One of the most challenging aspects of care in patients with neurogenic bladders (NGBs) is interpreting the finding of bacteriuria in order to properly diagnose and treat a potential urinary tract infection (UTI). Recurrent UTIs can cause significant patient morbidity in any population but have particular consequences in NGB patients. UTI is the most common infection in those with a spinal cord injury and NGB, with increasing number of UTIs independently associated with a worse quality of life.¹ In addition, UTI is the second leading cause of death in this patient population.² As such, accurately identifying an infection to enable proper treatment and prevention of future infections is of particular importance in this population to prevent such outcomes.

Yet the presence of bacteria in the urine alone does not necessarily indicate infection and may instead be reflective of asymptomatic bacteriuria (ASB). Patients with NGB have multiple risk factors for having bacteriuria, mainly as a result of their neurological insult, such as their regular need for bladder instrumentation, incomplete bladder emptying, neurogenic bowel dysfunction and prior urinary tract reconstruction. As a result, patients with NGB have a high incidence of bacteriuria even when asymptomatic.³ The general recommendations do not advise treating uncomplicated ASB as it is not associated with an increased risk of symptomatic UTI or deterioration of the upper urinary tract.³ In fact, treatment of ASB has been found to increase the risk of future symptomatic UTI in a study of young women without NGB.⁴ In addition, there is a real motivation to be more thoughtful and deliberate about antibiotic use given the rise in antibiotic resistance among bacteria, with patients with NGB having a particularly high rate of antibiotic-resistant bacterial carriage.⁵ Thus, it is of paramount importance to distinguish between bacteriuria suggestive of infection versus simply as a result of colonization in those with NGB. This distinction, however, can be difficult in this patient population.

Part of the problem is the lack of a unified definition of UTI in NGB patients. Various definitions have been used among guidelines (Infectious Diseases Society of America, European Association of Urology, National Institute on Disability, Independent Living, and Rehabilitation Research), with provider confusion on how to diagnose UTIs in NGB patients and a lack of consensus on the evaluation and management of bacteriuria between specialty centers caring for NGB patients.⁶

The diagnostic criteria for UTI in the NGB population broadly includes 1) presence of bacteriuria, 2) signs/symptoms compatible with UTI and 3) an abnormal urinalysis. Each criterion has its own set of problems, however. The presence of bacteriuria itself is necessary for the diagnosis of both UTI and ASB, with the magnitude of bacteriuria unable to distinguish between the 2 conditions.⁷ Symptoms in this population can be nonspecific or atypical due to altered sensation as a result of their neurological lesion. Various urinalysis findings used to potentially indicate infection, such as the presence of nitrites and leukocyte esterase, have poor sensitivity and specificity, respectively.⁸

As a result, there has been interest in other biomarkers that could distinguish between UTI and ASB. These have tended to focus on the innate host response to bacteriuria, through measuring interleukins like IL-6 and IL-8 and certain antimicrobial peptides, with studies primarily having been done in nonNGB patients. The research in NGB patients is quite limited, with neutrophil gelatinase-associated lipocalin being the only urinary marker showing some promise in discriminating between UTI and ASB specifically in the pediatric NGB population.^9,10 Findings related to characteristics of the bacteria itself and composition of the microbiome have not been illuminating thus far.

While work does continue to try and identify better means of distinguishing true infection from colonization, this still leaves clinicians with the dilemma of trying to interpret the finding of bacteriuria in this complex patient population. At this time, providers have to continue to rely on their level of clinical suspicion and make the most of the diagnostic test results at their disposal. In the meantime, it bears repeating that one should carefully assess the clinical question to be answered by even checking urine studies, remaining an important first step before the process of interpreting the subsequent results.