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
-------
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
Variant CJD
symptoms?
median survival and mean age of onset
cause?
diagnosis?
neuropathology?
psychiatric onset:
- dysphoria, anxiety, paranoia, hallucinations
then neurological:
- peripheral abnormal sensations
-ataxia
- myoclonus
- dementia
14 months, 26 years median onset
linked to mad cow disease, few cases linked to blood transfusion
MRI:
- positive pulvinar sign = high signal in posterior thalamus/putamen
EEG:
- non specifc slow waves
CSF markers not raised
Neurogenetics:
- almost everyone is MM at codon 129
Tonsil biopsy = 100% sensitive and specific
florid plaques in brain
Iatrogenic CJD causes?
symptoms?
1. human cadaveric growth hormone
2. corneal transplants
3. neurosurgical procedures
4. blood and blood products transfusions
progressive ataxia initially
dementia and myoclonus later stages
speed of progression depends on route of inocculation
Genetic prion disease
questions to ask?
symptoms
diagnosis
GSS, FFI, CJD
FH is important:
- dementia, MS, ataxia, psychiatric
GSS:
- slow progressive ataxia and dementia
- survival 2-10 years
FFI:
- untreatable insomnia, ataxia, dysautonmia (BP surges)
neurogenetics
CJD treatment?
1. myoclonus = clonazepam
research into antiprion antibodies, depleting prion protein
secretory diarrhea presentation?
organisms?
- no or low fever
- no wbc in stool
- cholera, ETEC, EPEC, EHEC, EAggEC
inflammatory diarrhea presentation?
organisms?
- fever
- wbc in stool - neutrophils
- campylobacter, shigella, non typhoidal salmonella, EIEC
Enteric fever diarrhea presentation?
organisms?
- fever
- wbc in stool - mononuclear cells
- typhoidal salmonella, enteropathogenic yersinia, brucella
s. aureus food poisoning
prominent vomiting and watery non-bloody diarrhea
self limiting
skin cells shedding into food
b cereus food poisoning
gram positive-rod spores
reheating rice
water non blooding diarrhea
can cause bacteremia
clostridium botulinum/ botulism
cause?
symptoms
treatment
canned or vaccumed packed foods/honey
blockage of ACh receptors -> paralysis
antitoxin
clostridium perfringens food poisoning
reheated food -> meat
superantigen
watery diarhea, cramps, vomiting
anaerobic infection!!!
c difficile
diarrhea
hospitalisation and antibiotics = risk
anaerobic infection!!!
listeria monocytogenes
symptoms?
sources?
treatment?
febrile gastroenteritis
b hemolytic bacteria with tumbling motility
unpasteurised dairy, refrigerated food
ampicillin
ecoli diarrhea
source
etec = travellers
EHEC = hemorrhagic
food/water contaminated with faeces
salmonella enteritidis presentation?
non bloody diarrhea, self limiting
poultry, eggs, meat
bacteremia and fever infrequent
salmonella typhi presentation?
typhoid fever
bacteremia
slow onset FEVER and CONSTIPATION
spleenomgaly, rose spots
anemia, leucopenia
positive blood cultures
ceftriaxone treatment
Shigella presentation?
dysentery
avoid antibiotics
vibrio cholera presentation and treatment
vibrio parahemolytics cause and treament
vibrio vulnificus presentation?
rice water stool
treat loss, electolyte and fluid replacement
raw or undercooked seafood, self limiting
cellulitis in shellfish handlers, risk of septicemia
campylobacter source?
presentations?
poultry, meat, unpasteurised milk
diarrhea -> GBS syndrome
Yersinia enterocolitica presentation?
enterocolitis, mesenteric adenitis
food contaminated with waste from domestic animals
abdominal symptoms +/- diarrhea -> always think could this be mycobacterium eg TB
entamoeba presentation?
dysentery, tenesmus, flatulence, liver abscess
metronidazole + paramomycin for luminal disease
Giardia presentation?
2 nuclei and flagella
malabsorption of protein and flat
stool microscopy - ova cysts and parasites
metronidazole
cryptospordium parvum
severe diarrhoea in immunocompromised
oocytes in stool
no treatment
Viruses that cause diarrhea?
norovirus - CAN CAUSE OUTBREAKS!! - big concern
rotavirus - Exposure can cause immunity
adenovirus
(polio, enteroviruses, hep A )
all forms of gasteroenteritis are notifiable
congenital toxoplamosis presentation
classic triad:
1. intracranial calcifications
2. hydrocephalus
3. chorioretinitis
+/- blueberry muffin rash
60% asymtomatic at birth but can develop -> deafness, low iq, microcephaly
*contrast to CMV which causes hearing loss and chorioretinitis but PERIVENTRICULAR calcifications and no hydrocephalus
congenital rubella presentation
Eyes: cataracts!!!; microphthalmia; glaucoma; retinopathy
Ears: deafness
Heart : PDA!!!; ASD/VSD ("Ruby red heart")
+/- blueberry muffin rash
name common organisms that cause neonatal infection
1. group b strep - meningitis, bacteremia, joint infection
2. E coli - bacteremia, meningitis, UTI
3. listeria monocytogenes
maternal sepsis risk factors
PROM/prem. Labour
Fever
Foetal distress
Meconium staining
Previous history
neonatal sepsis rfs
Birth asphyxia
Resp. distress
Low BP
Acidosis
Hypoglycaemia
Neutropenia
Rash
Hepatosplenomegaly
Jaundice
neonatal sepsis investigations?
