplant recipients. costovertebral angle tenderness. Urinary abnormality (anatomical or functional) or the presence of an underlying disease predisposing to a UTI is also necessary. For more details see chapter 6 on catheter-associated UTIs. with 82% of patients infected with urease-producing organisms (10).1. It also has to be recognised that symptoms. in the MSU of women and men. flank pain. The resultant increase in ammonia in the urine injures the glycosaminoglycan layer. 4. respectively (1. Among patients with staghorn calculus disease.15). the distribution of microorganisms is similar (16).1 General principles Treatment strategy depends on the severity of the illness. suprapubic pain and fever). which in turn increases bacterial adherence (11) and enhances the formation of struvite crystals. concomitant medical conditions. Proteus. tend to show a diversity of microorganisms with a higher prevalence of resistance against antimicrobials. but Klebsiella. are often present in a complicated UTI. However.

it has not been shown that any agent or class of agents is superior in cases in which the infective organism is susceptible to the drug administered. Patients can generally be treated as outpatients. In most countries.2 and Appendix 16. A new Group 1 oral carbapenem. E. Many therapeutic trials have been published on the use of specific antimicrobial therapies in complicated UTIs. 4. optimal management of the underlying urological abnormalities or other diseases. Bacteraemia is usually reported too late to influence the choice of antibiotics. Intense use of any antimicrobial. eventually in combination with an aminoglycoside. Therefore. has been shown to be as effective as ceftriaxone (16). in a prospective randomised trial. a Group 3b cephalosporin. are no longer sufficiently active against E. and the selection of an antimicrobial agent should be re-evaluated once culture results are available (7). empirical therapy should be replaced by a therapy adjusted for the specific infective organisms identified in the urine culture. Therapy has to be reconsidered when the infective strains have been identified and their susceptibilities are known. Fosfomycin trometamol is licensed only for a single-dose therapy of uncomplicated cystitis (18). Whenever possible. In patients with renal failure.4. a urine specimen for culture must be obtained before initiation of therapy. Similarly. but the duration should be closely related to the treatment of the underlying abnormality (1). a prolongation for up to 21 days. If empirical treatment is necessary. most reports are of limited use for the practical management of the patient in a day-to-day situation because of limitations such as: • poor characterisation of the patient populations • unclear evaluation of the severity of the illness • nosocomial and community-acquired infections are not accurately distinguished • urological outcome is seldom taken into consideration. Hospitalisation is often necessary depending on the severity of the illness. or. or if microbiological results are not yet available. in the case of parenteral therapy. or as initial therapy in the case of clinically severe infection. ampicillin or amoxicillin. If needed. especially when used on an empirical basis in this group of patients with a high likelihood of recurrent infection.management of the urological abnormality are mandatory. The severity of the associated illness and the underlying urological condition are still of the utmost importance for prognosis. an acylaminopenicillin (piperacillin) plus a BLI.4 Complicated UTIs associated with urinary stones If a nidus of a stone or an infection remains. as well as assessment of the severity of the underlying urological abnormality (including the evaluation of renal function). coli. according to the clinical situation. or a carbapenem. 4. To date. The antibacterial treatment options are summarised in Table 4.3 Duration of antibiotic therapy Treatment for 7-14 days is generally recommended. In the case of failure of initial therapy. ertapenem. are alternatives. stone growth will occur. treatment should be switched to an antibiotic with a broader spectrum that is also active against Pseudomonas.2 (Recommendations for antimicrobial therapy in urology). antibiotics have to be given parenterally. and sufficient life-supporting measures. supportive care is given. suspicion of bacteraemia must influence the empirical treatment. After a few days of parenteral therapy and clinical improvement. many experts concur that empirical therapy for the institutionalised or hospitalised patients with a serious UTI should include an intravenous antipseudomonal agent because of an increased risk of urosepsis (19). such as a fluoroquinolone (if not used for initial therapy).4. appropriate dose adjustments have to be made. Sometimes. will lead to the emergence of resistant microorganisms in subsequent infections. Unfortunately. An aminopenicillin plus a BLI. The aminopenicillins.4. whether related to a urological abnormality or not.2 Choice of antibiotics Empirical treatment of a symptomatic complicated UTI requires a knowledge of the spectrum of possible pathogens and local antibiotic resistance patterns. 4. Complete removal of the stones and 30 UPDATE MARCH 2011 . In more severe cases (e. The successful treatment of a complicated UTI always combines effective antimicrobial therapy. fluoroquinolones with mainly renal excretion are recommended because they have a large spectrum of antimicrobial activity that covers most of the expected pathogens. coli shows a high rate of resistance against TMP-SMX (18-25% in the latest evaluation in the USA) (17) and should therefore be avoided as a first-line treatment. is necessary (2). patients can be switched to oral treatment.g. hospitalised patients). A combination of an aminoglycoside with a BLI or a fluoroquinolone is widely used for empirical therapy. an aminoglycoside. and they reach high concentration levels both in the urine and the urogenital tissues. However. a Group 2 or 3a cephalosporin. Fluoroquinolones can be used orally as well as parenterally.

only a few studies have investigated the most appropriate agent and duration of therapy. based on culture and sensitivity results. because it will promote the emergence of resistant strains (22. ampicillin Trimethoprim-sulphamethoxazole (only if susceptibility of pathogen is known) Fosfomycin trometamol BLI = ß-lactam inhibitor 4.adequate antimicrobial therapy are both needed.4. Table 4. or for severe cases Fluoroquinolone (if not used for initial therapy) Ureidopenicillin (piperacillin) plus BLI Cephalosporin (Group 3b) Carbapenem Combination therapy: . antibiotics may delay the onset of bacteriuria. The optimal duration is not well established. This is not a priori related to the urinary abnormality.2. 7-10 days of therapy is most commonly used.6 Complicated UTIs in patients with spinal cord injury In case of persistent UTIs and suspicion of urinary retention.g.4.4. Eradication of the infection will probably eliminate the growth of struvite calculi (20). In short-term catheterisation. urine cultures must be obtained for the identification of the microorganisms and the evaluation of susceptibility testing. A symptomatic complicated UTI associated with an indwelling catheter is treated with an agent with as narrow a spectrum as possible. Long-term antimicrobial therapy should be considered if complete removal of the stone cannot be achieved (21).7 Follow-up after treatment The greater likelihood of the involvement of resistant microorganisms in complicated UTIs is another feature of these infectious diseases. a full urodynamic assessment to appraise bladder function is to be carried out.Aminoglycoside + fluoroquinolone Antibiotics not recommended for empirical treatment Aminopenicillins.2: Antimicrobial treatment options for empirical therapy Antibiotics recommended for initial empirical treatment Fluoroquinolones Aminopenicillin plus a BLI Cephalosporin (Groups 2 or 3a) Aminoglycoside Antibiotics recommended for empirical treatment in case of initial failure. e. It is generally accepted that asymptomatic bacteriuria in patients with spinal cord injury should not be treated (26). A 7-day course could be a reasonable compromise. 4. Antimicrobial treatment options are summarised in Table 4.23). but is related more to the fact that patients with a complicated UTI tend to have recurrent infection (7). before and after the completion of the antimicrobial treatment. There is no superiority of one agent or class of antimicrobials in this group of patients. UPDATE MARCH 2011 31 . Priority is to ensure proper drainage of the bladder to protect the urinary tract. 4. but do not reduce complications (24). For further details. For symptomatic episodes of infection in patients with spinal cord injury. even in cases of intermittent catheterisation. Treatment durations that are too short as well as too long may cause the emergence of resistant strains. Currently. either during short-term catheterisation (< 30 days) or during long-term catheterisation.Aminoglycoside + BLI . amoxicillin. see the EAU guidelines on Neurogenic LUTS (25). For these reasons.5 Complicated UTIs associated with indwelling catheters Current data do not support the treatment of asymptomatic bacteriuria.

nih.htm Reid G. http://www.15 Suppl 1:S216-S227.nlm. Once-daily fleroxacin versus twice-daily ciprofloxacin in the treatment of complicated urinary tract infections. http://www. Gaynes RP.nih. 11.gov/pubmed/8005688 Stamm WE.6(4):428-42. http://www.nlm. http://www. MD: Drug Information Branch. pp.62(7):2998-3003.nlm. Bischoff W. Childs S. double-blind.100(6A):76S-82S.nlm.nih. 10.ncbi. Infectious Diseases Society of America and the Food and Drug Administration.11(3-4):189-96.nih. et al. Treatment of urinary tract infections: selecting an appropriate broadspectrum antibiotic for nosocomial infections.gov/pubmed/11302802 2.gov/pubmed/8678101 Frankenschmidt A. Basel: Karger. including the role of the microbiology laboratory.21(1):86-92. Woods GL. Infect Immun 1994 Jun. Andriole VT.ncbi. 13. Epidemiological features of complicated UTI in a district hospital of Kuwait. Naber KG.nih. http://www.gov/pubmed/15150185 Sahm DF.ncbi. Infectiology.4.329(18):1328-34.nlm. Clin Infect Dis 1995 Jul.nih. Multidrug-resistant urinary tract isolates of Escherichia coli: prevalence and patient demographics in the United States in 2000. Rockville. In: Bergan T.nlm. Clin Microbiol Rev 1993 Oct.nlm. Antimicrob Agents Chemother.gov/pubmed/10394969 Sharifi R. Germany: The European Society of Clinical Microbiology and Infectious Diseases. Management of urinary tract infections in adults.gov/pubmed/8413414 US Department of Health and Human Services.ncbi. http://www.gov/pubmed/9302150 Nicolle LE. Food and Drug Administration.5 1. Hooton TM.nlm. 9. Division of Communications Management. Unique ability of the Proteus mirabilis capsule to enhance mineral growth in infectious urinary calculi.nlm.ncbi. Vol 1. 2001 May. http://www.ncbi. J Urol 1984 Aug. J Antimicrob Chemother 2004 Jun. ed. J Urol 1997 Oct. Complicated urinary tract infections and pyelonephritis-developing antimicrobial drugs for treatment.45(5):1402-6. Holloway WJ. Am J Med 1996 Jun. 14. 32 UPDATE MARCH 2011 . Mulholland SG. Drugs 1997 Apr.nih.ncbi. Stauffer C.ncbi. References Rubin RH. Thornsberry C. Dobardzic R. Shapiro ED. 8.13(4):465-70.132(2):365-6.nlm. Eur J Epidemiol 1997 Jun. et al.53(4):583-92. http://www. http://www.nih.gov/pubmed/6376829 Dumanski AJ. Edin-Liljergen A. et al. Geckler RW. http://www. Hedelin H. 3. 19-26. 1998. 15.ncbi.gov/pubmed/10394974 Wells WG.53 Suppl 2:ii67-74.gov/pubmed/9258554 Emori TG. A multicenter comparative study of meropenem and imipenem/ cilastatin in the treatment of complicated urinary tract infections in hospitalized patients.gov/pubmed/8269394 Parsons CL. General guidelines for the evaluation of new anti-infective drugs for the treatment of UTI. Biofilms in infectious disease and on medical devices. http://www. Taufkirchen.gov/pubmed/1477233 Rubin RH.nih. Clin-Anti. 240-310. Complicated UTIs. et al. Mayfield DC.11 (3-4):223-6. Clin Infect Dis 1992 Nov. 1997.nlm.nlm. pp.fda. et al.nih.nih. 7.nih.nlm. 17.gov/pubmed/7578765 Dobardzic AM. 1993. Andriole VT. 12. An overview of nosocomial infections.ncbi.nih.ncbi. Geckler R.nih. 4. multicentre trials comparing ertapenem and ceftriaxone followed by an appropriate oral therapy. Evaluation of new anti-infective drugs for the treatment of urinary tract infection. Jiang Q. A practical guide to the management of complicated urinary tract infection. Matsumoto T. http://www.ncbi. Center for Drug Evaluation and Research (CDER). Int J Antimicrob Agents 1999 May. Effect of ammonium on bacterial adherence to bladder transitional epithelium. Treatment of complicated urinary tract infection in adults: combined analysis of two randomized. Shapiro ED.gov/pubmed/9098661 Cox CE.gov/cder/guidance/2559dft.158(4):1494-9. Naber KG. Kumazawa J. et al. Int J Antimicrob Agents 1999 May.ncbi.nlm. N Engl J Med 1993 Oct. http://www.ncbi. Guidance for Industry. 16. 6. Experience with the new guidelines on evaluation of new anti-infective drugs for the treatment of urinary tract infections. UTIs. 5. et al. http://www. with modifications by a European Working Party. http://www.

J Urol 1991 Jun.nlm. Management of complicated urinary tract infection in older patients.ncbi.15(3):194-204. hyperleukocytosis or leukopenia. et al. Nicolle LE.nih. Carson C.ncbi. Severe sepsis is defined by the presence of symptoms of organ dysfunction. Most nosocomial urosepsis can be avoided by measures used to prevent nosocomial infection.nih.ncbi. Seeberg S. January 27-29. GR: A).g. GR: B). http://www. Infection (urease) stones. 20. Sepsis is diagnosed when clinical evidence of infection is accompanied by signs of systemic inflammation (fever or hypothermia. http://www. appropriate and prompt antibiotic therapy. sepsis or severe sepsis.13(4):278-85. tachypnoea). Blok B. hydrocortisone. The prevention and management of urinary tract infections among people with spinal cord injuries. Williams N. Scand J Infect Dis 1975.gov/pubmed/1984100 Alling B. JAMA 1982 Jul.nih. http://www. Miner Electrolyte Metab 1987. tachycardia. The fate of residual fragments after extracorporeal shock wave lithotripsy monotherapy of infection stones. Lerner SA.18. avoidance of unnecessary urethral catheterisation. 23.gov/pubmed/15200349 Griffith DP. reduction of hospital stay.1 SEpSIS SYNDROME IN UROLOgY (UROSEpSIS) Summary and recommendations Patients with urosepsis should be diagnosed at an early stage. Osborne CA. recombinant activated protein C) and the optimal management of urinary tract disorders (LE: 1a. 22. is recognised as the first event in a cascade to multi-organ failure. UPDATE MARCH 2011 33 .gov/pubmed/809837 Warren JW.g. known as SIRS (fever or hypothermia. Cephalexin for susceptible bacteriuria in afebrile. ed. Effect of consecutive antibacterial therapy on bacteriuria in hospitalized geriatric patients. The systemic inflammatory response syndrome. 26. Drugs 2004. 24. Price S. 1992.ncbi.nih.nlm.nlm. correct use of closed catheter systems. Naber KG. 19.nih. http://www. especially in the case of a complicated UTI. 21.56(1):81-8. sympathomimetic amines.gov/pubmed/19403235 National Institute on Disability and Rehabilitation Research. et al. http://www.nlm. Microbiological studies of fosfomycin trometamol against urinary isolates in vitro. pp. The treatment of urosepsis calls for the combination of adequate life-supporting care. depending on localised or systemic extension.ncbi. 121-129. Role of fluoroquinolones in the treatment of serious bacterial urinary tract infections. although the prognosis of urosepsis is globally better than that of sepsis from other infectious sites. et al.7(3):201-7. tachypnoea. 25. long term catheterized patients. and septic shock by the presence of persistent hypotension associated with tissue anoxia.248(4):454-8. tachycardia. and attention to simple daily asepsis techniques to avoid cross-infection (LE: 2a. e.nih. The drainage of any obstruction in the urinary tract is essential as first-line treatment (LE: 1b. Mortality is considerably increased when severe sepsis or septic shock are present. Riehle RA Jr. J Am Paraplegia Soc 1992 Jul. leukocyturia or leukopenia). blood glucose control. 2a. 2009 Jul.gov/pubmed/3306321 Beck EM. GR: A). adjunctive measures (e.nlm.ncbi.nlm. EAU Guidelines on Neurogenic Lower Urinary Tract Dysfunction.gov/pubmed/8856005 Stöhrer M. Anthony WC. National Institute on Disability and Rehabilitation Research Consensus Statement.nlm. Basel: Karger.ncbi.ncbi.145(1):6-9. http://www.44(10):1235-41. GR: B). Castro-Diaz D. 5.nih. Hoopes JM.nih.2 Background UTIs can manifest as bacteriuria with limited clinical symptoms. 1988. 5.64(12):1359-73. http://www. Norman DC.gov/pubmed/7045440 Yoshikawa TT. Brandberg A. early removal of indwelling urethral catheters. Eur Urol. J Am Geriatr Soc 1996 Oct. Kulkarni S. In: New trends in urinary tract infections. Urologists are recommended to treat patients in collaboration with intensive care and infectious diseases specialists (LE. Urosepsis is seen in both community-acquired and healthcare associated infections. http://www.nlm.gov/pubmed/1500945 5.

Systolic blood pressure < 90 mmHg or a reduction of > 40 mmHg from baseline in the absence of other causes of hypotension. pancreatitis.7% per year (1). In urosepsis.9% during 1995-2000) (4). Bacteria present in blood as confirmed by culture. physical examination. which should prompt urologists and intensive care specialists to search for and treat infection. Sepsis associated with organ dysfunction. 5. as in sepsis but may be non-infectious in aetiology (e. sonographic and radiological features.000 cells/mm3 or < 4. or endoscopic manoeuvres. • Septic shock is persistence of hypoperfusion or hypotension despite fluid resuscitation. burns. Response to a wide variety of clinical insults. or nonseptic shock) (5). oliguria or acute alteration of mental status. the rate of sepsis due to fungal organisms has increased while Grampositive bacteria have become the predominant pathogen in sepsis. For therapeutic purposes. patients receiving cancer chemotherapy or corticosteroids. or pancreatitis). The following definitions apply (Table 5.WBC > 12.6) Disorder Infection Bacteraemia Systematic inflammatory response syndrome (SIRS) Definition Presence of organisms in a normally sterile site that is usually.000 cells/mm3 or > 10% immature (band) forms Activation of the inflammatory process due to infection. such as urinary tract calculi. • Severe sepsis is sepsis associated with organ dysfunction.Severe sepsis is a severe situation with a reported mortality rate of 20-42% (1). and laboratory data. all patients can be affected by bacterial species that are capable of inducing inflammation within the urinary tract. congenital uropathy. Globally (this is not true for urosepsis). the diagnostic criteria of sepsis should identify patients at an early stage of the syndrome.Respiratory rate > 20 breaths/min or PaCO2 < 32 mmHg (< 4. and monitor for organ failure and other complications. • Refractory septic shock is defined by an absence of response to therapy. diabetics. Hypoperfusion and perfusion abnormalities may include but are not limited to lactic acidosis.8% to 17. such as bacteriuria and leukocyturia. such as transplant recipients. and patients with AIDS.1): • Sepsis is a systemic response to infection.g.3 kPa) . which suggests improved management of patients (total in-hospital mortality rate fell from 27. apply appropriate therapy.g. Many other clinical or biological symptoms must be considered. but the associated mortality has decreased. Patients who are more likely to develop urosepsis include: elderly patients. This systemic response is manifested by two or more of the following conditions: . May be transient. which can be infectious.Heart rate > 90 bpm . with UTIs accounting for only 5% (2). The symptoms of SIRS which were initially considered to be ‘mandatory’ for the diagnosis of sepsis (5). the incidence of sepsis has increased by 8. Most severe sepsis reported in the literature is related to pulmonary (50%) or abdominal (24%) infections. Moreover. However. even if Gram-negative bacteria remain predominant in urosepsis. Sepsis Hypotension Severe sepsis 34 UPDATE MARCH 2011 . the severity depends mostly upon the host response. as in other types of sepsis.3 Definition and clinical manifestation of sepsis in urology The clinical evidence of UTI is based on symptoms. but not necessarily. Urosepsis also depends on local factors. it is now recognized that SIRS may be present without infection (e.Temperature > 38°C or < 36°C . burns. are now considered to be alerting symptoms (6). accompanied by an inflammatory host response. In recent years.1: Clinical diagnostic criteria of sepsis and septic shock (5. Table 5. hypoperfusion or hypotension. neurogenic bladder disorders. Sepsis is more common in men than in women (3). obstruction at any level in the urinary tract. immunosuppressed patients.

during severe viral infections or inflammatory reactions of non-infectious origin. Other cytokines are involved such as interleukins (ILs). the condition develops in compromised patients (e. Refractory septic shock 5. cytokines change their behaviour in the inflammatory response. those with diabetes or immunosuppression). In contrast.4. An immunosuppressive phase follows the initial pro-inflammatory mechanism. • Prudent use of antimicrobial agents for prophylaxis and treatment of established infections. but is devoid of hormonal activity. oliguria. Septic shock that lasts for > 1 h and does not respond to fluid administration or pharmacological intervention.1 Preventive measures of proven or probable efficacy (9. with typical signs of generalised sepsis associated with local signs of infection. the pathogens have to reach the bloodstream. • Reduction in hospital stay. haematogenous. in response to various infectious stimuli. They are released from various cells including monocytes.and anti-inflammatory responses is modified in severe sepsis. In such a situation. P. Patients who are on inotropic or vasopressor agents may not be hypotensive at the time that perfusion abnormalities are measured. IL-1.2 Procalcitonin is a potential marker of sepsis Procalcitonin is the propeptide of calcitonin. Normally. They are peptides that regulate the amplitude and duration of the host inflammatory response. Sepsis initiates the cascade that progresses to severe sepsis and then septic shock in a clinical continuum. and appropriate antibiotic therapy (2). Most commonly. aeruginosa and Serratia sp. High procalcitonin levels. or both. or acute alteration in mental status. For urosepsis to be established. E. such as methicillin-resistant Staphylococcus aureus (MRSA). Some microorganisms are multiresistant. and therefore difficult to treat. The exact site of procalcitonin production during sepsis is not known. it is recommended that urologists collaborate with intensive care and infectious disease specialists for the best management of the patient. to avoid selection of resistant strains.1 Cytokines as markers of the septic response Cytokines are involved in the pathogenesis of sepsis syndrome. macrophages and endothelial cells. The risk of bacteraemia is increased in severe UTIs. levels are undetectable in healthy humans.Septic shock Sepsis with hypotension despite adequate fluid resuscitation along with the presence of perfusion abnormalities that may include.g. but are not limited to lactic acidosis. A fatal outcome is described in 20-40% of all patients. During severe generalised infections (bacterial.10) The most effective methods to prevent nosocomial urosepsis are the same as those used to prevent other nosocomial infections: • Isolation of all patients infected with multi-resistant organisms to avoid cross-infection. Procalcitonin monitoring may be useful in patients likely to develop a SIRS of infectious origin. 5. such as pyelonephritis and acute bacterial prostatitis. Urosepsis treatment calls for a combination of treatment of the cause (obstruction of the urinary tract).8). 5. some bacterial strains can be resistant to quinolones or third-generation cephalosporins. The complex balance between pro. When they become bound to specific receptors on other cells. Sepsis may indicate an immune system that is severely compromised and unable to eradicate pathogens or a nonregulated and excessive activation of inflammation. Tumour necrosis factor (TNF)-α. or an abrupt increase in levels in these patients. Genetic predisposition is a probable explanation of sepsis in several patients. 5. It is well known that long inpatient periods before surgery lead to a greater UPDATE MARCH 2011 35 . IL-6 and IL-8 are cytokines that are associated with sepsis. procalcitonin levels show only a moderate or no increase. adequate life-supporting care. 5. procalcitonin levels may rise to > 100 ng/mL. and is facilitated by obstruction of the urinary tract. Mechanisms of organ failure and death in patients with sepsis remain only partially understood (2).4 physiology and biochemical markers Microorganisms reach the urinary tract by way of the ascending.5 prevention Septic shock is the most frequent cause of death for patients hospitalised for community-acquired and nosocomial infection (20-40%). parasitic and fungal) with systemic manifestations.5. coli remains the most prevalent microorganism. should prompt a search for the source of infection. In several countries. Antibiotic agents should be chosen according to the predominant pathogens at a given site of infection in the hospital environment. Procalcitonin may be useful in differentiating between infectious and non-infectious causes of severe inflammatory status (7.4. or lymphatic routes.

which reduces the incidence of bacteriuria only for a few days and increases the risk of infection with multi-resistant bacteria (9. 5. see Section 15. 5. The potential side effects of antibiotics must be considered before their administration in a prophylactic regimen.5.2 Appropriate perioperative antimicrobial prophylaxis For appropriate perioperative antimicrobial prophylaxis. Early removal of indwelling urethral catheters. Ineffective or counterproductive measures Continuous or intermittent bladder irrigations with antibiotics or urinary antiseptics that increase the risk of infection with resistant bacteria (9. frequent hand disinfection. Attention to simple everyday techniques to assure asepsis. blood . adjunctive sepsis therapy. 5. as soon as allowed by the patient’s condition. Early goal directed therapy + Empirical antibiotic therapy 2.analysis/culture) 1.6 Algorithm for the management of urosepsis Figure 5.g. Use of closed catheter drainage and minimisation of breaks in the integrity of the system. Nosocomial UTIs are promoted by bladder catheterisation as well as by ureteral stenting (11). Use of least-invasive methods to release urinary tract obstruction until the patient is stabilised.1: Clinical algorithm for the management of urosepsis 6h 1h Clinical status indicative for severe sepsis yes SIRS criteria positive yes no Observation Observation no General ward Initial oxygen + fluid resuscitation High dependency unit Microbiology (urine. Antibiotic prophylaxis does not prevent stent colonisation. Routine administration of antimicrobial drugs to catheterised patients. if necessary Supportive.• • • • incidence of nosocomial infections. including the routine use of protective. and using infectious disease control measures to prevent cross-infections.5. for urine sampling or bladder wash-out. Early goal directed therapy + Empirical antibiotic therapy 2. Its use may be reserved for immunosuppressed patients. e.5. if necessary 36 UPDATE MARCH 2011 . Imaging Signs and symptoms indicative for urosepsis yes 1.4 • • Preventive measures of debatable efficacy Instillation of antibiotic or antiseptic drugs into catheters and drainage bags. disposable gloves. Use of urinary catheters coated with antibiotics or silver.12).3 • • 5.12). which appears in 100% of patients with a permanent ureteral stent and in 70% of those temporarily stented. Imaging Complicating factor in urogenital tract yes Source control no Transfer to alternative department no Supportive. adjunctive sepsis therapy.

