We report a case in a 65-year-old man receiving intravesical BCG therapy for superficial bladder cancer. He was admitted due to a prostate abscess accompanied by fever, liver dysfunction, and disseminated intravascular coagulation (DIC). During antibiotic therapy, he developed interstitial pneumonia with acute respiratory failure, which rapidly improved after steroid pulse therapy. Mycobacterium bovis (M. bovis) was isolated from blood and sputum cultures taken at the diagnosis of interstitial pneumonia, suggesting the involvement of hematogenous dissemination of BCG. Despite the absence of anti-tuberculosis therapy, repeat blood and sputum cultures were negative at discharge. Isolation of M.bovis from the blood culture is extremely rare. The clinical improvement and bacterial clearance observed following treatment with corticosteroids alone, despite the presence of bacteremia, suggest that the primary pathophysiology of this complication may be a hypersensitivity reaction rather than bacterial proliferation. We report this case as an instance of transient hematogenous dissemination and a severe systemic reaction following intravesical BCG therapy.

Acute bacterial prostatitis (ABP) typically presents with fever and urinary symptoms; however, its diagnosis can be challenging in patients who lack characteristic findings such as perineal pain or prostatic tenderness. Although postvoid residual (PVR) urine may be associated with voiding dysfunction in ABP, its potential role as a diagnostic clue has received little attention. A 44-year-old man presented with a 2-day history of fever ranging from 38 to 39°C, irritative urinary symptoms, back pain, and difficulty initiating urination. At presentation, the patient was afebrile and had no perineal tenderness. Noncontrast computed tomography (CT) performed approximately 1 min after urination revealed an estimated PVR volume of 170 mL. The CT also showed an enlarged prostate with irregular margins and a low-density area. Laboratory tests showed a white blood cell count of 17,700/μL, a C-reactive protein level of 7.01 mg/dL, and 3+ leukocytes on urinalysis. Urine culture subsequently yielded Escherichia coli. Based on the clinical, imaging, and laboratory findings, ABP was diagnosed, and antibiotic therapy was administered for 28 days. Following treatment, inflammatory markers and urinary findings improved, and the follow-up PVR volume was 36 mL when measured 10 min after urination. In this case, PVR volume measurement immediately after urination provided a clue to the presence of voiding dysfunction associated with ABP, despite the absence of typical clinical findings. Furthermore, the reduction in PVR volume following treatment was temporally associated with improvement in inflammatory findings and urinary symptoms, although a causal relationship cannot be established. In patients with urinary symptoms and suspected ABP despite the absence of characteristic clinical findings, assessment of PVR volume may provide additional information regarding associated voiding dysfunction and support the overall clinical assessment.

While acute bacterial prostatitis is seen occasionally in adult males, the development of a prostatic abscess (PA) is exceedingly rare in pediatric and adolescent populations. When PA does occur in younger patients, congenital anomalies, immune compromise, trauma, or genitourinary instrumentation are commonly associated. We report a unique case of a 16-year-old boy who developed a prostatic abscess after deliberately instilling shower water into his urethra. This report details the clinical presentation, diagnostic workup, and treatment course of this patient, followed by a literature review of the pathophysiology, diagnostic considerations, therapeutic paradigms, and operative management strategies for pediatric prostatic abscesses.

Recurrent urinary tract infections (rUTIs) represent one of the most common infectious conditions worldwide, yet their pathophysiology extends far beyond repeated episodes of acute bacterial cystitis. Increasing evidence indicates that recurrence may arise through overlapping mechanisms including reinfection from intestinal or periurethral reservoirs, intracellular bacterial persistence, microbial dysbiosis, impaired mucosal immunity and chronic inflammatory remodelling of the bladder microenvironment. Current diagnostic frameworks remain largely based on symptom-based definitions and standard urine culture, approaches that incompletely capture the biological complexity of recurrent disease. This limitation is evident even at the definitional level, where clinically pragmatic categories often fail to reflect the heterogeneous mechanisms underlying recurrence. Advances in expanded urine culture techniques, metagenomics and metabolomics have reshaped the understanding of the urinary tract as a dynamic ecological system interconnected with vaginal, intestinal and prostatic microbial compartments. These approaches have identified diverse microbial communities, virulence-associated functional profiles and host-microbe interactions linked to recurrence-prone phenotypes. Significant challenges continue to persist in elucidating the biological mechanisms driving recurrence. Addressing these gaps is essential to improve disease characterization and support the development of more effective diagnostic and therapeutic approaches.

