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Infectious Diseases > Infectious Diseases Basics P2 > Flashcards

Infectious Diseases Basics P2 Flashcards

1
Q

What are the three classifications of ARF?

A

Definitie
- fulfills jones criteria

Probably
- Does not fulfil Jones diagnostic criteria, missing one
major or one minor criterion or lacking evidence
of preceding streptococcal infection, but ARF is
still considered the most likely diagnosis

Possible
- Does not fulfil Jones diagnostic criteria for ARF, missing one major or one minor criterion or lacking evidence
of preceding streptococcal infection, and ARF is
considered uncertain but cannot be ruled out

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2
Q

How long should ben pen be continued after AFR for the prevention of RHD?

A

Possible ARF
- continue for 1 year then ECHO

Probable or definite
- at least 5 years following last episode OR until age 21 (whichever is longer) then ECHO
-> if ECHO abnormal then could consider continuing further

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3
Q

Which antibiotics can cause seratonin syndrome?

A

Linezolin in combination with other seratinergic drugs

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4
Q

Which antibiotics can prolongue the QTc?

A

Quinolones
- moxifloxacin, ciprofloxacin, levofloxacin, norfloxacin
Macrolides
- azithromycin, clarythromycin, arrythromycin

Should not be combined with other agents that prolong QTc such as amiodarone

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5
Q

Which antibiotics can interacti which colchicine and how does this occur?

A

Macrolides such as clarythromycin are inhibitors of CYP450 3A4 and teh P-Glycoprotien dependent handling of colchicine in the liver, which can increase levels of cochicine leading to toxicity

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6
Q

Statin should be dose adjusted when combined with which antimicrobial class?

A

azoles
- these are potent inhibitors of CYP450 3A4 which can lead to high statin levels (statins are metabolised by Cyp 3a4)

Also macolides and fluroquinolones for the same reason

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7
Q

What is the the imaging finding on CT with pseudomembranous colitis?

A

THumbprinting
-represent thickening od the bowel wall due to oedema

Other features include toxic megacolon, obstruction, performation

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8
Q

How is C Dif infection diagnosed?

A

Detect C dif:
- GDH ELISA - tests that is very sensitive at detecting teh presence of C dif (ie if neg can be used to rule out C dif)
- does not differentiate between toxin and non toxin

Detect toxin:
- PCR for C dif toxin B
- Culture and toxin detection in lab (gold standard test)

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9
Q

Which antibiotics is most associated with C dif infection?

A

Clindamycin

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10
Q

Is handwashing effective against C dif?

A

Yes but need to use soap and water (alcohol not effective against spores)

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11
Q

What is the definition of community onset / acquired C dif infection?

A

Nil overnight hospital stay in last 12 weeks

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12
Q

What are some biochemical and clinical markers of severe C dif?

A

Clinical:
- Febrile >38.5
- Haemodynamic instability
- Illeus, obstruction, toxic megacolon

Lab:
- Albumin <25
- WCC >15
- elevated Lactate
- AKI (>50% rise in Cr)

Colonoscopy:
- severity of inflammation / pseudomembranous colitis

Note number of stools per day is technically not a marker of severity

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13
Q

How is non severe C dif infection treated? Including first and second recurrance?

A

Metronidazole 400mg PO TDS for 10 days
(americans suggest initial therapy with Vanc 125mg Po QID)

First recurrance / refractory disease (ie not responding to metro
- Vancomycin 125mg PO QID for 10 days
- Fidaxomicin 200mg BD 10d (if prieviously treated with vanc)

Second recurrence or more:
- FMT (recomended therapy for second or more recurrance)
- Vanc 14 days + taper
- Fidaxomycin

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14
Q

How is severe C dif infection treated?

A

Vancomycin 125mg PO/NG QID 10 days + metronidazole 500mf 12hr if complicated
- Can use colonic vancomycin if complicated by ileus

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15
Q

Is antibiotics or FMT more effective at curing C dif infection?

A

FMT
- response is more durable too

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16
Q

Is there a difference in efficacy between the dif modes of FMT administration?

A

No, all equal currently

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17
Q

What are some severe AE of FMT?

