Urogenital Infections and Inflammations

T.E. Bjerklund Johansen, F. M.E. Wagenlehner, Y.-H. Cho, T. Matsumoto, J. N. Krieger, D. Shoskes, K. Naber

Asymptomatic bacteriuria in pregnancy - Is it still necessary to screen & treat?

 Caroline Schneeberger 1
Brenda Kazemier 2


1 Academic Medical Center (AMC), Amsterdam, Netherlands
2 Obstetrics & Gynaecology, Academic Medical Centre, Amsterdam, Netherlands

Abstract

Asymptomatic bacteriuria (ASB) in pregnancy occurs in 2–10% of pregnant women although higher frequencies have also been reported, up to 40%. Pregnant women are more prone to develop urinary tract infections (UTI) because of dilatation of the renal system and decreased peristalsis of the ureters and bladder facilitating bacterial colonisation and ascending infection in pregnancy.

Enterobacteriaceae comprise approximately the majority of urine isolates, of which Escherichia coli is the most common pathogen. A urine culture is considered the gold standard for diagnosing bacteriuria. The biggest challenge however is differentiating between significant (disease) and insignificant colonisation (not related to symptoms or adverse events) of the urinary tract. In addition, it is not clear which microorganisms are considered uropathogens and which are contaminants resulting in a wide range of reported incidences of ASB.

ASB when considered a latent stage and UTI as a symptomatic stage are both recognizable conditions that may be associated with an increased risk of adverse pregnancy outcomes. However, most pregnant women who developed a symptomatic UTI did not suffer from bacteriuria at the moment of screening (often performed in the first half of pregnancy) and not all women with ASB develop a UTI. In addition, the optimal timing of ASB screening remains unclear because ASB is often not a permanent stage and can dissolve spontaneously.

It has always been suggested that untreated ASB is an important risk factor for preterm birth, however when critically reviewing the literature, we found that currently there is no clear causal association between untreated ASB in pregnant women and preterm birth.

Recent studies showed that the incidence of antepartum pyelonephritis has decreased in developed countries with estimated incidences between 0.07% and 0.5%. This decrease is also notable in countries without a screen and treat program for ASB thereby questioning the effectiveness of current screening programs.

There is much debate about the best pharmacological and/or non-pharmacological treatment for ASB. There is no consensus or good quality evidence guiding clinicians in how to treat and how long to treat ASB in pregnancy.

The varying course of ASB in combination with the limited evidence for associations with negative long-term effects support the hypothesis that ASB is more likely a commensalism state than a disease. Possibly another not yet identified recognizable latent or early stage for pyelonephritis and/or preterm birth is present.

We conclude that the current evidence does not justify a screening programme for asymptomatic bacteriuria to prevent preterm birth or pyelonephritis.


Summary of recommendations

  • The distinction between significant disease and insignificant colonisation of the urinary tract in pregnancy is not clear, neither is clear which microorganisms are considered uropathogens and which contaminants (GoR B).
  • Causality between ASB in pregnancy and adverse pregnancy outcomes such as preterm birth, pyelonephritis and symptomatic UTI is not proven (GoR A).
  • The treatment of ASB in pregnancy could lead to harmful effects such as increase in antibiotic resistance and possible adverse effects on the newborn (GoR B).
  • Current evidence does not justify a screenings programme for asymptomatic bacteriuria to prevent adverse pregnancy outcomes (GoR B).

1 Introduction

The objective of this chapter is to elucidate why screening and treating of asymptomatic bacteriuria (ASB) in pregnancy is not desirable based on recent studies. The introduction of a screening and treating program of ASB is mainly based on outdated studies performed in the 70s and 80s, even before introduction of ultrasound for pregnancy dating. Screening is a valuable tool and may lead to early detection and treatment of disease, preventing subsequent disease and disease related sequelae. Unfortunately screening, like any other treatment has the potential to do harm. Therefore, the evaluation and re-evaluation of screening programs is a delicate process weighing the desirable and undesirable consequences [1], [2].

2 Methods

A systematic literature search was performed for the last 10 years (2005–2015) in PubMed using the following key words: “asymptomatic urinary tract infection” and “bacteriuria”. We limited search results to clinical studies of pregnant women written in the English language. A total of 159 publications were found and subsequently screened by title and, when appropriate, abstract. Only one clinical trial was found comparing pregnant women with ASB who were treated with pregnant women with ASB who were not treated.

The information identified through the literature review was supplemented by other papers identified by the authors. The studies were rated according to the level of evidence (LoE) and the grade of recommendation (GoR) using ICUD standards (for details see Preface).

3 Epidemiology

ASB in pregnancy occurs in 2–17% of pregnant women although higher frequencies have also been reported, up to 40% [3], [4], [5].

Pregnant women are more prone to develop ascending UTI because up to 90% of pregnant women develop dilatation of the renal system in combination with decreased peristalsis of the ureters and bladder thereby facilitating bacterial colonisation and ascending infection in pregnancy [6].

Risk factors for bacteriuria in pregnancy include underlying genitourinary anatomic or functional defects, diabetes, sickle cell disease, and history of recurrent urinary tract infections. Multiparity and disadvantaged socioeconomic status are also significant risk factors as were fertility treatments [7], [8], [9].

