UTI and urine processing Flashcards

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1
Q

What is NF in the distal urethra?

A
  • CoNS
  • Corynebacteria and diphtheroids (miscellaneous GPB) * Lactobacilli
  • Enterobacteriaceae (? transient colonisers ? normal)
  • 𝛂 haemolytic streptococci
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2
Q

when is nephrostomy performed?

A

Blocked ureter
- kidney stone
- tumour
- Stagnation = infection and/or kidney damage
* Hole in the ureter or bladder
- urine is leaking into the body
* To assess kidney anatomy * To assess kidney function

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3
Q

Many are endogenous in the gut and lower urinary tract of humans and animals
* Used to be assumed that they were a major component of large intestinal flora of humans
* Opportunistic pathogens - esp. nosocomial infections

A

enterobacteriaceae - salmonella shigella yersinia diarrhoea producing strains of e coli always significant

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4
Q

what does nitrite pos on a dipstick signify

A

enterobacteriacea present- but other stuff that cause UTI can also be nitrite neg

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5
Q

Persistent proteinuria has two principal renal causes

A

Glomerular damage
* Diminished tubular reabsorption

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6
Q

does normal urine have ketones?

A

no lol

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7
Q

when are hyaline casts seen

A

Can occur with low urine flow, in concentrated urine, or with acidic urine
* Can be seen normally in individuals suffering dehydration or following vigorous exercise

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8
Q

when are renal epithelial cell casts seen?

A

*
Renal tubular epithelial cells
- renal tubular necrosis
- viral disease (such as CMV nephritis) - kidney transplant rejection

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9
Q

when are red cell casts seen

A

Always pathological – i.e., kidney damage, glomerular nephritis, pyelonephritis, acute interstitial nephritis

can also have hb casts

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10
Q

when are Coarse and fine granular casts possible

A

Can be due to retention, but usually associated with chronic renal disease, acute tubular necrosis * Can be seen normally in individuals following vigorous exercise/dehydration (retention)
* With advanced cell breakdown become waxy casts

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11
Q

what are waxy casts

A

final stage of degeneration of a granular cast (often has indentations in the edge as it deteriorates – see bottom left image)
- Severe chronic renal disease
- Renal amyloidosis (the deposition of amyloid proteins in the kidney causes renal damage)

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12
Q

when is extra media needed?

A

when there is more than 10 x 10^6 WBC/L- use BA, MAC CLED SABC or chrome candida for yeast, sensitivity plate

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13
Q

when do we do direct sensitivity testing?

A

when there is more than 10 x 10^6 WBC/L May be performed on specimens with bacteria that have no squames or WBC

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14
Q

All usually have grey, moist, shiny looking colonies on BA
- Slightlymoreopaqueinthecentrethan the edge
- Usually,non-haemolytic
Yersinia-non-motileat37 ̊C
* most motile at 25-28 ̊C
* Y. pestis is always non motile
Motile genera all have peritrichous flagella
* Facultative anaerobes
Nil green/yellow pigments

A

Enterobacteriacae

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15
Q

what does indole production test

what is the colour difference for kovacs and DMACA reagant?

A

Tests if an organism produces the enzyme tryptophanase which breaks down AA Tryptophan

Kovac pos = pink neg= blue
DMACA pos= blue, neg= pink both less than 10 secs, use BA

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16
Q

Enterococcus are split into 5 groups
which does group II contain

which are the only motile species

A

group II has E.faecalis the most common species isolated from humans - E.faecium (5-25%of human isolates-up from historical 1-2%)
- other species(1-5%
) including e durans

The only Motile species
- E. gallinarum
- E. casseliflavus

17
Q

ENterococcus

_____ contain the Group D antigen in their cell wall
Normal gut (106-8 cfu/g faeces) and vaginal flora
- _____ ____ _____(usually animal sources),food(butchering and poor hand hygiene) _____________ pathogens - esp. as Nosocomial pathogens
- Use of broad-spectrum antibiotics has led to the development of resistance i.e., R to AMP, R to 3GC, R to lower activity aminoglycosides
- Use of glycopeptides as animal growth promoters * ~ _____ of all enterococci isolates are VRE
Increased incidence of nosocomial infection due to….
- Increasednumbersofimmunocompromisedpatients(HIV,transplant) - Increaseduseofsurgeryandimplantation,instrumentation

A

90%
soil and water
opportunistic
30%

18
Q

What is the most common infection caused by enterococci?
what are some other infections?

A

UrinaryTractInfection(UTI)

Abdominal infections,peritonitis–especially following any kind of GIT surgery * Endocarditis
* Septicaemia(50%mortality) * Meningitis
* Endometritis

19
Q

What are enterococci intrinsically resistant to?

