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BPT Written > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

What vaccinations do splenectomy patients require?

A

Pneumovax (13PPV then 23PPV 8 weeks later, then 23PPV 5y later), HiB, meningococcal ACWY + B + annual influenza

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2
Q

When are live vaccinations contraindicated?

A

Pred > 20mg daily
CD4 < 200
Primary immunodeficiency
Pregnancy

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3
Q

What are the live vaccines?

A

MMR, VZV, oral polio, BCG, oral typhoid, yellow fever, JEV

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4
Q

What vaccinations are contraindicated in egg anaphylaxis?

A

Q fever and yellow fever

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5
Q

What organism are hyposplenic sickle cell patients predisposed to?

A

Salmonella

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6
Q

What organism causes infection following dog bite?

A

Capnocytophagia

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7
Q

What antibiotic for prophylaxis post-splenectomy, and for how long?

A

Phenoxymethyl penicillin or amoxicillin, at least 2 years if healthy or lifelong if previous OPSI

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8
Q

Incubation period for Dengue

A

3-14 but usually 4-7 (short)

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9
Q

Incubation period for Zika

A

2-14 days (short)

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10
Q

Incubation period for Typhoid

A

5-21 days

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11
Q

Incubation period for malaria

A

1-6 weeks (can be much longer)

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12
Q

Incubation period for Ebola

A

6-12 days

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13
Q

What infections cause eschar?

A

Rickettsia, plague, trypanosomiasis

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14
Q

Treatment for severe falciparum malaria

A

IV artesunate, add IV quinine if from greater mekong

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15
Q

What gene confers resistance to artemesinin? Where found?

A

Kolch 13, SE Asia

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16
Q

What test must you do before treating vivax/ovale, and what treatment?

A

G6PD, primaquine for 7-14 days

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17
Q

Mosquito species for malaria

A

Anopheles

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18
Q

Treatment of non-severe malaria

A

Artemether + lumefantrine

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19
Q

List 4 flaviviruses

A

Dengue, Zika, Yellow fever, JEV

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20
Q

Mosquito for Dengue

A

Aedes aegypti - same as for Zika, Chikungunya

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21
Q

What is ADE with regards to Dengue?

A

Antibody dependent enhancement, meaning second infection with another Dengue serotype being a risk factor for severe Dengue

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22
Q

Viral protein that causes Dengue shock

A

NS1Ag

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23
Q

Test for diagnosis when < 5 days of illness in Dengue

A

NS1Ag

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24
Q

Diagnosis > 5 days of illness in Dengue

A

Serology

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25
Q

Who do you vaccinate against Dengue?

A

Seropositive individuals in endemic areas

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26
Q

What is clinical course of Dengue?

A

Biphasic, with defervescence of fevers after 5 days then get sick again

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27
Q

What is main complication of Zika in adults?

A

GBS

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28
Q

How do you diagnose Zika?

A

< 7 days = PCR

> 7 days = serology

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29
Q

Name three alphaviruses

A

Chikungunya, Ross River Virus, BF

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30
Q

Organism causing Typhoid

A

Salmonella enterica, serotypes typhi, paratyphi A/B/C

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31
Q

Key skin finding for Typhoid

A

Rose spots

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32
Q

Empiric treatment of typhoid

A

Ceftriaxone or azithromycin

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33
Q

Mechanism of action of triazoles

A

Inhibit C14alpha demethylase which is required for ergosterol synthesis in cell membrane. Fungistatic.

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34
Q

Mechanism of action of polyenes (amphotericin)

A

Bind to sterol ergosterol, forming pores in membrane

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35
Q

Echinocandins MOA

A

Inhibit B-1,3-D glucan synthase, inhibiting cell wall synthesis. Fungicidal.

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36
Q

Griseofulvin MOA

A

Inhibits nuclear division

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37
Q

First line antifungal for invasive aspergillus?

A

Voriconazole. Second line amphotericin/echinocandins

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38
Q

What is the vector for cutaneous leishmaniasis?

