Urinary tract infection, cystitis and pyelonephritis

• A urinary tract infection (UTI) is a bacterial infection anywhere from the urethra to the renal parenchyma. It splits clinically into a localised infection (cystitis, limited to the bladder) and a systemic infection (fever and systemic signs, such as pyelonephritis). ^[1]
• Most uncomplicated infections in women are caused by Escherichia coli, and are diagnosed from symptoms and a dipstick more often than from a culture. Fever, flank pain or vomiting mark a systemic infection that needs closer assessment and often imaging.
• Acute uncomplicated cystitis in women is treated for a few days with fosfomycin trometamol, nitrofurantoin or pivmecillinam, chosen according to local resistance. Fluoroquinolones are restricted because of their adverse-effect profile.
• Pyelonephritis needs urine culture and antimicrobial susceptibility testing, an ultrasound to exclude obstruction, and oral fluoroquinolone or cephalosporin treatment in mild cases, or intravenous therapy when the patient is systemically ill. ^[1]
• Asymptomatic bacteriuria is not an infection to be treated in most patients; the main exceptions are pregnancy and before urological procedures that breach the mucosa.

By the end of this page you should be able to:

1. Define localised and systemic UTI and name the common uropathogens and their usual hosts.
2. Take a focused history and examination, interpret dipstick and culture results, and decide when imaging is needed.
3. Treat uncomplicated cystitis in a woman, man or pregnant patient, with correct drug, dose and duration, and know when not to treat.
4. Manage acute pyelonephritis, including when to admit, which antibiotics to use by route, and switch criteria.
5. Prevent recurrence with non-antimicrobial and, when needed, low-dose antimicrobial strategies.
6. Recognise a complicated infection, catheter-associated infection, and urosepsis, and escalate appropriately.

Urinary tract infection is one of the commonest bacterial infections in adults. It ranges from a short, self-limiting bladder infection to a life-threatening systemic illness. The clinical problem is shaped by three forces: anatomy (the female urethra is short and close to the bowel), uropathogen virulence (most often Escherichia coli), and antimicrobial resistance (rising worldwide). ^{[1] [3]} The EAU 2026 guideline deliberately drops the old labels "uncomplicated" and "complicated" in favour of localised versus systemic disease, because the older labels could mislead early management. ^[1] The IDSA and ESCMID guideline, in contrast, builds its recommendations for uncomplicated cystitis and pyelonephritis around the classic premenopausal, non-pregnant woman with no known abnormality. ^[2] Both frameworks are still in clinical use, so the same patient may be described differently on different wards; what matters is whether there are systemic signs and whether risk factors are present. ^{[1] [2]}

The EAU 2026 scheme separates two groups by clinical signs rather than by host factors. ^[1]

Complicated in the older sense means infection in a patient who is not a healthy non-pregnant woman: male sex, pregnancy, diabetes, immunocompromise, obstruction, stones, catheter, neurogenic bladder, recurrence, or systemic signs all push an infection into the complicated or systemic group. ^{[1] [2]} In practice, "complicated" and "systemic" overlap, and the words are used interchangeably by many clinicians; the key distinction for safety is whether the patient is febrile or systemically unwell. ^[1]

Asymptomatic bacteriuria (ABU) is bacterial growth in an asymptomatic person. It is commensal colonisation rather than infection, and in most groups it should not be screened for or treated. ^[1] It is diagnosed from a properly collected urine specimen with a significant bacterial count in a person without urinary symptoms; the counts and confirmation rules are set by the guideline you follow. ^[1]

Catheter-associated urinary tract infection (CAUTI) is defined as a UTI in a person who is currently catheterised or has been catheterised within the previous 48 hours. ^[1]

Recurrent cystitis is defined as at least three episodes of cystitis in a year, or two in the last six months. ^[1]

