INTRODUCTION

UTIs are one of the most common bacterial infections in the United States. The clinical presentation ranges from completely asymptomatic to septic shock. All ages are affected and certain subgroups of the population are particularly vulnerable. A national survey in the mid-1990s estimated that UTIs resulted in 7 million office visits, 1 million emergency department visits, and 100,000 hospital admissions per year. It is an illness that primarily affects women. One in 3 women by age 24 years are treated with antibiotics for a UTI, and 50% of women have UTI symptoms at some point in their life. Figure 22.1 shows the incidence of UTI throughout life. Early in life (circle 1 in Figure 22.1) females are at higher risk than males largely as a result of ureteral reflux. During the reproductive years women are at much higher risk than men (circle 2 in Figure 22.1). With advancing age (circle 3 in Figure 22.1) the gap narrows as the incidence of UTI in men increases as a result of benign prostatic hyperplasia. The term UTI in this chapter refers generically to an infection in any of the components of the urinary tract—kidney, bladder, prostate, and urethra. Each is discussed individually. Additionally, UTI is referred to as uncomplicated or complicated depending on the presence of risk factors that predispose the patient to an adverse outcome.

Symptoms and Signs

UTI refers to bacterial infection of the urinary tract. Patients, however, present with symptoms referable to the site and nature of infection. They complain of urinary frequency and urgency resulting from spontaneous bladder contractions due to irritation of the trigone. Dysuria is caused by inflammation of the urethra that causes pain or a burning sensation when further irritated by urine. Flank pain results from stretching and irritation of the renal capsule that causes pain in the area of the costovertebral angle. Irritation of the bladder trigone and pain on defecation results from compression of the inflamed prostate. Finally, patients may report symptoms of systemic infection such as fever, rigors, malaise, nausea, vomiting, general muscle and joint ache, and lassitude. These symptoms suggest a bloodborne bacterial infection. Nausea and vomiting are also the result of increased vagal activity because vagal nerve fibers innervate the renal capsule, as well as the stomach. Stretching of the capsule is sensed as gastric distension and triggers nausea and vomiting.

Site of Infection

The urinary tract is composed of the kidney and ureters; bladder; prostate and epididymis in men; and urethra. Infection in any of these results in the above symptoms and causes the patient to seek medical attention. It is important to accurately diagnose the site of infection, as the type and duration of therapy differs.

The most common form of UTI in both men and women is cystitis. There is a distinction between asymptomatic bacteriuria and a symptomatic infection of the bladder or cystitis. The patient with asymptomatic bacteriuria has a sufficient number of bacteria to be consistent with infection, greater than 10⁵ colony forming units (CFU)/mL of a pathogenic bacteria, but no symptoms. Asymptomatic bacteriuria requires therapy only in specific patient populations. However, good practice dictates that all patients should be monitored for progression to symptomatic infection and undergo follow-up urine culture to demonstrate resolution.

Cystitis refers to a symptomatic bladder infection that in addition to having a significant number of urinary bacteria is associated with dysuria, lower abdominal cramping, urinary frequency, and urgency. Cystitis is not associated with fever. If fever is present, an invasive tissue infection exists. This implies infection of the renal parenchyma and is referred to as pyelonephritis.

When discussing cystitis or any infection of urinary tract components, it is useful to think in terms of uncomplicated versus complicated infection. Table 22.1 lists criteria that define a complicated UTI. An uncomplicated cystitis is one that occurs in a healthy outpatient. The primary pathogens that cause uncomplicated UTI are Escherichia coli (80%) and Staphylococcus saprophyticus (15%). The remaining 5% are composed of non-E. coli Gram-negative rods, Klebsiella, Proteus, Enterobacter, Pseudomonas, and Serratia, and Gram-positive cocci, Enterococci, Staphylococcus aureus, and group B streptococcus. Complicated cystitis occurs in a patient who is institutionalized, pregnant, diabetic, paralyzed, or a transplantation recipient. Additionally, the presence of an anatomic abnormality of the genitourinary tract or an indwelling urinary catheter makes a UTI complicated. The spectrum of pathogens in these populations is different and is discussed individually.

Pyelonephritis is an infection of the renal parenchyma. Its presentation is varied. If fever is present in a patient with cystitis, by definition the patient has an invasive infection of the kidney. This is one end of the spectrum of pyelonephritis. Often patients have fevers and pain on the affected side. If these symptoms are ignored, a systemic infection ensues with progression to multiple organ dysfunction and shock. Figure 22.2 illustrates the mechanism of renal parenchymal infection. Under most circumstances, bacteria ascend to the renal parenchyma by ureteral reflux from the bladder. One exception to this rule applies. If the causative organism is S. aureus, a source of hematogenous infection should be sought.

Factors distinguishing complicated pyelonephritis from uncomplicated pyelonephritis are the same as those for cystitis. The primary pathogens causing uncomplicated pyelonephritis are the same as those for uncomplicated cystitis. If a patient remains febrile for 72 hours on an antibiotic to which the causative organism is sensitive, then evaluation for a parenchymal or perinephric abscess is indicated.

Prostatitis occurs both acutely and chronically. It causes symptoms similar to cystitis. The patient has dysuria and pelvic pain and occasionally discomfort on defecation. Distinct from cystitis, patients with prostatitis are acutely ill with signs and symptoms of systemic infection including fever, rigors, malaise, myalgias, and in extreme cases sepsis. Prostatitis is distinguished from pyelonephritis by its typical history and a tender prostate on rectal examination. The spectrum of bacterial pathogens is similar to that of cystitis and pyelonephritis.

