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Microbiology Flashcards

1
Q

Choice of correct antimicrobial depends on what?

A 
CHAOS
Choice
Host characteristics
Antimicrobial susceptibilities of the 
Organism itself and also the
Site of infection
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2
Q

General rules for choice of antimicrobial drug

A 
Narrow spectrum if possible
Use bactericidal drugs if poss.
Ideally on bacterial dx but otherwise 'best guess'
Consider local sensitivities
Patient characteristics
Cost

Consider pharmacokinetics, route of administration and dosage

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3
Q

Preliminary identification of infecting organism

A

1) Gram stain
- CSF, joint aspirate, pus
2) Rapid antigen detection
- Immunofluorescence, PCR

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4
Q

Which route for delivery of antimicrobial

A

i.v. : serious or deep seated infection
p.o. :Usually easy but avoid if poor GI function or vomiting
- diff classes of antimicrobials have diff bioavailabilities
i.m. : Not an opotion for long term use. Avoid if bleeding tendency or irritant
Topical: Limited application and may cause local sensitisation

i.v. to p.o. switch recommended in hospital for most infections if patient has stabilised after 48hours i.v. therapy

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5
Q

Adverse effects of aminiglycosides

A

Ottotoxicity and nephrotoxicity

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6
Q

Type 1 antimicrobials

+ 2 examples

A

Concentration dependent killing

Aminoglycosides
Fluoroquinolones

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7
Q

Type 2 antimicrobials

+ examples

A

Time dependent killings + minimal persistent side effects

Penicillins
Carbapenems
Cephalasporins
Linezoid
Erthromycin
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8
Q

Type 3 antimicrobials

A

Time-dependent killing and moderate to prolonged persistent effects

Vancomycin
Azithryomycin
Tetracyclines

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9
Q

Recommended length of antimicrobial therapy for N. meningitides meningitis

A

7 days

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10
Q

Recommended length of antimicrobial therapy for simple cystitis (in women)

A

3 days

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11
Q

Recommended length of antimicrobial therapy for acute osteomyelitis (adult)

A

6 weeks

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12
Q

Recommended length of antimicrobial therapy for bacterial endocarditis

A

4-6 weeks

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13
Q

Recommended length of antimicrobial therapy for Group A streptococcal pharyngitis

A

10 days

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14
Q

Skin infections
Common causative organisms

Antimicrobial choice

A

S. aureus
Beta-haemolytic Streptococci

Flucloxacillin (unless penicillin allergy or MRSA)

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15
Q

iGAS Tx

A

Aggressive and early debridement
Antibiotics adjunctive use of protein synthesis inhibitors esp. clindamycin (good skin and soft tissue penetration
Use of IVIg

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16
Q

What is the eagle effect

A

Eagle effect describes a phenomenon in which bacteria or fungi exposed to concentrations of antibiotic higher than an optimal bactericidal concentration (OBC) have paradoxically improved levels of survival

Applies to beta lactams

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17
Q

Recommended antimicrobial therapy for pharyngitis

A

Benzyl penicillin x10days

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18
Q

Recommended antimicrobial therapy for community acquired pneumonia (mild)

A

Amoxicillin

or
Erythromycin/clarithromycin

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19
Q

Recommended antimicrobial therapy for community acquired pneumonia (moderate - severe)

A

Co-amoxiclav
&
Clarithromycin

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20
Q

Recommended antimicrobial therapy for hospital acquired respiratory tract infections

A

1st line: Ciprofloxacin + Vancomycin

ITU/2nd line: Piptazobactam + Vancomycin
Psuedomonas: Tazacoin or Cirprofloxacin + Gentamicin

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21
Q

Recommended antimicrobial therapy for bacterial meningitis

A

Ceftriaxone (+/- amoxicillin if Listeria likely)

Baby <3 months: Cefatoxamine PLUS amoxicillin (to cover for listeriosis)
- ceftriaxone not used in neonates as displaces bilirubin from albumin and can cause biliary sludging

Neisseria meningitidis: Benzylpenicillin (high dose) or Ceftriaxone/Cefotaxime

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22
Q

Main pathogens in bacterial meningitis

A

N. meningitidis
S. pneumoniae
+/- Listeria in v elderly/young/immunocompromised

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23
Q

Recommended antimicrobial therapy for simple cystitis (community)

A

Trimethopron x 3 days

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24
Q

Recommended antimicrobial therapy for hospital acquired UTI

A

Cephalexin or Augmentin

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25
Q

Recommended antimicrobial therapy for infected urinary catheter

A

Change under gentamicin cover

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26
Q

Recommended antimicrobial therapy for C. difficile colitis

A

STOP offending antibiotic (usually cephalosporin)
p.o. metronidazole 10-14days
If above fails, use vancomycin

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27
Q

Routes of entry for CNS infection

A

1) Haematogenous
2) Direct implantation
3) Local extension
4) PNS into CNS

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28
Q

Most frequent route of entry for CNS infection

A

Haematogenous

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29
Q

Meningitis
Region affected
Signs and symptoms
Causative agents

A

Meninges
Fever, headache, stiff neck, some brain function disturbance
Neisseria meningitidis, Strep pneumonia, Haemophilus influenza, Listeria, group B strep, E. coli

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30
Q

Encephalitis
Region affected
Signs and symptoms
Causative agents

A

Brain
Disturbance of brain function
Rabies virus, arboviruses, Prions, Amoeba, Trypansoma species

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31
Q

Myelitis
Region affected
Signs and symptoms
Causative agents

A

Spinal cord
Disturbance of nerve transmission
Poliovirus

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32
Q

Neurotoxin
Region affected
Signs and symptoms
Causative agents

A

CNS and PNS
Paralysis, rigid (tetanus) or flaccid (botulism)

Clostridium tetani, clostridium botulism

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33
Q

What processes produce septicaemia

A

Capillary leak
Coagulopathy
Metabolic derangement
Myocardial failure… multi-organ failure

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34
Q

Aseptic meningitis symptoms

Causative organisms

A

headache, stiff neck, photophobia. SELF-LIMITED and resolves in 1-2 weeks
No inflammatory markers
Most freq children <1

Coxackievirus group B and echovirus - responsible for 80-90%

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35
Q

Encephalitis transmission

A

Person to person
OR
Through vectors (mosquitoes, lice, ticks)

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36
Q

Encephalitis causative organisms

A

Viral - west nile virus etc.

Bacterial - listeria monoctogenes

Amboeic - naegleria fowleri, acanthamoeba species and Balamunthia mandrillaris

Toxoplasmosis

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37
Q

Brain abscess - where does the infection come from

Causative organisms

A

Mainly local extension: Ottitis media. mastoiditis/paranasal sinuses
Rarely: endocartitis, haematogenoisly

Streptococci, staphylocicci
Gram -ve organisms (neonates particularly)
Mycobacterium tuberculosis
Fungi
Parasites
Actinomyces
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38
Q

Spinal infections pathogenesis

Consequence if untreated

A

Direct open spinal trauma, from infections in adjacent structures, from haematogenous spread of bacteria to a vertebra

Permanent neurological deficits, significant spinal deformity, or death

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39
Q

Spinal infections risk factors

A 
Advanced age
Iv drug use
Long term steroids
DM
Organ transplantation
Malnutrition
Cancer
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40
Q

Difference between gram +ve and gram -ve bacteria

A

Gram+ve - thick peptidoglycan cell wall
- Stain purple

Gram-ve - outer membrane and thinner peptidoglycan layer
- Stain pink

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41
Q

Beta-lactams
Mechanism

Affective against which types of bacteria

Ineffective against which types of bacteria

A

Inactivate enzymes involved in terminal stages of cell wall synthesis (transpeptidases - penicillin binding proteins)
- so daughter cells have no peptide cross links and defective/weak peptidoglycan cell walls

Active against rapidly dividing bacteria

Ineffective against bacteria without peptidoglycan cell wall e.g. mycoplasma or chlamydia

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42
Q

Examples of beta-lactams

A

Penicillin
Cephalosporins
Carbapenems

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43
Q

Penicillin type of antibiotic

Organisms used against

Broken down by

A

beta lactam

gram +ve
Streptococci, Clostridia

Broken down by enzyme (beta lactamase) produced by S. aureus

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44
Q

Amoxicillin type of antibiotic

Organisms used against

Broken down by

A

Beta lactam

Broad spectrum penicillin - extends cover to Enterococci and some Gram -ve (esp E.coli)

Broken down by beta lactamases produced by S.aureus and many gram -ve organisms

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45
Q

Flucloxacillin type of antibiotic

Organisms used against

A

Beta lactam - similar to penicillin but less stable

Stable to beta-lactamases produced by S. aureus
Mainstay tx for S. aureus

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46
Q

What are clavulanic acid and tazobactam?

