UTI and urine processing Flashcards
What is NF in the distal urethra?
- CoNS
- Corynebacteria and diphtheroids (miscellaneous GPB) * Lactobacilli
- Enterobacteriaceae (? transient colonisers ? normal)
- 𝛂 haemolytic streptococci
when is nephrostomy performed?
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
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
enterobacteriaceae - salmonella shigella yersinia diarrhoea producing strains of e coli always significant
what does nitrite pos on a dipstick signify
enterobacteriacea present- but other stuff that cause UTI can also be nitrite neg
Persistent proteinuria has two principal renal causes
Glomerular damage
* Diminished tubular reabsorption
does normal urine have ketones?
no lol
when are hyaline casts seen
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
when are renal epithelial cell casts seen?
*
Renal tubular epithelial cells
- renal tubular necrosis
- viral disease (such as CMV nephritis) - kidney transplant rejection
when are red cell casts seen
Always pathological – i.e., kidney damage, glomerular nephritis, pyelonephritis, acute interstitial nephritis
can also have hb casts
when are Coarse and fine granular casts possible
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
what are waxy casts
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)
when is extra media needed?
when there is more than 10 x 10^6 WBC/L- use BA, MAC CLED SABC or chrome candida for yeast, sensitivity plate
when do we do direct sensitivity testing?
when there is more than 10 x 10^6 WBC/L May be performed on specimens with bacteria that have no squames or WBC
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
Enterobacteriacae
what does indole production test
what is the colour difference for kovacs and DMACA reagant?
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
Enterococcus are split into 5 groups
which does group II contain
which are the only motile species
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
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
90%
soil and water
opportunistic
30%
What is the most common infection caused by enterococci?
what are some other infections?
UrinaryTractInfection(UTI)
Abdominal infections,peritonitis–especially following any kind of GIT surgery * Endocarditis
* Septicaemia(50%mortality) * Meningitis
* Endometritis
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
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
First VRE in Australia (Melbourne) in 1994, >90% strains are E. faecium compared to 5-10% E. faecalis why?
- 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
in VRE how is glycopeptides prevented from binding to cell wall?
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
What are the vancomycin and teicoplanin resistant enterococci due to in
- vanA, vanB, vanD, vanM resistance
2.vanC1,vanC2,vanC3,vanE,vanG,vanL,vanN resistance
which are the most common?
- Due to replacement of D-alanyl-D-alanine with D-alanyl-D-lactate
- 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
which resistant genotypes for VRE have intrinsic chromosomal R to glycopeptides?
vanC1, vanC2 intrinsic chromosomal R to glycopeptides
- VanC1 E. gallinarum
- VanC2 and/or VanC3 E. casseliflavus/E. flavescens
Where is group D streptococcus NF
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
which group D strep group and subgroup is associated with colorectal malignancies
S. gallolyticus subsp. gallolyticus
What is s saphrophyticus associated with
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
virulence factors of S saprophyticus
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
what do you do if numerous WBCs seen but NG?
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
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
VRE
