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Julija's Path > Microbiology ✔ > Flashcards

Microbiology ✔ Flashcards

1
Q

how do penicillin antibiotics work?

A

beta-lactam ring

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2
Q

how do cephalosporins work?

A

beta-lactam ring

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3
Q

how do carbapenems work?

A

beta-lactam ring

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4
Q

what are the tree types of antibiotics which work by inhibiting cell wall binding via beta-lactam rings?

A

penicillin
cephalosporins
carbapenems

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5
Q

what are the two types of glycopeptide antibiotics?

A

vancomycin

teicoplanin

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6
Q

how do beta-lactam antibiotics work?

A

contain beta-lactam ring which interferes with cell wall synthesis by binding the penicillin-binding proteins (PBP) which normally work to cross link and strengthen bacterial cell wall. These PBPs bind to the beta-lactam antibiotics instead. These abx are bactericidal, especially against rapidly dividing bacterium

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7
Q

when are beta-lactam (eg. penicillin) antibiotics ineffective?

A

bacteria without peptidoglycan cell walls

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8
Q

what is the difference between gram positive and gram negative cell walls?

A

gram positive: peptidoglycan & cytoplasmic membranes

gram negative walls: peptidoglycan wall in between outer and inner cell membranes

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9
Q

what color do gram negative & gram positive bacteria stain?

A

gram negative - pink/red. the thinner peptidoglycan wall means it doesn’t keep the stain.
gram positive - purple

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10
Q

what organisms do penicillin antibotics work well against?

A

Gram positive organisms, Streptococci, Clostridia

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11
Q

what organisms does amoxicillin work well against?

A

Broad spectrum penicillin, extending coverage to Enterococci and Gram negative organisms

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12
Q

what is special about flucloxacillin as opposed to the other penicillins?

A

the only penicillin antibotic stable to staph aureus beta-lactamase

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13
Q

what organisms does pipericillin work well against?

A

similar to amoxicillin, extends coverage to Pseudomonas and other non-enteric Gram negatives

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14
Q

what is special about co-amoxiclav and tazobactam?

A

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

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15
Q

name a first generation, second generation, third generation cephalosporin:

A

first generation - cephalexin
second generation - cefuroxime
third generation - cefotaxime, ceftriaxone, ceftazidime

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16
Q

what organisms is cefuroxime effective against?

A

Stable to many β-lactamases produced by Gram negatives. Similar cover to co-amoxiclav but less active against anaerobes

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17
Q

what antiobiotic - resistant infection is ceftriaxone associated with?

A

c. difficile

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18
Q

what antibiotic resistant organism is sensitive to ceftazidime?

A

pseudomonas

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19
Q

what organisms are resistant to all cephalosporins?

A

Extended Spectrum β-lactamase (ESBL)

e.g. strains of E Coli or Klebsiella

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20
Q

what are the key drug metabolism facts about beta-lactams?

A

renally excreted – so decrease dose with renal impairment
short half life
will not cross BBB

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21
Q

how do glycopeptide antibiotics work?

A

active against gram positive bacteria but cannot penetrate gram negative bacterial cell walls. Inhibit cell wall synthesis by blocking glycosidic bonds and peptide cross links of bacteria (between NAM-NAM and NAG-NAG)

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22
Q

name two examples of glycopeptide antibiotics:

A

vancomycin

teicoplanin

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23
Q

what two antibiotic resistant infections can be treated wtih glycopeptide antibiotics (eg vancomycin)?

A

oral vanc - C. Diff

IV vanc - MRSA

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24
Q

what key organs can be affected by glycopeptide antibiotics?

A

cause renal toxicity

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25
Q

what classes of antibiotics inhibit protein synthesis?

A 
aminoglycosides
tetracyclines
macrolides
chloramphenicol
Oxazolidinones
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26
Q

how do aminoglycosides work?

A

bind to amino-acyl site of 30s ribosomal subunit to stop elongation of polypeptide chain and cause misreading of mRNA codons

  • rapid and concentration-dependent bactericidal action.
  • Works synergistically with beta-lactams but no effect on anaerobes as requires existence of certain channels to be able to pass through
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27
Q

what organs are aminoglycosides (eg gentamycin) toxic to?

A

ototoxicity

nephrotoxicity

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28
Q

when do we not give tetracyclines?

A

pregnant women & children

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29
Q

how do tetracyclines work?

A

Broad-spectrum agents with activity against intracellular pathogens, bind reversibly to ribosomal 30s subunit and thus prevent protein synthesis in bacteria by preventing aa-tRNA from binding to codons

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30
Q

what are examples of macrolides?

A

clarithromycin, azithromycin

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31
Q

what are particular uses for macrolide antibotics (eg azithromycin)?

A

Useful agent for mild Staphylococcal or Streptococcal infections in penicillin-allergic patients

Also active against Campylobacter and Legionella

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32
Q

what bacteria are macrolides ineffective against?

A

gram negative bacteria

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33
Q

how do macrolide antibiotics work? (eg clarithromycin)

A

binding to 50s subunit of ribosome in bacteria to interfere with translocation and stimulate the disassociation of peptidyl tRNA

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34
Q

how does chloramphenicol antibiotic work?

A

binds to the peptidyl transferase of the 50S ribosomal subunit and inhibits the formation of peptide bonds during translation

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35
Q

what is the risk associated with use of chloramphenicol antibiotics?

A

aplastic anemia

grey baby syndrome (in neonates)

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36
Q

how do Oxazolidinones (i.e. Linezolid) work?

A

bind to 23s component of 50s ribosomal subunit to prevent the formation of a functional bacterial 70s initiation complex for translation to occur

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37
Q

when is Linezolid active & when do we prescribe it?

A

highly active against gram positive organisms, but not gram negatives. active against MRSA and VRE.

we only prescribe it with consult with ID - may cause thrombocytopenia

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38
Q

what are some examples of quinolones?

A

ciprofloxacin
levofloxacin
moxifloxacin

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39
Q

what are some examples of nitroimadizoles?

A

metronidazole

tinidazole

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40
Q

how do quinolones (eg ciprofloxacin) and nitroimadizoles (eg metronidazole) work?

A

inhibit DNA synthesis

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41
Q

how do fluroquinolones work?

A

Act on alpha-subunit of DNA gyrase; bacteriocidal

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42
Q

what infections are fluoroquinolones used for?

A

UTIs, pneumonia, atypical pneumonia & bacterial gastroenteritis; especially gram negative

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43
Q

how does nitroimadizoles work?

A

Under anaerobic conditions, an active intermediate is produced which causes DNA strand breakage; bacteriocidal

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44
Q

what infections are nitroimadizoles used against?

A

Active against anaerobic bacteria and protozoa (e.g. Giardia)

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45
Q

how do rifamycins (eg rifampicin) work?

A

inhibit bacterial RNA synthesis; Inhibits protein synthesis by binding to DNA-dependent RNA polymerase thereby inhibiting initiation; bactericidal

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46
Q

what infections is rifampicin effective against?

A

certain bacteria, including Mycobacteria & Chlamydiae

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47
Q

what do you need to beware of when giving rifampicin?