A

Beta-lactamase inhibitors. Prevent penicillins from enzymatic breakdown and increase coverage to include S. aureus, Gram negatives and anaerobes

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47
Q

What is Augmentin/co-amoxiclav?

A

Amoxicillin + clavulanic acid

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48
Q

What is tazocin?

A

Piperacillin + tazobactan

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49
Q

Piperacillin type of antibiotic

Organisms used against

Broken down by

A

Similar to amoxicillin

Extends cover to psudomonas and otehr non-enteric gram -ve

Broken down by beta lactamase produced by S.aureus and many gram -ver

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50
Q

What are cephalopsorins

Generations and what does that mean for their activity

A

Beta-lactam antibiotics - stable to most of beta-lactamases so not broken down

  1. Cephalexin
  2. Cefuroxime
  3. Cefotaxime, ceftriaxone, ceftazidime

Later generations v active against gram -ves

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51
Q

What is cefuroxime?

A

2nd gen Cephalosporin
Stable to many beta-lactamases produced by gram -ve’s

Similar cover to co-amoxiclav but less active against anaerobes

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52
Q

What is ceftriaxone

Active against

Limitation

A

3rd gen cephalosporin

V active against pneumococci, N meningitidis, Haemophilus (mainstay of tx for meningitis)

Associated with C.difficile infection (limits use)

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53
Q

What is ceftazidime

Use

A

3rd gen cephalosporin
V active against gram -ve, v little against +ve

Anti-psuedomonas

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54
Q

What is the limit of cephalosporins

A

Extended specrtum beta-lactamase (ESBL) producing organisms are resistant to all cephalosporins

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55
Q

What are carbapenems?

Examples

Uses

A

Beta lactam antibiotics - stable to ESBL enzymes

Meropenem, Imipenem, Ertapenem

Alternative to penicillins and cephalosporins for ESBLs
- last line

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56
Q

Key features of beta-lactams

A

Relatively non-toxic
Renally excreted - so reduce dose if renal impairment
Short half life - multiple doses in a day
Will not cross BBB (can cross inflamed meninges)
Cross allergenic (penicillins approx 10% cross reactivity with cephalosporins or carbapenems - don’t give if anaphylactic)

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57
Q

What are glycopeptides?

MOA

Active against which organisms?

Examples

Side effect

A

Inhibitors of cell wall synthesis
- Active against only gram +ve organisms

  • Stop glycosidic bons and peptide bonds by binding to peptide chain and stopping enzyme from acting
  • Weakened cell wall and daughter cells will lyse during replication

Vancomycin
Teicoplanin

Nephrotoxic - monitor drug levels and adjust dose

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58
Q

Antimicrobial inhibitors of protein synthesis

A

1) Aminoglycosides
2) Tetracyclines
3) Macrolides
4) Chloramphenicol
5) Oxazolidinones

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59
Q

Aminoglycosides mechanism of action

Dosage

A

Concentration dependent bacterial action

  • prevent elongation of the polypeptide chain
  • cause misreading of the codons along the mRNA

1 big dose per day

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60
Q

Aminoglycosides uses

Side effects

Inhibited by?

A

With tazocin for severe pseudomonas
With amoxicillin for endocarditis

No activity against anaerobes

Ototoxic and nephrotoxic

Low pH (e.g. abscess needs draining)

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61
Q

Tetracyclines limitations

A

Widespread resistance limits use

NOT for children or pregnant women - teratogenic - deposit in growing bones

Light sensitive rash - wear sun cream

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62
Q

Tetracylines mechanism of action and uses

A

Reversibly bind to the ribosomal 30s subunit. Prevent binding of aminoacyl tRNA to the ribosomal acceptor site, so inhibiting protein synthesis

Broad spectrum activity against intraceullar pathogens and ones that don’t have a cell wall (chlamydia, rickettsiea and mycoplasma) + most conventional bacteria and MRSA

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63
Q

Macrolides mechanism of action and uses

Examples

A

Binds to 50s subunit of ribosomes. Interferes with translocation.

Minimal activity against gram -ve bacteria
Useful for mild Staphylococcus or Strep in penicillin allergic patients.
+ Campylobacter and Legionella
Used for community acquired pneumonoa

Azithromycin, clarithromycin

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64
Q

Chloramphenicol mechanism of action

USES

A

Binds to 50s ribosomal subunit

V broad antibacterial activity - may have use in MDR bacteria
- used in anaphylactic penicillin activity for meningitis

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65
Q

Chloramphenical limited to use in..

because..

A

Eye preparations

Risk of aplastic anaemia + grey baby syndrome in neonaes

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66
Q

Oxalidinones
Example

Mechanism of action

Uses

Limitations

A

Linezolid

Binds to 23s component of 50s subunit

Highly active against gram +ve organisms, inclusing MRSA and VRE
(Not against -ve)

Neurotoxic - don’t use > 4 weeks
Optic neuritis
Thrombocytopenia

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67
Q

Oxalidinones limitations

A

Neurotoxic - don’t use > 4 weeks
Optic neuritis
Thrombocytopenia

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68
Q

Mechanisms of antimicrobial resistance

A

1) vBypass antibiotic sensitive step in pathway
2) Enzyme mediated modification/inactivation of the antibiotic
3) Reduced antibiotic Accumulation
4) Modification/replacement of Target

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69
Q

Mechanism of resistance to beta lactams

A

1) Inactivation
2) Altered targets - MRSA + strep pneumoniae
3) Reduced accumulation

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70
Q

Reportable GI infections

A 
Campylobacter
Salmonella
Shigella
E. Coli 0157
Listeria
Norovirus
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71
Q

Secretory diarrhoea

Causative organisms

A

No fever or low grade. No WBC in stool sample

  • Vibrio cholera
  • ETEC
  • EPEC
  • EHEC
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72
Q

Inflammatory diarrhoea

Causative organisms

A

Fever, WBC in stool (neutrophilia)

  • Campylobacter jejunia
  • Shigella
  • Non typhoidal Salmonella serotypes
  • EJEC
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73
Q

Enteric fever

Causative organisms

A

Fever, WBC in stool sample (mononucleic cells)

  • Typhoidal salmonella serotypes
  • Eneteropathogenic
  • Brucella
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74
Q

Mechanism of secretory diarrhoea-toxin production (cholera toxin)

A

cAMP opens Cl channel at apical membrane of enterocytes –> efflux of Cl to the lumen; loss of H20 and electrolytes

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75
Q

Mechanism of secretory diarrhoea-toxin production (superantigens)

A

Superantigens bind directly to T-cell receptors and MHC molecules
OUTSIDE the peptide binding site
–> massive cytokine production by CD4 cells i.e systemic toxicity and suppression of adaptive response

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76
Q

S. aureus appearance on agar

Gram stain

A

Yellow colonies

+ve coccus, clusters

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77
Q

S. aureus food poisoning presentation

Spread

Tx

A

Enterotoxin in GI tract - releasing IL-1 and Il2
- prominent vomitting and watery non-bloody diarrhoea

Skin lesions on food handlers

Self limiting

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78
Q

Bacillus cereus food poisoning
Gram staining

Toxins

Caused by which food

A

Gram-positive motile, spore-forming, rod-shaped

Heat stabile emetic toxin
Heat labile diarrhoeal toxin

Reheated rice

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79
Q

Bacillius cereus food poisoning presentation

Tx

A

Watery non bloody diarrhoea
Rare cause of bacteremia in vulnerable
Can cause cerebral abscesses

Self limited

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80
Q

Clostridia GI infection
Gram staining

Types (not C.diff)

A

Large anaerobic, gram-positive, motile rods.

