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Cross reference - year 5 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

what is the most common route of entry of pathogens into CNS?

A

haematogenous

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2
Q

what are the causes of meningitis?

A

neisseria meningitides (3 serotypes)
streptococcus pneumoniae
haemophillus influenzae

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3
Q

what is the most common infection of CNS?

A

coxsackie B

echovirus

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4
Q

which is becoming the leading cause of encephalitis worldwide?

A

West Nile Virus

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5
Q

what is pyogenic vertebral oseteomyelitis?

A

common vertebral infection

e.g. staph/strep

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6
Q

which is the best imaging modality in detecting parenchymal abnormalities?

A

MRI

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7
Q

normal cell count (x106/l) in CSF

A

0-5 leucocytes

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8
Q

normal protein level in CSF in g/l

A

0.15-0.40

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9
Q

normal glucose levels in CSF mmol/l

A

2.2-3.3

60% blood glucose levels

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10
Q

purulent meningitis CSF findings (bacterial)

A
  • turbid
  • 1000-2000 polymorphs
  • gram stain
  • 0.5-3.0g/l protein (high)
  • 0-2.2 mmol/l glucose (low)
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11
Q

aseptic meningitis CSF findings

A
  • clear, slightly turbid
  • 15-500 lymphocytes
  • -ve gram stain
  • 0.5-1.0g (protein)
  • normal glucose
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12
Q

differentials for aseptic meningitis

A
  • viral meningitis
  • partially Abx treated bacterial meningitis
  • brain abscess
  • TB/fungal meningitis
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13
Q

TB meningitis findings CSF

A
  • clear, slightly turbid
  • 30-500 lymphocytes/some polymorphs
  • -ve gram stain
  • 1.0-6.0g/l protein
  • 0-2.2. mmol/l glucose
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14
Q

gram stain colours

A

gram positive = more purple

gram negative = more pink

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15
Q

gram-negative diplocci meningitis

A

neisseria meningitis

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16
Q

Ziehl-Neelson stain coloir

A

red and blue

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17
Q

stain for cryptococcal

A

India Ink

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18
Q

how does Cryptococcal appear on India Ink?

A

orbit structure (yeast in middle, capsule around edge)

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19
Q

high opening pressure on LP

A

cryptococcal meningitis

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20
Q

what is early indication of HIV infection?

A

chronic swelling of parotids

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21
Q

what is lymphoid interstitial pneuominitis?

A

lung condition associated with HIV

lymphoproliferation due to immune activation

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22
Q

when is HIV most commonly transmitted in pregnancy?

A

end of pregnancy when placenta is tired

when placenta is unhealthy (e.g. malaria)

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23
Q

which drugs work to stop HIV entry?

A
  • fusion inhibitors e.g. Enfurvirtide

- CCR5 coreceptor antagonists e.g. Maraviroc

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24
Q

what HIV drugs affect the pretranscriptional stage?

A
  • NRTI e.g. Zidovudaine, Eruticutabine
  • NtRTI e.g. tenofavir
  • NNRTI e.g. Efavirenz
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25
Q

what HIV drugs target postranscriptional ?

A

integrase inhibitors e.g. Raltegravir

PI e.g. ritonavir

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26
Q

what did the ARROW trial show?

A

no difference in outcome when clinical monitoring is compared to labaratory monitoring in HIV

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27
Q

what is immune reconstitution inflammatory syndrome (IRIS)?

A

revamping the immune system can lead to severe inflammatory response
= deterioration in clinical state

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28
Q

features of PCP pneumonia clinically and X-ray

A

X-ray: widespread bilateral ground glass shadowing

reduced exercise tolerance, low sats

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29
Q

how to confirm PCP pneumonia?

A

bronchoalveolar lavage cytology

= cysts using silver stain (Grocott-Gomoti stain)

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30
Q

T cell defects result in..

A
  • viral infections

- aggressive, opportunistic infections

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31
Q

B cell defects lead to..

A
  • bacteria: staph, pseudomonas

- fungi: candida, aspergillus

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32
Q

what is actinomyces?

A

gram +ve rod that branches as grows
basophillic sulphur granules
= lung abscess in immunocompromised/alcoholics
slow growing and difficult to treat

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33
Q

C. difficle severity score

A

1+ of
- T > 38.5
- HR > 90
WCC > 15
- rising creatinine
- clinical signs of severe colitis/ colitis on radiology
- failure to respond to therapy at 72 hours

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34
Q

severe C. diff treatment

A

Vancomycin

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35
Q

what is C. diff ribotype 027?

A

associated with increased severity of disease

produces more toxin A + B

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36
Q

why do PPIs cause increase risk of C. diff?

A

raise pH of stomach

- more GI flora and C diff spores survive stomach and travel down to colon

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37
Q

what do the 2 toxins produced by C. diff do?