Enterobacteriaceae comprise approximately 95% of urine isolates, of which E. coli is the most common pathogen [10].

4 Diagnosis

For a screening programme it is important that one agrees which women have to be considered as patients [1]. The distinction between significant (disease) and insignificant colonisation (not related with symptoms or adverse events) of the urinary tract is often not clear-cut.

A urine culture is considered the gold standard for diagnosing bacteriuria [11]. The biggest challenge related to the diagnosis of ASB (and UTI) is differentiating between true bacteriuria and contamination and especially during pregnancy also between ASB and symptomatic UTI [12].

The first question: Does ‘true’ bacteriuria exist and is it possible to distinguish ‘true’ bacteriuria from contamination? The urethra (the tube that drains urine from the bladder) and the vaginal and perineal skin surrounding the urethra are known to be colonized with a motley crew of commensal bacteria [13]. These bacteria are often considered as non-pathogens, bacteria that do not cause infection or disease in that specific area. However when these bacteria are introduced in a different environment like the bladder (via the urethra) they can become pathogenic (uropathogens). Especially in women, who have a short urethra compared to men, bacteria present on the vaginal and perineal skin can easily enter and colonize the urinary tract [13].

The variety of definitions and diagnostic criteria used for ASB underscore that it is not clear whom to treat as patients and whom not. As mentioned earlier urine culture is the gold standard used to diagnose bacteriuria. Growth of 105 colony forming units (cfu)/ml of one (or maximum two) uropathogens is a commonly used definition [14], [15]. Some argue that two consecutive urine cultures are desirable but the interval between the two urine cultures is not clearly defined [16].

Furthermore, it is not clear which microorganisms are considered as uropathogens and which as contaminants in ASB. This probably explains why studies report a wide range of ASB prevalence up to 40% [4]. The most common organism associated with bacteriuria is Escherichia coli. Examples of microorganisms alternately defined as uropathogen are coagulase negative staphylococci (CNS) and Acinetobacter spp. [10], [13].

The second question: Is it possible to distinguish between ASB and symptomatic UTI during pregnancy? The difference between ASB and UTI is often based on symptoms. The difficulty is that some symptoms of UTI such as urgency and frequency are also common pregnancy complaints, which can make it more difficult to recognize a UTI and to distinguish between ASB and a symptomatic UTI [11]. A more important difference is that ASB is considered to be colonization and UTI an infection. A consequence of infection may be symptoms for example inflammation of the bladder wall due to the presence of bacteria is associated with frequency. In clinical practice the presence of leukocytes in a urine samples is often investigated to underset the UTI diagnosis. However pyuria is nonspecific and not always indicates infection [11], [13]. Summarizing it remains difficult to differentiate between contamination, colonization (ASB) and true infection (UTI).

5 Pathogenesis

5.1 Is ASB the latent or early symptomatic stage?

ASB when considered a latent stage and UTI as a symptomatic stage are both recognizable conditions that may be associated with an increased risk of adverse pregnancy outcomes. However, ASB is an asymptomatic stage and not necessarily a latent stage since only a small percentage of pregnant women with ASB develop one of the diseases; symptomatic lower UTI, pyelonephritis and/or preterm birth. Moreover the strength of the association between ASB and the different diseases, especially preterm birth, is questioned. [10], [17], [18], [19].

Besides, most of the pregnant women who developed a symptomatic UTI did not suffer from bacteriuria at the moment of screening (often performed in the first half of pregnancy) [10], [17], [18], [19]. In an old study by Lawson and Miller they reported that only 19.1% of pregnant women who developed symptomatic UTI had bacteriuria on initial screening [18]. This was even lower in recent cohort study by Kazemier et al., in this study they found that of all women who suffered from a UTI al only 12.7% suffered from either treated or untreated ASB [10].

Another key issue while discussing the value of this criterion is that ASB is not a permanent stage since ASB can dissolve spontaneously. A long-term follow-up study in non-pregnant patients with DM showed that incidence of UTI is slightly increased in women with DM and untreated ASB compared to those without [20]. Even though an increased incidence of symptomatic UTI in women with ASB was found, still only one third of the women with ASB developed a symptomatic UTI. Moreover, a study by Nicolle and colleagues demonstrated that many women have intermittent ASB, either spontaneously or due to antibiotic treatment [21].

An old study from Gower et al. reported that of the 164 women who had bacteriuria during pregnancy, six to twelve months after pregnancy a quarter of these women still suffered from bacteriuria independently of antibiotic treatment [22].

5.2 Timing of screening

The changeable nature of the presence of bacteriuria makes it difficult to determine when pregnant women should be screened for ASB. In most countries screening takes place early in pregnancy [15]. Stenqvist et al. screened 3,254 pregnant women at each prenatal visit (minimal three visits) showing that the risk of bacteriuria increased from 0.8% at 12 weeks’ gestation to 1.93% at the end of pregnancy. They recommend screening for ASB around the 16th week of pregnancy. This recommendation is based on possible ‘number of bacteriuria-free gestational weeks gained by treatment’ however also later in pregnancy women developed bacteriuria [23]. McIsaac et al. showed that a urine culture before 20 weeks’ gestation only detected half of the ASB cases of all cases identified with three urine cultures: at fewer than 20 weeks’, at 28 weeks and 36 weeks’ gestation [24]. Unfortunately this study did not assess the association between one, two or three urine cultures and pyelonephritis or preterm birth.