Endogenous endophthalmitis is a rare but severe intraocular infection caused by hematogenous spread from distant infectious foci and is often associated with poor visual outcomes. Klebsiella pneumoniae is an important pathogen responsible for invasive infections with bacteremia and metastatic complications. Although liver abscess is a well-known source of K. pneumoniae bacteremia leading to endogenous endophthalmitis, prostatic abscess as the primary focus has rarely been reported. We report two cases of endogenous endophthalmitis associated with prostatic abscess caused by K. pneumoniae. The first patient was a 37-year-old man who presented with fever and lower urinary tract symptoms followed by acute visual loss. Blood and urine cultures grew K. pneumoniae. Imaging revealed a prostatic abscess and septic pulmonary embolism. The abscess resolved with systemic antibiotics without drainage, but severe visual impairment persisted. The second patient was a 68-year-old man with benign prostatic hyperplasia who developed fever and visual disturbance. Blood cultures were negative, but K. pneumoniae was isolated from urine, and CT showed a prostatic abscess with liver abscess. Despite treatment, ocular inflammation progressed with elevated intraocular pressure and severe pain, requiring enucleation. These cases highlight that prostatic abscess can be a source of invasive K. pneumoniae infection with metastatic spread including endogenous endophthalmitis. Early recognition and treatment are essential to prevent severe complications and irreversible visual loss.

Pancreatic calcification is a hallmark structural change of chronic pancreatitis. However, few reports have described extensive diffuse pancreatic calcification that develops within a relatively short period after acute pancreatitis and is incidentally detected during urological evaluations. We report the case of a 34-year-old man who presented with urinary frequency, gross hematuria, and the passage of sand-like material in his urine. He had smoked five cigarettes per day and consumed alcohol on approximately 10 occasions per month since the age of 29 years, when abnormal liver function was noted on routine tests, and he developed acute pancreatitis at the age of 31 years. Computed tomography (CT) and magnetic resonance cholangiopancreatography performed at that time revealed no pancreatic calcifications. At the current presentation, he was diagnosed with acute bacterial prostatitis, and a urine culture yielded Escherichia coli. A kidneys, ureters, and bladder (KUB) radiograph performed to evaluate suspected urolithiasis incidentally revealed multiple calcified densities in the pancreatic region. Moreover, noncontrast CT demonstrated extensive diffuse calcifications involving the entire pancreas, with mild pancreatic enlargement. Serum calcium, IgG4, intact parathyroid hormone, and HbA1c levels were within the normal ranges, suggesting that alcohol consumption and smoking were the most likely etiological factors. This case suggests that extensive calcific chronic pancreatitis can develop within a relatively short period following acute pancreatitis. Clinicians evaluating KUB radiographs and CTs performed for urological indications should systematically check for clinically significant incidental findings outside the urinary tract.

Acute and chronic bacterial prostatitis are clinically significant entities that can be difficult to diagnose and appropriately treat. Herein, we review when to suspect these clinical conditions, how to diagnose them, and how to effectively treat them based on the extant literature. Our aim was to equip the practicing clinician with the ability to proficiently diagnose and manage acute and chronic bacterial prostatitis, particularly in older patients.