A
  1. damages epithelial cells (cytotoxin) = neutrophil infiltration
  2. disrupts tight junctions = lots of fluid loss
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38
Q

some lab findings in C. diff

A

High WCC

low CRP

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39
Q

what is 14-3-3 protein a marker of?

A

marker of rapid neurodegeneration

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40
Q

what Chr is normal prion gene found on? what is its role?

A

Ch20

prion protein role in copper metabolism

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41
Q

what are the 3 polymorphisms of codon 129?

A

MM (predisposes to prion disease)
MV
VV

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42
Q

structure of normal prion protein vs abnormal?

A 
normal = alpha-helical
abnormal = beta pleated sheet
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43
Q

prion disease classification

A
  • sporadic: Creutzfelt-Jakob Disease
  • acquired: Kuru, vCJD (BSE), iatrogenic CJD
  • genetic (PRNP mutation): Familial Fatal Insomnia, GSS syndrome
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44
Q

investigation results in sporadic CJD

A

EEG: triphasic complexes
MRI: increase signal in basal ganglia
increase 14-3-3 protein
tonsillar biopsy = not useful

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45
Q

vCJD investigation results

A
  • MRI: pulvinar sign
  • EEG: non specific slow waves
  • 14-3-3 normal
  • MM at codon 129
  • tonsillar biopsy = 100% sensitivve
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46
Q

most common mutation in Gerstmann-Strausser-Sheinker Syndrome

A

PRNP P102L

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47
Q

features of Fatal Familial Insomnia

A

untreatable insomnia

BP/HR dyregulation. ataxia, thalamic degeneration

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48
Q

what is Kuru linked to?

A

cannabalism

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49
Q

symptomatic treatment of CJD

A

clonazepam for myoclonus

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50
Q

treatment of CJD - delaying prion conversion

A

quinacrine
pentosan
tetracycline

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51
Q

what is staphylococcus saprophyticus?

A

coag -ve
infections in younger women
virulence factor (P. fimbriae) = allows adhesion of epithelial

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52
Q

what are the neurogenic malfunction that can cause obstruction in renal tract?

A
  • poliomyelitis
  • tabes dorsalis
  • diabetic neuropathy
  • spinal cord injuries
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53
Q

what does white cell pyuria?

A

indicative of infection

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54
Q

what does squamous epithelial cells in urine culture signify?

A

contamination

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55
Q

how many CFU do you need to identify a UTI?

A

> 105 with urinary symptoms

organisms typical of UTI = >103 CFU/ml

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56
Q

what could cause a sterile pyuria (raised WCC but no growth)?

A
  • prior treatment with Abx
  • chlamydia
  • TB
  • calculi
  • catheterisation
  • bladder
  • neoplasm
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57
Q

what culture is used for UTIs?

A

chromogenic agar

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58
Q

colours that the agar can turn and cause

A
  • pink: E. coli
  • blue: other coliforms
  • light blue: gram +ve
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59
Q

what is the incubation period of Hep A?

A

2-6 weeks after get hepatitis

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60
Q

describe the Hep B virus

A

DNA virus

4 overlapping reading frames

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61
Q

what are the treatment options for Chronic Hep B?

A

interferon alpha
lamivudine
tenofavir
entevavir

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62
Q

what time of virus is Hep C

A

flavivirdiae virus

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63
Q

best way to check for Hep C

A

HCV RNA check for virus in blood

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64
Q

treatment for Hep C

A

early treatment with peginterferon alpha

response guided therapy

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65
Q

what to remember about treating genotype 1 Hep C?

A

high dose, longer lasting ribavirin needed

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66
Q

features of hep D infection

A

smallest virus
needs presence of Hep B to replication
Hep B + D = super infection

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67
Q

what type of virus of Hep E

A

hepeviridae family

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68
Q

genotypes of Hep E

A

1+2: human, epidemic

3+4: swine and other

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69
Q

sources of Hep E

A

shellfish
blood transfusion
sausages

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70
Q

what are the rare complication of Hep E?

A 
CNS disease (Bell's Palsy, GB)
Chronic infection
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71
Q

Treatment of Hep E

A

supportive

ribavirin

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72
Q

type of virus is Hep G

A

Pegivirus

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73
Q

3 levels of SSIs

A 
superficial incisional (skin and subcutaneous)
deep incisional (fascial, muscle layer)
organ/space infection
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74
Q

features of MRSA and tx

A

gram +ve cocci
haemolytic
Tx: Linezolid

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75
Q

preventing SSRs pre-operatively

A
  • age
  • underlying issues (obesity, low albumin, smoking etc)
  • pre-operative showering (shower with soap on day)
  • hair removal (micro-abrasions = multiplication of bacteria)
  • nasal decontamination (if found to carry S. aureus)
  • Abx prophylaxis (at induction of prophylaxis)
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76
Q