The varying course of ASB in combination with the limited evidence for associations with negative long-term effects support the hypothesis that ASB is more likely a commensalism state than a disease. It is not clear whether a recognizable latent or early symptomatic stage for pyelonephritis or preterm birth is present.

6 Consequences of untreated ASB in pregnancy

Colonization and related infections of the urinary tract have explicitly been identified as one of the risk factors for preterm birth with potential lifelong sequelae [14], [15], [25]. Therefore during the past decades several attempts have been made to reduce preterm birth with the use of screening (& treatment) programs including for ASB [10], [14], [15]. The question remains if screening (& treatment) programs for ASB truly lead to reduced preterm birth rates without unwanted negative effects for both the mother and newborn.

For a screenings program to be effective it should prevent the identified condition and therefore needs to meet certain criteria [1]. One of the essential criteria is that the natural history of the condition, including development from latent to stablished disease should be adequately understood.

ASB was considered the pre-clinical and possibly also pre-pathological stage of symptomatic UTIs including pyelonephritis [14], [25]. However this is not a correct assumption, since not all women with ASB develop a UTI and not all women who develop UTI had ASB prior thereto.

6.1 Preterm birth

Studies from the 60s, 70s and 80s show that around 30% to 40% of pregnant women with untreated ASB developed pyelonephritis compared to less than 2% of those without ASB [12], [26], [27], [28], [29]. The consequences of not treating ASB on preterm birth are less well established [17].

A meta-analysis of 14 randomized or quasi-randomised control trials showed that treatment of ASB with antibiotics was associated with reduced incidence of low birthweight babies (RR 0.6, 95% CI 0.5 to 0.9) and preterm birth (before 37 weeks) (RR 0.3, 95% CI 0.1 to 0.6).7 However the found relative risk of preterm birth was based on only two studies with poor quality and one of the studies included only women with group B streptococcal bacteriuria. The authors concluded that the overall quality of the studies were poor [17].

Moreover most trials were performed more than 25 years ago, before the widespread use of the ultrasound to measure the duration of pregnancy, which could have led to misclassification of preterm birth [30].

The described meta-analysis did not include a recent multicentre prospective cohort study with an embedded RCT by Kazemier et al., which could have changed the conclusion For this study 4,283 pregnant women were screened in the Netherlands where currently no ASB screening programme is in place. The prevalence of ASB was 5% (n=248). Forty women were randomly assigned to treatment with nitrofurantoin and 45 to placebo. The other 163 women with ASB did not receive any treatment. No differences was found in the proportion of women with pyelonephritis, preterm birth or both between women treated with nitrofurantoin and placebo-treated women (2.9% vs. 1.9% adjusted odds ratio (OR) 1.5, 95% CI 0.6–3.5) or untreated and placebo treated women (2.5% vs. 2.9%; risk difference –0.4, 95% CI –3.6 to 9.4). These results underscore that currently there is no known association between untreated ASB in pregnant women and preterm birth [10].

In a large prospectively studied cohort of 26,844 pregnancies performed in Wales, United Kingdom, bacteriuria was found to be significantly associated with preterm birth in the initial univariable analyses. However, after adjustments for medical factors, demographic and social factors, the relationship disappeared [31].

Concluding the recent study by Kazemier et al. reveals that earlier assumptions that ASB is associated with preterm birth needs to be reconsidered.

6.2 Pyelonephritis

Pyelonephritis was estimated to occur in 2% of pregnancies with a recurrence rate up to 23% within the same pregnancy or soon after birth [32], [33]. Recent studies showed that the incidence of antepartum pyelonephritis, often defined as a hospital admission for a UTI, has decreased in developed countries, now estimating an incidence of antepartum pyelonephritis between 0.07% and 0.5% [34], [35]. These recent studies concluded once more that antenatal pyelonephritis is associated with preterm birth (10.3%–20% vs. 7.8%–7.9%) [34], [35]. The reduced incidence of antepartum pyelonephritis may have various reasons including the introduction of ASB screening programmes and/or improved antenatal care. The previously mentioned meta-analysis showed that incidence of pyelonephritis was reduced in pregnant women with ASB who were treated with antibiotics compared to those who were not treated with antibiotics (relative risk (RR) 0.2, 95% CI 0.1 to 0.4) [17]. However the recent RCT by Kazemier et al. found a low absolute risk of pyelonephritis in both women with ASB including untreated (2.4%) and women without ASB (0.6%) [10].

7 Treatment options

7.1 Antibiotics

Currently the most common way to treat both ASB and symptomatic infections (UTI and pyelonephritis) of the urinary tract are antibiotics. The ability of antibiotics to restrain the growth or kill microorganisms causing infections of the urinary tract depends on the concentration of the antimicrobial achieved in the urine together with the sensitivity of the organisms to that antibiotic [11].

Although a Cochrane meta-analysis showed that antibiotic treatment of ASB compared to no treatment (placebo) reduced both the incidence of pyelonephritis (reduction varying between 1%–4% to 20–35%) and preterm birth [15], [17]. Treatment of ASB with antibiotics does not always lead to a disease free interval, in this case pregnancy due to relapse or recurrence of ASB [21], [22]. Moreover a recent study of Kazemier et al. showed that untreated ASB is associated with symptomatic UTI and pyelonephritis however not with preterm birth [10].

