Urinary tract infection and pyelonephritis

• Urinary tract infection is a bacterial infection anywhere along the pathway from the urethra to the renal parenchyma; pyelonephritis is the same infection process that has ascended to the kidney and now carries systemic signs such as fever and flank pain.
• The organisms are predictable: Escherichia coli dominates uncomplicated community infection, Staphylococcus saprophyticus is the classic organism of cystitis in young women, and Proteus mirabilis drives alkaline, struvite-producing infection, while Klebsiella, Enterococcus, Pseudomonas, Serratia and Enterobacter matter mainly with catheters, obstruction, stones, diabetes and hospital care.
• Urinalysis is a supportive, not decisive, test: leucocyte esterase signals inflammation, nitrite signals nitrate-reducing bacteria, and pyuria is present in both infection and colonisation, so it must always be read against symptoms.
• Pyelonephritis is suggested by fever above 38 degrees C, rigors, flank pain or costovertebral tenderness and vomiting, and it is confirmed by culture in every case; white cell casts, when present, point toward renal parenchymal infection rather than simple cystitis. ^[1][5]
• Outpatient pyelonephritis is treated with a fluoroquinolone or an oral cephalosporin, typically for about 7 to 14 days depending on the chosen drug and the patient, and never with nitrofurantoin, oral fosfomycin or pivmecillinam, which do not reach adequate tissue or blood levels for kidney infection.
• The dangerous errors are treating asymptomatic bacteriuria without indication, diagnosing infection from cloudy catheter urine or pyuria alone, and continuing to give oral agents that cannot reach the renal parenchyma.
• Obstruction turns any of these infections into an emergency: pressure rises, bacterial growth is rapid, and urosepsis can develop within hours, so imaging and drainage matter as much as the antibiotic.

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

1. Name the common urinary pathogens and match each one to the host factors and clinical settings that favour it.
2. Explain how a uropathogen ascends from the urethra to the kidney and why urease production changes both the urine and the risk of stone formation.
3. Interpret leucocyte esterase, nitrite, pyuria and culture results correctly, including the special rules for catheterised patients.
4. Choose empirical antibiotic therapy by route, drug, dose and duration for uncomplicated cystitis, uncomplicated pyelonephritis, complicated or systemic infection and infection during pregnancy.
5. Recognise pyelonephritis clinically and on urinalysis, decide who can be treated as an outpatient, and identify the switch criteria for intravenous therapy.
6. Identify the serious complications of pyelonephritis and state when cross-sectional imaging and drainage are required.
7. Adjust diagnosis and treatment when tests, recommended drugs or imaging are unavailable, and adapt the plan to special groups including children, men, older adults, pregnant patients, people with diabetes and catheterised patients.

The most useful bedside split is localised versus systemic disease rather than the older labels uncomplicated and complicated, because the older terms were sometimes misleading. ^[1]

• Localised infection (cystitis) stays in the bladder without systemic signs: dysuria, frequency, urgency and suprapubic discomfort, without fever or loin pain.
• Systemic infection is present when fever, rigors, flank pain, delirium, hypotension or tachycardia accompany urinary symptoms, whatever the underlying anatomy.
• Asymptomatic bacteriuria is bacterial growth in an asymptomatic person and is colonisation rather than infection in most groups.
• Catheter-associated urinary tract infection (CAUTI) is defined as a UTI in a person who is currently catheterised or has been catheterised in the previous 48 hours.

The same patient may carry risk factors that sit alongside either form: pregnancy, diabetes, obstruction, stones, a catheter or immunocompromise all need identifying and addressing rather than being used as a label.

Urinary tract infection is among the commonest bacterial infections in any setting. Women are affected far more often than men at most ages, driven by a short urethra and easy access of bowel flora rather than by a weaker immune system. ^[1] Cystitis affects roughly half of women during their lifetime and about one in three by the age of 24. ^[1] Asymptomatic bacteriuria rises with age, diabetes, catheter use and institutional care. In hospital, the urinary tract is the source of about 20 percent of hospital-acquired bacteraemias and catheter-associated infection dominates, with bacteriuria accumulating at 3 to 8 percent per catheter day. ^[1]

For infectious-disease practice the point of this epidemiology is simple: the organism isolated depends on the patient, the anatomy and the setting, and the wrong empirical antibiotic is more likely to be chosen when those three factors are ignored.

