Chapter 9: Genitourinary Tract Infections and Sexually Transmitted Diseases PDF

University of the East Ramon Magsaysay Memorial Medical Center Access Provided by: Infectious Diseases: A Clinical Short Course, 4e Chapter 9: Genitourinary Tract Infections and Sexually Transmitted Diseases Fre...

University of the East Ramon Magsaysay Memorial Medical Center Access Provided by: Infectious Diseases: A Clinical Short Course, 4e Chapter 9: Genitourinary Tract Infections and Sexually Transmitted Diseases Frederick S. Southwick INTRODUCTION GUIDING QUESTIONS 1. What are the virulence factors that allow bacteria to infect the urinary tract, and where do the bacteria come from? 2. What are the host factors that help to prevent infection of the urinary tract? 3. Which symptoms and signs help the clinician to differentiate upper tract (pyelonephritis) from lower tract disease (cystitis)? 4. How useful is the urinary sediment in diagnosing urinary tract infection? 5. When should a urine culture be ordered, and what represents a true positive culture? What does 105 CFU/mL mean? 6. How is prostatitis contracted, and which organisms are most likely to cause this infection? 7. How do the treatments of acute and chronic prostatitis differ? 8. How is urethritis differentiated from cystitis? 9. Does delay in treating urethritis lead to any serious complications in women? 10. What are the physical findings that accompany pelvic inflammatory disease (PID)? 11. Why should physicians have a low threshold for diagnosing and treating PID? 12. What are the most common causes of genital ulcers, and how can they be differentiated on clinical examination? 13. What are the three stages of syphilis, and how are they treated? 14. How do the VDRL (Venereal Disease Research Laboratory) and RPR (rapid plasma reagin) tests differ from the FTA­ABS (fluorescent treponemal antigen–antibody absorption) test, and how should these tests be utilized? 15. What is the leading cause of venereal warts, and what are the potential long­term consequences of having this infection? POTENTIAL SEVERITY Often outpatient infections; however, the development of pyelonephritis or pelvic inflammatory disease can lead to sepsis and death. These infections need to be promptly treated. GENITOURINARY TRACT INFECTIONS: URINARY TRACT INFECTION Urinary tract infections (UTIs) are the most common infections seen in outpatient practice. Clinicians must understand the different types of UTIs and Downloaded 2024­11­1 8:45 A Your IP is know how to diagnose and treat them. Chapter 9: Genitourinary Tract Infections and Sexually Transmitted Diseases, Frederick S. Southwick Page 1 / 35 ©2024 McGraw Hill. All Rights Reserved. Terms of Use Privacy Policy Notice Accessibility Pathogenesis  infections need to be promptly treated. University of the East Ramon Magsaysay Memorial Medical Center Access Provided by: GENITOURINARY TRACT INFECTIONS: URINARY TRACT INFECTION Urinary tract infections (UTIs) are the most common infections seen in outpatient practice. Clinicians must understand the different types of UTIs and know how to diagnose and treat them. Pathogenesis Any discussion of UTI must take into account bacterial virulence factors and host factors. The balance between the ability of a specific bacterium to invade the urinary tract and the ability of the host to fend off the pathogen determines whether the human host will develop a symptomatic UTI. Bacterial Factors Bacteria generally gain entry into the urinary system by ascending the urethra into the bladder and then, in some cases, ascending the ureters to the renal parenchyma. The organism that most commonly infects the urinary tract is Escherichia coli, and certain strains of E. coli are more likely to cause a UTI. These strains possess advantageous virulence characteristics, including increased ability to adhere to the epithelial cells of the urethra and increased resistance to serum cidal activity and hemolysin production. E. coli adhere by their fimbria or pili that are distinct protein hairlike structures on the bacterial surface. Pyelonephritis strains are the most adherent; cystitis strains tend to be intermediately adherent. Pathogenic strains that cause pyelonephritis are more likely to express P fimbriae, and these fimbriae adhere to glycophospholipids embedded in the outer surface of the plasma membrane of uroepithelial cells. P fimbriae represent a classic example of bacterial tropism. Trimethoprim–sulfamethoxazole (TMP­SMX), an agent used to prevent UTI, reduces the synthesis and expression of the fimbria adhesion molecules. E. coli also express adherence molecules not associated with fimbria that enhance virulence (e.g., AFA). A number of other virulence factors contribute to the ability of urinary pathogens to survive and grow in the urinary tract. Because urine is an incomplete growth media, bacteria must be capable of synthesizing several essential nutritional factors before they can grow in urine. Bacterial synthesis of guanine, arginine, and glutamine are required for optimal growth. Pathogenic Proteus mirabilis produces ureases that appear to play an important role in the development of pyelonephritis. Urease production generates ammonium raising the urine pH above 7. Alkaline urine enhances bacterial growth and also increases the likelihood of renal stones. Proteus also produces an immunoglobulin A (IgA) protease, as well as a hemolysin. Motile bacteria possessing flagella can ascend the ureter against the flow of urine. Both Proteus and E. coli possess operons that respond to conditions in the external environment turning on and off the expression of flagella. The ability to alter the expression of flagella and other surface molecules allows bacteria to alternate between migrating up the urethra and ureters and adhering to epithelial cells in the urinary tract. Endotoxins also contribute to the development of pyelonephritis by decreasing ureteral peristalsis, slowing the downward flow of urine and enhancing the ability of gram­negative bacteria to ascend into the kidneys. Host Factors Urine contains high concentrations of urea and generally has a low pH. These conditions inhibit bacterial growth. The urine of pregnant women tends to be more suitable for bacterial growth, and patients with diabetes often have glucose in their urine, making that urine a better culture medium. These factors help to explain why pregnant women and diabetic patients have an increased incidence of UTI. Mechanical factors probably are the most important determinants for the development of UTI. Mechanical factors can be grouped into three risk categories: 1. Obstruction. The flushing mechanism of the bladder protects the host against infection of the urinary tract. When bacteria are introduced into the bladder, the organisms generally are cleared from the urine. Obstruction of urinary flow is one of the most important predisposing factors for the development of a UTI. Prostatic hypertrophy and urethral strictures can lead to bladder outlet obstruction. Defective bladder contraction associated with spinal cord injury also results in poor bladder emptying. These conditions result in a significant volume of urine remaining in the bladder after voiding (“increased post­void residual”), which markedly increases the likelihood of infection. Intrarenal obstruction caused by renal calculi, polycystic kidney disease, and sickle cell disease also increase the risk of renal infection. Proteus and other urea­splitting organisms can cause stone formation and can become entrapped within the stones. Another mechanical problem that increases the risk of upper tract disease is vesicoureteral reflux (defective bladder–ureteral valves). 2. Urethra length. Women have a short urethra, which increases the risk of bacteria entering the bladder. The incidence of UTI in women is estimated to be 1–3% per year. By the age of 32 years, half of all women have had at least one UTI. Trauma to the urethra by sexual intercourse, spermicide use, and history of past UTI are risk factors. Colonization of the vaginal area near the urethra is another important risk factor for UTI in women. This Downloaded event is 8:45 2024­11­1 thought to precede A Your IP is the development of UTI. IgA and immunoglobulin G (IgG) antibodies against cell wall antigens have been described. Chapter The exact role 9: Genitourinary of immunoglobulins Tract in protecting Infections and Sexually against Transmitted colonization Diseases, and invasion Frederick of the urinary tract remains to be determined. S. Southwick Page As 2 / a35 ©2024 McGraw Hill. consequence All Rights of their Reserved. much longer Terms urethra, menof Usea much have Privacy Policy lower Notice incidence of UTI Accessibility (