1 and 16.2 Relief of obstruction Drainage of any obstruction in the urinary tract and removal of foreign bodies. and providing sufficient oxygen transport capacity are highly effective. These are key components of the strategy. Early intervention with appropriate measures to maintain adequate tissue perfusion and oxygen delivery by prompt institution of fluid therapy. The dosage of the antibiotic substances is of paramount importance in patients with sepsis syndrome and should generally be high. Glucocorticosteroids 3. 5.7. respiration 1. Activated protein C 2. Intensified insulin therapy 8-12 mmHg 65-90 mmHg > 70% > 30 % > 40 mL/h 5.5. Recombinant activated protein C (dotrecogin α) is a new drug that has been approved for therapy of severe sepsis since November 2002.2. The antibacterial treatment options are summarised in Appendix 16. stabilisation of arterial pressure.7 5. Airways. ‘Surviving Sepsis Guidelines’. Early recognition of the symptoms may decrease the mortality by timely treatment UPDATE MARCH 2011 37 . Antimicrobials must be administered not later than 1 h after clinical assumption of sepsis (see algorithm).3: Levels of therapy in sepsis Levels of therapy in sepsis Causal therapy Supportive therapy Adjunctive therapy 1.7.7. aimed at reducing mortality by 25% in the next few years has been published recently (18). A recent campaign. should lead to resolution of symptoms and recovery. Source control 1. 5. Antimicrobial treatment 2.7.13) The management of fluid and electrolyte balance is a crucial aspect of patient care in sepsis syndrome. as assessed by Acute Physiology and Chronic Health Evaluation (APACHE) II scores > 25 or dysfunction of more than two organs (17). such as urinary catheters or stones. The best strategy has been summarised and graded according to a careful evidence-based methodology in the recently published ‘Surviving Sepsis Guidelines’ (18).4 Adjunctive measures (12. This expensive treatment has been proven to be more effective in patients with more severe disease. Volaemic expansion and vasopressor therapy have a considerable impact on the outcome. The use of human albumin is debatable. Hydrocortisone (with a debate on dosage) is useful in patients with relative insufficiency in the pituitary gland-adrenal cortex axis (adrenocorticotropin test) (15). Tight blood glucose control by administration of insulin doses up to 50 U/h is associated with a reduction in mortality (16). with the exception of patients in renal failure.3 Antimicrobial therapy Empirical initial treatment should provide broad antimicrobial coverage and should later be adapted on the basis of culture results.1 Treatment Clinical algorithm for management of urosepsis Table 5. Early goal-directed therapy has been shown to reduce mortality (14).8 Conclusion Sepsis syndrome in urology remains a severe situation with a mortality rate as high as 20-40%. 5. Haemodynamic stabilisation 2. particularly when the clinical course is complicated by shock. This condition is an absolute emergency.2: Early goal directed therapy Early goal directed therapy Central venous pressure (CVP) Mean arterial pressure (MAP) Central venous oxygen (CVO2) Haematocrit (HKT) Urine output Table 5.

nlm.gov/pubmed/1580035 Glück T.nlm. severe sepsis and septic shock.177(4):287-90.39(5): 443-5. http://www. Havstad S. The ACCP/SCCM Consensus Conference Committee.nlm.nlm. N Engl J Med 2001 Nov. http://www. Eaton S. References Martin GS.nih. and interleukin-8 in critically ill patients admitted with suspected sepsis. Evaluation of a urinary catheter with a preconnected closed drainage bag. 15. http://www.ncbi. Wegscheider K.nlm.ncbi.ncbi.10 1.nih. 9. Wouters P.288(7):862-71.164(3):396-402.ncbi. or urolithiasis. Intensive insulin therapy in the critically ill patients.31(4):1250-6. N Engl J Med 2001 Nov.ncbi. (Guideliness for prevention of nosocomial infections in intensive care unit.nlm. Am J Respir Crit Care Med 2001 Aug. 5.) Arnette Ed Paris 1994:41-53. obstruction. et al. http://www. France. et al.nlm. http://www. http://www.g. The prevention of sepsis syndrome is dependent on good practice to avoid nosocomial infections and using antibiotic prophylaxis and therapy in a prudent and well-accepted manner. Suppl. Urinary tract infections in the critically ill patient with a urinary catheter. 5. 16.gov/pubmed/3343502 Persky L.nlm. Intensive Care Med 2000 Mar. Nguyen B. 12. Charpentier C. Holeckova K.gov/pubmed/18470710 Harbarth S. 8. Sebille V. Pinton P. Urology 1992 May.nih.ncbi.nih. Advances in sepsis therapy.30(4):580-8. Diagnostic value of procalcitonin. Bare RL. 7. Balk RA. et al.ncbi. et al. http://www. 38 UPDATE MARCH 2011 . Drugs 2004. http://www.of urinary tract disorders.26. Jones JM.nlm. 4. http://www.nih.345(19):1368-77.ncbi. et al. Meshaka P. Gottot S. [article in French] Riedl CR. 11.gov/pubmed/12700374 Hotchkiss RS. Karl IE. 6.36(1):53-9. Adequate life-support measures and appropriate antibiotic treatment provide the best conditions for improving patient survival. et al. Intensive Care Med 2004 Apr. Marshall JC. Yangco B. American College of Chest Physicians/Society of Critical Care Medicine.gov/pubmed/15059039 Rivers E.9(2):72-6. e. The epidemiology of sepsis in the United States from 1979 through 2000.nih. http://www. et al. Opal SM.gov/pubmed/12682500 Brunkhorst FM.gov/pubmed/14997295 Bone RC. Meredith JW. Infect Control Hosp Epidemiol 1988 Feb. Carlet. Early Goal-Directed Therapy Collaborative Group. Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock.64(8):837-59. Head of Intensive Care. 2001 SCCM/ESICM/ACCP/ ATS/SIS International Sepsis Definitions Conference.gov/pubmed/1303622 Levy MM.ncbi. 13. 14. JAMA 2002 Aug.nlm.345(19):1359-67. EPISEPSIS: a reappraisal of the epidemiology and outcome of severe sepsis in French intensive care units. Froidevaux C.gov/pubmed/11794169 Annane D. http://www. Liesen D. 5.gov/pubmed/12519925 Rosser CJ.gov/pubmed/11794168 2. Guse R.nlm. Procalcitonin for early diagnosis and differentiation of SIRS. Definitions for sepsis and organ failure and guidelines for the use of innovative therapies in sepsis.nih. et al. Hôpital Saint Joseph. Am J Surg 1999 Apr. http://www. N Engl J Med 2003 Jan. Cerra FB. Paris. Weekers F.gov/pubmed/10326844 Brun-Buisson C. sepsis.nih. EPISEPSIS Study Group.nlm. Mannino DM. http://www. et al. Forycki ZF. Fink MP. 10.9 Acknowledgements The authors are thankful to Jean M. 3. Geneva Sepsis Network. Eur Urol 1999. et al.gov/pubmed/11500339 Carlet J.nlm.101(6):1644-55. interleukin-6. Dumay MF. N Engl J Med 2003 Apr.ncbi.ncbi. http://www.ncbi.nih. The pathophysiology and treatment of sepsis.nih. Hübner WA.nlm. Reduced urosepsis in a veterans’ hospital. Early goal-directed therapy in the treatment of severe sepsis and septic shock.nih. et al.gov/pubmed/12186604 van den Berghe G.ncbi.nih.348(2): 138-50.2:S148-52 . Chest 1992 Jun.nih.nih. http://www. Plas E.ncbi.nlm.nih.gov/pubmed/10364656 DeGroot-Kosolcharoen J. SCCM/ESICM/ACCP/ATS/SIS. for reviewing this manuscript on urosepsis. Bacterial colonization of ureteral stents.ncbi. Crit Care Med 2003 Apr.348(16):1546-54.

the Asian Association of UTI/STD. suprapubic catheters. therefore. Surviving Sepsis Campaign guidelines for management of severe sepsis and septic shock. and gave preference to the Cochrane Central Register of Controlled Trials. Recombinant Human Protein C Worldwide Evaluation in Severe Sepsis (PROWESS) study group. Routine urine culture in an asymptomatic catheterised patient is also not recommended (GR: C) because treatment is in general not necessary. only the abstract and a summary of the recommendations are presented here. give a close-to-evidence-based guideline for all medical disciplines.1 Abstract We surveyed the extensive literature regarding the development. Studies were identified through a PubMed search. Carlet JM. rating them on the basis of their quality. http://www. 6. the following text presents the findings of a comprehensive update produced as a collaborative effort by the ESIU (a full EAU section office). We systematically searched for meta-analyses of randomised controlled trials available in Medline. and the International Society of Chemotherapy for Infection and Cancer. The use of nurse-based or electronic reminder systems to remove unnecessary catheters can decrease the duration of catheterisation and the risk of CAUTI (LE: 2a). A minority of patients can be managed with the use of the non-return (flip) valve catheters. Vincent JL. While the catheter is in place. Since the complete document is available online. Further organisms tend to be acquired by patients who are catheterised for > 30 days. The survey found that the urinary tract is the commonest source of nosocomial infection. thus avoiding the closed drainage bag.nlm. usually with broad-spectrum antibiotics based on local susceptibility patterns (GR: C). CATHETER-ASSOCIATED UTIs Based on the EAU guidelines published in 2007 (ISBN-13:978-90-70244-59-0). 18. Bernard GR. et al. no recommendation can be made (GR: C). Antibiotic treatment is recommended only for symptomatic infection (GR: B). therapy and prevention of catheter-associated UTIs (CAUTIs).ncbi. This text was recently published as “The European and Asian guidelines on management and prevention of catheter-associated urinary tract infections” (1). systemic antimicrobial treatment of asymptomatic catheter-associated bacteriuria is not recommended (GR: A).nih. There are sparse data about antibiotic prophylaxis in patients on long-term catheterisation. condom drainage systems and intermittent catheterisation are each preferable to indwelling urethral catheterisation (GR: B). Healthcare workers should be constantly aware of the risk of cross-infection between catheterised patients. et al. Laterre PF. http://www. rated according to a modification of the US Department of Health and Human Services (1992).17. with special emphasis on urology. and also considered other relevant publications. The drainage bag should be always kept below the level of the bladder and the connecting tube (GR: B).gov/pubmed/15090974 6. except for some special cases. the Urological Association of Asia. In case of short-term catheterisation. the Federation of European Societies for Chemotherapy and Infection. the Western Pacific Society for Chemotherapy. particularly when the bladder is catheterised (LE: 2a). They should observe protocols on hand washing and the need to use disposable gloves (GR: A). Antibiotic irrigation of the catheter and bladder is of no advantage (GR: A). Clinicians should always consider alternatives to indwelling urethral catheters that are less prone to causing symptomatic infection. Surviving Sepsis Campaign Management Guidelines Committee. in which catheter care is an important issue. Efficacy and safety of recombinant human activated protein C for severe sepsis.nih. The clinician should be aware of two priorities: the catheter system should remain closed and the duration of catheterisation should be minimal (GR: A). UPDATE MARCH 2011 39 .ncbi. The recommendations of the studies. Masur H. Crit Care Med 2004 Mar. N Engl J Med 2001 Mar. Patients with urethral catheters in place for > 10 years should be screened annually for bladder cancer (GR: C). After initiation of empirical treatment. routine antibiotic prophylaxis is not recommended (GR: B). the choice of antibiotics might need to be adjusted according to urine culture results (GR: B). routine prophylaxis with systemic antibiotics is not recommended (GR: B).32:858-73. For patients using intermittent catheterisation.gov/pubmed/11236773 Dellinger RP. The most important risk factor for the development of catheter-associated bacteriuria is the duration of catheterisation (LE: 2a). Such patients may exchange the convenience of on-demand drainage with an increased risk of infection.344(10):699-709. In appropriate patients. Most CAUTIs are derived from the patient’s own colonic flora (LE: 2b) and the catheter predisposes to UTI in several ways. Long-term antibiotic suppressive therapy is not effective (GR: A). Most episodes of short-term catheter-associated bacteriuria are asymptomatic and are caused by a single organism (LE: 2a).nlm.

they cannot be recommended routinely. 14. Urine. The catheter system should remain closed. 17. The duration of catheterisation should be minimal. therefore. 2. but removal of the catheter or stent should be considered. In case of asymptomatic candiduria. systemic antimicrobial treatment of asymptomatic catheterassociated bacteriuria is not recommended. but must be changed before blockage is likely to occur. 20. 12. Written catheter care protocols are necessary. antibiotic therapy should be adjusted according to pathogen B sensitivity. neither systemic nor local antifungal therapy is indicated. 21. and in septic patients. Febrile episodes are only found in < 10% of catheterised patients living in a long-term facility. 22. Routine urine culture in asymptomatic catheterised patients is not recommended. 4. B B B 6. 11. Therefore. B C A Treatment 18. Diagnostics 15. B Prevention 7. Antibiotic-impregnated catheters may decrease the frequency of asymptomatic bacteriuria within 1 week. 10. 23. 40 UPDATE MARCH 2011 . A A A A B B Long-term indwelling catheters should be changed at intervals adapted to the individual patient. A B 13. urethra or meatus are not recommended. There was some evidence of reduced risk for symptomatic UTI. A 19. broad-spectrum antibiotics should be given based on local susceptibility patterns. While the catheter is in place. Silver alloy catheters significantly reduce the incidence of asymptomatic bacteriuria. A/C B B C After culture results are available. however. except in certain circumstances. For empirical therapy. Antimicrobial treatment is recommended only for symptomatic infection. Benefits from prophylactic antibiotics and antiseptic substances have never been established.2 Summary of recommendations gR* B A Recommendation General aspects 1. 8. The drainage bag should always be kept below the level of the bladder and the connecting tube. no evidence that they decrease symptomatic infection. An indwelling catheter should be introduced under antiseptic conditions.6. there is no evidence for the exact intervals of changing catheters. Catheter insertion and choice of catheter 3. Urethral trauma should be minimised by the use of adequate lubricant and the smallest possible catheter calibre. especially before traumatic urinary tract interventions. they are not recommended. There is. Topical antiseptics or antibiotics applied to the catheter. however. It is therefore extremely important to rule out other sources of fever. Removal of the indwelling catheter after non-urological operation before midnight might be beneficial. also blood for culture must be taken before any antimicrobial therapy is started. In case of symptomatic CAUTI. Health care workers should observe protocols on hand hygiene and the need to use disposable gloves between catheterised patients. 16. they may be useful in some settings. it might be reasonable to replace or remove the catheter before starting antimicrobial therapy if the indwelling catheter has been in place for > 7 days. but only for < 1 week. 9. Chronic antibiotic suppressive therapy is generally not recommended. 5. Therefore.

25.g. It has been suggested that 5% of schoolgirls and up to 0. Patients with urethral catheters in place for > 10 years should be screened for bladder cancer.1 UTIs IN CHILDREN Summary and recommendations UTI in children is a frequent health problem.1% in boys. In case of candiduria associated with urinary symptoms.8% in preschool boys and girls (3). systemic therapy with antifungals is indicated. Although rare.2 Background The urinary tract is a common source of infection in children and infants. which requires dialysis treatment in a significant number of adults (2) (LE: 2a). renal damage and even chronic renal failure.31S: S68-S78. hospital admission is required and parenteral antibiotics are given initially (GR: A). et al. It represents the most common bacterial infection in children < 2 years of age (1) (LE: 2a).4% in neonates.7% in boys and 2. B C Alternative drainage systems 26.24. Surgical re-implantation or endoscopic treatment is reserved for the small number of children with breakthrough infection (GR: B). Delayed sequelae related to renal scarring include hypertension.5% of schoolboys undergo at least one episode of UTI during their school life. but in early infancy. vesicoureteric reflux (VUR) and dysfunctional voiding. 27.3% in infants < 3 months of age. it can progress to renal scarring. with the incidence only a little lower than that of upper respiratory and digestive infections. C *GR = grade of recommendation 6. Investigation should be undertaken after two episodes of UTI in girls and one in boys (GR: B). after which the incidence changes. Int J Antimicrob Agents 2008.3 1. intrarenal reflux and VUR. For treatment of UTI in children.pdf [Access date February 2011] 7. UTI is more common in boys (3. The objective is to rule out the unusual occurrence of obstruction.ischemo. renal scarring may lead to severe long-term complications such as hypertension and chronic renal failure. There is little evidence to suggest that antibiotic prophylaxis decreases bacteriuria in patients using intermittent catheterisation. http://www. 7. C B B Long-term follow up 29. No recommendation can be made. In appropriate patients. and 0. proteinuria.4). The incidence of UTI varies depending on age and sex. European and Asian guidelines on management and prevention of catheter-associated urinary tract infections. The overall recurrence rate for the neonatal period has been reported to be 25% (3. Chronic pyelonephritic renal scarring develops very early in life due to the combination of a UTI. 28. Elderly female patients may need treatment if bacteriuria does not resolve spontaneously after catheter removal.8% in girls aged < 6 months.7-1. 7. when it is more common in boys. UPDATE MARCH 2011 41 . mostly the first 3 months. short courses are not advised and therefore treatment is continued for 5-7 days and longer (GR: A). as caused by a neuropathic disorder.2-0. The incidence of asymptomatic bacteriuria is 0. VUR is treated with long-term prophylactic antibiotics (GR: B). The outcome of a UTI is usually benign. it is not recommended. The risk of UTI during the first decade of life is 1% in males and 3% in females (3). Reference Tenke P.14% in neonates. condom drainage system or intermittent catheter is preferable to an indwelling urethral catheter. a suprapubic. If the child is severely ill with vomiting and dehydration. The clinical presentation of UTI in infants and young children can vary from fever to gastrointestinal and lower or upper urinary tract symptoms. Kovacs B. Bjerklund Johansen TE. 0. The incidence of symptomatic bacteriuria is 0. There is limited evidence that postoperative intermittent catheterisation reduces the risk of bacteriuria compared with indwelling catheters. Paediatric UTI is the most common cause of fever of unknown origin in boys aged < 3 years.7-3. The incidence is different for children < 3 months of age. In the first year of life.7%) than in girls (2%). It sometimes arises in utero due to dysplasia. being 3% in girls and 1.org/abstracts/TenkeIJAA2008. therefore. with a further increase to 0. or if candiduria is the sign of systemic infection. especially when associated with congenital anomalies of the urinary tract. e.

intrarenal reflux and UTI. or VUR). The link between renal damage and UTIs is controversial. In the first weeks of life. Recurrent UTI may be subclassified into three groups (8): • Unresolved infection: subtherapeutic level of antimicrobial. ureteropelvic junction obstruction or non-obstructive urinary stasis (e. and vary with the age of the child and the severity of the disease. Neuropathic bladder dysfunction (e. Later on in childhood. such as vomiting and diarrhoea. spina bifida. Dysfunctional voiding in an otherwise normal child may result in infrequent bladder emptying aided by delaying manoeuvres. e. A wide variety of congenital urinary tract abnormalities can cause UTIs through obstruction. Almost certainly.g.7. Epididymoorchitis is extremely unusual. Gram-positive bacteria (particularly enterococci and staphylococci) represent 5-7% of cases. a UTI may present with gastrointestinal signs. urethral valves. testicular torsion has to be considered. 7. frequent voiding.6% of patients with fever have a UTI (14). From the clinical point of view.5 Signs and symptoms Symptoms are non-specific. The mechanism in obstructive nephropathy is self-evident. Surgical correction or medical treatment for urinary dysfunction may be needed. or sphincter dyssynergia) may lead to postvoid residual urine and secondary VUR (4). abdominal or lumbar pain may appear with or without fever. crossing legs.4 pathogenesis and risk factors The urinary tract is a sterile space with an impermeable lining. coli that express P fimbriae. A UTI in neonates may be non-specific and with no localisation. • Bacterial persistence: may be due to a nidus for persistent infection in the urinary tract. • Reinfection: each episode is a new infection acquired from periurethral. malabsorption.10) (LE: 2a). Rarely. e. severe and simple forms of UTIs should be differentiated because to some extent the severity of symptoms dictates the degree of urgency with which investigation and treatment are to be undertaken (Table 7. prune belly syndrome. non-compliance with treatment.g. the necessary components include VUR. but more subtle changes occur when there is VUR.1: Clinical classification of UTIs in children Severe UTI Fever > 39°C Persistent vomiting Serious dehydration Poor treatment compliance Simple UTI Mild pyrexia Good fluid intake Slight dehydration Good treatment compliance 42 UPDATE MARCH 2011 . the presence of bacteriuria seems irrelevant to the progression of existing scars or the very unusual formation of new scars. sitting on heels (12). Nosocomial infection and involvement as part of a systemic infection are less common (8).6 Classification UTIs may be classified as a first episode or recurrent. such as Klebsiella. Of these. Phimosis predisposes to UTI (9. but later on. More mundane but significant causes of UTIs include labial adhesion and chronic constipation (7). perineal or rectal flora. 7. although the role of this bacterium is still debatable (7).g. Signs of UTI may be vague in small children. glandular surface and the distal urethra. Among these bacteria are strains of E. which adhere to the inner layer of the preputial skin and to uroepithelial cells (11). Groups A and B streptococci are relatively common in newborn infants (6). resistant pathogens. saprophyticus in UTIs in children.g. coli is responsible for 90% of UTI episodes (5).3 Aetiology The common pathogenic sources are Gram-negative. There is an increasing trend towards the isolation of S. Serratia and Pseudomonas sp.1). Enterobacteria derived from intestinal flora colonise the preputial sac. Retrograde ascent is the most common mechanism of infection. E. or according to severity (simple or severe). Table 7. dysuria and suprapubic. 13. bacteria. when they are older than 2 years. In small children. 7. mainly enteric. With scrotal pain and inflammation. Hospital-acquired infections show a wider pattern of aggressive bacteria. Obstruction and dysfunction are among the most common causes of urinary infection. septic shock is the presentation. These must all work together in early childhood when the growing kidney is likely to be susceptible to parenchymal infection. Another confounding factor is that many so-called scars are dysplastic renal tissue which develop in utero (13).

A positive urine culture is defined as the presence of > 100. To obtain a urine sample in the best condition in children < 2 years of age (girls and uncircumcised boys without sphincteric control).1 Suprapubic bladder aspiration Suprapubic bladder aspiration is the most sensitive method. labial adhesion.000 and 50.000-50. In these cases.2. it is better to use suprapubic bladder aspiration or bladder catheterisation. In older children with sphincteric control. diuresis. 7. and moderate or severe dehydration. such a child should be managed as one with a severe UTI.7.1.000 cfu/mL.6. 7.1. nitrites or other biochemical markers (15).2. Urine must be obtained under bacteriologically reliable conditions when undertaking a urine specimen culture (16). when the urine is obtained by bladder catheterisation.7.1. and method of storage and transport of the specimen (15). and different methods are advised because there is a high risk of contamination (17. The classical definition of significant bacteriuria of > 105 cfu/mL is still used and depends on the clinical environment (15. but is able to take fluids and oral medication. there was a mixed growth pattern suggesting contamination. When a low level of compliance is expected. 7.19).7. The collection of MSU or in a collecting bag of >105 cfu/mL is considered positive (16) (Table 7. hairy patch on the sacral skin. and stigmata of spina bifida.g.3 Plastic bag attached to the genitalia Prospective studies have shown a high incidence of false-positive results.000 cfu/mL > 104 cfu/mL with symptoms >105 cfu/mL without symptoms Urine specimen from bladder catheterisation Urine specimen from midstream void UPDATE MARCH 2011 43 . the feeling of being ill. The child is only slightly or not dehydrated and has a good expected level of compliance. epididymo-orchitis.2 Simple UTI A child with a simple UTI may have only mild pyrexia. 7.15). persistent vomiting.7. ranging from 85 to 99% (8. such as pyuria.18). MSU collection is possible and reliable (18).7. Table 7.2. even though there is the risk of introduction of nosocomial pathogens (8.2. 7. It is helpful when the culture is negative (8. the urine culture is considered positive with > 104 cfu/mL.000 cfu/mL of one pathogen. Even though Hoberman (20) has identified a microorganism in 65% of cases with colony counts between 10. 7.18) and has a positive predictive value of 15% (16).2).1 Physical examination It is mandatory to look for phimosis.2 Quantification of bacteriuria The final concentration of bacteria in urine is directly related to the method of collection. The urine specimen may be difficult to obtain in a child < 4 years old.7 Diagnosis 7.1 Collection of the urine 7.2 Bladder catheterisation Bladder catheterisation is also a very sensitive method. 7.7. The presence of pyuria (> 5 leukocytes per field) and bacteriuria in a fresh urine sample reinforce the clinical diagnosis of UTI (17).7. e.2. signs of pyelonephritis. The absence of fever does not exclude the presence of an infective process. In boys. it is better to repeat the culture or to evaluate the presence of other signs.2: Criteria for UTI in children Urine specimen from suprapubic bladder puncture Any number of cfu/mL (at least 10 identical colonies) > 1.18).6.17).18).7.2 Laboratory tests The definitive diagnosis of infection in children requires a positive urine culture (8.1 Severe UTI Severe UTI is related to the presence of fever of > 39°C. even though urine may be obtained in 23-99% of cases (8.

2. It is considered significant at a concentration > 20 μg/mL. Chlamydia trachomatis. it is advisable to repeat the urinalysis after 24 h to clarify the situation.7. volume in which sediment is resuspended and subjective interpretation of results (23).3.2. the positive predictive value of significant Gram staining with pyuria is 85% (20) (LE: 2b).g. The test for leukocyte esterase has a sensitivity of 48-86% and a specificity of 17-93% (8. However.25).2. Even in febrile children with a positive urine culture. but a very good specificity of 85-98% (8. 7. Bacteriuria without pyuria is found in 0. P.g. or enterococci • even nitrite-producing pathogens may show a negative test result. This figure corresponds well with the estimated rate of asymptomatic bacteriuria in childhood (20.7.22) (LE: 2a). Limitations of the nitrite test include: • not all uropathogens reduce nitrate to nitrite. pyuria in febrile children is indicative of acute pyelonephritis. 7.7. Instead. bacteriuria or the nitrite test.16). e.26) (LE: 3). the findings of > 10 WBC/mm3 and > 50.17. according to Landau et al.g. 44 UPDATE MARCH 2011 . 7.1 Nitrite Nitrite is the degradation product of nitrate in bacterial metabolism. (24). but carries the risk of false-positive results (21).2.3. Pyuria without bacteriuria may be due to: • incomplete antimicrobial treatment of UTI • urolithiasis and foreign bodies • infections caused by M. aeruginosa. e.2. have minimal predictive value for UTI (25. For all of these reasons. provided both nitrite and leukocyte esterase tests are negative.7.000 cfu/mL in a specimen collected by catheterisation are significant for a UTI.21). It is increased in febrile UTI and may become a reliable diagnostic marker for UTIs.7.17. the test may be negative (8.7. it is better to confirm the results in combination with the clinical symptoms and other tests (17. method of specimen collection. although it is also elevated in VUR (27). tuberculosis and other fastidious bacteria. Their assessment can be influenced by other factors. In older children. 7.5% of specimens. In such cases.4 Urinary N-acetyl-ß-glucosaminidase Urinary N-acetyl-ß-glucosaminidase is a marker of tubular damage.2.3 Other biochemical markers The presence of other biochemical markers in a urine sample are useful to establish the diagnosis of UTI (8). mode of centrifugation.3 C-reactive protein Although non-specific in febrile children with bacteriuria. and discriminate between infection and contamination (20. in neonates and children < 6 months of age. asymptomatic bacteriuria with a concomitant septic focus responsible for the febrile syndrome has to be considered. either bacteriuria or pyuria may not be considered reliable parameters to diagnose or exclude UTI.21). In contrast. A combination of nitrite and leukocyte esterase testing improves sensitivity and specificity. separately.20.21). with a positive predictive value of 98%.3.3. Thus.3. Bacteriuria without pyuria may be found: • in bacterial contamination • in colonisation (asymptomatic bacteriuria) • when collecting a specimen before the onset of an inflammatory reaction. Combining bacteriuria and pyuria in febrile children. The dipstick test has become useful to exclude rapidly and reliably the presence of a UTI. such as the degree of hydration.5 IL-6 The clinical use of urinary concentrations of IL-6 in UTIs (28) is still at the research stage. due to the short transit time in the bladder in cases of high diuresis and urine dilution. When an infection is caused by Gram-positive bacteria. If the tests are positive. The most frequent markers are nitrite and leukocyte esterase usually combined in a dipstick test. pyuria with a positive nitrite test is more reliable for the diagnosis of UTI. C-reactive protein seems to be useful in distinguishing between acute pyelonephritis and other causes of bacteriuria. neonates The nitrite test has a sensitivity of only 45-60%.2 Leukocyte esterase Leukocyte esterase is produced by the activity of leukocytes. either pyuria. particularly in Gram-negative bacteria. 7.7. the absence of pyuria may cast doubt on the diagnosis of UTI. e.

