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Infectious Diseases > Infectious diseases Basics > Flashcards

Infectious diseases Basics Flashcards

1
Q

When should asymptomatic bacturia be treated?

A

Pregnancy
Pre urological procedure if bleeding is expected

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2
Q

Should you treat the colonised bacteria of a non infected appearing ulcer?

A

NO, Only treat if clinically infected

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3
Q

When should an upper resp tract infection be treated with antibiotics?

A

If the pt is suspected or confirmed to have strep pyogenes infection, or bordatella pertusis infection

Should not treat URTI with abx otherwise

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4
Q

How long is an abx course for IE generally speaking? What are the exceptions and how long should the course be in this situiations?

A

6 weeks generally EXCEPT:
- Confirmed right sided (ie TV) staph aureus IE -> treat for 2 weeks
- Highly penicillin susceptible streph (MIC <12) native valve without surgical indications -> 4 weeks (OR 2 weeks if 2 weeks of gentamycin is used)

  • Q fever, whipple’s disease associated (Tropheryma whipplei) IE -> treat for much longer than 6 weeks (months or years)
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5
Q

What is the indication for surgery in IE?

A
  • Acute heart failure
  • Abscess
  • Modifying factors (prosthetic valve; very virulent organism ie candida / staph aureus)
  • failing medical management (persistent bacterial despite appropriate abx)
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6
Q

How is IE diagnosed?

A

Dx pathologically (ie surgical specimen)
Dx clinically:
- 2 major OR 1 maj + 3 minor OR 5 minor

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7
Q

What are the Major and minor criteria for Dukes criteria?

A

Major criteria: Micro
- Typical organism in 2x separate blood cultures (staph aureus, staph lugdunesis, staph gallolyticus, any strep, enterococcus)
- Other organism in 3x seperate blood cultures
- Bartonella IgG positive (serology)/ Q fever 1 IgG positive (serology)
- PCR pos for Coxiella/Bartonella/Whipples (more difficult to grow

Major Criteria: Images
- ECHO or Cardiac CT showing new valve regurgitation, abscess/dehiscence of valve, vegetation
- PET uptake valve or device (>3m)

Major criteria: Surgeon impression of IE upon opening

Minor criteria:
- Fever >38
- Predisposition: Prosthetic valve, prev IE, CCF, RHD, IVDU etc
- Vascular phenomenon: Janeway, mycotic aneurysm, splinter hemorrhage / emboli event
- Immune: GN, RF, Oslers, Roth spots
- Micro: micro that is not satisfying maj criteria
- PET uptake <3m

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8
Q

When should IE prophylaxis be used?

A

Have to have a risk factor, and a surgical procedure that is high risk of bleeding/ infection

Risk factor:
- Prev IE
- Prosthetic valve
- Congenital disease AND repair <6m ago with prosthetic or incomplete repair
- RHD

Dental procedures:
- Extraction, periodontal surgery, re-implantation of tooth (ie MAJOR dental procedures)

Resp tract/ other surg
- Tonsil or adenoid surgery (not indicated for other surgeries)

GI/urinary tract:
- There is no specific operation in which to given IE prophylaxis. If surgical prophylaxis is normally indicated then give

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9
Q

What should be used for IE prophylaxis?

A

Amoxicillin 2g

OR for urological/GI procedures ensure to cover enterococci (ie ampicillin, vanc, tazocin, mero)

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10
Q

How is strep broadly categorized? Explain how a strep is identified as these classifications?

A

Alpha haemolytic - Incomplete / partial haemolysis of horse blood agar plate

Beta haemolytic - copmplete haemolysis if horse blood agar plate

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11
Q

What are the main classifications and species in these classification of beta haemolytic strep?

A

Beta haemolytic strep is divided into group A, B, C/G, D (although D is more often grouped with alpha haemolytic strep)

Group A:
- S pyogenes

Group B:
- S agalactiae

Group C/G:
- S dysgalactiae

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12
Q

What are the main classifications and species in these classification of alpha haemolytic strep? (Acronym)

A

Pneumonic
- GONDON was SANGUINE about his ORAL MITES.
- But he wanted to get out of the mouth and cause so endocarditis. so he SOBERLY, MUTATED and off he went
- meanwhile, in pus land, so IMTERMIDATE level STARS were giving each other ANGINA
- at least that was better than the hangers on in the VESTIBULE SALIVATING and doing generally not much

  • then I saw D. d was looking decidedly BOVINE, not lookign well at all like he was lying in the GALLOWs, just lying in the GALLOWs. D looks like he has got cancer, or endocarditis; we need to get a c scope PASTEURIANUS. Have you seen LUTICIA? she took the BABY and headed off to the gall bladder to cause some trouble
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13
Q

Which strep is most associated with bowel cancer?