Cystitis is among the most frequent bacterial infections encountered in primary care: roughly one in two women experiences at least one episode in her lifetime, and about one in three has had at least one episode by the age of 24. ^[1] Asymptomatic bacteriuria is found in 1 to 5 percent of healthy premenopausal women, rising to 4 to 19 percent of otherwise healthy older women and men, 0.7 to 27 percent of people with diabetes, 2 to 10 percent of pregnant women, 15 to 50 percent of institutionalised older people, and up to 23 to 89 percent of people with spinal cord injury. ^[1] In hospital, catheter-associated infection dominates: catheter-associated UTI is the leading cause of secondary healthcare-associated bacteraemia, with about 20 percent of hospital-acquired bacteraemias arising from the urinary tract and a mortality of about 10 percent. ^[1] A multistate survey put UTI at 12.9 percent of healthcare-acquired infections, and the incidence of bacteriuria with an indwelling catheter is 3 to 8 percent per day. ^[1]

Women are affected far more often than men at most ages. Young men have low rates unless there is an underlying urological problem; from middle age onward the male rate rises as prostate disease becomes commoner. ^[1] The female predominance reflects a shorter urethra and easier entry of bowel flora, not a weaker immune system. ^[1]

Almost all uncomplicated community-acquired infections are monomicrobial and most are caused by E. coli. ^{[1] [3]} The typical organisms and their clinical habits are:

• Escherichia coli (uropathogenic strains) is the dominant pathogen in uncomplicated cystitis and pyelonephritis in women. ^{[1] [3]}
• Klebsiella species, especially in people with diabetes or recurrent infection.
• Proteus mirabilis, a urease producer that raises urine pH, promotes stone formation and is common with catheters and stones.
• Staphylococcus saprophyticus, the classic cause of cystitis in young, sexually active women; it does not reduce nitrate.
• Enterococcus, often in complicated or catheter-associated infection and after manipulation; it does not reduce nitrate.
• Pseudomonas aeruginosa, more common with catheters, stones, recent antibiotics and obstruction, and notable for broad resistance.

Risk factors split into those that increase the chance of getting an infection and those that make it more likely to be severe or to resist treatment. ^[1]

• Female sex and anatomy. Short urethra, sexual activity and new sexual partner.
• Pregnancy, in which 2 to 10 percent of women develop asymptomatic bacteriuria. ^[1]
• Postmenopausal oestrogen deficiency, with atrophic vaginitis and incomplete emptying.
• Diabetes mellitus, even when well controlled. ^[1]
• Indwelling or intermittent urinary catheters; risk rises by 3 to 8 percent per catheter day. ^[1]
• Obstruction or poor emptying: stones, stricture, prostate enlargement, prolapse, neurogenic bladder, residual volume.
• Vesicoureteral reflux and other anatomical abnormalities, especially in children but relevant in adults with complicated infection.
• Previous infection, including childhood cystitis, in the same person or a mother with recurrent cystitis.
• Spermicide use and sexual intercourse.
• Immunocompromise, renal impairment and neurological disease.
• Recent instrumentation or antibiotic exposure, which selects resistant organisms. ^[1]

The EAU risk-factor table reminds the reader that male sex is not, by itself, a risk factor in the modern view; what matters is prostatic involvement and other comorbidities. ^[1]

Infection begins when a uropathogen gains a foothold at the urethral opening, ascends the urethra, and reaches the bladder. E. coli does this with adhesive fimbriae that bind uroepithelial receptors; type 1 fimbriae mediate bladder colonisation and P fimbriae help the organism reach the upper tract. ^[1] A catheter provides a foreign surface on which biofilm forms, protecting bacteria from both host defences and antibiotics and explaining why catheterised urine is often polymicrobial and resistant. ^[1]

The bladder normally clears bacteria by complete voiding and a mucosal glycosaminoglycan layer. Anything that reduces washout (residual urine, obstruction, reflux), damages mucosa (catheters, stones), or supplies nutrients (glycosuria) tips the balance toward infection. ^[1]

From the bladder, infection ascends the ureters to the renal parenchyma in pyelonephritis. Ascending infection is the usual route; haematogenous spread is rare and occurs mainly in sepsis or with obstruction. ^[1] Renal parenchymal infection produces the systemic signs: fever, flank pain, vomiting. If obstruction is present, pressure rises, bacterial growth is rapid, and urosepsis can follow within hours.