Almost all uncomplicated community-acquired infections are monomicrobial and most are caused by E. coli. ^[1][2] The organisms fall into clinically meaningful groups, as set out in the table, and the same groups reappear whenever the host changes.

Urease-producing organisms (Proteus, and sometimes Klebsiella and Pseudomonas) hydrolyse urea, raise urine pH and precipitate struvite stones; infection cannot be cured while the stone nidus remains. ^[1] This is one of the few situations in which the organism's biochemistry dictates both the stone and the management plan.

Other risk factors that change the likely organism and the severity of disease:

• Female sex and anatomy, sexual activity, new partner, spermicide use.
• Pregnancy, in which 2 to 10 percent of women develop asymptomatic bacteriuria. ^[1]
• Postmenopausal oestrogen deficiency, with atrophic change and incomplete emptying.
• Diabetes mellitus, even when well controlled, and particularly when glucosuria or autonomic neuropathy is present. ^[1]
• Indwelling or intermittent catheters, with risk rising by 3 to 8 percent per day. ^[1]
• Obstruction or poor emptying: stones, stricture, prostate enlargement, prolapse, neurogenic bladder, residual urine.
• Vesicoureteric reflux and other anatomical abnormalities, especially in children.
• Immunocompromise, renal impairment and neurological disease.
• Recent instrumentation or antibiotic exposure, which selects resistant organisms. ^[1]

Catheter-associated urine is typically polymicrobial and frequently multidrug-resistant. ^[1] Cloudy or offensive catheter urine on its own does not diagnose infection.

Infection begins at the urethral meatus, 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. ^[1]

The bladder normally clears bacteria by complete voiding and a mucosal glycosaminoglycan layer. Anything that reduces washout, damages mucosa or supplies nutrients, such as glycosuria, tips the balance toward infection. ^[1] From the bladder the infection ascends the ureters to the kidney in pyelonephritis; ascending infection is the usual route and haematogenous spread is rare, occurring mainly in sepsis or obstruction. ^[1] Renal parenchymal infection then produces the systemic signs.

Obstruction is the critical turning point. When a stone or stricture raises pressure, bacterial growth is rapid and the kidney is perfused poorly, so antibiotics penetrate badly; urosepsis can then follow within hours. This is why imaging and drainage are management, not just diagnosis.

The typical patient describes burning on passing urine, very frequent small voids, urgency, and sometimes lower abdominal or suprapubic cramping; the urine may be dark, cloudy or smell strong, and visible blood can occur. Fever, flank pain and vomiting are absent by definition. ^[1]

Pyelonephritis is suggested by fever above 38 degrees C, rigors, flank pain or costovertebral tenderness, nausea and vomiting, with or without the ordinary cystitis symptoms. ^[1][4] The patient looks unwell. Lower tract symptoms often coexist, especially early, which can mislead one into calling a rising illness cystitis until the fever and flank pain are elicited. ^[1] Costovertebral angle tenderness on percussion is a useful bedside sign. ^[1][4]

In young women with acute pyelonephritis, gross haematuria occurs in up to about 40 percent of cases, which is much less common in men. ^[4] A single bacterium seen on microscopic oil-immersion examination of unspun urine indicates at least 100,000 colony-forming units (CFU) per mL. ^[4]

• Children. Infants may have only fever, irritability or poor feeding, with no urinary complaint; in older children fever suggests ascent. Congenital abnormalities and vesicoureteric reflux must be sought. ^[1]
• Young women. Acute uncomplicated cystitis often follows sexual activity, and dysuria with a 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 by 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, fever or 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]

In cystitis the main alternatives are vaginal candidiasis, bacterial vaginosis, sexually transmitted urethritis and cervicitis, renal colic and the presence of asymptomatic bacteriuria 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]

Urinalysis is supportive, and its value varies between studies and populations. ^[5] Leucocyte esterase is an enzyme produced by neutrophils and indicates inflammation; nitrite indicates the presence of nitrate-reducing bacteria. ^[5] Both require interpretation against pre-test probability.