A

Strep Galolyticus gallolyticus

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14
Q

Which group D (Bovis strep) is most likely to cause IE? Which strep in gerneally is most likely to cause IE?

A

Strep Galolyticus gallolyticus
- All the group D (strep bovis group) can cause it at fairly high rates

Step mutans (on of the oral streps)

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15
Q

Which Aus demographic has the highest incidence of acute rheumatic fevers?

A

ATSI children 5-14yrs
Pacific island children 5-14 years

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16
Q

What bacteria causes rheumatic fevers?

A

Group A beta haemolytic strep (ie strep pyogenes)

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17
Q

GAS infection can lead to rheumatic fevers. What are the most common sites of initial infection with GAS?

A

Pharyngitis
Skin infection (scabies, impetigo)

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18
Q

Explain the psychophysiology of rheumatic fever?

A

GAS M protein and N-acetyl-beta-D-glucosamine epitope cross reactivity with myosin and laminin in the heart (leading teh heart disease) and basal gangli (leading to syndromes chorea)

Immune complexes form causing joint problems

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19
Q

How is rheumatic fever Dx?

A

Jones Criteria: Definitie Dx
- Evidence of GAS infection (usually culture, but can be antistreptolysin O titre, or anti DNase B) AND (2 major OR 1 major with 2 minor OR syndenham’s chorea)

Jones Criteria: Probable
- criteria falls short by 1 major, or 1 minor, or no serology/culture

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20
Q

How is ARF treated once it has been Dx?

A

Single dose benzathine penecillin (kills all GAS)
Manage heart (ACEI, possible HF drugs)
Manage joint pain (NSAIDs ie high dose aspirin)
Manage chorea (suportivly)

Prevention (usually monthly benzethine injections)

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21
Q

What are some sequelae of acute GAS infection?

A

ARF/RHD
Post strep GN
Bone and joint infections
GAS sepsis

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22
Q

What is the most effective way of preventing recurrent lower leg cellulitis?

A

Knee high compression stocking daily
- Not organism specific

Abx prophylaxis also works but is more expensive and complex and works less in obese or fluid overload etc pts

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23
Q

CMV negative recipient to get a CMV positive kidney. What should be used as prophylaxis?

A

Oral valgancyclovir

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24
Q

What time frame should osetalmavir be started and how much does it shorten the flu illness?

A

Needs to commence in 48hrs of symptoms
Shortens illness by 24hrs

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25
Q

Can osetalmavir be used in preg woman?

A

Yeas

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26
Q

List the most relevant herpesviruses and their associated conditions?

A

HSV1 - encephalitis, liver failure
HSV2- aseptic meningitis, mollarets, STI

HHV3 = VZV - Chickenpox, shingles
HHV4 = EBV - Amoxicillin rash, Atypical lymphocytosis, hepatitis, severe lymphadenopathy, neutropenia (or neutrophilia)
HHV5 = CMV - atypical lymphocytosis, hepatitis
HHV6,7 - roseola
HHV8 - karposi sarcoma

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27
Q

How do pts with HSV encephalitis present?

A

Prodrome of malaise, fever, headache, and nausea, followed by acute or subacute onset of an encephalopathy (lethargy, confusion, and delirium, seizures)

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28
Q

What demographic usually gets HSE due to HSV1 and HGSV2?

A

Children and adults - HSV1
Infants HSV2 (vertical transmission)

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29
Q

Which lobes are typically affected by HSV 1 and HVS 2?

A

Adults with HSV1 HSE - Temporal and frontal lobes
Infants with HSV2 HSE - generalised brain

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30
Q

How is HSE managed?

A

IV acyclovir
Anticonvulsants
Manage increased intracranial pressure

Supportive care

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31
Q

What is the most common cause of aseptic meningitis?