preventing SSRs intra-operatively

A 
\+ve pressure ventilation
sterilisation instruments
aseptic prep
normothermia (dec temp = dec oxygen)
oxygenation >95%
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77
Q

pathophysiology of septic arthritis

A
  • bacterial proliferation in synovial fluid = host inflammatory response
  • joint damage = host derived protein (e.g. fibronectin) exposed –> bacteria adhere
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78
Q

bacterial factors that influence in septic arthritis

A
  • S. aureus: fibronectin-binding protein (recognises selected host proteins)
  • Kingella Kinga: bactieral pili (help adhere to synovium)
  • some S. aureus strains = cytotoxin PVL = fulminant infection
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79
Q

what joint is mostly affected in septic arthritis?

A

50% knee

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80
Q

rarer causes of septic arthritis

A

lyme disease
brucellosis
mycobacteria
fungi

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81
Q

chronic osteomyeltiis presentation

A

pain
brodies abscess
sinus tract

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82
Q

treatment for chronic ostemyelitis

A
  • radical debridement
  • remove sequestra (dead bony tissue)
  • Lautenbach technique
  • Papineau technique
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83
Q

Lautenbach technique

A
  • debridement to healthy bleeding bone
  • double lumen irrigation system inserted
  • fluid and Abx irrigated for 3 weeks
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84
Q

Papineau technique

A

complete excision of infected tissue/necrotic bone

bone grafting of osseous defect

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85
Q

most common cause of prosthetic join infection

A

coagulase negative staphylocci

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86
Q

single stage revision of PJI

A
  • remove dead bone/material

- replant new prosthesis with Abx impregnated cement

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87
Q

two stage revision of PJI

A
  • remove, put in spacer
  • Abx for 6 weeks
  • re-debride
  • implant with Abx impregnated cement
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88
Q

what is the most common HAI?

A

pneumonia

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89
Q

features of C. difficle

A

gram +ve

spore forming anaerobe

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90
Q

features of S. aureus

A

gram +ve cocci in clusters

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91
Q

differentials for PUO

A
  • infection
  • AI/ inflammatory, vasculitides
  • malignancy
  • medication
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92
Q

extra tests to remember to do in PUO

A
  • HIV test
  • EBV/CMV test
  • extended serology tests (Q-fever, Bartonella, Brucella)
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93
Q

parasites that can cause PUO

A
  • malaria
  • amoebic liver abscess
  • schistosomasis
  • toxoplasmosis
  • trypanosomiasis
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94
Q

fungi that can cause PUO

A
  • cryptococcus

- histoplasmosis

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95
Q

EBV serology

A
  • viral capsid antigen (appear quickly when symptomatic)

- EBNA-1 IgG appear late on in disease

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96
Q

how does a PET-CT scan work?

A
  • fluoro-D glucose accumulates in cells with increased rate of glycolysis
  • kidney light up as where FDG is excreted
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97
Q

what is a very high ferritin associated with?

A
  • adult onset Still’s disease (salmon pink rash)

- macrophage activation syndrome

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98
Q

what is the test for latent TB?

A

IGRA

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99
Q

Duke’s criteria for IE

A

2 major
or
1 major + 3 minor

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100
Q

major criteria for IE

A

persistent bacteraemia (>2 BCs)
echo - vegetations
+ver serology for Bartonella, Coxiella or Brucella

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101
Q

minor criteria for IE

A
  • predisposition (murmur, IVDU)
  • inflammatory markers (fever, CRP high)
  • immune complexes (splinters, haematuria)
  • embolic phenomena (janeway lesion, CVA)
  • atypical ECHO
  • 1 +ve BC`
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102
Q

reservoir, source and symptoms of Campylobacter

A

reservoir: poultry, cattle
contaminated food
Presentation: diarrhoea, bloating, cramps

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103
Q

salmonella reservoir, symptoms and management

A

reservoir: poultry
symptoms: diarrhoea, vomiting, fever
Mx: supportive, ciprofloxacin, azithromycin

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104
Q

Bartonella henselae:

reservoir, source, causes what

A
  • reservoir: kittens > cats
  • scratches, bites
  • causes cat scratch disease or bacilliary angiomatosis
  • diagnosed via serology
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105
Q

cat scratch disease and management

A
  • macule at site, becomes pustular
  • regional adenopathy
  • systemic Sx
  • Mx: erythromycin, doxycycline
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106
Q

bacilliary angiomatosis and Mx

A
  • immunocompromised
  • skin papules
  • disseminated multi-organ and vasculature involvement
  • Mx: erythromycin + doxycycline + RIFAMPICIN
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107
Q 
TOXOPLASMOSIS
reservoir
symptoms
investigation
management
A

cats/sheep
fever, adenopathy, still birth, seizures
serology
Mx: spiramycin, pyrimethamine + sulfadiazine

