Uti
Uti
Uti
Infections
(UTIs)
Effort By: Zeeshan Akbar
Overview read that
Any site or structure within the urinary tract can become infected, but the bladder
(cystitis) and kidney (pyelonephritis) are most frequently involved.
In men, the prostate, epididymis, and testis can also become infected by bacteria
originating from the urinary tract.
The presence of bacteria or fungi in the urine is termed bacteriuria or funguria,
respectively.
However, the detection of bacteria or fungi in the urine does not always imply
infection or a clinically significant condition.
Bacteria in the urine without signs and symptoms of infection is termed
asymptomatic bacteriuria.
Urinary tract infections (UTIs) are classified as either uncomplicated or
complicated.
This distinction is important since management strategies often differ between
these two groups.
Uncomplicated UTIs include acute cystitis and pyelonephritis in otherwise healthy
individuals.
These patients have the lowest risk of complications or treatment failure.
Complicated infections can be acute or chronic and occur in a diverse mix of
patients with metabolic, functional, or structural abnormalities of the urinary
tract or kidneys.
Metabolic factors include diabetes mellitus, renal failure, and kidney
transplantation.
Examples of functional abnormalities are neurogenic bladder and vesicoureteral
reflux. Structural abnormalities result from stones, tumors, strictures, or foreign
objects such as catheters, stents, and other forms of instrumentation.
Recurrent infection in a patient with a previous UTI can be due to either a relapse
or reinfection.
Relapses are caused by the same microorganism as in the preceding infection and
usually occur within 2 to 4 weeks after treatment has ended.
Reinfections typically occur after a greater length of time and may be due to a new
strain or species.
Patients who never improve or who immediately relapse following completion of
treatment have persistent infection.
Urosepsis is a serious condition in which the bacterial species found within the
urinary tract is also recovered from the patient's blood in conjunction with the
clinical picture of sepsis.
Patients who develop urosepsis are usually physically debilitated or have an
underlying immunodeficiency.
Etiology make list of microbes
names
Enteric bacteria are the most common organisms causing urinary tract infections.
This is due to the anatomic proximity of bowel flora to the urethra, particularly in
women.
More important is the pathogenicity specific to the urinary tract that certain species
of enteric organisms have acquired.
Such organisms are called uropathogens for their ability to cause infection even in
the healthy host.
The most prevalent causative agent is Escherichia coli among all patient groups in
both upper and lower tract infections.
Uropathogenic E. coli (UPEC) may possess one or more virulence factors that
allow for colonization and persistence within the urinary tract. The number of
factors expressed may correlate with the severity of infection.7
A key virulence factor is the presence of bacterial structures named adhesins,
which mediate bacterial attachment to urinary epithelium.
UPEC strains with the greatest capacity for attachment to uroepithelial receptors
succeed more frequently in establishing infection.
Close attachment to epithelial cells improves the chances for cellular invasion and
results in higher exposure to cytotoxic or inflammatory compounds released by
UPEC strains.
Strong affinity for urinary tract epithelium also correlates with bacterial persistence
within the vagina and periurethral area in women.
Subsequently, the same strain can be responsible for recurrent UTI in women if
therapy is not effective against UPEC strains harbored outside the urinary tract.4
The most pathogenic strains of E. coli are those that have filamentous adhe- sins
termed p-pili or p-fimbriae.
E. coli with p-pili are responsible for almost all cases of bacteremic pyelonephritis
in previously healthy patients.
Other UPEC virulence factors include diminished susceptibility to phagocytosis,
iron extraction from host sources, and adaptations to the nutrient-poor environment
of the urine.
In uncomplicated UTI in women, Staphylococcus saprophyticus is the next most
common causative organism.
S. saprophyticus is a coagulase-negative staphylococcus that does not originate
from the bowel.
This organism causes cystitis and pyelonephritis clinically similar to E. coli.
Risk factors for UTI due to S. saprophyticus include use of spermicide-coated
condoms, young age, previous UTI, and multiple sexual partners.
Other bacteria known to cause UTIs in a small but significant number of patients
are Klebsiella spp. and Proteus mirabilis.
These enteric organisms are often difficult to eradicate from the urinary tract,
particularly when the kidney is involved.