A

HSV2
- note HSV1 causes HSV encephalitis, not so much meningitis

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32
Q

What is Mollarets meningitis?

A

This is at l;east 3x episodes of recurrent aseptic meningitis with at least 1x proven HSV2 (ie PCR for CSF during an episode)

The meningitis is usually much less severe than bacterial meningitis and is managed with supportive care alone. Nil antivirals needed

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33
Q

Who is recommended to get varicella containing vaccine?

A

Children >12 months to <14 years should get 2x doses of a varicella containing vaccine at least 4 weeks apart

All ppl >14 years who are not immune (or unclear if immune) should receive 2x doses or a varicella containing vaccine at least 4 weeks apart

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34
Q

Who is eligible for the shingles vaccine (shingrex)?

A

2 dose course is available for adults >65 years, and indigenous adults >50 years

Also availible for immunocompremised pts >18yrs with following conditions:
- SCT
- solid organ transplant
- Haem malignancy
- Advance untreated HIV

Cant be given in pregnancy

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35
Q

Explain the relationship between shingles infection and stroke?

A

Pts with shingles infection in the last 6 months are at increased risk of stroke (esp if shingles infection is in V1 distribution)
- Receiving the vaccine for shingles significantly mitigated this risk

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36
Q

At what time does the rash appears following commencement of antibiotics in a pt with EBV infection?

A

2-10 days after stating antibiotics (usually amoxicillin, but can also be other abx)

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37
Q

Describe the EBV - amoxicillin rash?

A

drug eruption is an itchy maculopapular or morbilliform rash

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38
Q

What is atypical lymphocytosis? in what infections does this classically occur?

A

Atypical lymphocytes is lyphmocytosis (high lymphocytes) with atypical appearance, mainly due to increased production fo CD8 T

It typically occurs in primary EBV and CMV infection, however lower numbers of atypical lymphocytes can be seen in other viral infections

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39
Q

What is the difference between atypical lypmhocytosis and leymphocytic leumkaemias?

A

the atypical lymphocyutes in atypical lymphcytosis are heterogenous unlike leukaemia

40
Q

What malignancies is EBV causally associated with?

A

Burkits lymphoma
Primary CNS lymphoma (in severe AIDs pts)
Post transplant lymphoproliferative disorders (PTLD)
nasopharyngeal cancer

41
Q

Who gets systemic CMV disease?

A

Immunocompremised pts:
- severe HIV infection with CD4 count <50
- Solid organ transplant pts (esp CMV non immune host receiving CMV positive donor)

42
Q

What is the treatment of systemic CMV disease?

A

for hospitalized pts, treat with IV gancyclovir +/- forcanet (if severe)
- then switch to oral course of valgancyclovir

43
Q

How does covid enter the cell?

A

It has viral spike (S) prteins that bind to host ACE2 receptors and the co-receptor TMPRSS2

44
Q

At what stage of the natural covid lifecycle do MABs work? Why are these not routinely used anymore?

A

MABs used in the treatment of covid target the spike pretein which prevents covid from entering cells)

They have lost activity (no longer work as they once did)

45
Q

What is paxlovid? At what stage of the natural covid lifecycle does paxlovid work?

A

Paxlovid is a combination drug for covid infection
- it contains nirmatrelvir and ritonavir (these are both protease inhibitors)

The stop viral primary translation and polyprotein processing

46
Q

At what stage of the natural covid lifecycle does remdesevir and molnupiravir work?

A

Remdesevir and molnupiravir are both viral RdRP inhibitors (RNA dependant RNA polymerase inhibitors)
- they stop viral RNA systhesis

47
Q

What role (generally speaking) do baracitinib and toculizumab play in covid 19 infection? when are these medications used generally?

A

these are both immune modulator drugs
They are typically used in the second week of infection as the inflammatory response / immune response becomes the predoiminate response at this time

48
Q

What drugs are used as immune modulators in covid 19 infection?

A

Inhaled budesonide
Dexamethazone
Baracitinib
Toculizumab

49
Q

Define critical, severe, moderate and mild covid 19 infection?