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108
Q 
BRUCELLOSIS
reservoir
symptoms
investigation
management
A 
cattle/goats
unpasturised milk, undercooked meat
Px: fever, back pain, orchitis, focal absecess
Blood culture
Mx: doxycycline + gentamicin
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109
Q 
COXIELLA BURNETII - Q FEVER
reservoir
symptoms
investigation
management
A 
goats/sheep/cattle
aerosolisation, unpasturised milk
Px: flu like, pneumonia, hepatitis, endocarditis, focal absecess
Serology
Mx: doxycycline
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110
Q 
RABIES (LYSSA VIRUS)
reservoir
symptoms
investigation
management
A

dogs/cats/bats
seizures, excessive salivation, agitation, confusion
serology
Mx: Ig, vaccine

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111
Q

RAT BLUE FEVER
organisms
symptoms
management

A
  • streptobacillus moniliformis
  • fevers, polyarthralgia, rash
  • can progress to endocarditis
  • Mx; penicillin
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112
Q

causes of viral haemorrhagic fever

A
  • ebola (bats)
  • lass (rats)
  • crimean congo haemorrhagic fever (ticks)
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113
Q

sail sign

A

double heart border

LLL collapse

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114
Q

features of strep pneumoniae

A

gram +ve cocci
alpha-haemolytic
optochin-sensitive

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115
Q

main organisms causing CAP

A 
S. pneumoniae
H. influenzae
Moraxella catarrhalis
Staph aureus
Klebsiella pneumoniae
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116
Q

atypical causes of CAP

A

legionella
mycoplasma
Coxiella burnetti (Q fever)
chlamydia psittaci

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117
Q

urea and RR cut offs in CURB

A

urea >7

RR > 30

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118
Q

bronchitis causing organisms

A

viruses
S. pneumoniae
H. influenzae
Moraxella catarrhalis

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119
Q

causes of cavitation on CXR

A

staph aureus
Klebsiella pneumoniae
TB

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120
Q

features of H. influenzae

A

gram -ve cocco bacilli

chocolate agar plate

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121
Q

what investigations in legionella pneumophilia?

A

grown on buffered charcoal yeast extract

urinary antigen

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122
Q

stains in TB and coloir

A

auramine stain + Ziehl Neelson stain

red rods = acid fast bacilli

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123
Q

causes of HAP

A

Enterobacteriae (e.g. E coli, K. pneumoniae)
Staph aureus
Pseudomonas sp

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124
Q

PCP type of organism and Ix

A

protozoan
walk test = de sat on exercise
CXR: bat wing shadowing

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125
Q

3 lung diseases caused by aspergillus fumigatus

A
  • allergic bronchopulmonary aspergillosis (chronic wheeze, eosinophilia, bronchiectasis)
  • aspergilloma
  • invasive aspergillosis (immunocompromised)
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126
Q

treatment of invasive aspergillosis

A

amphotericin B

127
Q

treatment of HAP

A
  1. ciprofloxacin +/- vancomycin

2. piptazobactum + vancomycin

128
Q

MRSA and Pseudomonas treatment

A

MRSA: vancomycin
Pseudomonas: Tazocin or cipro +/- gentamicin

129
Q

what percentage of world population is infected with TB

130
Q

categories of mycobacterium

A
  • TB complex (TB, bovis)
  • avium complex (avium, intraceullare)
  • abscessus complex
  • ungrouped (leprae)
131
Q

describe the features of mycobacteria

A

non motile rod shaped

mycolic acid, complex waves, glycoprotein cell wall

132
Q

what stain is used for MTB screening?

133
Q

types of slow growing Non-TB mycobacteria

A
  • avium complex (disseminated in immunosuppressed)
  • marinum (swimming pool granuloma)
  • ulcerans (Brului ulcer)
134
Q

2 types of mycobacterium leprae

A
  1. Paucibacillary tuberculoid: few skin lesions, robust T cell response
  2. Multibacillary lepromatous: lots of bacilli, multiple skin lesions, poor T cell response
135
Q

what is primary TB?

A

Ghon focus

granuloma in lungs

136
Q

what is post-primary TB?

A
  • reactivation/ re-infection
  • > 5 years after initial infection
  • pulmonary/ extra-pulmonary
137
Q

forms of extra-pulmonary TB

A
  • lymphadenitis (scrofula)
  • GI
  • peritoneal (ascitic or adhesions)
  • GU
  • bone and joint (Spine = Potts)
  • mililary TB
  • TB meningitis
138
Q

investigation requirement for TB

A

3 sputum samples for culture

139
Q

what does tuberculin skin test (TST) look for?