Prostatitis is an inflammatory disease of the prostate gland that can present with lower abdominal pain, urinary incontinence, and sexual dysfunction. The diagnosis of prostatitis encompasses two main conditions: acute bacterial prostatitis (ABP) and chronic bacterial prostatitis (CBP). Urinary dysfunction is a key factor in the pathogenesis of chronic prostatitis. Overactive contraction of the urinary sphincter can cause bladder outlet obstruction and residual urine, which can lead to urinary reflux into the prostate. Alpha-1-adrenergic receptor antagonists (alpha blockers) are a class of drugs that inhibit smooth muscle contraction in the prostate and bladder neck. Tamsulosin is the first selective 1-adrenergic receptor antagonist, primarily the 1A and 1D subtypes, which are found in the smooth muscle of the prostate, bladder neck, and prostatic urethra. Blockade of these receptors reduces smooth muscle tone in these structures, which, in turn, improves urine flow from the bladder. We carried out a systematic review of the literature to evaluate the efficacy of tamsulosin in the treatment of acute and chronic bacterial and abacterial prostatitis, as well as chronic pelvic pain syndrome (CPPS). A search for clinical trials was carried out in the PubMed database, the clinical trials registry clinicaltrials.gov, and the Russian electronic library elibrary.ru by two independent researchers using keywords describing treatments that potentially included tamsulosin. The search yielded information on 21 publications, 20 of which were included in the systematic review. Five studies were non-comparative, meaning they analyzed only patients receiving tamsulosin in addition to background therapy. The remaining studies had different comparison groups and could include active strategies such as antibacterial, analgesic, anti-inflammatory, herbal (urological) medications, and others. Treatment duration ranged from 4 to 52 weeks. The prescribed dose of tamsulosin was 0.4 mg orally once daily. Most studies used the NIH-CPSI (National Institute of Health Chronic Prostatitis Symptom Index) scores to evaluate outcomes. The average age of the participants ranged from 28.9 to 59.1 years. The quality of the included studies was highly variable. Of the 20 studies included in this review, 19 examined the use of tamsulosin in patients with CP/CPPS. Positive treatment outcomes were observed in all studies using tamsulosin. Increases in maximum urinary flow rate, significant symptom regression, as measured by standardized scales, and improvements in quality of life were observed. The greatest differences in symptom regression were observed early in treatment, up to 45 days. This is likely due to the fact that urinary dysfunction, pain, and decreased quality of life become more prominent early in the disease course. The safety of the treatment was assessed in 15 of the 20 studies. No standardized scales were used to assess safety. The safety of tamsulosin was assessed based on the reporting of adverse reactions. The development of serious adverse reactions (defined in Roszdravnadzor Order No. 1071 of February 15, 2017) was reported in two studies, but it was not possible to reliably link them to tamsulosin use. CONCLUSION: The results of this systematic review confirm that tamsulosin is an effective drug for inclusion in combination treatment regimens for various forms of prostatitis, including CBP, chronic abacterial prostatitis, and CPPS. Its use significantly reduces symptoms such as pain and dysuria, which in turn improves patients' quality of life.

The management of male urinary tract infections (UTIs) has historically been based on a monolithic approach, under which every episode was treated as acute prostatitis, leading to prolonged antibiotic courses. To address rising bacterial resistance and promote antimicrobial stewardship, the French Infectious Diseases Society (SPILF) updated its guidelines in 2026, introducing a stratified management framework. This review outlines the scientific evidence underlying these updated recommendations. A comprehensive review of recent literature, including randomized controlled trials and large-scale retrospective cohorts, was conducted so as to evaluate antibiotic efficacy, resistance patterns, and optimal treatment durations for male cystitis, febrile UTIs (prostatitis/pyelonephritis), and acute epididymo-orchitis. Evidence validates distinguishing male cystitis from febrile UTI. For male cystitis, 7-day regimens using narrow-spectrum oral agents-such as fosfomycin trometamol, nitrofurantoin, or pivmecillinam-achieve satisfactory clinical success with minimal risk of complications. Conversely, febrile UTIs require initial parenteral third-generation cephalosporins or oral fluoroquinolones. For targeted oral step-down therapy in prostatitis, cotrimoxazole is preferred over fluoroquinolones so as to minimize ecological impact, while amoxicillin remains the drug of choice for enterococcal coverage. Although recent data show that seven days can be sufficient for selected bacteremic presentations, to prevent relapses a conventional 14-day duration remains the standard for acute prostatitis. Non-sexually transmitted orchitis and epididymitis require a 10-day course of fluoroquinolones or cotrimoxazole. The 2026 SPILF guidelines represent a paradigm shift toward a tailored, stratified approach.