A present issue that may have an effect on antibiotic treatment of ASB and prevention of other infectious diseases is the increasing prevalence of antimicrobial resistance [36]. Screening for ASB and subsequent treatment with antibiotics may cause an increase of the use of antibiotics, especially if the number needing treatment needed to treat is high. This again may subsequently undermine the effectiveness of a screening programme because one of the main causes of antimicrobial resistance is the overuse of antibiotics.

Emerging evidence showing possible long-term consequences of antibiotic use in pregnant women are reason for concern [37], [38], [39]. Recent studies showed several associations between antibiotics used during pregnancy and adverse neonatal outcomes including increased risk for cerebral palsy, early onset sepsis with antibiotic-resistant micro-organisms, malformations and epilepsy [37], [38], [39]. Also maternal exposure to certain antibiotics is associated with childhood asthma and childhood obesity by 7 years of age [40], [41]. Significant alterations in overall microbiota community structure, as well as a reduction in microbiota richness and a depletion of Bacteroides has been noted after intrapartum antibiotic prophylaxis [42].

Moreover antibiotics may cause several side-effects such as gastro-intestinal symptoms and vaginal candidiasis [43], [44]. These side-effects may be worse than the disease, especially since it is not clear that the treatment causing the side-effects is preventing preterm birth.

But what should a clinician prescribe when ASB is present? A Cochrane review addressing antibiotic regimens for treatment of ASB in pregnancy could not draw any definite conclusion based on the five included studies [45]. Another Cochrane review on the duration of treatment of ASB during pregnancy analysing 13 studies could only conclude that a single-dose treatment of antibiotics may be less effective than a four to seven-day treatment. However, a single-dose regimen was associated with less side-effects. The authors note that the overall quality of included trials was low [46].

7.2 Non-pharmacological treatment

Many other interventions have been proposed to treat bacteriuria besides antibiotics such as cranberry products, probiotics and behavioural interventions [43].

One of the possible non-pharmacological interventions are cranberry products [47]. So far little evidence of the effect and side-effects of cranberry products during pregnancy are known. A meta-analysis of studies in non-pregnant women showed that cranberries are effective in reducing urinary tract infection recurrence (2 trials, sample size 250, RR 0.5, 95% CI 0.3-0.8) [47]. A pilot study found a good compliance and tolerability of cranberry capsule ingestion also during pregnancy [48] and currently a Cochrane review is being performed to determine the role of cranberries in the treatment of ASB in pregnant women [49]. However this study is not needed when ASB screening and treatment is not considered worthwhile. A recent study investigated the safety of cranberry product use during pregnancy using the Norwegian Mother and Child cohort including almost 70,000 pregnancies. No increased risk for malformations and other adverse pregnancy outcomes were observed [50]. Nevertheless, in this same study an association was found between the use of cranberry in late pregnancy and vaginal bleeding after pregnancy week 17, which should be investigated in appropriate clinical studies more carefully.

8 The costs of screening

Preterm birth is extremely costly due to increased maternal and neonatal admissions [51]. Therefore screening and treatment of ASB in pregnant women would prevent preterm birth it will almost always outweigh the costs of a ASB screening programme even with a high number of patients to treat since. Studies showed that the cumulative costs for children born preterm during the first 10 years of life doubled or more compared those who are born term [51], [52].

Not only preterm birth but also pyelonephritis in pregnant women is costly since a hospital admission is often needed. Rouse and colleagues concluded based on an analytic decision model that screening for ASB to (only) prevent pyelonephritis with either a urine culture or a leukocyte esterase-nitrite dipstick is cost-effective when the prevalence of ASB is 6% or higher [53].

However mainly due to lacking evidence on the effectiveness of ASB screening and treating policies we conclude that it is currently not clear whether the cost of case-finding is economically balanced in relation to possible expenditure on medical care as a whole.

9 Conclusions

New insights challenge the preconception that ASB in pregnant women is a disease of great importance associated with preterm birth [10]. Recent studies suggest that ASB might be more an expression of commensalism than a disease [54]. If this is the case, an ASB screening programme may not be effective to reduce the burden of preterm birth.

An association does not always represent a causal relationship; the association between ASB during pregnancy and preterm birth, established a long time ago, may have been confounded by other (yet) unidentified risk factors for preterm birth.

The question remains how can we explain the results of studies that have shown that treatment of ASB with antibiotics reduces the incidence of preterm birth compared to treatment with placebo [27], [55]? This finding seems to support the hypothesis that there is a direct association between colonization of the urinary tract and preterm birth. However preterm birth is thought to be the result of a combination of factors including several infectious diseases and antibiotics may achieve this reduction in preterm birth rate, by indiscriminate reduction of bacterial colonization and/or infectious loads elsewhere in the body [25], [56], [57].

In addition, even though antibiotic treatment of ASB seems to decrease the risk of pyelonephritis during pregnancy, the majority of women with pyelonephritis were screened negative for ASB. Furthermore, recent studies showed that the overall risk of pyelonephritis is small, which questions the need for a screening program even further.