A
  • interactions with other drugs metabolized in liver (eg COCP)
  • may turn urine or contact lenses orange
  • resistance develops rapidly so don’t give by itself!
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48
Q

what is daptomycin?

A

a new abx that is a cyclic lipopeptide with activity limited to G+ve pathogens. Likely to be used like linezolid (eg MRSA, VRE)

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49
Q

what is colistin?

A

a new polymyxin antibiotic that is active against Gram negative organisms (including klebsiella and pseudomonas). Should be reserved for multi-drug resistant organisms.

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50
Q

what two antibiotics work by inhibiting folate synthesis?

A

Diaminopyrimidines

Sulfonamides

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51
Q

what two medications are combined in co-trimoxazole?

A

sulphamethoxazole+trimethoprim

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52
Q

when is trimethoprim used?

A

treating community acquired UTIs

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53
Q

what are the 4 mechanisms of developing antibiotic resistance?

A

1) chemical modification/inactivation of abx
2) modification/replacement of abx target
3) reduced antibiotic accumulation (impaired uptake or enhanced efflux)
4) bypassing the step in bacterial growth that is sensitive to the abx

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54
Q

how are Staphylococcus aureus and Gram Negative Bacilli penicillin resistant?

A

chemical modification/inactivation of abx –> beta lactamases

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55
Q

how is MRSA antibiotic resistant?

A

new mecA gene encodes a novel PBP (2a) with a low affinity for binding ß Lactams so the antibiotic is ineffective at therapeutic doses

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56
Q

what animals are the natural hosts for influenzae organisms?

A

birds

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57
Q

what antivirals are available for influenza?

A

1) Amantadine: Targets M2 ion channel, but a single amino acid mutation in M2 (S31N) renders virus resistant
2) Neuraminidase inhibitors and mode of administration:
Tamiflu (oseltamivir) oral
Relenza (zanamivir) inhaled
Peramivir iv

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58
Q

describe influenza vaccines in use today:

A

trivalent or quadrivalent inactivated vaccine given to those at risk which has a short-term strain specific immunity mediated by antibody to HA head. Required adjuvant to produce robust immune response.

Other option is tri or quadrivalent live attenuated vaccine given to children. Broader more cross reactive immunity including cellular response

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59
Q

what are the most common organisms in hospital acquired UTI?

A

Lactose fermenting - E Coli (MOST COMMON), also klebsiella spp
Non-lactose fermenting - pseudomonas

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60
Q

what is c. difficile?

A

a gram positive spore forming anerobe that usually infects in hospital or patients on antibiotics. The spores persist so that contamination can persist for long periods of time. This produces coilitis & diarrhea. Manage with metronidazole or vancomycin

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61
Q

do we use this for gram positive or gram negative? flucloxacillin

A

gram positive

narrow spectrum

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62
Q

do we use this for gram positive or gram negative? co-amoxiclav

A

gram positive; community gram negative; anerobes

broad spectrum

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63
Q

do we use this for gram positive or gram negative? metronidazole

A

anaerobes

narrow spectrum

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64
Q

do we use this for gram positive or gram negative? piperacillin-tazobactam

A

hospital gram negative; some gram positive; anaerobes; pseudomonas
(broad spectrum + anti-pseudomonal)

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65
Q

do we use this for gram positive or gram negative? amoxicillin

A

gram positive, gram negative, anerobes

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66
Q

do we use this for gram positive or gram negative? ciprofloxacin

A

mainly gram negative, ok for pseudomonas

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67
Q

do we use this for gram positive or gram negative? gentamicin

A

gram negative

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68
Q

do we use this for gram positive or gram negative? meropenem

A

hospital gram negative; gram positive; anaerobe; pseudomonas
(broad spectrum)

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69
Q

do we use this for gram positive or gram negative? colistin

A

hospital gram negative including carbapenem resistant

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70
Q

describe mycobacterium (in contrast to gram negative or gram positive):

A
  • non-motile rod-shaped bacteria that grow slowly
  • long chain fatty acids, complex waves, glycolipids in cell walls
  • acid alcohol fast – stain on Ziehl-Neelsen and Auramine
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71
Q

name 3 slow growing non-TB mycobacterium:

A

M. ulcerans – causes slowly growing painless ulcer
M. marinum - swimming pool granuloma
M. avium intracellulare-

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72
Q

name 3 fast growing non-TB mycobacterium:

A

M. abscessus
M. chelonae
M. fortitum

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73
Q

what is the natural history of myco. TB?

A

primary phase - usually asymptomatic; will have ‘Ghon focus’
latent phase
reactivation

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74
Q

what changes do we see in pulmonary TB?

A

caseating granuloma
with changes in mediastinal LNs
often issue in upper lobe

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75
Q

what are the potential extra-pulmonary forms of TB?

A
  • lymphadenitis - cervical LNs most commonly
  • GI - swallowing of tubercles
  • peritoneal - ascitic/adhesive
  • genitourinary - becomes renal disease
  • bone & joint - Pott’s disease
  • miliary TB - progressive disseminated hematagenous TB
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76
Q

what is 1st line treatment for TB?

A

RIPE

Rifampicin - p450 inducer; can turn urine/lenses orange
Isoniazid - peripheral neuropathy, hepatotoxicity
Pyrazinamide - hepatotoxicity
Ethambutol - visual disturbance
Take all four RIPE drugs for 2 months, then just RI for 4 months. Cure rate is 90%

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77
Q

what drugs is multi-drug resistant TB resistant to?

A

rifampicin/isoniazid

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78
Q

what drugs is extremely drug resistant TB (XDR TB) resistant to?

A

rifampicin, isoniazid, fluoroquinolones, and at least 1 injectable antibiotic

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79
Q

what are the 4 potential routes of entry for meningitis?

A

1) hematogenous spread
2) direct implantation
3) local extension
4) PNS into CNS

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80
Q

what are the potential causative agents for meningitis?

A 
Neisseria meningitidis
Strep pneumoniae
Hemophilus influenzae
TB
viruses
cryptococcus neoformans
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81
Q

what are the potential causative organisms for an encephalopathy?

A 
rabies virus
prions
amoeba
trypanosomas
Listeria monocytogenes
Toxoplasmosis
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82
Q

what are the potential causative organisms for myelitis (spinal cord) or neurotoxin disturbance (CNS/PNS)?

A

myelitis - polio virus

neurotoxins - clostridium tetani, clostridium botulinum

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83
Q

what are the four aspects of meningicoccal septicemia?

A

1) capillary leak (albumin/plasma proteins –> hypovolemia)
2) coagulopathy (via protein C pathway; bleeding/thrombosis)
3) metabolic derangement (acidosis)
4) HF/multi organ failure

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84
Q

what are the 3 main types of meningitis?

A

bacterial
TB
viral (aseptic)

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85
Q

what is the most common form of CNS infection?

A

Aseptic meningitis. Coxsackievirus group B and echoviruses are responsible for 80-90% cases in which a causative organism of aseptic meningitis is identified.

It most frequently occurs in children younger than 1 year.

The clinical course of aseptic meningitis is self-limited and resolves in 1-2 weeks.

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86
Q

what can west nile virus cause & has been producing outbreaks of?

