UNCOMPLICATED URINARY TRACT INFECTION

I. ETIOLOGY

Escherichia coli , a gram negative bacilli, accounts for ~80% of uncomplicated

urinary tract infection (UTI). Staphylococcus saprophyticus is a distant second with 5-
20% of the reported cases. Other etiologic agent accounting for small percentage of the
overall infections are Klebsiella Pneumoniae and Proteus mirabilis.

Although less cases of S. saphrophyticus are reported, it is found to be more

aggressive and more likely to cause recurrent infections.

II. PATHOGENESIS ( brief)

III. DRUG TREATMENT

Treatment for uncomplicated UTI include the combination drug trimethoprim

and sulfamethoxazole, trimethoprim, β-lactams, fluoroquinolones and nitrofurantoin.
However increasing resistance of E. coli strains causing acute cystitis have become
resistant to amoxicillin, sulfa drugs and cephalexin. Recent studies based on the
Surveillance Network (TSN) database reported that E. coli had an overall resistance
rate of 38 percent to ampicillin, 17.0 percent to TMP-SMX, 0.8 percent to nitrofurantoin,
and 1.9 to 2.5 percent to fluoroquinolones ( mehnert-Kay, 2005)

Trimethoprim-sulfamethoxazole (TMP-SMX) has long been considered the

standard of therapy for acute and recurrent urinary tract infections because of its activity
against the most common uropathogens and its low cost and tolerability. ( Jancel and
Dudas, 2002). But because of E.coli’s rapidly developing resistance, fluoroquinolones
have become a popular treatment. The use of fluoroquinolones however are reserved for
treatment failures or patients allergic to TMP-SMX because of resistance concerns.
TRIMETHOPRIN- SULFAMETHOXAZOLE

Trimethoprim and sulfamethoxazole are both

folate antagonists. Trimetophrin, a potent inhibitor of
bacterial dihydrofolate reductase whereas
sulfamethoxazole, a sulfonamide , is a competitive
antagonists of para-aminobenzoic acid inhibitng the
formation of tetrahydrofolic acid. The synergistic
combination of trimethoprim and sulfamethoxazole
works at two separate steps of the bacterial folate
metabolism, resulting in the inhibition of DNA synthesis.
( Jancel and Dudas, 2002). The resulting combination of
these two drugs, called CO-TRIMOXAZOLE, shows
greater antimicrobial activity than equivalent quantities of
either drug used alone as shown in Figure ()

A. PHARMACOKINETICS Figure 1. Synergism between

trimethoprim
and sulfamethoxazole on the

B. MECHANISM of ACTION

C. CLINICAL USE

D. ADVERSE DRUG REACTION

E. DOSAGE INDICATIONS

F. CONTRAINDICATIONS