Insight into the natural course of ASB during pregnancy is lacking, the borderline-group is large, test results ambiguous, the effectiveness of ASB treatment with antibiotics or any other treatment to prevent preterm birth or pyelonephritis not established and the possible harms of antibiotic use during pregnancy may be worse than the disease.

We conclude that the current evidence does not justify a screenings programme for ASB to prevent preterm birth or pyelonephritis.


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[41] Mueller NT, Whyatt R, Hoepner L, Oberfield S, Dominguez-Bello MG, Widen EM, Hassoun A, Perera F, Rundle A. Prenatal exposure to antibiotics, cesarean section and risk of childhood obesity. Int J Obes (Lond). 2015 Apr;39(4):665-70. DOI: 10.1038/ijo.2014.180
[42] Azad MB, Konya T, Persaud RR, Guttman DS, Chari RS, Field CJ, Sears MR, Mandhane PJ, Turvey SE, Subbarao P, Becker AB, Scott JA, Kozyrskyj AL; CHILD Study Investigators. Impact of maternal intrapartum antibiotics, method of birth and breastfeeding on gut microbiota during the first year of life: a prospective cohort study. BJOG. 2016 May;123(6):983-93. DOI: 10.1111/1471-0528.13601
[43] Epp A, Larochelle A; SOGC Urogynaecology Committee, SOGC Family Physicians Advisory Committee. Recurrent urinary tract infection. SOGC Clinical Practice Guideline No. 250, November 2010. J Obstet Gynaecol Can 2010;32(11):1082-1090. J Obstet Gynaecol Can. 2011 Jan;33(1):14. DOI: 10.1016/S1701-2163(16)34779-X
[44] Albert X, Huertas I, Pereiró II, Sanfélix J, Gosalbes V, Perrota C. Antibiotics for preventing recurrent urinary tract infection in non-pregnant women. Cochrane Database Syst Rev. 2004;(3):CD001209. DOI: 10.1002/14651858.CD001209.pub2
[45] Guinto VT, De Guia B, Festin MR, Dowswell T. Different antibiotic regimens for treating asymptomatic bacteriuria in pregnancy. Cochrane Database Syst Rev. 2010 Sep 8;(9):CD007855. DOI: 10.1002/14651858.CD007855.pub2
[46] Widmer M, Lopez I, Gülmezoglu AM, Mignini L, Roganti A. Duration of treatment for asymptomatic bacteriuria during pregnancy. Cochrane Database Syst Rev. 2015 Nov 11;(11):CD000491. DOI: 10.1002/14651858.CD000491.pub3
[47] Beerepoot MA, Geerlings SE, van Haarst EP, van Charante NM, ter Riet G. Nonantibiotic prophylaxis for recurrent urinary tract infections: a systematic review and meta-analysis of randomized controlled trials. J Urol. 2013 Dec;190(6):1981-9. DOI: 10.1016/j.juro.2013.04.142
[48] Wing DA, Rumney PJ, Hindra S, Guzman L, Le J, Nageotte M. Pilot Study to Evaluate Compliance and Tolerability of Cranberry Capsules in Pregnancy for the Prevention of Asymptomatic Bacteriuria. J Altern Complement Med. 2015 Nov;21(11):700-6. DOI: 10.1089/acm.2014.0272
[49] Eke AC, Akarolo-Anthony SN, Enumah AP. Cranberries for treating asymptomatic bacteriuria during pregnancy. Cochrane Database of Systematic Reviews. 2012;4:CD009793. DOI: 10.1002/14651858.CD009793
[50] Heitmann K, Nordeng H, Holst L. Pregnancy outcome after use of cranberry in pregnancy–the Norwegian Mother and Child Cohort Study. BMC Complement Altern Med. 2013 Dec;13:345. DOI: 10.1186/1472-6882-13-345
[51] Russell RB, Green NS, Steiner CA, Meikle S, Howse JL, Poschman K, Dias T, Potetz L, Davidoff MJ, Damus K, Petrini JR. Cost of hospitalization for preterm and low birth weight infants in the United States. Pediatrics. 2007 Jul;120(1):e1-9. DOI: 10.1542/peds.2006-2386
[52] Petrou S. The economic consequences of preterm birth during the first 10 years of life. BJOG. 2005 Mar;112 Suppl 1:10-5. DOI: 10.1111/j.1471-0528.2005.00577.x
[53] Rouse DJ, Andrews WW, Goldenberg RL, Owen J. Screening and treatment of asymptomatic bacteriuria of pregnancy to prevent pyelonephritis: a cost-effectiveness and cost-benefit analysis. Obstet Gynecol. 1995 Jul;86(1):119-23. DOI: 10.1016/0029-7844(95)00097-B
[54] Wagenlehner FM, Naber KG. Editorial commentary: asymptomatic bacteriuria--shift of paradigm. Clin Infect Dis. 2012 Sep;55(6):778-80. DOI: 10.1093/cid/cis541
[55] Romero R, Oyarzun E, Mazor M, Sirtori M, Hobbins JC, Bracken M. Meta-analysis of the relationship between asymptomatic bacteriuria and preterm delivery/low birth weight. Obstet Gynecol. 1989 Apr;73(4):576-82.
[56] Romero R, Espinoza J, Chaiworapongsa T, Kalache K. Infection and prematurity and the role of preventive strategies. Semin Neonatol. 2002 Aug;7(4):259-74. DOI: 10.1053/siny.2002.0121
[57] Bansal M, Khatri M, Kumar A, Bhatia G. Relationship between maternal periodontal status and preterm low birth weight. Rev Obstet Gynecol. 2013;6(3-4):135-40.