1) Clostridium botulinum: botulism
Canned/vacuum packed food
Ingestion of preformed toxin
Blocks ACh release from peripheral nerve synapses - paralysing
Tx : antitoxin

2) Clostridia perfringens: food poisoning
Reheated food (meat)
Normal flora of colon but not small bowel where the enterotoxin acts (superantigens)
Incubation 8-16hrs
Watery diarrhoea, cramps, little vomiting lasting 24

  • Perfringens is a gram positive bacillus that produces alpha toxin causing gas gangrene in infected wounds
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81
Q

Pseudomembranous colitis caused by

Related to what

Treatment

A

C. difficile

Antibiotic related (any but mainly cephalosporins)

PO Metronidazole, vancomycin, stop antibiotics where possible

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82
Q

Listeria monocytogenes

Source

Presentation

At risk groups

Treatment

A

Gram +ve, nonspore-forming, motile, facultatively anaerobic, rod - beta haemolytic

Refrigerated food i.e. dairy

Watery diarrhoea, cramps, headache, fever, little vom

Perinatal, immunocompromised

Ampicillin

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83
Q

E. coli gram stain

Source

Tx

Enterotoxins action

A

Gram -ve rod

Food/water contaminated with human faeces

Avoid antibiotics

Heat labile stimulates adenyl cyclase and cAMP
Heat stabile stimulates guanylate cyclase

Act on jejenum, ileum not colon

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84
Q

Types of E.coli and characteristics

A

ETEC: toxigenic - main cause of travellers diarrhoea
EPEC: pathogenic - infantile diarrheoa
EIEC: invasive, dysentry
EHEC: haemorrhagic 0157:H7 EHEC: shiga like verocytotoxin causes HUS

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85
Q

Salmonellae gram stain

Antigens

Species

A

Gram -ve rods

Cell wall O (groups A-I)
Flaggellar H
Capsular Vi

S. typhi
S.enteriditis
S. cholerasuis

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86
Q

Salmonella enteritidis

Transmission

Presentation

Treatment

Test

A

Poultry, eggs, meat

Invassion of epi- and sub-epitherlial tissue of SMALL and LARGE bowel. Loose stool, diarrhoea (like cholera) Self limiting and resolves within 3-7days. Bacteremia infrequent, no fever

Self limited

Stool positivity

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87
Q

Salmonella typhi

Transmission

Presentation

Treatment

Test

A

By humans, multiplies in Payer’s patches, spreads endoreticular system

Enteric fever (typhoid)
Slow onset high fever and constipation, splenomegaly, rose spots, anaemia, leucopaenia, bradycardia, haemorrhage and perforation

Ceftriaxone IV and then Azithromycin 500mg BD 7 days

Blood culture positive

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88
Q

Shigella gram stain

Antigens

Types

Tx

A

Gram -ve rods, non lactose fermenters, non H2S producers, non-motile

Cell wall O antigens
Polysaccharide (groups A-D)

S.dysenteriae, S. flexneri (MSM)

Avoid antibiotics

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89
Q

Vibrios gram stain

Associated with

A

Curved, comma shaped, gram negative, oxidase positive, late lactose fermenters

Seafood raw/undercooked

Massive diarrhoeaa (rice water stools without inflammatory cells)

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90
Q

Campylobacter gram stain

Transmission

Presentation

tx

Complications

A

Curved, comma gram -ve, oxidase +ve

Contaminated food/water with animal faeces

Enterotoxin (watery diarrhoea) ?invasion (+/- blood)
Watery foul smelling diarrhoea, bloody stool, fever and severe abdo pain

Erythromycin or cipro on first 4/5 days
Self limiting but can last for weeks
Only tx if immunocompromised

GBS, reactive arthritis, Reiter’s

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91
Q

Viral gastroenteritis causes

A

Norovirus - notifiable
Adenovirus <2 non-bloody
Rotavirus - dsDNA (by 6 yrs - most have antibodies)

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92
Q

Protozoa gastroenteritis causes

A

Entamoeba histolytica
- Killed by boiling water, removed by water filters
Flask shaped ulcer, dysentry, flatulence, tenesmus. Chronic wt loss, liver abscess

Giardia lamblia
2 nuclei, pear shaped
Tx metronidazole
Foul smelling, non bloody diarrhoea

Cryptosporidium
Infects jejenum. Severe in immunocompromised.
Profuse watery diarrhoea
Tx: reconstitution of immune system

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93
Q

Bacteriuria definition

Cystitis definition

A

Bacteria in the urine

Inflammation of bladder, often due to infection

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94
Q

Classifying UTIs

A

Uncomplicated - infection in a structurally and neurologically normal urinary tract

Complicated - infection in a urinary tract with functional or structural abnormalities (including catheters and calculi)

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95
Q

Types of patients that get complicated UTI

A

Men, pregnant women, children, patients in hospital

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96
Q

Most common organism causing UTI

A

E. coli

Others:
Proteus, Klebsiella, Pseudomonas, Enterobacter, enterococci, staphylococci

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97
Q

Host defences in the urinary tract

A

Urine (osmolality, pH, organic acids)
Urine flow and micturition
Urinary tract mucosa

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98
Q

Why do females more commonly get UTIs

A

Female urethra short and is colonised with bacteria

Proximity to warm moist vulvar and perianal areas - contamination likely

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99
Q

Why does obstruction of renal tract cause UTIs

A

Inhibits normal flow of urine. Resulting stasis is important in increasing susceptibility to infection

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100
Q

Types of renal tract obstruction

A

1) Mechanical
- Extrarenal: valves, stenosis; calculi; extrinsic ureteral compression from variety of causes;BPH
- Intrarenal: nephrocalcinosis, polycystic kidney, uric acid nephropathy, renal lesions of sickle cell trait or disease

2) Neurogenic malformations
- Polyomyelitis
- Tabes dorsalis
- Diabetic neuropathy
- Spinal cord injuries

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101
Q

What is reflux in the kidney and what can it cause

A

Vesicoureteral reflux - perpetuates infections as residual pool of infected urine in bladder after voiding

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102
Q

Symptoms of UTI

A

Under 2yrs - non specific
Failure to thrive
Vomiting
Fever

Over 2
Frequency
Dysuria
Abdo/flank pain

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103
Q

How do we get UTI

A

Most common: ascending UTI
female urethra short and close to vulvar/perianal areas
- contamination likely
Sexual activity can force bacteria into bladder and multiplies, passes up ureters, particularly if VUR, to renal pelvis and parenchyma

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104
Q

Renal tract abnormalities that predispose to UTI

A

OBSTRUCTION: Intrarenal; renal; neurogenic malformation
Reflux - residual pool of urine in bladder
Haematogenous route - S.aureus abcess ore endocaditis

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105
Q

Renal tract obstruction causes

A

Extrarenal
- valves, stenosis, bands; calculi; extrinsic renal compression; BPH
Intrarenal
- Nephrocalcinosis, uric acid nephropathy, analgesic nephprhopathy, PKD, hypokalaemic nephropathy, renal lesions of sickle cell

Neurogenic malformations
- Poliomyelitis; tabes dorsalis; diabetic neuropathy; spinal cord injuries

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106
Q

Investigation of UTI

A

Urine dip
MSU urine
Bloods: FBC, UE, CRP

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107
Q

Interpreting UTI culture result

A

100,000 CFU /mL
Pyuria (10,000/mL) = inflammation - may be absent in children
If epithelial cells - indicates perineal containation