A

encephalitis

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87
Q

which organisms can produce a brain abscess?

A
  • Streptococci (both aerobic and anaerobic)
  • Staphylococci,
  • Gram-negative organisms. (particularly in neonates)
  • Mycobacterium tuberculosis
  • fungi
  • parasites
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88
Q

what are the risk factors for spinal infections?

A
  • IVUD
  • age (elderly)
  • long-term steroid use
  • diabetes mellitus
  • malnutrition
  • cancer
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89
Q

what is a normal CSF result?

A

appearance: clear
cells: 0-5 leukocytes
gram stain: negative
protein: 0.1-0.4
glucose: 2.2-3.3

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90
Q

spot diagnosis- CSF

appearance: turbid
cells: polymorphs
gram stain: positive
protein: 0.5-3.0 (low/normal)
glucose: low

A

purulent (bacterial) meningitis

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91
Q

what is a CSF result for bacterial meningitis?

A

appearance: turbid
cells: polymorphs
gram stain: positive
protein: low/normal
glucose: low

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92
Q

what is a CSF result for viral meningitis?

A

appearance: clear/slightly turbid
cells: lymphocytes
gram stain: negative
protein: high
glucose: normal

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93
Q 
spot diagnosis- CSF
appearance: clear/slightly turbid
cells: lymphocytes
gram stain:  negative
protein: high
glucose: normal
A

viral meningitis

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94
Q

what is a CSF result for TB meningitis?

A

appearance: clear/slightly turbid
cells: lymphocytes/polymorphs/maybe acid-fast bacilli
gram stain: negative
protein: high
glucose: low

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95
Q 
spot diagnosis - CSF:
appearance: clear
cells: lymphocytes & polymorphs
gram stain:  negative
protein: high
glucose: low
A

TB meningitis

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96
Q

what stains with indian ink stains?

A

cryptococcus

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97
Q

what is generic therapy for meningitis (i.e. before any CSF results)?

A

ceftriaxone 2g IV BD
(if >50 years old or immunocompromised, add amoxicillin 2g IV 4 hrly)

Once you know the exact causative organism, then you can change antibiotics to target that, if bacterial.

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98
Q

what is generic therapy for meningo-encephalitis?

A

aciclovir 10mg/kg IV TDS
ceftriaxone 2g IV BD
(if >50 years old or immunocompromised, add amoxicillin 2g IV 4 hrly)
Once you know the exact causative organism, then you can change antibiotics to target that, if bacterial.

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99
Q

if someone has really severe malaria, what treatment should be given asap?

A

IV artesunate

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100
Q

describe dengue fever:

A

aedes mosquito transports this flavivirus into humans - presenting with a rash in 50% of people. this is usually a mild self-limited illness worse at day 4-5 (shock, bleeding, organ impairment)

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101
Q

what is the management for dengue fever?

A

EXCLUDE MALARIA!

serology to confirm, and then supportive

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102
Q

what happens in typhoid fever?

A

High prolonged fever
Headache
Rose spots (rare)
low/normal WCC

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103
Q

how do we treat typhoid fever?

A

rx - ceftriaxone IV

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104
Q

what are pathological signs of mononucleosis?

A 
EBV,  CMV,  HIV
Tonsillar enlargement with exudates
Atypical lymphocytosis
Monospot
IgM+ EBV/CMV
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105
Q

describe Rickettsial disease & diagnosis:

A

Fever, headache, myalgia +/- eschar
Obligate intracellular bacteria
Invades endothelial cells -> vasculitis
dx - serology

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106
Q

how do we treat Rickettsial disease?

A

doxycycline

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107
Q

name some examples of bacteriostatic & bacterioicidal antibiotics -

A

BACTERIOSTATIC: tetracyclines, macrolides, chloramphenicol
BACTEROCIDAL: aminoglycosides, penicillins, cephalosporins, carbapenems, fluoroquinolones, nitroimadizoles, rifamycins,

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108
Q

what is the difference between bacteriostatic and bacteriocidal antibiotics?

A

bacteriostatic - stops growth of bacterium; helps body to fight it off with natural immune system. good for rapidly growing infections

bacteriocidal - kills/lyses bacteria that are already exisiting and active so they cannot keep growing or propagate

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109
Q

name some protozoa -

A

malaria, leishmaniasis, trypsanosomiasis

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110
Q

name some helminth -

A

round worms (nematodes), tape worms (cesatodes), flukes (trematodes)

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111
Q

what is Chagas disease?

A

Trypanasoma cruzi :

  • spread by triatomine bugs
  • Cardiac disease: cardiomyopathy & arrhythmias
  • GI Disease: achalasia, megacolon
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112
Q

what is Trypanasoma brucei?

A

sleeping sickness spread by tsetse flies

-often present late with neuro signs: drowsiness, sleep/wake cycle inversion, confusion, psych symptoms

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113
Q

how do we treat leischmaniasis?

A

pentavalent antimonials and prevention (not nets; but rather DEET and collars)

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114
Q

what is enterobius vermicularis?

A

threadworm infection

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115
Q

how do we diagnose threadworm infections?

A

sellotape slide test for eggs

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116
Q

how do you treat enterobius vermicularis (threadworm)?

A

mebendazole x2

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117
Q

what is toxocara canis?

A

visceral or ocular helminth invasion from dogs

  • Non-specific presentation
  • Eosinophilia
  • Positive serology
  • Treat with albendazole; steroids; surgery
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118
Q

how do people get hookworms?

A

through the skin - eg. walking barefoot - prevention is key!
We are a dead end host so they may wander the skin (cutaneous larva migrans) but will die eventually. Drugs can speed up this process.

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119
Q

what is a strongyloides infection?

A

Common cause of eosinophilia
Treatment/prevention like hookworm
Helminth

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120
Q

what happens in strongyloidiasis?

A

hyperinfection syndrome - HTLV-1; steroids; biologics (infliximab, entanercept)
Leads to bowel perforation, meningitis/encephalitis, or even death

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121
Q

what does hydatid disease cause?

A

usually liver cysts with few other symptoms

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122
Q

how do we treat hydatid disease?

A

long term medication with albendazole or praziquantel, aspirate the cyst and then inject the medication

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123
Q

what is katayama fever?

A

infection by schistosomiasis water snails into lungs causing cough, wheeze, urticaria, eosinophilia

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124
Q

what can chronic schistosomiasis infection cause?

A

hematuria, bladder cancer, diarrhea, colitis, weight loss, liver fibrosis, portal HTN, or spinal/cerebral disease

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125
Q

how do we treat schistosomiasis?

A

praziquantel

126
Q

what is Onchocerciasis?

A

river blindness disease from black flies in Africa and South America. The adult worms hide in subcutaneous nodules and cause symptoms of pruritis, scratching, or in the eyes keratitis from the microfilariae

127
Q

what do bancroftian filariasis worms cause?

A

elephantiasis; lymph blockage

128
Q

how do we diagnose bancroftian fillariasis?

A

clinically - ‘dance sign’ on uss
blood film
serology

129
Q

what does dracunculiasis cause? (aka the guinea worm)

A

‘little dragon’ of central africa

the adult grows up to 1m long and migrates to the feet where it forces its way out - very painful event!