The ZB MED – Information Center for Life Sciences, Germany, together with the European Association of Urology (EAU) provided the opportunity to publish a “Living Textbook” on “Urogenital Infections and Inflammations” in an open access form. This “Living Textbook” represents also an update of the Textbook on Urogenital Infections published 2010 by the International Consultation on Urological Infections and the EAU: http://www.icud.info/urogenitalinfections.html.

The “Living Textbook” will cover infections and inflammations of the kidney, the urinary tract, as well as the male and female genital tract considering pathogenesis, diagnostics, treatment, prophylaxis and future aspects. The “Living Textbook” will be structured into about 26 Sections each with two section co-chairs responsible for peer review of the chapters of each section. Each chapter should reflect the background to the topic and highlight all of the critical evidence relating to the subject. The intention is to provide an up to date, concise synthesis of the literature on that topic, and for clinical topics also recommendations based on levels of evidence for contemporary clinical practice, as well as suggested research recommendations.

The editors hope that this “Living Textbook” may become a useful instrument for physicians of different specialties taking care about patients suffering from these diseases.

Truls E. Bjerklund Johansen (Norway),

Florian ME Wagenlehner (Germany),

Yong-Hyun Cho (South Korea),

Tetsuro Matsumoto (Japan),

John N Krieger (USA),

Daniel Shoskes (USA),

Kurt G. Naber (Germany).

Publishing at PUBLISSO

Your chapter will be published at the PUBLISSO platform (https://books.publisso.de).

Information for corresponding authors

It is necessary for all corresponding authors to register at PUBLISSO.
To register at PUBLISSO please click the following link: http://books.publisso.de/publisso_gold/register

After registration, please complete your user profile. Information from your user profile will appear in the published chapter and the authors board of the book (http://books.publisso.de/publisso_gold/book/52). If you are displayed in the authors board, you can be contacted by readers and other professionals. You can also contact other authors of the book for exchange and to build a network.
(If you do not want to be displayed in the authors board, but stay registered, you can disable this feature in your profile settings. In this case, your affiliation (publication data) will be displayed in the published chapter only.)

We kindly ask you to provide the co-authors email addresses in the manuscript so that we can contact them in case of queries.

Information for co-authors

After publication of your chapter, your affiliation (publication data) will be displayed in the published chapter.

If you also want to be displayed in the authors board of the book (http://books.publisso.de/publisso_gold/book/52), we kindly ask you to register at PUBLISSO. If you are displayed in the authors board, you can be contacted by readers and other professionals. You can also contact other authors of the book for exchange and to build a network.

To register at PUBLISSO please click the following link: http://books.publisso.de/publisso_gold/register

If you do not want to be displayed in the authors board of the book, you do not have to register. Your affiliation (publication data) will be displayed in the published chapter only.

Support

If you have any further questions please don’t hesitate to contact the PUBLISSO editorial office:

E-Mail: livingbooks@zbmed.de
Phone: +49 221 478-7093

General

The textbook will be structured in sections with two co-chairs each. Each section will start with an introductory chapter written by the two respective co-chairs presented like an editorial commentary in regard to the following chapters (see proposed contents of the book). The two co-chairs of each section will also peer review all chapters in their section and stimulate a consensus discussion within their section together with the authors and the main editors if needed.

Chapters

Each chapter should reflect the background to the topic and highlight all of the critical evidence relating to the subject. The intention is to provide an up to date, concise synthesis of the literature on that topic, and for clinical topics also recommendations based on levels of evidence for contemporary clinical practice, as well as suggested research recommendations.

Manuscript

Each manuscript should have up to approximately 3,000 words (excluding abstract, tables/figures and references). The abstract should count about 300 words.

Structure

The outline of each chapter should be structured as follows (similar as in the edition 2010, which can be downloaded for free: http://www.icud.info/urogenitalinfections.html):

  1. Abstract
  2. Summary of recommendations*/key notes*
    (*which ever term is more appropriate)
  3. Introduction
  4. Methods
  5. Results
  6. Further research
  7. Conclusions
  8. Acknowledgement
  9. Conflict of interest of each author
  10. References

Citation style

As a citation style, the Vancouver style is preferred.

Please mark your references in the text with square brackets ([1], [2], ...).

Summary of recommendations

We would like to have the Summary of recommendations at the beginning after the abstract (as in the edition 2010). However, we do not expect as in the edition 2010, that each recommendation is also specified according to Level of Evidence and Grade of Recommendation, because such a claim would not only need a systematic literature search (see below), but also a structured discussion in a defined group of experts.

Systematic literature search

A systematic literature search should be performed, at least of PUBMED/MEDLINE but ideally of several relevant databases in addition (like Cochrane CENTRAL) to find recent, high quality systematic reviews and/or primary research studies. It is not expected to perform for all chapters a de novo systematic review, if such reviews are already published recently, but it still may be indicated for some items. For questions relating therapy, it should be focused on evidence from (systematic reviews of) randomized controlled trials if available.