Full blood count
C-reactive protein (CRP)
Blood culture
Deep ear swab
Lumbar puncture (CSF)
Surface swabs
Chest X-ray (full body)
neonatal sepsis treatment
Ventilation
Circulation
Nutrition
Antibiotics: e.g. benzylpenicillin & gentamicin
what is late onset sepsis?
features?
investigations?
treatment
after 48 -72 hours
Bradycardia
Apnoea
Poor feeding/bilious aspirates/ abdominal distension
Irritability
Convulsions
Jaundice
Respiratory distress
Increased CRP; sudden changes in WCC/platelets
Focal inflammation – e.g. Umbilicus; drip sites etc.
FBC
CRP
Blood culture(s)
Urine
ET secretions if ventilated
Swabs from any infected sites
1st line: cefotaxime & vancomycin
2nd line: meropenem
Learn CSF to diagnose type of meningitis - viral fungal bacterial
list the organisms that cause meningitis in children by age group
<3/12: N. meningitidis; S. pneumoniae; (H. influenzae (Hib) if unvaccinated); GBS; E. coli; Listeria sp.
3/12 - 5 years:N. meningitidis; S. pneumoniae; (Hib if unvaccinated)
>6 years: N. meningitidis; S. pneumoniae
common causes of respiratory infections in children
1. s pneumonia = most important bacterial cause
2. mycoplasma = >4 years old, treat with macrolide. cold aggluttinins (IgM Antibodies). neurological signs in 1% eg encephalitis
3. also consider whooping cough, tb
causes of UTI in children
managment?
E. coli = MOST COMMON
Other coliforms e.g. Proteus species, Klebsiella Enterococcus sp.
Coagulase negative Staphylococcus
Staph saprophyticus
treatment
renal tract imaging
antibiotics as prophylaxis
recurrent may be sign of immunodeficiency either congenital or acquired - HIV, SCID
Risk factors for fungal disease?
diagnostic tests?
3 targets of antifungals and types of drugs for each?
1. immunocompromised
2. inhaled steroids
3. malignancy, burns, complicated post ops, long lines -> invasive candida
4. diabetes -> mucormycosis
5. moisture, gentetics, CMI -> dermatophytes
MC&S, Bx- Histology, serology, PCR, imaging
cell membrane - polyene (eg ambisome, amphoceritin B ), Azoles
DNA/RNA synthesis - pyrimidine analogues (flucytosine)
cell wall - echinocandins
what are yeasts? give examples
single cell fungi, reproduce by budding
1. candida
2. cryptococcus
3. Histoplasma - dimorphic
what are moulds? give examples
multicellular hyphae fungi. grow by branching and extension
1. dermatophytes
2. aspergillus
3. agents of mucormycoses
what is the most common cause of fungal infections in humans?
what infections does it cause? treatments for each?
candida
1. oral thrush = topical nystatin
2. candida oesophagitis = oral fluconazole
3. vulvovaginitis = topical clotrimazole or oral fluconazole
4. cutaneous -> localised or generalised = topical clotrimazole
5. invasive candida infections
list types of invasive candida infections
candidemia
cns
endocarditis
bone and joint
urinary tract eg vulvovaginitis
intraabdominal
which animal is cryptococcus associated with?
rfs?
presentation?
diagnosis?
management
pigeons
immunodeficiency
c gatti -> meningitis in immunocopetent, space occupying lesions in brain and lung (sob, cough)
imaging eg brain
india ink staining of CSF
serum/CSF Ag
amphotericin b and flucytosin
then consolidation and maintenance with fluconazole
Aspergillosis
diagnosis?
management?
- can colonize preformed cavities and debilitated tissues eg tb cavity
imaging, sputum
looking for antibodies = precipitins
OR serology for galactomannan (polysaccharide)
voriconazole
ambisome
why might antifungals targeting cell wall not work in PCP?
pcp symptoms
it lacks ergosterol in cell wall
pneumnia -> fever cough sob
name some dermatophytes
tinea corporis
tinea cruris
tinea pedis
tinea capitis
pityriasis versicolor -> Malassezia furfur
amphotericin B key side effect?
nephrotoxicity
azoles key side effect?
abnormal LFTs
polyenes key side effect?
nephrotoxicity
pyrimidine analogues key side effect?
blood disorders
what is the most likely organism causing intracranial abscesses?
MRSA
Diagnosis of septic arthritis requirement?
> 50,000 White cells on synovial fluid analysis
negative culture does not exclude
most likely organism causing a prosthetic joint infection?
coagulase negative staphylococcus
adult onset stills disease
most common cause of lobar pneumonia?
strep penumoniae
CRB-65 score
50 year old man
LLL pneumonia
Hemoptysis
cavitation of CXR
patient not particularly unwell
what organism would you suspect?