A

Transmission of infectious agents (ie transmission of infectious agents ie E coli, ESBL, norovirus)

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18
Q

When can neurosyphilus develop following an acute infection?

A

A singificant number of pts will develop neurosyphilus early
- need to be aware and treat is evident

This is different to the traditional way of thinking (ie tirtiary syphilus down the line)

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19
Q

Describe the natural history of syphillus infection?

A

Primary infection
can develop into secondary infection however primary infection can also develop into early latent infection (ie no secondary infection)

Early latent infection is asymptomatic latent infection <1 yrs following acute infeciton

Early latent infection can develop into secondary infection, however it can also go on to become late latent infection (asymptomatic, >1yrs following acute infection)

Most of these late latent infection will remain latent for life. Minority will develop tirtiary syphiluis.

Note a significant portion (40%) of people will develop early neurosyphilus following acute infection. Can also develop occular and otic syphillus at this time.

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20
Q

What are some symptoms / clinical findings in primary syphilus?

A

Chancre + regional lyphadenopathy (inguinal)
- Be wary if someone presents with isolated lymphadenopathy in the right demographic

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21
Q

What are some symptoms / clinical findings in secondary syphilus?

A

Presents 2-10 weeks following initial infection usually

Rash, fever, generalized lymphdenopathy
Mucosal leisions
Allopecia

Can present as nephritis, hepatitis

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22
Q

What syphilus test is non treponeal? What does this mean for furture testing?

A

RPR is the only non-treponeal test
- means it will not always remain positive (like the treponeal tests will once exposed to syphillus)

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23
Q

What are the two syphillus tests? what do they test for?

A

RPR (rpaid plasma reagin)
- Non specific cardiolipin antibody tests
- very sensitive (so if negative then dont have acute infection, but may have latent or past infection)

Treponeal specific tests (TPPA/TPHA/ FTA-Abs)
- FTA-abs and TPHA measure specific antibodies to Treponema pallidum antigens (will always be present post exposure)

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24
Q

What is considered a high RPR titre?

A

> 1:32

(ie 1:64 would be positive, 1: 200 would be very positive)

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25
Q

Negative RPR, postive TPHA. Possible interpretation?

A

Prievious infection, treated
Latent infection
Tertiary infection
- need to obtain CSF if concerned for tertiary neurosyphillus

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26
Q

High titre (>1:32) RPR, postive TPHA. Possible interpretation?

What if the titre was coming down but then rebounded?

A

Acute infection = infectious pt

Consider re-infection if rebound RPR titire

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27
Q

Low titre (< 1:32) RPR, postive TPHA. Possible interpretation?

A

Treated / resolving infection
Any stage

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28
Q

Low titre (< 1:32) RPR, negatiuve TPHA. Possible interpretation?

A

Very early infection (ie prior to seroconversion)
- repeat in 5 days time
False negative

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29
Q

Treatment of early syphylis (acute, secondary, early latent)?

A

Single dose of benazthine penecillin 2.4g IM

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30
Q

Treatment of late latent syphylis?

A

Benzathine penecillin 2.4g IM weekly for 3 weeks

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31
Q

Treatment of tertiary syphillus?

A

If nil evidence of CNS, otic or optic inv
-Benzathine penecillin 2.4g IM weekly for 3 weeks

If evidence of involvment
- IV ben pen q4h

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32
Q

Treatment for Uncomplicated genital or anorectal gonnococal infection?

Treatment for Uncomplicated pharyngeal gonnococal infection?

A

Ceftriaxine 500mg IM stat
Azithromycin 1g PO stat

Ceftriaxine 500mg IM stat
Azithromycin 2g PO stat

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33
Q

Why is azithromycin added to treatment regimes for gonnoicocal infections?

A

2 reasons:
- assume chlamydia is co-infection
- gonnococal resistance to ceft monotherapy is prevenlent

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34
Q

TImeframe of acute pelvic inflammatory disease?

A

<30 days

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35
Q

Treatment of acute pelvic inflammatory disease?

A

Ceftriaxone 500mg IM stat
+ metronidazole 400mg 12hrly 14 days
+ Doxy 100mg q12h 14d OR azithromycin 1g PO stat then reapeated 1 week later (for preg, or likely to be non compliant

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36
Q

Treatment of severe acute pelvic inflammatory disease?