• Leucocyte esterase is sensitive for the neutrophiluria of infection but cannot distinguish infection from stones, contamination, glomerular or tubular inflammation.
• Nitrite requires bacteria that possess nitrate reductase. Enterococcus species and Staphylococcus saprophyticus do not reduce nitrate, and other organisms may produce negative or weak results; a negative nitrite therefore never excludes infection. ^[1][5]
• Nitrate conversion can take up to about 30 hours to reach useful concentration. ^[1][5]
• 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.
• White cell casts on microscopy, normal range absent, point to renal inflammatory disease rather than bladder infection: pyelonephritis, interstitial nephritis, glomerulonephritis or other renal inflammatory processes. ^[5] Cellular casts dissolve within 30 minutes depending on urine pH, so the specimen must be examined promptly. ^[5]
• Red cell casts are not a feature of simple pyelonephritis and suggest glomerular disease; their presence should redirect the differential. ^[5]
• Dysmorphic (acanthocyte) red cells point to glomerular bleeding.

Observation on units: urine microscopy reports cells per high-power field; the normal range for white cells is 0 to 5 per high-power field. ^[5] Dipstick specific gravity, pH and protein add context but are not diagnostic.

• All pyelonephritis, systemic infection, catheterised patients and complicated infection require culture with antimicrobial susceptibility testing. ^[1][3]
• A valid count on a properly collected specimen in a person without symptoms defines asymptomatic bacteriuria; in systemic infection no single threshold applies because lower counts are significant when the patient is symptomatic and febrile. ^[1]
• In catheter-associated infection, a lower colony count than for voided specimens can be significant, provided there are clinical features; follow the threshold of the guideline in use. ^[1]
• One bacterium on oil-immersion microscopy of unspun urine indicates at least 100,000 CFU/mL. ^[4]
• Pyuria is worth testing even when a catheter is in place, but its greatest value is negative: absence of pyuria makes infection unlikely and suggests that a positive culture reflects colonisation or contamination. ^[1]
• Blood cultures are obtained in sepsis or severe illness, and whenever Staphylococcus aureus grows in the urine, because urinary S. aureus is a marker for bloodstream infection. ^[1] In straightforward pyelonephritis blood cultures are frequently obtained but rarely change management, because the urine culture provides the result. ^[4]

In systemic infection blood tests are always worth considering. The full blood count may show leucocytosis or leucopenia in severe sepsis; urea and creatinine assess renal function; C-reactive protein and (where available) procalcitonin support severity assessment.

Imaging finds obstruction, stones and complications, and thereby changes management rather than the diagnosis. ^[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]
• Cross-sectional imaging (CT or MRI) is used when the patient remains febrile after 48 to 72 hours of appropriate treatment, when obstruction is suspected, or on deterioration. ^[1]
• In pregnancy ultrasound or MRI is preferred to avoid fetal radiation. ^[1]
• Chest and abdominal imaging may be needed when sepsis is suspected from another source.

No single test diagnoses a UTI; the diagnosis is a clinical judgement combining symptoms, signs and laboratory support. ^[1]

• Cystitis in a woman without risk factors is diagnosed from a focused history of dysuria, frequency and urgency and the absence of vaginal discharge; 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][3]
• Systemic UTI is suspected when urinary symptoms are accompanied by fever, chills, flank or pelvic pain, or general unwellness. ^[1]
• Complicated or catheter-associated infection 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]

The management of the whole infection (definitions, diagnosis, treatment of cystitis and lower tract infection) is treated in the Renal-chapter topic; the algorithm below concentrates on infection that has ascended to the kidney, on drug selection by group, and on the points where choice of drug changes the outcome. All dose values that follow come from the guideline tables of the EAU 2026 urological infections guideline and the NICE pyelonephritis guideline, and are best checked against the formulary in force where you work.