A

looks for previous exposure to bacteria

140
Q

second line meds for TB

A

quinolones
injectables e.g. amikacin
linezolid
ethionamide

141
Q

rifampicin SEs

A

reduced transaminases
induces CYP450
orange secretions

142
Q

Isonaizid SEs

A 
peripheral neuropathy (give with pyroxidine)
hepatotoxicity
143
Q

side effect of pyrazinamide

A

hepatotoxic

144
Q

ethambutol SEs

A

visual disturbance

145
Q

multi-drug resistant TB definition

A

resistant to rifampicin and isoniazid

146
Q

extremely drug resistant TB

A

also resistant to fluoroquinolones and 1 injections

147
Q

natural reservoir for influenza A

148
Q

how does flu virus attaches to cell ?

A

sialic acid receptors

149
Q

what is the purpose of the haemaglutinin protein?

A
  • needs to be cleaved for virus to be able to fuse with endosome and release genome
  • human airway tryptase in lung capable of cleaving HA
150
Q

what does the PB2 627K mutation allow?

A

mutation that allows bird flu to cross into human (polymerase protein)

151
Q

amantadine target and use

A

M2 channel

influenza A

152
Q

NA inhibitors

A

Oseltamivir (oral)

Zanamivir (inhaled/IV)

153
Q

what does the seasonal flu vaccine contain?

A

NA + HA of inactivated virus

154
Q

MoA of Aciclovir

A
  • nucleoside analogue
  • gets incorporated into growing chain of viral DNA
  • chain termination
  • needs activation by viral thymidine kinase
155
Q

what are the indications for treatment for VZV?

A

chicken pox in adults
shingles in adults
immunocompromised
neonates

156
Q

where does CMV remain latent?

A

blood, monocytes, dendritic cells

157
Q

CMV appearance

A

Owl’s eye inclusions

158
Q

different treatment options for CMV

A
  • ganciclovir
  • valganciclovir
  • foscarnet
  • cidofovir
159
Q

how is ganciclovir activated? SE

A

activation UL97 kinase enzyme

SE: bone marrow toxic

160
Q

what is valganciclovir?

A

prodrug of ganciclovir

can be taken PO

161
Q

MoA of foscarnet

A

non-competitive inhibitor of viral DNA polymerase
used when ganciclovir is contraindicated (e.g. neutropaenia)
SE: nephrotoxic

162
Q

MoA of cidofovir and SE

A

nucleotide analogue
competitive inhibitor of viral DNA synthesis
does not require activation
SE: nephrotoxic

163
Q

HA purpose

A

HA medicated virus binding and entry into target cell

164
Q

NA purpose

A

allow release of progeny virus particles from host cell

165
Q

RSV drugs

A

ribavirin (inhibits viral RNA synthesis)

IVIG

166
Q

RSV prophylaxis

A

Palivizumab

167
Q

BK virus effects in BM transplant and tx

A

haemorrhagic cystitis

Tx: cidofovir

168
Q

BK virus effects in renal transplant

A

BK nephritis

Tx: reduce immunosuppression, IVIG

169
Q

what is a quasispecies?

A

population of virus are genetically heterogenous rather than clonal

170
Q

cause of HSV drug resistance

A

mutations in viral thymidine kinase

171
Q

cause of CMV drug resistance

A

mutations in protein kinase gene (UL97)

172
Q

what is R0?

A

number of people that 1 sick person will infect on average

173
Q

what is the herd immunity threshold?

174
Q

examples of inactivated vaccines

A

influenza
polio
cholera

175
Q

examples of toxoid vaccines

A

diptheria

tetanus

176
Q

subunit vaccines

177
Q

which exams can cause anaphylaxis?

A

DTP
T/DT/Td
Hep B

178
Q

side effect of measles and rubella vaccines

A

Measles: thrombocytopaenia
Rubella: acute arthritis

179
Q

congenital toxoplasmosis S/S

A

40% babies symptomatic at birth

  • chorioretinitis
  • microcephaly
  • intracranial calcifications
  • seizures
  • hepatosplenomegaly
180
Q

congenital rubella triad

A
  1. cataracts
  2. congenital heart disease (PDA)
  3. deafness
181
Q

which is a particularly problematic E.coli in neonates?

A

E. coli K antigen

182
Q

treatment of late onset neonatal sepsis

A

cefotaxime + vancomycin

183
Q

pneumococcal conjugate vaccine number of serotypes

184
Q

how do you classify streptococci?

A

alpha-haemolytic: blood agar turns green (partial haemolysis) e.g. strep pneumoniae, strep viridans

beta-haemolytic: blood agar turns clear (full haemolysis)
Lancefield grouping

185
Q

Lancefield grouping

A

A: strep pyogenes
B: strep agalactiae
D: enterococci

186
Q

H. influenza features

A

gram -ve

grows glossy colonies on blood agar

187
Q

extra-pulmonary features of mycoplasma pneumoniae

A
  • haemolysis (IgM Abs, cold agglutins)
  • neurological
  • polyarthralgia
  • otitis media
  • bullous myringitis (vesicles on tympanic membrane)
188
Q

which are the yeasts?