A

Sandflies

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39
Q

What are key words for biopsy of cutaneous leish lesion?

A

Rod-shaped kinetoplasts

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40
Q

How does HIV attach to CD4?

A

Via Gp120

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41
Q

What are HIV attachment coreceptors?

A

CCR5 early, CXCR4 late

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42
Q

What cells are CD4 positive and susceptible to HIV

A

Lymphocytes, macrophages, DCs

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43
Q

Mutation that confers immunity to HIV infection

A

CCR5delta32

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44
Q

HLA type with slowest progression to AIDS in HIV

A

HLAB5701

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45
Q

What are side effects of tenofovir?

A

Osteoporosis and RTA. TAF less toxic than TDF due to longer plasma half-life.

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46
Q

What drug classes are used to treat HIV in general?

A

2x NRTI + integrase inhibitor (ends in -tegravir)

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47
Q

When should you give PEP?

A

Best if < 24h, no longer than 72h

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48
Q

What drugs do you give for PEP? How long?

A

Tenofovir, emtricitabine, integrase (dolutegravir, raltegravir). 28 days

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49
Q

What drugs for PrEP?

A

Tenofovir and emtricitabine

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50
Q

What are the AIDS defining illnesses?

A

PJP, toxoplasmosis, CMV, TB/MAC, oesophageal candidiasis, Cryptosporidium/microsporidium, Kaposi’s

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51
Q

When should you start HIV treatment assuming no infection?

A

ASAP

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52
Q

What prophylaxis needs to be given at what CD4 counts for HIV?

A

< 200 PJP -> Bactrim
< 100 Toxo -> Bactrim
< 50 MAC, Crypto - Azith

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53
Q

What are RFs for IRIS?

A

High VL, high pathogen burden, low CD4 count

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54
Q

Top causes of IRIS?

A

TB, Crypto, MAC, CMV, PML

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55
Q

When to start ART with OI?

A

If TB and CD4 > 50, delay until 4-8 weeks of TB treatment
If TB and CD4 < 50, delay 2-4 weeks
Crypto - Delay until 4-6 weeks post amphotericin, sooner if mild and CD4 < 50
If crypto meningitis or other neurological OI - optimum time to start unclear

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56
Q

When do you treat a pregnant woman with HIV?

A

ASAP - risk to baby is 25% if untreated

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57
Q

WHen do you give zidovudine to pregnant woman?

A

If VL > 1000 at birth give IV zidovudine and deliver via C-section

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58
Q

What is ecthyma gangrenosum?

A

Ecthymatous skin lesions associated with Pseudomonas bacteraemia

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59
Q

Risk factors for invasive moulds?

A

AML, neutrophils < 0.1 for 2-3/52, neutropaenic + steroids, ALL, HSCT, cytarabine/fludarabine

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60
Q

What is Nocardia?

A

Gram positive rod, long chains of acid fast bacilli, branching like a mould. Causes lung and brain abscesses.

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61
Q

What is PTLD?

A

Post transplant lymphoproliferative disorder. High risk if EBV D+/R-, lymphoid rich transplant, ATG use.

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62
Q

What organism causes PML?

A

Progressive multifocal leucoencephalopathy- JC Virus (John Cunningham)

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63
Q

What drugs are highest risk for PML?

A

Natalizumab, TNFa inhibitors, rituximab

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64
Q

What is treatment for Stronglyoides stercoralis?

A

Ivermectin and repeat in 14 days

65
Q

What are examples of yeasts?

A

Candida (no capsule), Cryptococcus (polysaccharide)

66
Q

What are examples of moulds?

A

Aspergillus (septated hyphae), Rhizo, Mucor (non-septated)

67
Q

How do aminoglycosides (Gentamicin, tobramycin, neomycin, kanamycin, plazomycin) and tetracyclines (doxy, minocycline, tigecycline) work?

A

Protein synthesis inhibitors (bind 30s)

68
Q

How do macrolides (erythro, oxithro, azithro, clarithromycin) and chloramphenicol work?

