Genitourinary infections Flashcards
What are most common organisms causing UTIs?
E. coli 70% Klebsiella Proteus Enterobacter spp Enterococcus faecalis
Which patients require imagining of urinary tract, if pyelonephritis suspected?
All male patients
Females if >2 episodes of pyelonephritis
any patient with Proteus species isolated
Patient on CAPD for chronic renal failure. Last 24 hours noted dialysis fluid is cloudy, with mild abdominal pain.
What is most likely cause of this infection?
Staph aureus/ CoNS - 50% infections
gram neg including pseduomonas
fungi (candida) 5% - particularly if culture results are negative
Patient on CAPD for chronic renal failure. Last 24 hours noted dialysis fluid is cloudy, with mild abdominal pain.
Fluid sent for analysis
What criteria are used to confirm microbiological diagnosis of infection?
Cell count >100mm3, usually >50% polymorphs
fluid also grown in blood culture bottles
Patient on CAPD for chronic renal failure. Last 24 hours noted dialysis fluid is cloudy, with mild abdominal pain.
What is empirical treatment?
Intraperitoneal vancomycin and gentamicin
Patient on CAPD for chronic renal failure. Last 24 hours noted dialysis fluid is cloudy, with mild abdominal pain.
Pseudomonas isolated.
Patient on vancomycin and gentamicin.
Does organism alter antibiotic management?
Can stop vancomycin
Once improved, switch to ciprofloxacin for 21 days total treatment
Need to exchange PD line, as pseudomonas forms biofilms
Renal transplant patient has rising creatinine, concerns about rejection.
Urine microscopy shows “decoy cells”
What does this mean?
Decoy cells are infected epithelial cells, which have large, abnormal nuclei. Can sometimes look like cancer cells
In this case, like due to BK virus
What is usual natural history of BK virus infection?
50% of children infected by age 4 - most asymptomatic
80% of adults infected
transmitted respiratory, faecal-oral, sexual, transplant
remains latent in renal tubular epithelial cells. First sigsn of re-activation include slowly rising creatinine
What are symptoms of BK virus reactivation in immunosuppressed/ renal transplant patients?
Tubule-interstitial nephritis
haemorrhagic cystitis
pneumonitis
meningoencephalitis
How to diagnose BK reactivation
renal biopsy gold standard
BK virus DNA PCR - blood or urine
BK virus decoy cell microscopy - can be useful as screening tool
19 year old with fever, flank pain.
Urinalysis showed >50 white cells, 10 red cells, 3+ bacteria
gram negative rod seen, which is beta haemolytic
What is significance of WCC?
normal urine <10 white cells
> 50 suggests infection/ inflammation
bacteria colonies help point towards infection
19 year old with fever, flank pain.
Urinalysis showed >50 white cells, 10 red cells, 3+ bacteria
gram negative rod seen, which is beta haemolytic
What is causative organism?
E. coli can often be beta haemolytic
Pseudomonas is only other GNEG which is beta-haemolytic. But this would be less likely as young, and no catheter
Can differentiate between these, as E. coli will be lactose fermenter, and Pseudomonas will not
19 year old with fever, flank pain.
Urinalysis showed >50 white cells, 10 red cells, 3+ bacteria
E. coli in culture
Had amoxicillin with GP, which she failed to complete.
What is explanation for deteriorating?
Amoxicillin selected for resistance organism e.g E. coli
This pressure likely caused move of antimicrobial resistance plasmid ESBL
This provides resistance to penicillin and cephalosporins
What are treatment options for ESBL UTI?
Meropenem IV
Nitrofurantoin/ fosfomycin oral
Need to check sensitivities, as can be sensitive to other agents e.g tazocin, co-trimoaxozle, cipro, get
ESBL provides resistance to penicillin/ cephalosporins, but often confers resistance to multiple other antibiotics
What are features which indicate pyelonephritis over cystitis?
Cysitis - bladder
Pyelonephritis - kidney
Systemic symptoms - fever flank pain hypotension tachycardia
urinalysis - white blood cell casts
Why is it important to differentiate cystitis from pyelonephritis?
cystitis treatment duration is 3 days female, 7 days male
pyelonephritis is 7-14 days treatment
pyelonephritis will require imaging to assess for renal stone obstruction
What are virulence factors, which allow E. coli to infect urinary tract?
P fimbriae - adhesion, and resistance to phagocytosis
haemolysin - directly cytotoxic
aerobactin - siderophore which is molecule which scavenge iron, an essential nutrient for bacteria
What are reasons that a gonococcal vaccine cannot be produced?
Vaccines normally target exotoxins or cell surface component
Gonorrhoea does not produce conventional exotoxin
Gonorrhoea can re-arrange pilin genes, called antigenic variation. Which changes the pili expressed on surface
Chlamydia used detected via NAAT
What media can be used for culture?
McCoy cells
fluorescin stain can show intracellular chlamydia
What is life cycle of chlamydia?
infectious elementary body is endocytosed
bacteria develop into reticulate bodies, which are reproductive form
reticulate bodies then reproduce, and condense to form elementary bodies, which are released when cell lyses
What infections do different serovars of chlamydia trachomatis cause?
Chlamydia trachomatis A/ B/ C - trachoma
Chlamydia trachomatis D-K - genital chlamydia
Chlamydia trachomatis L1 -L 3 - LVG
Chlamydia psitacci - pneumonia
Chlamydia pneumoniae - pneumonia
16 years old presents with crampy abdo pain, vaginal bleeding, abnormal discharge.
Considering PID
Swabs for chlamydia/ gonorrhoea NAAT are negative.
Why does treatment still need to cover for these organisms?