Uncomplicated cystitis in women. Antimicrobial treatment succeeds much more often than placebo. ^[1] First-line empirical choices in Europe are fosfomycin trometamol, nitrofurantoin and pivmecillinam. ^[1] Co-trimoxazole or trimethoprim are first choice only where local E. coli resistance is under 20 percent. ^[1][2] Aminopenicillins and fluoroquinolones are not recommended for empirical treatment of cystitis, because they add little over the first-line agents and select resistance. ^[1]

Treatment of cystitis in men. Empirical oral treatment of acute uncomplicated cystitis in younger men uses pivmecillinam or nitrofurantoin, the latter only when prostatic involvement has been reliably excluded, because it penetrates prostatic tissue poorly. ^[1] Any febrile or complicated infection in a man should instead be treated as systemic infection, with a longer fluoroquinolone-based course (see below).

Pregnancy. Penicillins, cephalosporins, fosfomycin and nitrofurantoin can be considered, with nitrofurantoin avoided in glucose-6-phosphate dehydrogenase deficiency and toward the end of pregnancy, trimethoprim avoided in the first trimester and sulphonamides in the last trimester. ^[1] Screening for and treating asymptomatic bacteriuria in pregnancy is recommended, with short-course therapy or single-dose fosfomycin trometamol. ^[1]

Renal impairment. Most antibiotics need no dose change until glomerular filtration rate falls under 20 mL/min, but nitrofurantoin is contraindicated under 30 mL/min per 1.73 m2 because accumulation increases side effects and reduces efficacy. ^[1]

Fluoroquinolone restriction. European regulators restricted fluoroquinolone use in March 2019 because of disabling and potentially persistent side effects. ^[1] In cystitis a fluoroquinolone is reserved for cases in which other standard agents are unsuitable. In pyelonephritis, where only oral cephalosporins and fluoroquinolones reach adequate tissue levels, a short fluoroquinolone course remains common first-line practice, especially where local fluoroquinolone resistance is low; hypersensitivity or known resistance pushes the choice toward trimethoprim-sulfamethoxazole or an oral beta-lactam with an initial single intravenous dose of a long-acting agent such as ceftriaxone. ^[1]

The oral and intravenous regimens below are the EAU suggested regimens. ^[1] Oral cephalosporins achieve lower blood and tissue levels than intravenous formulations, which is taken into account when choosing dose and duration. ^[1]

Outpatient pyelonephritis is appropriate only in a mild case with a patient able to take oral medication. ^[1][3] Nitrofurantoin, oral fosfomycin and pivmecillinam should not be used for pyelonephritis at all, because they do not achieve adequate tissue or blood levels. ^[1] Where an initial single intravenous dose of a long-acting cephalosporin is given before oral therapy, as is common when susceptibility is unknown, the total treatment course is planned accordingly. ^[1]

Inpatient pyelonephritis, for the systemically ill, vomiting or complicated patient, starts intravenously with 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 cases where culture shows multidrug-resistant organisms. ^[1] In critically ill or obstructed patients, broad-spectrum coverage including carbapenems is used, with MRSA cover added as indicated. ^[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 carry a higher early recurrence rate. ^[1]

Complicated and systemic urinary tract infection. Empirical treatment must start promptly, without waiting for cultures, and then be de-escalated on results. ^[1] Recommended empirical intravenous options include amoxicillin plus an aminoglycoside, a second-generation cephalosporin plus an aminoglycoside, or a third-generation cephalosporin. ^[1] Ciprofloxacin can be used only where local resistance is under 10 percent and where beta-lactams or aminoglycosides are unsuitable. ^[1] Fluoroquinolones should not be used empirically in patients coming from urology departments or who have taken one in the previous 6 months. ^[1] Treatment duration is generally 5 to 10 days based on response, with seven days non-inferior to fourteen days in bloodstream infection, but in men seven days is inferior to fourteen. ^[1] Underlying obstruction must be identified and relieved, because antibiotics alone are not enough. ^[1]

Catheter-associated infection. Management is to remove the catheter when it is no longer needed, replace a catheter that has been in place for two weeks or more at the onset of infection, obtain culture before starting antibiotics, and treat according to localised or systemic disease. ^[1] Duration is seven days if symptoms resolve promptly, fourteen days if response is delayed; a five-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 three days. ^[1] Asymptomatic bacteriuria in a catheterised patient is not treated. ^[1]