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108
Q

IVDU hepatitis

A

B or C

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109
Q

Hepatitis transmitted from mother

A

B more than C

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110
Q

Hepatitis transmitted sexually

A

B more than C

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111
Q

Hepatitis related to blood transfusion

A

C

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112
Q

Hepatitis acute only, no chronic infection

A 
A 
sRNA virus
Prodromal illness 3-10d then icteric stage for 1-3 weeks
ALT rises
Faeco-oral transmisison
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113
Q

Hepatitis food and water contamination

A

A and E

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114
Q

Natural hx of hep B infection

A

Healthy, hepatic fibrosis, cirrhosis, HCC

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115
Q

Elevated serum HBV DNA level (10 000 copies/mL) is a strong risk predictor of what

A

HCC

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116
Q

Chronic Hep B tx

A

• Interferon alpha - if only boost of own immune system needed
• Lamivudine
• Adefovir
• Tenofovir
- - any of 3 for if heading into or got cirrhosis
• Entecavir
• Emtricitabine

Truvada= tenofovir + emtricabine if HIV + too

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117
Q

Acute Hep C tx

A

IFN

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118
Q

Define PUO

A

Pragmatic

Fever of 3 days with no diagnosis despite investigation

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119
Q

Initial tests to do for fever

A 
FBC
U&amp;E
Total protein
LFTs
CRP
CXR
Blood cultures x 3
Urine culture
HIV test - do it!!

Extra
CK, ANA, ANCA, RhF, Ferritin, Abdo USS/CT, CMV EBV serology, stool cultures and OCP

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120
Q

Criteria for dx of infective endocarditis

A

Dukes criteria
2 major or 1 major and 3 minor or 5 minor

Major:
Persistent bacteraemia (>2BC +ve)
Echo: vegetation
Positive serology for Bartonella, Brucella or Coxiellia

Minor
Predisposition (Murmur, IVDU)
Inflammatory markers (fever, CRP high)
Immune complexes: splinters, RBC in urine
Embolic phenomena: Janeway lesions, CVA
Atypical echo
1 +ve BC
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121
Q

Salmon pink rash

V high ferritin

A

Adult onset Stills disease

Type of inflammatory arthritis

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122
Q

Malignancies associated with fevers

A

Lymphoma (esp Non-hodgkin)
Leukaemia (BM biopsy)
Renal cell carcinoma
HCC (or any that metastasise to the liver)

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123
Q

Unpasteurised milk infections

A

Brucella, Campylobacter, Cryptosporidium, E. coli, Listeria, and Salmonella.

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124
Q

What does HAI stand for

A

healthcare asociated infections

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125
Q

Catheter associated blood stream infection organisms

A

MRSA
MSSA
Resistant gram -ve’s

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126
Q

Surgical site infection organisms

A

MRSA
MSSA
Resistant gram -ve’s

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127
Q

Incidence of HAI in UK

A

8%

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128
Q

Most common syndrome of HAI

A 
Pneumococcal pneumonia
Then
Surg site infections
UTI
Bloodstream
Gastro
129
Q

C. difficile gram stain

A

Gram +ve spore forming anaerobe

130
Q

Why is E. coli bacteraemia increasing

A

UTI
Catheter use
Antibiotics
Antibiotic resistance

131
Q

What influences surgical site infection risk?

A

Host defence
Wound environment
Pathogens - S.aureus most common

132
Q

What is CPE

A

Carbapenemase producing Enterovacteriaceae

133
Q

Building works organism

A

aspergillus

134
Q

Water/cooling tower associated organism

A

Legionella pneumophilia

135
Q

Negative pressure vs positive pressure isolation

A

Negative pressure - protection of others from an infectious patient with airborne infection
Positive pressure - Protection of transplant patients from organisms from outside the room

136
Q

What % of world has TB

A

33%

137
Q

TB type of bacteria

A

Aerobic, non-motile rod
Cell wall made of long chain fatty acids (structure and staining characteristics)
- Acid alcohol fast (resists discolouration with acid)

= AAFB

138
Q

Slow growing NTM

A

M. avium intracellulare

  • Immunocompetent but propensity for lung abnormalities
  • Disseminated in immunocompromised

M. marinum
- in cold water, usually cutaneous

M. ulcerans
- seen in W Africa, likes cold areas of

139
Q

Rapidly growing NTM

A

M. absessus
M. chelonae
M. fortuitum

These typically cause skin and soft tissue infection
In hospital, isolated from blood cultures.
Relatively easier to treat

140
Q

Diagnosis of NTM lung disease

A

Clinical + microbiological findings + excluding other dx

C: pulmonary symptoms, nodular cavities/opacities, bronchiectasis

M: 2 sputum cultures or 1 BAL
OR + biopsy with granulomata

141
Q

Bacteria causing leprosy

A

Myobacterium leprae

142
Q

If exposed to a smear +ve pulmonary TB person, what is lifetime risk of developing active TB?

A

10%

143
Q

What is Ghon focus?

What is Ghon complex?

A

Primary TB - subpleural caseating granuloma

Ghon focus + ipsilateral hilar lymphadenopathy

144
Q

Presentation of primary TB

A 
usually asymptomatic
Ghon focus/complex
Limited by cell mediated immunity
Rare allergic reactions e.g erythema nodosum
Ocassionally dissemination/miliary
145
Q

Risk factors for re-activation of TB

A

Immunosuppression
Chronic alcohol use
Malnutrition
Ageing

146
Q

Post-primary TB presentation

A

Pulmonary or extra pulmonary
>5yrs after primary infection

Pulmonary TB
Caseating granulomas
- lung parenchyma
- Mediastinal LN
Upper zones

Extra-pulmonary

  • Lymphadenitis (scrofula, cervical)
  • GI
  • Peritoneal
  • Genitourinary
  • Bone and joint (spinal most common - Pott’s disease)
  • Miliary TB (millet seeds on CXR, increasing due to HIV)
  • TB meningitis
147
Q

Investigations for TB

A

CXR

Sputum x3 (induced)
Bronchoscopy
Biopsies
EMU
Stain for AAFB (smear)
Culture
NAATT
Histology

Tuberculin skin test
IGRAs - Elispot

148
Q

TB treatment side effects

A

R: CyP450 inducer, orange secretions
I: Peripheral neuropathy (give B6 - pyridoxine), hepatitis
P: Hepatotoxicity
E: Visual disturbance

149
Q

Length of Tb treatment

A

RIPE 2 months
RI: extra 4 months

CNS TB: 10/12

Adherence checked with direct observation or video observed

150
Q

Define MDR TB and worse

A

MDR: Resistant to R and I
XDR: Also resistant to fluroquinolones and at least 1 injectable

151
Q

Causes of MDR TB

Treatment of MDR TV

A 
Previous TB tx
HIV +ve
Kniwn contact of MDR TB
Failure to respond to conventional Rx
>4 months smear positive, >5 months vulture positive

4/5 drug regime, longer duration
- Quinolones, aminoglycosides, PAS…

152
Q

Streptococcus pneumoniae gram stain

A

Gram +ve diplococci

Alpha haemolysis (green) + Sensitive to optochin

153
Q

Severe, acute onset pneumonia presenting with fevers, rigors, lobar consolidation.

Causative organism
Treatment

A

Streptococcus pneumonia

Almost always penicillin sensitive
- Check travel hx (resistance in south europe)

154
Q

Fever, cough, pleuritic chest pain, SOB

Cause and define

A

Pneumonia - inflammation of lung alveoli

155
Q

Pneumonia classification

A

CAP or HAP

156
Q

Main CAP organisms

A 
Streptococcus pneumoniae
Stapylococcus aureus
Hamemophilus influenzae
Moraxella catarrhalis
Klebsiella pneumoniae
157
Q

Haemophilus influenzae gram stain

A

-ve cocco-bacilli

Grow on chocolate agar

158
Q

Moraxella catarrhalis gram stain

A

-ve coccus

159
Q

Staphylococcus aureus gram stain

A

+ve cocci

160
Q

Klebsiella pneumoniae gram stain

A

-ve rod, enterobacter

161
Q

Pneumonia causative organisms based on age of pt

A

0-1 month: Listeria, E.coli, GBS
1-6months: Chlamydia, S.aureus, RSV
6months-5yrs: Mycoplasma, Influenza
16-30yrs: M. pneumonia, S. pneumoniae

162
Q

Atypical causes of CAP

A

Organisms with no cell wall (don’t respond to penicillin Abx. Use macrolides and tetracylcines)

Legionella pneumophilia
Mycoplasma pneumonia
Coxellia burnetti (Q fever) - farm animals, hepatitis
Chlamydia psittaci - Bird exposure, splenomegaly, haemolytic anaemia, rash

163
Q

How do atypical CAP present differently to typical CAPs

A

No signs on chest exam or signs not in keeping with CXR. May have extrapulmonary features.