A

candida
cryptococcus
histoplasma

189
Q

what are the moulds?

A

aspergillus
dermatophytes
agents of mucormycosis

190
Q

describe candida

A

form individuals cells

grow in colonies

191
Q

which candida is sensitive to first line antifungals?

A

C. albicans

192
Q

what are the problems with C. glabrata and C. krusei?

A

resistant to first line drug

193
Q

what does candida albicans form on screening?

194
Q

what happens if candida affects eyes?

A

endopthalmitis

195
Q

why should you give anti-fungal in upper GI perforation?

A

candida leaks into mediastinum = mediastinitis

196
Q

agar and serology for Candida

A

sabouraud agar

Beta D Glucan assay (serology)

197
Q

management of candida

A

2 weeks of antifungals

flucanazole: C. albicans
echinicandins: non C. albicans

198
Q

features of crypotococcus

A

caused by cryptococcus neoformans
primary pulmonary infections = subclinical
dissemination = predilection to CNS

199
Q

treatment of cryptococcus

A

choice: ambisome
resistant to echinicandins
susceptible to fluconazole, amphotericin

200
Q

life cycle of cryptococcus

A
  • birds excreta
  • spores inhaled
  • lodges into alveoli
  • disseminated into CNS
201
Q

microscopy of cryptococcus

A

India Ink

Enzyme immunoassay

202
Q

Management of cryptococcus

A

3 weeks of amphotericin +/- flucytosine

203
Q

diseases caused by aspergillus

A
  • mycotoxicosis (ingestion of contaminated food)
  • allergy
  • colonisation
  • invasive disease
  • systemic/fatal disseminated disease
204
Q

diagnosis of aspergillosis

A

serology
IgE allergic response = ABPA
antigen detection = galactomannan

205
Q

management of aspergillosis

A

amphotericin

at least 6 weeks

206
Q

examples of dermatophyte infections

A

ringworm
tinea
nail infection

207
Q

cause of tinea pedis

A

athletes foot

Trichophyton rubrum

208
Q

cause of tinea cruris

A

groin area

trichophyton rubrum

209
Q

tinea corporis

A

body

ring worm

210
Q

cause of tinea capitis

A

head

trichophyton rubrum

211
Q

cause and treatment of onychomycosis

A

Trichiphyton species

Tx: nail lacquers and terbinafine

212
Q

Pityrasis versicolor

A

skin discolouration

malassezia furfur

213
Q

symptoms of mucromycosis

A

severe/invasive disease
cellulitis of orbit = discharge, black pus from palate/nose
dec level of consciousness id brain involved (rhinocerebral)

214
Q

cause of mucormycosis

A

Rhizopum spp
Rhizomucor spp
Mucor spp

215
Q

Tx of mucormycosis

A

surgical emergency debridement

high dose amphotericin

216
Q

MOA of Azole antifungals

A
  • inhibit ergosterol production
  • accumulation of toxic steroids
  • cell death
217
Q

issue with azoles

A

cross reactivity with human CYP450 enzymes (drug interactions)

218
Q

Voriconazole coverage

A

candida, cryptococcus, aspergillus

219
Q

itraconazole coverage

A

dermatophytes

220
Q

posaconazole coverage

221
Q

Echinocandin MOA

A

inhibit production of Beta-D GLucan (component of fungal cell wall)
= osmotic fragility

222
Q

Echinocandin examples and active against

A

e.g. caspofungin, andiulafungin

active against: candida, aspergillius

223
Q

main Polyene

A

Amphotericin B

Ambisome = amphotericin within phospholipid bilayer

224
Q

MOA of amphotericin

A

binds to ergosterol in fungal cell membrane

creates transmembrane channels = fungal cell death

225
Q

which fungis are amphotericin not active against?

A

Aspergillus Terreus

Scedosporum spp

226
Q

MOA of flucytosine

A

inhibits DNA in fungal cells
restricted spectrum of activity
monotherapy limited

227
Q

type of virus: Rubella

A

Togovirdae family

228
Q

Congenital Rubella Syndrome

A

most likely <12 weeks

  • sensorineural hearing loss
  • microcephaly
  • PDA
  • cataracts
229
Q

congenital CMV

A

most common congenital infection
90% asymptomatic at birth
leading cause of hearing loss - give audiology F/U

230
Q

when is the highest risk of HSV neonatal infection? presentations?

A

primary HSV in 3rd trimester
SEM disease
CNS disease
disseminated disease

231
Q

VZV virus type

232
Q

Congenital Varicella Syndrome

A 
13-20 weeks
LBW
Cutaneous scarring
Limb hypoplasia
Microcephaly
Chorioretinitis
233
Q

measles virus type and rash

A

RNA paramyxovirus

maculopapular rash = starts behind ears

234
Q

what is the problem with measles in pregnancy? Tx?

