Usual bacteria
UPEC/ ExPEC
Enterococcus spp.
Proteus mirabilis
Staphylococcus saprophyticus
Entry for UPEC
Host factor for entry
Host factor for spread
Bacterial factor for damage
Hemolysin: tissue damage
Lipopolysaccharide: inflammation
Polysacharide: prevent phagocytosis
Urease: stone formation (break urea into NH3, raised pH and ppt)
Treatment for uncomplicated cystitis
First line: nitrofurantoin, co-amoxiclav
Second line: fluoroquinolones, cefuroxime, Sulfamethoxazole-trimethoprim
Treatment for uncomplicated UTI in children
Co-trimethoxazole, cefuroxime
avoid co-trimethoxazole, nitrofurantoin in <3 months
Treatment for pyelonephritis
IV co-amoxiclav or piperacillin-tazobactam
Treatment for enterobacter clocae
PO/IV fluoroquinolone
IV cefepime
IV piperacillin-tazobactam
Treatment for ESBL-E Coli
Fosfomycin trometamol (act like beta lactam)
Treatment for symptomatic candida cystitis
Oral fluconazole for susceptible
Resistance: Amphotericin B deoxycholate or flucytosine
Treatment for symptomatic ascending candida pyelonephritis
Oral fluconazole
Resistant: AmB deoxycholate with or without flucytosine
Fungus ball
surgical intervention + antifungal treatment
Chlamydial infection (urethritis/ cervititis)
Gonococcal infection (urethritis or cervititis)
Prostatitis
Antifolate mechanism of action
trimethoprim and sulfamethoxazole are structurally similar to folate intermediate of DNA synthesis thus compete with them to inhibit. Bacteriostatic.
Antifolate formula and Cons
1:5 trimethoprim: sulfamethoxazole
skin rashes, hemolytic anemia in G6PD deciency
Mechanism of DNA synthesis inhibitors
metronidazole: diffuse and metabolised in cell, form unstable complex with DNA, break
rapid bactericidal effect
effective against anaerobes
Nitrofurantoin
Mechanism of fosfomycin