164
Q

Low Na, in a hotel, pneumonia picture, hepatitis

A

Atypical CAP - Legionella

165
Q

Systemic symptoms, joint pain, cold agglutin test, erythema multiforme, pneumonia picture

A

Atypical CAP - Mycoplasma

- Risk factors - SJS, AIHA

166
Q

Invesrigations for pneumonia

A

FBC
U+Es
CRP (high can indicate S.pneumo - 500ish)
Blood culture, sputum (often not sent, often no dx)
ABG
CXR

167
Q

Assessment score for pneumonia

A 
Confusion (abbreviated Mental Test score 8 or less, or new disorientation in person, place or time)
Urea >7 mmol/litre)
RR > 30 
BP <90 S, <60 D
>65yrs

Consider
Home if 0-1
Hospital 2 and above
ICU 3 and above

168
Q

Definition of bronchitis and causative organisms

A

Inflammation of medium sized airways

Viruses, S,pneumoniea, H. influenzae, M.catarrhalis

169
Q

CXR in bronchitis

A

normal

170
Q

Cavitating lesion cxr causes

A

S. aureus
K. pneumoniae
TB

171
Q

Ddx of failure to improve on pneumonia treatment

A 
Empyema/abscess
Proximal obstruction (Tumour)
Resistant organism (TB)
Not receiving/absorbing Abx
Immunosuppression
172
Q

ground glass shadowing cxr
bat’s wing appearance

test to do
Treatment

A

Pneumocystitis jiroveci

Walk test - desaturate
Immunofluorescence on BAL
Silver stain

Septrin (co-trimoxazole)

173
Q

Neutropenia + on lots of antibiotics

Intersititial change on cxr/ nothing much

A

Aspergillus (invasive)

174
Q

Immunosuppresion (BMT) and LRTI

A

CMV pneumonitis

175
Q

Immunosuppresion (splenectomy)

A

Encapsulated organisms (NHS), malaria

176
Q

Investigations of LRTI

A

Before antibiotics: Sputum, blood cultures

BAl
Pleural fluid
Antigen tests (urine - one for MCS, one for legionella)
Antibody tests
Immunofluorescence
PCR
177
Q

Candida diagnosis

A

Culture - selective agar plate (with antibiotic to kill bacteria)
B D glucan assay (serology for component of fungal wall)
Imaging e.g. for hepatosplenic candidiasis

178
Q

Candidiasis management

A

Minimum 2 weeks antifungals from first -ve blood cultures
Echo and fundoscopy
Enchinicandin empirically and for non albicans Candida
Fluconazole for Candida albicans

179
Q

Aspergillus spectrums of disease

A

1) Mycotoxicosis due to ingestion of contaminated food
2) Allergic sequelae - allergic bronchopulmonary aspergillosis - wheeze, eosinophilia, bronchiectasis
3) Colonisation without invasion - aspergilloma
4) Invasion, inflammation, granulomatous disease in lungs
- Rx: amphotericin B
5) Disseminated systemic (in immunocompromised)

180
Q

Aspergillus dx

A

Microscopy mainstay - hyphi
- Can stain with methenamine silver

IgE bloods: to look for allergic response
- can look for antigen - galactaman - blood or BAL
PCR
Histology sample
Culture (slow)

181
Q

Antifungal agents targets and examples

A

1) Cell membrane
- polyene antibiotics: Amphotericin B, lipid formulations, nystatin (topical)
- Azole antifungals: Ketoconazole, itraconazole, fluconazole…

2) DNA synthesis
- Pyrimidine analogues, flucytosine
3) Cell wall
- Echinocandins

182
Q

Azoles mechanism

SEs

A

Target cell membrane of funguses
- inhibit fungal P450 enzymes that help synthesise ergosterol (main component of fungal cell membrane)

Some cross reactivity with mammalian P450

  • Drug interactions esp warfarin
  • Impairment of steroidneogenesis (keto and itroconazole)
183
Q

Echinocandins mechanism

A

e.g. Anidulafungin
Target cell wall of fungus
- Specific inhibitors of beta 1 3 glucan synthase (needed for b glucan synthesis - structures in fungal cell wall)

Remember cryptococcus is inherently resistant

184
Q

Amphotericin B mechanism

Active against

A

Targets cell membrane of fungus - polyene antibiotic
- Binds sterols in fungal cell membrane, creates transmembrane channel and electrolyte leak

Active against most fungi except aspergillus terreus, Sceedosporium spp
Used in cryptococcal meningitis

185
Q

Side effects of amphotericin B

A

Nephrotoxic (delayed toxicity)

  • Drop in GFR, azotemia (vascular decrease in renal blood flow)
  • Wasting of K, Na and Mg (distal tubular ischaemia)
186
Q

Flucytosine mechanism

Indications

A

Targets fungal DNA synthesis

Not really montherapy
But used in combinations with amphotericin B or fluconazole for Candidiasis, Cryptococcosis or ?Aspergillosis

187
Q

Flucytosine SEs

A

Liver function, blood disorders, D&V

Blood conc needs monitoring when used in conjunction with Amphotericin B

188
Q

Assessment of patient with fever

A

B symptoms, localising clues
Medications
Foreign travel - exact, what doing, where, how lonh
Unwell contacts, animal expo, Iv drug use, sexual hx
Examination - eyes, mouth, palpate back , rash

189
Q

V high ferritin caused by

A

Adult onset stills disease
Maacrophage activation syndrome

Also infective causes

190
Q

Aciclovir mechanism of action

A

Guanosine analogue - chain terminator of viral DNA

  • activated by viral thymidine kinase so restricted to virally infected cells
  • affinity for viral DNA polymerase more than host

low drug toxicity. rarely neuro and nephro toxic

191
Q

HSV encephalitis treatment

A

As soon as suspected 10mg/kg tds aciclovir

21 days

192
Q

HSV meningitis treatment

A

Only treat if unwell enough for admission or immunocompromised

ACV iv 2-3 days then oral for further 10 days

If immunocompromised can use valciclovir to avoid cannula

193
Q

VZV treatment

A 
Only for 
Chicken pox in adults
Shingles in adults
Immunocompromised
Neonatal chickenpox
Increased risk of complications
194
Q

CMV course of infection

Histology

A

latent in blood monocytes and dendritic cells in primary infection
Reactivation following immunosuppression

Owl’s eye inclusions

195
Q

CMV risk

A 
Immunocompromised. Causes:
Marrow suppression
Retinitis
Pneumonitis
Hepatitis
Colitis
Encephalitis
196
Q

CMV treatment

A

1st line) Ganciclovir (iv) or valganciclovir (po)

2) Foscarnet
3) Cidofovir

2 and 3 don’t need activation by viral kinase but 1 does

197
Q

CMV pneumonitis treatment

A

Ganciclovir (iv) + IVIg

198
Q

Ganciclovir indications

SE

CI

A

CMV disease in immunocompromised or newborns with congenital CMV

BM toxicity
Renal toxicity

BM suppression (i.e. BM transplant patient)

199
Q

Foscarnet indications

SE

A

CMV and occasionally HSV (e.g. if ACV resistance)