A

measles in pregnancy = risk to mother (foetal loss, preterm delivery)
no congenital abnormalities
Tx: measles Ig within 6 days of exposure

235
Q

Parvovirus B19 virus type and biggest risk

A

DNA virus

biggest risk <20 weeks

236
Q

what does Parvovirus attack?

A

erythrocyte precursors

virus needs P blood antigen receptor to enter cell

237
Q

inhibitors of cell wall synthesis (groups and examples)

A
  • beta lactam (penicillins, cephalosporins, carbapenems)

- glycopeptide (vancomycin, teicoplanin)

238
Q

glycopeptide coverage

A

only gram +ve

239
Q

gram +ve vs gram -ve structure

A

gram +ve: thick peptidoglycan wall

gram -ve: outer membrane

240
Q

what is the MOA of Beta-Lactam Abs?

A

inactivate transpeptidases/pen binding proteins involved in terminal stages of cell wall synthesis
active against rapidly dividing bacteria

241
Q

amoxicillin coverage

A

broad spec

extends coverage to enterococci and gram _ve

242
Q

important to remember about flucloxacillin

A

does not get broken down by beta lactamases

243
Q

piperacillin coverage

A

amoxicillin and coverage to Pseudomonas and other non-enteric gram -ve

244
Q

1st gen cephalsporin

A

cephalaxin

245
Q

2nd generation of cephalosporin

A

cefuroxime

246
Q

3rd generation of cephalosporin

A

cefotaxime
ceftriaxone
ceftazidine

247
Q

issue with cephalosporin

A

C. diff (esp Ceftriaxone)

248
Q

Ceftazidine importance

A

good anti-pseudomonas

249
Q

MOA of glycopeptides

A

large molecules
binds to amino acid chain
prevents glycoside bonds and crosslinks

250
Q

use of glycopeptides

A

MRSA

but nephrotoxic

251
Q

inhibitors of protein synthesis

A 
aminoglycosides (gentamicin, amikacin)
tetracyclines
chloramphenicol
oxazolidnoes (e.g. Linezolid)
macrolides
252
Q

aminoglycoside MOA and SE

A

30S subunit of ribosome

ototoxic, nephrotoxic

253
Q

tetracycline MOA and danger

A

30S subunit of ribosome

do not give to children/ pregnancy

254
Q

MOA of macrolides, warning

A

50S subunit

minimal activity against gram -ve

255
Q

chloramphenicol MOA and SEs

A

50S subunit of ribosomes

SE: aplastic anaemia, grey Baby syndrome

256
Q

Oxazilidinedions MOA and coverage

A

binds to 23S component of 50S subunit of ribosomes

gram +ve (MRSA, VRE)

257
Q

inhibitors of DNA synthesis

A
  • Fluroquinoles: ciprofloxacin

- Nitroimidazoles: metronidazole

258
Q

Fluroquinoles MOA and cover

A

act of alpha subunit of DNA gyrase

broad cover: gram -ve and pseudomonas

259
Q

MOA of nitroimidazole

A

DNA strand breakage in anaerobic conditions

260
Q

Rifampicin MOA

A

inhibits protein synthesis

binds to DNA dependent RNA polymerase

261
Q

SEs of rifampicin

A

monitor LFTs
interactions with other drugs, metabolised in liver
orange secretions

262
Q

cell membrane toxin Abx

A
  • daptomycin: cyclic lipopeptide (gram +ve)

- colisitin: polymyxin, gram -ve

263
Q

inhibitors of folate metabolism

A

sulphinamides

diaminopyrimine (e.g. trimethoprim)

264
Q

mechanism of resistance

A

chemicals modifications/inactivation of Abx
modification/replacement of target
dec antibiotic accumulation
bypass Abx-sensitive sensitive step

265
Q

which enzymes gain resistance through inactivation? exception

A

beta lactamases

exception pen-resistant pneumococcus + MRSA

266
Q

how does MRSA get resistance?

A

altered targets

MRSA has mecA gene encodes PBP2a (low affinity for beta lactamases)

267
Q

how does strep pneumoniae gain resistance?

A

mutations in PBP genes

can over come by increasing dose

268
Q

how does macrolide gain resistance?

A

erm genes cause modification of 23S RNA

reduces binding or macrolide

269
Q

what is the MIC?

A

minimum inhibitory concentration

minimum drug conc to inhibit growth of organism

270
Q

aim of type I abx

A

maximise conc
e.g. aminoglycosides
(measure trough concentration)

271
Q

aim of type II abx

A

maximise time above MIC
e.g. penicillins
need to take frequently

272
Q

aim of type III abx

A

amount of drug above MIC is most important
e.g. vancomycin
(time and conc dependent effects)

273
Q

what is haemophagocytic lymphtohistiocytosis>

A

perforin deficiency

increased incidence of EBV

274
Q

what mutation is HHV8 associated with?

