According to Moore, Day & Albers (2002) pathogenesis of Urinary Tract Infections (UTIs) is not a widely known infection. Current research has shown that most UTIs cases result when bacteria gains access to the bladder via the urethra. This is due to ascending infection, through a single gram-negative enteric bacterium some of which include Escherichia coli, Klebsiella, Proteus, Enterobacter, Pseudomonas, or Serratia. Research has shown that out of UTI cases by Enterobacteriaceae, about 80% of community-acquired infections are caused by Escherichia coli (Ronald & Toye, 2002). In addition, other gram-negative organisms, including Klebsiella, Proteus, Enterobacter, Pseudomonas, or Serratia, together represent 10 % of community-acquired infections. As a result, patients with recurrent infections are highly prone to these pathogens (Ronald & Toye, 2002). Similarly, Staphylococcus saprophyticus is the second most common cause of acute cystitis in young and sexually active females. On the other hand, Enrerococcus faecalis is a gram-positive pathogen in the elderly and in patients who have undergone genitourinary tract instrumentation (Ronald and Toye, 2002). In children, Enterobacteriaceae is the primary cause of UTI, while etiologic pathogens associated with diabetic patients are Klebsiella, Group B streptococci, Enterococcus and E coli. For patients with indwelling urethral catheters but not receiving antimicrobial agents, a different etiology exists for them because they are at the greatest risk of acquiring multiple resistant bacteria. For patients being treated with Cephalosporins infection due to E. faecalis has become more common nowadays (Ronald and Toye, 2002).
Although infection through the hematogenous is a rare occurrence, the ascending route is still the most rampant. Before the development of UTI, migration of uropathogens from the rectum to the vagina with urethral colonization occurs (Ronald and Toye, 2002). Consequently, a bacterial entry into the bladder is facilitated by sexual intercourse hence allowing the bacteria to proceed to the upper tract and kidneys. In contrast, a special zone within the urethra creates a natural barrier to the ascent of organisms colonized in the distal urethra and the bladder. Therefore, this interaction of the host defenses with bacteria determines the occurrence of the infection (Moore et al, 2002). The major host defense evident in the flushing effect of micturition is an elaborately normal urinary flow. The normal functioning of the ureterovesical junction coupled with inherent antibacterial properties of bladder mucin help in preventing infection.
Physiologically, the P fimbriae of E coli are a virulence determinant and permit their adherence to epithelial cells. While women with recurrent infections experience increased incidences of the Lewis blood-group non-secretor phenotype, females without vesicoureteral reflux have increased susceptibility to pyelonephritis due to the PI blood group. In response to infection with virulent bacteria, IL-6 and IL -8 cytokines are produced locally by epithelial cells. These cytokines not only produce acute-phase proteins but also act as a chemoattractant for neutrophils. Surprisingly, most women with complicated and recurrent infections have normal urinary tracts. Cases of interruption of the normal flow of urine such as obstruction, neurogenic bladder, or calculi result in residual urine and instrumentation, thereby increasing the incidents of infections. The findings of a recent study showed that the high incidence of UTI among women resulted from the shortness of the female urethra, which predisposes women to infection caused by bacteria from the vagina, perineum, rectum, or from a sexual partner (Harrington & Hooton, 2000).
In a positive light, recent advancements in molecular biology will highly facilitate the identification of new etiologic agents for UTI.