Acquired resistance varies from isolate to isolate,place to place and species to species
- 90% of E. faecium strains are resistant to Ampicillin compared with 10% strains E. faecalis - High level resistance to aminoglycosides in certain species:
* E. gallinarum, E. casseliflavus, E. avium, E. raffinosus, E. mundtii

A

Low level resistance to:
- Aminoglycosides (an exception: Enterococcus faecium is intrinsically resistant to tobramycin)
- Lincosamides
* Moderate level of resistance to:
- Penicillins
- Cephalosporins * Resistant to:
- Sulphonamides
- E. gallinarum, E. casseliflavus, E. flavescens intrinsically resistant to glycopeptides

20
Q

First VRE in Australia (Melbourne) in 1994, >90% strains are E. faecium compared to 5-10% E. faecalis why?

A
  • This is not because the incidence of E. faecalis infection has decreased - Emergence postulated due to- high use of vancomycin and cephalosporins
  • use of avoparcin as an animal growth promoter in pig & poultry farming - Avoparcin is a glycopeptide from the same family as Vancomycin
  • Resistance mechanism mediates resistance to both drugs
  • Has led to antibiotic-resistant enterococci in human food and
  • Colonised patients spread in the nosocomial setting

Over exposure to vancomycin has also led to the emergence of VRD strains

21
Q

in VRE how is glycopeptides prevented from binding to cell wall?

A

Vancomycin and Teicoplanin are glycopeptides
* The AA modification in the cell wall leads to decreased binding affinity for glycopeptide antibiotics = resistance
* Glycopeptides normally bind to the terminal D-alanyl-D-alanine residue in the cell wal

22
Q

What are the vancomycin and teicoplanin resistant enterococci due to in

  1. vanA, vanB, vanD, vanM resistance
    2.vanC1,vanC2,vanC3,vanE,vanG,vanL,vanN resistance

which are the most common?

A
  1. Due to replacement of D-alanyl-D-alanine with D-alanyl-D-lactate
  2. Due to replacement of D-alanyl-D-alanine with D-alanyl-D-serine

most common= vanA vanB- Carried on transposons that can be inserted into either plasmids or the chromosome
* PCR ‘Gold standard’ for vanA, vanB

23
Q

which resistant genotypes for VRE have intrinsic chromosomal R to glycopeptides?

A

vanC1, vanC2 intrinsic chromosomal R to glycopeptides
- VanC1 E. gallinarum
- VanC2 and/or VanC3 E. casseliflavus/E. flavescens

24
Q

Where is group D streptococcus NF

A

Normal GIT flora in vertebrates (i.e., non-fastidious, can tolerate bile) - Generally,cause similar infections to enterococci

?S.equinus(from horses) is now considered to be a variant of S.bovis (fromcattle)

Accurate identification may require combinations of the following: * Biochemical tests
* Genetic analysis
* MALDI-TOF

25
Q

which group D strep group and subgroup is associated with colorectal malignancies

A

S. gallolyticus subsp. gallolyticus

26
Q

What is s saphrophyticus associated with

A

Most commonly associated with community acquired UTI
- Especially in young sexually active females
- Second most common cause of uncomplicated cystitis after E.coli
* Cause of UTI and urethritis in men
* Prostatitis (elderly men)
* Commensal of rectum, urethra and cervix

27
Q

virulence factors of S saprophyticus

A

Virulence factors
- adherence to epithelial cells
* inc specificity for uroepithelial, urethral and peri-urethral cells - urease production-?contributes to bladder tissue invasion
- produces a slimelayer in the presence of urine and urease
* Therefore, is very sticky in urinary system–not flushed out

28
Q

what do you do if numerous WBCs seen but NG?

A

Centrifuge 10ml of well mixed urine. Pour off the supernatant. Prepare a Gram smear using a portion of the sediment.
- If bacteria can be visualised, consider extended incubation of the culture plates and testing for antimicrobial activity
- If “Bacteria NOT Seen” then report this finding as part of the microscopy result and record No Growth for the culture result

29
Q

First VRE in Australia (Melbourne) in 1994
* >90% strains are E. faecium compared to 5-10% E. faecalis
- This is not because the incidence of E. faecalis infection has decreased - Emergence postulated due to
- high use of vancomycin and cephalosporins
- use of avoparcin as an animal growth promoter in pig & poultry farming - Avoparcin is a glycopeptide from the same family as Vancomycin
- Resistance mechanism mediates resistance to both drugs
- Has led to antibiotic-resistant enterococci in human food and
- Colonised patients spread in the nosocomial setting

A

VRE