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Urinary tract infections Flashcards

1
Q

what is a urinary tract infection

A

a symptomatic infection within the urinary tract.

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2
Q

why is Asymptomatic bacteriuria not treated

A

Because of increasing antimicrobial resistance, it is important not to treat patients with asymptomatic bacteriuria unless there is evidence of potential benefit

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3
Q

what is Asymptomatic bacteriuria

A

significant numbers of bacteria in the urine but no symptoms of infection.

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4
Q

what parts of the urinary system relate to lower and upper UTIs

A

Lower UTIs = the bladder or urethra

Upper UTIs = kidneys or ureters

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5
Q

what are the disease names of lower UTIs (of the bladder or urethra)

A

bladder (cystitis) or urethra (urethritis).

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6
Q

what are the disease names of upper UTIs (kidneys or ureters)

A

kidneys (pyelonephritis) or ureters (ureteritis).

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7
Q

what is the main component of urine

A

urea

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8
Q

what is the normal pH of urine

A

pH of 6.5-6.7 just below neutral normally.

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9
Q

give two examples of bacteria that make urine alkaline (pH what?) by producing urease

A

Proteus mirabilis and Pseudomonas aeruginosa - break down urea to make pH 8.8 - 8.9

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10
Q

what antimicrobial agent can be a component of urine (in the other category)

A

lysozyme

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11
Q

list some examples of components of urine

A

urea, chloride, sodium, sulphate, phosphate, amino acids, potassium, creatine, uric acid, phospholipids, ammonia, calcium, other (albumin, cholesterol, triglycerides, sugars, immune globulines, 5-HIAA, VMA, peptides, lysozyme, amylase, serotonin)

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12
Q

what is the prevalence of UTIs treated in women

A

about 1 in 2 women will be treated for a symptomatic UTI

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13
Q

why are UTIs more common in women

A
  • Primary difference due to Anatomy – shorter urethra, closer to the bladder.
  • Birth control – use of spermicidal agents or diaphragms can increase risk of infection.
  • Menopause – decline in circulating oestrogen, causes changes to urinary tract, more vulnerable to infection.
  • Sexual activity – more common in sexually active women.
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14
Q

what is an odd manifestation of UTIs in the elderly

A

symptoms of dementia (confusion)

must be along with two other UTI symptoms

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15
Q

what ways can UTIs be classified

A

Single episode or recurrent. For recurrent UTIs, either a relapse by the same organisms or reinfection with a different organism. Timeframe undefined.

Uncomplicated or complicated. Uncomplicated - otherwise healthy, with no additional urinary tract problems. Complicated – associated with other factors including urinary obstruction, renal failure, urinary retention, presence of indwelling catheters, etc.

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16
Q

what are the risk factors of UTIs

A

Iatrogenic/ drugs
Behavioural
Anatomic/ Physiologic
Genetic

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17
Q

what is vesicoureteral reflux

A

urine flow backwards from bladder into ureters/kidneys

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18
Q

what are the stages of parthenogenetic ascension of untreated UTIs

A

colonization, uroepithelium penetration, ascension, pyelonephritis, acute kidney injury

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19
Q

what ability does Proteas bacteria have that help them ascend

A

Proteas has swarming capabilities, can become highly motile and ascend catheter.ureter really quickly

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20
Q

what cell do uropathogen invade in the bladder

A

superficial umbrella cells (by pilli and adhesins)

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21
Q

how do uropathogens evade host immune system in the bladder

A

through host cell invasion or through morphological changes that result in resistance to neutrophils

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22
Q

when do untreated UTIs progress to bacteraemia

A

if the pathogen crosses the tubular epithelial barrier in the kidneys

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23
Q

what is the most common cause of compromised bladder

A

catheterzation

24
Q

what robust immune response induced by catheterisation provides an ideal environment for uropathogen attachment

A

fibrinogen accumulation (for pathogens with fibrinogen binding proteins)

