[CP]
Medicine
Microbiology referral framework:
History.
Dx.
Microbiology.
ABX/allergies.
Plan.
Infective endocarditis:
Take 3 sets of blood cultures at different times within a 24 hr period.
Echocardiogram to view valves.
Coagulase -ve Staph (CNS) is predominant cause of early-onset PVE. Viridans Strep (usual
cause of NATIVE valve IE) is predominant in late-onset infn.
For prosthetic valve endocarditis flucloxacillin (/vancomycin) + rifampicin + gentamicin.
CAUTI:
Clinical Dx – not microbiological Dx as nearly all CSUs will grow bacteria due to catheter
colonisation.
Sx – fever, suprapubic tenderness, altered mental status.
o If pt has loin pain or severity of Sx not in keeping with lower UTI treat as upper
UTI not CAUTI.
ESBL +ve E. coli is sensitive to nitrofurantoin but not trimethoprim.
o ESBLs are enzymes capable of breaking down most β-lactam ABX, making the
organism MDR.
o They are carried on plasmids which can spread from 1 bacteria to another.
Teicoplanin, vancomycin, linezolid are all effective against MRSA.
Trimethoprim, meropenem, ciprofloxacin are all active against ESBLs. Co-amoxiclav is not.
Typical serological response to hepatitis B:
In persistent hep B infn, HBsAg remains detectable for > 6 mo.
Persistence of HBsAg and HBeAg is aw high infectivity.
Detection of anti-HBc provides evidence of natural infn with hep B.
o Immunisation presence of anti-HBs alone.
Hepatitis B is more likely than hepatitis C to cause an acute hepatitis. Hepatitis C accounts for 10 –
15% of acute viral hepatitis. Both are BBVs and transmitted pareneterally.
, [CP]
Primary Care
Flora of the urinary tract:
Urine and the UT are normally sterile.
The anterior urethra may be colonised by coagulase -ve Staph, Strep, enteric flora
(enterococci + coliforms).
UTI PATHOGENESIS – enteric flora ascends the urethra and causes infn.
Bacterial classification and diseases:
UTI – investigations:
DIPSTICK:
o Nitrites – prod of bacterial nitrate reduction. Not all bacteria prod nitrate reductase
e.g. enterococci, GBS, Staph, PAER.
o Leucocyte – leucocyte esterase is prod by neuts. May reflect pyuria aw UTI, but also
+ve in chlamydia, urethritis, TB, bladder tumours, viral infn, nephrolithiasis, foreign
bodies, corticosteroid use.
o Haematuria – can occur in stones, malignancy, vasculitis, GN. +ve dipstick for
blood in absence of RBCs via microscopy = Mburia/Hburia (not true haematuria).
o Proteinuria – common.
URINE CULTURE:
o MSU – often WCC > 105 bacteria. Infn caused by gram +ve organisms, fastidious
organisms and fungi rarely reach > 104.
o CSU – almost always have ↑ WCC so not diagnostic.
RENAL USS – to look for pyelonephritis, hydronephrosis, renal abscess.
PR EXAM – if prostatitis suspected.
UTI – management:
PO – trimethoprim, nitrofurantoin, pivmecillinam, Fosfomycin, amoxicillin, co-amoxiclav,
cefalexin, ciprofloxacin.
IV – gentamicin, aztreonam, cefuroxime, piperacillin-tazobactam, temocillin.
Asymptomatic bacteriuria:
Presence of bacteria in urine of an asymptomatic patient.
RFs – ↑ age, sexually active F, DM.
Bacteria isolate are similar to those causing UTIs (E. coli, Klebsiella, Proteus, Enterobacter).
ONLY treat patients at risk of developing complications i.e. pregnant women, those
undergoing urological procedures, those in the first 3 mo post-renal transplant.
Colonisation – presence of bacteria on body sites that are exposed to the enviornemtn which do
not cause infn.
Infection – presence of microorgansims causing damage to body tissues (usually occur in presence
of acute inflammation).
Upper UTI – organisms:
GRAM -ve – most commonly Enterobacteriaceae (E. coli, Proteus, Klebsiella); P. aeruginosa
if catheter present/abnormal renal tract.