The method of the systematic literature search needs to be fully described in the section “Methods”, e.g.:

“A systematic literature search was performed for the last ... (usually 10) years in MEDLINE, Cochrane etc. with the following key words ... and the following limitations: e.g. UTI, age (adult?), ... clinical studies ... English ... abstract available ... only peer reviewed ...

A total of ... publications were identified, which were screened by title and abstract ... After exclusion of duplicates ... a total of ... were included into the review (analysis), supplemented by citations or known to the authors ... ”.

Clinical topics

Clinical topics should be focused on the importance to clinical practice according to the up to date scientific knowledge as presented in the literature. It should relate to questions/complaints/symptoms of patient/population concerning definition, diagnosis, therapy/prevention, intervention, and outcome in comparison, if different approaches are feasible. Please choose patient-important outcomes and focus on those, which you deem critical for decision-making.

Level of evidence and grade of recommendations

Any recommendation should be based on the level of evidence and the grade of recommendation. For this purpose the following system, modified from the Oxford Centre for Evidence-based Medicine should be used (EAU guidelines 2015):

Level of evidence (LE)

Level Type of evidence
1a Evidence obtained from meta-analysis of randomised trials
1b Evidence obtained from at least one randomised trial
2a Evidence obtained from one well-designed controlled study without randomization
2b Evidence obtained from at least one other type of well-designed quasi-experimental study
3 Evidence obtained from well-designed non-experimental studies, such as comparative studies, correlation studies and case reports.
4 Evidence obtained from expert committee reports or opinions or clinical experience of respected authorities.

Grade of Recommendations (GoR)

Grade Nature of recommendations
A Based on clinical studies of good quality and consistency addressing the specific recommendations and including at least one randomised trial
B Based on well-conducted clinical studies, but without randomised clinical trials
C Made despite the absence of directly applicable clinical studies of good quality

Comments (EAU guidelines 2015)

The aim of assigning a LE and grading recommendations is to provide transparency between the underlying evidence and the recommendation given.

It should be noted that when recommendations are graded, the link between the level of evidence and grade of recommendation is not directly linear. Availability of randomized controlled trials may not necessarily translate into a grade “A” recommendation where there are methodological limitations or disparity in published results.

Alternatively, absence of high level evidence does not necessarily preclude a grade A recommendation, if there is overwhelming clinical experience and consensus. In addition, there may be exceptional situations where corroborating studies cannot be performed, perhaps for ethical or other reasons and in this case unequivocal recommendations are considered helpful for the reader. The quality of the underlying scientific evidence - although a very important factor – has to be balanced against benefits and burdens, values and preferences and costs when a grade is assigned.

Since the same rating system should be used in all chapters, for the sake of brevity the same sentence could be used in “Methods” for all manuscripts, because the rating system will be described in details in the Preface of the book:

“The studies were rated according to the level of evidence and the strength of recommendations graded according to a system used in the EAU guidelines modified from the Oxford Centre for Evidence-based Medicine [1].”

References

[1] European Association of Urology. Guidelines. Methodology section. 2015 ed. Arnhem: European Association of Urology; 2015. p. 3. ISBN/EAN: 978-90-79754-80-9. Available from: http://uroweb.org/wp-content/uploads/EAU-Extended-Guidelines-2015-Edn..pdf

The Living Handbook of Urogenital Infections and Inflammations is issued by:

European Association of Urology
att. Maurice Schlief, EAU executive manager business affairs

P.O.Box 30016
NL-6803 AA Arnhem, The Netherlands

Phone: 0031-26-38.90.680
E-mail: m.schlief@uroweb.org

Editor in Chief

responsible for the contents according to § 5 TMG and § 55 Abs. 2 RStV (Germany):

Kurt G. Naber, MD, PhD
Assoc. Professor of Urology

Technical University of Munich
Karl-Bickleder-Str. 44c
94315 Straubing, Germany

E-mail: kurt.naber@nabers.de

John N. Krieger MD, PhD

University of Washington Section of Urology

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Daniel Shoskes MD, PhD

Cleveland Clinic Glickman Urological and Kidney Institute

more

Yong-Hyun Cho MD, PhD

St. Mary's Hospital, The Catholic University of Korea Department of Urology

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Tetsuro Matsumoto MD, PhD

University of Occupational and Environmental Health Department of Urology

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Florian M. E. Wagenlehner MD, PhD

Justus-Liebig University of Giessen Clinic of Urology and Andrology

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Truls Erik Bjerklund Johansen MD, PhD

Oslo University Hospital Urology Department

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Kurt G. Naber MD, PhD

Technical University of Munich

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Riccardo Bartoletti

University of Pisa
Department of Translational Research and New Technologies

more

Truls Erik Bjerklund Johansen MD, PhD

Oslo University Hospital
Urology Department

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PD Dr. med. Gernot Bonkat

University Basel
alta uro AG, Merian Iselin Klinik, Center of Biomechanics & Calorimetry (COB)

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Prof. Tommaso Cai MD

Santa Chiara Regional Hospital
Dept. of Urology

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Dr Leyland Chuang

Ng Teng Fong Hospital, National University Health System
Department of Medicine

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Prof. Milan Cizman

University Medical Centre
Department of Infectious Diseases

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Alison Crawford MSc

Queen's University
Department of Psychology

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Pfofessor Svetlana Dubrovina MD, PhD