Hemophilus influenzae
- gram negative coccobacillus
coxiella burnetti pneumonia typically caused by contact with?
domestic/farm animals
74 year old woman, penumonia, on antibiotics but not getting better. most likely diagnosis?
empyema
64 year old treated for lymph node TB
increasing SOB and cough
ground glass diffuse shadowing on CXR
Most likely organism?
pneumocysitis jirovecii
22 year old man. chemo for leukemia
prolonged neutropenia
ongoing fevers and raised inflammatory markers
what is the likely organism?
aspergillus fumigatus (patient immunosuppressed)
which antibiotics inhibit cell wall synthesis? give examples from each class
B-lactams = Penicillins, cephalosPorins, carbaPenems (carbapenems stable to ESBLs)
Glycopeptides = vancomycin and Teicoplanin
B lactams mechanism of action?
what are they inefective against?
inactivate transpeptidases/penicillin binding proteins which are involved in cell wall synthesis
only effective against rapidly dividing bacteria
ineffective for organisms without peptidoglycan cell wall - mycoplasma, chlamydia
function of clavulanic acid and tazobactam?
B-lactamase inhibitors. protect penicillins from enzymatic breakdown
name examples of cephalosporins from each generation. how do they change with generation
1st generation = cephalexin
2nd generation = cefuroxime
3rd = cefotaxime, ceftriaxone, ceftazidime
as generation increases, more gram negative cover and less gram positive
What bacteria are glycopeptides active against?
mechanism of glycopeptides action
gram+ve only - too large to penetrate gram negative cell walls
binds to peptide chain -> prevents formation of glycosidic bonds and peptide cross linkes
name antibiotic classes that inhibit protein synthesis
state their mechanisms of action.
aminoglycosides - gentamicin, amikacin, tobramycin - bind to 30s ribosomal subunit, prevent elongation of polypeptide chain
tetracylines - bind 30s subunit and prevent trna binding to ribosomal site. active against intracellular pathogens eg chlamydia, rickettsia, mycoplasma. may cause light-sensitive rash
macrolides(bind 50s subunit, interfere with translocation, stimulate dissociation of trna), lincosamides eg clindamycin, streptogramins eg synercid ( the MSL group)
Chloramphenicol - binds peptidyl transferase of 50s subunit. rarely used due to risk of aplastic anaemia and grey baby syndrome
Oxazolidinones eg linezolid - highly active against gram positives mostly, including MRSA and VRE. optic neuritis and thrombocytopenia risk!
name an antibiotic class that is ototoxic
aminoglycoside
name antibiotic clases that inhibit DNA synthesis
Quinolones - ciprofloxacin, levofloxacin, movifloxacin. act on DNA Gyrase
nitroimidazoles - metronidazole, tinidazole - active against anaerobes and protozoa
what antibiotic class inhits RNA synthesis?
Rifamycins - rifamipicin (inhibits dna dependent rna polymerase), rifabutin
State 2 cell membrane toxins used
Daptomycins - complex gram +ve eg MRSA
Colistin - gram -ves
state 2 antibiotics that inhibit folate synthesis
sulfonamides
diaminopyrimidines eg trimethoprim
describe mechanisms of resistance to antibiotics
1. modification/ inactivation of antibiotic = penicillin resistance, ESBL ecoli resistance to ceftriaxone
2. modification/replacement of target - MRSA Have a MecA gene making them resistant to flucloxacillin!! -> new PBPs with low affinity for B-lactams, strep pneumonia acquires multiple mutations in PBPs genes. fluclox was developed to not be broken down by beta lactamases
3.reduce antibiotic accumulation
- impared uptake
- increased efflux
4. bypass antibiotic sensitive step - eg in trimethprim and sulfonamides
avibactam mechanism of action?
inhibits ox-48 and most kpc enzymes
meropenem verobactam mechanism?
inhibit kpc enzymes
cefiderecol mechanism of action?
enters through ion channels
make notes for antimicrobial 2 lecture
Covid 19 treatment
Kaletra = lopinavir + ritonavir
hydroxychloroquine
Remdesivir
dexamethasone
host proteins in influenza infection
butrophilin a3 = inhibits influenza polymerase
ANP32 = host proteins - copted by influenza virus
Oral thrush treatment?
Topical nystatin
Oseophagitis treatment?
Oral fluconazole
Which organism is cryptococcus associated with ?
Pigeons ! = infects lungs and can disseminate into blood
C gattii = particular strain that can cause meningitis in immunocompetent patients
PCP cxr findings?
Diffuse ground glass changes
Microscopy
Pcr
Beta d glucan
Co trimoxazole to treat
Tinea cruris affects where?
Groin
Most common side effects with
1. Azoles
2. Polyenes
3. Echinocandins
4. Pyrimidine analogues
Learn what each antifungal targets!
Azoles = abnormal lfts
Polyenes = nephrotoxicity
Echinocandins = relatively safe
Pyrimidine analogues = blood disorders
fever in a returning traveller
dengue - transmitted by aedes mosquito
typhoid
malaria