Both organisms are capable of possessing various adhesins and other
uropathogenic virulence factors.
Proteus mirabilis often produces urease, which mediates the conversion of urea to
ammonia.
This raises urinary pH, which can then initiate the formation of urinary stones or
encrustations on catheters.
Stones can become a continuous nidus for infection and a cause of treatment
failure by obstructing urine flow or by harboring organisms.
In complicated UTIs, a broader spectrum of microbial species is encountered.
A greater variety of organisms can cause infection because the required degree of
microbial virulence is lower in patients with structural or functional abnormalities of
the urinary tract.
Many of these patients have received multiple courses of antimicrobial therapy and
have become colonized with microorganisms that are intrinsically resistant or have
acquired resistance to standard treatment regimens.
Also, recovery of more than one organism from culture is not uncommon.
Although E. coli is most frequently identified as the causative agent in complicated
UTI, other organisms such as Candida spp., Pseudomonas aeruginosa,
enterococci, Enterobacter spp., and other gram-negative aerobic bacilli are
common pathogens in this patient population.
Fungal UTIs are common among hospitalized patients, particularly those with
diabetes mellitus, urinary catheterization, malignancy, recent broad-spectrum
antibacterial therapy, and kidney transplantation.
In addition to Staphylococcus aureus and Candida spp., Mycobacterium
tuberculosis and Salmonella spp. can infect the urinary tract via dissemination from
the bloodstream.
Pseudomonal UTI may be acquired via the bloodstream or the urethra.
Asymptomatic bacteriuria and funguria are usually due to a variety of relatively
nonvirulent bacteria or fungi.
Patients with functional or structural defects often harbor organisms intermittently
or chronically.
These nonpathogenic strains do not effectively invade or attach to uroepithelium,
so a full immune response with subsequent clinical symptoms does not develop.
The presence of these nonpathogenic organisms may actually protect against
infection by more virulent bacteria.
Risk Factors
Pathophysiology
Organisms enter the urinary tract primarily via an ascending route from the
urethra.
Less commonly, organisms from the blood infect one or both kidneys and then
descend into the bladder with the flow of urine.
The organisms infecting via the ascending route originate almost exclusively
from the bowel.
These organisms spread to the perineum and, in women, colonize the vaginal
introitus and vagina.
Once the vaginal introitus and periurethral area are colonized, bacteria can
readily gain entry into the urethra and bladder.
Since vaginal colonization with potential urinary pathogens is an important
intermediate step in pathogenesis, changes in vaginal flora or pH that
promote colonization of urinary pathogens dramatically increase the risk of
developing a UTI.
In healthy adult men, UTIs are very uncommon due to the greater distance
organisms must travel from the perineum to urethra.
Also, the longer urethra in males further discourages entry into the bladder.
After bacteria (or fungi) reach the bladder, the balance between host
defenses and bacterial virulence will determine whether the bacteria will be
able to survive, replicate efficiently, and invade the bladder mucosa.
Most bacteria introduced into the bladder of healthy individuals are normally
cleared by host defenses within 2 to 3 days.
However, if patients have high postvoid residuals, alterations in urine flow
from stones or strictures an abnormal narrowing of a bodily passage (as from
inflammation, cancer, or the formation of scar tissue), or prolonged urethral
catheterization, bacteriuria may never spontaneously resolve.
Chronic or intermittent bacteriuria may remain asymptomatic if the organisms
are not able to adhere to and invade the bladder mucosa.
The presence of these nonpathogenic strains within the bladder may protect
these high-risk individuals from infection by discouraging subsequent
colonization with more uropathogenic organisms.
UPEC strains, however, readily attach to and invade bladder
epithelial cells, where the organisms may replicate intracellularly
or become quiescent (quiescence is the state of not dividing).
The infected host cells may then respond by undergoing
exfoliation or apoptosis such that the intracellular bacteria are
mechanically removed with urination.
Persistence of viable microbes harbored within epithelial cells
may be a source of relapsing UTIs.
Mucosal attachment and invasion also triggers a host immune
response.
The mucosal cells release chemokines that attract neutrophils to
the affected tissues.
Recruited neutrophils cross the mucosa and are released into
the urine (pyuria) to phagocytose infecting organisms.