Its main drawbacks are the risk of infection. scars can be identified. but its use in UTIs is debatable unless preliminary imaging has demonstrated abnormalities that require further investigation. the need for retrogrades filling of the bladder.52). and the possible deleterious effect of radiation on children (48). Up to 23% of these patients may reveal VUR (50).3. especially when following patients with reflux. The major disadvantages in infants are the risks of side effects from exposure to contrast media and radiation (53). (37) have stated that significant renal scarring may develop.3.30) (LE: 2a).3. It represents an attractive alternative to conventional cystography. VCU is mandatory in the assessment of febrile childhood UTI. although not as well as with Tc-99m DMSA scanning (29. Disadvantages are poor image resolution and difficulty in detecting lower urinary tract abnormalities (51. and have minimal or no radiation.3. tailored low-dose fluoroscopic VCU has been used for the evaluation of VUR in girls to minimise radiological exposure (49). and may show areas of focal defect in the renal parenchyma. However. regardless of the existence or absence of VUR.36). half of the dose remains in the renal cortex after 6 h.3. defects lasting > 5 months are considered to be renal scarring (41) (LE: 2a). However. It is subjective and therefore operator-dependent.7. which indicates lack of function.1 Ultrasonography Ultrasonography (US) has become very useful in children because of its safety. painless.7. 7. About 50-85% of children show positive findings in the first week. It is considered mandatory in the evaluation of UTIs in children < 1 year of age.1 Conventional voiding cystourethrography Voiding cystourethrography (VCU) is the most widely used radiological exploration for the study of the lower urinary tract and especially of VUR. even in the presence of normal US.3.3. because of its lower dose of radiation. the role of excretory urography is declining with the increasing technical superiority of CT (54) and UPDATE MARCH 2011 45 . when characterised by a slight area of hypoactivity.7.52). A UTI interferes with the uptake of this radiotracer by the proximal renal tubular cells. 7.7.7. A star-shaped defect in the renal parenchyma may indicate an acute episode of pyelonephritis. Rushton et al. 7. 7.3 Cystosonography Contrast-material-enhanced voiding ultrasonography has been introduced for the diagnoses of VUR without irradiation (47. as well as have the ability to detect any significant structural anomaly. However.7. and gives no information on renal function.3 Cystourethrography 7. A focal defect in the renal cortex usually indicates a chronic lesion or a renal scar (32-34) (LE: 2a). 7. Current techniques do not fulfil all such requirements.7. 7.7.47).7. speed and high accuracy in identifying the anatomy and size of the renal parenchyma and collecting system (29). Minimal parenchymal defects. Ransley and Risdon (38) have reported that Tc-99m DMSA shows a specificity of 100% and sensitivity of 80% for renal scarring.3. This technique has been shown to be very sensitive and excretory urography must be reserved only for when images need to be morphologically clarified (31) (LE: 2a).2 Radionuclide studies Tc-99m DMSA is a radiopharmaceutical that is bound to the basement membrane of proximal renal tubular cells. can resolve with antimicrobial therapy (39. However.3. In recent years. Tc-99m DMSA scans are considered more sensitive than excretory urography and ultrasonography (US) in the detection of renal scars (42-45).3 Imaging of the urinary tract A gold standard imaging technique has to be cost-effective. The use of Tc-99m DMSA scanning can be helpful in the early diagnosis of acute pyelonephritis. This technique is helpful in determining functional renal mass and ensures an accurate diagnosis of cortical scarring by showing areas of hypoactivity.4 Additional imaging Excretory urography remains a valuable tool in the evaluation of the urinary tract in children.2 Radionuclide cystography (indirect) This investigation is performed by prolonging the period of scanning after the injection of Tc-99m diethylene triamine pentaacetate (DTPA) or mercaptoacetyltriglycine (MAG-3) as part of dynamic renography. Focal scarring or a smooth uniform loss of renal substance as demonstrated by Tc-99m DMSA is generally regarded as being associated with VUR (reflux nephropathy) (35.40). Further studies are necessary to determine the role of this new imaging modality in UTI. safe.3. It remains questionable whether radionuclide scans can substitute for echography as a first-line diagnostic approach in children with a UTI (46.

Antimicrobial treatment has to be initiated on an empirical basis. correction of associated urological lesions. In patients with an allergy to cephalosporins. If a Gram-positive UTI is suspected by Gram stain. amphotericin B and quinolones should be avoided. 46 UPDATE MARCH 2011 .8 Schedule of investigation Screening of infants for asymptomatic bacteriuria is unlikely to prevent pyelonephritic scar formation. However.61). Figure 7. urodynamic evaluation with uroflowmetry. but when present. but should be adjusted according to culture results as soon as possible. incontinence. It is also less expensive. sulphonamides. 7. residual urine. This provides some advantages. e. such as less psychological impact on the child and more comfort for the whole family. but not in the case of asymptomatic bacteriuria (51-58).9. elimination of symptoms and eradication of bacteriuria in the acute episode 2. preferably with cephalosporins (third generation). 7. Only a minority of children with a UTI have an underlying urological disorder. 7. because musculoskeletal adverse events are of moderate intensity and transient (60. serum levels should be monitored for dose adjustment. such a disorder can cause considerable morbidity.9 Treatment Treatment has four main goals: 1. co-trimoxazole (TMP plus sulphamethoxazole).MRI. it is useful to administer aminoglycosides in combination with ampicillin or amoxycillin/clavulanate (59) (LE: 2a). but if necessary. he/she may be given an oral agent to complete the 10-14 days of treatment. A wide variety of antimicrobials can be used in older children.3. with the exception of tetracyclines (because of tooth staining). rifampicin. the indications for their use is still limited in UTI. aztreonam or gentamicin may be used. Chloramphenicol. (video) cystometry. Fluorinated quinolones may produce cartilage toxicity (58). well tolerated and eventually prevents opportunistic infections (20). The preferred oral antimicrobials are: trimethoprim (TMP). For a safety period of 24-36 h.1). VCU = voiding cystourethrography. which may be continued on an outpatient basis. The need for DTPA/MAG-3 scanning is determined by the ultrasound findings.1 Severe UTIs A severe UTI requires adequate parenteral fluid replacement and appropriate antimicrobial treatment. after a maximum of two UTI episodes in a girl and one in a boy. an oral cephalosporin. When the child becomes afebrile and is able to take fluids. When aminoglycosides are necessary.1: Schedule of investigation of a UTI in a child Physical examination + Urinalysis/urine culture > 2 UTI episodes in girls Echography + VCU > 1 UTI episode in boys Optional : Intravenous urography DMSA scan DMSA = dimercaptosuccinic acid. The use of ceftriaxone must also be avoided due to its undesired side effect of jaundice. tetracyclines. particularly if there is suspicion of an obstructive lesion. including pressure flow studies. parenteral therapy should be administered. prevention of renal scarring 3. and electromyography should be considered. investigations should be undertaken (Figure 7. 7.7.5 Urodynamic evaluation When voiding dysfunction is suspected. as these usually develop very early in infancy. increased bladder wall thickness. Thus. may be used as second-line therapy in the treatment of serious infections. UTI = urinary tract infection.g. prevention of a recurrent UTI 4.

or amoxycillin/clavulanate. However, the indications for TMP are declining in areas with increasing resistance. In children < 3 years of age, who have difficulty taking oral medications, parenteral treatment for 7-10 days seems advisable, with similar results to those with oral treatment (62). If there are significant abnormalities in the urinary tract (e.g. VUR, or obstruction), appropriate urological intervention should be considered. If renal scarring is detected, the patient will need careful followup by a paediatrician in anticipation of sequelae such as hypertension, renal function impairment, and recurrent UTI. An overview of the treatment of febrile UTIs in children is given in Figure 7.2 and the dosing of antimicrobial agents is outlined in Table 7.3 (63). Figure 7.2. Treatment of febrile UTIs in children

Severe UTI parental therapy until afebrile • adequate hydration • cephalosporins (third generation) • amoxycillin/clavulanate if cocci are present

Simple UTI oral therapy parenteral single-dose therapy (only in case) of doubtful compliance) • cephalosporins (third generation) • gentamicin

oral therapy to complete 10-14 days of treatment • amoxycillin • cephalosporins • trimethoprim

oral therapy to complete 5-7 days of treatment

• daily oral prophylaxis • nirofurantoin • cefalexin • trimethoprim 7.9.2 Simple UTIs A simple UTI is considered to be a low-risk infection in children. Oral empirical treatment with TMP, an oral cephalosporin or amoxycillin/clavulanate is recommended, according to the local resistance pattern. The duration of treatment in uncomplicated UTIs treated orally should be 5-7 days (64,65) (LE: 1b). A single parenteral dose may be used in cases of doubtful compliance and with a normal urinary tract (66) (LE: 2a). If the response is poor or complications develop, the child must be admitted to hospital for parenteral treatment (67). 7.9.3 Prophylaxis If there is an increased risk of pyelonephritis, e.g. VUR, and recurrent UTI, low-dose antibiotic prophylaxis is recommended (68,69) (LE; 2a). It may also be used after an acute episode of UTI until the diagnostic work-up is completed. The most effective antimicrobial agents are: nitrofurantoin, TMP, cephalexin and cefaclor (68).

7.10

Acknowledgement

With our grateful thanks, the chapter on UTIs in children was updated also by Jorge Caffaratti Sfulcini, Paediatric Urology, Fundació Puigvert, Barcelona, Spain, as co-author.

UPDATE MARCH 2011

47

Table 7.3: Dosing of antimicrobial agents in children aged 3 months to 12 years* Antimicrobial agent Ampicillin Ampicillin Amoxycillin Amoxycillin/clavulanate 12 years Amoxycillin/clavulanate Cephalexin Treatment Prophylaxis Cefaclor Treatment Prophylaxis Cefixime Oral Oral Oral 3 months to 12 years 1-12 years 3 months to 12 years 3 months to 12 years 3 months to 12 years 3-12 months 1-2 years 50-100 mg/kg BW 10 mg/kg BW 8-12 mg/kg BW 3 1-2 1-2 Oral Oral 3 months to 12 years 1-12 years 50-100 mg/kg BW 10 mg/kg BW 3 1-2 Application Intravenous Intravenous Oral Intravenous 60-100 mg/kg BW Oral Age 3-12 months 1-12 years 3 months to 12 years 3 months to 3 3 months to 12 years 37.5-75 mg/kg BW 2-3 Total dose per day 100-300 mg/kg BW 60-150 (-300) mg/kg BW 50-100 mg/kg BW No. of doses per day 3 3 2-3

Cetriaxone

Intravenous

50-100 mg/kg BW

1

Aztreonam

Intravenous

(50)-100 mg/kg BW

3

Gentamicin Gentamicin Trimethoprim Treatment Prophylaxis Nitrofurantoin Treatment Prophylaxis BW = body weight. * Adapted from ref. 63.

Intravenous Intravenous

5-7.5 mg/kg BW 5 mg/kg BW

1-3 1-3

Oral Oral

1-12 years 1-12 years

6 mg/kg BW 1-2 mg/kg BW

2 1

Oral Oral

1-12 years 1-12 years

3-5 mg/kg BW 1 mg/kg BW

2 1-2

7.11
1. 2.

References
Jodal U. The natural history of bacteriuria in childhood. Infect Dis Clin North Am 1987 Dec;1(4):713-29. http://www.ncbi.nlm.nih.gov/pubmed/3333655 Jacobson SH, Eklöf O, Eriksson CG, et al. Development of hypertension and uraemia after pyelonephritis in childhood: 27 year follow up. BMJ 1989 Sep;299(6701):703-6. http://www.ncbi.nlm.nih.gov/pubmed/2508881

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Foxman B. Epidemiology of urinary tract infections: incidence, morbidity, and economic costs. Am J Med 2002 Jul;113 Suppl1A:5S-13S. http://www.ncbi.nlm.nih.gov/pubmed/12113866 Schulman SL. Voiding dysfunction in children. Urol Clin North Am 2004 Aug;31(3):481-90, ix. http://www.ncbi.nlm.nih.gov/pubmed/15313057 Shapiro ED. Infections of the urinary tract. Pediatr Infect Dis J 1992 Feb;11(2):165-8. http://www.ncbi.nlm.nih.gov/pubmed/1741197 Richards MJ, Edwards JR, Culver DH, et al. Nosocomial infections in pediatric intensive care units in the United States. National Nosocomial Infections Surveillance System. Pediatrics 1999 Apr;103(4):e39. http://www.ncbi.nlm.nih.gov/pubmed/10103331 Abrahamsson K, Hansson S, Jodal U, et al. Staphylococcus saprophyticus urinary tract infections in children. Eur J Pediatr 1993 Jan;152(1):69-71. http://www.ncbi.nlm.nih.gov/pubmed/8444210 Ma JF, Shortliffe LM. Urinary tract infection in children: etiology and epidemiology. Urol Clin North Am 2004 Aug;31(3):517-26, ix-x. http://www.ncbi.nlm.nih.gov/pubmed/15313061 Craig JC, Knight JF, Sureshkuman P, et al. Effect of circumcision on incidence of urinary tract infection in preschool boys. J Pediatr 1996 Jan;128(1):23-7. http://www.ncbi.nlm.nih.gov/pubmed/8551417 To T, Agha M, Dick PT, et al. Cohort study on circumcision of newborn boys and subsequent risk of urinary-tract infection. Lancet 1998 Dec;352(9143):1813-6. http://www.ncbi.nlm.nih.gov/pubmed/9851381 Fussell EN, Kaack MB, Cherry R, et al. Adherence of bacteria to human foreskins. J Urol 1988 Nov;140(5):997-1001. http://www.ncbi.nlm.nih.gov/pubmed/2902235 Wan J, Kaplinsky R, Greenfield S. Toilet habits of children evaluated for urinary tract infection. J Urol 1995 Aug;154(2 Pt 2):797-9. http://www.ncbi.nlm.nih.gov/pubmed/7609183 Yeung CK, Godley ML, Dhillon HK, et al. The characteristics of primary vesico-ureteric reflux in male and female infants with pre-natal hydronephrosis. Br J Urol 1997 Aug;80(2):319-27. http://www.ncbi.nlm.nih.gov/pubmed/9284209 Lin DS, Huang SH, Lin CC, et al. Urinary tract infection in febrile infants younger than eight weeks of Age. Pediatrics 2000 Feb;105(2):E20. http://www.ncbi.nlm.nih.gov/pubmed/10654980 Zorc JJ, Kiddoo DA, Shaw KN. Diagnosis and management of pediatric urinary tract infections. Clin Microbiol Rev 2005 Apr:18(2):417-22. http://www.ncbi.nlm.nih.gov/pubmed/15831830 Cavagnaro F. [Urinary tract infection in childhood.] Rev Chilena Infectol 2005 Jun:22(2):161-8. http://www.ncbi.nlm.nih.gov/pubmed/15891797 Watson AR. Pediatric urinary tract infection. EAU Update Series 2, 2004 Sep, pp. 94-100. http://www.journals.elsevierhealth.com/periodicals/euus/article/PIIS1570912404000406/abstract Koch VH, Zuccolotto SM. [Urinary tract infection: a search for evidence.] J Pediatr (Rio J) 2003 May;79 Suppl 1: S97-S106. [article in Portuguese] http://www.ncbi.nlm.nih.gov/pubmed/14506522 Hellerstein, S. Urinary tract infection in children: pathophysiology, risk factors and management. Infect Med 2002;19:554-60. Hoberman A, Wald ER. Urinary tract infections in young febrile children. Pediatr Infect Dis J 1997 Jan;16(1):11-7. http://www.ncbi.nlm.nih.gov/pubmed/9002094 Devillé WL, Yzermans JC, van Duijn NP, et al. The urine dipstick test useful to rule out infections. A meta-analysis of the accuracy. BMC Urol 2004 Jun;4:4. http://www.ncbi.nlm.nih.gov/pubmed/15175113 Wettergren B, Jodal U. Spontaneous clearance of asymptomatic bacteriuria in infants. Acta Paediatr Scand 1990 Mar;79(3):300-4. http://www.ncbi.nlm.nih.gov/pubmed/2333743 Stamm WE. Measurement of pyuria and its relation to bacteriuria. Am J Med 1983 Jul;75(1B):53-8. http://www.ncbi.nlm.nih.gov/pubmed/6349345

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Renal radionuclide studies. et al.ncbi. Gold RH. et al. 38. Imaging in acute pyelonephritis.nih.13(9):777-81.nih.gov/pubmed/1640534 Pickworth FE.nih. Majd M.ncbi. Curr Opin Urol 1994 Jan.ncbi.gov/pubmed/3153344 Risdon RA. Gordon I. eds. 1998. Rosenberg AR.nih.nlm. 27.nlm.gov/pubmed/1335226 Rushton HG. http://www. Brydon MP.gov/pubmed/1331546 Jakobsson B. Keller DM.nih. 76-103.gov/pubmed/8320616 Piercey KR. http://www. 30.nlm.nih. et al. 41. et al. Jantausch B. 25. Chao HP. Ditchfield MR. http://www. 31. 28.86(8):803-7.nih. http://www. et al.com/co-urology/Abstract/1994/01000/Imaging_in_acute_pyelonephritis. J Urol 1992 May. Cacciarelli AA. et al. Pediatr Nephrol 1992 Jan.gov/pubmed/1189138 Risdon RA. Pediatr Infect Dis J 1994 Sep.ncbi.gov/pubmed/1311185 Britton KE.gov/pubmed/3880909 Kass EJ.nih. Pediatr Infect Dis J 1994 Jul. Sonographic measurement of renal enlargement in children with acute pyelonephritis and time needed for resolution: implications for renal growth assessment. Curr Opin Urol 1993 Feb.1(4):632-7.nih.gov/pubmed/7618567 Kangarloo H. et al. 36.nih. In: Whitfield HN. Kirby RS. http://www. Oxford: Blackwell Science.151(3):767-73.g.nih. et al. Transient pyelonephritic changes on 99mTechnetium-dimercaptosuccinic acid scan for at least five months after infection. http://www. Berg U. 40. 43. Söderlundh S. http://www. 29. http://www.gov/pubmed/2846898 Bircan ZE.gov/pubmed/8309003 Jakobsson B.nlm. J Urol 1988 Nov. J Urol 1992 Nov. http://www. Urinary tract infection in infants and children evaluated by ultrasound. Evaluation of acute urinary tract infection in children by dimercaptosuccinic acid scintigraphy: a prospective study. Vesico-ureteric reflux in the damaged non-scarred kidney.nih. Diagnosis and management of urinary tract infections.ncbi. Jodal U. The value of urinalysis in differentiating acute pyelonephritis from lower urinary tract infection in febrile infants.27(1):27-32. Andreasson A. Acta Paediatr 1997 Aug. Khoury AE. Carlin JB. 35.148(5 Pt 2):1746-9.nlm. Duckett JW. Rossleigh MA. Fink-Bennett D.67(11):1338-42. Arch Dis Child 1992 Nov. Rifai N. The sensitivity of renal scintigraphy and sonography in detecting nonobstructive acute pyelonephritis.gov/pubmed/7615367 50 UPDATE MARCH 2011 . pp.nih.3(3):111-3. et al.147(5):1327-32. Fine RN. Urol Res 1975 Oct. http://www. Svensson L. Textbook of genitourinary surgery. et al.3:25-9.nlm.140(5 Pt 2):1169-74. 42.ncbi. Prevalence of urinary tract infection in febrile infants.aspx Stutley JE.nlm. http://www. Renal scarring following reflux and nonreflux pyelonephritis in children: evaluation with 99mtechnetium-dimercaptosuccinic acid scintigraphy.6(1):25-9. Jantausch BA. Pediatr Nephrol 1987 Oct. Brennan J. Radiology 1985 Feb. 39.4:39-44. Landau D. Parkhouse HF. A congenital or an acquired lesion.123(1):17-23. Buyan N.nlm. Hasanoglu E. Radiologic evaluation of urinary tract infection.gov/pubmed/7970949 Kass EJ.nlm. Chandra R. http://www.nih. Int Urol Nephrol 1995.nih. 26. Pediatr Infect Dis J 1994 Apr.ncbi.13(4):294-9. Majd M.nlm. http://www. http://www.nih.nlm. Interleukin 6 response to urinary tract infection in childhood. Godley ML.gov/pubmed/1314912 Ransley PG.165(2):405-8.ncbi. Turner ME.ncbi. 34. http://www.ncbi. http://journals.ncbi. et al. et al.148(2 Pt 2):606-8.nlm. The small scarred kidney of childhood.gov/pubmed/7808845 Hoberman A.13(7):612-6. J Urol 1994 Mar.154(2):367-73.ncbi. Risdon RA.24.ncbi. http://www. Evaluation of 99mtechnetium-dimercapto-succinic acid renal scans in experimental acute pyelonephritis in piglets.nlm.lww. Diagnostic significance of 99mTc-dimercaptosuccinic acid (DMSA) scintigraphy in urinary tract infection.ncbi. Renal papillary morphology in infants and young children.gov/pubmed/8036046 Benson M.gov/pubmed/9307157 Rushton HG. McLorie GA.nih. AJR Am J Roentgenol 1995 Aug. Urinary N-acetylbetaglucosaminidase and beta-2-microglobulin in the diagnosis of urinary tract infection in febrile infants.nlm. 33. Hendry WF.nlm. 37. J Urol 1992 Aug. Getson P.ncbi. http://www. J Pediatr 1993 Jul. Renal pathology and the 99mTc-DMSA image during the evolution of the early pyelonephritic scar: an experimental study.nlm.nlm.ncbi.ncbi. et al. 32.

48.162(5):1151-6.gov/pubmed/1524081 Majd M.gov/pubmed/15499700 Bloomfield P.nlm. 62. http://www. http://www. Karellas A. 54. et al. http://www.nih.nih.nih. Maguire B.5(4):401-2.nlm.49(5):324-5. http://www.44. http://www.(1):CD003772. http://www. Madrid: Ed Aula Medica. AJR Am J Roentgenol 1994 May. 56. Arch Dis Child 1995 Mar. Pediatr Nephrol 1991 Jul.nlm.13(73):184-6.72(3):247-50.72(3):251-8. Elison BS.nlm. Br J Urol 1992 Mar.nih. Carey JM. How good is technetium-99m mercaptoacetyltriglycine indirect cystography? Eur J Nucl Med 1994 Mar. et al.5(1):2.93(3):289-98. http://www.gov/pubmed/8166001 Kass EJ. Relationship among vesicoureteral reflux. Pediatr Infect Dis J 2003 Mar.nih. 499-507. Degl’ Innocenti ML. Comparison of DMSA scintigraphy with intravenous urography for the detection of renal scarring and its correlation with vesicoureteric reflux.] In: Broseta E. pp. http://www. Cystosonography and voiding cystourethrography in the diagnosis of vesicoureteral reflux. Jimenez-Cruz JF. Antibiotics for acute pyelonephritis in children. Pfimbriated Escherichia coli.nih.gov/pubmed/12488985 Vela Navarrete R.gov/pubmed/1327798 Smellie JM. http://www. http://www.nih. Chen KW.nlm. A practical approach to evaluating urinary tract infection in children. The value of ultrasound in the child with an acute urinary tract infection.69(3):294-302.nih. 49. http://www. [Urinary tract infection in children.gov/pubmed/7741578 [No authors listed. 55. [article in Spanish] Grady R.ncbi.nlm.nih.ncbi. Infeccion urinaria.nlm. Whiting PF.86(1):94-6. 50. Rigden SP. 47. 59. 1993. De Boe V. et al. Fowler K.ncbi. Pediatr Nephrol 2003 Jan. J Pediatr 1991 Oct.18(1):18-22. Tailored low-dose fluoroscopic voiding cystourethrography for the reevaluation of vesicoureteral reflux in girls.ncbi.gov/pubmed/8200390 Piaggio G.74(2):240-4. et al.ncbi. Barcelona: Ed Prous. Paediatric urinary tract infection and the necessity of complete urological imaging. Rigden SP. Safety profile of quinolone antibiotics in the pediatric population.nlm. 61. et al.gov/pubmed/7741579 Smellie JM. Taylor D. BMC Pediatr 2005 Mar.22(12):1128-32. Hollman AS.gov/pubmed/1314684 MacKenzie JR. Kernen KM. Keuppens F. Diamond BA.nlm.ncbi. Rioja LA.nlm. Hoskens C. Acute bacterial nephritis: a clinicoradiologic correlation based on computer tomography. Pitfalls in the investigation of children with urinary tract infection.nih.] Fluoroquinoles in children: poorly defined risk of joint damage. Does routine ultrasound have a role in the investigation of children with urinary tract infection? Clin Radiol 1994 May. http://www. http://www. et al. Cohrane Database Syst Rev 2005 Jan. 45. 57.ncbi.gov/pubmed/7741578 Broseta E.119(4):578-85. Rushton HG. http://www. et al.gov/pubmed/8013196 Westwood ME. Jiménez Cruz JF.nih.nih. 52.ncbi. 185-194.ncbi. Urinary tract infection: a comparison of four methods of investigation. Arch Dis Child 1995 Mar. [article in Spanish] Huang JJ.nih. Cooper J. Sung JM.gov/pubmed/15769296 Haycock GB. eds. Involvement of the renal parenchyma in acute urinary tract infection: the contribution of 99mTc dimercaptosuccinic acid scan. 58. 46. pp. http://www. Jantausch B. [Urinary tract infections in children. Vandevivere J.nlm. http://www.gov/pubmed/1654977 Kleinman PK. Prescod NP. 51.gov/pubmed/7921944 Mucci B. 53. http://www.nlm. Van der Wall H. and acute pyelonephritis in children with febrile urinary tract infection.ncbi.nlm.gov/pubmed/10886091 De Sadeleer C. et al. 60.nih. Br J Urol 1994 Aug. eds. et al. Hodson EM.ncbi. Tomà P.ncbi.nih.] In: Tratado de urología tomo I. Jimenez-Cruz JF. BJU Int 2000 Jul.ncbi.nih. Am J Med 1992 Sep. Prescrire Int 2004 Oct. Further investigation of confirmed urinary tract infection (UTI) in children under five years: a systematic review.nlm.gov/pubmed/1681043 Melis K. Eur J Pediatr 1992 Jul.ncbi. Craig JC.nih.nlm.ncbi.ncbi.ncbi.151(7): 536-9.gov/pubmed/15674914 UPDATE MARCH 2011 51 .nlm.nlm. 1999.21(3):223-7.

ncbi.ncbi. Typically. http://www. It is arguable that diabetic patients are susceptible to rapid progression of parenchymal infection.42(6): 1433-57. DIABETES MELLITUS AND IMMUNOSUppRESSION Summary and recommendations 8.1.ncbi. (DGPI) (ed).nlm.gov/pubmed/11713435 8. In patients with VUR and UTI in end-stage chronic renal failure. and rarely.nih.86(9):690-6. J Pediatr 2001 Nov. if in the adult the kidney is normal beforehand. http://www.ncbi. In diabetes mellitus. Pediatr Nephrol 1988 Jan.gov/pubmed/12535494 Tran D. Bantock HM. Urinary tract infections. http://www. overwhelming infection can predispose to pyogenic infection with intrarenal perinephric abscess formation. Pediatr Clin North Am 1995 Dec. Hodson EM. Short versus standard duration oral antibiotic therapy for acute urinary tract infection in children. TRANSpLANT RECIpIENTS. UTIs IN RENAL INSUFFICIENCY. but there is little evidence that vigorous treatment of lesser degrees of infection or prophylaxis will slow renal functional impairment once it is established (GR: C). Clearly.139(5):620-1.nih. 69.nih.1. including the loss of several urinary defence mechanisms and a degree of immunosuppression. http://www. pp. 66. There is no evidence that prolonged or intensive antibiotic treatment of acute pyelonephritis shortens the episode or prevents complications. Cochrane Database Syst Rev 2003. http://www. Prophylactic co-trimoxazole and trimethoprim in the management of urinary tract infection in children.gov/pubmed/11445800 Khan AJ. emphysematous pyelonephritis. 8. adult polycystic kidney disease (APCKD). Aronoff SC.139(1):93-9. very dramatic changes can occur with focal reduction in perfusion on imaging and corresponding renal tubular dysfunction.V.nlm.nih.nih. J Nalt Med Assoc 1994 Sep. 68.1 Acute effects of UTI on the kidney In acute pyelonephritis. [article in German] Michael M. Deutsche Gesellschaft für pädiatrische Infektiologie e.gov/pubmed/3152984 Arant BS Jr. severe UTI with accompanying bacteraemia can hasten progression of renal failure. et al. J Pediatr 2001 Jul.nlm. 64. 52 UPDATE MARCH 2011 . Women are more prone to asymptomatic bacteriuria than men with diabetes.1. 2003. http://www.(1):CD003966.2(1):12-7. but in both sexes. [Textbook for infections in children and adolescents. et al. progression to clinical pyelonephritis is more likely than in normal individuals.nlm. a specific form of infective interstitial nephropathy. Old and new concepts.1 APCKD In patients with acute pyelonephritis and infected cysts (presenting as recurrent bacteraemia or local sepsis). 148-157. However.ncbi.2. Short-course versus conventional length antimicrobial therapy for uncomplicated lower urinary tract infections in children: a meta-analysis of 1279 patients.nlm. gross VUR and end-stage obstructive uropathy harbour infective foci or promote ascending infection. chronic renal damage is unlikely.gov/pubmed/7966433 Hellerstein S. Futuramed: Munich.63.ncbi. followed by prophylaxis. treatment requires a long course of high-dose systemic fluoroquinolones. the clearance of asymptomatic bacteriuria should not be attempted if the intention is to prevent complications. 8. Papillary necrosis is a common consequence of pyelonephritis in patients with diabetes. bilateral nephroureterectomy should only be undertaken as a last resort (GR: B). but not invariably so.1 8. Efficacy of single-dose therapy of urinary tract infection in infants and children: a review.] 4th edn. Gruneberg RN. However.nih. The risk factors for developing asymptomatic bacteriuria differ between type 1 and type 2 diabetes. Muchant DG.gov/pubmed/8614594 Smellie JM.nlm. Vesicoureteral reflux and evidence-based management. notably acute pyelonephritis (GR: A).2 Chronic renal disease and UTI There are several factors of general potential importance that predispose to infection in uraemia. Bilateral nephrectomy should be utilised as a last resort (GR: B). 67. Craig JC. 65.

e. Immunosuppression is of secondary importance.1. There are also important scientific issues to be considered concerning the cause.1. Obstruction may be covert and require specific diagnostic tests. Does chronic renal disease progress more quickly as a result of infection.4 Antibiotic treatment for UTI in renal insufficiency and after renal transplantation The principles of antibiotic treatment for UTI in the presence of renal impairment. although if this is extreme. 8.g.1-8.4. but immunosuppression is only one of many factors that are mainly classified as ‘surgical’. What are the acute effects of UTI on the kidney and do the lesions become chronic? 2. or upper urinary tract pressure flow studies. even if the reflux has not already been successfully treated (6) (GR: A).2 Background Whenever UTI is present in patients with renal insufficiency. and do particular renal diseases predispose to UTI? 3. in almost all cases.1. Pathologically. to clear the stones if possible and to minimise antibiotic treatment if the calculus cannot be removed. Even so. special susceptibilities. a similar process may occur in such fundamentally different situations as obstructive and reflux nephropathy. immunosuppression can promote persistent bacteriuria. Nephrectomy should be performed as a last resort.3. Although acute infection is important in the early stages of this disease. 8. video-urodynamics. it may cause renal scarring in a previously normal kidney (1.2 Obstructive neuropathy Obstruction occurring through a voiding disorder or supravesically causes renal tubular dysfunction and ultimately renal damage. and the contribution of ascending infection are still unresolved. angiotensin-converting enzyme (ACE) inhibitors and highly active retroviral therapy appear to reduce progression to end-stage renal disease. 8. Steroids. the combination of obstruction and infection is dangerous and should be treated vigorously. possibly through the mechanisms of thrombotic microangiopathy and immune-mediated glomerulonephritis. 8.3 Acute effects of UTI on the kidney Some authors regard acute pyelonephritis as complicated because.3 UTI in renal transplantation and immunosuppression The need to correct uropathy or to remove a potential focus of infection in an end-stage disease kidney is more pressing in patients enlisted for renal transplantation. although the distribution and extent of the lesions may be different (3-5) (LE: 2a). Renal scarring can certainly be acquired as a result of these three factors. i. However. In this narrow age range. Infection enhances the process of UPDATE MARCH 2011 53 . mainly through the process of apoptosis. during dialysis treatment and after renal transplantation are discussed in the text and summarised in Tables 8. 8. the results of nephrectomy for a scarred or hydronephrotic kidney may be disappointing.e.8. further discussion of reflux nephropathy is beyond the scope of these guidelines.2 Calculi and UTI Management is similar to that for patients without renal impairment.2. HIV infection is associated with acute and chronic renal disease. 8.1.3. developmental renal dysplasia must be a major consideration in the pathogenesis of chronic pyelonephritis. particularly in the immunosuppressed patient.3 Obstruction of the urinary tract and UTI As in all other situations. Prophylactic antibiotics therefore offer little benefit in preserving renal tissue in reflux nephropathy in older children and adults. in their view. Which problems arise in antibiotic therapy in patients with renal insufficiency and after renal transplantation? 8. which may become symptomatic.1 VUR and intrarenal reflux The effects of VUR and intrarenal reflux on the renal parenchyma. In the context of renal transplantation. 1. This part of the guidelines can be subdivided into four sections. but even residual renal function may be of vital importance (GR: B). particularly in the context of renal transplantation? Is UTI a significant cause of graft failure? 4.2. although. UTI is very common.2) (LE: 2a). Are immunosuppressed patients prone to UTI. problems arise in both the treatment of infection and the management of renal disease. effects and complications of renal parenchymal infection. this usually occurs very early in life. the status of either recurrent acute UTI or asymptomatic bacteriuria specifically in the progression of scar formation is tenuous.

