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36 Cards in this Set

  • Front
  • Back
COmmon clinical syndrome characterized by alterations in vaginal flora
bacterial vaginosis
Where is prevalence highest for BV?
STD clinics and sex workers (although not exclusively sexual problem)
Changes in BV flora
absence of lactobacilli
Large number of gram- or gram variable coccobacilli
Epithelial cells studded with bacteria: clue cells
2 changes for BV
Garnderella vaginalis (gram-variable, facultative anaerobes) and mobiluncus spp. (gram- anaerobes)
Clinical signs and symptoms of BV
odor from anaerobes, elevated pH, changes in vaginal discharge
criteria for diagnosis of BV
at least 3 of:
-presence of clue cells
-vaginal pH >4.5
-Homogenous adherent discharge
-fishy odor with addition of KOH on slide
BV associations
Acquisition and transmission of HIV
Other STIs
Developing PID from gonococcal or chlamydial infections
Recommended tx for BV
metronidazole or clindamycin (anaerobes)
-only moderately effective, high relapse
Potential tx for BV down the road
probiotics for Lactobacilli
What causes bacterial vaginosis?
No specific bacteria, disappearance of Lactobacillus
What goes on with vulvovaginal candidiasis?
vaginal yeast infection (lactobacilli eliminated by antibiotics)
What does candida normally exist as?
yeast
What is vulvovaginal candidiasis prevalence higher in?
Pregnant women
Women with uncontrolled diabetes
Women with impaired immunity
Common complaint with VVC
Vulvar itching or irritation
-discharge often absent, but when present is thick
Pathogenesis of VVC
hyphae associated with active disease
allergic reaction may cause severe symptoms
How do you diagnose VVC?
Culture/wet mount
Tx of VVC
Uncomplicated: Short course of oral antifungals
Complicated: Culture to confirm, longer antifungals
How is VVC different from other STIs discussed thus far?
Candida is sometimes part of normal flora; organisms causing STIs are not.
Main classifications of UTIs
Lower (cystitis) vs. Upper (acute pyelonephritis)
Symptoms of cystitis
frequency
dysuria
urgency
strangury (muscle spasms)
hematuria
suprapubic pain
Change in smell of urine
Symptoms of acute pyelonephritis
fever
rigors
vomiting
loin pain or tenderness
(rapid onset)
Anti-adherence protein in urogenital tract
Tamm-Horsfall protein (binds uropathogenic E. coli UPEC, comp inhibitor of binding)
Reason why women are more suscetible to UTIs
shorter urethra
anus and urethra close by
pregnancy inc risk
inc with common behaviors
Recurrent UTIs occur when: (4)
greater density of receptors for binding of UPEC
Structural abnormality resulting in reflux
Urinary tract stones (site to adhere)
Conditions affecting nerve supply (like spinal cord injury)
Main two causes of UTI
Uropathogenic E.coli (UPEC) (have fimbrial adhesins)
Staphylococcus saprophyticus
Movement of UPEC during UTI
intestine -> periurethra -> urethra -> bladder
What causes the inflammatory response for UPEC UTIs?
LPS (received by TLR4)
How do UPEC usually start the infection of the bladder?
Form biofilm and "pods"
What is the key to the UPEC virulence?
Pili (recurrent bind more)
What aspect of UPEC is responsible for establishing cystitis? It also binds to Tamm-Horsfall protein.
Type 1 pili
What role do Tamm-Horsfall proteins play in UTIs?
Anti-UTI factor b/c it binds some Type I pili because it binds mannose
These types of pili are required to cause pyelonephritis. What do they bind?
Pap pili; galactose-containing glycolipid R on kidney epithelial cells
What forms on urinary catheters?
biofilms
Dx of UTI
Quantitative urine culture, but usually signs, symptoms, urine dipstick
Tx of UTIs
3 days of antibiotics for cystitis, long course for pyelonephritis (watch out for yeast infection in women)
Preventing UTIs?
Goal: Block adherence
Vaccines: Tamm-Horsfall protein like to block binding