Approximately 40%–80% of CRBSIs are caused by gram-positive organisms. Coagulase-negative Staphylococci, Staphylococcus aureus, and Enterococcus are the most common organisms. Methicillin-resistant staphylococcus is frequently seen.
Full Answer
Complicated UTIs are usually associated with indwelling catheters, urinary tract abnormalities, immunosuppression or exposure to antibiotics. The most common causative agent for both uncomplicated and complicated UTIs is uropathogenic Escherichia coli(UPEC).
Definition A UTI is classified as uncomplicated if there are no functional or anatomical anomalies in the urinary tract, no renal functional impairment, and no concomitant disease that would promote the UTI (3).
Guideline implementation in care Because it is done so often, treating uncomplicated UTIs with antibiotics exerts enormous selective pressure not only on the bacteria involved, but also on the collateral flora, resulting in a significant influence on the selection of antibiotic-resistant bacteria.
Uncomplicated UTIs: occur in normal urinary tract and usually involve only the bladder. Note: complicated infection: increase risk for pyelonephritis, urosepsis, and renal damage. How sterile is the urinary tract? The urinary tract above the urethra is normally sterile.
By far, the most common uropathogen identified in uncomplicated UTIs is Escherichia coli, accounting for about 85% of all cases. The remaining 15% are caused primarily by Staphylococcus saprophyticus and Klebsiella and Proteus species.
The most common UTIs occur mainly in women and affect the bladder and urethra. Infection of the bladder (cystitis). This type of UTI is usually caused by Escherichia coli (E. coli), a type of bacteria commonly found in the gastrointestinal (GI) tract. However, sometimes other bacteria are responsible.
The most common bacterium to cause UTIs is Escherichia coli (E. coli). It is usually spread to the urethra from the anus.
What causes a urinary tract infection (UTI)? Urinary tract infections are caused by microorganisms — usually bacteria — that enter the urethra and bladder, causing inflammation and infection. Though a UTI most commonly happens in the urethra and bladder, bacteria can also travel up the ureters and infect your kidneys.
The most common cause of a UTI in the urethra is a sexually transmitted disease. Chlamydia and gonorrhea are two STDs that can cause a UTI. STDs are also the most common cause of UTIs in younger men. Prostate problems can also cause UTIs.
Women are particularly at risk for UTIs because their urethra sits close to the anus, where E. coli is present. It's also shorter than a man's, giving the bacteria easier access to the bladder, where the majority of UTIs occur, and the rest of the urinary tract.
The distinctive E. coli strains that cause most UTIs have been designated uropathogenic E. coli (UPEC).
A urine culture is performed to confirm the presence of bacteriuria and the antimicrobial susceptibility of the infecting uropathogen. This test is indicated in all women with suspected pyelonephritis but is not necessary for the diagnosis of cystitis, given the reliability of the patient's history in establishing the diagnosis and the delayed availability of culture results. 20,22 Moreover, studies comparing voided urine specimens and bladder-aspirate specimens in women with cystitis have shown that the traditional criterion for a positive culture of voided urine (10 5 colony-forming units per milliliter) is insensitive for bladder infection, and 30 to 50% of women with cystitis have colony counts of 10 2 to 10 4 colony-forming units per milliliter in voided urine. 23 Since most clinical laboratories do not quantify bacteria below a threshold of 10 4 colony-forming units per milliliter in voided urine specimens, a culture report of “no growth” in a woman with urinary symptoms should be interpreted with caution.
New treatment guidelines for cystitis from the Infectious Diseases Society of America recommend that ecologic adverse effects of an antimicrobial agent (selection for antimicrobial-resistant organisms) be considered along with efficacy in selecting antimicrobial therapy.