A

Protein synthesis inhibitors (binds 50s)

69
Q

How do oxazolidinones (linezolid, tedizolid) and lincosamides (clindamycin) work?

A

Binds to 23S portion of 50S subunit of bacterial ribosomes, inhibiting protein synthesis

70
Q

How do colistin (Classified as polymyxin antibiotic), glycopeptides (Vancomycin, teicoplanin) and daptomycin (Lipopeptide class) work?

A

Cell membrane synthesis inhibitor

71
Q

How does fusidic acid work?

A

Protein synthesis inhibitor, blocks factor G

72
Q

How do quinolones work? (ciprofloxacin, moxifloxacin, levofloxacin, norfloxacin)

A

DNA gyrase, replication inhibitors

73
Q

How do rifamycins work? (rifabutin, rifampin, rifapentine)

A

Inhibit DNA-dependent RNA synthesis by inhibiting RNA polymerase

74
Q

How do nitrofurantoin, sulphonamides and trimethoprim work?

A

DNA synthesis inhibitor

75
Q

How do beta lactams work?

A

Inhibit cell wall synthesis - binds to penicillin binding proteins, which are bacterial transpeptidases required for cell wall peptidoglycan assembly

76
Q

How does metronidazole work? (Nitroimidazole class)

A

Free radicals fragment DNA

77
Q

What is the only antibiotics in class monobactam?

A

Aztreonam - useful against gram negatives, cross-reactive allergy with ceftazidime

78
Q

What is a new cephalosporin with MRSA cover?

A

Ceftaroline

79
Q

Which 3rd generation cephalosporin has Pseudomonas cover?

A

Ceftazidime (like tazocin)

80
Q

What classes of drugs are cell membrane inhibitors?

A

Colistin (polymyxin class), beta lactams, daptomycin, glycopeptides (vanc, teico),

81
Q

Side effects of daptomycin?

A

Myopathy (check CK), eosinophilic pneumonia

82
Q

What is the mechanism of MRSA resistance?

A

mecA gene producing PBP2a, low affinity for beta lactams. Must acquire this mutation from other bacteria (conjugation), isn’t a sporadic mutation produced under long-term beta lactam pressure.

83
Q

What is the Panton-Valentine Leucocidin toxin?

A

Exotoxin produced by particular MRSA strains, causes leucocyte destruction and tissue necrosis, and associated with skin boils, necrotising pneumonia and increasing virulence.

84
Q

What is mechanism of resistance for VRSA?

A

VanA plasmid from VRE. Mutations of genes encoding for vancomycin binding site, changes from D-ala-D-ala to D-ala-D-lac

85
Q

What is mechanism of resistance for VRE?

A

VanA/VanB/VanC genes, transferrable via plasmid (conjugation). More common in E. faecium than E. faecalis

86
Q

What are the ESCAPPM organisms?

A

Enterobacter, Serratia, Citrobacter koseri, Acinetobacter and Aeromonas, Proteus vulgaris, Providencia, Morganella morganii

87
Q

What is the NDM-1 enzyme with regards to Enterobacteriaceae?

A

New Delhi Metallo-beta-lactamase-1, a beta lactamase that hydrolyses carbapenems, rendering Enterobacteriaceae resistant to carbapenems. Produced by gene blaNDM-1, transferred via plasmids.

88
Q

What are ESBLs?

A

Gram neg organisms (E. coli, Kleb) with extended spectrum beta lactamase enzymes that hydrolyses later generation cephalosporins. Treat with carbapenems. CTX-M most common gene, present on plasmids

89
Q

How can the genes encoding for ESBLs be transferred?

A

Via plasmids

90
Q

What is the mechanism of ESCAPPM organism resistance?

A

ampC gene, present on chromosome, encodes for beta-lactamase enzyme. Beta-lactamase production inducible in presence of beta lactams.

91
Q

What is most common organism causing cellulitis?

A

Strep pyogenes or dysgalactiae, then Staph (particularly if purulent)

92
Q

Prophylaxis for recurrent cellulitis?