A

IV ceft + azithro + metro

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37
Q

Presentation (Hx and Ex) of PID?

A
  • Lower abdo pain / pelvic pain
  • Pelvic organ tenderness (ie cervical hyperexcitability or pain during sex)
  • evidence of inflamation of genital tract

Onset of pain shortly after or during menstruation is suggestive

cute cervical motion, uterine, and adnexal tenderness on bimanual pelvic examination are the defining characteristic of acute symptomatic PID [7,8]. Purulent endocervical discharge and/or vaginal discharge is also common.

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38
Q

What needs to be excluded before considering Dx PID?

A

acute abdomen (ie apendicitis)
Ectopic pregnancy

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39
Q

Investigations for PID?

A

Speculum for endocervical swab
- NAAT for CHlamydia trachamonis, Neisseria gonorrhoea, Mycoplasma genitalium
- Gram stain and culture for Gonnorhoea for susceptibility testing

BC if hospitalized or severe

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40
Q

How is PID due to M genitalium treated?

A

moxiflox 400mg OD 14d

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41
Q

How is PID, chlamydia and gonnorhoea followed up?

A

Test of Cure 3 weeks

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42
Q

How is chlamydia treated?

A

doxycyclin 100mg q12h 7d
OR
azithromycin 1g oral as single dose (if preg)

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43
Q

Common organism causing urethritis in men?

A

N. Gonorrhoeae
Mycoplasma genitalium
Neisseria Meningitis (no capsule)

Should recommenced MSM (esp MSM with HIV) to get meningococcal vax

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44
Q

Common organism causing proctitis (STI)? How does this inform teh work up investigations?

A

Chlamydia trachomatis L1,2,3 (causes Lymphogranuloma venereum)
N gonorrhoeae
HSV
Monkeypox

Need to rest for all of these, including monkey pox
Need to test for L1,2,3 if Ct positive

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45
Q

What is lymphogranuloma venereum? How is it different from Chlamydia infection?

A

This is an ulcerative disease of the genital area (STI). It is caused by specific strains of the gram-negative bacteria Chlamydia trachomatis (L1, L2, L3)

Chlamydia is also caused by Chlamydia trachomatis but not by the L1,2,3 strains. It is limited to the local mucosa whereas lymphogranuloma venereum invades lymphatics.

46
Q

How is proctitis in men empirically treated?

A

Ceftriaxone + Doxycycline + valacyclovir

47
Q

What is monkey pox (Mpox)?

A

Mpox is a rare disease caused by the DNA monkeypox virus (also known as monkeypox and MPV). The monkeypox virus belongs to the Orthopoxvirus genus (same as small pox)

48
Q

Presentation of Mpox infection (immunocompetent pt)?

A

appox 7 day incubation (3-21d) +/- flu like prodrome
Rash (similar to chickenpox)
- simialr to cheicklen pox, starts maculopapular, then develops into vesiculo-pustular
- Rash is over face mainly, can be on palms and soles, and dorsum of hands (unusual in chicken pox)
- Can have mucosal leison + anogenital leisions
- Can have few or even a single leision

Self resolving in 2-4 weeks

49
Q

Who gets severe mokeypox infection? What is the main way of preventing severe infection?

A

HIV pts with CD4 count <0.2
- increased chance of death

Vaccine

50
Q

What is meliodosis? what causes it?

A

This is a severe lung or systemic (septic) bacterial infection caused by Burkholderia pseudomallei which is an endemic soil borne organism i NT and north QLD

51
Q

Risk factors for meliodosis?

A

NT, wet season, playing in mud, poor living conditions

Diabetes, alcoholism, renal failure (immunocompremised)

52
Q

How does meliodosis present (generally)?

A

Severe pneumonia, sepsis, any other organ can be effected (think TB)

53
Q

How does meliodosis treated? How is it erradicated following acute managment?

A

Meropenum OR ceftazadime
If severe/neuro/bone/jone/GI involved then add:
- trimethoprim+sulfamethoixazole + folic acid

Erradiacation:
- 3-6 months of trimethoprim+sulfamethoixazole

54
Q

Is vestibular or cochlear toxicity more common with gent? How does this manifest clinically?

