Biology Reference
In-Depth Information
Treatment
UTIs are commonly treated with oral antibiotics based on the symptoms
described by patients before the diagnosis is confirmed ( Mishra et al., 2012 ).
However, urine dipstick testing or wet mount microscopy to test for pyuria
are quick confirmatory tests that can be conducted prior to antibiotic therapy
to ensure that the diagnosis is correct. Antibiotics are selected based on local
resistance profiles and those commonly prescribed include sulfamethoxa-
zole-trimethoprim, nitrofurantoin, ciprofloxacin, norfloxacin, or ofloxacin
( Kodner and Thomas Gupton, 2010 ). Symptoms usually resolve within a few
days of treatment. Treatment lasts from three to ten days. Women who suffer
from recurrent UTI are often treated with continuous or postcoital antibiot-
ics to prophylactically prevent subsequent infections ( Kodner and Thomas
Gupton, 2010 ).
Control and prevention
Currently there is no effective vaccine to prevent UTI caused by E. coli . To
prevent UTI, physicians recommend use of contraceptives that do not include
spermicides. For recurrent infections, antibiotics taken continuously or prophy-
lactically after sexual intercourse is a common preventative practice ( Kodner
and Thomas Gupton, 2010 ). A non-prescription preventative method is drink-
ing cranberry juice, however, there is no clear correlation between dose or fre-
quency of intake and a reduction of incidence of UTI ( Sen, 2006 ).
CONCLUSIONS
Uropathogenic E. coli utilize a variety of virulence factors to ascend and colo-
nize the urinary tract ( Table 9.1 and Figure 9.1 ). Flagella are necessary to pro-
pel bacteria from the periurethral space to the bladder, where UPEC then use
multiple fimbrial and afimbrial adhesins to colonize the uroepithelium. The
host responds to UTI by exfoliation of bladder epithelial cells and stimula-
tion of the inflammatory response. Further limitation of infection occurs by
iron sequestration. To overcome iron limitation, UPEC produce several sid-
erophores that chelate iron from the host proteins and heme receptors to take
up iron from the host. To evade killing by neutrophils, UPEC produce TcpC
to reduce the TLR4 response, as well as secrete toxins that reduce leukocyte
motility. Flagella can also direct UPEC up the ureters to the kidneys, where
damage from the robust inflammatory response can cause renal scarring and
ultimately renal failure. Fimbrial and afimbrial adhesins again are used to bind
to the kidney epithelial cells. While several virulence factors are now known
for UPEC, the mechanism of action is still to be determined for some newly
recognized factors. UPEC are highly versatile pathogens, able to commensally
colonize the human gastrointestinal tract, while opportunistically causing dis-
ease in the urinary tract.
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