Urinary symptoms that persist or recur within a week or two of treatment for uncomplicated cystitis suggest infection with an antimicrobial-resistant strain or, rarely, relapse. In such women, a urine culture should be performed and treatment should be initiated with a broader-spectrum antimicrobial agent, such as a fluoroquinolone. Episodes of cystitis that occur at least 1 month after successful treatment of a urinary tract infection should be treated with a first-line short-course regimen ( Table 2 ). If the recurrence is within 6 months, one should consider a first-line drug other than the one that was used originally, especially if trimethoprim–sulfamethoxazole was used, because of the increased likelihood of resistance. 22
Clinical manifestations suggestive of pyelonephritis include fever (temperature >38°C), chills, flank pain, costovertebral-angle tenderness, and nausea or vomiting, with or without symptoms of cystitis. Dysuria is also common with urethritis or vaginitis, but cystitis is more likely when symptoms include frequency, urgency, or hematuria; when the onset of symptoms is sudden or severe; and when vaginal irritation and discharge are not present. 19,20 The probability of cystitis is greater than 50% in women with any symptoms of urinary tract infection and greater than 90% in women who have dysuria and frequency without vaginal discharge or irritation. 20 The only finding on physical examination that increases the probability of urinary tract infection is costovertebral-angle tenderness (indicating pyelonephritis). 20
The dipstick test is most accurate for predicting UTI when the presence of either leukocyte esterase or nitrite is considered a positive result, with a sensitivity of 75% and a specificity of 82%. 20,21 However, results of the dipstick test provide little useful information when the history is strongly suggestive of urinary tract infection, since even negative results for both tests do not reliably rule out the infection in such cases. 20
With respect to both ecologic adverse effects and efficacy, nitrofurantoin, trimethoprim–sulfamethoxazole, fosfomycin, and pivmecillinam (not approved in the United States) are considered first-line agents for cystitis, even though there are concerns about increasing resistance (to trimethoprim–sulfamethoxazole) and suboptimal efficacy (of fosfomycin and pivmecillinam).
The patient described in the vignette appears to have recurrent cystitis on the basis of her symptoms and history. A 3-day course of trimethoprim–sulfamethoxazole is generally my choice of a first-line empirical regimen for cystitis in women who are not allergic to the medication, given that it is inexpensive and effective and that there are no reliable data in my community to suggest a high prevalence of resistance. In this case, however, I would prescribe a different first-line antimicrobial agent, nitrofurantoin (5-day course), since the patient's recent exposure to trimethoprim–sulfamethoxazole increases the likelihood that the current infecting strain will be resistant to this agent. I would also offer her a urinary analgesic (e.g., phenazopyridine [over-the-counter], three times daily as needed) until her dysuria diminishes, which often occurs within a few hours after the start of antimicrobial therapy. 53 An office visit is not required for management, and there is no need for a follow-up urine culture if her symptoms resolve.
Other factors that can increase the risk of UTIs: A previous UTI. Sexual activity, and especially a new sexual partner. Changes in the bacteria that live inside the vagina (vaginal flora), for example caused by menopause or use of spermicides. Pregnancy.
What is a urinary tract infection (UTI)? UTIs are common infections that happen when bacteria, often from the skin or rectum, enter the urethra, and infect the urinary tract. The infections can affect several parts of the urinary tract, but the most common type is a bladder infection (cystitis).
Call your doctor if you develop any side effects while taking your antibiotic. Sometimes other illnesses, such as sexually transmitted diseases, have symptoms similar to UTIs. Your doctor can determine if a UTI or different illness is causing your symptoms and determine the best treatment.
Do you have pain or burning when you urinate? You might have a urinary tract infection (UTI).
Age (older adults and young children are more likely to get UTIs) Structural problems in the urinary tract, such as prostate enlargement. Poor hygiene, particularly in children who are potty-training.
Fever. Chills. Lower back pain or pain in the side of your back. Nausea or vomiting that your child may have a UTI. Younger children may not be able to tell you about UTI symptoms they are having. While fever is the most common sign of UTI in infants and toddlers, most children with fever do not have a UTI.
Kidney infection (pyelonephritis) is another type of UTI. They’re less common, but more serious than bladder infections.
1). The most common causative agent for both uncomplicated and complicated UTIs is uropathogenic Escherichia coli(UPEC).
The uropathogens that cause uncomplicated UTIs, including UPEC, K. pneumoniaeand S. saprophyticus, have the ability to bind directly to the bladder epithelium, which is composed of the umbrella cells (also known as superficial facet cells), intermediate cells and basal cells19(TABLE 1). UPEC and K. pneumoniaebind to uroplakins, which are the major protein components of the umbrella cell apical membrane19and which form a crystalline array protecting the mammalian bladder tissue from damaging agents in urine20. In addition to uroplakins, α3β1integrins, which are expressed at the surface of uroepithelial cells, can also serve as receptors for UPEC21. By contrast, complicated UTIs are initiated when the bacteria bind to a urinary catheter, a kidney stone or a bladder stone, or when they are retained in the urinary tract by a physical obstruction. Some pathogens (for example, UPEC) can cause both uncomplicated and complicated UTIs. However, others such as P. mirabilis, P. aeruginosaand Enterococcusspp. predominantly cause complicated UTIs (FIG. 2). Subsequently, these uropathogens often form biofilms that are responsible for colonization and persistence22,23(BOX 1).