A

Vestibular

Manifest:
- hearing loss and vertigo rare
- Can detect with head impulse test bedside

55
Q

Risk factors for gent tox?

A

Cumulitive dose (can occur after 1 dose)
Elderly pt

56
Q

What gene is gent tox associated with?

A

Mitochondrial gene coding for ribosime MT-RNR1

57
Q

Presentation of Buruli ulcer?

A

Single isolated ulcer, with underminded edges
- systemic feature nearly always absent

58
Q

How is Buruli ulcer Dx?

A

PCR of wound swab (cultures take ages)

59
Q

Treatment for buruli ulcer?

A

Rifampicin + clarythromycin 8-12 weeks +/- surgery

60
Q

What is causative agent of buruli ulcer?

A

Mycobacterium ulcerans

61
Q

Causative agent in Q fever?

A

Coxiella Burnetii

62
Q

Demographic that gets Q fever?

A

Vets
Abattoir workers
farm workers

63
Q

Vector for Q fever?

A

Cattle/sheep/goats (many others too)
- found in the placenta&raquo_space; faeces/urine/milk

64
Q

Presentation acute Q fever?
presentation of chronic / untreated Q fever?

A

Acute infection:
- 2-3 week incubation period
- followed by fever, myalgia etc (non specific signs)
- May have pneumonia, may have hep (not always)

Chronic infection / sequela of untreated infection:
- Osteoarticular: peripheral arthritis, spondylitis, sacroileitis
- Genitourinary: Orchiditis, epidydimitis
- Neuro: meningitis
- CVS: Endocarditis

65
Q

How is Q fever Dx? Explain antibody testing in Q fever?

A

PCR in acute infection
Detection of Phase 2 antibodies occurs before phase 1 antibodies
- If detect Phase 1 antibodies then need to go looking for sequaela of chronic disease (ie osteoarticular, endocarditis etc)

66
Q

How is acute Q fever empirically treated?
How is long term Q fever treated (ie detected Phase 1 antibodies)?

A

Doxycycline upfront
Then confirm or not confirm Dx with serology

Long term:
- long term doxycycline +/- Hydroxychloroquine +/- surgery ie for endocarditis

67
Q

Vaccination is routinely used for Q fever. What is teh most concerning side effect of teh Q fever vaccine specifically?

A

Pts with past Q fever exposure can get hypersensitivity reaction
- therefor need to have negative skin test and serology before vaccinate

68
Q

Main toxicities of linezolid?

A
  • Serotonin syndrome (interaction)
  • Anaemia and thrombocytopenia (develops a few weeks later)
  • Neuropathy (develops weeks to months later)
  • Lactic acidosis (elderly pts)
69
Q

Main toxicities of Voriconazole?

A
  • Visual symptoms: blue green aura
  • PHotosensativity
  • Purpilish skin discolouration
  • FLurosis orthosis
70
Q

Main toxicities of Qinolones?

A
  • Tendiopathy (bilateral tendinopathy only 3-4 days into Rx)
  • QTc prolonge
  • C dif
71
Q

Main toxicities of daptomycin?

A
  • raised CK (rhabdo)
  • Eosinophilic pneumonia
72
Q

Main toxicities of nitrofurantoin?

A
  • Pul fibrosis
73
Q

Main toxicities of metro?

A
  • peripheral neuropathy
74
Q

Main toxicities of azithro?

A

hearing loss
QTC increased

75
Q

What is gene responsible for MRSA resistance?

Treatment of MRSA

A

penicillin-binding protein mutation coded by the mecA gene +/- Panton-Valentine Leukocidin (PVL) Gene

Vancomycin, ticoplanin, cipro

76
Q

What are the three resistance level of staph aureus?

A

MRSA - methacillin resistance SA
VISA - vancomycin intermediate SA
h-VISA - heteroresistant vancomycin intermidate SA
VRSA - vancomycin resistance SA

77
Q

Treatment for VISA / hVISA?

A

teicoplanin, linezolid

78
Q

What is MSRE? What gene is responsible for the resistance?