Rostov Medical State University
Obstetrics and Gynaecology

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Dr Valerie Huei Li Gan MBBS (S'pore), MRCS (Edin), MMed (Surg), FAMS (Urology)

Singapore General Hospital
Department of Urology

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Philip Hanno

University of Pennsylvania

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Ass prof MD Gundela Holmdahl

Queen Silvia Childrens Hospital, Sahlgrens Academy
Pediatric surgery and urology

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Udo B. Hoyme

HELIOS Hospital Erfurt Ltd.
Department of Gynecology and Obstetrics

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David Hunstad

Washington University School of Medicine
Pediatrics / Molecular Microbiology

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Gitte M. Hvistendahl

Aarhus University Hospital

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Prof. Michael KOGAN M.D., PhD

Rostov State Medical University
Department of Urology

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Dr Akihiro Kanematsu

Hyogo College of Medicine
Department of Urology

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Frieder Keller

University Hospital Ulm
Department Internal Medicine 1, Nephrology

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Professor Katarzyna Kilis-Pstrusinska PhD, MD

Wroclaw Medical University
Department of Pediatric Nephrology

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MD, PhD Tae-Hyoung Kim

Chung-Ang University
Urology

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John N. Krieger MD, PhD

University of Washington
Section of Urology

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Prof Ekaterina Kulchavenya

Novosibirsk Research TB Institute, Novosibirsk State Medical University

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Dr Christina Kåbjörn Gustafsson

Ryhov Hospital Jönköping
Pathology

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Dr. Bela Köves

South Pest Teaching Hospital
Department of Urology

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Dr. med. Giuseppe Magistro

Ludwig-Maximilians-University of Munich
Department of Urology

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Vittorio Magri

ASST-North
Urologic Clinic

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András Magyar

South-Pest Hospital
Department of Urology

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Professor Emeritus Brian Morris

University of Sydney
School of Medical Sciences

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Baerbel Muendner-Hensen

ICA-Deutschland e.V.

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Stephen F. Murphy

Feinberg School of Medicine, Northwestern University
Department of Urology

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Kurt G. Naber MD, PhD

Technical University of Munich

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Prof. Yulia Naboka

Rostov State Medical University
Department of Microbiology

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Dr. J. Curtis Nickel MD

Queen's University
Department of Urology

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Professor Ralph Peeker MD PhD

University of Gothenburg
Department of Urology

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Tamara Perepanova

N.A. Lopatkin Research Institute of Urology and Interventional Radiology

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Prof. Gianpaolo Perletti M. Clin. Pharmacol.

University of Insubria
Department of Biotechnology and Life Sciences

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Felice Petraglia

Department of Biomedical, Experimental and Clinical Sciences, University of Florence
Obstetrics and Gynecology

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Dr. Jörgen Quaghebeur PhD. Med. Sci.

University Hospital Antwerp and University Antwerp
Department of Urology

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Yazan F. Rawashdeh

Aarhus University Hospital
Paediatric Urology Section, Department of Urology

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Professor Claus Riedl MD

-
Urology

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Matthew Roberts

The University of Queensland
Faculty of Medicine

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PD Dr. med Guido Schmiemann MPH

Institut für Public Health und Pflegeforschung, Universität Bremen
Abteilung Versorgungsforschung

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Caroline Schneeberger MD PhD

Academic Medical Center (AMC)

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Prof. Dr. med. Peter Schneede

Klinikum Memmingen
Department of Urology

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Aaron C. Shoskes

Des Moines University Medical College of Ostheopathic Medicine

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Daniel Shoskes MD, PhD

Cleveland Clinic
Glickman Urological and Kidney Institute

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Prof. Dr. Roswitha Siener

University of Bonn
University Stone Centre, Department of Urology

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Sofia Sjöström

Queen Silvia Childrens Hospital, Sahlgrens Academy
Pediatric surgery and urology

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Mathew Sorensen

University of Washington School of Medicine
Department of Urology

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Prof. Dr. Dr. Walter Ludwig Strohmaier FEBU

Regiomed-Klinikum Coburg. Medical School Regiomed
Urology and Paediatric Urology

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Satoshi Takahashi

Sapporo Medical University School of Medicine
Department of Infection Control and Laboratory Medicine

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Professor Paul Anantharajah Tambyah

Yong Loo Lin School of Medicine, National University Hospital
Department of Medicine

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Peter Tenke

South-Pest Hospital
Department of Urology

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Praveen Thumbikat


Department of Urology

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Dr. Jose Tiran Saucedo

IMIGO / Universidad de Monterrey
Obstetrics and Gynaecology

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Dominic Tran-Nguyen

Des Moines University

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Dean Tripp

Queen's University
Psychology, Anesthesia & Urology

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Prof. SEONGHEON WIE

The Catholic University of Korea, St. Vincent's Hospital
Division of Infectious Diseases, Department of Internal Medicine

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Florian M. E. Wagenlehner MD, PhD

Justus-Liebig University of Giessen
Clinic of Urology and Andrology

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Assoc. Prof. Christian Wejse

Aarhus University, Aarhus University Hospital
Department of Infectious Diseases/Center for Global Health, Dept of Public Health

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Prof. Dr. Mete Çek

Trakya University, School of Medicine
Urology

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