130
Q

what is the basic principle on which vaccines work?

A

The humoral response to a specific antigen is faster and more effective upon re-exposure

131
Q

name 4 types of vaccine:

A

live attenuated -
subunit/inactivated -
conjugate - increase immunogenecity
toxin (inactivated)-

132
Q

what are some examples of live and attenuated vaccines?

A

MMR
yellow fever
rotavirus

133
Q

what are some examples of inactivated vaccines?

A

Hep A
Hep B
pneumococcus
HPV

134
Q

what are some examples of conjugate vaccines?

A

DTAP
Hib (5-in-1)
Pneumococcal
Meningicoccal

135
Q

what are examples of inactivated (toxin) vaccines?

A

tetanus

diptheria

136
Q

what are some of the advantages to live vaccines?

A

single dose is often sufficient to induce long-lasting immunity; a strong immune response is evoked and local/systemic immunity produced

137
Q

what are some of the disadvantages to live vaccines?

A

potential to revert to virulence and contraindicated in immunosuppressed patients. Other viruses, vaccines can interfere and they have poor stability for transport

138
Q

what are some of the advantages of inactivated vaccines?

A

stable, constituents clearly define, unable to cause infection themselves

139
Q

what are some of the disadvantages to inactivated vaccines?

A

need several doses for immunity and shorter lasting immunity. Local reactions are common. An adjuvant is often needed to keep vaccine at the injection site and activate APCs.

140
Q

when are vaccines contraindicated?

A

ONLY if a confirmed anaphylactic reaction to a previous dose of the vaccine or one of its components

141
Q

when is DTP contraindicated?

A

precautioned if evidence of evolving neuro abnormality or current neuro deterioration (e.g. poorly controlled epilepsy)

142
Q

when is influenza vaccine contraindicated?

A

if a confirmed anaphylactic reaction to a previous dose of vaccine/component of vaccine and additionally in individuals with confirmed anaphylactic hypersensitivity to eggs

143
Q

when are live vaccines contraindicated?

A

any pregnant or immunocompromised patient

144
Q

what about vaccines in HIV patients?

A

SHOULD be given MMR if susceptible.
SHOULD be given inactivated vaccines

SHOULD NOT be given BCG.
SHOULD NOT be given Yellow fever vaccine.

145
Q

what is the definition of a complicated UTI?

A

infection in urinary tract with functional or structural abnormalities (including indwelling catheters and calculi)

146
Q

what sorts of patients get complicated UTIs?

A

men, pregnant women, children, patients who are hospitalized

147
Q

what sorts of organisms cause UTIs?

A 
(>95%) E Coli
Klebsiella aerogenes
Enterococcus faecalis
Staph saprophyticus
Staph epidermus
148
Q

what are the potential obstructive causes to ureters causing ascending UTI?

A
  • mechanical
  • extrarenal: valves, stenosis, calculi, extrinsic ureteral compressoin; BPH
  • intrarenal: nephrocalcinosis, uric acid nephropathy, PCKD, hypokalemic nephropathy
149
Q

what 3 investigations do you want to do for UTI?

A

-urine dip and MSU
-bloods: FBC, U&Es, CRP
(can move on to IV urography, renal USS)

150
Q

what sorts of patients do we check MC&S for in suspected or confirmed UTI?

A
  • pregnany
  • children
  • suspected pyelonephritis
  • suspected in men
    (esp. consider chlamydia)
  • catheterized patients
  • failed Abx treatment or persistant
  • ESBL organisms
  • renal impaired
151
Q

what are causes of sterile pyuria?

A
  • prior treatment with antibiotics
  • calculi
  • catheterisation
  • bladder neoplasms
  • TB
  • STDs
152
Q

what is the empirical treatment for UTI?

A

cefalexin or nitrofurantoin first line
*Dosage depends on gender, age, if systemically unwell.
(second line - co-amoxiclav or consider adding gentamicin/amikacin if severe and unwell)

153
Q

how long do we treat UTI with antibiotics for?

A

3 days if uncomplicated, female patient, well systemically. Otherwise 7 days.

154
Q

how do we treat fungal UTI infections?

A

most candida (yeast) UTIs occur in patients with indwelling catheters. Removal of the catheter may cure but oral fluconazole is no more effective than no therapy.

155
Q

what are the complications of pyelonephritis?

A
  • perinephric abscess
  • chronic pyelonephritis (scarring, chronic renal impairment)
  • septic shock
  • acute papillary necrosis
156
Q

what is pyelonephritis?

A

Infection of the kidney that is commonly associated with sepsis and septicaemia. Requires more aggressive treatment with broad spectrum antibiotics

157
Q

how do we treat pyelonephritis?

A

Co-amoxiclav +/- gentamicin

158
Q

where is Hep A most prevalent?

A

south america, africa, asia

159
Q

what is hep A virus?

A

acute hepatitis for 2-6 weeks, notifiable disease but often stays subclinical

160
Q

what is the serology progress of Hep A virus?

A

infection
then Hep A virus in stool 2-3 weeks later
ALT raises after 3-4 weeks
IgM raises first, then IgG after infection dies down. So IgM for current infection, IgG for past.

161
Q

how do we check for Hep A virus in someone?

A

Anti-HAV IgM -recent infection
Anti-HAV IgG -previous infection

(NOTE - vaccines can raise IgM and IgG)

162
Q

how is Hep A transmitted?

A

faecal - oral

163
Q

how is Hep B transmitted?

A

sexual; vertical; blood products

164
Q

what are the consequences of chronic Hep B infection?

A

healthy liver –> hepatic fibrosis –> cirrhosis –> liver cancer

165
Q

what is the serology timeline for Hep B infections?

A

Hep B sAg spikes first ( 8 weeks)
Hep B eAg spikes after
Anti-HBc will grow around 12 weeks after infection and stay raised
Anti-Hbs grows later
Anti-HBC IgM will spike around 20 weeks and then decrease back to lower levels.
Anti-HBe takes over a year to decrease to old levels

166
Q

what are the possible disease stages of Hep B virus?

A
  • immune, tolerant
  • immune, reactive
  • inactive HBV carrier
  • HBeAg negative (chronic HBV)
  • HBsAg negative
167
Q

what is the treatment for chronic HBV?

A
  • interferon alpha
  • lamivudine
  • tenofovir
  • entecavir
168
Q

how is Hep C virus spread?

A

mainly blood products; 60-80% end up chronic infection

169
Q

what is the serology timeline for acute hep C infection?

A

ALT spikes, then anti-HCV antibodies raise and stay raised

170
Q

what treatments can be used for Hep C infections?

A

interferon
ribavirin
peginterferon alfa-2b

171
Q

what is the serologic course of Hep D CO-infection?

A

only can infect after HBsAg present (i.e. with Hep B chronic infection)!

IgM anti-HDV rises first with ALT (liver enzymes), then total anti-HDV and IgM anti-HDV drop but anti-HBs continues risen

172
Q

Hep D can only infect in the presence of Hep B. What happens in Hep D super infection?

A

patient appears jaundiced & has symptoms with ALT spike.
The total anti-HDV levels keep rising but IgM anti-HDV spikes and then lowers down again.
This whole time HBsAg and HDV RNA are present.