A

Critical
- Resp failure
- Severe resp failure (based on blood gas)
- Failing NIV/HFNP (ie requires invasive ventilation)
- ARDS
- Hypotension / shock
- Other organ failure (CNS eg impaired consciousness)

Severe:
- requiring O2 to maintain >92%
- resp rate >30 on RA
- >50% lung infiltrates

Moderate
- Stable pt is evidence of lower resp tract disease on imaging
- maintaining 92-94% on RA
- desaturation with minimal exersise

Mild:
- Not any of the others

50
Q

How is severe covid infection managed?

A
  • Dexamethasone 6mg daily for 10 days
  • Remdesevir 200mg loading then 100mg daily for total course of 5 days
  • Baracitinib 4mg daily for up to 14 days OR Tocilizumab 1x dose (IV infusion)
51
Q

How is mild to moderate covid managed?

A

If 1x risk factror and <14 days of infection then given inh Budensonide/ciclosenide +/- ONE of the following:
- Remdesevvir for 3 days course (if <7/7 sx)
- Paxlovid (nirmatrelvir/ritonavir) for 5 day course (if <5/7 sx)
- Molnupiravir if <5 day sx

52
Q

What are some important aspect of respiratory care / supportive resp care in covid 19 pts?

A

Proning (>3hrs/d or >12h/day in intubated pts)
Higher PEP (10-12), recruitment procedures
Aim O2 sats 92-96%

53
Q

Should theraputic or prophylactic clexane be given for covid 19 infection? how long after DC from hospital should it be continued?

A

Aus guidelines say prophylactic regardless of severity
Should continue 2 weeks after DC

54
Q

Which covid medication has the most drug interaction? Which ones have the least?

A

Paxlovid (nirmatrelvir + ritonavir) has the most
- esp with CYP3A4 inhibitors
Remdsesevir and molnupiravir have the least

55
Q

What is vaccine induced thrombotic thrombocytopenia? What is the characteristic presentation and lab test? what is the pathophysioology?

A

Vaccine induced thrombotic thrombocytopenia (VITT) is a MAHA similar to heparin induced thombocytopenia
- It was relevant because the VAZ COVID vaccine caused it (no longer in aus)

Presentation:
- Pt with vaccine 4-42 days ago presents with symptoms of thrombosis or bleeding
- Found to have low plt count and fibrinogen, and elevated D dimer
- Imaging consistent with thrombosis somewhere
- Test for anti platlet factor 4 antibody is positive

It is due to the development of antiplatlet factor 4 antibodies (similar to HIT)

56
Q

Who usually gets covid vaccine related myocardiaits and myocarditis?

A

Results post RNA vaccine
Usually teenage males post second dose of vaccine
Self resolves with supportive management

57
Q

What is a side effects of long term treatment of Voriconazole?

A

Voriconazole is a triflurinated azole (triazole)
- Long term intake of fluorine can result in skeletal fluorosis and petrosis. Presents as diffuse, asymmetric periostitis usually of the wrists. It is reversible
- Long term use can result in alopecia and skin bronzing

58
Q

What is the most common organism causing human candida infection? What is its susceptibility pattern?

A

Candida albicans
- usually very suceptible to all agents, but still need to do suceptibility testing

59
Q

What are some other candida species (aside from albicans)? and what are some susceptibility considerations for each?

A

C. Glabrata
- then the azoles have nada (fluconazole, itraconazole). Susceptible to the other antifungals (ie echinocandins such as caspofungin)

C. Krusi
- dont use the Fluzi (fluconazole), but can use most other things

C. parapsilosis
- then dont use the Echino (echinocandins) and pull out the lino. Can use azole

C. Auris
- time to call the greek chorus (azoles dont work, amp B dosent work. Echinocandins do work but not always)

60
Q

What are some examples of azole antifungals (5)? What are some examples of echinocandins (2)? What are some other antifungal drugs not in these catagories?

A

Azoles:
- Fluconazole
- itraconazole
- voriconazole
- Posaconazole
- Isavaconazole

Echinocandins:
- caspofungin
- micafungin
- anidulafungin

Others:
- Amphoterecin B
- Flucytosine

61
Q

Explain the molecular changes resolonsible for azole resistance in aspergilosis and candida spp?

A

Aspergilosis
- CYP51A mutation

Candida spp
- ERG1 mutaiton

62
Q

Explain how amphoterecin B resistance develops?

A

Bypass of the ergosterol biopsynthesis pathway usually used for lipid metabolism

63
Q

Explain how echionocandin resistance develops?