  • GCV CI
  • CMV retinitis

nephrotoxic - need to keep well hydrated and correct electrolytes

200
Q

Cidofovir indications

A

3rd line tx of CMV in immunocompromised

Nephrotoxic - need to keep hydrated and probenicid

201
Q

Managing CMV in transplant patients

A

1) Prophylaxis with GCV - for solid organ transplant. SE - nephrotoxic
2) Pre-emptive therapy: Surveillance - weekly blood CMV PCR, GCV or foscarnet when PCR +ve. mostly for stem cell transplant pts

202
Q

Main surface proteins of influenza virus

  • which one is targeted by anti-influenza drugs
A

Haemagluttinin

Neuraminidase - inhibited by e.g. oseltamavir (tamiflu) or zanamavir (dry powder inhaler)

203
Q

Indications of anti-infleunza drugs

MOA

Examples

A

Any pt admitted for flu-like illness
In community for at risk groups, within 48 hrs of symptom onset

Target neuraminidase

Oseltamavir, zanamavir

204
Q

Pavilizumab use

A

Monoclonal Ab against RSV. Can be used in winter months by high risk infant groups as prophylaxis

205
Q

BK virus clinical picture

A

In BMT patients: haemorrhagic cystitis

In renal transplant: BK nephritis and ureteric stenosis

206
Q

Treatment of BK haemorrhagic cystitis

A

Bladder washout and reduce immunosuppression if poss
Cidofovir iv + probenicid if significant morbidity
Intravsecal cidofovir if nephrotoxic
? future: brincidofovir

207
Q

Treatment of BK nephropathy

A

Reduce immunosuppression if poss
IVIg
? future: brincidofovir

208
Q

Adenovirus clinical picture

Treatment

A

Paeds transplant recipient - severe multi-organ involvement

Tx: Cidofovir + IVIg
? future: brincidofovir

209
Q

Brincidofovir MOA

A

Pro drug of cidofovir. Less toxic.

Main potensh is for tx or adenovirus and BK virus in immunocompromised

210
Q

Immunodeficiency associated with HSV encephalitis

A

UNC93B deficiency

TLR3 deficiency

211
Q

Immundofeiciency associated with HPV

A

Epidermodysplasia verruciformis (primary immunodeficiency - EVER1/2)

212
Q

neisseria meningitis gram stain

A

Gram -ve coccus

213
Q

Most common causative organism of prosthetic joint infections

A

1) Coagulase -ve staph

2) S. aureus

214
Q

Hep A epidemuiology

A

Countries with poor sanitation of water supply

Also MSM and school outbreaks

215
Q

Hep A incubation period

A

2-6 weeks

216
Q

HBV transmission

A

Sexual, blood products and mother to baby

217
Q

Hep B incubation period

A

2-6 months

218
Q

HCV serology

A

ALT high in acute reaction
Anti-HBV may come years after - not in acute phase at all + lag

Sooo diagnostic test is HCV RNA

219
Q

HCV treatment

A

Peginterferon + ribavarin

220
Q

Natural reservoir of influenza A virus

A

Ducks, geese, swans

221
Q

Why does influenza virus cause respiratory disease

A

Needs activation by proteases (human airway tryptase) which cleaves haemagglutinin and this allows virus to leave first infected cell and enter new cell

222
Q

Mutation in influenza viruses that can lead to switch to it becoming transmittable in humans
- why worry about these?

A

PB2 627K

627 switch can lead to hypercytokinaemia: MCP, IL-8, IL-10 –> ARDS

223
Q

Chicken vaccinations in China for?

A

H7N9 influenza

224
Q

Influenza virus, how does it get through mucuc

A

Neuraminidase breaks down mucus

225
Q

Gene linked with more severe influenza

A

Loss of IFITM3

226
Q

What does seasonal influenza vaccine contain

A

Purified fraction containing HA and NA of an inactivated virus

To children: Live attenuated

227
Q

Current screening of mothers during pregnancy

A

Hep B, HIV, Rubella, Syphillis

228
Q

What bacteria is the most common cause of early onset neonatal sepsis?

A

Group B Strep by far (1/3 of women colonized with)

Then E. coli

229
Q

Most common type of meningococcal disease in UK

A

Men B
(because vaccinated for men c)
But now is a men B one

230
Q

Most common cause of death WW in children under 5

A

Prematurity

231
Q

Most common cause of congenital deafness in UK

A

CMV

232
Q

Congenital toxoplasmosis presentation

A

Can cause still birth

60% asymptomatic at birth. May get long-term sequelae - deafness, low IQ, microcepahly

40% symptomatic at birth - choroidoretinitis, microcephaly, hydrocephalus, intracranial calcifications, seizures, hepatosplenomegaly, jaundice

233
Q

Congenital rubella presentation

A

Depends on time of infection. Worst in 1st 12 weeks.
13 - 20 weeks - >15% have deafness and retinopathy

Eyes: Retinitis, cataracts, glaucoma
Ears: Deafness
CVS: PDA; ASD, VSD
Ears: Deafness
Brain: Microcephaly, meningoencephalitis, DD
Other: Bone disease, hepatosplenomegaly, rash, thrombocytopenia

Classic triad: Microcephaly, PDA, cataracts

234
Q

Early onset sepsis risk factors (maternal)

A 
PROM, prem
fever
Foetal distress
Meconium staining
PH

CAUSE IS: GBS, E.coli, Listeria

235
Q

Early onset sepsis in neonate treatment

A

Ventilation
Circulation
Nutrition
Antibiotics: Benpen (Group B Strep) + Gent (E.coli)

236
Q

Late onset sepsis neonate causative organisms

A 
By far the most - Coagulase negative staphylococcus.
LEG
S. aureus
Enterococcus
Gram -ves - kelbsiella, pseudomonas
Candida
237
Q

Late onset sepsis in neonate treatment

- examples only

A

1st line: Cefotaxime + Vancomycin
2nd line: Meropenem

If community acquired: cefotaxine, amoxicillin+/- geny

238
Q

What kind of organism is rubella

Congenital rubella moa

A

RNA virus

Stops rate of cell division, decreases no of overall cells, interferes with development of key organs

239
Q

Rubella dx

A

Rubella IgG - 90% +ve antenatally - if -ve, consider aaaa

  • Seroconversion
  • Avidity

Rubella IgM

PCR - blood, resp, urine,

240
Q

Pre-natal diagnosis of rubella

A

Should consider termination in 1st trimester because of congenital rubella syndrome risk

241
Q

CMV transmission

A

Horizontally

Vertically: Transplacental (any stage of pregnancy), during delivery, breastfeeding

242
Q

Congenital CMV infection diagnosis

A

In neonate. Can be smptomless at birth and develop sequelae.

Detection of CMV from bodily fluids or tissues within 3 weeks of birth (urine and saliva tested) - PCR best, can do serology

243
Q

Congenital CMV treatment

A

6/12 ganciclovir or valganciclovir
Audiology follow up for 6 yrs
Opthalmology review

244
Q

Classification of maternal HSV infection and risk

A

1st episode primary - 57%
1st episode non-primary - 25%
Recurrent infection - 2%

Symptomatic/asymptomatic

245
Q

congenital HSV transmission risks

A

No maternal neutralising Ab
Duration of rupture of membranes
Loss of integrity of mucocutaneous barriers
Vaginal vs c-section

246
Q

When during pregnancy is HSV infection the greatest risk

A 
3rd trimester (particularly within 6 weeks of delivery) as mum continuously shedding virus
- c-section recommended
247
Q

HSV congenital disease picture in neonate

A

SEM - skin, eye and mouth in 45%
CNS in 30% - 10d-4weeks post natal
Disseminated infection involving multi-organ in 25% - most serious, mortality of 30%

248
Q

Congenital HSV investigations

A

HSV cultures/PCR of anything blood, CSF, urine

ALT good marker

249
Q

Congenital HSV treatment

A

IV aciclovir 60mg/kg/day in 3 divided doses

  • 21 days in CNS or disseminated
  • 14 days in SEM

Monitor neutrophils

250
Q

Varicella infection in pregnancy may cause

A 
In mother: pneumonia/encephalitis
Intrauterine VZV:
- congenital varicella syndrome
- neonatal varicella
- HZ during infancy or early childhood