173
Q

where does Hep E infection come from?

A

blood transfusions
shellfish
sausage/pig liver consumption
very little person-person spread

174
Q

what is the treatment for Hep E infection?

A

supportive

- ribavirin might help

175
Q

what is the incubation period for Hep E infection?

176
Q

what is the serology timeline for Hep E infections?

A

HEV RNA is detectable in stool & serum from 4 weeks.
ALT Spikes at about 6 weeks.
IgM anti-HEV antibody spikes around 4-6 weeks and then keeps dropping after
IgG anti-HEV antibody keeps growing until 24 weeks (6 months infection)

177
Q

what complications do we worry about with Hep E virus?

A
  • CNS disease - bell’s palsy, Guillan-barre

* Chronic infections

178
Q

what types of immune deficiencies occur in the host?

A

primary: SCID, common variable immunodef.
acquired: malignancy (lymphoma), viral infections, iatrogenic (drugs)

179
Q

Viral infections are the leading cause of mortality in allogenic stem cell transplants and a major cause of morbidity in autologous stem cell transplants. What are the risk factors associated?

A
  • allogenic BMT
  • mismatched related or matched unrelated
  • acute/chronic GvHD
  • immunosuppressive therapy
  • in vitro T cell depletion
  • delayed CD4 cell recovery time
180
Q

how can viral infections even infect a transplant recipient?

A
  • viruses acquired from graft (eg Hep B)
  • viruses reactivated from the host
  • novel infection from infected invidiual
181
Q

how do we detect opportunistic viral?

A

-serology has limited dx value
-virus detected: nucleic acids (PCR) or antigens
-

182
Q

what are the types of human herpes viruses?

A

-HSV 1/2
-Varicella zoster virus
-Epstein barr virus
-CMV
-HHV-6
HHV-8

183
Q

what happens in latent herpes virus infection?

A

only a small subset of genes expressed, reactivation can occur leading to expression of viral genes, production of progeny virus and destruction of host cells

184
Q

where do the herpes viruses lie latent? (HSV 1/2, VZV, EBV, CMV, HHV)

A 
HSV 1/2 - sensory nerve ganglia
VZV - sensory nerve ganglia
EBV - leucocytes, epithelial cells
CMV - b lymphocytes
HHV -  T lymphocytes, epithelial cells
185
Q

what happens with varicella in the immunocompromised?

A

varicella carries an increased risk of complications –> secondary bacterial infection of rash, bullous/hemorrhagic skin lesions (‘purpura fulminans’), pneumonitis, hepatitis

186
Q

what is shingles and what patterns does it come in?

A 
VZV = Herpes Zoster 
*reactivation of endogenous virus
*late complication -- >100 days post BMT
*comes in one of 3 patterns:
dermatomal skin eruptions
varicella like skin lesions w/o dermatome distributions ('atypical)
or reactivation without skin lesions
187
Q

how is varicella and herpes simplex treated in the immunocompromised?

A

acyclovir (oral or IV) or valaciclovir

188
Q

how does EBV virus present in the immunocompetent?

A

acutely - mono (fever, hepatitis, lymphadenopathy); mainly infecting B cells
chronic - lifelong low-grade replication, kept in check by cellular immune system

189
Q

how does EBV virus present in the immunocompromised?

A
  • oral hairy leukoplakia (in HIV infected)

- lymphomas (predisposed)

190
Q

how do you manage EBV virus in the immunocompromised?

A
  • confirm by biopsy of LNs
  • reduce immunosupression (helps in 50%)
  • anti-CD20 monoclonal Ab therapy (rituximab)
191
Q

how does CMV present in the immunocompromised?

A
  • kept in B lymphocytes
  • fever
  • bone marrow suppressoin
  • graft failure/delayed engraftement
  • hepatitis
  • gastritis, enterocolitis
  • interstitial pneumonitis
  • CMV retinitis (esp. in HIV patients)
192
Q

what viruses can cause retinitis in immunocompromised?

A

CMV, HSV, VZV

193
Q

how do you diagnose CMV?

A
  • PCR

- ‘owl’s eye’ inclusions on histopathology

194
Q

how do you treat CMV in the immunocompromised?

A 
-IV ganciclovir 
(risk of bone marrow suppression)
-oral valganciclovir
-iv foscarnet (nephrotoxic)
-CMV hyperIg
195
Q

how does HHV-8 present in the immunocompromised?

A

-particular issue for HIV infected patients

  • Kaposi’s sarcom
  • Primary Effusion lymphoma (PEL)
  • multicentric Castleman’s disease
196
Q

what is Kaposi’s sarcoma?

A
  • angioproliferative disorder
  • characterized by spindle cell proliferation, neo-angiogenesis, inflammation
  • preceded by HHV8 infection
  • involves lymphatic endothelium
  • dx only by biopsy (spindle cells)
197
Q

how does adenovirus present in the immunocompromised?

A

-fever
-bone marrow suppression
-hemorrhagic cystitis
-necrotising pneumonitis
-hepatitis
-colitis
This virus leads to high mortality with a disseminated infection.

198
Q

what is Progressive multifocal leukoencephalopathy and how does it present?

A
  • from polyomavirus ‘JC’
  • seen in AIDS patients, as well as those on high dose steroids, or on humanised monoclonal ab treatment
  • the demyelination of white matter with focal neuro deficits corresponding to the areas of brain affected
    dx: MRI/PCR on CSF
199
Q

which respiratory viruses present with increased risk of complications & high mortality in the immunocompromised?

A
  • Influenza A and B
  • Parainfluenza 1, 2, 3 and 4
  • RSV infection
  • Adenovirus
  • Novel coronavirus: MERS coronavirus
200
Q

how do we diagnose respiratory viruses in the immunocompromised?

A

multiplex PCR

201
Q

how is influenza treated in the immunocompromised?

A

osteltamivir for 5 days

202
Q

how does measles present in the immunocompromised?

A

FATAL. Either from…

  • giant cell pneumonia or
  • subacute measles encephalitis
203
Q

how do we treat measles in the immunocompromised?

A
  • don’t; supportive

- PEP –> normal human Ig

204
Q

what does human parvovirus B19 cause in the immunocompromised?

A

chronic anemia

dx: PCR on blood

205
Q

how do we treat parvovirus B19 in the immunocompromised?

A
  • human normal Immunoglobulin

- blood transfusion if indicated

206
Q

what is the serology difference between chronic Hep B virus infection in immunocompetent & immunocompromised?

A

HbsAg doesn’t go down. Acute infections continue.

  • Those with chronic infection may have flare of disease.
  • Those who have had past infection (ie core Ab+/surface antigen negative) may revert to positive surface antigen
207
Q

how do we treat hep B infection in immunocompromised?

A
  • Hep B Ig In liver transplant

- nucleoside/nucleotide analogues

208
Q

what tests can we do to check for viral transaminitis in post-transplant or otherwise immunocompromised patients?

A 
Hepatitis A IgM 
Hepatitis B surface antigen 
Hepatitis C virus PCR  
Hepatitis E virus PCR 
CMV PCR and EBV PCR 
Adenovirus PCR for paediatric patients
209
Q

which antibiotic is empirically most appropriate in skin infections?