Obstruction has to be cleared if infection is to be eradicated (7) (GR: A). such as CT or DMSA scanning.3. ß2-microglobulin and N-acetyl-ß-D-glucosaminidase. Urinary calculi and pregnancy can cause urinary stasis and an intermittent increase in pressure in the upper urinary tract. Bacterial adhesion may be of variable benefit to the bacterium. but not with standard intravenous urography (IVU). compared with a much smaller proportion of those who have had cystitis or asymptomatic bacteriuria (18) (LE. There are many identifiable factors relating to virulence of the bacterial cell and to its ability to adhere to the mucosa as a preliminary to invasion (17). at least in children in whom 90% of individuals with acute pyelonephritis express these bacteria. E. a group of 160 patients who had recently suffered acute UTI all developed reduced concentrating power. which can cause subtle and persistent damage. and therefore. Metastatic infection rarely causes renal infection. hypotension and poor renal perfusion. the infiltrating bacteria had reduced adhesive characteristics. 8. and may be intrinsically deficient in converting asymptomatic bacterial colonisation to clinical infection. but the kidney that is permanently damaged by any cause has less reserve to withstand the effects of reflux. 8. IL-6 and IL-8) are responsible for inducing leukocyte migration. Various cytokines (e. reduced adhesiveness can facilitate silent penetration into the renal parenchyma. It is sometimes difficult to exclude an element of obstruction when discussing the pathogenesis of putative infective renal damage in the alleged normal kidney. because its attachment may mean that it is easier for host defence mechanisms to localise and abolish it (19).parenchymal loss. Bacterial infection in the urinary tract can induce fever and elevate acute phase reactants. Paradoxically. 2b). as a result of UTI in the absence of reflux. Type 2 or P fimbriae bind to glycolipids of the blood group substances that are secreted by the host urothelium. pyonephrosis.15) (LE: 2b). such as C-reactive protein. E. such as α2-macroglobulin. obstruction and infection. obstruction or calculi. perinephric abscess and widespread systemic sepsis develop. In the majority of these patients.13) (LE: 2b). In any circumstances.3. In functional terms. The fact that there is a serological immune response and bacteria become coated with antibodies to various antigenic components of the microorganism is regarded as evidence of an immune response. For example. the combination of obstruction and infection is a surgical emergency and both must be relieved without delay.4 Acute effects of UTI on the normal kidney The acute effects of UTI on the normal kidney are complex. type 1 pili or fimbriae combine with mannose receptors on the uromucoid. there may be a loss of concentrating power that can persist in the long term (14. 8. Virulent microorganisms cause direct cellular injury. usually after colonising the renal pelvis. The cellular and humoral inflammatory host response is also a crucial part of host defences. It is agreed that dramatic reduction in renal perfusion and excretion can occur acutely and so-called ‘lobar nephronia’ has been demonstrated with the newer methods of imaging.3 Renal effects of severe UTI Severe infection can lead to renal functional impairment through sepsis. coli. which is pathological to the kidney. In practical terms. 54 UPDATE MARCH 2011 . coli is lower in adults than children (69% vs. appears to express P (or pyelonephritis-associated) or type 2 fimbriae. In extreme cases. which is part of the protective mucopolysaccharide layer found on uroepithelial cells lining the urinary tract. They are worth reviewing because they may provide a lead in deciding how chronic changes can occur and therefore a basis for the development of guidelines on the prevention of renal damage. as part of the process of multiorgan failure. 80%) (9) (LE: 2b). In particular. serum levels of IL-6 and IL-8 are elevated (12. is controversial (20) (LE: 2a). coli is the most common of the Gram-negative bacteria that are isolated in the majority of patients with acute pyelonephritis. In a Swedish study. Damage can also occur indirectly from the effects of inflammatory mediators.g. The presence of renal calculi and diabetes mellitus further reduces host defences (8). Tissue damage is reflected by urinary secretion of tubular proteins and enzymes.5 Renal scarring The possible development of scarring. perhaps facilitating their penetration into the renal parenchyma and promoting more permanent structural and functional damage (15) (LE: 2b). A detailed discussion of obstructive nephropathy is not appropriate here. and usually only in susceptible individuals (see the sections below on Diabetes mellitus and Immunosuppression) (10).3. Bacterial infection also elicits immunoglobulin A and cytokine responses (11) (LE: 2b). which presents as cortical abscesses. and erythrocyte sedimentation rate (ESR). even though a significant proportion (40%) did not develop a febrile illness. of exposure to microorganisms that are potentially damaging to the renal parenchyma (16) (LE: 2b). endotoxaemia. The proportion of infections caused by E.

with evidence of increasing renal damage and chronic pyelonephritis upon biopsy (LE: 3). However.6. This is characterised histologically by acute pyogenic infiltration with micro-abscesses and the development of acute renal failure. Other subtle factors may be present. a low body mass index and a past history of recurrent UTIs (23) (LE: 2a).A study has shown that 55% of patients with no pre-existing lesions developed acute parenchymal lesions during an episode of acute pyelonephritis (2) (LE: 2a). This important issue is clarified by a recent more critical study of DMSA scanning during the acute phase of acute pyelonephritis. as in uncomplicated acute pyelonephritis. These patients will have been identified as having an intrinsic genetic defect in the host response of cytokine release to infection. diabetic women with asymptomatic bacteriuria can have good glycaemic control. The mechanism is ill-understood and. such patients do not develop chronic renal failure and the scar is a very different lesion from the typical scar of reflux nephropathy. of which. the rare occurrence of renal damage apparently arising from acute or recurrent uncomplicated UTI may be prevented by targeting long-term treatment at selected patients. 26% had significant bacteriuria (> 105 cfu/mL) compared with 6% of controls.6 Specific conditions in which an acute UTI causes renal damage There are several specific conditions in which acute UTI can cause renal damage: 8. which sometimes includes infection by gas-forming organisms. Poor glycaemic control has not been shown to increase the risk of bacteriuria (26). Even in the absence of obstruction. and diabetes should not therefore be regarded as an indication for screening or treatment of asymptomatic bacteriuria. Impaired host resistance is thought to predispose to persistence of nephropathogenic organisms. Diabetic patients are also prone to an under-reported and probably unusual form of infective interstitial nephritis. Asymptomatic bacteriuria is common in women with diabetes (though not in men). In summary. This is reflected in clinical experience. such as underlying diabetic nephropathy (25) and autonomic neuropathy that causes voiding dysfunction. Over such a long period. it may lead to renal functional impairment (24). However. the majority resolved within 3 months. should discourage the clinician from prescribing excessive antibiotic treatment beyond that needed to suppress the acute inflammatory reaction (GR: A). Diabetes mellitus increases the risk of acute pyelonephritis from infection by Enterobacteriaceae That originate in the lower urogenital tract. The poor correlation between the severity of the symptoms in an episode of acute pyelonephritis and the risk of permanent damage. but specific evidence is lacking for the development of renal complications. which has concluded that treatment does not reduce complications. The origin of the organisms may be haematogenous. double-blind randomized trial (27) (LE: 1b). which might not have identified pre-existing disease. Risk factors in patients with type 2 diabetes were old age. In future. with a high mortality (emphysematous pyelonephritis) (29). Such a genetic defect would be even more important if a patient also had structural abnormalities that cause complicated UTI. An earlier study by Alwall (21) has described 29 women who were followed for 20-30 years. proteinuria. further imaging invariably showed evidence of reflux or obstructive nephropathy that must have predated the acute infective episode (22) (LE: 2a). particularly peripheral neuropathy and proteinuria. a direct causal link is dubious. IVU or DMSA scanning during an acute urinary infection can have alarming and dramatic results. In lesions that persisted. 37 of 81 patients had one or more perfusion defects. In the study. treatment and prophylaxis of asymptomatic bacteriuria. therefore. but in practical terms the observed changes mostly resolve. In a prospective study of non-pregnant women with diabetes mellitus. The findings from this trial have been subsequently recognised in the guidelines published by the Infectious Diseases Society of America (IDSA) on the diagnosis and treatment of asymptomatic bacteriuria in general (28).g. e. but still show reduced urinary cytokine and leukocyte concentrations (although polymorph function is normal). these issues have been addressed in a placebo-controlled. in acute pyelonephritis. These lesions were found to have persisted after 3-6 months follow-up in 77% of patients (9) (LE: 3). Klebsiella infection is particularly common (25% compared with 12% in nondiabetics). acute parenchymal infection may progress insidiously to form an intrarenal abscess UPDATE MARCH 2011 55 .3. However. Thus. Women with type 1 diabetes are particularly at risk if they have had diabetes for a long time or complications have developed. 8. Glycosuria inhibits phagocytosis and perhaps cellular immunity. analgesic abuse.3. That study would have used cruder diagnostic techniques. small parenchymal scars demonstrated by modern imaging may develop as a result of acute non-obstructive pyelonephritis. It has always been recognised that diabetic patients are particularly susceptible to rapid progression of renal parenchymal infection and ensuing complications. there was no consensus on the questions of pre-emptive screening. it was impossible to exclude other causes of renal impairment and interstitial nephropathy. If left untreated.1 Diabetes mellitus Asymptomatic bacteriuria is common in diabetic women. and encourages bacterial adherence. patients may have had renal damage initially. which is very small. Until recently.

Uraemic patients are also mildly immunosuppressed and the formation of protective uroepithelial mucus may be inhibited (36-38) (LE: 2b). Cephalosporins. due to urea or low pH and high osmolality. Tuberculosis and leprosy can cause renal damage through the development of amyloid and a form of proliferative glomerulonephritis (32. clearly does promote infection.that ruptures. particularly in the later stages of disease progression. this can lead to end-stage renal failure. The issue of whether urological complications including UTI affect the progression of renal failure in polycystic disease or in any other renal pathology is controversial. apart from a few exceptions. The few exceptions include the following. although not always. it is doubtful whether vigorous treatment of asymptomatic bacteriuria or even mild clinical UTI makes any difference to the progression of renal disease (43) (LE. 2b). 8. After transplantation. which have lowered the dose of immunosuppressive therapy and prophylactic antibiotics (45). calcification or obstruction (30. overall graft and patient survival rates do not differ between ADPKD and control groups (42) (LE: 2a). 8. The presentation can occasionally be indolent.2 Tuberculosis Tuberculosis can cause acute and chronic renal damage through bilateral renal infiltration. are often ineffective (41) (LE. Bacteriuria is present in 35-80% of patients. Acute pyelonephritis is common and may originate from pyogenic infection in the cysts (40) (LE: 3). which has no predisposition to UTI.31) (LE: 3). Papillary necrosis is common in diabetics. It is disappointing that. 8. such that bilateral nephrectomy may be the only option. Polycystic disease is not to be confused with acquired renal cystic disease of the end-stage kidney. Severe symptomatic UTIs may indicate an adverse prognosis. although the risk has been reduced by improvements in donation surgery. The antibacterial properties of normal urine. 3). 8.4. which is sufficient to cause renal failure in the absence of fibrosis. However.4 Chronic renal disease and UTI There are good reasons why all uraemic patients should be prone to UTI.1 Adult dominant polycystic kidney disease (ADPKD) UTI is a prominent complication of ADPKD. Fluoroquinolones are generally the most effective (GR: A).4. particularly in association with acute pyelonephritis. The efficacy of antibiotic treatment may depend on whether cysts are derived from proximal (active secretion) or distal tubules (passive diffusion) and on the lipid solubility of the agent used. However. with symptomatic UTI being the presenting feature in 23-42% of patients. It is certainly associated with permanent renal parenchymal scarring.3. which even occasionally included progressive renal scarring. It was concluded that even patients whose reflux prevention surgery had been successful were prone to recurrent UTI. In this respect. particularly in men with ADPKD. who are usually female (39). obstructive uropathy and gross reflux. 56 UPDATE MARCH 2011 . UTI and septicaemic episodes are still a significant cause of morbidity. 8. Rarely. However. hypertension and complications. there is little evidence for a causal relationship between preexisting chronic renal disease and persistent UTI (7). particularly from infective struvite stones. a more subtle form of interstitial granulomatous disease can occur. For more details see the EAU guidelines on genitourinary tuberculosis (34). gentamicin and ampicillin. which leads to a perinephric collection and a psoas abscess. However. few studies have provided long-term serial data that identify renal damage and its causal relationship with infection. and why UTI should increase the rate of deterioration of renal function. Such consequences should at least inform the patient’s decision in deciding between surgical and medical treatment of VUR. as yet.5 UTI in renal transplantation UTI is common after renal transplantation. may be lost (35). but pyuria is common. It may be difficult to obtain a positive culture on standard laboratory media.33).6. which are standard treatments of acute pyelonephritis and require active transport.2 Renal calculi Nephrolithiasis. despite close monitoring of patients. Antibiotic prophylaxis for the treatment of asymptomatic bacteriuria is probably required (GR: C). although it is difficult to exclude obstruction by the sloughed papillae as the cause of the nephropathy. it is of some interest that a study of 100 patients who underwent reflux prevention surgery at least 20 years before has recently been published (44). (LE: 2b). The results of removing a scarred or hydronephrotic kidney in the hope of curing infection are often disappointing.

and infective calculi. Detailed discussion of this process is beyond the limits of these guidelines. chemical urethritis and bladder calculi of sufficient severity to warrant cystoenteric conversion. Urinary diversions and bladder augmentation and substitution have also been successfully completed in patients on dialysis treatment and after transplantation.1 Donor organ infection Early factors predisposing to UTI include infection in the transplanted kidney. residual urine. massive infective VUR. can promote UTI through bacterial colonisation of dead tissue. only the most obvious renal or ureteric abnormality will be detected. organ donation will be abandoned at this late stage. In the first 3 months. and a better response to antibiotics unless there are urological complications (e.5.2 Graft failure There are several potential mechanisms by which severe UTI can cause graft failure. For many years. These may include recurrent UTI. these findings have not been confirmed and most surgeons do not make a special effort to perform an antireflux anastomosis. Sometimes it can be very difficult to distinguish rejection from infection (48) (LE: 2b). fistula. This often occurs by commensal or fastidious pathogens. particularly in diabetes mellitus (46). which should either be avoided or given at much higher doses.8. Infection can theoretically induce graft failure by three other mechanisms. There is also concern about the increasing number of children with congenital uropathy. Very occasionally. poor bladder compliance. After the kidney is removed from its storage box. However. Infarction. The infection may be impossible to eradicate until the kidney or at least the dead segment is removed. but also with interstitial nephropathy progressing to graft loss in possibly 5% of recipients.6 Antibiotic therapy in renal failure and transplant recipients Much of the detailed information on antibiotic prescribing in renal failure is summarised in Tables 8.3. 8. the polyomavirus type BK has been listed as a possible candidate for causing transplant ureteric stenosis. There was an early suggestion that reflux into the graft could lead to pyelonephritis and parenchymal scarring. and VUR. The virus is susceptible to treatment with the antiviral agent cidofovir (49) (LE: 2a). as well as providing a source of microorganisms within the mucous biofilm that covers the foreign body. are identified and corrected well in advance of the transplant procedure (50) (LE: 3).5. such as by the direct effect of cytokines. Improved detection of so-called ‘decoy cells’ in urine and of virus DNA by polymerase chain reaction has confirmed the causal relationship between infection and obstruction. even if the mid-stream urine (MSU) culture is positive.5. The risk of such complications is minimised if urodynamic abnormalities. either of the whole kidney or of a segment due to arterial damage. often associated with neuropathic bladder dysfunction and the sinister combination of intravesical obstruction. UTI is more likely to be symptomatic with a high rate of relapse.g. Later on. UTIs can also reactivate cytomegalovirus infection. It is important to note that peritoneal dialysis and haemodialysis clear certain antibiotics. the following problems are most troublesome: papillary necrosis. growth factors (e. Antibiotics are given empirically. A full urodynamic assessment.1-8. which can lead to acute transplant rejection. the organ donor should be screened for a variety of viral and bacterial infections. there is a lower rate of pyelonephritis and bacteraemia. Clearly.g. or obstruction of the urinary tract). UPDATE MARCH 2011 57 . 8. the effluent from the renal vein and surrounding fluid in the sterile plastic bags that contain the excised kidney should ideally be cultured because microorganisms are likely to have been introduced during the donation process. it must be acknowledged that the urinary tract of the cadaver donor is rarely investigated. but usually the first suspicion of occurrence of a renal tract abnormality is raised during the organ donation operation. 8. Bladder catheters and ureteric stents promote the loss of the glycosoaminoglycan layer from the uroepithelium. However. polycystic disease. e. establishing a routine of intermittent selfcatheterisation and any necessary bladder surgery must be completed well in advance of renal transplantation. In renal transplant recipients.g. Infection in the native kidneys may worsen considerably as a result of maximum immunosuppression.3 Kidney and whole-organ pancreas transplantation Simultaneous kidney and whole-organ pancreas transplantation can present specific urological complications when the bladder is chosen for drainage of exocrine secretions. obstruction. although bacteriuria is common and may require antibiotic treatment (47). tumour necrosis factorTNF) and free radicals as part of the inflammation cascade (45). Also.5 and Appendix 16. there are important interactions to consider between immunosuppressive agents and antibiotics. Under these circumstances.

However.1 Treatment of UTI in renal transplant recipients The treatment of a symptomatic UTI is similar to treatment given to non-transplant patients.1: Use of antibiotics for UTI with renal impairment Most antibiotics have a wide therapeutic index. No adjustment of dose is necessary until GFR < 20 mL/min. aminoglycoside.g. but not doxycycline. Combination of loop diuretics (e.6. Table 8. and in most cases a 10-14-day course of treatment is given.5: Drug interactions with cyclosporin and tacrolimus Rifampicin Erythromycin Aminoglycosides TMP-SMX Amphotericin B TMP-SMX = trimethoprim-sulphamethoxazole. Slightly dialysed Fluoroquinolones* Co-trimoxazole Erythromycin Not dialysed Amphotericin Methicillin Teicoplanin 58 UPDATE MARCH 2011 . Drugs removed by dialysis should be administered after dialysis treatment. Give pyridoxine. GR: A). Perioperative antibiotic prophylaxis. e. Table 8. TMP-SMX for 10-14 days). Table 8.Table 8. 8.g. The choice of antibiotic is dictated by the special need for penetration into the renal parenchyma rather than for merely a ‘mucosal’ antibiotic. 6 months low-dose TMP-SMX (co-trimoxazole) (LE: 1b.3: Treatment of tuberculosis in renal failure Rifampicin and isoniazid (INH) not cleared by dialysis. Avoid rifampicin with cyclosporin. furosemide) and a cephalosporin is nephrotoxic. Fluoroquinolones seem to be particularly effective. Nitrofurantoin and tetracyclines are contraindicated. Ethambutol not dialysed. Table 8. Empirical treatment of overt infection (quinolone.4: Recommendations for prevention and treatment of UTI in renal transplanation Treat infection in recipient before transplantation. TMX = trimethoprim-sulphamethoxazole. Reduce dose if GFR < 30 mL/min. except antibiotics with nephrotoxic potential.2: Clearance of antibiotics at haemodialysis Dialysed Amoxycillin/ampicillin Carbenicillin Cephalosporins* Aminoglycosides* Vancomycin Trimethoprim Metronidazole Aztreonam* Fluconazole* * Drugs cleared by peritoneal dialysis. GFR = glomerular filtration rate. Culture donor tissue sample and perfusate. a short course of treatment has yet to be established.

However. In these patients. This will cover the high-risk period when infection is more likely to be symptomatic and associated with acute graft impairment. in whom there is a close relationship between CD4 counts and the risk of bacteriuria. It is wise to treat all patients with antifungal agents (fluconazole.6. A number of other drug interactions need to be considered. Fairley KF. and to chronic renal failure through a variety of nephropathies. Renal transplantation is possible. 186-205.8 1. 8.There is good evidence for the beneficial effects of treating asymptomatic bacteriuria in the first 6 months after renal transplantation (51) (LE: 2a). It will also prevent Pneumocystis carinii pneumonia (PCP) and infection with other rare fastidious organisms. primarily to the glomerular epithelial cell. Combination therapy using corticosteroids.1 HIV infection HIV infection can lead to acute renal failure through non-specific severe systemic illness. (54). In most units. Rifampicin and erythromycin also interact with calcineurin inhibitors by increasing cytochrome p450 synthetase and inhibiting hepatic cyclosporin A metabolism. provided they are treated. Oxford: Oxford Medical Publications (Oxford University Press). such as a urological complication in the transplant kidney or recipient bladder dysfunction. adverse interactions with cyclosporin do not occur. At a low dose. particularly in patients whose counts are < 200 cells/mL (57). HIV infection is therefore no longer a contraindication to renal replacement therapy. however.2 Viral and fungal infections Viral and fungal infections are relatively common in immunosuppressed patients. pp. UPDATE MARCH 2011 59 . 1996. immunemediated glomerulonephritis and nephropathy due to virus-induced cellular damage. the situation is a little clearer in male patients with HIV and AIDS. For further details on schistosomiasis in genitourinary tract infections see Bichler et al. ed. it was concluded that active schistosomiasis did not preclude transplantation (53) (LE: 3). although evidence from randomised trials is not available (55). although they may acquire unusual and granulomatous infections. amphotericin B plus flucytosine) even when they are asymptomatic.3 Schistosomiasis Schistosomiasis is a familiar problem for patients treated for end-stage renal failure from locations where the disease is endemic.7 Immunosuppression It is well known that viral and fungal infections are common in immunosuppressed patients. must be considered and treated vigorously. However. Despite this. In any patients with relapsing or recurrent infection. although the higher dose advocated by some units results in synergistic nephrotoxicity with trimethoprim. ACE inhibitors and highly active antiretroviral therapy seems to delay and prevent progression of nephropathy. 8. Infections of the kidney and urinary tract. the combination of trimethoprim and sulphamethoxazole (co-trimoxazole) is effective in preventing UTI (52) (LE: 1b). Removal of the catheter or stents is usually necessary (GR: B).6. 8.g. gentamicin. an anatomical cause.2 Fungal infections Candidal infections can occur in any immunosuppressed patient. In a trial that compared infected patients with those free of schistosomiasis. These include HIV-induced thrombotic microangiopathy. 8. Complicated urinary tract infection in adults. there was no difference between the incidence of acute and chronic rejection. 8. Patients with end-stage renal failure are generally not particularly susceptible to the usual Gram-negative urinary pathogens. Low-dose antibiotic prophylaxis with co-trimoxazole has been recommended for 6 months after transplantation. In: Cattell WR.7. even when live donors and recipients have active lesions. References Kincaid-Smith P. Combined medication (praziquantil and oxaminoquine) is recommended for 1 month. PCP prophylaxis of the type used in transplant patients may not reduce the rate of bacteriuria. Patients have evidence of reduced cellular and humoral immunity. perhaps due to the previous development of resistant organisms. The place of immunosuppression per se in the development of UTI remains unresolved (56). but are more common in diabetic patients and those with chronic residual urine and in whom there is an indwelling catheter or stent. e.7. About 40% of patients with bacteriuria are asymptomatic. UTI and urological complications occurred in the infected group and a higher cyclosporin dose was required. 8. Patients must be investigated for surgical complications. co-trimoxazole and amphotericin B promote cyclosporin and tacrolimus toxicity.

