Microbiology Flashcards
Meningitis
Acute - key = Neisseria meningitidis, Strep pneumonia Hemophilia influenzae. Others - listeria, group B strep, ecoli
chronic - CT here will show changes (thickening of dura)
aseptic - enterovirus - cocksackie group B, echovirus
Mortality - 10%
Morbidity - 5, deafness most common
Encephalitis
Rabies virus, arbovirus eg West Nile
Amoeba - Naegleria fowleri
Bacteria - listeria
Trypansoma species
Prions
Toxoplasmosis
Brain abscess
Otitis media, mastoiditis etc
Staph etc
Spinal
CSF studies, how to Interpret results
Listeria meningitis management?
Viral hepatitis A B C D E
Jaundice dark urine , pale stools, pruritus
Check what antibodies/ surface markers mean
HbsAg = surface antigen most important. Positive means current infection
HbcIgM = recent infection
AntiHbc = exposure to HbV, could be past or present
AntiHbs = surface antibody = immunity due to vaccination or cleared infection
Which immunoglobulin class shows recent infection?
IgM
IgG = past/ chronic
Insert table interpreting hep B findings
Hep B medications
Nucleoside/tide analogues
Entecavir, tenofovir
If treatment history is unknown , what assay will help establish previous patients HBV status
HBV DNA viral load
Why are genotypes 1 and 2 of hep B important?
30% mortality in pregnant women
Chronic infection of hep e only happens in immunocompromised
Hep D requires infection with hep what to enter?
Hep B
Diagnosing pyrexia of unknown origin (PUO)]
History taking?
examination
investigation
definition = Fever >38.3 lasting for at least 3 weeks
1. B symptoms, localising symptoms
2. Medications - doses and initiation date
3. Contact history, pets/animal exposures
4. injecting drug use, sexual history
5. foreign travel
physical including fundoscopy (e.g roth spot endocarditis), look at spine
PET scan, Echo, brucella serology e.g patient from lebanon, HIV test for all patients, must test malaria if travel in last 2 days
if BP is 75/50 -> start Antibiotics immediately!!!!, this is sepsis and not PUO.
Infective causes of PUO
Inflammatory causes of PUO
SLE
rheumatoid arthritis
sjogrens syndromes
vasculitis syndromes
Malignant causes of PUO
lymphoma - especially non-hodgkins
leukaemia
renal cell carcinoma
Miscellaneous causes of PUO
endocrine - thyroiditis, addisons disease
TFTs screening
4 urgent causes of PUO
1. infective endocarditis
2. disseminated TB
3. central nervous system TB
4. Giant cell/ temporal arteritis
specific zoonoses
- farm/wild animals - UK or tropical
- companion animals - UK or tropical
managing patients with zoonoses
classic zoonoses
- campylobacter - chicken - diarrhoea - stool pcr for diagnosis - self resolving
- salmonella - chicken
- bartonella henslae - cats- bacilliary angiomatosis if immunosuppressed
- cats - toxoplasmosis
- brucellosis - unpasteurised milk from cattle/goat - fever, back pain, night sweats/weight loss - can present like TB. psoas abscess. psoas pus culture important
- coxiella burnetii - goat and sheep feces/milk, is aerosolised. learn presentation
- rabies - dogs, bats, cats
- rat bite fever -athralgia, fever
- hantavirus - rodents/rates - pulmonary-renal syndrome
- viral hemorrhagic fever - ebola, marburg, lassa, CCHF
opportunistic viral infections
51 year old with recent HSCT is unwell with ALT=800, what is the important test to do?
serology tests e.g EBV, hepB are not useful in immunosuppressed.
HEV PCR is useful
which type of immunosuppression carries the greatest relative risk of developing a viral infection?
allogenic stem cell transplant
EBV
in tansplant patients, you worry about lymphoma (post-transplant lymphoproliferative disease)
Rituximab treatment
CMV
HIV/AIDS
- retinitis
- polyradiculopathy
- pneumonitis
- GI tract
inclusion bodies seen
Ganciclovir
JC virus
polyomavirus
progressive multifocal leukoencephalopathy - personality change, motor deficit, cognitive dysfunction
- demyleination of white matter -> MRI
BK virus
polyomavirus
cystits post SCT
Nephropathy post renal transplant
Hepatitis B
tenofovir
Herpes simples 1,2
immunoglobulins given to bone marrow transplant patients
varicella zoster
chicken pox -purpura fulminans, hepatitis, encephalitis, pneumonitis
shingles - reactivation
SOT vs HSCT
CMV
SOT CMV concern = positive donor and negative recipient. give prophylaxis ganciclovir (can cause bone marrow suppression)
HSCT CMV concern = positive recipient and negative donor
Influenza A and B treatment in immunosuppresed
oseltamivir
the natural reservoir of influenza A virus is?