Urease-producing organisms (Proteus, Klebsiella, Pseudomonas) hydrolyse urea to ammonia, raise urine pH, and precipitate magnesium ammonium phosphate (struvite) stones; such infection can persist in a stone nidus and recur until the stone is removed. ^[1]

In the patient's own words, typical cystitis is a burning or stinging pain on passing urine (dysuria), passing small amounts very often (frequency) and with urgent, hard-to-defer need (urgency), sometimes with lower abdominal or suprapubic cramping, dark or cloudy urine and occasional visible blood. ^[1] The urine smells stronger than usual. Fever, flank pain and vomiting are absent by definition. ^[1] The diagnosis can be made with high confidence from this pattern and the absence of vaginal discharge. ^[1]

Pyelonephritis is suggested by fever above 38 degrees C, chills and rigors, flank pain or costovertebral angle tenderness, nausea and vomiting, with or without the ordinary cystitis symptoms. ^[1] The patient looks unwell. Lower tract symptoms often coexist, especially early, which can mislead one into calling the illness cystitis until the fever and flank pain are elicited by history or examination. ^[1]

• Children. In infants a UTI may present only as fever, irritability or poor feeding, without any urinary complaint. In older children, dysuria and frequency are clearer; fever suggests ascent. Congenital abnormalities and vesicoureteral reflux must be sought. ^[1]
• Young women. Acute uncomplicated cystitis often follows sexual activity; dysuria with new partner or spermicide use is common. ^[1]
• Pregnancy. Cystitis may be asymptomatic; pregnancy is one of the few settings in which asymptomatic bacteriuria must be sought and treated, because of the risks of pyelonephritis in the mother and preterm birth. ^[1]
• Men. A UTI in a man is usually complicated because of prostatic involvement; fever and prostatic tenderness point to acute prostatitis rather than simple cystitis. ^[1]
• Older and frail patients. Genitourinary symptoms in older women are not necessarily infection. ^[1] New confusion, delirium, fever or a functional decline may be the only presentation of a UTI in a frail older person, and these are easily attributed to other causes. ^[1]
• Catheterised patients. CAUTI is suspected from new fever, rigors, altered mental state, malaise, flank pain or suprapubic tenderness, not from cloudy or offensive urine alone. ^[1]

Palpation of the suprapubic region for tenderness and firmness, percussion of the costovertebral angles (a positive test elicits deep, dull flank pain), and in men a digital rectal examination when prostatitis is suspected. ^[1] In women a pelvic examination is useful when the diagnosis is unclear, to look for vaginal discharge or cervical tenderness that points to a sexually transmitted or pelvic infection. ^[1]

In cystitis the main alternatives are vaginal candidiasis, bacterial vaginosis, sexually transmitted urethritis and cervicitis, a kidney stone, and the presence of ABU in a patient with non-infective dysuria. ^[1] In systemic infection one must separate pyelonephritis from other causes of fever and flank pain: renal colic, appendicitis or gynaecological sepsis, and sepsis of another source. ^[1] A careful history, dipstick and, where appropriate, culture separate these.

For a typical acute cystitis in a woman without risk factors, the diagnosis is clinical and a dipstick adds little. ^[1] When the diagnosis is unclear, or in pyelonephritis and systemic infection, dipstick testing is used: leucocyte esterase is an enzyme produced by neutrophils and indicates inflammation, and nitrite indicates the presence of nitrate-reducing bacteria. ^[4] Both require interpretation against pretest probability: their diagnostic value varies between studies and populations. ^[4] Nitrate reduction can take up to 30 hours to reach saturation, and as noted above, Enterococcus and S. saprophyticus do not reduce nitrate at all. ^[4]

In systemic UTI, urinalysis is standard and includes white and red blood cells and nitrite. ^[1] Urine culture with antimicrobial susceptibility testing is performed in all cases of pyelonephritis, in catheterised patients and in systemic infection. ^[1]

• Asymptomatic bacteriuria: a significant bacterial count on a valid specimen in a person without symptoms, with the confirmation rule of your guideline. ^[1]
• Catheter-associated UTI: symptoms plus a lower colony count than for voided specimens in a catheter specimen (or a voided sample shortly after catheter removal); follow the guideline's threshold. ^[1]
• Pyelonephritis and systemic infection: cultured in every case; no single threshold is used because lower counts are significant in the presence of symptoms and systemic illness. ^[1]

Pyuria alone is unreliable in catheterised patients; in a catheterised patient, pyuria does not distinguish infection from colonisation. ^[1] In non-catheterised patients pyuria supports infection but does not prove it.

