Lecture 8 Flashcards

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1
Q

likelihood of experiencing a UTI for women and men, and is secondary infection more likely after experiencing a UTI?

A

women = 40-50%
men = 10-12%
- yes, secondary infection is more probable

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2
Q

downfalls of antibiotic treatment for UTI’s

A

costly, disrupts normal flora, increased likelihood of drug resistance

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3
Q

what is the endpoint of treatment for UTI’s?

A

sterilisation of urine and loss of symptoms

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4
Q

Bacteria that is responsible for most community-acquired UTI’s, and most susceptible gender and age groups

A
A uropathogenic Escherichia coli (UPEC) called Proteus mirabilis is responsible for most CA-UTI's 
Young women (opening of the anus is close to the urethra) and old men (enlarged prostate --> pooling of liquid (stasis) allows bacteria to grow)
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5
Q

Bacteria that is responsible for most hospital-acquired UTI’s, and most susceptible gender and age groups, mode of transmission, are they more or less drug-resistant than CA-UTI’s?

A

UPEC and other bacteria (Proteus mirabilis)
non-gender specific
device-related transmission - urinary catheter
more drug-resistant

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6
Q

signs of a CA-UTI

A

bad smelling urine, cloudy urine, hematuria (blood in urine)

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7
Q

symptoms of a CA-UTI

A

frequent toilet breaks, dysuria (pain when urinating), cystitis (infection of the urinary system and bladder), pyelonephritis (kidney infection, causes fever), flank pain (kidney), hesitancy to urinate, urgency to urinate

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8
Q

diagnostics of UPEC E.coli

A

Gram-negative, rod, oxidase negative

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9
Q

CA-UPEC source of bacteria

A

Colon (colonise there)

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10
Q

CA-UPEC infection route of transmission

A

Ascending route off infection (colon –> urethra –> bladder (cystitis) –> ureter (pyelonephritis) –> kidney)

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11
Q

risk factors for CA-UPEC infection

A

sex (women), sexual activity women (20-40), previous UTI’s, antibiotics that disrupt vaginal flora, underlying disease that leads to stasis

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12
Q

virulence factors of Proteus mirabilis colonisation

A

siderophore (iron uptake), pili (attachment to bladder, type 1 fimbriae bind to mannose residues, S-fimbriae (SFA-1), P-related fimbriae (prf), curli bind to amyloid, P-pili bind to globobiose in the membrane of kidney cells)

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13
Q

virulence factors of Proteus mirabilis immune evasion

A

flagella (motility), invades cells and colonises, escapes sick cells to infect others, form QIR (quiescent intracellular reservoirs)

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14
Q

toxin to cells by Proteus mirabilis

A

alpha-hemolysin (punctures membrane of RBC’s), cytotoxic necrotising factor (affects WBC’s)

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15
Q

progression of symptoms for CA-UTI Proteus mirabilis

A

frequency, urgency and dysuria problems, urine is smelly and cloudy - cystitis –> develops into pyelonephritis, mild fever (38degrees), pain in the suprapubic region (no higher than kidneys)

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16
Q

sample tested for identification of Proteus mirabilis

A

urine (mid-stream so there isn’t much skin bacteria, usually sterile but if it touches the walls then there will be some bacteria) analysis immediately or stored <4degrees

17
Q

microscopy of urine in Px with CA-UTI

A

sediment, bacteria, WBC’s (neutrophils), epithelial cells (bladder sheds cells with bacteria on them) seen

18
Q

type of culture used to diagnose UTI and CFU requirement for UTI

A

CLED agar: cysteine (requirement of UPEC), electrolyte-deficient (prevents swarming), lactose (UPEC causes blue –> yellow colour change due to change in pH)
10^5CFU/mL or 10^8CFU/L = infection

19
Q

further tests to diagnose CA-UTI

A

MALDI-TOF (mass spectrometry for microorganisms), dipstick test: positive for nitrites (bacteria convert nitrates –> nitrites), positive for leukocyte esterase (presence of WBC’s, present in infections of the bladder)

20
Q

treatment options for CA-UTI’s

A

fluids and pain relief, give advice to Px (hygiene, don’t hold on, go to the toilet, drink lots of fluids*, dietary changes (cranberry juice, mannose tablets (attaches to mannose so bacteria can’t), live yoghurt)

21
Q

advice for antibiotic use for CA-UTI’s

A

advise fluid uptake, ensure antibiotic reaches kidneys and are excreted in urine, be aware of resistance issue and of persistent infections, if there is a reoccurrence it is better to change drugs to prevent resistance than to use the same drug (use non-penicillin antibiotics, e.g. trimethoprim or ciprofloxacin)

22
Q

why and when no antibiotics should be used for UTI’s

A

increases resistance, if Px is a healthy young woman fluids and her immune system should be sufficient)
Px should return if symptoms persist or worsen (blood in urine, fever, flank/loin pain are signs of pyelonephritis)

23
Q

why and when antibiotics should be used for UTI’s

A

If there is a clinically established infection (enumeration - 10^5CFU/mL - significant bacteriuria), UPEC infection

24
Q

what disease is commonly seen for community-acquired and hospital-acquired UPEC infections?

A

Cystitis

25
Q

main source of HA-UPEC infection

A

urinary catheter

26
Q

risk factors for HA-UPEC infection

A

countries with high bacterial prevalence (e.g. India), antibiotics that disrupt vaginal flora, ESBL (Extended spectrum beta-lactamase - antibiotic resistant strain of E.coli)

27
Q

progression of symptoms of HA-UPEC infection

A

fever, cloudy & smelly urine, ESBL –> no recovery/symptoms worsen, E.coli resistant to: penicillins, cephalosporins, carbapenems (beta-lactam antibodies)

28
Q

sample tested to identify HA-UPEC infection

A

rectal swab

29
Q

culture test for HA-UPEC infection

A

Agar with antibiotic which selects for ESBL’s (strains E.coli) –> bacterial growth = positive result, as it shows resistance to drugs

30
Q

treatment options for HA-UPEC infection

A

remove catheter (source), give broad spectrum antibiotics (as Px will have multiple diseases in them), monitor recovery, culture bacteria from catheter tip, urine (to identify bacteria) and blood (not ensure no bacteremia)

31
Q

prevention options for HA-UPEC infection

A

screen and segregate Px’s

32
Q

what are ESBL’s and in which population are they usually found?

A

microorganisms (mainly enterobacteriaciae and some strains of E.coli) which have plasmids with antibiotic resistnace genes (extended spectrum beta lactamases in this case) spread by conjugation. The genes for the beta lactamase enzyme allows resistance to penicillin, cephalosporin and carbapenem antibiotics.
Px’s in hospitals and travellers to India

33
Q

how are ESBL’s managed?

A

screen Px’s –> separate ESBL carriers from non-carriers –> polymyxin B or drug administered –> monitor renal polymyxin toxicity (measure levels of serum urea and creatinine), monitor Px’s recovery, time to recovery extended, emphasis on hygiene

34
Q

treatment of ESBL’s

A

polymyxin B or E (colistin): forms pores in membranes –> kills bacteria, cationic polypeptide antibiotic, not used any more due to renal toxicity, only reconsidered where it is the only drug that works