Ducks
influenza
hemaglutinn
neuraminidase
PB2E627K virus
antigenic shift - alone is not sufficient to cause a pandemic. you need antigenic shift + hemaglutinn adaptation (to allow transmission)
influenza entry to human is also pH dependent
influenza drugs are used separately and not together - neuraminidase inhibitors
The influenza vaccine given to those at greater risk of complications from flu in the UK is
inactivated virus
the live attenuated is given instead to children, not adults
*children are the key flu spreaders
hemaglutinnin has been the molecule used for vaccines
most likely origin of SARS COV2?
bats
Treatment for Covid
dexamethasone
monoclonal antibodies - Sotrovimab, remdesivir etcmRNA vaccines encoding stabilized spike - omicron variant less well controlled by this
antibiotics that inhibit cell wall syntheisis
beta lactam antibiotics eg penicillins, cephalosporins, carbapenems(carbapenems stable to ESBL enymes) - ineffective against bacteria that lack peptidoglycan cell walls eg mycoplasma, chlamydia. only kill bacteria actively dividing - may be ineffective against abscess, biofilm
glycopeptides - vancomycin, teicoplanin - used for MRSA infections
antibiotics that inhibit protein synthesis
Aminoglycosides (e.g. gentamicin, amikacin,tobramycin)
Tetracyclines
Macrolides (e.g. erythromycin) / Lincosamides (clindamycin) / Streptogramins (Synercid) – The MSL group
Chloramphenicol
Oxazolidinones (e.g. Linezolid)
finish antimicrobials notes
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bacteria that cause TB
m tuberculosis
m bovis
m africanum
m microti
m caneti
(m avium complex does not cause TB)
not all AFB is TB!
what percentage of world population has latent TB?
post latent infection, what is lifetime risk for active TB?
1/4 to 1/3
10%
HSV in pregnancy and neonates
neonates - SEM -> SEM + CNS -> disseminated
Maternal varicella and congenital VZV
treat maternal infection with oral acyclovir
entervoviruses in pregnancy and neonates
most commonly cocksackie
rash, hand foot and mouth disease, encephalitis, myocarditis
neonates are at higher risk of myocarditis, encephalitis, meningitis
Rubella in pregnancy, congenital, neonates
rash that spreads from head down to trunk
congenital rubella:
cataracts, hearing loss, hepatospleenomegaly
Measles in pregnancy
conjuctivitis, rash from head to trunk, koplik spots
SSPE risk in neonates
Parvovirus B19
slapped cheek, polyarthropathy, aplastic crisis
fetal hydrops
CMV
maculopapular rash, infectious mono
congenital - microcephaly, retinitis, IUGR,
zika virus
send a serum and save and alert obstetric team if 4 week pregnant with recent travel to antigua and worried about zika if NO symptoms. -> if symptoms do serum and urine sample
Hep B, HIV in pregnancy
pregnant woman presents with a rash, what do you do?
gestation
date of onset, clinical features
past history of infection/antibody testing
past immunisation testing
tests:
antibody
blood samples
pcr
HIV in children
describe certain presentations
how to prevent
molluscum contagiosum
tb of spine
rashes
HIV encephalopathy - basal ganglia calcification, cortex atrophy
CMV - retinitis - blindness
First born twin is more at risk than second twin -> sits in birth canal and dilates it
16% excess risk of HIV with breastfeeding in Nairobi study - balance against increased rissk from formula feeding only in certain places in world
triple therapy for pregnant women, infant should get prophylaxis for 6 weeks, uninfected infants should be exclusively BF for 6 months
what is prion disease?
what gene is prion protein found on? what polymophism predisposes to disease?
presentation?
an infectious protein
chromosme 20 - condon 129 MM polymorphism predisposes to disease (3 polymoprhisms MM, MV, VV)
Rapid neurodegeneration (cjd maximum survival 6 months), spongiform enceophalopathies
paresethesia
unseteadiness
jerky tremor
state the different types of prion disease
1. Sporadic - CJD - 80%
2. Acquired <5%
- Kuru - papua new guinea, cannibalisms. ataxia & myocolonus. dementia late or absent
- Variant CJD - mad cow disease
- Iatrogenic CJD - GH, blood, surgery
3. Genetic 15%
- PRNP mutations eg Gerstmann-Straussler-Sheinker Syndrome, Familial fatal insomnia
what is the most common form of prion disease?
symptoms?
median survival and mean age of onset
cause?
diagnosis?
neuropathology?
Sporadic CJD
rapid dementia with:
- myoclonus!!
- cortical blindness - problem with occipital cortex, optic nerve normal
- akinetic mutism
- LMN signs
<6 months, 65 years
cause is unclear - may be environmental exposure, PRNP mutation etc
EEG:
periodic triphasic complexes - non specific, not always present
MRI:
- increased signal in basal ganglia, cortex
CSF:
- elevated markers of rapid neurodegeneration; 14-3-3 protein, S100
neurogenetics to rule out mutation
tonsillar biopsy NOT useful - only useful in variant CJD
spongiform vacuolation, Prp amyloid plaques
- Alzheimers
- vascular dementia
- CNS neoplasm
- Cerebral vasculitis
- Paraneoplastic syndrome