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If an amplification system is used for identifying the pathogens. However. Urinary tract infections. C. trachomatis. Mycoplasma genitalium and Trichomonas vaginalis. pp.6 Therapy 9.4 Clinical course Mucopurulent or purulent discharge. 1 g intramuscularly (with local anaesthetic) as a single dose UPDATE MARCH 2011 63 .5 Diagnosis A Gram stain of a urethral discharge or a urethral smear that shows more than five leukocytes per high power field (× 1. In: Bergan T. gonococci located intracellularly as Gram-negative diplococci. or 400 mg by suspension (200 mg/5 mL) • ceftriaxone. GR: B). The frequency of the different species varies between patient populations (1-5). The following antimicrobials can be recommended for the treatment of gonorrhoea: As first-choice treatment • cefixime.6. many infections of the urethra are asymptomatic. gonorrhoeae. chlamydiae and gonococci can spread further through the urogenital tract to cause epididymitis in men or cervicitis.57. Information has been derived from the following standard reference sources: 1. indicate pyogenic urethritis (7)(LE: 3.org. 1997. non-specific urethritis is much more frequent than gonorrhoeal urethritis. British national formulary. 2004. ed. It is highly sensitive and specific for documenting urethritis and the presence or absence of gonococcal infection. 9. Currie A. The renal drug handbook. endometritis and salpingitis in women. Borleffs JC. Treatment of gonorrhoeal urethritis The following guidelines for therapy comply with the recommendations of the US Centers for Disease Control and Prevention (8-10). In most cases. Available from http:// emc. Schneider MM. and when sexual transmission is suspected. Infection is spread by sexual contact. BMA and RPSGB.1 Further reading Antibiotic prescribing in renal failure: evidence base of guidelines. 8. gonorrhoeae and C. A positive leukocyte esterase test or > 10 leucocytes per high power field (× 400) in the first voiding urine specimen is diagnostic. the aim should be to identify the pathogenic organisms. 2nd edn. et al. 9. Van Dooyeweert DA. trachomatis) and cause pyogenic infection.1. Datapharm Communications Ltd. the first voiding urine specimen can be taken instead of a urethral smear. 9. In Central Europe. 9.3 Route of infection and pathogenesis Causative agents either remain extracellularly on the epithelial layer or penetrate into the epithelium (N. Oxford: Radcliffe Medical Press. There is a correlation between promiscuity and low socioeconomic status and the frequency of infections due to Neisseria gonorrhoeae and C. 37-45. 9. can usually be identified microscopically. Bacteriuria in male patients infected with human immunodeficiency virus type 1.uk Ashley C. clinical evidence of Mycoplasma or Ureaplasma is caused by asymptomatic colonisation of the urogenital tract. In all patients with urethritis. Trichomonas sp. Mycoplasma hominis probably does not cause urethritis. and Ureaplasma urealyticum is an infrequent cause. Although arising from urethritis. Summary of product characteristics from electronic medicines compendium for individual drugs. Recent evidence has suggested that Myc.000) and eventually.8. 400 mg orally as a single dose.1 URETHRITIS Epidemiology From a therapeutic and clinical point of view. genitalium can also cause cervicitis and pelvic inflammatory disease in women (6) (LE: 3) 9. dysuria and urethral pruritus are symptoms of urethritis. 9. trachomatis. The Gram stain is the preferred rapid diagnostic test for evaluating urethritis.2 pathogens Pathogens include N. Basel: Karger. alguria. gonorrhoeal urethritis has to be differentiated from non-specific urethritis. 2.medicines.

sexual lifestyle.2. et al. 9. http://www. the treatment of sexual partners is necessary. Trichomoniasis in men: old issues and new data. et al.gov/pubmed/9634302 Evans BA. 5.gov/pubmed/9634303 Krieger JN.Alternative regimens • ciprofloxacin.20(4):325-32. References Borchardt KA. Persons who have been diagnosed with a new STD should receive testing for other STDs. Prevalence of Trichomonas vaginalis in a male sexually transmitted disease clinic population by interview.nih. this class of antibiotics is no longer recommended for the treatment of gonorrhoea in the United States. As in other STDs. and genital infection among women attending a genitourinary medicine clinic in London (1992). Detection of Mycoplasma genitalium and Chlamydia trachomatis DNAs in male patients with urethritis using the polymerase chain reaction.gov/pubmed/7624817 2.gov/pubmed/9385602 Evans BA. 500 mg orally as single dose • ofloxacin. 400 mg orally as single dose • levofloxacin.nih. In Europe. however. http://www.8 1. Sex Transm Infect 1998 Feb. sexual behaviour.gov/pubmed/8566985 Busolo F. besides erythromycin and azithromycin. 250 mg orally as single dose.ncbi. 500 mg orally four times daily for 14 days erythromycin ethylsuccinate.ncbi. Racial origin. provided their symptoms have resolved and their sexual partners have been adequately treated.ncbi. an active antichlamydial therapy should be added. New Microbiol 1997 Oct. and the InPouch TV test. 4. vaginalis and/or Mycoplasma with a combination of metronidazole (2 g orally as single dose) and erythromycin (500 mg orally four times daily for 7 days).nlm. Bond RA. a regimen with amoxicillin 500 mg three times daily for 7 days is also recommended. 800 mg orally four times daily for 7 days ofloxacin.nlm.nlm. 500 mg orally once daily for 7 days Doxycycline and azithromycin are considered to be equally effective in the treatment of chlamydial infections.71(6):405-6. 3. gonorrhoeae.nlm. Patients should be instructed to abstain from sexual intercourse until 7 days after therapy is initiated.74(1):40-4. infections with Myc. Sex Transm Dis 1995 Mar-Apr. Genitourin Med 1995 Dec. http://www.ncbi. one should consider treating infections by T. Maida N. Because gonorrhoeae is frequently accompanied by chlamydial infection. Bond RA. Erythromycin is less effective and causes more side effects. Racial origin. therefore. 64 UPDATE MARCH 2011 . 100 mg orally twice daily for 7 days As second choice of treatment: erythromycin base. As a result of the continuous spread of fluoroquinolone-resistant N. wet mount microscopy. http://www.6.nih. Bordignon G.nlm. Kell PD. 300 mg orally twice daily for 7 days levofloxacin. Treatment of non-gonorrhoeal urethritis The following treatment has been successfully applied to non-gonorrhoeal urethritis: As first choice of treatment: azithromycin. knowledge of local susceptibility patterns is mandatory for the correct treatment of gonorrhoeal urethritis. 1 g orally as single dose doxycycline.nih. Note that fluoroquinolones are contraindicated in adolescents (< 18 years) and pregnant women.7 Follow-up and prevention Patients should return for evaluation if symptoms persist or recur after completion of therapy.22(2): 83-96. If therapy fails. fluoroquinolones and doxycycline are contraindicated. MacRae KD. In pregnant women. Sex Transm Infect 1998 Feb. 9. and genital infection among heterosexual men attending a genitourinary medicine clinic in London (1993-4). including syphilis and HIV. 1b A 1b A LE 1b 1b gR A A 9.nih.74(1):45-9. Camposampiero D. al-Haraci S.ncbi. http://www. genitalium may respond better to azithromycin (11).

nlm.48(2):96-104. In chronic bacterial prostatitis. GR: B). 2008 Feb. J Midwifery Womens Health 2003 MarApr. The CDC 2002 guidelines for the treatment of sexually transmitted diseases: implications for women’s health care. UPDATE MARCH 2011 65 . A total treatment period of 4-6 weeks is recommended (LE: 3. This chapter reviews documented or suspected bacterial infections of the prostate.gov/pubmed/213495 Workowski KA. Diagnosis and etiology of nongonococcal urethritis. CDC sexually transmitted diseases treatment guidelines. Haggerty CL.ncbi.gov/pubmed/12902584 10. Jensen JS. According to the duration of symptoms.138(4):445-54. pROSTATITIS AND CHRONIC pELVIC pAIN SYNDROME 10. 11. more recently. and for whom antimicrobial therapy therefore has a rational basis. Despite the existence of some scientifically valid studies. a fluoroquinolone or trimethoprim should be given orally for 2 weeks after the initial diagnosis. Evidence for a role of Mycoplasma genitalium in pelvic inflammatory disease.1 Summary and recommendations Bacterial prostatitis is a disease entity diagnosed clinically and by evidence of inflammation and infection localised to the prostate. http://www.ncbi.ncbi.nih. is detected by routine methods in only 5-10% of cases (2). http://www. The remainder of patients are treated empirically with numerous medical and physical modalities.79:318-9.gov/pubmed/12686941 Falk L. http://www. Curr Opin Infect Dis.gov/pubmed/18192788 Swartz SL. A causative pathogen. in which an infective origin is accepted. the term prostatitis has included both acute and chronic bacterial prostatitis. GR: B).35(Suppl 2):S135-7. 8.nih. which may include a broad-spectrum penicillin. 7. http://www. Berman SM.ncbi.nlm.nih. However. Sex Transmit Infect 2003 Aug. 10. including molecular biology.gov/pubmed/12891051 Scharbo-Dehaan M. Clin Infect Dis 2002 Oct 15. Acute bacterial prostatitis can be a serious infection. in which no infective agent can be found and whose origin is multifactorial and in most cases obscure.gov/pubmed/12353199 Burstein GR.nlm.nlm. 10. Fredlund H.6. however. http://www. Treatment is required until there is defervescence and normalisation of infection parameters (LE: 3.ncbi. Patients with CPPS are treated empirically with numerous medical and physical modalities. Kraus SJ. http://www. no specific recommendations have been made until now. Curr Opin Pediatr 2003 Aug. It is recommended that European urologists use the classification suggested by the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) of the National Institutes of Health (NIH). 9.ncbi.15(4):391-7. Sexually transmitted diseases treatment guidelines.nih.nlm.2 Introduction and definition Traditionally. All of these agents can be combined with an aminoglycoside for initial therapy. bacterial prostatitis is described as either acute or chronic. a third-generation cephalosporin. recent improvement in classification and application of modern methods.nih. and if infection is strongly suspected in CPPS.21(1):65-9. J Infect Dis 1978 Oct. The patient should then be reassessed and antibiotics only continued if pretreatment cultures are positive and/or the patient has reported positive effects from the treatment. should allow proper systematisation of treatment (3-5). when symptoms persist for at least 3 months. Anderson DG. In less severe cases. This has been because patients with CPPS probably represent a heterogeneous group of diseases and therapeutic outcome is always uncertain. GR: B). Parenteral administration of high doses of a bactericidal antibiotic is usually required. CPPS. Prostatitis and CPPS are diagnosed by symptoms and evidence of inflammation and infection localised to the prostate (1). Tetracycline treatment does not eradicate Mycoplasma genitalium. and the term prostatitis syndrome or. Herrmann KL.nlm. or a fluoroquinolone. Workowski KA. et al.nih. in which bacterial prostatitis with confirmed or suspected infection is distinguished from chronic pelvic pain syndrome (CPPS). a fluoroquinolone may be given orally for 10 days (LE: 3.

Prostatitis symptom questionnaires have therefore been developed for the quantification of symptoms (10. the prostate may be swollen and tender on digital rectal examination (DRE). initiated by the NIH (USA) (12). Prostatic massage is contraindicated. Otherwise.3).3.11).3. They include the Chronic Prostatitis Symptom Index (CPSI). which was recently developed by the International Prostatitis Collaborative Network (IPCN). bacterial prostatitis is described as either acute or chronic. Chronic bacterial prostatitis is the most frequent cause of recurrent UTI in men (9). as described by Meares and Stamey (1) (see Appendix 16.3 Diagnosis 10.1 and 10.2: LUTSs in prostatitis and CppS* Frequent need to urinate Difficulty urinating. The inclusion of leukocytes in the ejaculate as part of the new consensus CPPS concept allows almost twice as many patients to be reclassified into group IIIA as were formerly included in the category abacterial prostatitis using the earlier Drach’s classification (13).1: Localisation of pain in prostatitis and CppS* Site of pain Prostate/perineum Scrotum and/or testes Penis Urinary bladder Lower back *Adapted from Zermann et al. Table 10.3 Urine cultures and expressed prostatic secretion The most important investigations in the evaluation of the patient with prostatitis are quantitative bacteriological localisation cultures and microscopy of the segmented urine and of expressed prostatic secretion (EPS).3. Clinical examination should include evaluation of the pelvic floor musculature. An essential consideration in the clinical evaluation is to exclude differential diagnoses.3. two regarding urination. weak stream and straining Pain on urination. Table 10. Although the CPSI has been validated. 10.1. According to the classification developed by the NIDDK/NIH (Table 10. such as other diseases in the urogenital organs and anorectal disorders.2) (6-8).1 History and symptoms According to the duration of symptoms. percentage of patients 46% 39% 6% 6% 2% 66 UPDATE MARCH 2011 . (8) 10. the latter being defined by symptoms that persist for at least 3 months (3-5).10. the presence of leukocytes in post-massage urine and ejaculate are also included in the definition of inflammatory chronic prostatitis or CPPS (group IIIA) (3). The predominant symptoms are pain at various locations and LUTSs (Tables 10. to date. 10. its benefit in clinical studies is still uncertain. (6). the prostate is usually normal on palpation. and three related to quality of life (see Appendix 16. The questionnaire contains four questions regarding pain or discomfort.g.6).2 Clinical findings In acute prostatitis.1 Symptom questionnaires Symptoms appear to have the strongest basis for use as a classification parameter in bacterial prostatitis as well as in CPPS (10). e. or that increases with urination *Adapted from Alexander et al.5).

Non-inflammatory CPPS (no white cells in semen/EPS/VB3) Asymptomatic inflammatory prostatitis (histological prostatitis) IV CPPS = chronic pelvic pain syndrome.CPPS A. C. VB3 = voided bladder urine 3 (urine following prostatic massage). mirabilis Enterococcus faecalis P. especially E. Blastomyces dermatitidis and Histoplasma capsulatum (16). Prostatic biopsy is not indicated in the routine management of prostatitis/CPPS. tuberculosis. EPS = expressed prostatic secretion. Other inflammatory markers include elevated pH. urealyticum Myc.4 Perineal biopsy Perineal biopsies may be taken to help in the detection of difficult-to-culture microorganisms. 10. and rare pathogens. and seminal fluid. In patients with immune deficiency or HIV infection. they are classified in the new category of asymptomatic prostatitis (type IV) (Table 10. 10.Table 10. but these results do not differ from the findings in asymptomatic controls (19). Candida sp.4: Most common pathogens in prostatitis Aetiologically recognised pathogens* E. such as M. patients with clearly defined chronic bacterial prostatitis were excluded. If such patients are asymptomatic. In both studies. aeruginosa Organisms of debatable significance Staphylococci Streptococci Corynebacterium sp. Bacteria have been cultured from perineal prostate biopsies in 36% of men with CPPS. trachomatis. and cannot be recommended as part of the routine work-up. However.3. histological prostatitis is frequently diagnosed in biopsies taken for suspected prostate cancer.3). trachomatis U. coli Klebsiella sp. The Enterobacteriaceae. (2) and Schneider et al. are the predominant pathogens in bacterial prostatitis (Table 10. Inflammatory CPPS (white cells in semen/EPS/VB3) B. but perineal biopsy should be reserved for research purposes.4) (14). lactate dehydrogenase (LDH) and immunoglobulins UPDATE MARCH 2011 67 . hominis *Adapted from Weidner et al.3. It has also been shown that culture. Table 10. leukocyte and antibody status does not predict antibiotic response in this group of prostatitis patients (18). such as Coccidioides immitis. however.5 Other tests The main parameter for diagnosis of inflammation in the male urogenital tract is increased leukocyte counts in the prostatic fluid. such as C. (14) There is no correlation between leukocyte and bacterial counts and the severity of symptoms in men with chronic prostatitis/CPPS (17). post-prostate massage urine. coli. Prot.3: Classification of prostatitis and CppS according to NIDDK/NIH (3-5) Type I II III Name and description Acute bacterial prostatitis Chronic bacterial prostatitis Chronic abacterial prostatitis . is uncertain (15). prostatitis may be caused by fastidious pathogens. The significance of intracellular bacteria.

10. and eventually prevent the prostatitis syndrome’ (4). and the distance from the patient’s home to the urologist. or isolation of an organism whose aetiological significance is debatable No significant prostatic inflammation Failure to isolate an organism from the prostatic fluid/urine In 1995. Ten years later. IL-1ß and TNF-α. A suggested algorithm for diagnostic evaluation is presented in Table 10. and positive cultures in EPS and in segmented urine samples. This classification is now used as a logical basis for choice of treatment. which has been accepted by the IPCN. A new category (type IV) of asymptomatic prostatitis (histological prostatitis) was added (Table 10. because it is unreliable for diagnosis. The NIDDK recommended a new classification of the prostatitis syndrome. uroflowmetry and residual urine Four-glass test according to Meares and Stamey Microscopy Culture Try antibiotics if signs of inflammation 10. treat.(20).6 Classification systems The purpose of the culture technique described by Meares and Stamey in 1968 was to decide whether bacteriuria originated from the urethra.3. the NIDDK of the NIH (USA) convened a workshop to ‘develop a plan which would enable clinicians and research investigators to effectively diagnose.e. and is still included in the latest WHO classification of diseases (ICD 10) (24). Table 10. VB2) and urine following prostatic massage (third voided bladder urine-3.3.7 Diagnostic evaluation The content and order of procedures in the diagnostic evaluation of a patient with suspected prostatitis depends on previous examinations undertaken by GPs. However. An experienced urologist should decide which investigations are relevant for each 68 UPDATE MARCH 2011 . coeruloplasmin or polymorphonuclear (PMN) elastase in the ejaculate. The cytokines. calcification in the prostate.5: Classification of prostatitis according to Drach et al (23) Classification Acute bacterial prostatitis Chronic bacterial prostatitis Chronic abacterial prostatitis Prostatodynia Clinical and laboratory findings Clinically significant infection of the prostate Significant inflammation of the prostate Isolation of an aetiologically recognised organism from the prostatic fluid/urine Significant prostatic inflammation Failure to isolate an organism from the prostatic fluid/urine. the established routines in different hospitals and countries. Table 10. cannot be considered to be part of routine diagnostic work-up (21).6. The terms abacterial prostatitis and prostatodynia were exchanged for CPPS. This has been the most widely used classification of prostatitis for almost three decades (Table 10. mid-stream urine (second voided bladder urine-2.3. Drach et al. (23) suggested a classification of prostatitis based on the work of Meares and Stamey. respectively. and dilatation in the seminal vesicles. with or without inflammation. i.6: Algorithm for diagnostic urological work-up in prostatitis Clinical evaluation Urinalysis and urine culture Exclude STDs Micturition chart. TRUS is not an important classification parameter in prostatitis (22). may be identified in EPS (20) and complement C3.5). however. prostate or bladder. Transrectal ultrasound (TRUS) may reveal intraprostatic abscesses.8 Additional investigations The EAU working group believes that guidelines on prostatitis should not contain a set of minimum differential diagnostic examinations. in which various types of prostatitis were differentiated according to the number of leukocytes. VB3). 10. first voided bladder urine-1 (VB1). These tests. Seminal secretion was added to segmented urine and EPS as an additional parameter.3).

and the detection rate for positive cultures is significantly reduced (26).4 Treatment 10. many clinical studies report a beneficial effect of antibiotics in inflammatory CPPS (37. serum PSA will normalise after antimicrobial treatment for 4 weeks in about 50% of patients (30). are listed in Table 10. even though bacteria have not been detected by routine methods (35. Relatively high doses are needed and oral therapy is preferred (33. or endoscopy. A combination treatment of β-blockers and antibiotics is reported to have a higher cure rate than antibiotics alone in inflammatory CPPS (Type IIIA+B) (39) (LE: 1b. Parenteral administration of high doses of bactericidal antibiotics. GR: B).individual patient. Bladder outflow and urethral obstruction should always be considered and ruled out by uroflowmetry. The patient should then be reassessed and antibiotics continued only if cultures are positive or the patient reports positive effects from the treatment. e. nor the combination of ciprofloxacin and tamsulozin was superior to placebo in reducing symptoms in men with moderate to severe symptoms (40) (LE: 1b. together with their advantages and disadvantages. such as ciprofloxacin and levofloxacin. UPDATE MARCH 2011 69 . It is difficult to differentiate between spermatocytes and leukocytes. Anorectal examination is carried out whenever indicated. In addition. Fluoroquinolones.28).4. unless specific methods are applied. Interstitial cystitis is diagnosed by means of a micturition chart. and general symptoms.7 (33). tetracyclines or erythromycin should be given (33. in this study. 10. levofloxacin is active against Gram-positive and atypical pathogens. in a recent randomised. Furthermore. peroxidase staining (25). For initial therapy. In chronic bacterial prostatitis and in inflammatory CPPS. cystoscopy and biopsy. A delay of at least 3 months should be allowed before it can be assumed that a stable level of PSA has been reached. Acute bacterial prostatitis can be a serious infection with fever. This is a treatment option that is favoured by many urologists.38) (LE: 2b. GR: B). such as a broad-spectrum penicillin. However. trachomatis and genital mycoplasmas (LE: 2b. The reason for administration of antibiotics in inflammatory CPPS is that there may be a bacterial infection.g. GR: B). GR: B). are considered drugs of choice because of their favourable pharmacokinetic properties (33) (LE: 2b.36).1 Antibiotics Antibiotics are life-saving in acute bacterial prostatitis. A total treatment period of 4-6 weeks is recommended. 10. their generally good safety profile. GR: B).4. After defervescence and normalisation of infection parameters. and may be tried in inflammatory CPPS. The duration of antibiotic treatment is based on experience and expert opinion and is supported by many clinical studies (34). including P. many patients were included who had already been heavily pretreated with different drug regimens. GR: B). double-blind. If intracellular bacteria have been detected or are suspected. intense local pain. oral therapy can be substituted and continued for a total of 2-4 weeks (32). a fluoroquinolone may be given orally for 10 days (5) (IVC).38) (LE: 2a. Measurement of free and total PSA adds no practical diagnostic information in prostatitis (31). bladder cancer must be excluded by urine cytology and cystoscopy. If a patient has elevated PSA and evidence of prostatic inflammation. and antibacterial activity against Gramnegative pathogens. If suspected.2 Antibiotics and β-blockers in combination therapy Urodynamic studies have shown increased urethral closing pressure in patients with chronic prostatitis (5). may be administered. The measurement of cytokines and biofilms in EPS has research interest only (6. although intriguing results have been obtained in some studies (27). recommended in chronic bacterial prostatitis. The recommended antibiotics in chronic bacterial prostatitis and inflammatory CPPS (NIH type IIIA). a third-generation cephalosporin or a fluoroquinolone. antibiotics should be given for 2 weeks after initial diagnosis. GR: B). aeruginosa. Ureteric calculus is ruled out by unenhanced spiral CT or intravenous pyelography. In less severe cases. such as C. it was shown that neither ciprofloxacin.34) (LE: 3. these regimens may be combined with an aminoglycoside. tamsulozin. Microscopic examination of ejaculate is inferior to microscopy of EPS. placebo-controlled multicentre study. Video-urodynamics and advanced urodynamic examination with measurement of urethral closing pressure are not justified in the routine evaluation of patients with prostatitis. retrograde urethrography. However. Prostatespecific antigen (PSA) values may be elevated in both symptomatic and asymptomatic prostatitis (29).

and enterococci • Contraindicated in renal and liver failure • Risk of skin sensitisation • Minimal supporting data from clinical trials • Unreliable activity against Gram-negative bacteria Reserve for special indications • No activity against Pseudomonas. Reserve for special indications 70 UPDATE MARCH 2011 . In general. aeruginosa • In general.4. Aeruginosa • Unreliable activity against coagulase-negative staphylococci.47) (LE: 2a. GR: B). except for drainage of prostatic abscesses. good safety profile Trimethoprim • Good penetration into prostate • Oral and parenteral forms available • Relatively cheap • Monitoring unnecessary • Active against most relevant Pathogens Tetracyclines • Cheap • Oral and parenteral forms available • Good activity against Chlamydia and Mycoplasma • No activity against P. some patients need bladder drainage. Pentosan polysulphate sodium may reduce symptoms and improve quality of life in patients with CPPS (42) (LE: 2a.Table 10.45). coli.4. GR: B). A positive effect of transurethral resection of the prostate (TURP) and transurethral needle ablation has been observed in patients with severe discomfort (46. the results of which are dubious (48). some enterococci and some Enterobacteriaceae Consider Disadvantages • Depending on the substance: • Drug interactions • Phototoxicity • Central nervous system adverse events Recommendation Recommend Fluoroquinolones Macrolides • Reasonably active against Gram-positive bacteria • Active against Chlamydia • Good penetration into prostate • Relatively non-toxic *Adapted from Bjerklund Johansen et al. GR: B).7: Antibiotics in chronic bacterial prostatitis* Antibiotic Advantages • Favourable pharmacokinetics • Excellent penetration into the prostate • Good bioavailability • Equivalent oral and parenteral pharmacokinetics (depending on the substance) • Good activity against typical and atypical pathogens and P. Even radical prostatovesiculectomy has been carried out to relieve the pain of chronic prostatitis. 10. surgery should be avoided in the treatment of prostatitis patients. preferably with a suprapubic catheter.4 Intraprostatic injection of antibiotics This treatment has not been evaluated in controlled trials and should be considered only if oral treatment fails to eradicate the infection (44. other Enterobacteriaceae. GR: B).4.5 Surgery In acute prostatitis. 10. E. (33) 10.3 Other oral medication The β-blocker terazosin has been found to be superior to placebo in reducing symptoms for patients with CPPS (41) (LE: 1b. Finasteride will provide some improvement for patients with category IIIA prostatitis (43) (LE: 1b.

35(5):258-62. McNaughton-Collins M. 12. http://www. Int J Antimicrob Agents 1999 May.ncbi.nlm. Prostatitits.gov/pubmed/10022711 Alexander RB. Andrologia 2003 Oct. Trissel D.5 1.nlm. 11.gov/pubmed/11025703 Schneider H.gov/pubmed/10026774 Litwin MS.nlm. there is no evidence of an infection. eds.282(3):236-7. 3.nih.25(4): 677-84. In: Armstrong D. Urology 1996 Oct. 10. 9. Chronic prostatitis workshop.nlm. Schiefer HG.gov/pubmed/10394972 Zermann DH.6 Other treatment forms Microwave energy delivered from Prostatron 2. 2. Aghajanyan IG.nih. London: Mosby. Krauss H.nih. Fanarjyan SV.nlm. however. J Urol 1999 Mar.gov/pubmed/9801092 Alexander RB.164(5):1554-8. 5. Dec 7-8. that symptoms resolve within 1 year in about 30% of men with CPPS (51) (2).gov/pubmed/10422990 Workshop Committee of the National Institute of Diabetes and Digestive and Kidney Disease (NIDDK).nih.ncbi. Chlamydial and ureaplasmal infections in patients with nonbacterial chronic prostatitis.nih. TUMT is still considered an experimental treatment option in patients with a suspected infection.11(3-4):205-11.35(5):263-5. The 2001 Giessen Cohort Study on patients with prostatitis syndrome . Weidner W. 10. Fowler FJ Jr. therefore.nlm.ncbi. Urol Clin North Am 1998 Nov. 16. 15. The National Institute of Health chronic prostatitis symptom index: development and validation of new outcome measure. Jacobs RR.gov/pubmed/8886062 Krieger JN.gov/pubmed/8911515 Nickel JC. Schaeffer AJ. 13. et al. Chapter 58. References Meares EM. Does the chronic prostatitis/pelvic pain syndrome differ from nonbacterial prostatitis and prostatodynia? J Urol 2000 Nov. Ross SO.ncbi.ncbi.ncbi. et al. and the reader is referred to other publications. Ishigooka M.nih. http://www. 14.nlm. coli and Enterobacter cloacae (49). Andrologia 2003 Oct. Hossain HM.gov/pubmed/2055646 Krieger JN. et al. http://www. Chronic prostatitis: a thorough search for etiologically involved microorganisms in 1. Infectious diseases.nlm. Maryland. 7. and transurethral microwave thermotherapy (TUMT) in inflammatory CPPS has been proven to be superior to sham-treated controls (50) (LE: 1b.10. J Urol 1999 Aug.nlm. Chronic prostatitis: results of an Internet survey.nlm. In this condition.nlm.ncbi.ncbi.an evaluation of inflammatory status and search for microorganisms 10 years after a first analysis. 8. epididymitis and orchitis.nih.gov/pubmed/14535852 Naber KG.52(5):744-9. Nyberg L Jr. http://www. Invest Urol 1968 Mar. Ludwig M. UPDATE MARCH 2011 71 .48(5):715-21. http://www. Recurrent lower urinary tract infections in men. Bacteriologic localization patterns in bacterial prostatitis and urethritis. Cohen J. Egan KJ.5(5):492-518. Urology 1996 Nov. http://www.461 patients. It should be recalled. Doggweiler R. 1999. Nickel JC.nih.nih.ncbi. Neurourological insights into the etiology of genitourinary pain in men. Infection 1991.nlm. NIH consensus definition and classification of prostatitis.47:4-15.162(2):369-75. http://www. Elevated levels of proinflammatory cytokines in the semen of patients with chronic prostatitis/chronic pelvic pain syndrome. A number of other medical and physical treatment modalities have been suggested in non-inflammatory CPPS.48(4): 568-74. JAMA 1999 Jul.nih. et al. Bethesda.nlm. J New Rem Clin 1998. http://www. http://www. full coverage of this topic lies beyond the scope of this review.gov/pubmed/14535851 Badalyan RR. http://www. et al.nih. 1995. Prostatitis: US perspective. 4.161(3):903-8.ncbi. Chronic pelvic pains represent the most prominent urogenital symptoms of ‘chronic prostatitis‘. However. Ross SO. Effective office management of chronic prostatitis. Krieger JN.ncbi.4. http://www. Stamey TA.gov/pubmed/10411041 Krieger JN.0 has an in vitro bactericidal effect on laboratory-cultured E. http://www.nih. Hasday J.nih.gov/pubmed/4870505 Weidner W. http://www. Urology 1998 Nov. Chronic Prostatitis Collaborative Research Network.ncbi. 6. GR: B). Ponniah S.ncbi. et al.19 Suppl 3:S119-25.