In systemic infection blood tests are always worth considering, and blood cultures are taken in sepsis or severe illness, or when Staphylococcus aureus is grown in the urine, because urinary S. aureus is a marker for bloodstream infection. ^[1]

The role of imaging is to find obstruction, stones or complications that will delay recovery. ^[1]

• Ultrasound is the first study in suspected systemic or complicated infection. ^[1]
• In pyelonephritis, upper-tract ultrasound is done to rule out obstruction or stone disease in patients with a history of urolithiasis, renal impairment or a high urinary pH. ^[1]
• CT or MRI cross-sectional imaging is used when the patient remains febrile after 48 to 72 hours of appropriate treatment, if obstruction is suspected, or on deterioration. ^[1]
• In pregnancy, ultrasound or MRI is preferred to avoid fetal radiation. ^[1]
• In systemic UTI, the aim is to find hydronephrosis, obstruction, abscess or prostatic abscess; ultrasound first, cross-sectional imaging if blockage is suspected or the patient stays unwell after 48 to 72 hours of antibiotics. ^[1]

No single test diagnoses a UTI: the diagnosis is a clinical judgement combining symptoms, signs and laboratory support. ^[1] Useful shorthand for the bedside:

• Cystitis in a woman without risk factors is diagnosed from a focused history of dysuria, frequency and urgency and the absence of vaginal discharge; a dipstick helps when the diagnosis is uncertain. ^[1]
• Pyelonephritis is suspected from fever, chills, flank or costovertebral angle pain, with or without cystitis symptoms, and confirmed by culture. ^[1]
• Systemic UTI is suspected when urinary symptoms are accompanied by fever, chills, flank or pelvic pain, or general unwellness. ^[1]
• Complicated or CAUTI requires the microbiological threshold plus clinical features, and must not be diagnosed from urine appearance or pyuria alone. ^[1]
• Asymptomatic bacteriuria is a laboratory diagnosis only, in a patient with no urinary symptoms. ^[1]

Antimicrobial treatment is much more likely to succeed than placebo. ^[1] The EAU position is that, in a shared decision, non-antimicrobial options can be offered to non-geriatric women. ^[1] First-line empirical antibiotics, chosen according to Europe's susceptibility patterns, are fosfomycin trometamol, nitrofurantoin and pivmecillinam. ^[1] Co-trimoxazole or trimethoprim are only first choice where local E. coli resistance is under 20 percent. ^[1] Aminopenicillins and fluoroquinolones are not recommended for empirical treatment of cystitis. ^[1]

Non-antibiotic alternatives for uncomplicated acute cystitis (cranberry products, D-mannose, selected herbal preparations, xyloglucan-gelose, and NSAIDs for symptom control) reduce antibiotic use but have lower success rates and are inappropriate for frail older adults. ^[1] They are offered through shared decision making after explaining the evidence. ^[1]

Pregnancy. Short courses of appropriate antibiotics can be used. Penicillins, cephalosporins, fosfomycin and nitrofurantoin can be considered, with nitrofurantoin avoided in glucose-6-phosphate dehydrogenase deficiency and at the end of pregnancy; trimethoprim is avoided in the first trimester and sulphonamides in the last trimester. ^[1] Screening for and treating ABU in pregnancy is recommended, with standard short-course therapy or single-dose fosfomycin trometamol. ^[1]

Renal impairment. Most antibiotics have a wide therapeutic index and need no dose change until the glomerular filtration rate falls under 20 mL/min; nitrofurantoin is contraindicated under 30 mL/min per 1.73 m² because accumulation raises side-effects and lowers efficacy. ^[1]

Men. Empirical oral treatment of acute uncomplicated cystitis in younger men uses pivmecillinam or nitrofurantoin, the latter only once prostatic involvement is excluded; nitrofurantoin has limited evidence for the best duration and poor prostatic penetration. ^[1] In practice any febrile or suspected complicated infection in a man should prompt a longer, fluoroquinolone-based course (see below).