Complications are usually tied to obstruction, stones, diabetes or catheter use. ^[1]

• Urosepsis, the systemic illness from a urinary source, requires immediate resuscitation and broad-spectrum antibiotics; management details follow the surviving sepsis guidance used at your institution. ^[1]
• Renal abscess (lobar nephronia or intrarenal abscess) and perinephric abscess: suspect when fever persists despite 48 to 72 hours of appropriate therapy, or on clinical deterioration. ^[1][6] A perinephric abscess in particular should be suspected when fever remains after 4 to 5 days of adequate antibiotics for pyelonephritis. ^[6] Urinalysis may be normal when the abscess does not communicate with the collecting system. ^[6] Diagnosis is by cross-sectional imaging, management by drainage as well as antibiotics.
• Emphysematous pyelonephritis, a severe necrotising infection with gas in the renal parenchyma or collecting system, occurs almost exclusively in people with diabetes and is a surgical emergency. ^[1][4]
• Obstructive pyelonephritis can progress to urosepsis within hours because of the pressure effect; early imaging and drainage are critical. ^[1]
• Chronic pyelonephritis is the disease process of pyogenic scarring and long-term inflammatory change following persistent or recurrent renal infection, usually with a major anatomical anomaly, calculi or an abnormal inflammatory response such as xanthogranulomatous pyelonephritis. ^[4]
• Urease-driven stone formation complicates Proteus and other urease producers; 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] The dangers are delay in a febrile or vomiting patient, an unrelieved obstruction, and failure to treat or remove an infected stone.

• Do not screen for or treat asymptomatic bacteriuria in most groups; do screen in pregnancy and before urological procedures that breach the mucosa. ^[1]
• Avoid unnecessary catheters and remove them promptly. ^[1]
• Treat stones, obstruction and incomplete emptying to prevent recurrence.
• Increase non-antibiotic fluid intake in low-intake women with recurrent infection; consider vaginal oestrogen after menopause. ^[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 apply adult uncomplicated terminology to children; 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 follow-up because of risks to mother and fetus. ^[1]

Men. Any UTI in a man is presumed complicated until proven otherwise, because prostatic involvement is common; men require at least two weeks of therapy, preferably with an agent that penetrates prostatic tissue such as a fluoroquinolone. ^[1]

Older adults. Older patients may present with confusion rather than dysuria, and pyuria and asymptomatic bacteriuria are common, so do not treat urine without infection signs. NSAID-only strategies for symptom control are inappropriate for frail older adults because of renal and gastrointestinal risk. ^[1]

Diabetes. Diabetes increases both frequency and severity of infection, predisposes to rare complications such as emphysematous pyelonephritis and xanthogranulomatous pyelonephritis, and is associated with use of SGLT2 inhibitors that raise glucosuria. ^[1][4]

Immunocompromised patients, those with catheters, stones or neurogenic bladder, and renal transplant recipients. These need individualised management and are outside the uncomplicated pathway; treating asymptomatic bacteriuria in transplant recipients does not reduce UTI and selects resistance. ^[1]

Catheters. (see above) Diagnosis and treatment follow clinical signs; pyuria does not diagnose infection; treatment duration follows severity.

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 rotate or avoid drugs with documented local resistance; check local patterns rather than importing them. ^[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]
• Pyuria's absence is a useful rule-out; a positive culture with no pyuria usually reflects colonisation. ^[1][5]
• Stewardship is especially important: a large share of hospital antibiotics are unnecessary or inappropriate. ^[1]

• Urinary infection, cystitis, and pyelonephritis (renal chapter): for the full diagnostic and lower-tract management pathway, which is deliberately not repeated here.
• Nephrolithiasis: for struvite stones driven by urease producers and the surgical steps needed to clear infection.
• Acute kidney injury: for the deteriorating renal patient with urinary sepsis.
• Prostatitis and interstitial cystitis: for men with urinary symptoms and for non-infective bladder pain.
• Antimicrobial stewardship: for resistance patterns and empirical choice.
• Sepsis and septic shock: for resuscitation when urosepsis develops.
• Pregnancy and infection: for screening and treatment during pregnancy.