With the onset of this local inflammatory response, the patient
may experience symptoms of infection.
Systemic responses such as fever or leukocytosis rarely
occur with uncomplicated cystitis.
Spontaneous resolution of infection may occur in 70% of
previously healthy females within 30 days.
Pyelonephritis results when bacteria ascend the ureters and infect one or both
kidneys.
The entire kidney is rarely involved; instead, patchy areas of necrosis and scarring
are found adjacent to normal tissue.
Local inflammation occurs with neutrophil recruitment, but in pyelonephritis,
the host also experiences a systemic response resulting in leukocytosis,
cytokine release, and immunoglobulin M (IgM) and immunoglobulin G
(IgG) elevations.
A significant number of patients will be bacteremic, and urosepsis may
develop in those with comorbidities.
Full recovery and sterilization of the kidney tissue may take as long as 6
to 10 weeks, even in previously healthy patients.
For both cystitis and pyelonephritis, neutrophil response is crucial to the successful
clearance of organisms from the urinary tract.
Genetically based variations in host response that result in suboptimal neutrophil
recruitment, activation, and phagocytosis of uropathogens may predispose some
seemingly healthy individuals to UTIs or frequent reinfections.
Acquisition of a UTI from the descending route appears to account for only 3% of all
UTIs.
Bacteremia or fungemia from a non-urinary tract source rarely results in clinically
significant kidney infection.
The exception is for organisms with a special affinity for kidney tissue such as S.
aureus or Candida spp.
Complete ureteral obstruction or preexisting renal injury substantially increases the risk
of kidney infection in the presence of bacteremia.
Once the kidney is infected, bacteria or fungi can enter the urine stream and proceed to
the bladder, where bacteriuria may then be detected.
Host Defenses
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The host defenses that deter bacteria from colonizing the urinary tract are primarily
mechanical and not immunologic.
Urination washes out microorganisms that have entered the urethra and bladder.
Since normal postvoid bladder residuals are only 0.09 to 2.4 mL, the vast majority
of colonizing organisms are physically removed with each void.
The peristaltic action of the ureters and the one-way vesicoureteral valve at the
junction with the bladder dissuades (detachment/ separation) pathogens from
ascending from the bladder to the kidneys.
Other host defenses discourage replication or attachment of microorganisms.
Tamm-Horsfall protein, low-molecular-weight sugars, secretory immunoglobulin A
(IgA), and uromucoid (a phosphatidylinositol-linked membrane protein.) can act as
false ligands for bacterial attachment, leaving fewer bacteria to attach to the
mucosa.
In men, prostatic secretions contain compounds with antibacterial properties.
The pH and osmolarity of urine can alter bacterial growth in that both very dilute
urine and concentrated urine with low pH can inhibit growth.
Tamm-Horsfall glycoprotein (THP) is the most abundant urine protein, with
multiple roles in renal physiology and bladder protection. THP protects against
bacterial UTI by blocking bacterial adherence to the bladder epithelium, but its role
in defense against fungal pathogens is not yet described.
Tamm-Horsfall (TH) glycoprotein is a major protein of normal urine and is the
primary component of waxy nephron casts. Tamm-Horsfall protein is of renal origin
and has been localized in the thick ascending limb of the loop of Henle and in the
distal convoluted tubule.
Tamm–Horsfall protein is made in the thick ascending limb of the loop of Henle and
released to the urine by proteolytic cleavage. It is believed to play a key role
in prevention of stone formation.
Waxy or pre-waxy casts are closely related to impaired renal function.
Waxy casts can be found in people with advanced kidney disease and long-term
(chronic) kidney failure .
Individuals with abnormal urine dynamics are at greater risk of UTI.
For example, patients with neurogenic bladder have higher postvoid residual urine
volumes and so are less efficient at removing bacteria with urination.
Also, the dilated ureters of women in the later stages of pregnancy cannot prevent
organisms from reaching the kidneys.
In healthy people, therefore, an uncomplicated UTI results when the virulence of the
pathogen is sufficient to overcome normal host defenses.
Conversely, a complicated UTI often results from the inadequacy of host defenses to
prevent even low-virulence organisms from establishing infection.
The immune system has no significant role in preventing UTIs but is activated only after
bladder mucosa or kidney tissue has been invaded.
