C h a p t e r 2 7
Disorders of the Bladder and Lower Urinary Tract
667
UrinaryTract Infections
Urinary tract infections (UTIs) include several distinct
entities—asymptomatic bacteriuria, symptomatic lower
UTIs such as cystitis, and upper UTIs such as pyelone-
phritis. Because of their ability to cause renal damage,
upper UTIs are considered more serious than lower
UTIs. Acute pyelonephritis (discussed in Chapter 25)
represents an infection of the renal parenchyma and
renal pelvis. The discussion in this chapter focuses on
lower urinary tract infections.
Etiologic Factors
Most uncomplicated lower UTIs are caused by
Escherichia coli
.
35–39
Other common uropathic patho-
gens include
Enterococcus faecalis
,
Staphylococcus sap-
rophyticus
,
Klebsiella pneumoniae
,
Proteus mirabilis
,
and
Pseudomonas
species. Most upper and lower UTIs
are caused by bacteria that enter through the urethra.
Although the distal portion of the urethra often contains
pathogens, the urine formed in the kidneys and found in
the bladder normally is sterile or free of bacteria. This
is because of the
washout phenomenon
, in which urine
from the bladder normally washes bacteria out of the
urethra during urination.
There is an increased risk for UTIs in persons with uri-
nary obstruction and reflux, in people with neurogenic
disorders that impair bladder emptying, in women who
are sexually active, in postmenopausal women, in men
with diseases of the prostate, and in elderly persons.
Instrumentation and urinary catheterization are the most
common predisposing factors for nosocomial, or hospi-
tal-acquired, UTIs. Urinary tract infections occur more
commonly in women with diabetes than in women with-
out the disease. People with diabetes are also at increased
risk for complications associated with UTIs, including
pyelonephritis, and they are more susceptible to fungal
infections (particularly
Candida
species) and infections
with gram-negative pathogens other than
E
.
coli
, both of
which are accompanied by increased severity and unusual
manifestations.
Host–Agent Interactions
Because certain people tend to be predisposed to devel-
opment of UTIs, considerable interest has been focused
on host–pathogen interactions and factors that increase
the risk for UTI.
35,36
Host Defenses.
In the development of a UTI, host
defenses are matched against the virulence of the patho-
gen. The host defenses of the bladder have several com-
ponents, including the washout phenomenon, in which
bacteria are removed from the bladder and urethra during
urination; the protective mucin layer that lines the bladder
and protects against bacterial invasion; and local immune
responses. Immune mechanisms, particularly secretory
immunoglobulin (Ig) A, appear to provide an important
antibacterial defense. Phagocytic blood cells further assist
in the removal of bacteria from the urinary tract.
There has been a growing appreciation of the protec-
tive function of the bladder’s mucin layer. It is thought
that the epithelial cells that line the bladder produce
protective substances that subsequently become incor-
porated into the mucin layer that adheres to the bladder
wall. One theory proposes that the mucin layer acts by
binding water, which then constitutes a protective bar-
rier between the bacteria and the bladder epithelium.
Elderly and postmenopausal women produce less mucin
than younger women, suggesting that estrogen may play
a role in mucin production in women.
Other important host factors include the normal flora
of the periurethral area in women and prostate secretions
in men. In women, the normal flora of the periurethral
area, which consists of organisms such as
Lactobacillus
,
provides a defense against the colonization of uropathic
bacteria.
40
Alterations in the periurethral environment,
such as occurs with a decrease in estrogen levels dur-
ing menopause or the use of antibiotics, can alter the
protective periurethral flora, allowing uropathogens to
colonize and enter the urinary tract. In men, the pros-
tatic fluid has antimicrobial properties that protect the
urethra from colonization.
Pathogen Virulence.
Pathogen virulence derives from
its ability to gain access to and thrive in the environment
■■
Neurogenic disorders of the bladder commonly
are manifested by a neurogenic overactive or
spastic bladder dysfunction, in which there is
failure to store urine, or an aflexic or flaccid
bladder dysfunction, in which bladder emptying
is impaired. Neurogenic overactive bladder
dysfunction results from neural lesions above the
level of the sacral cord that allow neurons in the
micturition center to function reflexively without
control from higher central nervous system
centers; in contrast, areflexic bladder dysfunction
results from neural disorders affecting the motor
neurons in the sacral cord or peripheral nerves
that control detrusor muscle contraction and
bladder emptying.
■■
Incontinence represents the involuntary loss
of urine. Stress incontinence is caused by the
decreased ability of the vesicourethral sphincter
to prevent the escape of urine during activities,
such as lifting and coughing, that raise bladder
pressure above the external sphincter pressure.
Urge or overactive bladder incontinence is
caused by disorders that result in hyperactive
bladder contractions. Overflow incontinence is
caused by overfilling of the bladder with escape
of urine.