A

common organisms are staph aureus & beta-hemolytic streptococci –> flucloxacillin abx

210
Q

which antibiotic is empirically most appropriate in pharyngitis?

A

benzyl-penicillin for 10 days

211
Q

which antibiotic is empirically most appropriate in CAP? (mild)

A

amoxicillin

212
Q

which antibiotic is empirically most appropriate in CAP (severe)?

A

co-amoxiclav & clarithromycin

213
Q

which antibiotic is empirically most appropriate in HAP?

A

cephalosporin; ciprofloxacin; pipercillin/tazobactam

If MRSA risk - consider adding Vancomycin

214
Q

which antibiotic is empirically most appropriate in bacterial meningitis?

A

neisseria meningitidis & strep pneumoniae most common –> ceftriaxone

215
Q

how do we treat meningitis in a baby under 3 months?

A

cefotaxime + amoxicillin

216
Q

why don’t we use ceftriaxone in neonates?

A

displaces bilirubin from albumin; can cause biliary sludging

217
Q

how do we treat neisseria meningitidis as cause of meningitis?

A

ceftriaxone/cefotaxime or benzylpenicillin (high dose)

218
Q

which antibiotic is empirically most appropriate in community acquired simple cystitis?

A

trimethoprim (3 days)

219
Q

which antibiotic is empirically most appropriate in hospital- acquired UTI?

A

cephalexin or augmentin

220
Q

what are the major pathogens of surgical site infections?

A 
staph aureus (eg MRSA)
E Coli
pseudomonas aeruginosa
221
Q

what are risk factors for septic arthritis?

A
  • Rheumatoid arthritis, osteoarthritis
  • joint prosthesis
  • IVDU
  • diabetes
  • CKD
  • liver disease
  • on steroids long term
  • trauma
222
Q

what are the causative organisms of septic arthritis?

A
  • staph aureus (about 50%)
  • streptococci (pyogenes, pneumoniae, agalactiae)
  • gram negative organisms (E Coli, hemophilus influenzae, neisseria gonorrhea, salmonella)
  • rarely: brucellosis, mycobacteria, fungi
223
Q

what are the clinical features of septic arthritis?

A

*1-2 week history of red, painful, swollen & restricted joints
(monoarticular in 90%, knee involved in 50%)

224
Q

how do we investigate septic arthritis?

A
  • blood culture
  • synovial fluid aspiration for MCS
  • ESR, CRP bloods
  • imaging - for needle aspiration
225
Q

what are the causative organisms of vertebral osteomyelitis?

A
  • Staph aureus (in almost 50%)
  • streptococcus
  • coagulase negative staphylococci
  • gram negative bacilli
226
Q

how do we diagnose vertebral ostemyelitis?

A
  • present with back pain & fever

- dx with MRI, blood cultures

227
Q

what food gives campylobacter infections?

228
Q

what food gives vibrio parahemolyticus infection?

229
Q

what food gives bacillus cereus infections?

A

reheated rice

230
Q

how do superantigen toxins work?

A

Superantigens bind directly to T-cell receptors and MHC molecules outside the peptide binding site, keeping them active and causing a….
» massive cytokine production by CD4 cells (ie systemic toxicity and suppression of adaptive response)

231
Q

how would staph aureus give food poisoning?

A

catalase, coagulase positive gram positive coccus that produces a new enterotoxin that can act as a superantigen in the GI tract (releasing IL2/IL1) and causing prominent vomiting and watery, non-bloody diarrhea. you have to just give supportive treatment and let it be self-limited.

232
Q

how does bacillus cerues cause food poisoning?

A

spore-forming gram positive rods, where the spores germinate when you reheat the food. There are two toxins involved… a heat stable emetic toxin (vomiting even from reheating), and a heat labile diarrheal toxin (when food not cooked to high enough temperature). This causes watery, non bloody diarrhea in a self-limited course.

233
Q

how can clostridium botulinum cause botulism?

A

found in canned/packed vacuum food. when we ingest the preformed toxins (usually inactivated by cooking), then Ach release is blocked from peripheral nerve synapses.

234
Q

how can clostridium perfringes cause food poisoning?

A

reheated meat is ingested and the enterotoxin acts as as a superantigen in the colon –> incubated for 8-16 hours and watery diarrhea ensues.

235
Q

how does listeria cause food poisoning?

A

ß haemolytic, aesculin positive with tumbling motility.
from refrigerated food (“cold enhancement”) (ie unpasteurised dairy, vegetables.) and causes GI watery diarrhoea, cramps, headache, fever, little vomiting.

Treat with ampicillin, ceftriaxone

236
Q

how does e coli cause food poisoning?

A

Escherichia coli is also known as traveller’s disarrhea. It’s from feces contaminated food. The heat labile toxin stimulates adenyl cyclase and cAMP where Heat stable stimulates guanylate cyclase. They act on the jejeunum & ileum, but not on colon.
The exact toxin determines if it’s a bit of traveler’s diarrhea or as bad as dysentery

237
Q

how does salmonella enteriditis cause food poisoning?

A

Enterocolitis, transmitted from poultry, eggs, meat. Bacterial invasion of epi- and sub-epithelial, tissue of small and large bowel causing self limited non bloody diarrhoea ,usually no treatment (Cipro if required)

238
Q

how does salmonella typhi cause food poisoning?

A

Typhoid (enteric) fever, transmitted only by humans
multiplies in Payer’s patches and causes lots of problems. Fever, constipation, anemia/leucopenia, rose spots, splenomegaly, bradycardia, hemorrhage, perforation. Treatment : ceftriaxone

239
Q

how does shigella cause food poisoning?

A

Non lactose fermenters, non motile. Produce cell wall O antigens, and polysaccharide antigens. Cause dysentery from invading cells of mucosa of distal ileum and colon and producing enterotoxin (Shiga toxin)

Avoid antibiotics (ciprofloxacin if required)

240
Q

how does vibrio cause food poisoning?

A

Transmitted by contamination of water and food from human faeces ( shellfish, oysters, shrimp).
Leads to colonisation of small bowel and secretion of enterotoxin with A and B subunit, causing persistent stimulation of adenylate cyclase and massive diarrhoea (rice water stool) without inflammatory cells..

Treat cholera supportively; treat vulnificus and parahemolyticus with doxycycline.

241
Q

how does Yersinia cause food poisoning?

A

Yersinia enterocolitica is a non-lactose fermenter, which is enriched in the fridge and transmitted via food contaminated with domestic animals feces. It causes an enterocolitis, mesenteric adenitis. It is associated with reactive arthritis , Reiter’s

242
Q

how does entamoeba histolytica cause food poisoning?

A

Entamoeba histolytica is usually killed by boiling water but ingestion of cysts&raquo_space; trophos in
ileum&raquo_space; colonize cecum, colon&raquo_space; “flask shaped” ulcer. Presents with dysentery,flatulence, tenesmus.
If chronically infected - wt loss,+/- diarrhea, can cause liver abscesses

Diagnosis

  • stool micro (wet mount, iodine and trichrome )
  • serology in invasive disease

Treat : metronidazole + paromomycin in luminal disease

243
Q

how does giardia (lambia) cause food poisoning?