Fluoroquinolone caution. European regulators (March 2019) restricted fluoroquinolone use because of disabling and potentially persistent side-effects. In cystitis a fluoroquinolone is reserved for cases where other standard agents are inappropriate. ^[1]

Outpatient (mild, patient able to take oral medication): fluoroquinolones and oral cephalosporins are the only agents recommended for oral empirical treatment; nitrofurantoin, oral fosfomycin and pivmecillinam should not be used because they do not achieve adequate tissue or blood levels. ^[1] Where local fluoroquinolone resistance is low, a short fluoroquinolone course is the usual first choice. In fluoroquinolone hypersensitivity or known resistance, trimethoprim-sulfamethoxazole or an oral beta-lactam may be used, and if susceptibility is unknown an initial single intravenous dose of a long-acting agent such as ceftriaxone is given. ^[1]

Inpatient (systemically ill, vomiting, or complicated infection): start with intravenous therapy such as a fluoroquinolone, an aminoglycoside with or without ampicillin, or an extended-spectrum cephalosporin or piperacillin-tazobactam. ^[1] Carbapenems and newer broad-spectrum agents (ceftolozane-tazobactam, ceftazidime-avibactam, meropenem-vaborbactam, cefiderocol, plazomicin) are reserved for early culture results indicating multidrug-resistant organisms. ^[1] In critically ill or obstructed patients, broad-spectrum coverage including carbapenems is used, with MRSA coverage added as indicated; advanced agents are reserved for highly resistant cases. ^[1]

Switch from intravenous to oral therapy once the patient has improved and can tolerate oral fluids, guided by culture results. ^[1] In pregnancy, outpatient parenteral therapy is acceptable for mild disease with close follow-up; after improvement a switch to oral therapy gives a total duration of 7 to 10 days. ^[1] In men, and whenever a complicating factor is suspected, the minimum duration is 2 weeks, preferably with a fluoroquinolone because prostatic involvement is common. ^[1] Short outpatient courses equivalent to longer ones exist, but with a higher early recurrence rate. ^[1]

Empirical treatment must be started promptly, without waiting for cultures, and then de-escalated on the results. ^[1] The choice depends on severity, risk factors for resistance, prior cultures, patient factors and local patterns. ^[1] Recommended empirical intravenous options include amoxicillin plus an aminoglycoside, a second-generation cephalosporin plus an aminoglycoside, or a third-generation cephalosporin. ^[1] Ciprofloxacin (if local resistance is under 10 percent) can be used when there are contraindications to cephalosporins or aminoglycosides. ^[1] Fluoroquinolones should not be used empirically in patients coming from urology departments or who have taken them within the last 6 months. ^[1] Treatment duration is generally 5 to 10 days based on response, with seven days non-inferior to 14 in bloodstream infection. ^[1] In men seven days is inferior to 14. ^[1] Underlying obstruction must be identified and relieved, because antibiotics alone are not enough. ^[1]

Clinically unwell patients need imaging to find the obstruction or complication. ^[1] Follow up outpatients with pyelonephritis by phone or in person within 48 to 72 hours. ^[1] Post-treatment dipsticks or cultures in asymptomatic patients are not indicated. ^[1]

CAUTIs are usually polymicrobial and often involve multidrug-resistant organisms. ^[1] Management is to remove the catheter when it is no longer needed (and to avoid catheters being placed unnecessarily), replace a catheter that has been in place for two weeks or more at the onset of infection, obtain a culture before starting antibiotics, and treat according to localised or systemic disease recommendations. ^[1] Duration is 7 days if symptoms resolve promptly, 14 days if the response is delayed; a 5-day levofloxacin course may be considered if the patient is not severely ill; women under 65 without upper-tract symptoms after catheter removal can be treated for 3 days. ^[1] ABU in catheterised patients is not treated. ^[1]