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141(8):581-9.nlm. 50. et al.ncbi.gov/pubmed/8618295 Nickel JC. A randomized placebo-controlled multicentre study to evaluate the safety and efficacy of finasteride for male chronic pelvic pain syndrome (category IIIA chronic nonbacterial prostatitis). double-blind trial. Transrectal ultrasonography directed intraprostatic injection of gentamycin-xylocaine in the management of the benign painful prostate syndrome. et al.nlm. A report of a 5 year clinical study of 75 patients.(1):18-23. EpIDIDYMITIS AND ORCHITIS 11.ncbi.nih.37. Alpha-blockers for the treatment of chronic prostatitis in combination with antibiotics. Propert KJ. [Transurethral electroresection in chronic prostatitis and its complications. develops in 20-30% of post-pubertal patients with mumps virus infection. Jung PB. 42.159(3):883-7. BJU Int 2002 Nov. Sorensen R. Johnston B. BJU Int 2004 May. Downey J. If mumps orchitis is suspected.52(3):411-5.nih.nlm. 51. Nikiforidis G. BJU Int 2002 Feb.83(4):347-9.nih.gov/pubmed/15142149 Mayersak JS. 47. Liong ML.1 Summary and recommendations Orchitis and epididymitis are classified as acute or chronic processes according to the onset and clinical course.nlm. 43. http://www. Yuen KH.nih. Pentosan polysulfate therapy for chronic nonbacterial prostatitis (chronic pelvic pain syndrome category IIIA): a prospective multicenter clinical trial.ncbi.93(7):991-5. Downey JA.89(3):226-9.ncbi.90(7):678-81. http://www.nlm. de la Rosette JJ.56(3):413-7. [article in Russian] http://www. 40.gov/pubmed/2470185 Lee KC. Transurethral microwave thermotherapy for nonbacterial prostatitis: a randomized double-blind sham controlled study using new prostatitis specific assessment questionnaires. Prostatitis-like symptoms: one year later.nlm. Urol Int 1993.169(2):592-6.nih. placebo controlled trial. et al.ncbi. 38.nih. discussion 1954-5. Ann Intern Med 2004 Oct. J Urol 1996 Jun. Kuz’min GE. Total prostatoseminal vesiculectomy in the treatment of debilitating perineal pain. Nickel KR.nih. The most common type of orchitis.51(3):129-32. Downey J. Gómez JG. The in vitro bactericidal effect of microwave energy on bacteria that cause prostatitis. Chronic Prostatitis Collaborative Research Network. Simonov VIa. http://www. et al. Treatment of chronic prostatitis: intraprostatic antibiotic injections under echography control. et al. Terazosin therapy for chronic prostatitis/chronic pelvic pain syndrome: a randomized. et al. http://www.nlm. 45.nih. Urology 2000 Sep. http://www.ncbi.nih.nih. 48.ncbi. Spalding TH. Tokunaga S. Yamaguchi K.gov/pubmed/1635150 Sahin A. mumps orchitis.gov/pubmed/9474175 Alexander RB. J Urol 1998 Mar. 49.gov/pubmed/11856102 Frazier HA.nih.ncbi.nih.ncbi. 39. Int Surg 1998 Oct-Dec. http://www. http://www.148(2 Pt 1):409-11.139(5):967-70.nlm. J Urol 1992 Aug. J Urol 2003 Feb. et al. http://www. Hubregtse MR.nlm. Diagnosis and treatment of 409 patients with prostatitis syndromes. http://www. Urology 1998 Sep. Tormo FB. Eiley D. 41. Goldfischer ER.gov/pubmed/12544314 Nickel JC.nih.ncbi.41(4):301-7. 44.ncbi. et al.nlm. 46. Paulson DF.nih. et al.gov/pubmed/10962305 Nickel JC.gov/pubmed/12410746 11. http://www. http://www. Antimicrobial treatment for chronic prostatitis as a means of defining the role of Ureaplasma urealyticum.gov/pubmed/10096759 Jiménez-Cruz JF. et al.ncbi. Meuleman EJ. Park HS. Liatsikos EN.gov/pubmed/8249222 Barbalias GA.ncbi. Pontari MA.nlm.155(6):1950-5.gov/pubmed/3283385 Darenkov AF.nih. Transurethral needle ablation for chronic nonbacterial prostatitis.gov/pubmed/15492337 Cheah PY. http://www.] Urol Nefrol (Mosk) 1989 Jan-Feb. Schaeffer AJ. Urology 1993 Apr. http://www.gov/pubmed/9730452 Nickel JC. Ciprofloxacin or tamsulosin in men with chronic prostatitis/chronic pelvic pain syndrome: a randomized.ncbi.nlm.nlm.nlm. J Urol 1988 May.ncbi.gov/pubmed/8470312 Ohkawa M. http://www. a history of parotitis and evidence of IgM antibodies in UPDATE MARCH 2011 73 .nlm.

4 Morbidity Complications in epididymo-orchitis include abscess formation. inflammation of the epididymis. The spermatic cord is usually tender and swollen.the serum supports the diagnosis. the infection is spread from the urethra or bladder. and that in older men. trachomatis is usually causative. Bladder outlet obstruction and urogenital malformations are risk factors for this type of infection. whereas in elderly patients. The most common type of orchitis. treatment could also be continued with doxycycline. acute epididymitis has been a major cause for admission to hospitals of military personnel (2) (LE: 3). and a rare condition with uncertain aetiology that has been reported in about 100 cases in the literature (5). Antimicrobials should be selected on the empirical basis that in young.2 Definition and classification Epididymitis. In non-specific granulomatous orchitis.2). It is imperative for the physician to differentiate between epididymitis and spermatic cord torsion as soon as possible using all available information. Epididymitis is almost always unilateral and relatively acute in onset. 11. 11.6) (LE: 3). According to older data. Acute epididymitis in young men is associated with sexual activity and infection of the consort (3) (LE: 3). In young males it is associated with sexual activity and infection of the consort (LE: 3). it is usually due to common urinary pathogens (LE: 3). A urethral swab and MSU should be obtained for microbiological investigation before antimicrobial therapy (GR: C). lues. Macrolides may be used as alternative agents (GR: C). Fluoroquinolones with activity against C. 11. the inflammation and swelling usually begin in the tail of the epididymis. The microbial aetiology of epididymitis can usually be determined by examination of a Gram stain of a urethral smear and/or an MSU for the detection of Gram-negative bacteriuria (LE: 3). In case of C. the most common uropathogens are involved. causes pain and swelling which is almost always unilateral and relatively acute in onset. On the other hand.7). should be the drugs of first choice. mumps orchitis. and the organisms can lie dormant for months before the onset of symptoms. Paediatric orchitis and mumps orchitis are of haematogenous origin (7). inflammatory processes of the testicle. The spermatic cord is usually tender and swollen. brucellosis and cryptococcus disease. testicular infarction. If C. up positioning of the testes and anti-inflammatory therapy. 200 mg/day. The incidence depends upon the vaccination status of the population (4). chronic inflammation may result in testicular atrophy and the destruction of spermatogenesis (1. for a total of at least 2 weeks. testicular atrophy. Orchitis and epididymitis are classified as acute or chronic processes according to the onset and clinical course. which are also the most common cause of bacteriuria (2.5 pathogenesis and pathology Typically. Abscessforming epididymitis or orchitis needs surgical treatment. ofloxacin and levofloxacin). Supportive therapy includes bed rest.6 Diagnosis In acute epididymitis. 11. the testes are involved in the inflammatory process (epididymoorchitis). trachomatis (e. C. and may spread to involve the rest of the epididymis and testicular tissue. often involve the epididymis. the sexual partner should also be treated (GR: C). in epididymitis due to common bacteria and sexually transmitted organisms. Chronic disease with induration develops in 15% of acute epididymitis cases. trachomatis has been detected. Primary chronic orchitis is a granulomatous disease. Epididymo-orchitis is also seen in systemic infections such as tuberculosis. develops in 20-30% of post-pubertal patients with mumps virus infection. Epididymitis caused by sexually transmitted organisms occurs mainly in sexually active males aged < 35 years (2. All men with epididymitis that is caused by sexually transmitted organisms have a history of sexual exposure. trachomatis epididymitis. In the case of testicular involvement. especially virally induced orchitis.6) (LE: 3).g. autoimmune phenomena are assumed to trigger chronic inflammation (5. If the patient is examined immediately after undergoing urinalysis. which begins in the tail of the epididymis. development of chronic epididymal induration and infertility (2). Chronic epididymitis can sometimes be the first clinical manifestation of urogenital tuberculosis. urethritis and urethral discharge may be missed because WBC and 74 UPDATE MARCH 2011 .3 Incidence and prevalence There are no new data available concerning the incidence and prevalence of epididymitis. The majority of cases in sexually active males aged < 35 years are due to sexually transmitted organisms. 11. sexually active men. Epididymitis causes pain and swelling. The majority of cases of epididymitis are due to common urinary pathogens. and may spread to involve the rest of the epididymis and testicular tissue. In some cases.

7. 3). Acute epididymitis: why patient and consort must be investigated. 650-662. 3. should be the drugs of first choice. for a total period of at least 2 weeks. If uropathogens are found as causative agents. because of their broad antibacterial spectra and their favourable penetration into the tissues of the urogenital tract. fluoroquinolones.nih. Paniagua R.bacteria have been washed out of the urethra during urination. Robinson AJ. epididymitis. Granulomatous orchitis. trachomatis epididymitis. Schiefer HG. Drugs 1987. London: Mosby.ncbi.gov/pubmed/2207549 Weidner W. Chronic epididymitis can sometimes be the first clinical manifestation of urogenital tuberculosis. Successful interferon-alpha 2.ncbi. Azoospermia due to complete obstruction of both epididymides is a rare complication (8). If C. Grant JB. 1984. In many cases. 200 mg/day.66(6):642-5. Farrell J. 5. Eur Urol 1995. the fluoroquinolones have shown favourable properties (9) (LE: 2a). the sexual partner should also be treated (GR: C). Berger RE.gov/pubmed/3481311 Nistal M. Infectious diseases. http://www. with BPH or other micturition disturbances. 1999. clinical evaluation and Doppler (duplex) scanning of testicular blood flow. In young men. Nunnensiek C.nih. Abscess-forming epididymitis or orchitis also needs surgical treatment. 1984.gov/pubmed/2265337 Rüther U.nlm. The presence of intracellular Gram-negative diplococci on the smear correlates with infection with N. a history of parotitis and evidence of IgM antibodies in the serum supports the diagnosis. a urethral swab and MSU should be obtained for microbiological investigation (GR: C). orchitis. and that in older men. Weidner W. The microbial aetiology of epididymitis can usually be determined by examination of a Gram stain of a urethral smear and/or an MSU for the detection of Gram-negative bacteriuria. Aetiological and therapeutic aspects. http://www. Br J Urol 1990 Dec. 11. et al. a therapy for a patient with acute mumps orchitis. pp.27(2):174-6. 1-58. Prostatitis. Harcourt Publishers Ltd. If mumps orchitis is suspected. Stilz S. http://www. Röhl E. In case of C. 11. trachomatis (e. Of these. transient decreased sperm counts and forward motility can be found. preferably those with activity against C. In: Sexually transmitted diseases. http://www. Supportive therapy includes bed rest. Epididymitis. et al. UPDATE MARCH 2011 75 . 40 mg/day. Macrolides may be used as alternative agents (GR: C). trachomatis is isolated in approximately two-thirds of these patients (2. Again.nih. therefore. Testicular and Epididymal Pathology. C. New York: McGraw-Hill. Studies that have compared microbiological results from puncture of the epididymis and from urethral swabs as well as urine have shown very good correlation.8 1. 2. before antimicrobial therapy. In about 20% of mumps orchitis cases. gonorrhoeae.ncbi.66(3):312-4. 4. Br J Urol 1990 Sep.nlm. Mardh P-A. epididymitis can lead to permanent occlusion of the epididymal ducts and thus to infertility. the disease occurs bilaterally in post-pubertal men with a risk of testicular atrophy and azoospermia (3) (LE: 3). Cohen J.nih. a thorough search for micturition disturbances should be carried out to prevent relapse (GR: C).1 Differential diagnosis It is imperative for the physician to differentiate between epididymitis and spermatic cord torsion as soon as possible using all available information. Antimicrobials should be selected on the empirical basis that in young. C.6. up-positioning of the testes and antiphlogistic therapy. Mufti GR. Review of 15 cases. ofloxacin and levofloxacin). Therefore. sexually active men. treatment could also be continued with doxycycline. the most common uropathogens are involved. In: Armstrong D. The presence of only WBC on a urethral smear indicates the presence of non-gonorrhoeal urethritis. References Naber KG. Spencer RC. 6. including the age of the patient.ncbi.nlm. Stuttgart: Thieme. Holmes KK.34 Suppl 1:111-7. 11. Sparling PF. trachomatis has been detected as an aetiological agent. and reduce the dose by half every second day (GR: C).nlm. eds. pp. et al.7 Treatment Only a few studies have measured the penetration of antimicrobial agents into the epididymis and testes in humans. one should consider antiphlogistic therapy with methylprednisolone.6) (LE. trachomatis is usually causative. Garbe C.g. Ejaculate analysis according to WHO criteria including leukocyte analysis indicates persistent inflammatory activity.gov/pubmed/7744163 Aitchison M. Acute nongonococcal epididymitis. history of urethritis. Wiesner PJ (eds).

nih. Special considerations (i. and external genitalia. particularly of obese patients. including S. Andrological findings. http://www.nih. all STDs are caused by > 30 relevant pathogens. Adjunctive treatment such as pooled immunoglobulin and hyperbaric oxygen are not recommended. aureus.1 1. SEXUALLY TRANSMITTED INFECTIONS The classical bacteria that cause venereal diseases. 13. or a recent history of catheterisation..ncbi. References Schneede P. Tissue penetration of sparfloxacin in a rat model of experimental Escherichia coli epididymitis.1 1.nlm. Sexually transmitted diseases (STDs)--a synoptic overview for urologists.e. Klebsiella sp.g.gov/pubmed/12814668 13. 9.nih. http://www. chancroid and inguinal granuloma. http://www. Summary of recommendations Full.nlm. Other bacteria and viruses as well as yeasts. 3. 12.gov/pubmed/9181388 12. Evidence regarding investigation and treatment is predominantly from case series and expert opinion (level 3/4). 2. the onset is more insidious with undiagnosed pain often resulting in delayed treatment. not all pathogens that can be sexually transmitted manifest genital diseases. Wolf S. syphilis. However.gov/pubmed/2120839 Ludwig M. gonorrhoea. FOURNIER’S gANgRENE 13. Weissbach L.25(3):178-84. with subsequently refinement according to culture and clinical response (LE: 3. GR: B). protozoa and epizoa must also be regarded as causative organisms of STD.29(5):277-80. E. e. In up to 40% of cases.2 Background Fournier’s gangrene describes an aggressive and frequently fatal polymicrobial soft tissue infection of the perineum. coli and anaerobic bacteria. GR: B). Typically there is painful swelling of the scrotum or perineum associated with signs of severe sepsis. Risk factors include immuno-compromised patients.nlm. Infection 1997 May-Jun.. GR: C). is required. Jantos CA. together with emergence of multi-resistant pathogens.44(1):1-7.8.] Urologe A 1990 Sep. and allergy) and recommended regimens may be looked up here. II. only account for a small proportion of all known sexually transmitted deceases (STDs) today.3 Clinical presentation Fournier’s gangrene remains rare but its incidence is increasing with an ageing population and higher prevalence of diabetes. Urinary Tract Infection Working Group of the Health Care Office of the European Association of Urology. HIV infection. is 76 UPDATE MARCH 2011 . Concise information and tables that summarise the diagnostic and therapeutic management of STDs in the field of urology allow a synoptic overview and are in agreement with recent international guidelines of other specialities. Weidner W.4 Microbiology Fournier’s gangrene is typically a type 1 necrotising fasciitis that is polymicrobial in origin. pregnancy. Hofstetter AG. 13. et al. A high index of suspicion and careful examination. instrumentation or perineal surgery. Taken together. Examination shows a small necrotic bulla with surrounding erythema and oedema. et al. Garbe C. Crepitus on palpation and a foul-smelling exudate occurs with more advanced disease. and not all genital infections are exclusively sexually transmitted. [Initial therapy of acute unilateral epididymitis using ofloxacin. 13. It is an anatomical sub-category of necrotising fasciitis with which it shares a common aetiology and management pathway. repeated surgical debridement should commence within 24 h of presentation (LE: 3. most commonly diabetes or malnutrition. Tenke P. Eur Urol 2003 Jul. involvement of Clostridium sp. Streptococcus sp.ncbi. perianal region.ncbi. infants. except in the context of clinical trials (LE: 3. Treatment with broad-spectrum antibiotics should be started on presentation.

bibliographic review and assessment of the Fournier’s gangrene severity index.75(5):1193-8. et al. Sonmez Y.nih.nlm. Garcia JD. et al. Lopez JA. Care pathway Diagnosis • History . GR: B). Fournier’s gangrene: overview of prognostic factors and definition of new prognostic parameter. Consensus from case series suggests that surgical debridement should be early (< 24 h) and complete. Fournier’s gangrene: our experience in 5 years. Ozturk E. Recently.62(7): 532-40.SP cathether . Subsequent inflammatory reaction by the host contributes to multi-organ failure and death if untreated. not recommended grade C). 13. This can then be refined following surgical cultures. [Epub ahead of print] PMID: 20579084 http://www. Urology.gov/pubmed/20579084 UPDATE MARCH 2011 77 . to appreciate that the degree of internal necrosis is much greater than suggested by the external signs.gov/pubmed/20451745 2.Colostomy • Cultures Resuscitation • Critical care • Assessment of vital organ function • Agressive fluid replacement Antibiotics • Vancomycin/Linezolid . http://www.now less common. repeated surgical debridement is necessary to save life (LE: 3. What are the indications for a stoma in Fournier’s gangrene? Colorectal Dis. survival rates are > 70% depending upon patient group and availability of critical care (LE: 3).MR gram +ve • Clindomycin .Gram -ve • Metronidazole . These organisms secrete a variety of endotoxins that cause tissue necrosis and severe cardiovascular impairment.nlm. Yilmazlar T. GR: B). The benefit of pooled immunoglobulin therapy and hyperbaric oxygen remains uncertain (LE: 3. severity scoring systems have been devised based on laboratory parameters to aid management.Risk factors • Examination • Assessment of sepsis .ncbi. which suggests the need for colostomy (LE: 3. 2009 Sep. first.nih. Tuncel A.Risk score Surgical debridement • Early < 24 hours • Complete • Diversion . that adequate.5 Management It is essential.Strep • Fluoroquinolone . Concurrent parenteral antibiotic treatment should be given that covers all causative organisms and can penetrate inflammatory tissue (LE: 3. GR: C). 2010 Jun 23. 2010 May.nlm. Morua AG.Anaerobes Wound inspection • Further debridement • Dressing change Critical care • Organ support • Immunoglobulin Rehabilitation • Skin graft • Undiversion • Reconstruction Hyperbaric Oxygen References 1. Following resolution. http://www. GR: B). Arch Esp Urol.ncbi.ncbi. and cross-sectional imaging using CT or MRI can help define para-rectal involvement. because delayed and/or inadequate surgery results in higher mortality (LE: 3/4. reconstruction using skin grafts is required. Hanci V. Erol B. and second.nih.gov/pubmed/19815967 3. With aggressive early surgical management.

et al. Reference Mete Cek M. genetic factors. Redorta JP. Before surgery. In a world of globalisation. 2009. Eur Urol 2006 Jun. http://www. biopsy material on conventional solid media may occasionally be required.nlm. For the population in endemic areas.nih. evidence for the best choice of antibiotics and prophylactic regimens is limited (Table 15. 78 UPDATE MARCH 2011 .1 Summary and recommendations The aim of antimicrobial prophylaxis in urological surgery is to prevent infective complications that result from diagnostic and therapeutic procedures. 14. it is essential to categorise the patients in relation to (1): • general health status according to American Society of Anesthesiology (ASA) score P1-P5.1 1. Although not endemic in Europe.49(6):998-1003. precautions are most important. impaired immune system. et al. there is a direct link to these published guidelines.nih. For travellers. Eur Urol 2005 Sep.1 Urogenital tuberculosis Nearly one third of the world’s population is estimated to be infected with M. surgery in the form of ablation or reconstruction may be unavoidable. which can be consulted for free. SpECIFIC INFECTIONS Urogenital tuberculosis and bilharziasis are two infections that may affect the urogenital tract. Lobel B. EAU guidelines for the management of urogenital schistosomiasis. previous instrumentation. BjerklundJohansen TE. 208: 279-88. which is caused by Schistosoma heamatobium.48(3):353-62. Effective pharmacological treatment is available.nlm. Cek M.4. Botto H. diabetes mellitus. extreme weight. Necrotizing fasciitis: Current concepts and review of the literature. Savatovsky I. Strong M.gov/pubmed/15982799 14. the Members of the Urinary Tract Infection (UTI) Working Group of the Guidelines Office of the European Association of Urology (EAU):. Naber KG. • presence of general risk factors such as older age. Sarani B.nih. the Members of the Urinary Tract Infection (UTI).gov/pubmed/16519990 15. Lenk S.1). Grabe M. travellers are regularly confronted with situations in which they may be infected. Treatment regimens of 6 months are effective in most patients. Pascual J.2 Urogenital schistosomiasis More than 100 million people worldwide are affected by bilharziasis. bacterial burden. however.2. 14. an integrated approach including health education is necessary. 14. Following the abstract printed here.ncbi. tuberculosis. J Am Coll Surg. Tenke P. tuberculosis is the most common opportunistic infection in AIDS patients. Bischop MC. http://www. EAU Guidelines for the Management of Genitourinary Tuberculosis.gov/pubmed/19228540 14. However.1. http://www.ncbi. pERIOpERATIVE ANTIBACTERIAL pROpHYLAXIS IN UROLOgY 15.ncbi. Drugs are the first-line therapy in urogenital tuberculosis. Although chemotherapy is the mainstay of treatment. malnutrition. Moreover.1 1. Reference Bichler KH. Naber KG. The diagnosis of urogenital tuberculosis is made based on culture studies by isolation of the causative organism.nlm. Urogenital tuberculosis is not very common but it is considered as a severe form of extra-pulmonary tuberculosis. indwelling catheters. cases of urogenital tuberculosis are occasionally diagnosed in all communities. Both radical and reconstructive surgery should be carried out in the first 2 months of intensive chemotherapy. • presence of specific endogenous or exogenous risk factors such as a history of UTI or urogenital infection. Guidelines on the diagnosis and management of these two infections have been published elsewhere.

No concern given to burden of tumor. fluoroquinolones. Table 15.5) procedure Diagnostic procedures Cystoscopy Urodynamic study Transrectal core biopsy of prostate Diagnostic ureteroscopy Therapeutic procedures TURB TURP ESWL (standard. There is no evidence for any benefits of antibiotic prophylaxis in standard non-complicated endoscopic procedures and extracorporeal shockwave lithotripsy (ESWL). aminopenicillins plus a beta-lactam inhibitor. Many antibiotics are suitable for perioperative antibacterial prophylaxis. Best practice includes surveillance and an audit of infectious complications. GR: A) are well documented. second-generation cephalosporins. multiplicity. Broader-spectrum antibiotics including fluoroquinolones should be used cautiously and reserved for treatment. For open and laparoscopic surgery. the same rules as in abdominal and gynaecological surgery can be applied. and aminoglycosides. This applies also to the use of vancomycin.• • type of surgery and surgical field contamination burden. prolongation of perioperative antibiotic prophylaxis is not recommended. no risk factors such as the presence of a stent or nephrostomy tube) Ureteroscopy stone Percutaneous stone management Open and laparoscopic surgery Clean operations (no opening of urinary tract) Nephrectomy Scrotal surgery Prosthetic implants Clean-contaminated (opening of urinary tract) Nephroureterectomy Ureteropelvic junction repair Total (radical) prostatectomy 3 4 2a B C B Poor documentation No studies detected No RCT. The use of antimicrobials should be based on knowledge of the local pathogen profile and antibiotic susceptibility pattern. Only transrectal core prostate biopsy (LE: 1b. size. Opening of the urinary tract is considered as clean-contaminated surgery.1: Level of evidence and grade of recommendation for standard urological procedures (The consequences in terms of antibiotic prophylaxis are given in Table 15. GR: A) and TURP (LE: 1a.e. A single dose or a short course of antimicrobials can be given parenterally or orally. necrosis Good documentation Low frequency of infections Contradictory findings Literature does not distinguish between severity of stone management High risk of infection 1b 1a 1b 4 A A A C Low frequency of infections Contradictory findings Low frequency of infections Contradictory findings High risk of infection Assess carefully risk factors No available studies LE gR Remarks UPDATE MARCH 2011 79 . In a case of continuous close urinary drainage. e.g. Oral administration requires drugs that have good bioavailability. whereas a single or 1-day dose is recommended in clean-contaminated/contaminated operations. although it is recommended in complicated procedures and patients with identified risk factors. i. co-trimoxazole. expected level of surgical invasiveness. No antibiotic prophylaxis is recommended for clean operations. poor documentation 3 3 3 C C B SSI poorly documented Catheter-related UTI Review studies contradictory Limited documentation Regimen not well defined 2b 1a 1a/1b 2b 2b C A A B B Poor data. The administration route depends on the type of intervention and patient characteristics. duration and technical aspects.

such as the Paul Ehrlich Society for Chemotherapy. e. The survey illustrated the need for a stringent antibiotic policy throughout Europe. including > 200 urological services or units.2 Introduction Antibiotic prophylaxis in urology has been controversial for many years. however. Antibiotic prophylaxis is only one of several measures to prevent infections and can never compensate for poor hygiene and operative technique. Clearly. TURP = transurethral resection of the prostate. Several surveys among urologists in Europe have revealed wide differences in regimens and choice of antibiotics for prophylaxis.7% of patients had a healthcare-associated UTI (10).2 illustrates the different types of infectious complications encountered in urological surgery. there is a need for evidence-based guidelines (2-6). These definitions have also been used in the recent panEuropean study on nosocomial UTI (10). SSI = surgical site infection. Antibiotic prophylaxis aims to prevent healthcareassociated infections that result from diagnostic and therapeutic procedures.g. There is also a dilemma regarding the definition of infections. In contrast. and that recommendations for antibiotic prophylaxis should be included in the general antibiotic policy of each hospital. One systematic review of antibiotic prophylaxis in urological surgery has been published (9). French Association of Urology (8) and of an international consensus working group (1).2: Main types of healthcare-associated infections encountered in urological practice Site of infection Minor Major Deep wound infection Wound rupture (abdominal dehiscence) Deep abdominal or surgical site abscess Febrile UTI Pyelonephritis Renal abscess SIRS or sepsis with signs of systemic response Acute bacterial prostatitis (type I) Pneumonia Surgical wound Superficial wound infection Incision/surgical site infection (SSI) UTI or organ-specific infection Asymptomatic bacteriuria (bacterial colonisation) Symptomatic lower UTI Bacteremia without signs of systemic response Epididymitis (Orchitis) Blood stream Septic embolism Other urogenital sites Other sites 80 UPDATE MARCH 2011 . TURB = transurethral resection of the bladder. RCT= Randomised Controlled Trials 15. The present section aims to clarify the current state of knowledge and to propose practical recommendations based on clinical studies. Table 15. The US Centers for Disease Control and Prevention (CDC) have presented definitions that are currently the most comprehensive. Urological practice has changed particularly in the last decade and older studies are no longer relevant. patients with long-term indwelling catheters and bacteriuria.Partial bladder resection Cystectomy with urine deviation 3 2a C B No specific RCT studies Limited documentation Clean-contaminated/contaminated (opening of bowel. There are some clinical situations. antibiotic therapy is the treatment of a clinically suspected or microbiologically proven infection. The results of the review strengthen the underlying documentation for the present recommendations. the corresponding working groups of the German Society of Urology (7). Table 15. The survey found that 9. These patients must receive antibiotics at the time of surgery. Most studies in the past have been poorly designed and have lacked statistical power. There has been inconsistency concerning definitions and assessment of risk factors. Revision of definitions and recommendations are ongoing in some countries (12). The section also considers the recommendations of societies. urine deviation) ESWL = extracorporeal shockwave lithotripsy. that are not easily classified as either prophylaxis or therapy.3 goals of perioperative antibacterial prophylaxis Antibiotic prophylaxis and therapy are two different issues. 15. expert opinion and professional consensus. A recent pan-European survey was carried out by the EAU Section for Infection in Urology (ESIU) in a large number of European countries. and are recommended for the evaluation of infectious complications (11). regardless of how they are classified.