Any pregnant women - 10 days IV aciclovir

251
Q

Varicella neonatal infection

A

Occurs just prior or just after delivery - no time for VZV antibodies to pass

May result in:

  • mild course of infection
  • disseminated skin lesions
  • visceral infections
  • pneumonia
252
Q

Congenital varicella syndrome risk

A

Highest at 13-20 weeks gestation - 2%

0.4% before

253
Q

What type of vaccine is VZV

A

Live (can’t give in pregnancy)

254
Q

VZV exposure in pregnant woman

A

Determine if contact significant
Then do serology, if negative then treat:

VZ immune globulin if within 10d of exposure (better <20wk gestation)
Aciclovir if 7-14d post exposure (>20 week gestation)

255
Q

Measles type of virus

Symptoms

Complications

A

RNA

Prodrome: Fever, conjunctivitis, Koplik spots
Rash on face moving down

Pneumonia, bronhcitis, otitis media
Encephalitis
SSPE

256
Q

Measles exposure by pregnant woman

A

Measle immunoglobulin within 6 day window of exposure

NO CONGEITAL ABNORMALITIES TO FETUS

Does cause

  • Preterm
  • Fetal loss
  • Increases maternal morbidity
257
Q

Hydrops fatalis if in 1st 20 weeks of pregnancy

A

Parvovirus B19

Hydrops fetalis - due to severe anaemia

After 20 weeks, no documented risk

258
Q

Source animal classification in zoonoses

A

1) Farm/wild animals:
- Cattle, poultry, pigs, goats
2) Companion
- Dogs, cats (ticks, mice rodents)
- Reptiles
- Fish

259
Q

UK zoonoses

A

Farm/wildlife: Camplyobacter + Salmonella

Companion: Bartonella, Toxoplasmosis, Ringworm, Psitticosis

260
Q

Tropical zoonoses

A

Farm/wildlife: Brucella, Coxiella, Rabies, VHF

Companion: Rabies, tickborn diseases, Spirilum minus

261
Q

Diarrhoea bloating cramps after uncooked chicken

Investigations

Management

A

Camplyobacter

Stool culture

Supportive

262
Q

Cat at home, bit/licked ot and has fever, night sweats and adenopathy. Cause

Treatment

A

Bartonella henselae - cat scratch disease
- In immuncompotent. Can progress to more severe symptoms in 15%.

If immunocompromised - bacilliary angiomatosis
Skin papules, disseminated and vascular involvement

Erythromycine + Doxycycline (+ rifampicin if angiomatosis)

263
Q

Toxoplasmosis treatment

A

Pregnant: Spiramycin

Non-pregnant: Pyramethamine + sulfadiazine

264
Q

Pt from abroad went to cattle/goat farm and milked some cows, drank some unpasteurised milk, mucosal splash, aerolisation/ inhalation. Now has fevers similar to extra-pulmonary TB + back pain, orchitis, focal abscess.

Cause

Investigation

Managament

A

Brucellosis

Blood/pus culture (say suspected brucella)
Serology

Doxycycline
+ Gent or rifampicin

265
Q

Coxiella burnetti presentation

Investigation

Treatment

A

Fever, ‘Flu like illness’, pneumonia, hepatitis, endocarditis, focal abscesses (paravertebral/discitis)

Serology

Doxycycline
(hydroxychloroquine)

266
Q

Rabies presentation

Treatment

A

Seizures, excessive salivation, agitation, confusion, fever, headache

Treatment helps before symptomatic stage
- Immunoglobulin + vaccine

267
Q

Rat zoonoses

A

Rat bite fever - fevers, polyarthralgia, maculopapular –> purpuric rash, can get endocarditis
Due to spirillum minus and streptobacillus moniformis
- penicillin

Hentavirus pulmonary syndrome - Resp failure in US, renal failure in SE Asia

268
Q

non-falciparum malaria treatment

A

Chloroquine then primaquine

269
Q

19yo male returns from Spain. 4 weeks later hot swollen painful red knee joint. Knee tapped and 20ml cloudy fluid stains as gram -ve intracellulular diplococci

A

Neisseria gonorrhoea

Most common cause of septic monoarthritis in a 18-30yo who has monarthritis.

270
Q

Meningitis symptoms in 19yo boy. LP reveals gram -ve intraceullar diplococci

A

Neisseria mengitidis

271
Q

6yo meningitis picture. LP reveals gram -ve rods

A

H. influenzae

272
Q

19yo PUO. After 2 months, bloods show gram +ve cocci

A 
Endocarditis
Signs will slowly appear 
- Splenomegaly
- Splinter heamorrhages
- Roth spots
- Clubbing
- Microscopic haematuria
- Janeway lesions

Step viridan - chooses aortic valves because higher pressure, already bit of damage there - settles there

273
Q

Iv drug user endocardit

A

S. aureus.

V agressive, lands on first valve and grows there - tricuspid valve - die of septicaemia in 3 weeks. Much quicker disease progression than s.viridans

274
Q

CF with respiratory tract infection

- Organisms responsible

A

Pseudomonas aeruginosa, Burkholderia

275
Q

HIV respiratory tract infection

A

Pneumocystitis jiroveci (PCP)
TB
Cryptococcus neoformans

276
Q

Respiratory tract infection following splenectomy

- responsible organisms

A

NHS (encapsulated)

277
Q

PCP presentation

A

Dry cough, weight loss, SOB, malaise

278
Q

neutropenic patient develops respiratory tract infection

- causative organism?

A

Aspergillus spp.

279
Q

Fungal infections

A

Yeasts

  • Candida
  • Cryptociccus
  • Histoplasma

Moulds

  • Aspergillus
  • Dermatophytes
  • Agents of mucormycosis
280
Q

Cryptococcosis diagnosis and management

A

Presents as meningitis with insidious onset in HIV.
Associated with birds, particularly pigeons

Diagnosis

  • detection of cryptococcal antigen in blood/CSF + india ink stain = mainstay
  • Can often culture but slower (2 days)

management
- 3/52 amphotericin B +/- flucytosine

281
Q

Classification of PUO

A

Durack and street

1) Classical. >38.3 temp. Lasting >3/52. 3 or more visits/days in hospital
- Infection
- Malignancy
- Collagen vascular disease

2) Nosocomial. >38.3 temp. Hospitalised 24h but no fever on admission. 3 or more days investigation
- C. difficile enterocolitis
- Drug induced
- PE
- Septic thrombophlebitis
- Sinusitis

3) Immune deficient. >38.3 temp. Neutrophils <500. 3 or more days investigation
- Opportunistic bacterial infections
- Aspergillosis
- Candidiasis
- Herpes

4) HIV associated
- CMV
- PCP
- Kaposi/N-H lymphoma

282
Q

How does PET-CT work

A

Fluoro-D glucose accumulates in cells with an increased rate of glycolysis (all activated leukocytes)

  • Infection
  • Inflammation
  • Cancer

Caution in patients with poor glucose control

283
Q

Malaria definition

Carried by which mosquito

Life cycle

A

RBCs parasitized –> ineffective –> haemolysis

Anopheles mosquito

Mosquito stage + human stage.
Human stage divided into erythrocytic (in RBCs) and exoerythrocytic.
Sometimes a liver stage too (hypnozoite stage) - non-falciparum types sleep in liver (chloraquine doesn’t kill liver stage hence need primaquine)

284
Q

Malaria species

A

5 plasmodium species:

  1. P. falciparum - invades erythrocytes of all ages, may be drug resistant and can be life threatening
  2. P. vivax
  3. P. ovale
  4. P. malaria
  5. knowlesi
285
Q

Malaria symptoms

A 
Fever + rigors
Headache
Back pain
Myalgia
N&amp;V
286
Q

Severe malaria features

A 
Impaired consciousness/seizures
Renal impairment
Acidosis 
Hypoglycaemia
Pulmonary oedema/ARDS
Anaemia
DIC/bleeding
Shock
Haemoglobinuria
Parasitaemia >2%, pregnancy, vomiting
287
Q