ABU does not cause renal damage, and in most groups treating it brings no benefit and can cause harm. ^[1]

• Do not treat: women without risk factors; well-controlled diabetes; postmenopausal women; institutionalised older people; people with reconstructed or neurogenic lower tracts; renal transplant recipients (treatment does not reduce UTI and selects resistance); recipients before arthroplasty or cardiovascular surgery. ^[1]
• Do treat: all pregnant women, because of maternal and fetal benefit, using a standard short course or single-dose fosfomycin trometamol (recognising that the evidence is old and of low quality, and that national guidance should be followed); and before urological procedures that breach the mucosa, with culture and targeted treatment rather than empirical therapy. ^[1]
• Harmful: treating ABU in women with recurrent UTI actually increases the risk of the next symptomatic episode, because ASB can be protective. ^[1]
• Decisions in immunocompromised patients, candiduria and other complex groups are individualised. ^[1]
• If treatment is given, it must be directed by the organism's susceptibility, not empirical. ^[1]

Prevention of recurrent cystitis is stepped. First exclude risk factors and treat abnormalities and residual urine. Then behavioural and non-antimicrobial measures: increased fluid intake (1.5 litres per day additional reduced episodes and antibiotic use in low-intake premenopausal women over 12 months), post-coital voiding, avoidance of spermicides and occlusive underwear. ^[1] Vaginal oestrogen is recommended for postmenopausal women. ^[1] Other options with weaker and mixed evidence include immunomodulatory vaccines, proven Lactobacillus probiotic strains, cranberry products, D-mannose, methenamine hippurate (non-inferior to daily antibiotic prophylaxis when the urinary tract is normal), xyloglucan/hibiscus/propolis or herbal preparations, and glycosaminoglycan replenishment intravesically. ^[1] Continuous or post-coital low-dose antimicrobial prophylaxis is the most effective option when non-antimicrobial measures fail; regimens include nitrofurantoin 50 or 100 mg once daily, fosfomycin trometamol 3 g once weekly and trimethoprim 100 mg once daily, with cephalosporins in pregnancy. ^[1] No evidence establishes the optimal duration; studies range from 3 to 12 months, and episodes tend to recur after stopping. ^[1] Post-coital prophylaxis is especially useful in pregnancy. ^[1] Self-diagnosis and self-treatment suit compliant patients. ^[1]

Complications are the reason a routine infection earns its systemic or complicated label, and they are usually associated with obstruction, stones, diabetes or catheter use. ^[1]

• Urosepsis, the systemic illness from a urinary source, requires immediate resuscitation and broad-spectrum antibiotics; the EAU currently directs clinicians to the Surviving Sepsis Campaign 2021 guidelines for management detail. ^[1]
• Renal and perinephric abscess, suggested by persistent fever despite 48 to 72 hours of appropriate therapy or deterioration, diagnosed by cross-sectional imaging and managed with drainage as well as antibiotics. ^[1]
• Emphysematous pyelonephritis, a severe necrotising infection with gas in the renal parenchyma or collecting system, typically in people with diabetes, is a surgical emergency. It is rare and described in case reports and small series rather than guideline randomised trials.
• Obstructive pyelonephritis can progress to urosepsis within hours because of the pressure effect; early imaging and drainage are critical. ^[1]
• Urease-driven stone formation complicates Proteus and other urease producers, and infection cannot be cured until the stone is removed. ^[1]

Uncomplicated cystitis treated appropriately resolves quickly in almost all cases. ^[1] Pyelonephritis treated early with the right antibiotic has a good outcome; short courses of about 5 to 7 days are effective for systemic infection, although men need at least 14 days. ^[1] Recurrent attacks are common in susceptible women (recurrent cystitis) and CAUTI drives repeated infections, resistance and sepsis. ^[1]