Medicine
Microbiology referral framework:
History.
Dx.
Microbiology.
ABX/allergies.
Plan.
Infective endocarditis:
Take 3 sets of blood cultures at different times within a 24 hr period.
Echocardiogram to view valves.
Coagulase -ve Staph (CNS) is predominant cause of early-onset PVE. Viridans Strep (usual
cause of NATIVE valve IE) is predominant in late-onset infn.
For prosthetic valve endocarditis flucloxacillin (/vancomycin) + rifampicin + gentamicin.
CAUTI:
Clinical Dx – not microbiological Dx as nearly all CSUs will grow bacteria due to catheter
colonisation.
Sx – fever, suprapubic tenderness, altered mental status.
o If pt has loin pain or severity of Sx not in keeping with lower UTI treat as upper
UTI not CAUTI.
ESBL +ve E. coli is sensitive to nitrofurantoin but not trimethoprim.
o ESBLs are enzymes capable of breaking down most β-lactam ABX, making the
organism MDR.
o They are carried on plasmids which can spread from 1 bacteria to another.
Teicoplanin, vancomycin, linezolid are all effective against MRSA.
Trimethoprim, meropenem, ciprofloxacin are all active against ESBLs. Co-amoxiclav is not.
Typical serological response to hepatitis B:
In persistent hep B infn, HBsAg remains detectable for > 6 mo.
Persistence of HBsAg and HBeAg is aw high infectivity.
Detection of anti-HBc provides evidence of natural infn with hep B.
o Immunisation presence of anti-HBs alone.
Hepatitis B is more likely than hepatitis C to cause an acute hepatitis. Hepatitis C accounts for 10 –
15% of acute viral hepatitis. Both are BBVs and transmitted pareneterally.
, [CP]
Primary Care
Flora of the urinary tract:
Urine and the UT are normally sterile.
The anterior urethra may be colonised by coagulase -ve Staph, Strep, enteric flora
(enterococci + coliforms).
UTI PATHOGENESIS – enteric flora ascends the urethra and causes infn.
Bacterial classification and diseases:
UTI – investigations:
DIPSTICK:
o Nitrites – prod of bacterial nitrate reduction. Not all bacteria prod nitrate reductase
e.g. enterococci, GBS, Staph, PAER.
o Leucocyte – leucocyte esterase is prod by neuts. May reflect pyuria aw UTI, but also
+ve in chlamydia, urethritis, TB, bladder tumours, viral infn, nephrolithiasis, foreign
bodies, corticosteroid use.
o Haematuria – can occur in stones, malignancy, vasculitis, GN. +ve dipstick for
blood in absence of RBCs via microscopy = Mburia/Hburia (not true haematuria).
o Proteinuria – common.
URINE CULTURE:
o MSU – often WCC > 105 bacteria. Infn caused by gram +ve organisms, fastidious
organisms and fungi rarely reach > 104.
o CSU – almost always have ↑ WCC so not diagnostic.
RENAL USS – to look for pyelonephritis, hydronephrosis, renal abscess.
PR EXAM – if prostatitis suspected.
UTI – management:
PO – trimethoprim, nitrofurantoin, pivmecillinam, Fosfomycin, amoxicillin, co-amoxiclav,
cefalexin, ciprofloxacin.
IV – gentamicin, aztreonam, cefuroxime, piperacillin-tazobactam, temocillin.
Asymptomatic bacteriuria:
Presence of bacteria in urine of an asymptomatic patient.
RFs – ↑ age, sexually active F, DM.
Bacteria isolate are similar to those causing UTIs (E. coli, Klebsiella, Proteus, Enterobacter).
ONLY treat patients at risk of developing complications i.e. pregnant women, those
undergoing urological procedures, those in the first 3 mo post-renal transplant.
Colonisation – presence of bacteria on body sites that are exposed to the enviornemtn which do
not cause infn.
Infection – presence of microorgansims causing damage to body tissues (usually occur in presence
of acute inflammation).
Upper UTI – organisms:
GRAM -ve – most commonly Enterobacteriaceae (E. coli, Proteus, Klebsiella); P. aeruginosa
if catheter present/abnormal renal tract.