A

Methicillin-Resistant Staphylococcus epidermidis (MRSE)
penicillin-binding protein mutation coded by the mecA gene as per MRSA

79
Q

What is VRE?
What are the subtypes of VRE and what are these subtypes resistant to?

A

Vancomcyin resistnt encterococcus
- enterococcus faecium, enterocuccus faecalis

Usually low virulence organisms, but can cause significant disease in immunocompremised pts on bread spektrum abx

Van A - resistant to vancomycin and teicoplanin
Van B - resistant to vanc, teicoplanin my work but resistance likely to develop
Van C - partly resistant to Vanc

80
Q

Explain the vancomycin resistance mechanism of VRE?

A
  • Altered peptidoglycan terminus (d-ala-d-lac instead of the usual d-ala-d-ala), resulting in reduced vancomycin binding and failure to prevent cell wall synthesis. THis is encoded for by Tn1546 or Tn1547, two transposons
  • also resistant through changes to the penicillin binding proteins from high affinity to low affinity
  • Aminoglycoside modifying enzymes
81
Q

Treatment of VRE?

A
  • Linezolid
  • Daptomycin (not used for lung infections as does not penetrate lungs)
  • Tigecyclin is used for tissue / intrabdominal infection (inferior for septisaemia)
82
Q

What is VRSA and VRSE? How did the acquire resistance?

A

Vancomycin resistant staph aureus (VRSA)
Vancomcyin resistance staph epididimis (VRSE)

Resistance aquired through transfer of resistance gene from Van A (VRE) + penecilin binding protein mutations (as with MRSA/MRSE)

83
Q

Treatment for VRSA/VRSE?

A

linezolid
quinupristin-dalfopristin

84
Q

What are the ESCAPPM organisms? What is the underlying resistance feature that unifies these organisms and what is the implication for treatment?

A

ESCAPPM is a group of gram negative rods in which beta lactamase production is chromosomal medited. Treatment with cepholosporin (even if susceptible) will iunduce resistance. This empirical therapy involves carbopenums or aminoglycosides or cefepime

  • Enterobacter species
  • Serratia species
  • Citrobacter freundi
  • Aeromonas
  • Proteus vulgaris (non-mirabilus) + Pseudomonas
  • Providencia
  • Morgonella Morganii
85
Q

Example of a multi drug resistant gram negative bacilli that is one of the leading causes of infection worldwide?
Whop usually gets this and what does it cause?
How to treat empirically?

A

Acinetobacter baumanii
- often can be multi drug resistant

Tropical wet season in northern australia
Affects individual with predisposing factors such as etoh use, lung disease or DM

Causes pneumonia

Treat with meropenum empirically

86
Q

Give some examples of multidrug resistant enterobacteriaceae?

A

ESBL producing enterobacteracieae
AmpC beta lactamase producing enterobacteriaceae
Carbepenemase producing enterobacteracieae

87
Q

Treatment for ESBL producing enterbacteriaceae?

A

Carbopenums
Ciprofloxacin
Gentamycin

88
Q

Which cephalasporin have activity against pseudomonas?

A

4th generation and newer
- ceftazidime, cefepime

89
Q

Most carbopenums have activity against pseudomonas. Which one does not?

A

Ertapenum

90
Q

Which cefalasporin does not cover gram positive bacteria well (ie staph Aureus)?

A

Ceftazadime
- it has psudomonal activity but not gram positive cover unlike the rest of the cefalasporins

91
Q

Quinolones generally have good psudomonal cover? What is the exception?

A

Moxifloxacin
- ciprofloxacin has good action

92
Q

What group of gram positive is inherently resistant to cepohalasporins?
In what situation can cephalasporin be used to treat this organism?

A

Enterococcus (E facium, E faecalis)
- used to treat in combination with ampicillin (synergy)

93
Q

First line treatment of E faecalis (nil resistance)?

A

First line:
- ampicillin, amoxicillin (better than penecillin)

94
Q

What are the resistance mechanisms of pseudomonas?

A

Poor outer membrane permiability to antibiotics medicated by porins
- Additional mutations to porins leading to loss of porins can reduce the permiability

Efflux pumps pump abx out of the cell

Formation of a biofilm that protects the multidrug resistance persister cells resulting in highly recalcitrant infection (comes back even after treated)

95
Q

Basic management of staph aureus bacteramia?