a |Uncomplicated urinary tract infections (UTIs) begin when uropathogens that reside in the gut contaminate the periurethral area ( step 1) and are able to colonize the urethra. Subsequent migration to the bladder (step 2) and expression of pili and adhesins results in colonization and invasion of the superficial umbrella cells (step 3). Host inflammatory responses, including neutrophil infiltration (step 4), begin to clear extracellular bacteria. Some bacteria evade the immune system, either through host cell invasion or through morphological changes that result in resistance to neutrophils, and these bacteria undergo multiplication (step 5) and biofilm formation (step 6). These bacteria produce toxins and proteases that induce host cell damage (step 7), releasing essential nutrients that promote bacterial survival and ascension to the kidneys (step 8). Kidney colonization (step 9) results in bacterial toxin production and host tissue damage (step 10). If left untreated, UTIs can ultimately progress to bacteraemia if the pathogen crosses the tubular epithelial barrier in the kidneys (step 11). b |Uropathogens that cause complicated UTIs follow the same initial steps as those described for uncomplicated infections, including periurethral colonization (step 1), progression to the urethra and migration to the bladder (step 2). However, in order for the pathogens to cause infection, the bladder must be compromised. The most common cause of a compromised bladder is catheterization. Owing to the robust immune response induced by catheterization (step 3), fibrinogen accumulates on the catheter, providing an ideal environment for the attachment of uropathogens that express fibrinogen-binding proteins. Infection induces neutrophil infiltration (step 4), but after their initial attachment to the fibrinogen-coated catheters, the bacteria multiply (step 5), form biofilms (step 6), promote epithelial damage (step 7) and can seed infection of the kidneys (steps 8 and 9), where toxin production induces tissue damage (step 10). If left untreated, uropathogens that cause complicated UTIs can also progress to bacteraemia by crossing the tubular epithelial cell barrier (step 11).
Uropathogens also adopt morphological changes, such as filamentation, to circumvent the host immune system130,138. During IBC maturation, expression of suppressor of lon(SulA) inhibits FtsZ polymerization in a subpopulation of UPEC, blocking septation ring formation and cell division138. When the resulting filamentous bacterial cells emerge from epithelial cells, they are resistant to killing by neutrophils and can colonize other naive uroepithelial cells and re-enter the IBC cycle129,138(FIG. 3). Alternatively, during colonization by P. mirabilis, the bacteria adopt a filamentous morphology as a result of the sensor activities of flagella on contact with a urinary catheter. Contact creates a torsional change in the outer membrane, and this is sensed by upregulator of the flagellar master operon (Umo) proteins, which induce the expression of flagella to produce the highly flagellated cells that are required for swarming during a UTI6,23,53,139(FIG. 4).
An increased susceptibility to recurrent UTIs can occur not because of a deficient host response to UPEC infection, as is commonly accepted, but rather as a result of an unrestrained lymphocyte-dependent innate inflammatory response to acute infection, leading to severe acute injury to the mucosal uroepithelium and potentiating subsequent infections39.
Enterococci encode several adhesion factors, including the collagen adhesin Ace, enterococcal surface protein (Esp), enterococcal polysaccharide antigen (Epa), and endocarditis- and biofilm-associated (Ebp) pili54(TABLE 1) . Of these, Ebp pili contribute to CAUTIs54–56and are required for persistence during infection55,56. Clinical studies have shown that mechanical stress induced by urinary catheterization produces histological and immunological changes in the bladder, resulting in a robust inflammatory response, exfoliation, oedema, and mucosal lesions of the uroepithelium and kidneys57,58. Importantly, a mouse model of CAUTI seems to recapitulate these immunological changes that are induced by urinary catheterization, exhibiting catheter-induced inflammation, severe uroepithelial damage, exfoliation and the onset of bladder wall oedema, which is exacerbated by increased catheterization time59. Urinary catheters provide a surface for E. faecalisattachment and biofilm formation, which promotes E. faecalispersistence in the bladder and further dissemination to the kidneys55(FIG. 4). However, E. faecalisis unable to bind to catheter material in vitroand is unable to grow in urine60. This apparent paradox was resolved by the finding that urinary catheterization induces fibrinogen release into the bladder as part of the inflammatory response; this fibrinogen subsequently accumulates in the bladder and is deposited on the implanted catheter60(FIGS 2,,4).4). Following fibrinogen deposition, the Ebp pilus adhesin — EbpA, which contains an N-terminal fibrinogen-binding domain — mediates catheter colonization and biofilm formation during CAUTIs caused by E. faecalis60,61(FIG. 4). Furthermore, E. faecaliscan use fibrinogen for growth, enhancing biofilm formation on the catheter60(FIG. 4). This resolution of the paradox has been recapitulated in vitroby the demonstration that E. faecalisattaches to fibrinogen-coated catheters and grows in urine supplemented with fibrinogen60.