Swabs are often endocervical, so cannot exclude upper genital infection e.g ovaries/ fallopian tubes
What are differential diagnoses for ulcerating genital lesions?
Painful -
HSV
LVG
Chancroid
Painless
Syphilis
Donovanosis
HSV2 is usual culprit of encephalitis
Why are cases of HSV1 encephalitis rising?
Unclear
Possibly higher rates of oral sex, leading to higher HSV1 transmission
Primary HSV1 genital infection may then lead to encephalitis
26 year old female with white genital discharge.
Wet mount prepared, which shows organism.
What is diagnosis?
What other genital infections can be detected by wet mount prep?
Trichomonas - NAAT testing now more commonly used, which does Chlamydia/ gonorrhoea as well
Candida - yeast and pseudohyphae will be seen
What are consequences of untreated trichomonas infection in pregnancy?
Preterm labor
Premature rupture of membranes
LBW baby
Why HPV types causes -
genital warts
cancer - cervical/ anal/ oropharyngeal
genital warts - 6/ 11
cervical cancer - 16/ 18 cause 70% of cancers
HPV causing cervical cancer
What classification systems are used to grade pre-malignant changes?
Bethesda system - cytological findings
Urine culture on chromogen plate suggests staph aureus. This is sub-cultured onto other plates to help identify what type of staph
What plate is useful?
Novobiocin disc
Sensitive - Staph aureus
Resistant - Staph saprophyticus (CoNS)
Patient with tape worm coming out of anus.
Worm is quite wide and flat.
What species of tape worm is this?
Diphyllobothrium latum
Latum is latin for broad or wide
Which part of tape worms contain eggs?
Scolex (head) attached to segments called proglottids
These rectangular proglottids contain eggs. They are broken off and passed in stool.
In lab can crush proglottid which release eggs, can be viewed microscopy
What is definitive host of Diphyllobothrium latum?
Fish tape worm - but humans are definitive host. Worm replicates in humans
uncooked white fish/ sushi are common sorke
What are common tape worms which infect humans?
Diphyllobothrium latum - fish
Taenia solium - pork. Causes cysticercosis
Taenia saginata - beef
Humans are definitive hosts for all 3. It is a naming convention irony, that they are named after the species which they use as intermediary host
E. coli
E. histolytica
E. moshkovskii
All appear similar microscopically. How can we distinguish species?
E. histolytica will have phagocytosed red cells.
Blood culture positive
Gram neg bacilli
Macconkey - non-pigmented colonies
H2S producing
Non-pigmented colonies on Macconkey suggests non-lactose fermenters
Patient with gastroenteritis - this would suggest non-typhoidal salmonella
Humans are natural host and reservoir for salmonella. But can be zoonosis from birds/ reptiles
Salmonella species have increasing resistance to fluoroquinolones
What is most common mechanism of resistance?
Mutation of binding site of DNA gyrase - gyrA gene
Ceftriaxone and azithromycin are other options for treatment
STEC producing E. coli can cause HUS.
What is pathophysiology which causes death in HUS?
5% mortality - usually children <5
Haemolysis - anaemia
Thrombocytopenia
Uraemia and raised creatinine
Shiga toxin bind to and damage endothelial cells of renal tubules
What are sources of E. coli infection?
uncooked beef is most common. It is common commensal/ pathogen in bovine
Run-off water from cattle, can affect crops. So leaf vegetables - lettuce, spinach, sprouts. Impossible to wash thoroughly before eating
Petting zoos are also common sources of outbreaks
Severe sepsis can cause DIC.
What is pathophysiology?
systemic activation of coagulation cascade in an unregulated manner
Causes intravascular deposition of fibrin - resulting in occlusive thrombi of microvasculature
Causes consumption of platelets and clotting factors - can lead to bleeding and bruising
infection can cause activation of cytokines. But non-infectious causes such as trauma, burns, malignancy can cause DIC
Neiserria meningitidis has lipopolysacchardie on outcer capsule, which can lead to DIC, and meningococal rash. Bacteria + antibody complex depositon also contributes to rash. DIC can cause also adrenal haemorrhage and Waterhouse-Friedrichsen syndrome
Filter feeders such as shellfish and oysters can harbour GI pathogens - as they ma filter raw sewage.
What are some examples?
HAV
Vibrio species
Cirrhosis patients are at greatly increased risk of infection with vibrio species e.g V. vulnifucus
Why is this?
Greatly reduced levels of complement - causing reduced chemotaxis and phagocytosis
Some bacteria have quorom sensing. What is this?
Different bacteria in population can have different gene expression.
One set of quorom sensing-regulated genes are expressed at low bacterial concentrations, and another at high bacterial concentrations
This means best genes are present, at correct time, for optimisation - symbiosis, virulence, motility, biofilm formation, antibiotic production
HBeAg appears shortly after HBsAg, and persists for 3-6 weeks before disappearing (before HBsAg disappears)
HBeAg is a marker of viral replciation.
What is significance of any mutations which affect HBeAg?
core/ pre-core promoter mutations render HBeAg negative, or reduce its expression.
These mutations are associated with higher liver disease, and higher rates of HCC
Treatment guidelines have lower threshold for treatment in these patients
Patient has been fully vaccinated against HBV.
They then acquire HBV infection, and hepatitis.
How can we explain this?
Vaccine used is a recombinant vaccine
- some people do not respond to vaccine, so we should measure anti-HBs levels
- mutation of S gene in HBsAg, can cause infection, but vaccine will not protect. This is termed a vaccine-escape mutant. It is very rare. Usually results in reduced transmissibility, so less-fit virus