Another question is whether perioperative prophylaxis should also be concerned with the prevention of non-urological infections. previous instrumentation.3: generally accepted risk factors for infectious complications general risk factors Older age Deficient nutritional status Impaired immune response Diabetes mellitus Smoking Extreme weight Coexisting infection at a remote site Lack of control of risk factors The pan-European study on nosocomial UTI (10) has identified the three most important risk factors for infectious complications as: • an indwelling catheter. as well as serious wound infections directly related to surgery (Table 15. Furthermore. The wide spectrum of interventions further complicates the provision of clearcut recommendations. It is generally agreed that its main aim is to prevent symptomatic. bacterial burden. asymptomatic bacteriuria after TURP or other endourological procedures can disappear spontaneously and is usually of no clinical significance.e. epididymitis and urosepsis. In some circumstances. e. even in the presence of sterile urine (6. which could easily be treated on an outpatient basis. prostatitis. or surgery of the renal pelvis and ureter) should be classified as clean or clean-contaminated surgery in cases of negative urine culture. Sepsis can be seen with all types of procedures. the surgeon’s skill.15). febrile urogenital infections such as acute pyelonephritis. 15. extreme weight.3) are underestimated in most trials. • presence of general risk factors such as older age.SSIs are seen after open surgery and to some extent after laparoscopic surgery. However. contaminated. They are related to: • general health of the patient as defined by ASA score P1-P5. The same applies to endoscopic and transurethral surgery. • presence of specific endogenous or exogenous risk factors such as a history of UTI or urogenital infection. clean-contaminated. bladder surgery. impaired immune system. • long preoperative hospital stay. The traditional classification of surgical procedures according to Cruse and Foord (13) into clean. Table 15. radical prostatectomy. the duration and difficulty of the operation. and dirty operations applies to open surgery but not to endourological interventions. genetic factors.4 Risk factors Risk factors (Table 15.g. • expected level of surgical invasiveness. even minor wound infections can have serious consequences. It is still debated whether opening of the urinary tract (i. • type of surgery and surgical field contamination. Perioperative antibacterial prophylaxis in urology must go beyond the traditional aim of prophylaxis in surgery. • previous urogenital infection. they are important in the preoperative assessment of the patient. However. indwelling catheters. the bacterial load. Febrile and complicated UTIs are mainly complications of endoscopic surgery and the use of indwelling catheters and stents. The risk of infection varies with the type of intervention. and perioperative bleeding may also influence the risk of infection (6). However. malnutrition.14. They can also occur following open surgery of the urinary tract. as in implant surgery. members of the EAU Expert Group consider these procedures as clean-contaminated because urine culture is not always a predictor of bacterial presence. duration and technical aspects. The endpoints of perioperative prophylaxis in urology are debatable. and the lower genitourinary tract is colonised by microflora. which is the prevention of wound infections. This might be extended to asymptomatic bacteriuria and even minor wound infections.2). Special risk factors associated with an increased bacterial Load Long preoperative hospital stay or recent hospitalisation History of recurrent urogenital infections Surgery involving bowel segment Colonisation with microorganisms Long-term drainage Urinary obstruction Urinary stone UPDATE MARCH 2011 81 . endocarditis and postoperative pneumonia. diabetes mellitus.

1.6.4 and the empirical relationship between the level of invasiveness and risk for infective complications is illustrated in Figure 15. ideally to a single preoperative antibiotic dose. target organ.5. aminoglycosides and fluoroquinolones. co-trimoxazole.a and 15. 15. resistance is correlated with an up to fourfold difference in sales of antibiotics (25).1 Timing There is a given time-frame during which antibiotic prophylaxis should be administered. 15.5. Antimicrobial resistance is usually higher in Mediterranean compared with Northern European countries. Fluoroquinolones should be avoided as far as possible for prophylaxis. a tentative classification of the urological procedures in relation to the surgical field contamination level is given in Table 15. many antibiotics are suitable for perioperative antibacterial prophylaxis. These timings allow antibiotic prophylaxis to reach a peak concentration at the time of highest risk during the procedure. 15. it is necessary to consider the procedurespecific risk factors. However. duration of antibiotic prophylaxis has not yet been adequately addressed and rarely can a defined regimen be recommended. knowledge of the local pathogen profile. as there are considerable variations in Europe regarding both bacterial spectra and susceptibility to different antibiotics. For practical purposes. aminopenicillins plus a BLI. Administration of the drug several hours before surgery is probably less effective.5.5 principles of antibiotic prophylaxis Antibiotic prophylaxis aims at protecting the patient but not at the expense of promoting resistance. susceptibility and virulence is mandatory in establishing local antibiotic guidelines. Perioperative prophylaxis should be prolonged only where there are significant risk factors (see Section 15. 15.4 Choice of antibiotics No clear-cut recommendations can be given. The optimal time for antibiotic prophylaxis is from 2 h before but not later than 3 h after the start of an intervention (21-23). Thus. Unfortunately. e. oral antibiotic prophylaxis should be given approximately 1 h before the intervention. contamination load.3 Duration of the regimen For most procedures. there is good reason to believe that the same findings apply to urological surgery. Antibiotics cannot replace other basic measures to reduce infection (18-20). the duration of perioperative prophylaxis should be minimised.4). In other cases.2 Route of administration Oral administration is as effective as the intravenous route for antibiotics with sufficient bioavailability. When choosing an antimicrobial agent.16). 82 UPDATE MARCH 2011 . It is essential to individualise the choice of antibiotic prophylaxis according to each patient’s cumulative risk factors (17).b. Broader-spectrum antibiotics should be used sparingly and reserved for treatment. In general.6 prophylactic regimens in defined procedures The list of major urological diagnostic and therapeutic procedures is given in Table 15. This applies also to the use of vancomycin.5. Urine culture prior to surgery is strongly recommended.15. there is good evidence that intelligent use of prophylaxis can lower the overall consumption of antibiotics (15. and the role of local inflammation.g. It is also essential to define the predominant pathogens for each type of procedure.6. In principle. Intravenous antibiotic prophylaxis should be given at the induction of anaesthesia. Moreover. intravenous administration is recommended. and an effective concentration shortly afterwards (24). Local irrigation of the operating field with antibiotics is not recommended. This is recommended for most interventions when the patient can easily take the drug between 1 and 2 h before intervention. second-generation cephalosporins. It is worth noting that a bloodstream infection can develop in less than an hour (21). 15. the benefit of antibiotic prophylaxis for most modern urological procedures has not yet been established by well-designed interventional studies. Although the following guidelines are based on research into skin wounds and clean-contaminated and contaminated bowel surgery.

e. i.4: List of urological interventions Diagnostic procedures • Fine-needle biopsy of the prostate • Core-needle biopsy of the prostate Cystoscopy • Urodynamic examination • Radiological diagnostic intervention of the urinary tract • Ureteroscopy Deviation procedures • Insertion of indwelling catheter • Insertion of suprapubic catheter • Insertion of nephrostomy tube • Insertion of ureteric stent Endourological operations • Resection of bladder tumour • Resection of prostate • Minimal invasive prostatic operation. enucleation of prostatic adenoma • Open stone surgery • Pyeloplasty • Nephrectomy and nephron-sparing surgery of the kidney • Nephro-ureterectomy.Table 15.e. including bowel surgery Open surgery • Open surgery of the prostate. including bladder resection • Bladder resection • Urethroplasty • Implantation of prosthetic devices • Urinary diversion procedures using intestinal segments UPDATE MARCH 2011 83 . microwave thermotherapy • Ureteroscopy for stone or tumour fulguration • Percutaneous stone or tumour surgery ESWL Laparoscopic surgery • Radical prostatectomy • Pyeloplasty • Nephrectomy and nephron-sparing surgery of the kidney • Other major laparoscopic surgery. i.

such as simple diagnostic and distal stone treatment. GR: C). randomised and controlled studies. 15. bleeding.1 Diagnostic procedures Antimicrobial prophylaxis in core biopsy of the prostate is generally recommended (GR: A). However.4.1).000 patients. due to the increased bacterial burden (e. it seems reasonable to manage laparoscopic surgical procedures in the same manner as the corresponding open procedures (LE: 4. A meta-analysis of 32 prospective. indwelling catheter. the choice of regimens remains debatable. indwelling catheters. showed a benefit of antibiotic prophylaxis with a relative risk reduction of 65% and 77% for bacteriuria and septicaemia.57. No standard prophylaxis is recommended. 15. 15. including cephalosporins. Most regimens used are effective. nephrostomy tube. and a history of urogenital infection are risk factors that must be considered (42-56) (LE: 1b.6. Most antibiotic groups have been evaluated. ESWL is one of the most commonly performed procedures in urology. Other risk factors (i.2 Endourological treatment procedures (urinary tract entered) There is little evidence for any benefit of antibiotic prophylaxis in TURB. or infectious stones) (71-79) (LE: 1a-1b. GR: C).58) (LE: 2b.1 Level of invasiveness and risk of infection in urological procedures (empirical scheme) (5) Open: clean contaminated Endourological: complex TRUS biopsy prostate TURp Endourological: simple Open: open UT Laparoscopic surg Cystoscopy+ Cystoscopy ESWL Open: clean Laparoscopic surg The recommendations for antibiotic prophylaxis in standard urological surgery are summarised in Table 15. bacteriuria. and recent studies have suggested that 1-day and even single doses are sufficient in low-risk patients (26-41) (LE: 1b. and surgeon’s experience) also need to be considered in the choice of regimen (63-70) (LE: 2b. However. There have been few studies that have defined the risk of infection following ureteroscopy and percutaneous stone removal. however. antibiotic prophylaxis is not recommended in standard cases. However.59-61) (LE: 1a.e.5 and Appendix 16. and no clear-cut evidence exists (62). It is reasonable.1) (5).Figure 15. GR: A). The use of antibiotic prophylaxis is still debated and the results are controversial. but comparative studies are limited. prophylaxis is recommended in cases of internal stent and treatment. In view of the very large number of cystoscopic examinations and the potential adverse effect on bacterial sensitivity. respectively (15. urodynamic studies and diagnostic simple ureteroscopy is low. including > 4. 84 UPDATE MARCH 2011 .6. GR: B). and with risk factors (43. antibiotic prophylaxis should be considered in patients with large tumours with a prolonged resection time. length. such as fluoroquinolones. from higher-risk procedures. and co-trimoxazole. There is a difference between smaller resections in healthy patients and large resections in at-risk patients (Figure 15. size. to distinguish low-risk procedures. GR: A). GR: A). such as treatment of proximal impacted stones and intrarenal interventions (Figure 15. BLIs.6. GR: A).3 Laparoscopic surgery There has been a lack of sufficiently powered studies in laparoscopic urological surgery. large necrotic tumours. The frequency of infectious complications after cystoscopy.g. However. However. TURP is the best-studied urological intervention.

prolongation of perioperative antibacterial prophylaxis is not recommended. although prolonged operation and other morbidity risk factors might support the use of a prolonged regimen.7 Postoperative drainage of the urinary tract When continuous urinary drainage is left in place after surgery. which should be < 72 h. Diabetes mellitus is considered a specific risk factor for infection. Skin-related staphylococci are responsible for most infections. 15. The choice of antibiotic should focus on aerobic and anaerobic pathogens. but experience is limited as for specific urological interventions (90-93) (LE: 2a. GR: B). as for clean-contaminated operations in general surgery. 15.6.4 Open or laparoscopic urological operations with open urinary tract (clean-contaminated procedures) In cases of opening the urinary tract.6.8 Implantation of prosthetic devices When infectious complications occur in implant surgery. unless a complicated infection that requires treatment is suspected.Open or laparoscopic urological operations without opening of the urinary tract (clean procedures) No standard antibiotic prophylaxis is recommended in clean operations (80-84) (LE: 3. GR: B).5 Open urological operations with bowel segment (clean-contaminated or contaminated procedures) Antibiotic prophylaxis is recommended. This is valuable for standard procedures such as total (radical) prostatectomy (85-88). GR: C). 15.5 Recommendations for perioperative antibiotic prophylaxis in urology pathogens (expected) Enterobacteriaceae Anaerobes? prophylaxis Antibiotics Remarks procedure Diagnostic procedures Transrectal biopsy of the prostate All patients Fluoroquinolones TMP ± SMX Metronidazole?1 Single dose effective in low-risk patients. GR: B). Single or 1-day dosage is recommended. a single perioperative parenteral dose of antibiotics is recommended (LE: 3. GR: C). they are usually problematic and often result in removal of the prosthetic device. Consider prolonged course in high-risk patients Consider in high-risk patients Consider in high-risk patients Cystoscopy Urodynamic examination Ureteroscopy Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci No TMP ± SMX Cephalosporin 2nd Generation TMP ± SMX Cephalosporin 2nd generation TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLIa No Endourological surgery and ESWL ESWL No ESWL with stent or nephrostomy tube Enterobacteriaceae Enterococci All patients TMP ± SMX Risk patients Cephalosporin 2nd or 3rd generation Aminopenicillin/BLIa UPDATE MARCH 2011 85 .6. Asymptomatic bacteriuria (bacterial colonisation) should only to be treated before surgery or after removal of the drainage tube (LE: 3. the risk of postoperative infection is particularly high (89) (LE: 2b.6 15. GR: B). GR: A).6.6. The antibiotics used must be chosen to target these strains (94-97) (LE: 2a. Evidence is based on colorectal surgery (LE: 1a. 15. 15. In open enucleation of prostatic adenoma.

g. e. staphylococci Catheterassociated uropathogens Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci Anaerobes Skin-related bacteria Skin-related bacteria.g. e.Ureteroscopy for uncomplicated distal stone Enterobacteriaceae Enterococci Staphylococci No TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Fluoroquinolones TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Fluoroquinolones TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Consider in risk patients Enterobacteriaceae Ureteroscopy Enterococci of proximal or impacted stone and Staphylococci percutaneous stone extraction TURP Enterobacteriaceae Enterococci All patients Short course Length to be determined Intravenous suggested at operation Low-risk patients and small-size prostate probably do not require prophylaxis Consider in high-risk patients and large tumours All patients TUR of bladder tumour Enterobacteriaceae Enterococci No Open or laparoscopic urological surgery Clean operations Skin-related pathogens. staphylococci No Consider in high-risk patients Short postoperative catheter requires no treatment TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Cephalosporin 2nd or 3rd generation Metronidazole Single perioperative course Cleancontaminated (opening of urinary tract) Cleancontaminated/ contaminated (use of bowel segments) Implant of prosthetic devices Recommended All patients As for colonic surgery All patients Cephalosporin 2nd or 3rd generation Penicillin (penicillinase stable) 1No a evidence for metronidazole in core biopsy of the prostate = gram-negative bacteria excluding Pseudomonas aeruginosa 86 UPDATE MARCH 2011 .

ileal conduit) TURB (major. fulguration)* ESWL* Urogenital tract not entered No evidence of inflammation No break in technique Blunt trauma Urogenital tract entered with no or little (controlled) spillage No major break in technique Clean-contaminated (4-10%) Pelvio-ureteric junction repair Nephron-sparing tumour resection Total/radical prostatectomy Bladder surgery and partial cystectomy Incl.Table 15. Tentative classification of urological instrumentation and procedures in relation to the different classes.6.a: Surgical Wound Classes and risk of wound infection modified for urological procedures.6. EAU/ICUD. p 674-75) Category of intervention (risk of surgical wound infection) Clean (1-4%) Description Open or laparoscopic urological surgery (Examples) Simple nephrectomy Planned scrotal surgery Vasectomy Varicocele surgery Endoscopic urological instrumentation and surgery (examples) Cystoscopy Urodynamic study TURB (minor.b UPDATE MARCH 2011 87 . Vaginal surgery Urine diversion (orthotopic bladder replacement. (Urogenital infections. fresh accidental wounds Pre-existing infection Perforated viscera at surgery Old traumatic wound Urine deviation (colon) and small intestine/spillage Trauma surgery Concomitant gastrointestinal disease Core prostate biopsy* TURP* Impacted proximal stone management Complicated PCNL Dirty (15-40%) Drainage of abscess Large dirty trauma surgery Infectious stone surgery *Detailed description in table 15. 2010. The risk of wound infection as expressed in per cent is that of classical wound infection and not bacteriuria or clinical UTI in urological surgery. necrotic)* TURP* Diagnostic URS* Uncomplicated URS* and PCNL stone management ESWL* Gastrointestinal tract entered with no or little (controlled) spillage No break in technique Contaminated (10-15%) Spillage of Gastrointestinal content Inflammatory tissue Major break in technique Open.

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Infectious Diseases Society of America and the Food and Drug Administration.1 Criteria for the diagnosis of UTI.gov/pubmed/1477233 Rubin RH. Taufkirchen.nlm. 94 UPDATE MARCH 2011 . with modifications by a European Working Party (Norrby SR). acute uncomplicated cystitis in women Acute uncomplicated pyelonephritis Clinical features Dysuria. no structural/functional abnormalities All pyuria counts refer to unspun urine. Naber KG. et al. http://www. Evaluation of new anti-infective drugs for the treatment of urinary tract infection. General guidelines for the evaluation of new anti-infective drugs for the treatment of UTI. one or more factors associated with a complicated UTI (see text) No urinary symptoms Laboratory investigations > 10 WBC/mm3 > 103 cfu/mL* 2 > 10 WBC/mm3 > 104 cfu/mL* 3 Complicated UTI > 10 WBC/mm3 > 105 cfu/mL* in women > 104 cfu/mL* in men. Int J Antimicrob Agents 1999 May. other diagnoses excluded.nih. no urinary symptoms in 4 weeks before this episode Fever. or in straight catheter urine in women > 10 WBC/mm3 > 105 cfu/mL* in two consecutive MSU cultures > 24 h apart < 103 cfu/mL* 4 Asymptomatic bacteriuria 5 Recurrent UTI (antimicrobial prophylaxis) At least three episodes of uncomplicated infection documented by culture in past 12 months: women only. Shapiro ED. Andriole VT.ncbi. frequency.nlm.ncbi. radiography) Any combination of symptoms from categories 1 and 2 above.1 1.15 Suppl 1:S216-27. Experience with the new guidelines on evaluation of new anti-infective drugs for the treatment of urinary tract infections. 294-310.11(3-4):189-96. suprapubic pain. 16. Andriole VT. 1993. http://www. no history or clinical evidence of urological abnormalities (ultrasonography. flank pain. et al. 3. as modified according to IDSA/European Society of Clinical Microbiology and Infectious Diseases guidelines (1-3) Category 1 Description Acute uncomplicated UTI in women. References Rubin RH.gov/pubmed/10394969 2. urgency.1. chills. discussion 213-6. AppENDICES 16. *Uropathogen in MSU culture. Germany: The European Society of Clinical Microbiology and Infectious Diseases.16.nih. Clin Infect Dis 1992 Nov. pp. Shapiro ED.

2 Recommendations for antimicrobial therapy in urology Most frequent pathogen/species • E. if not used initially • Acylaminopenicillin/BLI • Cephalosporin (group 3b) • Carbapenem • ± Aminoglycoside In case of Candida: • Fluconazole • Amphotericin B UTI with complicating factors Nosocomial UTI • E. empirical antimicrobial Therapy duration therapy Diagnosis Cystitis acute. coli < 20% • TMP-SMX • Trimethoprim 3 days 5 days 7-10 days (1-)3 days 3 days 1 day (3-)7 days (5-)7 days Initial. chronic • E. coli • Other enterobacteria • Fluoroquinolone* Alternative in acute bacterial prostatitis: Acute: 2-4 weeks UPDATE MARCH 2011 95 . uncomplicated Pyelonephritis acute. coli • Enterococci • Pseudomonas • Staphylococci • Klebsiella • Proteus 3-5 days after defervescence or control/elimination of complicating factor Pyelonephritis severe acute. uncomplicated • E. coli • Proteus • Klebsiella • Other enterobacteria • Staphylococci • Fluoroquinolone* • Cephalosporin (group 3a) Alternatives: • Aminopenicillin/BLI • Aminoglycoside • Fluoroquinolone* • Aminopenicillin/BLI • Cephalosporin (group 2) • Cephalosporin (group 3a) • Aminoglycoside In case of failure of initial therapy within 1-3 days or in clinically cases: Anti-Pseudomonas active: • Fluoroquinolone. complicated • Enterobacter • Other enterobacteria • (Candida) Prostatitis acute. coli • Klebsiella • Proteus • Staphylococci • Fosfomycin trometamol • Pivmecillinam • Nitrofurantoin Alternatives • Fluoroquinolone* Cepodoxime proxetil If local resistance rate of E.16.

°Only in areas with resistance rate < 20% (for E. 16. normal normal 250-500 mg 6 h 75% 250 mg 6 h (500 mg 6 h) 20-50% Max. Consider using liposomal/lipid complex amphotericin.and 1 h post-dose levels after 3rd dose and adjust dose as required Amoxicillin po Amphotericin (Liposonal + lipid complex) Ampicillin IV Benzylpenicillin normal normal normal normal 250 mg 8 h (normal) Give post-HD normal Amphotericin is highly NEPHROTOXIC.6 g/day (1. coli).2 g qds) normal 1 g stat then 50% 250 mg 6 h Give post-HD Give post-HD Give post-HD Give post-HD Refer to microbiology for dosing in SBE Caspofungin Cefotaxime Cefradine normal normal normal normal normal Normal 96 UPDATE MARCH 2011 .• Pseudomonas Epididymitis Ureaplasma: Acute • Enterococci Chronic: • Staphylococci • Chlamydia • Ureaplasma Urosepsis • E.multiresistant pathogens: • Pseudomonas • Proteus • Serratia • Enterobacter • Cephalosporin (group 3a/b) In case of Chlamydia or • Doxycycline • Macrolide 4-6 weeks or longer • Cephalosporin (group 3a/b) • Fluoroquinolone* • Anti-Pseudomonas active acylaminopenicillin/BLI • Carbapenem • ± Aminoglycoside 3-5 days after defervescence or control/elimination of complicating factor *Fluoroquinolone with mainly renal excretion (see text).3 Recommendations for antimicrobial prescription in renal failure gFR (mL/min) Mild 50-20 Moderate 20-10 normal dose every 24 h Herpes simplex: normal Herpes zoster: 800 mg Total Dissolved Solids tds 3-4 mg/kg 24 h HD: 5mg/kg post HD and monitor levels Severe < 10 50% of normal dose every 24 h Herpes simplex: 200 mg bid Herpes zoster: 800 mg bd 2 mg/kg 24-48 h Give post-HD Give post-HD Comments Antibiotic *Aciclovir Aciclovir po normal dose every 12 h normal Amikacin 5-6 mg/kg 12 h Give post-HD Monitor pre. coli • Other enterobacteria After urological interventions . Daily monitoring of renal function (GFR) essential. 3.

BOTH METHODS Give post-HD Monitor blood levels: Once daily: pre only Conventional: pre and 1 h post level required.2 g 12 h) 375-625 mg 12 h (375 mg 8 h) Normal for 3/7 then 50% normal 500 mg 24 h (1 g 24 h) normal Max. 4 g/day 50% Give post-HD No adjustments in single-dose therapy required Give post-HD Levels should be monitored predialysis.2 g stat then 600 mg 12 h) 375 mg 12 h (375 mg 8 h) 50% normal Give post-HD Give post-HD Give post-HD Give post-HD Co-amoxiclav po (Augmentin) *Co-trimoxazole IV Doxycycline normal normal normal Give post-HD Give post-HD All other tetracyclines contraindicated in renal impairment Erythromycin IV + po *Ethambutol normal normal normal Max.Ceftazidime Ceftriaxone Cefuroxime IV Ciproflazin IV + po Clarithromycin IV + po Clindamycin IV + po Co-amoxiclav IV (Augmentin) 1 g 12 h normal normal normal normal normal normal 1 g 24 h normal 750 mg-1. 2 g/day 750 mg 24 h (750 mg 12 h) 50% 50% normal 1.5 g/day (500 mg qds) 48 h Give post-HD normal 24-36 h Monitor levels if GFR < 30mL/min (contact Mirco) Flucloxacillin IV + po Fluconazole normal normal normal normal normal Max.use Meropenem: see below Fusidic acid 1) Gentamicin ONCE DAILY normal normal gFR 10-40 mL/min 3 mg/kg stat (max. 200 mg) redose according to levels 80 mg 24 h HD: 1-2 mg/kg Post-HD: redose according to levels Risk of convulsions .5 g 12 h 50% normal normal 1. 1. Give post-HD *Flucytosine 50 mg/kg 12 h 50 mg/kg 24 h 50 mg/kg stat then dose according to levels normal gFR < 10 mL/min 2 mg/kg (max.2 stat then 50% 12 h (1.2 stat then 50% 24 h (1. 300 mg) Check pre-dose levels 18-24 h after first dose Redose only when level < 1 mg/L 80 mg 12 h 80 mg 48 h 2) Gentamicin CONVENTIONAL Imipenem 500 mg 8-12 h 250-500 mg bid UPDATE MARCH 2011 97 .

5 g 12 h Do NOT use in renal impairment normal normal 100% 48 h normal normal 100% 72 h normal 50-100% 100% 72 h Dose reduction after day 3 of therapy Give post-HD Monitor pre-dose levels and adjust dose as required Tetracycline Trimethoprim Vancomycin normal See Doxycycline Normal for 3/7 then 50% 18 h 1 g 48 h Check pre-dose level before 2nd dose 50% 24 h 1 g stat (or 15 mg/ kg.5 g 12 h normal 50% 24 h 12 h (normal) normal 4. up to max. qid = four times daily. SBE = subacute bacterial endocarditis. HD = haemodialysis. od = once daily. five reduced doses daily Give post-HD Give post-HD Give post-HD Give post-HD Give post-HD Linezolid Meropenem Metronidazole Nitrofurantoin Penicillin V Piperacillin/ Tazobactam (Tazocin) Pyrazinamide Rifampicin *Teicoplanin normal 12 h normal normal 4. Recheck level after 4-5 days ONLY give subsequent dose when level < 12mg/L normal 1 g od Check pre-dose level before 3rd dose Vorinconazole normal normal Give post HD bid = twice daily. tds = total dissolved solids. 2 g).5 g 8 h normal 50% 12 h normal normal 4. qds = Quantum Dots 98 UPDATE MARCH 2011 .Isoniazid Itraconazole Levoflaxacin normal normal 500 mg stat then 250 mg bid** normal normal 500 mg stat then 125 mg bid** 200-300 mg 24 h normal 500 mg stat then 125 mg od Give post-HD **Applies if full dose is 500 mg bid If full dose is 500 mg od. po = by mouth.

e. staphylococci Catheterassociated uropathogens No Consider in high-risk patients Short postoperative catheter requires no treatment UPDATE MARCH 2011 99 .16. Consider prolonged course in high-risk patients Consider in high-risk patients Consider in high-risk patients Cystoscopy Urodynamic examination Ureteroscopy Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci No TMP ± SMX Cephalosporin 2nd Generation TMP ± SMX Cephalosporin 2nd generation TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLIa No Endourological surgery and ESWL ESWL No ESWL with stent or nephrostomy tube Enterobacteriaceae Enterococci All patients TMP ± SMX Risk patients Cephalosporin 2nd or 3rd generation Aminopenicillin/BLIa TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Fluoroquinolones TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Fluoroquinolones TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Consider in risk patients Ureteroscopy for uncomplicated distal stone Enterobacteriaceae Enterococci Staphylococci No Enterobacteriaceae Ureteroscopy Enterococci of proximal or impacted stone and Staphylococci percutaneous stone extraction TURP Enterobacteriaceae Enterococci All patients Short course Length to be determined Intravenous suggested at operation Low-risk patients and small-size prostate probably do not require prophylaxis Consider in high-risk patients and large tumours All patients TUR of bladder tumour Enterobacteriaceae Enterococci No Open or laparoscopic urological surgery Clean operations Skin-related pathogens.4 Recommendations for perioperative antibiotic prophylaxis in urology pathogens (expected) Enterobacteriaceae Anaerobes? prophylaxis Antibiotics Remarks procedure Diagnostic procedures Transrectal biopsy of the prostate All patients Fluoroquinolones TMP ± SMX Metronidazole?1 Single dose effective in low-risk patients.g.

staphylococci Recommended TMP ± SMX Cephalosporin 2nd or 3rd generation Aminopenicillin/BLI Cephalosporin 2nd or 3rd generation Metronidazole Single perioperative course All patients As for colonic surgery All patients Cephalosporin 2nd or 3rd generation Penicillin (penicillinase stable) 1No a evidence for metronidazole in core biopsy of the prostate = gram-negative bacteria excluding Pseudomonas aeruginosa 100 UPDATE MARCH 2011 .Cleancontaminated (opening of urinary tract) Cleancontaminated/ contaminated (use of bowel segments) Implant of prosthetic devices Enterobacteriaceae Enterococci Staphylococci Enterobacteriaceae Enterococci Anaerobes Skin-related bacteria Skin-related bacteria.g. e.