Therefore, immunocompromised patients do not have a greater incidence of UTIs but
are at higher risk of severe forms of infection and treatment failure when they do occur.
Clinical Presentation
Signs and Symptoms
in clinical presentation learn only symptoms of
Acute Uncomplicated Cystitis
Complicated UTIs occur in a diverse mix of patients who have an increased risk of
either acquiring a UTI or experiencing a severe or persistent UTI.
This category includes patients with mild lower tract disease as well as those with
significant kidney infection and urosepsis.
The clinical presentation may include the hallmark symptoms of dysuria,
frequency, and urgency.
However, vaguer symptoms of fatigue, headache, temperature instability, and
irritability may be the only clues.
Immunocompromised persons may not exhibit the usual symptoms due to their
dampened inflammatory response to infection.
An important example of this is the debilitated elderly patient, who may have UTI-
associated bacteremia in the absence of fever or leukocytosis.
Men with prostatic enlargement and UTI may complain only of obstructive
symptoms, but further questioning can reveal symptoms referable to a UTI.
Therefore, the clinician must hold a greater degree of suspicion for possible UTI in
these individuals, since treatment delays may lead to more serious infections.
In the patient suspected of having urinary abnormalities, an extensive workup may be
indicated to delineate the extent of the abnormality and to determine whether it is
correctable.
Without amelioration [the act of making something better; improvement] of the
underlying problem, relapses or reinfections are to be expected.
Some infections may never be cured without corrective action, as in the presence of
kidney stones or urinary stents.
For patients with known or suspected complicated UTIs, a urinalysis, urine culture,
blood count, and serum creatinine should be performed.
For those who are sicker or are immunocompromised, blood culture and imaging
studies of the upper tract may be indicated to determine the extent and severity of
infection.
Diabetics in particular have an increased risk of perinephric abscess or
emphysematous pyelonephritis.
Pyuria is expected but is less specific, since the primary urinary abnormality may be
responsible for the presence of white blood cells.
An appropriately obtained urine culture is crucial to effective treatment, since a
multitude of non-uropathogens with varied antimicrobial susceptibilities can infect the
urinary tract in individuals with hampered host defenses.
Colony counts are usually 105 CFU or more per mL.
Negative culture results may necessitate further testing for fastidious organisms.
It may be reasonable to wait for culture and sensitivity results before initiating
treatment in the stable patient with lower tract infection.
Because persistence and relapse of infections are common, a repeat urine culture
1 or 2 weeks after therapy may be helpful.
Hospitalization is indicated for patients who cannot take oral medications, need
other intravenous therapy, or have probable kidney involvement or possible
urosepsis.
The diagnosis of urosepsis is made when bacteremia originating from a urinary
source is associated with fever, tachycardia, hypotension, and general
decompensation.
Urosepsis occurs most frequently in debilitated elderly patients,
immunocompromised persons, and those with chronic urinary obstruction.
Nosocomial and Catheter-
Associated Urinary Tract Infection
complete
The majority of nosocomial UTIs are associated with indwelling (inside your body)
urinary catheters.
This catheter drains urine from your bladder into a bag outside your body.
Common reasons to have an indwelling catheter are urinary incontinence
(leakage), urinary retention (not being able to urinate), surgery that made this
catheter necessary, or another health problem.
Other confounding factors in nosocomial UTI include the severity of the underlying
illness causing hospitalization; antimicrobial therapy for other infections, which
increases the risk for resistant or unusual organisms; multiple medications being
administered, which may interact with UTI treatment; and possibly the inability of
the patient to describe symptoms of UTI due to altered mental status.
Confounding occurs when a competing cause of illness is associated with one or
more of the factors being examined under the study hypothesis.
Management of catheter-associated UTI varies considerably depending on
whether catheterization is short term or chronic.
Even with good insertion and maintenance techniques, the incidence of bacteriuria
among catheterized patients increases with time at a rate of 3% to 10% per day of
catheterization.
Thus, a large percentage of patients will be bacteriuric after a week and virtually all
will be bacteriuric after a month of catheterization.
The organisms are believed to gain entry via the space between the catheter and
the urethral mucosa.
The biofilm that develops on catheters may allow organisms within it to elude (to
not be caught by someone) leukocytes and antimicrobials.
