UTIS & TREATMENT EXAM QUESTIONS
WITH COMPLETE ANSWERS
Urolithiasis - Answer-- formation of stones
- due to formation of infectious or non-infectious causes
Infectious Urolithiasis - Answer-- associated w/ Proteus spp & other UREASE producing
organisms --> bring pH of urine up (alkalinizes) & give bacteria opportunity to grow
- Urease --> causes precipitation of struvite stones
- stones can serve as growth niche for bacteria
Calculi formation - Answer-- partially d/t diet & dehydration
- bacteria increase pH
- attach
- produce extracellular polysaccharide
- crystals start attaching & precipate, getting bigger & bigger
- they will dis-attach & reattach & then form a stone
** ONLY 10% are due to infection
E. coli virulence factors - Answer-- has Adhesins = P-pili & Type-1 pili
Dysuria causes - Answer-- vaginitis
- urethritis
- cystitis
- non-infectious
Which infectious agent is the 2nd most common cause of ascending UTIs? - Answer--
Staph saprophyticus, 2nd to E. coli
Etiology of UTIs= - Answer-almost always E. coli
- have intestinal normal flora
- intestinal pathogens
- extraintestinal pathogens
Most common cause of Community-acquired UTI - Answer-E. coli - can cause to
Malakoplakia (rare presentation of yellow plaques in bladder due to lack of functioning
macrophages)
Most common cause of Hospital-acquired UTI - Answer-E. coli - BUT other gram-
negatives are a close 2nd
CAUTI - Answer-Catheter-associated UTI - b/c catheters are the perfect niche for
biofilm colonization
, Pathogens of CAUTI - Answer-Bacterial = E. coli
Non-bacterial = candida (create proper environment for bacteria to attach, not really
causing infection) --> so you STILL want to treat for bacteria not w/ antifungals
Pathogenesis involves 3 things - Answer-Host innate immunity - Urinary tract function -
Bacterial virulence traits
** together they cause UTIs, and can lead to renal damage (pyelonephritis)
How does bacteria act? - Answer-- comes from colon, attaches & resists urine flush,
can be internalized in bladder or kidney, then release cytokines causing inflammation
- different strains produce different inflammatory results
Type-1 pili - Answer-- present in a lot of the E. coli found in our intestines
- virulence factor that is also found in people w/o UTIs
- but allows bacteria to bind to urethra, & bind to epithelium of bladder/kidney/ureters
- attach to mannose-containing glycoproteins
- proteinaceous appendages - just like hair - but tip is STICKY
- usually peritrichous = expressed evenly on the surface
P-pili - Answer-- just the RECEPTORS are different from Type-1 pili
- binds to digalactosides on human urinary tract cells
- encoding gene = PAP --> pyelonephritis associated pili (a lot of cases w/
pyelonephritis, are associated w/ PAP, but not all)
- P-pilus binds host cell & induces synthesis of other virulence factors
- PAP genes are clustered on bacterial chromosome in Pathogenicity Islands
Phase variation - Answer-- gene expression of Type 1 & P pili is subject to this
- can turn pili on or off depending on the environment
- formation of the "on" complex depends on inversion (type 1) or differential methylation
(P-pili)
Alkanization = - Answer-has nothing to do with the attachment of the pili
Type 1 pili mediated invasion - Answer-- bacteria induces cytoskeletal rearrangement
- recruitment & activation of inflammatory cells (PMNs)
- cell dies
- bacteria is exfoliated
- invasion of underlying epithelium, where it can remain for long periods of time by
forming IBCs
IBC - Answer-* intracellular bacterial communities
- stay, change morphology, become filamentous, resist phagocytosis
WITH COMPLETE ANSWERS
Urolithiasis - Answer-- formation of stones
- due to formation of infectious or non-infectious causes
Infectious Urolithiasis - Answer-- associated w/ Proteus spp & other UREASE producing
organisms --> bring pH of urine up (alkalinizes) & give bacteria opportunity to grow
- Urease --> causes precipitation of struvite stones
- stones can serve as growth niche for bacteria
Calculi formation - Answer-- partially d/t diet & dehydration
- bacteria increase pH
- attach
- produce extracellular polysaccharide
- crystals start attaching & precipate, getting bigger & bigger
- they will dis-attach & reattach & then form a stone
** ONLY 10% are due to infection
E. coli virulence factors - Answer-- has Adhesins = P-pili & Type-1 pili
Dysuria causes - Answer-- vaginitis
- urethritis
- cystitis
- non-infectious
Which infectious agent is the 2nd most common cause of ascending UTIs? - Answer--
Staph saprophyticus, 2nd to E. coli
Etiology of UTIs= - Answer-almost always E. coli
- have intestinal normal flora
- intestinal pathogens
- extraintestinal pathogens
Most common cause of Community-acquired UTI - Answer-E. coli - can cause to
Malakoplakia (rare presentation of yellow plaques in bladder due to lack of functioning
macrophages)
Most common cause of Hospital-acquired UTI - Answer-E. coli - BUT other gram-
negatives are a close 2nd
CAUTI - Answer-Catheter-associated UTI - b/c catheters are the perfect niche for
biofilm colonization
, Pathogens of CAUTI - Answer-Bacterial = E. coli
Non-bacterial = candida (create proper environment for bacteria to attach, not really
causing infection) --> so you STILL want to treat for bacteria not w/ antifungals
Pathogenesis involves 3 things - Answer-Host innate immunity - Urinary tract function -
Bacterial virulence traits
** together they cause UTIs, and can lead to renal damage (pyelonephritis)
How does bacteria act? - Answer-- comes from colon, attaches & resists urine flush,
can be internalized in bladder or kidney, then release cytokines causing inflammation
- different strains produce different inflammatory results
Type-1 pili - Answer-- present in a lot of the E. coli found in our intestines
- virulence factor that is also found in people w/o UTIs
- but allows bacteria to bind to urethra, & bind to epithelium of bladder/kidney/ureters
- attach to mannose-containing glycoproteins
- proteinaceous appendages - just like hair - but tip is STICKY
- usually peritrichous = expressed evenly on the surface
P-pili - Answer-- just the RECEPTORS are different from Type-1 pili
- binds to digalactosides on human urinary tract cells
- encoding gene = PAP --> pyelonephritis associated pili (a lot of cases w/
pyelonephritis, are associated w/ PAP, but not all)
- P-pilus binds host cell & induces synthesis of other virulence factors
- PAP genes are clustered on bacterial chromosome in Pathogenicity Islands
Phase variation - Answer-- gene expression of Type 1 & P pili is subject to this
- can turn pili on or off depending on the environment
- formation of the "on" complex depends on inversion (type 1) or differential methylation
(P-pili)
Alkanization = - Answer-has nothing to do with the attachment of the pili
Type 1 pili mediated invasion - Answer-- bacteria induces cytoskeletal rearrangement
- recruitment & activation of inflammatory cells (PMNs)
- cell dies
- bacteria is exfoliated
- invasion of underlying epithelium, where it can remain for long periods of time by
forming IBCs
IBC - Answer-* intracellular bacterial communities
- stay, change morphology, become filamentous, resist phagocytosis