A

Penicillin VK 250mg BD

93
Q

Empirical treatment for nec fasc

A

Mero/vanc/clinda

94
Q

Most common organisms causing meningitis over 60yo?

A

Pneumococcus, Listeria

95
Q

Most common organisms causing meningitis < 60 years old?

A

Pneumococcus, Neisseria

96
Q

Risk factors for Listeria meningitis?

A

> 50 years old, pregnant, impaired cell-mediated immunity (T2DM)

97
Q

What organism causes recurrent aseptic/lymphocytic meningitis?

A

HSV-2, Mollaret’s meningitis

98
Q

Empiric therapy for meningitis?

A

Ceftriaxone 2g BD, dex 10mg QID. If gram pos diplococci/RF for S. pneumo, add vanc. If old/immunocompromised, add benpen.

99
Q

When are steroids used in meningitis?

A

Pneumococcal meningitis

100
Q

Most common causes of viral meningitis?

A

Enteroviruses, HSV1, HSV2

101
Q

What species of Cryptococci affects immunocompromised and immunocompetent?

A

HIV - C. neoformans

Immunocompetent - C. gattii

102
Q

What serotype of N. meningitidis causes most severe infection?

A

B (for BAD)

We vaccinate against ACWY

103
Q

Who can we give meningococcal B vaccination to?

A

Asplenics, complement deficiencies

104
Q

When to treat asymptomatic bacteriuria?

A

Pregnant, prior to procedures. NOT renal transplant

105
Q

Most common predisposing cardiac condition for IE?

A

MVP with regurgitation, if no regurg then not a RF

106
Q

Most common organism for prosthetic valve IE?

107
Q

Most common organisms for IE?

A

S. aureus, viridans Strep, coag-negative Staph, Enterococci

108
Q

What are HACEK organisms and their significance?

A

Cause IE. Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella corrodens, Kingella

109
Q

Empiric therapy for IE?

A

Benpen, fluclox, gent

110
Q

Treatment for E. faecalis IE?

A

Amox + ceftriaxone

111
Q

Prophylactic antibiotics for IE, which patients? Which procedures?

A

Prosthetic valves, RHD, previous IE, unrepaired congenital heart disease.
Procedures - Dental/oral surgery, respiratory mucosal breaks, surgery at site of established infection.

112
Q

Antibiotics used for IE prophylaxis?

A

Amoxicillin 2g or clindamycin 600mg

113
Q

Most common organisms causing culture negative IE?

A

Q fever, Bartonella hensellae

114
Q

Organisms causing pneumonia in tropical regions

A

Mellioidosis and acinetobacter

115
Q

Define MDR TB

A

Resistance to isoniazide + rifampicin

116
Q

Define XDR TB

A

Resistance to fluoroquinolone + aminoglycisides

117
Q

Standard treatment regime for TB?

A

RIPE (other letters for drugs in same order = RHZE) for 2 months then RI for 4 months (rifampicin, isoniazide, ethambutol, pyrazinamide)

118
Q

What are issues/side effects from rifampicin?

A

Drug interactions, hepatotoxicity

119
Q

What are side effects of isoniazid?

A

Hepatotoxicity, peripheral neuropathy

120
Q

Key side effect of ethambutol

A

Optic neuropathy

121
Q

Key side effects of pyrazinamide

A

Hepatotoxicity, arthralgia/gout

122
Q

Most hepatotoxic TB treatment drugs? (in order)

A

Pyrazinamide, isoniazid, rifampicin (RIPE backwards without the E)

123
Q

When do you treat latent TB?

A

<35 years old, healthcare workers, HIV, immunosuppressed, recent acquisition

124
Q

Options for latent TB treatment?