Patients with long-term catheters often have polymicrobial bacteriuria.
Differentiating between infection and colonization can be difficult because
bacteriuria is present in almost all patients with prolonged catheterization.
Among hospitalized patients, symptoms may not be clearly associated with the
urinary tract, since they may have other reasons for lower abdominal discomfort,
leukocytosis, and fevers.
Also, the usual symptoms of dysuria, hesitancy, and urgency are not seen in
catheterized patients.
Difficulty starting or maintaining a urine stream is called urinary hesitancy.
Often the only symptoms manifested are confusion or fever.
In spinal cord-injured patients, symptoms may include fever, diaphoresis,
abdominal pain, or increased muscle spasticity.
Overall, only 30% to 50% of infected patients undergoing short-term
catheterization will experience symptoms.
For patients who have symptoms, a urinalysis and culture of urine and blood
should be obtained.
Screening for bacteriuria in asymptomatic individuals is generally discouraged
because antimicrobial treatment in this situation can lead to recolonization with
more resistant strains.
Antimicrobial treatment of catheter-associated UTI has relatively high failure and
relapse rates.
Catheter-associated urinary tract infections (CAUTIs) represent the most common
type of nosocomial infection and are a major health concern due to the
complications and frequent recurrence. These infections are often caused
by Escherichia coli and Proteus mirabilis.
Removing the catheter increases cure rates, but for patients who require chronic
catheterization, replacement with a new catheter does not always improve the
odds/chances for success.
Recurrence rates in patients chronically catheterized may be improved with
suprapubic bladder catheterization, because bacterial colonization on the
abdominal wall is less than in the periurethral area/ being the tissues surrounding
the urethra..
Suprapubic catheters provide an alternate method
to drain the urinary bladder. These are commonly
utilized to manage bladder dysfunction and urinary
retention not amenable/preventable to urethral
catheterization.
Diagnosis
important and complete
Diagnostic tests are used when the clinical presentation or physical examination
does not yield a clear diagnosis.
The most frequently used tests are dipstick urinalysis, urine microscopy with or
without Gram stain, and quantitative urine culture with antimicrobial susceptibility.
Such tests help to determine whether the patient's symptoms are consistent with
UTI and to identify the infecting organism.
Other diagnostic procedures include localization tests such as bilateral ureteral
catheterization, bladder washout techniques, and antibody-coated bacteria assays.
These procedures are used to differentiate upper tract infections from lower tract
ones, but they are rarely necessary in the management of most patients.
Ultrasound and computed tomography (CT) studies may help to identify renal
abscesses or structural abnormalities of the kidneys.
Intravenous pyelograms are performed less frequently but may also help to assess
possible structural defects and urine flow patterns.
Collecting the urine specimen correctly is important to ensure the accuracy of the
results for both urinalysis and urine culture.
In non-catheterized patients, urine is collected in a sterile container midway
through urination.
Using a midstream voided urine sample is preferred, although some data show
that contamination rates are similar without this precaution.
Although rarely done in routine cases, specimens obtained via urethral
catheterization or suprapubic bladder aspiration have the lowest risk of
contamination.
Urinalysis
A complete urinalysis consists of biochemical dipstick testing of fresh urine and a
microscopic examination of the urine sediment.
Urine dipsticks have multiple reagent pads that undergo color changes when
dipped in the urine sample.
The pad colors are then compared to a standardized color reference.
Most dipsticks can determine pH and can give a quantitative value for red blood
cells, protein, nitrites, and leukocyte esterase.
Leukocyte esterase, an enzyme produced by activated leukocytes, is used as a
marker for the presence of leukocytes in the urine sample.
The dipstick urinalysis is often the only diagnostic test used by the office- or clinic-
based practitioner to confirm the clinical diagnosis of uncomplicated cystitis.
On microscopic examination of the urine sediment, the number of leukocytes,
erythrocytes, bacteria, fungi, and other solid elements can be quantified.
The most important aspects of the urinalysis in diagnosing urinary tract infections
are pH and the presence of nitrites, blood (hematuria), bacteria (bacteriuria), fungi
(funguria), and particularly leukocytes (pyuria) or white blood cell casts.
A high pH may indicate the presence of urea-splitting organisms such as Proteus
spp.