A

STIM1 mutation

275
Q

when do you normally suffer from viral infections after solid organ transplant?

A

normally after 1 month

276
Q

when do viral infections happen following BM transplant?

A

early due to intense immunosuppression

277
Q

what are the different human herpes viruses?

A 
HSV 1+ 2
VZV
CMV
HHV6
HHV8
EBV
278
Q

what are Owl’s eyes?

A

appearance of lung pneumocytes caused by inclusion bodies

279
Q

when is the risk of reactivation of CMV greatest in solid transplant?

A

greatest risk is when donor has had past CMV but recipient is naive

280
Q

when is the risk of reactivation of CMV greatest in BM transplant?

A

greatest risk of when recipient has had past CMV but donor is naieve

281
Q

different disease HHV8 is associated with

A

Kaposi sarcoma
Primary effusion lymphoma
Multicentric Castleman disease

282
Q

Histological findings of Kapsoi sarcoma

A

spindle cell proliferation
neo-angiogenesis
inflammation and oedema

283
Q

what is JC virus associated with?

A

progressive multifocal leukoencephalopathy

= demyelination of white matter

284
Q

what monoclonal Ab increasing risk of PML?

A

Natalizumab (used in MS)

285
Q

BK virus

A

polyamivirus, dsDNA

BK cystitis, BK nephritis

286
Q

HBV serology if infected

A

develop Ab against core and surface Ag

287
Q

HBV serology if acute infection becomes chronic

A

HBsAg will persist

288
Q

HBV serology if vaccinated

A

Ab against surface Ag (NOT core)

289
Q

what is the classification of worms (based on shape)?

A
  • cestodes (tape worm): hydatid disease, pork/fish/beef tapeworm
  • trematodes (flushes): e.g. schistosmasis
  • nematodes (roundworms): e.g. Hookwarms, Ascarids, Stronglyodides
290
Q

when do pork/beef tapeworm become problems?

A

humans are definitive host

cause trouble when humans become accidental/immediate host

291
Q

pork tapeworm and consequence

A

taenia solum

can invade human tissue causing cystericosis

292
Q

beef tapeworm

A

taneia saginata

293
Q

treatment and prevention of worms

A 
treatment = praziquental
prevention = hygiene
294
Q

how do people get infected by Schistosomiasis and where can the eggs affect?

A

contaminated water with cercariae from snails
damage caused by laying of eggs
eggs to bladder = bladder cancer
eggs to liver = cirrhosis

295
Q

treatment of schistosomiasis

A

praziquantel

296
Q

different soil transmitted helminths

A
  • ascaris lumbricoides (eggs hatched in intestine = adult worm)
  • hookworm
  • stronglyoides stercoralis
297
Q

important fact about strongyloids

A

only helminth capable of auto infection (via perineal skin)

Tx: Ivermectin

298
Q

filariasis spread by

A

blackflies and mosquitoes

299
Q

how is filariasis categorised

A

on where adult worm lives

lymphatic/ subcutanoues/serous cavity

300
Q

symptoms of lymphatic filarisis

A

scotal swelling
elephantasis
oncho-nodule

301
Q

what is myiasis

A

parasitisation of human flesh by fly larvae

e.g. Bot (S. America), Tumbu (Africa)

302
Q

what is the most common cause of adult onset seizures in world?

A

Brain worms

303
Q

how percentage of the population is infected with latent TB?

304
Q

what is taenia solium cystericosis?

A

infection of tissues with pork tapeworm
brain worms = ingestion of eggs
Sx manifest due to cyst degeneration

305
Q

Neurocystericosis management

A

anticonvulsant
VP shunt
cestocidal drugs (e.g. Praziquantel)
Steroids

306
Q

RFs for TB

A 
malnutrition
HIV
Poverty
Underweight
past TB
307
Q

stain for malaria

A

Fields

Giemsa stain

308
Q

treatment of Non-Falciparium

A

chloroquine

primaquine (check G6PD)

309
Q

treatment of non-falciparium

A

oral malarone
Artermisinin combination therapy
quinine

310
Q

treatment of severe falciparum

A

IV artesunate

311
Q

cause and features of dengue

A

aedes mosquito

fever, headache, myalgia, erythrofermic rash, hepatitis

312
Q

how does chikungunga present?

A

similar to dengue but worse arthralgia

313
Q

what is Faget sign?

A

sphygomothermic dissociation

HR should go up with fever

314
Q

Salmonella typhi organism and treatment

A

gram -ve rod

Tx: ceftriaxone + azithromycin

Cross reference - year 5 (22 decks)

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