A

Mutations in Beta-(1,3)- Glucansynthase complex (FKS1 and FKS2) - f*ck sake 1 and 2

64
Q

Which antifungals penetrate the BBB?
Which work best in urine tract infection?

A

FLuconazole, voriconazole, 5 flucytosine (5FC), amphoB
- just think of what youd treat cryptococcus with)

Fluconazole and 5FC are both concentrated into urine

65
Q

Which azoles interact with P-glycoproein inhibitor / substrate drugs?

Which azole interacts with CYP2C19 drugs (inhibitor and substrate) the most?

Which azole interacts with CYP3A4 drugs (inhibitor and substrate) the most?

A

Itraconazole, posaconazole
- fluconzaole interacts with p glycoprotin substrate drugs only

Voriconazole

Itraconazole

66
Q

How is invasive candidiasis Managed?

A

Echinocandins first line empirically, then can switch to azole if suceptible strain isolated (esp for C parasilosis)
- need to remove the source (often a line or presthetic)

67
Q

What are the three main aspergilosis spp and what ares of the body do they typically affect?

A

A fumigatus
- Lung (fumes into the lugs)

A Flavus
- sinus (smell is main part of flabour)

A niger/flavus
- burn (burnt tiger prawn is favourful)

68
Q

What are the main catragories of diseases caused by aspergilosis?

A

Invasive disease
- usually due to a neutrophil deficit (ie immunocompremised)

Allergic disease
- ie allergic bronchopulmonary aspergillosis

Anatmoic disease
- bronchiectasis, TB, CF

69
Q

What are some examples of health care relates situations that predispose to aspergilosis infection?

A
  • Long ICU stay
  • Severe viral infection (ie covid, flu)
  • BTK inhibitors such as ibrutinib; venetoclax (BCL2); ? fludarabine (antimetabite)
  • prolongued neutropenia
70
Q

What investigations are typically inveolved in Dx of aspergilosis?

A
  • Radiology tests - many different findings eg halo sign
  • serum galactomannan (in neurotrpenis), BAL galacomannan
  • PCR for aspergilosis
  • beta1-3-d-Glucan
71
Q

What is the treatment of allergic disease related to aspergilosis?

A

Steroids +/- omalizumab

72
Q

What is the treatment of invasive aspergilosis?

A

Voriconazole monotherapy (may use combination with echinocandins if severe)
- If voriconazole is contraindicated or not tolerated the itraconazole or posaconazole is second line

Can also use lipid ampB but this has additional nephrotoxicity and is IV formulation

73
Q

How are fungal balls (aspergiloma) managed (in the abscence of invasive aspergilosis)?
What is a complication of aspergilomas?

A

Observation with serial imaging if minimal or no haemoptysis.
Surgery is definitive managment, used when there is worsening or severe haemoptysis

Main complication is life threatening haemoptysis

74
Q

What is the preferred long term treatment of aspergilosis?

A

Itraconazole (avoids long term side effects of voriconazole)

75
Q

What are some chronic forms of aspergilosis (3)?

A

Aspergiloma
- pt with structural lung disease
Chronic cavitating pulmonary aspergilosis
Recalcitrant Allergic bronchopulmonary aspergillosis (ABPA)

76
Q

Which form of central line (femoral, sub calv, IJV) is associated with the most infections?

A

femoral

77
Q

Which form of central line (femoral, sub calv, IJV) is associated with the most pneumoT?

A

subclavian

78
Q

What is Strongyloidiasis?

A

This is infection by the soil borne helminth Strongyloides stercoralis

79
Q

Is strongyloides found in Aus? Where?

A

Yes it is endemic in parts of australia (NT and north QLD)
- otherwise located in USA, mexico, south ameria and parts of africa

80
Q

What are the various ways in which infection with strongyloides stercolaris manifest?

A
  • Acute infection
  • Chronic asymptomatic infection
  • Disseminated/ hyperinfection in the event of future immunosupression (autoinfection)
81
Q

Explain briefly the lifecycle of strongyloides?

A

Skin contact with infected soil or other human faeces contaminated material

filariform larvae penetrate skin, migrate via blood/lymph to lungs

Penetrate into alveolar sacs, ascend teh resp tract, then are swallowed

Matuyre into adult worm, burrow into duodenum/jejunum (can live there for five years)

Adults make eggs, passed in stool (cycle starts again)

82
Q

How does strongyloides acute infection present?