• Do not screen or treat asymptomatic bacteriuria in most groups; screen in pregnancy and before urological mucosal procedures. ^[1]
• Avoid unnecessary catheters and remove them promptly; catheter restriction protocols and nurse-driven protocols reduce CAUTI. ^[1]
• Increase fluid intake in low-intake women with recurrent infection. ^[1]
• Offer vaginal oestrogen after menopause, and systematic management of stones and obstruction. ^[1]
• Antimicrobial stewardship matters: in acute care hospitals, roughly 20 to 50 percent of prescribed antibiotics are unnecessary or inappropriate. ^[1]

Children. A UTI in a child needs evaluation for congenital abnormalities, reflux and obstruction. Do not assume the terminology of adult uncomplicated infection applies; paediatric protocols are separate. ^[1]

Pregnancy. All pregnant women are screened and treated for asymptomatic bacteriuria; cystitis and pyelonephritis are treated with pregnancy-compatible drugs, and pyelonephritis may need hospitalisation, parenteral therapy and early follow-up because of risks to mother and fetus. ^[1]

Older adults. Older patients may present with confusion rather than dysuria. Pyuria and ABU are common, so do not treat urine unless infection signs are present. NSAID-only symptomatic strategies are inappropriate for frail older adults because of renal and gastrointestinal risk. ^[1]

Immunocompromised and patients with catheters, stones or neurogenic bladder, and recipients of renal transplants. These need individualised management and are outside the uncomplicated pathway. ^[1]

Where culture, imaging and newer agents are unavailable, the clinical syndromes still guide care.

• Treat a febrile patient with flank pain as pyelonephritis, and give a broad-spectrum parenteral antibiotic such as ceftriaxone (or an aminoglycoside where monitoring is feasible) until oral therapy can be used. ^[1]
• Use inexpensive first-line oral agents (nitrofurantoin, trimethoprim where resistance is known to be low, fosfomycin trometamol, pivmecillinam) and check local resistance patterns; rotate or avoid drugs with documented local resistance. ^[1]
• Do not treat asymptomatic bacteriuria or cloudy catheter urine without symptoms; cultures and antibiotics are wasted and select resistance. ^[1]
• Ultrasound, where available, is the single most useful imaging test for obstruction and abscess; if imaging is impossible, a patient who does not improve within 48 to 72 hours should be referred. ^[1]
• Stewardship is especially important: a large share of hospital antibiotics are unnecessary or inappropriate. ^[1]

Related subjects in this library (not yet linked): nephrolithiasis and ureteric calculus, acute kidney injury, prostatitis, interstitial cystitis and bladder pain syndrome, sepsis, antimicrobial stewardship, pregnancy and infection. Plain-text cross-references are used here because per-topic linking is not yet enabled.

• Classify by localised versus systemic disease: fever, flank pain, vomiting or delirium move a UTI out of simple cystitis.
• E. coli dominates uncomplicated infection; Proteus, Klebsiella, Enterococcus and Pseudomonas become commoner with catheters, stones and comorbidity.
• Dipstick leucocyte esterase and nitrite support the diagnosis, but a negative nitrite does not exclude infection, especially with Enterococcus or S. saprophyticus.
• Culture and susceptibility testing are mandatory in pyelonephritis, systemic and complicated infection, and before urological mucosal surgery.
• First-line cystitis regimens: fosfomycin trometamol 3 g once, nitrofurantoin 100 mg twice daily for 5 days, or pivmecillinam 400 mg three times daily for 3 to 5 days; trimethoprim or co-trimoxazole only where local E. coli resistance is under 20 percent.
• Pyelonephritis is treated orally with fluoroquinolones or cephalosporins, never with nitrofurantoin, oral fosfomycin or pivmecillinam; severe cases need intravenous therapy and usually admission. ^[1]
• Fluoroquinolones are restricted in Europe for cystitis and require justification in pyelonephritis.
• Asymptomatic bacteriuria is not treated except in pregnancy and before urological mucosal procedures; treating it in recurrent cystitis is harmful.
• Women with recurrence need stepped care: behavioural and non-antimicrobial measures first, then low-dose or post-coital antimicrobial prophylaxis.
• Catheter care (avoid, remove early, culture before treating) is the most effective prevention of CAUTI and its sepsis.