The conversion of nitrates in urine to nitrites has been associated with the
presence of enteric bacteria.
In patients who are not menstruating, the presence of hematuria can localize the
problem to the urinary tract.
Finding microorganisms on urinalysis may assist in making the diagnosis of UTI
but may also represent contamination from organisms residing in the distal urethra
or periurethral area.
The leukocyte count is of primary importance when determining the significance of
bacteriuria and confirming UTI as the cause of dysuria.
Pyuria usually is defined as eight leukocytes or more per mm3, which correlates to
two to five leukocytes per high-power field.
However, most patients with UTIs have 20 or more leukocytes per mm3.
Pyuria in the absence of bacteriuria or a positive urine culture can occur in patients
with vaginal infections or urethritis due to Chlamydia or other fastidious organisms.
Urine Culture
Several culture techniques are available, but the biplate method is used most
commonly.
With the biplate method, a selective medium on one side of the culture dish is used to
isolate possible gram-negative urinary pathogens, while the other side usually contains
nonselective culture medium.
Use of the selective culture medium often allows for more rapid identification of
potential uropathogens.
The microorganism colony count is determined using the nonselective side of the plate.
The number of colonies can be correlated to the number of organisms or CFU per mL
in the original urine sample.
Using the standard inoculum size, this method can detect bacterial concentrations of
103 CFU or more per mL.
Antibacterial susceptibility testing is then performed on the predominant organisms
recovered from the biplate.
BluEcoli™ Urine Biplate is a urine culture media, consisting of Blood Agar on one
side and BluEcoli™ Agar on the other side, which is used for the isolation of
urinary pathogens and for the identification of E. coli.
Features and Benefits:
• A revolutionary agar bi-plate for screening urine specimens for E. coli, which
causes about 85% of all urinary tract infections (UTI).
• Blood Agar (side 1) is recommended as a primary plating medium when culturing
urine specimens. All common bacteria and yeasts will grow on this medium.
• BluEcoli™ (side 2) is a urine culture medium used for the selective culture and
isolation of urinary pathogens and for the identification of E. coli which turns blue
within 24 hours by using chromogenic substrates. No further testing is needed!
• Inoculate both sides of the biplate with the urine specimen. If the infecting
organism is E. coli, the colonies on the chromogenic side of the biplate will turn
blue.
• The blue color of E. coli is confirmatory! No further confirmation or indole testing is
required. Save time and money by not using an expensive identification system. All
other Gram-negative bacteria will appear as they would on a MacConkey plate
(pink for lactose fermentors and clear for non-fermentors).
• With the BluEcoli™ Urine Biplate, you can select a colony from the blood agar side
of the biplate for susceptibility testing.
• Helpful in spotting mixed infections.
Traditionally, a single-species microorganism count of 105 CFU or more per mL from a midstream
urine specimen was considered indicative of infection.
Multiple studies have shown, however, that as few as 102 CFU per mL in a symptomatic patient
with pyuria represents true infection.
Up to half of all young women with true uncomplicated cystitis will have bacterial counts of 102 to
104 CFU per mL.
According to the Infectious Diseases Society of America guidelines, a midstream urine culture of
103 CFU or more per mL of a single uropathogen is indicative of cystitis in patients with pyuria and
symptoms consistent with lower tract infection.
However, for unspeciated coagulase- negative staphylococci, 105 CFU per mL is used as a cutoff
due to the potential for contamination by these organisms.
In a symptomatic patient with pyuria, a midstream urine culture with less than 102 CFU per mL can
be seen in patients with chlamydial urethritis, infections due to other fastidious organisms, early
infection, partially treated infection, and candidal or bacterial vaginitis.
In symptomatic women without pyuria, 105 CFU or more per mL is still required for the diagnosis of
UTI. However, any sample with 102 CFU or more per mL obtained by suprapubic bladder aspiration
or urethral catheterization is considered significant.
For patients without risk factors for complicated UTI, any urine culture result with mixed organisms
or with a nonuropathogen is probably due to contamination.
Urine cultures are not routinely done for presumed cases of uncomplicated lower
UTI, because the causative agent is reliably E. coli and occasionally S.
saprophyticus.