1d. and 9 1 0 2. O’Leary MP. Alexander RB.8.16. Area between rectum and 1 0 testicles (perineum) b. Pain or burning during 1 urination? b. over the last week? 0 1 NO PAIN 2 3 4 5 6 7 8 9 10 PAIN AS BAD AS YOU CAN IMAGINE Urination 5. In the last week.2a. How much did you think about your symptoms. How often have you had to urinate again less than two hours after you finished urinating. How often have you had pain or discomfort in any of these areas over the last week? 0 Never 1 Rarely 2 Sometimes 3 Often 4 Usually 5 Always 4. McNaughton-Collins M. Pain or discomfort during or after sexual climax (ejaculation)? 1 No 0 0 3. Calhoun MA.369375. Tip of penis (not related to urination) d. over the last week? 0 None 1 Only a little 2 Some 3 A lot Quality of life 9. Nickel JC.2b. J Urol 1999:162. In the last week. Farrar JT. The National Institute of Health chronic prostatitis symptom index: development and validation of new outcome measure. If you were to spend the rest of your life with your symptoms. Testicles c. How often have you had a sensation of not emptying your bladder completely after you finished urinating over the last week? 0 Not at all 1 Less than 1 time in 5 2 Less than half the time 3 About half the time 4 More than half the time 5 Almost always = __________ = __________ UPDATE MARCH 2011 101 . How much have your symptoms kept you from doing the kinds of things you would usually do over the last week? 0 None 1 Only a little 2 Some 3 A lot 8. have you experienced any pain or discomfort in the following areas? Yes No a.3 and 4 = __________ Urinary Symptoms: Total of items 5 and 6 Quality of Life Impact: Total of items 7. Fowler FJ Jr. Chronic Prostatitis Collaborative Research Network. just the way they have been during the last week.1b. have you experienced: Yes a. how would you feel about that? 0 Delighted 1 Pleased 2 Mostly satisfied 3 Mixed (about equally satisfied and dissatisfied) 4 Mostly dissatisfied 5 Unhappy 6 Terrible Scoring the NIH-CPSI Prostatitis Symptom Index Domain Pain: Total of items 1a. Pontari MA.5 CpSI from: Litwin MS. over the last week? 0 Not at all 1 Less than 1 time in 5 2 Less than half the time 3 About half the time 4 More than half the time 5 Almost always Impact of Symptoms 7. in your pubic or bladder area 1 1 0 0 6.1c. Which number best describes your AVERAGE pain or discomfort on the days that you had it. Below your waist. NIH-Chronic prostatitis Symptom Index (NIH-CpSI) Pain or Discomfort 1.

co-tetroxoprime (trimethoprim plus sulfametrol) groups Trimethoprim-sulphonamide combinations Fluoroquinolones1. 16. fleroxacin. clarithromycin. 1999. London: Mosby. In: Armstrong D. azithromycin Doxycycline. moxifloxacin Erythromycin.16. tetracycline Fosfomycin sodium.idreference. lomefloxacin. eds. co-trimoxazole.com * Naber KG. minocycline.www.2 Group 1 Group 2 Group 3 Group 4 Macrolides Tetracyclines Fosfomycin Nitrofuran4 Norfloxacin. pefloxacin Enoxacin. Weidner W. roxithromycin. ofloxacin. Infectious Diseases. orchitis. Harcourt Publishers Ltd. 1-58. ciprofloxacin Levofloxacin Gatifloxacin. epididymitis. Prostatitis. Cohen J. pp.7 Antibacterial agents Agents Trimethoprim. fosfomycin trometamol3 Nitrofurantoin 102 UPDATE MARCH 2011 .6 Meares & Stamey localisation technique* © Elsevier 2004 Infections Disease 2e .

bacampicillin Ampicillin/sulbactam. piperacillin Piperacillin/tazobactam. propicillin and azidocillin. cefixime Cefazolin Cefamandole. Because of their narrow spectrum of activity. ceftriaxone Cefoperazone. these penicillins do not have any role in the treatment of urogenital infections. azidocillin Oxacillin. cefaclor Loracarbef.1. teicoplanin Linezolid according to the Paul Ehrlich Society for Chemotherapy (1-3). and Salmonella and Shigella sp. netilmicin. 7In solution. Indications UPDATE MARCH 2011 103 . However. 16. or sulbactam). However. Moraxella catarrhalis. have a high intrinsic activity against streptococci and pneumococci. Haemophilus influenzae. they cover enterococci. ampicillin and amoxycillin.1 Penicillins Penicillin G and the oral penicillins.. coli. dicloxacillin. cloxacillin. flucloxacillin Ampicillin. the resistance rate of pneumococci may vary considerably between countries. meropenem. 5In cases of resistance. 16. cefadroxil. sulbactam6 Cefalexin. E. have a broader spectrum of activity. They are therefore not sufficiently active against certain species.7. in adults. amikacin Vancomycin. cefetamet pivoxil. tobramycin. cefuroxime. the pathogen is most likely to be a ß-lactamase producer. This gap in the spectrum of activity can be closed by the use of a BLI (clavulanic acid. In Germany. such as staphylococci. Amoxycillin/ clavulanic acid and ampicillin/sulbactam are available on the market as fixed combinations. 3Only in acute. except pregnant and lactating women. penicillin V. amoxycillin. Apart from streptococci and pneumococci. resistance may occur. cefotaxime. uncomplicated cystitis as a single dose. cefpirome Cefoxitin Aztreonam Imipenem.1 Aminopenicillins Aminopenicillins. penicillin resistance in pneumococci is still < 1%. cefotiam Cefodizime.g. Bacteroides fragilis and many enterobacteria. e. mirabilis. cefuroxime axetile Cefpodoxime proxetile. Pr.7. Aminopenicillins are sensitive to ß-lactamases. Listeria sp. amoxycillin/clavulanic acid7 Mezlocillin. ceftazidime Cefepime. 4Contraindicated in renal failure and in newborns.penicillins Benzylpenicillin Phenoxypenicillins Isoxazolylpenicillins Aminobenzylpenicillins5 Aminopenicillins/BLI6 Acylaminopenicillins ±BLI6 Cephalosporins1 Group 1 (oral) Group 2 (oral) Group 3 (oral) Group 1 (parenteral) Group 2 (parenteral) Group 3a (parenteral) Group 3b (parenteral) Group 4 (parenteral) Group 5 (parenteral) Monobactams Carbapenems Aminoglycosides glycopeptides Oxazolidones 1Classification 2Only Penicillin G Penicillin V. Haemophilus parainfluenzae. propicillin. 6BLIs can only be used in combination with ß-lactam antibiotics. ceftibuten. ertapenem Gentamicin. storage instability.

for aminopenicillins and their combinations with a BLI are mild respiratory tract infections, UTIs, as well as infections of the skin and soft tissues. 16.7.1.2 Acylaminopenicillins The acylaminopenicillins include apalcillin, azlocillin, mezlocillin and piperacillin. They are characterised by their high activity against enterococci, enterobacteria and Pseudomonas (weaker activity of mezlocillin). Acylaminopenicillins are hydrolyzed by ß-lactamases and are therefore active only against ß-lactamaseproducing strains of staphylococci, B. fragilis, and if used in combination with a BLI, some of the enterobacteria. The acylaminopenicillin/BLI combination provides a broad spectrum of activity and may be used for a large number of indications, including complicated UTIs and urosepsis. A selection of free combinations with sulbactam is available, or there is the fixed combination of tazobactam and piperacillin, which has the advantages of being easy to use and a well-documented database drawn from qualified clinical studies. 16.7.1.3 Isoxazolylpenicillins Isoxazolylpenicillins are available as parenteral drugs with oxacillin and flucloxacillin, and have a narrow spectrum of activity. Their indications are limited to infections caused by S. aureus. Due to their suboptimal pharmacokinetic parameters, isoxazolylpenicillins are preferably used in milder infections of the skin and soft tissues, and of the ear, nose and throat area. They play no role in the treatment of UTIs, but may be used for staphylococcal abscesses in the genital area. 16.7.2 Parenteral cephalosporins According to the Paul Ehrlich Society for Chemotherapy (1), the parenteral cephalosporins have been classified into five groups, according to their spectrum of activity (Table 16.7.2). 16.7.2.1 Group 1 cephalosporins Group 1 cephalosporins (cefazolin and cefazedone) are very active against streptococci and staphylococci (including penicillin-G-resistant strains). They have only weak activity against Gram-negative microorganisms. Like all cephalosporins, cefazolin is not active against enterococci and MRSA and methicillin-resistant coagulase-negative staphylococci (MRSE). 16.7.2.2 Group 2 cephalosporins Compared with Group 1 cephalosporins, Group 2 cephalosporins, e.g. cefuroxime, cefotiame and cefamandole, exhibit markedly improved activity against Gram-negative pathogens and maintain high activity against staphylococci. 16.7.2.3 Group 3a cephalosporins Group 3a cephalosporins have high activity against Gram-negative bacteria and less activity against staphylococci. They differ mainly in their pharmacokinetic characteristics. 16.7.2.4 Group 3b cephalosporins Group 3b cephalosporins, e.g. ceftazidime and cefoperazone, have added high anti-pseudomonal activity. However, the activity of cefoperazone against P. aeruginosa is markedly inferior to that of the other substances in this group. 16.7.2.5 Group 4 cephalosporins Group 4 cephalosporins, e.g. cefepime and cefpirome, have a comparable activity against Gram-negative bacteria, but are more stable against extended-spectrum β-lactamases, and a better activity against Grampositive bacteria. 16.7.2.6 Group 5 cephalosporins The Group 5 cephalosporins are characterised by their anti-anaerobic activity. These cephalosporins have superior activity against Gram-negative bacteria compared with Group 1 and 2 cephalosporins, but most of them are weaker than Group 3 drugs. At present, cefoxitin is the only drug of that group available on the market in some countries.

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Table 16.7.2: Classification of parenteral cephalosporins (2) group group 1 (1st generation) generic names Cefazolin Cefazedone Features of the group • Active against Gram-positive and partly against Gram-negative bacteria • Stable against staphylococcal penicillinases • Unstable against ß-lactamases of Gram-negative bacteria • Activity against Gram-positive bacteria good, but weaker than Group 1 • Activity against Gram-negative bacteria superior to that of Group 1 • Stable against staphylococcal penicillinases • Limited stability against ß-lactamases of Gramnegative bacteria • Activity against Gram-negative bacteria clearly superior to that of Groups 1 and 2 • Stable against numerous ß-lactamases of Gramnegative bacteria • Microbiologically less active against staphylococci • Spectrum of antibacterial activity similar to that of Group 3a • Additional activity against P. aeruginosa • Spectrum of antibacterial activity similar to that of Group 3a • Additional activity against P. aeruginosa • Higher stability against beta-lactamases than group 3b • With anti-anaerobic activity • Superior activity against Gram-negative bacteria than Group 1 and 2 • Weaker than Group 3

group 2 (2nd generation)

Cefuroxime Cefotiame Cefamandole

group 3a (3rd generation)

Cefotaxime Ceftriaxone Ceftizoxime Cefmenoxime Cefodizime Ceftazidime Cefoperazone

group 3b (3rd generation)

group 4 group 5

Cefepime Cefpirome Cefoxitin

16.7.3 Oral cephalosporins Oral cephalosporins are classified into three groups, based on their spectrum of activity, according to the recommendations of the Paul Ehrlich Society for Chemotherapy (1) (Table 16.7.3).

Table 16.7.3: Classification of oral cephalosporins (1) Oral cephalosporins Group 1 Drug names Cefalexin Cefadroxil Cefaclor Cefprozil Loracarbef Cefuroxime axetile Cefpodoxime proxetile Cefetamet pivoxile Ceftibuten Cefixime

Group 2

Group 3

16.7.3.1 Group 1 oral cephalosporins Group 1 oral cephalosporins include cefalexin, cefadroxil and cefaclor. They are mainly active against Grampositive cocci with limited activity against H. influenzae (cefaclor). Their main indications are skin and soft tissue infections and, with limitations, respiratory tract infections. Their activity against enterobacteria is limited,

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therefore, they can only be recommended for the treatment or prophylaxis of uncomplicated UTIs in children or pregnant women, for whom the use of other antibiotics is limited. 16.7.3.2 Group 2 oral cephalosporins The activity of cefprozil against S. aureus, Streptococcus pyogenes, Streptococcus pneumoniae, H. influenzae and Mor. catarrhalis is somewhat higher than that of cefaclor. However, cefprozil is less active than cefaclor against E. coli, Klebsiella pneumoniae and Pr. mirabilis. Loracarbef is structurally close to cefaclor. In contrast to cefaclor, it is stable in solution, has better pharmacokinetics and a broader antibacterial spectrum. However, its activity against staphylococci is lower than that of cefaclor. The main indications are respiratory tract, skin and soft-tissue infections and uncomplicated UTIs. Cefuroxime axetile has a higher ß-lactamase stability and thus a broader spectrum than others in this group. It can be used mainly for bacterial infections of the upper (including otitis media) and lower respiratory tract, for skin and soft-tissue infections, and UTIs. 16.7.3.3 Group 3 oral cephalosporins Group 3 oral cephalosporins have a higher activity and a broader spectrum against enterobacteria than group 2 cephalosporins. In contrast, their activity against Gram-positive bacteria is lower. Against staphylococci, the activity of cefpodoxime proxetil is intermediate, whereas cefetamet pivoxil, ceftibuten and cefixime are inactive. The main indications for the oral cephalosporins of group 3 are complicated infections of the respiratory tract (provided that staphylococci can be excluded) and infections due to enterobacteria, e.g. UTIs or infections in immunocompromised patients. Group 3 oral cephalosporins are also suitable for oral switch therapy, i.e. when initial parenteral therapy (using a parenteral group 3a cephalosporin) needs to be continued orally. In addition, cefixime is licensed also for treatment of gonorrhoea. 16.7.4 Monobactams Among the monobactams, only aztreonam is available. It is active only against Gram-negative aerobes. In this respect, its spectrum and activity are similar to those of the parenteral group 3b cephalosporins. 16.7.5 Carbapenems Carbapenems are broad-spectrum antibiotics with good activity against Gram-positive and Gram-negative bacteria, including anaerobes. They are preferably used in the treatment of mixed infections and in the initial therapy of life-threatening diseases, including urosepsis. Imipenem/cilastatin, meropenem and doripenem are also active against P. aeruginosa. However, ertapenem is not active against P. aeruginosa. Ertapenem has a longer half-life than imipenem/cilastatin and meropenem, and is therefore, suitable for once-daily dosing. 16.7.6 Fluoroquinolones Non-fluorinated quinolones are no longer recommended because of their poor antibacterial activity. According to the Paul Ehrlich Society for Chemotherapy, the fluoroquinolones are classified into four groups, based on their spectrum of activity, their pharmacokinetics and indications (Table 16.7.4). Table 16.7.4: Classification of fluoroquinolones, as modified according to the paul Ehrlich Society for Chemotherapy (3) generic name group 1 Trade name* / features of the group Indications essentially limited to UTIs in some countries, e.g. germany Norfloxacin Pefloxacin** group 2 Broad indications for systemic use Enoxacin Fleroxacin*** Lomefloxacin Ofloxacin Ciprofloxacin

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UPDATE MARCH 2011

to date. 16. coli can vary between countries. * Listed according to increasing in vitro activity (minimum inhibitory concentration) against indicative pathogens. UPDATE MARCH 2011 107 . In complicated UTIs. due to its high renal elimination rate. The only group 3 fluoroquinolone available for parenteral use is levofloxacin. group 3 and group 4 fluoroquinolones have comparable activity against Gram-negative pathogens. ciprofloxacin.group 3 Improved activity against gram-positive and atypical pathogens Levofloxacin group 4 Improved activity against Gram-positive and atypical pathogens and anaerobes Gatifloxacin Moxifloxacin UTI = urinary tract infection. pneumococci. These include infections of the urinary tract. gonorrhoea and gastrointestinal infections.7.7.7. However. can lead to severe although rare adverse events. ofloxacin and fleroxacin are also available for parenteral use. 16. pneumococci and enterococci. Group 2 fluoroquinolones exhibit good activity against enterobacteria and H. However. UTIs. pefloxacin is also used for systemic oral and parenteral use.8 Fosfomycin Fosfomycin is active against Gram-negative and Gram-positive bacteria. group 4 fluoroquinolones have improved anti-anaerobic activity. Mycoplasma and Legionella sp. bones and joints. the left enantiomer of the ofloxacin racemate. 16. It is therefore also the most suitable for the treatment of uncomplicated and complicated UTI. Apart from respiratory tract infections. e. UTIs. these broad-spectrum fluoroquinolones are appropriate for treatment of skin.g. ** In France and other countries.7 Co-trimoxazole The treatment of UTIs is the main indication for trimethoprim alone or in combination with a sulphonamide. in June 1999. and. However.g. Urinary excretion of moxifloxacin after oral administration is only in the range of about 20%. respiratory tract. Trimethoprim with or without sulphamethoxazole can also be used for the prophylaxis of recurrent cystitis.7. as well as systemic infections and even sepsis. such as Lyell syndrome. The main indications for levofloxacin are respiratory tract infections.g.6. such as Chlamydia. e. moxifloxacin and trovafloxacin have been licensed. In France and some other countries. co-trimoxazole should only be used in accordance with sensitivity testing. 16. In addition.6. Legionella and Mycoplasma sp. as well as skin and soft-tissue infections. In addition. with ciprofloxacin being most active in vitro. Thus. skin and soft tissues. soft-tissue and intra-abdominal infections. Gatifloxacin has the highest renal excretion (about 84%) after oral administration. pefloxacin is also available for systemic use. *** Investigated in acute exacerbations of chronic bronchitis. especially in combination with sulphamethoxazole. The sodium salt is only for parenteral use. In addition. Chlamydia. Among group 4 fluoroquinolones. influenzae. streptococci. trovafloxacin was taken off the market because of severe side effects. Germany.3 Group 3 fluoroquinolones The main difference in the spectra of activity of group 3 fluoroquinolones (levofloxacin) and group 4 fluoroquinolones (gatifloxacin and moxifloxacin) is that the former have a higher intrinsic activity against Grampositive pathogens.7. gatifloxacin (not on the market in Europe). such as staphylococci.1 Group 1 fluoroquinolones The indications for group 1 fluoroquinolones are limited to UTIs in some countries. Trimethoprim. The resistance rate against E. Fosfomycin trometamol is licensed for single-dose (3 g) treatment of uncomplicated cystitis in women. Norfloxacin is not available as parenteral antibiotic. when the resistance rate in the area is > 10-20% (4). Their activity against P. e. Stevens-Johnson syndrome and pancytopenia. aeruginosa varies. they have improved activity against the so-called atypical pathogens. no parenteral fluoroquinolone of this group has been made available.2 Group 2 fluoroquinolones Group 2 fluoroquinolones includes fluoroquinolones for systemic use with a broad spectrum of indications. final judgement of their position in the treatment of these diseases is not yet possible. 16.6. It is therefore not recommended for empirical therapy of acute uncomplicated cystitis or pyelonephritis. sulphamethoxazole. with less activity against staphylococci. enterococci and atypical pathogens. and oral treatment of gynaecological infections.

Resistance data for tobramycin. coli. Their effective levels of activity are close to toxic borderline concentrations. The newer macrolides. Newer aminoglycosides include netilmicin.7. trachomatis. and streptococci. • In infections caused by ampicillin-resistant enterococci or oxacillin-resistant staphylococci. trachomatis. 16. therefore. such as non-gonococcal urethritis due to C.). Little development of resistance has been observed over many years. H. influenzae is not satisfactory. Their use is indicated: • In infections caused by the above-mentioned pathogens in case of allergy against all other suitable antibiotics. though rare adverse events. making a strict therapeutic indication mandatory.wissenschaftliche-verlagsgesellschaft. [Classification of oral cephalosporins. Due to the risk of selection of glycopeptide-resistant enterococci and staphylococci. staphylococci (including oxacillin-resistant strains). streptococci. including methicillin (oxacillin)-resistant strains. i.16.9 Nitrofurantoin The antibacterial activity of nitrofurantoin is limited to the urinary tract because of its low serum concentrations. Short-term therapy for this indication has not been proven in sufficiently large studies. and Chlamydia.14 Oxazolidinones The only substance of this group is linezolid. to metronidazole for the treatment of pseudomembranous colitis.7. Bordetella pertussis. e. Proteus. because this combination has a marked synergistic effect against certain bacterial species. whereas the resistance situation is more favourable for amikacin against many enterobacteria.12 Aminoglycosides Aminoglycosides are for parenteral use only. 16. Naber KG. It has good activity against Gram-positive cocci. are better tolerated than erythromycin.13 Glycopeptides The glycopeptides vancomycin and teicoplanin are active against Gram-positive pathogens. It is active against E. e. Their activity against streptococci.7. The macrolides are not active against Gram-negative rods. It is suitable only for the treatment or prophylaxis of uncomplicated UTIs. 16. Citrobacter and most strains of Klebsiella and Enterobacter. clarithromycin and azithromycin. including vancomycin-resistant strains. Similar to the aminoglycosides. Scholz H. influenzae and E.10 Macrolides Erythromycin is the only macrolide that is available for both oral and parenteral use. they may be used as alternative antibiotics in infections caused by these microorganisms. Tetracyclines are therefore only suitable for initial empirical therapy if the local resistance situation is sufficiently well known and justifies their use. gentamicin and netilmicin are almost identical. aeruginosa and Acinetobacter are almost always resistant. 16.7. They have good activity against enterobacteria and Pseudomonas (especially tobramycin). in oral form. [article in German] http://www. such as staphylococci. such as chronic desquamative interstitial pneumonia with fibrosis. Streptomycin is one of the older aminoglycosides and is used only for the treatment of tuberculosis. Mycoplasma and Legionella sp. • As an alternative. whereas Providencia and Serratia are mostly resistant. They are inactive against Gram-negative pathogens. Ideal partners are ß-lactam antibiotics.g. roxithromycin. Clostridium difficile.de/CTJ/CTJ2000/scholz. Chlamydia and Mycoplasma sp. 16. diphtheria bacteria and Gram-positive aerobes. streptococci.11 Tetracyclines The resistance against doxycycline and tetracycline of pneumococci.] Chemotherapie Journal 1999. or multiresistant corynebacteria. P. As a result of their high activity against the so-called atypical pathogens (Legionella. pneumococci. the use of glycopeptides should be highly restricted. coli shows marked regional differences.8:227-9. aminoglycosides should only be used in combination with another appropriate antibiotic. gentamicin.pdf 108 UPDATE MARCH 2011 . It is active against Gram-positive cocci. enterococci. enterococci. and an expert group of the Paul Ehrlich Society for Chemotherapy. their use in the treatment of UTIs is limited to special indications.7. Treatment can lead to severe. treatment of UTIs). glycopeptides have a narrow therapeutic window. which can be administered parenterally and orally. With few exceptions (e. but can only be administered orally.g. These drugs have a narrow therapeutic window. The macrolides have good activity against streptococci.7.g. enterococci and staphylococci. anaerobes and H.15 References 1.e. in non-gonococcal urethritis due to C.7. tobramycin and amikacin. 16.

13:46-105. and an expert group of the Paul Ehrlich Society for Chemotherapy. Guidelines for antimicrobial treatment of uncomplicated acute bacterial cystitis and acute pyelonephritis in women.] Chemotherapie Journal 2004.29(4):745-58. [Classification of fluoroquinolones. [article in German] http://www. Adam D.wissenschaftliche-verlagsgesellschaft.gov/pubmed/10589881 UPDATE MARCH 2011 109 . [Recommendations for empiric parenteral initial therapy of bacterial infections in adults.de/CTJ/CTJEMPF. 4. Abrutyn E. Clin Infect Dis 1999 Oct.ncbi.] Chemotherapie Journal 1998. Vogel F.wissenschaftliche-verlagsgesellschaft. [article in German] http://www. Hebel JR. http://www.nlm. et al.HTM Warren JW.pdf Naber KG.7:66-8. Bodmann K-F and the expert group of the Paul Ehrlich Society for Chemotherapy.de/CTJ/CTJ2004/CTJ2-2004/Consensus-par.2. 3.nih. Infectious Diseases Society of America (IDSA).

urealyticum Rods* Ziehl-Neelsen Postivie Gram-positive Aerobic Gram-negative aerobic Enterobacteriacaeae Mycobacteria .M. tuberculosis Corynebacteria .Proteus .T.Pseudomonas .Gardnerella vaginalis Streptococcus α-haemolytic .M.S. saprophyticus group Obligate intracellular bacteria Chlamydia . .Klebsiella .Xanthomonas .S.Hafnia (.S.Acinetobacter . urealyticum (Listeria) (Bacilli) .Enterobacter .Burgholderia Staphylococcus . pyogenes group A .S.C.16. trachomatis Mykoplasma . pallidum Cocci* Gram-positive aerobic Parvobacteria Neisseria .Serratia .S.8 Relevant bacteria for urological infections 110 No cell wall Spirochetes Treponema . faecalis .Escherichia .others . aureus . epidermidis group . agalactiae group B non-hemolytic Enterococcus .Shigella) UPDATE MARCH 2011 *Anaerobic bacteria not considered. hominus .U. genitalium Ureaplasma .Salmonella) (. viridans ß-hemolytic .Pantoea .Providencia .S.Citrobacter . gonorrhoeae Gram-negative aerobic Non-Fermenter Haemophilus .C.N.E.M. faecium .E.

This information is kept on file in the EAU Central Office database. No external sources of funding and support have been involved.17. The EAU is a non-profit organisation and funding is limited to administrative assistance and travel and meeting expenses. ACE ADPK APACHE APCKD BLI BPH CPPS CPSI CT CAUTI’s DMSA DTPA EPS ESWL EUCAST G6PD GFR IDSA IL IPCN IVU LUTS MAG-3 MRI MRSA MSU NCCLS NIDDK NIH PCP PSA SIRS SMX SSI STD TMP TNF TRUS TURP US UTI VB1 VB2 VB3 VCU VUR WBC angiotensin-converting enzyme adult dominant polycystic disease acute physiology and chronic health evaluation adult polycystic kidney disease ß-lactamase inhibitor benign prostatic hyperplasia chronic pelvic pain syndrome Chronic Prostatitis Symptom Index computed tomography catheter-associated urinary tract infections dimercaptosuccinic acid diethylenetriaminepentaacetate expressed prostatic secretion extracorporeal shockwave lithotripsy European Committee for Antimicrobial Susceptibility Testing glucose-6-phosphate dehydrogenase glomerular filtration rate Infectious Diseases Society of America interleukin International Prostatitis Collaborative Network intravenous urography lower urinary tract symptom mercaptoacethylglycine magnetic resonance imaging methicillin-resistant Staphylococcus aureus mid-stream sample of urine National Committee for Clinical Laboratory Standards National Institute of Diabetes and Digestive and Kidney Diseases National Institutes of Health Pneumocystis carinii pneumonia prostate-specific antigen systemic inflammatory response syndrome sulphamethoxazole surgical site infection sexually transmitted disease trimethoprim tumour necrosis factor transrectual ultrasound transurethral resection of the prostate ultrasonography urinary tract infection first-voided urine mid-stream urine voided bladder urine-3 voiding cysto-urethography vesicoureteric reflux white blood cells Conflict of interest All members of the Urological Infections guidelines working group have provided disclosure statements of all relationships which they have and which may be perceived as a potential source of conflict of interest. UPDATE MARCH 2011 111 . No honoraria or other reimbursements have been provided. ABBREVIATIONS USED IN THE TEXT This list is not comprehensive for the most common abbreviations. This guidelines document was developed with the financial support of the EAU.

112 UPDATE MARCH 2011 .

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