Malaria diagnosis

Treatment

A

Thick and thin blood film x 3
Malaria antigen tests

Non-falciparum:

  • 3 days chloraquine
  • Primaquine for 14days (hypnozoites)

Mild faclciparum (no vomit, parisataemia <2%)

  • oral malarone 3 days
  • Oral quinine + doxycycline
  • artemisinin combination therapies e.g. riamet

Severe falciparum

  • ABC
  • Correct hypoglycemia
  • IV artesunate
288
Q

Denque cause

A

Aedes mosquito

Fever, headache, myalgia, arthralgia, rash in 50%
Usually mild/self limiting
Dengue haemorrhagic fever

Investigations: Serology (IgM 5-7days), PCR
Treatment = supportive

289
Q

Schistosomiasis presentation

Treatment

A 
Asymptomatic
Acute schistosomiasis:
- High temp
- Blotchy, itchy red rash
- Cough
- Diarrhoea
- Myalgia
- Arthralgia

Permanent organ damage if not treated

Praziquantel

290
Q

Filiarisis

A 
Nematode infections spread by blackflies and mosquitoes
Classified by location of adult worm
- Lymphatic
- Subcutaneous
- Serous cavity

Diagnosis by finding microfilariae (blood films, skin snips), antibodies, finding adults (US)

291
Q

Worm classification

A

Cestodes (tapeworm)
e.g. hyatid, pork/beef tapworms

Trematodes (flukes)

e. g. lung, liver, intestinatl
- schistosomiasis (blood)

292
Q

Cognitive disturbance, personalty change, motor deficits

Demyelination of white matter with neurologial deficits corresponding to areas of brain affected

A

Progressive multifocal encephalopathy
Causd by JC virus
- acquired in childhood, latent in BM, circulates to blod

Used to mostly be seen in AIDS and patients on natalizumab (for MS)

Diagnosis on MRI and PCR of CSF

293
Q

Brown/purple vascular lesions in HIV patient

A 
Kaposi sarcoma
Characterised by:
- Spindle cell proliferation
- Neo-angeogenesis
- Inflammation and oedema

Chemo + initiate antiretroviral therapy

294
Q

HBV sAG +ve
HBV core Ab +ve
HBV s Ab -ve

A

Current HBV infection

295
Q

HBV sAG -ve
HBV core Ab +ve
HBV s Ab +ve

A

Past HBV infection

296
Q

HBV sAg -ve
HBV core Ab -ve
HBV s AB +ve

A

Vaccination against HBV

297
Q

What is prion disease

A

Protein-only infectious agent.
Rare transmissable spongiform encephalopathies in humans and animals –> rapid neurodegeneration and death in months
Untreatable
Prion protein gene on Chr 20

Normal protein structure PrP. Abnormal PrP^sc abnormally folds –> beta sheet configuration and protease/radiation resistant. PrP^sc promotes irreversible conversion of PrP to insoluble PrP^sc

298
Q

Prion disease classification

A

Sporadic: trigger for prion disease unknown

Acquired

  • vCJD
  • kuru
  • iatrogenic: GH, blood, surgery

Genetic: Familial CJD, GSS, Familial fatal insomnia

299
Q

Sporadic CJD cause

Presentation

Diagnosis

A

Cause uncertain:
– ? somatic PRNP mutation
– ? spontaneous conversion of PrPc to PrPsc
– ?? Environmental exposure to prions

Rapid progressive dementia with

  • Myocolonus
  • Cortical blindness
  • Akinetic mutism
  • LMN signs

Age of onset ~ 45-75
Mean survival = within 6/12 of symptoms starting

Diagnosis of sporadic CJD
•	EEG: periodic, triphasic complexes (non-specific)
•	MRI: basal ganglia – increased signal
•	CSF: 14-3-3 protein +ve
•	Neurogenetics to r/o genetic cause
•	Tonsillar biopsy NOT useful
•	Brain biopsy
•	Autopsy – by experienced pathologist: Spongiform vacuolation, PrP amyloid plaques
300
Q

vCJD

Cause

Presentation

Diagnosis

A

Cause: Exposure to bovine spongiform encephalopathy

Younger age of onset than sCJD ~ 26yo
Psychiatric onset: anxiety, paranoia, hallucinations
Then neurological
- peripheral sensory symptoms
- ataxia
- myoclonus
- chorea
- dementia

Diagnosis of vCJD
• EEG – non-specific slow waves
• MRI brain - positive pulvinar sign (posterior thalamus highlighted)
• CSF – 14.3.3, can be normal
• Neurogenetics (almost 100% are MM at codon 129)
• Tonsil biopsy 100% sensitive and specific
• (Brain biopsy)
• Autopsy: PrPSc type 4t detectable in CNS + most lympo-reticular tissues, florid plaques

301
Q

Iatrogrenic CJD

Cause

A

Innoculation with human prions, most commonly from surgery

  • Progressive ataxia initially
  • Dementia and myoclonus later
  • Speed of disease depends on route of innoculation

Diagnosis
- No mutations

302
Q

Antimicrobial inhibitors of DNA synthesis

A

Fluoroquinolones e.g. ciprofloxacin.
- against gram -ve’s

Nitroimidazoles
- against anaerobes and protozoa (Giardia)

303
Q

Conjugate vaccinations

MOA

Examples

A

N. meningitis
Haemophilus influenzae
Pneumococcal

Polysacharide + protein carrier (promotes T cell immunity + therefore enhances B cell/antibody response)

304
Q

Subunit vaccinations

MOA

Examples

A

Hep B - made using recombinant DNA

HPV
Influenza (haemaglutinin + neuraminidase)

305
Q

Live attenuated vaccines

MOA

Examples

A

Achieves immunisation with single dose
Not suitable for immunocompromised OR PREGNANT

MMR
BCG
Yellow fever
Typhoid
Oral poliomyelitis
Chickenpox
306
Q

Inactivated/killed vaccinations

A

Hep A
Cholera
Rabies
Polio (salk)

307
Q

What is Alum

A

Induces mild inflammatory response
- promotes predominantly antibody response through Il-4 release (eosinophil activation) and (primes naive B cells)

Used in

  • Hep A
  • Hep B
  • Hib
308
Q

What is ISCOM

A

Immune Stimulatory COMplexes

Antigen assembled in multimeric form and saponin that promotes a strong serum antibody response

309
Q

Leptospiriosis

A

Spiral shaped gram -ve
- Urine or tissue of an infected animal. From swimming in contaminated water

  • Hepatitis, jaundice, conjunctival infections, renal impairment

AGGLUTININ TEST = gold standard

310
Q

Bacillus anthralics

A

Gram +ve rod. Blood agar culture
Ulcerating papule - black and necrotic centre
Responds to high dose penicillin

311
Q

Vaccine given every 5 years to splenectomy patients

A

Pneumococcal

312
Q

Inhibitors of RNA synthesis

A

Rifampicin

Watch out for LFTs and orange urine
Never use as a single agent because of resistance

Used for TB

313
Q

Inhibitors of folate metabolism

A

Sulphonamides + diaminopridines

Sulphonamide e.g. Co-trimoxazole for PCP

314
Q

Painless ulcer, dark brown medium growth

Snail tracks in mouth now

A

Syphilis

315
Q

SSI organisms

A

MSSA, MRSA
E. coli
Psesomonas

316
Q

Early neonatal infection in order

Late onset sepsis (>48-72h)

A

Group B streptococci
E.coli
Listeria

CoN Staphyloccous

317
Q

Wet slide prep +ve

Discharge in woman, no other symptoms

A

Trichomonas. Flagellated protozoa
Rx with metronidazole

In meny: asymptomatic or urethritis

318
Q

Fever onset 6 weeks after holiday

A

Vivax malaria
Acute hep (B, C, E)
TB
Amoebic liver abscesses

Path (6 decks)

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