As with cystitis and pyelonephritis, prostatitis can also be complicated. The same populations at risk for complicated cystitis and pyelonephritis are also at risk for complicated prostatitis. Additionally, there are 2 primary anatomic complications that occur in prostatitis, prostatic abscess and chronic prostatitis. The rate of abscess formation has declined significantly since the middle 1970s as a result of antibiotic therapy that allows for better prostatic tissue penetration and higher antibiotic concentration.

Chronic prostatitis results from inappropriate or incomplete therapy of acute prostatitis or without any recognized cause. Symptoms are similar to cystitis without evidence of systemic infection. The diagnosis should be considered with recurrent bouts of cystitis in the absence of bladder catheterization.

In both sexes urethral inflammation causes symptoms of dysuria, urgency, and pelvic pain. Signs of systemic infection are absent. A high index of suspicion is required. In the setting of symptoms consistent with cystitis, a negative urine culture should raise suspicion for urethritis. The patient is carefully questioned regarding new sexual partners and urethral discharge. In both women and men, the most common organism responsible is Chlamydia trachomatis followed by Neisseria gonorrhoeae. The percentage of episodes of dysuria caused by these pathogens depends on the population studied. It can be as high as 20% in an individual with multiple sexual partners and from the urban indigent populations.

Finally, vaginitis causes symptoms of dysuria and can be mistaken for cystitis. Dysuria occurs when urine comes into contact with inflamed vaginal tissues. The reported symptoms are often perceived by the patient as being more external and sharp. It is common, however, that patients do not mention vaginal symptoms spontaneously and, therefore, should be questioned specifically. As with urethritis, a negative urine for leukocytes and a negative culture should raise suspicion of this diagnosis.

KEY POINTS

RISK FACTORS FOR AND PATHOGENESIS OF URINARY TRACT INFECTION

Patient-Specific Factors

For a UTI to occur, bacteria must first gain access to the urogenital system. This happens through introduction of bacteria into the urethra during sexual intercourse or insertion of urinary catheters or other objects. The exception to this rule is infection with S. aureus that results from hematogenous spread. Infection of the urinary tract with S. aureus should prompt a search for an endovascular infection. Women are at greater risk for UTI because the vaginal introitus can become colonized with fecal bacteria. Use of spermicides and diaphragms increase the risk of UTI by altering the vaginal flora and allowing overgrowth of pathogenic bacteria. Sexual intercourse mechanically introduces bacteria into the bladder. Men are at low risk for UTI compared to women because the periurethral environment is drier and not colonized by bacteria, their urethra is longer, and prostatic fluid contains antibacterial substances. In both men and women, complete bladder emptying following voiding is a primary defence against infection.

Once in the bladder, inadequate emptying of the bladder, as occurs with prostatism or patients with neurogenic bladder allows bacteria to multiply, as illustrated in Figure 22.3. With small residual volumes (1 mL), over time, bacteria are cleared from the bladder. As the residual volume increases (8 mL), this is no longer the case. Anatomic abnormalities or nephrolithiasis provide sites for bacterial adherence and prevent expulsion. Why one individual is susceptible to UTI while another is not is dependent on the genetic, biologic, and behavioral factors shown in Table 22.2. Women who have recurrent UTIs have been found to have higher density, up to 3 times more, E. coli adhering to vaginal, buccal and voided uroepithelial cells when compared to women with out recurrent UTIs. Additionally, uropathogenic E. coli can colonize the colon. Previous antibiotic use can alter protective vaginal and perineal flora and allow overgrowth of pathogenic organisms.

Pathogen-Specific Factors

Bacteria contain virulence factors that contribute to pathogenicity. The primary virulence factor is the ability of bacteria to adhere to cell surfaces. It is important to note that microbial virulence is not related to antimicrobial resistance. The most adherent bacteria, unless acquired in the hospital setting, are sensitive to antibiotics. Bacteria that do not have an adhesion system do not cause infection. This is because enteric bacteria have negatively charged cell surfaces and are, therefore, repelled by the negatively charged cell membrane. The primary adhesion system used by bacteria is adhesins, which are lectin molecules located on their fimbriae. Adhesins bind oligosaccharides on epithelial cell surfaces and mediate internalization of bacteria into epithelial cells, where they replicate avoiding the host immune system. Other virulence factors include flagella that are necessary for motility and the production of an enzyme, hemolysin, that forms pores in the cell membrane. These pores allow bacteria to gain access to the cytosol of the renal epithelial cell where they multiply in an environment shielded from local defense mechanisms. Finally, the presence of aerobactin, which is necessary for iron acquisition, is an additional virulence factor. Iron is responsible for many processes in bacteria including upregulation of genes that enhance virulence and the formation of superoxides that degrade cell walls.

A virulence factor unique to Proteus mirabilis is urease. This enzyme converts urea into ammonia and carbon dioxide. The ammonia buffers hydrogen ions in the urine increasing pH. The alkaline pH results in the precipitation of phosphate, carbonate, and magnesium forming struvite stones. These stones allow P. mirabilis to colonize the genitourinary tract and cause obstruction and urinary stasis further promoting bacterial multiplication.

KEY POINTS

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