How does it present chronically?

A

Irritation at site of skin penetration
Dry cough may develop within a week
GI symptoms develop as early as one week
- diarrhea, constipation, abdominal pain, or anorexia may occur

Non specific GI symptoms
Cutaneous manifestations larva currens, pruritus, urticaria, and angioedema
Resp symptoms

83
Q

A man presents with cough and vague GI symptoms. The cough paradoxically worsens with steroids. What is this concerning for?

A

Chronic strongyloides infeciton

84
Q

How does hyperinfection present?

A

Unwell pt
- manifestation in GI, lung, skin (ie cough, dysponea, lung infiltrates, non specific abdo symptoms, bright red skin rash)

85
Q

How is chronic infection (not hyperinfection) with strongyloids treated?

A

2 doses of ivermectin 0.2mg/kg PO separated by 1 week

86
Q

How is hyperinfection with strongyloids treated?

A

Daily Ivermectin
- often until have pathological (ie BAL or GI aspirate sample) evidence that parasites are dead

87
Q

What virus most increases risk of severe stroingyloids infection?

A

HTLV1
- larger risk factor than HIV1

88
Q

What does high eosinophils typically represent in parasite infeciton?

A

usually means that parasite is crossing tissue planes (ie from liver into lung)

89
Q

What drug can causes PML (progressive multifocal leukoencephalopathy)? How does this occur?

A

Natalizumab (cell adhesion alpha 4 integrin)
- treatment of crohns and MS

Causes reactivation of JC virus which can cause progressive multifocal leukoencephalopathy)

90
Q

What is progressive multifocal leukoencephalopathy?

A

Progressive multifocal leukoencephalopathy (PML) is a disease of the white matter of the brain, caused by a virus infection (polyomavirus JC) that targets cells that make myelin—the material that insulates nerve cells (neurons). Polyomavirus JC (often called JC virus) is carried by a majority of people and is harmless except among those with lowered immune defenses.

91
Q

Waht is eculizumab? What is an infectious complication of treatment with eculizumab?
- How is this potential complication prevented?

A

Eculizumab is a MAB used to treat paroxysmal nocturnal hemoglobinuria, atypical HUS, generalized myasthenia gravis, and neuromyelitis optica

It is a MAB against C5 (terminal pathway)

Side effect is fulminant neisseria meningitidis due to diablinmg the terminal complement pathway
- MAC used to control encapsulated organisms

Need to vaccinate: ACWY vaccine and MenB
- this only protects against typable strains, therfore need to give amocycillin prophylaxis to protect from no typable strains

92
Q

What are 4 organisms with a capsule? What is the most clinically relevant of these?

A

Step pneumniae (most relevant)
Neiseria meningitidis
Haemophilus influenzae
Capnocytophaga canimorsus

93
Q

What vaccinations are recommended for this without a spleen (in adults)?

What time are these given?

A

haemophilus influenza vaccine
- If never had -> give one dose
- If not completed course - > given one dose
- If complete course -> nil need

Influenza vaccine
- give 1 dose every year (as usual)

menACWY vaccine
- 2 doses >8 weeks appart, then booster every 5 years

MenB vaccine
- 2 doses >8 weeks apart, then booster every 5 years

Pneumococcal vaccine
- (if not had prievious vaccinations) given congugate vaccine, then 12 months later give 23vPPV vaccine, then 5 years later given second dose 23vPPV vaccine

94
Q

What ab prophylaxis is used in asplenism?

A

Amoxycillin 250mg daily for at least 3 years (preferably lifelong)
- abx proph not required after splenic artery embolization

95
Q

What is a typical emergency plan in a pt without a spleen?

A

amox 2g PO stat, then ongoing every 6hrs until medical review
Medical bracelet

96
Q

What is used for meningococcal prophylaxis (ie family member has menigococcal disease)?

A

Rifampacin usually
Ceftriaxone if preg

97
Q

What are some examples of live vaccines to be cautious of in immunocompremised hosts?

A

Live vaccinations:
- MMRV
- BCG
- Yellow fever

All the other vax have non live alternative

Infectious Diseases (3 decks)

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