A

usually from feces contaminated food. Can lead to foul smelling non bloody diarrhoea, cramps, flatulence, no fever
Diagnosis : stool micro, ELISA, “string test”
Treatment :metronidazole

244
Q

what’s the basis of antiviral medications? (think of immunomodulation)

A

Viral replication detected PRRs to trigger innate immune responses leading to production of restriction factors such as IFNs. Antiviral immune response can be boosted by exogenous immunomodulators (eg Interferon Rx for HBV/HCV)

245
Q

which antiviral drugs are used for treatment of herpes simplex & varicella?

A

po/iv acyclovir
valacyclovir or famciclovir
2nd line: foscarnet

246
Q

how does acyclovir work?

A

It is a guanosine analog. Further elongation of the chain is impossible because acyclovir lacks the 3’ hydroxyl group necessary for the insertion of an additional nucleotide after it fits in for the Guanosine in the viral replication.

247
Q

what antiviral drugs are used in the treatment of CMV?

A 
Ganciclovir
Valganciclovir
Foscarnet
Cidofovir
Brincidofovir
248
Q

Ganciclovir is also an antiviral drug. How does it work?

A

The same as acyclovir, a guanosine analog. It inhibits viral DNA synthesis and has activity against CMV.
Also activity against HSV, VZV, EBV and HHV6, but seldom used

249
Q

how does foscarnet work as an anti viral?

A

it’s a non-competitive inhibitor of viral DNA polymerase that does NOT require activation by phosphorylation. It has activity against CMV, and is used occasionally for HSV

250
Q

how does cidofovir work as an anti viral?

A

Nucleotide (cytidine) analogue acts as competitive inhibitor of viral DNA synthesis, but also does NOT require activation by phosphorylation. It has activity against CMV, and also occasionally used for HSV (or other viruses)

251
Q

How do oseltamivir or zanamivir work as anti virals?

A

they inhibit neuraminidase on the influenza or RSV viruses, an enzyme required in order for the virus to propagate infection.

252
Q

how does ribavirin work as an antiviral?

A

it’s a guanosine analogue so it Inhibits viral RNA synthesis (exact mechanism unclear) – broad activity in vitro: effective for Lassa fever and HEV. Used in combination with other drugs for HCV.

253
Q

when is palivizumab used for RSV treatment?

A

Palivizumab is a monoclonal antibody against RSV
Indication. It’s used for the prevention of serious lower respiratory tract disease caused by RSV in infants at high risk (eg preterm and severe underlying heart or lung disease, SCID)

254
Q

what are the 4 types of anti-retrovirals used in HIV treatment (by mechanism)?

A

reverse transcriptase inhibitors (NRTIs)
fusion/entry inhibitors
integrase inhibitors
protease inhibitors

255
Q

what parvovirus fetal sequelae can come from infection during pregnancy?

A

in first 20 weeks: increased risk of IUD/miscarriage
between 9-20 weeks: increased risk of hydrops fetalis
>20 weeks: low risk of fetal sequelae

256
Q

what are the potential fetal sequelae of rubella infection during pregnancy?

A
  • congenital rubella infection
    -Foetal loss
    -Congenital rubella syndrome at birth:
    (cardiac defects, deafness, ocular defects, IUGR, thrombocytopenic purpura, haemolytic anaemia, hepatosplenomegaly, meningoencephalitis)

Nearly 100% if infection before 11 weeks (congenital heart defects and deafness ++), but risk of fetal damage negligible after 16 weeks

257
Q

what are the signs of CMV congenital infections?

A 
Screen for CMV in neonate if... 
-Any Evidence of maternal seroconversion
-IUGR, prematurity
-Hepatosplenomegaly
-Prolonged jaundice with transaminitis
-Failed neonatal hearing screen
Cataract, retinitis
-Unexplained thrombocytopenia, petechiae and purpura (“blueberry muffin rash")
258
Q

how is neonatal CMV diagnosed?

A

urine or saliva PCR

259
Q

how is neonatal CMV treated, and when?

A

if infection confirmed: FBC, creatinine, LFTs, U&E, CMV viral load. Do cranial USS/brain MRI, refer for ophthalmologist review, and refer for auditory assessment.

Treatment is offered if there is significant organ involvement or any CNS disease. If treatment is decided: IV Ganciclovir

260
Q

where on the body does chicken pox rash begin?

A

vesicular rash starts on face and scalp, but spreads to trunk, abdomen, and the limbs.

261
Q

what is the infectious period of chickenpox?

A

2 days before the appearance of the rash until the vesicles are dry, but may be prolonged in immunosuppressed patients

262
Q

what fetal sequelae are at risk if mother contracts chicken pox during pregnancy?

A

First 20 weeks: risk of congenital (fetal) varicella syndrome (limb hypoplasia, microcephaly, cataracts, growth retardation, skin scarring)
2nd and 3rd trimester: herpes zoster
Chickenpox between 1 week before and
1 week after delivery: risk of severe disseminated haemorrhagic neonatal chickenpox with high mortality rate

263
Q

what are the potential complications of measles?

A
  • Opportunistic bacterial infections
  • Otitis media, pneumonia, bronchitis
  • Encephalitis
  • Sub-acute sclerosing pan-encephalitis (SSPE)
264
Q

what is the infectious period of measles?

A

from about 4 days before appearance of rash to 4 days after the appearance of the rash

265
Q

what congenital infections do we screen for?

A 
“TORCH” screen:
Toxoplasmosis
Other - syphilis; HIV; Hepatitis B/C etc
Rubella
CMV (cytomegalovirus)
HSV (herpes simplex virus)
266
Q

what symptoms appear due to congenital toxoplasmosis infections?

A 
40% symptomatic at birth: 
-choroidoretinitis; 
-microcephaly/hydrocephalus; 
-intracranial calcification;
-seizures
-jaundice; 
hepatosplenomegaly
267
Q

what is congenital rubella syndrome?

A

Effect on foetus -dependent on time of infection
Mechanism: Mitotic arrest of cells; angiopathy; growth inhibitor effect

Eyes: cataracts; microphthalmia; glaucoma; retinopathy
Cardiovascular syndrome: PDA; PAS; ASD/VSD
Ears: deafness
Brain: microcephaly; meningoencephalitis; developmental delay
Other: growth retardation; bone disease; hepatosplenomegaly; thrombocytopenia; rash

268
Q

what organisms are associated with early onset neonatal infection (within 48 hours)?

A

Group B streptococci
E. coli
Listeria

269
Q

how does group B strep present in the neonate?

A
  • Bacteraemia, Meningitis, Disseminated infection

* positive cocci bacteria, catalase negative, beta hemolytic

270
Q

what are risk factors for early onset sepsis?

A

Maternal: PROM, premature labor, fever, fetal distress, meconium staining
Fetal: birth asphyxia, respiratory distress, low BP, acidosis, hypoglycemia, neutropenia

271
Q

what organisms are associated with late onset (after 48 hours) sepsis?