A

9H (9 months isoniazid)
4R (4 months rifampicin)
3RH (weekly rifapentine/isoniazid for 3 months)
All equally efficacious, 3RH less hepatotoxic but more hypersensitivity

125
Q

Characteristic pathology finding for CMV infection

A

Owl eyes inclusions

126
Q

Greatest risk of CMV in SOT

127
Q

Greatest risk of CMV in BMT

128
Q

Mechanism of CMV resistance to valgan/gan

A

UL97 mutation

129
Q

Mechanism of CMV resistance to most antivirals

A

UL54 (alters DNA polymerase causing pan-resistance)

130
Q

Mechanism of action of ganciclovir/valgan

A

Guanosine analogue, inhibit CMV DNA polymerase - utilises UL97 to be phosphorylated and activated

131
Q

Mechanism of action of foscarnet

A

Pyrophosphate analogue binds directly to UL54 site on CMV DNA polymerase

132
Q

Mechanism of action of marabavir

A

Inhibits UL97

133
Q

Mechanism of action of cidofovir

A

Cytosine analogue

134
Q

VZV PEP in pregnant/immunocompromised/non-immune

A

VZVIg if < 4/7, PO valaciclovir if > 4/7

135
Q

Which influenza type has pandemic potential and why?

A

Influenza A- has 16H/9N possibilities and can undergo antigenic shift, whereas fluB only has 1H/1N and can only undergo antigenic drift

136
Q

What type of diarrhoea does cholera cause?

137
Q

What is a bacterial cause of aortitis?

A

Salmonella; syphilis

138
Q

What infection is most commonly associated with GBS?

A

Campylobacter

139
Q

Most common STEC organism?

A

E. coli 0157:H7

140
Q

Two most significant RFs for C. diff

A

Antibiotics and hospitalisation

141
Q

How does C. diff cause disease?

A

Via toxins (Tcd A, Tcd B). A severe strain B1/NAP1/027 also produces binary toxin.

142
Q

What is C. diff B1/NAP1/027 strain and significance?

A

Produces binary toxin in addition to Tcd A/B, more severe, fluoroquinolone resistant, more toxic megacolon, associated with outbreaks

143
Q

What drugs are used to treat HBV?

A

Tenofovir and entecavir

144
Q

How to prevent maternal-foetal transmission of HBV?

A

Treat mother with tenofovir, give baby HBVIg and vaccine

145
Q

Why does HCV not clear while HBV does (in adults)?

A

HCV more error prone, mutates rapidly, evades immune system

146
Q

Genotypes of HCV common in Aus?

147
Q

Standard classes of drugs for treament of HCV?

A

NS5A + NS3/4 inhibitors, add ribavirin if cirrhotic

148
Q

Neurological manifestations of HSV?

A

Mollaret’s, encephalitis, transverse myelitis

149
Q

Indications for HSV prophylaxis/suppression?

A

> 6 episodes/y, Mollaret’s, MSM at risk

150
Q

What are the stages of syphillis infection?

A

Primary = chancre
Secondary = skin lesions (mostly generalised maculopapular rash), maybe non-tender lymphadenopathy and fever. May have meningitis, hepatitis, osteitis, arthritis, iritis
Latent
Tertiary = gummatous, CV, or neurosyphilis

151
Q

What are manifestations of neurosyphillis?

A

GPI (General Paresis of the Insane)
Tabes dorsalis
CN palsies

152
Q

How do you diagnose syphillis?

A

Serology - EIA positive first, then confirm with TPPA. These stay positive for life. Then use RPR (rapid plasma reagent) which is not positive for life, therefore used to track treatment response/recurrence.

153
Q

What is successful treatment of syphillis defined as on RPR?

A

4 fold (2 titre) reduction in 6 months

154
Q

Most common HPV types to cause warts?

155
Q

Most common HPV types to cause SCC?

156
Q

Treatment of Chlamydia?

A

Azithromycin 1g PO or doxy 100mg BD for a week

157
Q

Treatment of gonorrhoea?

A

IM ceftriaxone 500mg

+ give azith 1g PO

158
Q

What causes chancroid, and are the ulcers painful or not?

A

Haemophilus ducreyi, very painful ulcers. Treat azith or cef

BPT Written (21 decks)

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