Risk factors for developing a CAUTI include prolonged catheterization, female gender, older age and diabetes11.
An uncomplicated urinary tract infection (UTI) is a bacterial infection of the bladder and associated structures. These are patients with no structural abnormality and no comorbidities, such as diabetes, immunocompromised state, or pregnancy. Uncomplicated UTI is also known as cystitis or lower UTI. …
E.coli causes the vast majority of UTIs but other organisms of importance include proteus, klebsiella, and enterococcus. The diagnosis of UTI is made from the clinical history (symptoms) and urinalysis with confirmation by a urine culture, but the proper collection of the urine sample is important.
Uncomplicated urinary tract infection ( UTI) is a bacterial infection of the bladder and associated structures. These are patients with no structural abnormality and no comorbidities, such as diabetes, immunocompromised, or pregnant. Uncomplicated UTI is also known as cystitis or lower UTI. Forty percent of women in the United States will develop ...
Many cases of uncomplicated UTIs will resolve spontaneously, without treatment, but many patients seek therapy for symptom relief. Treatment is aimed at preventing spread to the kidneys or developing into upper tract disease/pyelonephritis, which can cause the destruction of the delicate structures in the nephrons and eventually lead to hypertension.
Uncomplicated UTI is also known as cystitis or lower UTI. Forty percent of women in the United States will develop a UTI during their lifetime, making it one of the most common infections in women. UTI is uncommon in circumcised males, and by definition, any male UTI is considered complicated. Many cases of uncomplicated UTI will resolve ...
Pyelonephritis is usually caused by the bacteria Escherichia coli, Proteus, or Pseudomonas.
Hypercalciuria is usually attributable to intestinal hyperabsorption of dietary calcium and less commonly to a defect in renal calcium reabsorption. Hyperparathyroidism and bone demineralization associated with prolonged immobilization are also known to cause hypercalciuria but too a much lesser degree.
Neurologic disorders that develop above the pontine micturition center result in detrusor hyperreflexia, also known as an uninhibited or reflex bladder. This selection is the only option responsible for detrusor hyperreflexia.
The most common infecting microorganisms are uropathic strains of E. coli (80% to 85%).
Oncogenes of the ras gene family and tumor-suppressor genes including TP53 mutations and the inactivation of the retinoblastoma gene (pRb) are implicated in bladder cancer. This process is not associated with the other options.
The thickening of the glomerular capillary wall characterizes only membranous lesions.
b. Pyrophosphate, potassium citrate, and magnesium stimulate the supersaturation of salt.
Uncomplicated UTIs: occur in normal urinary tract and usually involve only the bladder.
Bacteria count result that indicate clinically significant UTI? Bacterial countsof 105 colony forming units per milliliter (CFU/mL) or higher typically indicate a clinically significant UTI. However, counts as low as 102 to 103 CFU/mL in a person with signs and symptoms are indicative of UTI.
Frequent urination (more than every 2 hours) Urgency. Suprapubic discomfort or pressure. Urine: may contain grossly visible blood (hematuria) or sediment, giving it a cloudy appearance. Flank pain, chills, and fever indicate an infection involving the :upper urinary tract (pyelonephritis).
Uncomplicated cystitis can be treated by a short-term course of antibiotics, typically for 1 to 3 days.
Pyelonephritis: implies inflammation (usually caused by infection) of the renal parenchyma and collecting system. Cystitis: indicates inflammation of the bladder. Urethritis: means inflammation of the urethra.
Hematogenous route blood-borne bacteria secondarily invade the kidneys, ureters,or bladder from elsewhere in the body.
A specimen obtained by catheterization provides more accurate results than a clean-catch specimen.