A

Group B streptococci
E. coli
Listeria monocytogenes
S. aureus
Enterococci
Gram negatives – Klebsiella spp. /Enterobacter spp.
/Pseudomonas aeruginosa/Citrobacter koseri

272
Q

what antibiotics are 1st line and 2nd line for neonatal sepsis?

A

Early onset sepsis: BenPen + Gentamicin
Late onset in NICU: Flucloxacillin & gentamicin
Late onset from community: amoxicillin/cefotaxime

273
Q

what shows up in bacterial meningitis on CSF?

A

Raised WCC –mainly polymorphs
Gram stain negative
High protein and low glucose
Rapid Antigen test on CSF may be positive.

274
Q

what is the most likely organism to cause meningitis before 3 months of age?

A 
N. meningitidis; 
S. pneumoniae;
(H. influenza (Hib) if unvaccinated); 
GBS; 
E. coli; 
Listeria sp
275
Q

what is the most likely organism to cause meningitis after 3 months of age?

A

N. meningitidis;

S. pneumoniae;

276
Q

what vaccinations do we give at 8 weeks?

A
  • TDAP
  • Polio
  • Hib (DTap, IPV, Hib)
  • Pneumococcal Conjugate vaccine
277
Q

what vaccinations do we give at 12 weeks?

A
  • DTaP
  • IPV
  • Hib
  • Men C
278
Q

what vaccinations do we give at 16 weeks?

A
  • DTap
  • IPV
  • Hib
  • PCV
  • Men C
279
Q

what vaccinations do we give at 12 months?

A
  • Hib

- Men C

280
Q

what vaccinations do we give at 13 months?

281
Q

what vaccinations do we give at 3 years 4 months?

A
  • MMR
  • TDAP
  • IPV
282
Q

what vaccinations do we give at 13+ years?

A
  • HPV 16&18 (girls)
  • Tetanus
  • Diptheria
  • IPV
283
Q

when do we treat children with ART who are HIV infected?

A

regardless of clinical symptoms, immune status or viral load - TREAT

284
Q

define zoonoses & give some examples:

A

-infections acquired from vertebrates
-by direct contact or indirect contact by vector/environmental contamination
Eg. dystentry, cholera, plague, lyme disease, leishmania, brucellosis

285
Q

which infections are closely associated with cats?

A

Toxoplasmosis
Leptospirosis
Rabies
Q-fever

286
Q

which infections are closely associated with dogs?

A 
Hydatid disease
Brucellosis
Leptospirosis
Rabies
Q-fever
287
Q

which infections are associated with birds?

A
  • Psitticosis
  • Cryptococcus
  • Influenzae A
288
Q

which infections are associated with cattle & pigs?

A
  • Anthrax
  • Bovine TB
  • Anaplasmosis
  • Toxoplasmosis
  • Brucellosis
  • Leptospirosis
289
Q

what is the clinical course of rabies?

A
  • contact with infected animal (dog/bat) usually bitten
  • variable incubation
  • slow migration to CNS –> death
290
Q

how do we diagnose rabies?

A
  • IFA in frozen skin/brain tissue
  • RT-PCR
  • history
  • no previous rabies vaccine
291
Q

what is brucellae and how is it spread?

A

Gram-negative intracellular bacteria in different species. Human infection follows contact with infected animals/consumption of infected animal products. No person-to person spread.

292
Q

how does brucellosis present?

A

-caused by brucella infection
Incubates: 3-4 weeks
Non specific onset with complications of osteomyelitis.
>90% positive in bone marrow culture and 70% in blood cultures.

293
Q

how do we treat brucellosis?

A

Prolonged therapy of 4-6 weeks with tetracycline or doxycycline + streptomycin.

294
Q

what causes plague and how does the bubonic plague present?

A
  • Caused by yersinia pestis
  • primary pneumonic plague
  • dx via PCR
295
Q

how do we treat plague now?

A

Streptomycin
Doxycycline
Gentamicin

296
Q

how does lyme disease present?

A

Early: erythema migrans (non specific flu like)
Early Disseminated: secondary EM, palsies/arthritis, carditis
Late: arthritis, ACA, encephalopathy

297
Q

how do we treat lyme disease?

A
  • remove any ticks

- doxycycline

298
Q

what is the most likely pathogen of pneumonia at…

a) 0-1 months
b) 1-6 months
c) 6 months - 5 years
d) Adult

A

a) E Coli, Group B strep, listeria
b) Chlamydia, Staph Aureus, RSV
c) Mycoplasma, influenza
d) strep pneumoniae, mycoplasma pneumonia

299
Q

what pathogens are the cause of typical CAP?

A

strep pneumoniae

hemophilus influenzae

300
Q

what are causes of atypical CAP?

A

Legionella
Mycoplasma
Q fever - Coxiella burnetii
Psittacosis - Chlamydia psittaci

-All organisms without a cell wall (so penicillins don’t work)

301
Q

what is the CURB-65 score and when do we worry?

A 
C - confusion
U - urea >7 mmol/L
R - RR> 30
B - BP <90 sys, <60 dias
>65 years of age

If score 2-5 then manage as severe CAP

302
Q

what organisms cause bronchitis?

A

Strep pneumoniae
Hem. Influenzae
M. catarrhalis

303
Q

when someone has chest infection and hyponatremia - what organism do we suspect?

A

Legionella pneumophilia

304
Q

what is the most common aetiology of hospital acquired pneumonias?

A

Enterobacteriae
Pseudomonas
Staph aureus

305
Q

which organism shows on CXR as ‘bat’s wing’ and how do we treat it?

A
  • pneumocystis carinii
  • also may show CXR bilateral ground-glass shadowing
  • Rx - co-trimoxazole
306
Q

which organism is the most common cause of infective endocarditis in IVDU?

A

Staph aureus (usually tricuspid valve)

307
Q

which organisms are the most common causes of infective endocarditis overall?

A

Viridans strep
Enterococci
Staph aureus

308
Q

what is Duke criteria?

A

-used for measuring the severity of infective endocarditis
A) Pathological criteria
B) Clinical criteria: 2 major, or 1 major + 3minor, or 5 minor

309
Q

what is the empiricaltreatment for infective endocarditis?

A

Acute (or staph aureus) - flucloxacillin
Indolent (or viridians strep)- penicillin + gentamicin
Prosthetic Valve - vancomycin + gentamicin + rifampicin

310
Q

what are the potential causes of pyrexia of unknown origin classified with?

A 
Abscesses
Endocarditis
TB
Complex UTIs
Fever in returning traveller
HIV
Vasculitis
Malignancy
Inherited disorders (eg familial Mediterranean fever)
311
Q

which antibotic is used in infants less than 3 months old vs more than 3 months old?

A

<3 months: Cefotaxime

>3 months: Ceftriaxone

312
Q

which are the major and which are the minor in Duke’s criteria?

A

Major

  • Persistent bacteraemia
  • Echocardiogram: vegetation
  • Positive serology Bartonella, Coxiella or Brucella

Minor

  • Predisposition (eg IVDU)
  • Inflammatory markers
  • Immune complexes: splinters, RBCs in urine
  • Embolic phenomena: Janeway lesion, stroke
  • Atypical echocardiogram
  • Only 1 positive BC

Julija's Path (6 decks)

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