A

Cease the empirical fluclox and vanc
- If PSSA treat with penecillin
- If MSSA treat with fluclox (or cefazolin) - most common
- if MRSA - vancomycin

Remove the source (mostly caused by lines)
Blood cultuires q48h until cleared
Perform TTE/TOE (high IE risk)
Decide duration:
- minimum 2 weeks, longer if complicated

96
Q

How is vanc dosed? how is it monitored (practically and ideally) ?

A

Critically ill
- give loading dose 25mg/kg stat
- then follow with maintainance 15-20mg/kg BD
-> consider renal function and obesity dose adjustment

Monitor with trough level every 4th dose
Ideally measure AUC/MIC but not practical

Consider infusion for better control of levels

97
Q

Why is treatment of MSRA with a vancomycin MIC >2.0 difficult?

A

because with a MIC this high, it is basically impossible to achieve a AUC/MIC ratio that is not nephrotoxic

98
Q

What alternatives are there for MRSA bacteramia aside from vanc?

A

Linezolid, daptomycin, ceftaroline

Dont use bactrim, clindamycin, teicplanin as these are inferior in bacteramia specifically (good for tissue infections)

99
Q

What are common types of CRE seen in Australia? What are the most common enterobacteriaceae that produce carbopenemase?

A
  • New Delhi metallo-betalactamase (NDM-1)
  • IMP (metallo beta lactamase common in aus)

Usually klebsiella or E coli
- can transdfer to other gram negative such as Acinetobactor baumannii (big problem)

100
Q

How is CRE treated?

A
  • Cefiderocol
  • Colistin (in combination with carbopenum, maybe rifampacin)
  • Tigecyclin
101
Q

What is the mechanism of colistin resistance?

A

LPS changes in cell wall

102
Q

There can be cross reactivity between cefalexin and What other drug?

A

Amoxicillin (very similar structure (more so than jjust the simiularity between cefalasporins and penecillins)

103
Q

What is vancomycin red man syndrome? WHat is teh pathyphys briefly? how to manage?>

A

It is a histamine medicated reaciton to vancomycin (not IgE mediated)
Treat by slowing infusion to <10mg/min and given antihistamines

104
Q

Initial therapy for TB?

A

RIPE therapy
- Rifampacin, isoniazid, pyrazinamide, ethambutol
- consists of intensive phase and continuation phase

Intensive phase
- RIF, INH, PZA, EMB daily for 2months

Continuing phase
- RIF and INH daily for 4 months

105
Q

When should steroid be used for TB?

A

Severe disease, including but not limited to pericarditis, CNS disease

106
Q

How long before clinical improvement should be expected with RIPE treatment of TB?

A

2-3 weeks
- If nil improvement then investigate why (MDR, non compliant etc)

107
Q

Monitoring TB treatment?

A

AFB and sputum culture at 2 months (end of intense phase)
- If sputum pos at 2 months -> Ix MDR

Sputum shouyld then be obtained every 2 months until cleared
- If not cleared by 4 months then suspect Rx failure

108
Q

Side effects of TB drugs?

A

Hepatotocicity is main SE
- Rifamycins, INH and pyrizinamide can all cause hepatotoxicity

  • Rifamycins cause cholestatic derrangment
  • INH and pyrazinamide cause tranaminitis
109
Q

Treatment of latent TB?

A

INH daily for 6-9 months (WHO favoured)
- has sig hepatotoxicity and non compliance so instead can use other regimes

Rifampicin daily for 4 months
Rifampicin + INH daily for 3 months
Rifapentine + INH weekly for 3 months

110
Q

What is japanese encephalitis? Presentation? Prevention ? treatment?

A

Mosquito born flavivirus
- found in torres strain and north queensland and now in norther NSW and VIC

Water birds and pigs are amplifying hosts, humans are dead end hosts

5-15d incubation, presents mostly asymptomatic
1/100-200 develop encephalitis

Manage with supportive care

Prevention:
- mosquito avoidance
- Vaccination

Infectious Diseases (3 decks)

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