25
what bacterial component causes tissue damage in the kidneys
toxins
26
what is the most common bacterial cause of uncomplicated and complicated UTIs
UPEC - uropathogenic E.coli (primary causative agent)
27
give examples of causative agents of uncomplicated UTIs
UPEC, Klebsiella pneumoniae, Staphylococcus saprophyticus, Enterococcus faecalis, group B Streptococcus (GBS), Proteus mirabilis, Pseudomonas aeruginosa, Staphylococcus aureus and Candida spp.
28
give examples of causative agents of complicated UTIs
UPEC, Enterococcus spp., K. pneumoniae, Candida spp., S. aureus, P. mirabilis, P. aeruginosa and GBS
29
what led people to think urine was sterile, when did this idea originate
idea originated in the 1800s based on an experiment where urine was placed in a sealed flask and remained clear. when urine was put in an open flask or tap water was added it became cloudy
30
in the 1950s what was the suggested measure to differentiate between contamination and infection
100000 colony forming units ml-1
31
what is dysuria
pain/discomfort on passing urine
32
what is polyuria
excessive urine production
33
what is pyuria
presence of pus/white blood cells (6 – 10 neutrophils per high magnification field of view from unspun, mid-stream urine) indicating inflammation and immune response
34
what is haematuria
blood in urine
35
what are the general diagnostic tests for UTIs
chemical tests(dipstick) and bacterial culture
36
what are the most common urinary dipsticks testing for
leukocytes and nitrites
37
what are other components of the urine that dipsticks test for
Urobilinogen, proteins, pH, blood, ketones, bilirubin, glucose
38
what species reduce nitrate (and can be tested by nitrite dipsticks)
Gram negative uropathogens like E. coli, Enterobacter, Klebsiella, Citrobacter, Proteus
39
what do nitrite dipsticks test for
test for asymptomatic (urinary) infections caused by nitrate-reducing bacteria
40
what are the disadvantages of Nitrite dipstick testing
– not very sensitive – Negative in presence of non-nitrate reducing organisms – Nitrate-reducing bacteria need to be in contact with reagents for long enough to get visible reaction – Often bacteria are able to reduce nitrate to nitrogen, leading to false negative results (ones that aren’t normally capable)
41
what are some problems with the way we currently diagnose UTIs
Culture result can be interpreted in different ways issues with contact time specificity and sensitivity some symptoms indicative of other disease (chlamydia) so many diff types of pathogens can cause UTIs, cant test for all methods focus on planktonic free flowing bacteria no identification of multi pathogen causing UTIs kass threshold may be too high
42
what three categories are there of virulence mechanisms of UPEC
* Adhesion – prevent removal in flow of urine.(the primary defence) * Survival – able to acquire iron and can evade host defences. * Toxicity – leads to inflammation.(helps invasion of tissues)
43
what are the primary adherence mechanisms of UPEC
pili and fimbriae (good at crossing the initial reversible attachment distance)
44
what are the common adhesive organelles of UPEC
• Common adhesive organelles are type 1, P, S and FIC pili.
45
what are quiescent intracellular reservoirs (QIR)
groups of 4-10 non replicating bacteria in membrane bound compartments covered in F actin. have long term viability, sit as stock and reactivate when conditions are viable ( in the acute phase of bladder infections )
46
what adhesin molecule does type 1 pili have - what does it do
Adhesin FimH: targets uroplakin and allows ecoli to attach to urothelilum and start invasion process
47
what occurs as a result of Rho GTPase activation by type 1 pili on UPECs
actin rearrangement (membrane ruffling) and internalisation, (plasma membrane engulfs bacterium)
48
where/how do pyelonephritis-associated (P) pilli bind - what immune effect do they have
P pili bind to globosides in the kidneys with help of P fimbriae (with PapG adhesin tip). they interact with toll like receptor 4 to reduce polymeric receptor expression and affect IgA transport through cells to kidney lumen
49
in addition to Pili, what other virulence factors do UPEC have
siderophores (scavenge Fe3+) α-haemolysin (HylA) - causes pore formation in umbrella cells, promoting lysis and release of nutrients Cytotoxic necrotising factor 1 (CNF1) - affect actin modeling causing membrane ruffling, aid internalisation (corregation)
50
how do proteus initially attach to the bladder
expression of mannose-resistant Proteus-like (MR/P) pili
51
how does Enterococcus faecalis begin pathogenesis in catheter associated Urinary tract infection (CAUTIs)
Catheter implantation causes bladder inflammation and so fibrinogen release. E. faecalis uses this fibrinogen as a food source by the production of proteases. E. faecalis also binds fibrinogen through the endocarditis- and biofilm-associated (Ebp) pilus
52
what two toxins are produced by Proteus if in contact with host tissues
– Haemolysin (HpmA) – inserts into cell membrane and induces pore formation. – Proteus toxic agglutinin (Pta) – punctures host membrane, cytosol leakage leads to osmotic stress and depolymerisation of actin filaments.
53
what happens after the initial attachment of proteus in the bladder
production of urease which elevates pH and causes crystals to form. EPS traps crystals, bacteria colonise the crystals causing formation of crystalline biofilm
54
what gene in E.coli confers protection against colistin
mcr-1 gene (detected in a UTI sample in 2016)
55
what is colistin (aka polymyxin E)
an antibiotic medication used as a last-resort treatment for multidrug-resistant Gram-negative infections including pneumonia.

Microbiology (12 decks)

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