The finding of typical clinical symptoms in patients with pyuria or hematuria is
usually sufficient to make the diagnosis and start empiric treatment.
However, with unclear symptoms, complicated cases, treatment failure, or
pyelonephritis, a urine culture should be done to confirm the diagnosis and to
ensure effective treatment.
Also, patients with urinary tract symptoms who do not demonstrate pyuria by
urinalysis should have a urine culture performed.
A urine Gram stain may be useful to guide initial treatment for complicated UTIs.
Treatment
Pharmacotherapy
The ability to eradicate bacteria from the urinary tract is directly
related to the sensitivity of the organism and the achievable
concentration of the antimicrobial agent in the urine.
The therapeutic management of UTIs is best accomplished by first
categorizing the type of infection: acute uncomplicated cystitis,
symptomatic abacteriuria, asymptomatic bacteriuria, complicated
UTIs, recurrent infections, or prostatitis.
Acute Uncomplicated Cystitis
nii krnaaa
These infections are predominantly caused by E. coli, and antimicrobial
therapy should be directed against this organism initially.
Because the causative organisms and their susceptibilities are generally
known, a cost-effective approach to management is recommended that
includes a urinalysis and initiation of empiric therapy without a urine culture.
Short-course therapy (3-day therapy) with trimethoprim–sulfamethoxazole
or a fluoroquinolone (e.g., ciprofloxacin or levofloxacin, but not
moxifloxacin) is superior to single-dose therapy for uncomplicated infection.
Fluoroquinolones should be reserved for patients with suspected or possible
pyelonephritis due to the collateral damage risk.
Instead, a 3-day course of trimethoprim–sulfamethoxazole, a 5-day course
of nitrofurantoin, or a one-time dose of Fosfomycin should be considered as
first-line therapy.
In areas where there is more than 20% resistance of E. coli to trimethoprim–
sulfamethoxazole, nitrofurantoin or Fosfomycin should be utilized.
Nitrofurantoin is an antibiotic medication that is used for the treatment of
uncomplicated lower urinary tract infections. It is effective against most
gram-positive and gram-negative organisms. Nitrofurantoin's primary use
has remained in treating and prophylaxis of urinary tract infections.
Fosfomycin was safe and significantly more efficacious in treating
uncomplicated UTI versus ciprofloxacin.
Amoxicillin or ampicillin is not recommended because of the high
incidence of resistant E. coli.
Follow-up urine cultures are not necessary in patients who respond.
Complicated Urinary Tract Infections
ACUTE PYELONEPHRITIS
The presentation of high-grade fever (>38.3°C [100.9°F]) and severe flank pain
should be treated as acute pyelonephritis, and aggressive management is
warranted.
Severely ill patients with pyelonephritis should be hospitalized and IV drugs
administered initially. Milder cases may be managed with oral antibiotics in an
outpatient setting.
At the time of presentation, a Gram stain of the urine should be performed,
along with urinalysis, culture, and sensitivities.
In the mild to moderately symptomatic patient for whom oral therapy is
considered, an effective agent should be administered for 7 to 14 days,
depending on the agent used.
Fluoroquinolones (ciprofloxacin or levofloxacin) orally for 7 to 10 days are the
first-line choice in mild to moderate pyelonephritis.
Other options include trimethoprim–sulfamethoxazole for 14 days.
If a Gram stain reveals gram-positive cocci, Streptococcus faecalis should be
considered and treatment directed against this pathogen (ampicillin).
In the seriously ill patient, the traditional initial therapy is an IV
fluoroquinolone, an aminoglycoside with or without ampicillin, or an
extended-spectrum cephalosporin with or without an aminoglycoside.
If the patient has been hospitalized in the last 6 months, has a urinary
catheter, or is in a nursing home, the possibility of P. aeruginosa and
enterococci infection, as well as multiple-resistant organisms, should be
considered.
In this setting, ceftazidime, ticarcillin–clavulanic acid, piperacillin,
aztreonam, meropenem, or imipenem, in combination with an
aminoglycoside, is recommended.
If the patient responds to initial combination therapy, the aminoglycoside
may be discontinued after 3 days.
Follow-up urine cultures should be obtained 2 weeks after the completion
of therapy to ensure a satisfactory response and to detect possible relapse.
Recurrent Infections