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Viruses Flashcards

1
Q

How do arboviruses survive a long time in vector populations?

A

can be passed from mosquito to its eggs

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2
Q

Diagnostics for arboviruses

A

PCR - short window of viremia
Serology

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3
Q

What is the natural host for dengue

A

humans and primates

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4
Q

How many serotypes does dengue have?

A

4 serotypes

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5
Q

Stages of dengue

A

Old:
Dengue fever
Dengue haemorrhagic fever
Dengue shock syndrome

New:
Dengue without warning signs
Dengue with warning signs
Severe dengue

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6
Q

Symptoms of dengue

A

Incubation 5-8 days
“break-bone fever” - fever, headache, retro-orbital pain, arthralgia
haemorrhagic manifestations - petechiae, frank bleeding, rash
other - sore throat, nasal congestion, nausea, vomiting, encephalopathy, hepatomegaly.
“saddleback fever” - re-emergence of fever after 48hrs

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7
Q

Dengue rash appearance

A

islands of white on a sea of red

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8
Q

Management for dengue

A

supportive only

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9
Q

With which infection does dengue haemorrhagic fever occur?

A

2nd infection
(or 1st infection in babies who have maternal antibodies)

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10
Q

Symptoms of dengue haemorrhagic fever

A

Fever
Narrow pulse pressure
Temperature drop
Marked thrombocytopenia
Can have haemorrhage (not required)
Plasma leakage syndrome

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11
Q

Issues with current dengue vaccine

A

If patient has had one episode of dengue before, they can be antibody primed to have a reaction (similar to having second infection)
Vaccine ideally needs to be tetravalent.
Currently only recommended in older children (no maternal Abs) and travellers (never had dengue)

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12
Q

What is the natural host for yellow fever

A

primates

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13
Q

Vector for yellow fever

A

Aedes Egypti
(Haemagogous in South america)

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14
Q

What is Fagets sign

A

Heart rate does not rise when temperature rises

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15
Q

Pathogenesis of yellow fever

A

Replicates initially in dendritic cells
Primary replication is then in APCs
Spread to lymph nodes, liver and spleen
Leads to liver failure and eosinophillic degranulation
Can get shock due to cytokine storm

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16
Q

Symptoms of yellow fever

A

Stage 1:
Fagets sign
Fever and malaise
Headache, photophobia
Nausea, vomitting, epigastric tenderness
Lumbosacral pain
Conjunctival redness

Stage 2:
Remission

Stage 3:
Day 3-6 of symptoms
fever, nausea, vomitting
jaundice, renal failure
haemorrhage from thrombocytopenia
myocardial injury
shock

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17
Q

Zika type of virus

A

Flavivirus

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18
Q

Methods of Zika transmission

A

Mosquito
Sexually
Vertically
Blood transfusion

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19
Q

Zika incubation

A

2-14 days (though most asymptomatic

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20
Q

Symptoms of Zika

A

Usually asymptomatic
Low grade fever
macular papular rash
small joint arthralgia
Conjunctivitis
facial swelling
Uveitis
Myocarditis
Pericarditis

Significant symptoms/complications:
- Guillian-Barre Syndrome
- Congenital Zika - zika crosses placenta causing microcephaly, still birth.

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21
Q

What type of virus is JEV

A

Flavivirus

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22
Q

Complications of JEV

A

Childhood neurological symptoms and disability

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23
Q

Normal hosts for JEV

A

Pigs (amplifying) and birds
Humans are dead end hosts

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24
Q

Mosquito that transmits JEV

A

Culex

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25
Q

Symptoms of JEV

A

Asymptomatic
Fever
Headache
GI symptoms

Neurological symptoms
Parkinsonian symptoms
Asymmetric limb paralysis
SIADH
Coma
Seizures common in children

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26
Q

JEV findings on MRI-B

A

Lesions in thalamus and basal ganglia

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27
Q

Chikungunya hosts

A

Humans
Sylvatic animals

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28
Q

Chikungunya incubation period

A

1 week

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29
Q

Chikungunya symptoms

A

Headache
Fever
Rash
myalgia and arthralgia

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30
Q

Chikungunya mosquito

A

Aedes Egypti

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31
Q

Ebola type of virus

A

Filovirus (RNA)

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32
Q

CCHF type of virus

A

Bunya virus (RNA)

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33
Q

Lassa fever type of virus

A

Arena virus (RNA)

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34
Q

CCHF symptoms

A

Fever - low grade
Low platelets
Profuse bleeding - with normal obs (platelets <50 = severe) - bleed early, bleed when they still look well.
Malaise
GI symptoms
Severe headache
DIC

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35
Q

Management of CCHF

A

Supportive management only
Blood products
Can trial ribavirin (SE of haemolytic anaemia)
Favipiravir

Ribavirin should be used as post-exposure prophylaxis!

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36
Q

CCHF vector

A

Tick bite - multiple types
Needle stick/ IVDU/ Nosocomial
Animal slaughter

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37
Q

CCHF endemic areas

A

Spain
Turkey
South Asia
Russia
Africa - poorly documented

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38
Q

CCHF incubation

A

2-21 days

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39
Q

CCHF diagnostics

A

Serology
PCR

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40
Q

Lassa fever symptoms

A

CNS infection
Hearing loss (sensory neural)
thrombocytopenia
renal failure
elevated LFTs

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41
Q

Lassa fever location

A

Nigeria
Sierra leone
Liberia
Only countries in West Africa (where the rat lives)

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42
Q

Vector for lassa fever

A

multimammate rat - from rats feeding on your food or from rat urine.
Aresolised when sweeping

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43
Q

incubation for lassa fever
and viral shedding period

A

1-3 weeks
continues for shed for 3 months in the semen

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44
Q

Treatment for Lassa fever

A

Ribavirin

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45
Q

Ebola symptoms

A

Stage 1:
Conjunctivitis
Fever
Lethargy

Stage 2:
Severe GI symptoms - massive diarrhoeal and vomiting losses.
Severe lethargy
Electrolyte imbalance

Stage 3: 33%
coagulopathy
ESRF
encephalopathy
seizures
hypoglycaemia

long term - cataracts

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46
Q

Post exposure prophylaxis for Ebola

A

Ribavirin
monoclonal antibodies

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47
Q

Treatment for Ebola

A

supportive management
antibiotics - risk of gut bacterial translocation
Antivirals - remdesevir
monoclonal antibodies

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48
Q

Investigations for Ebola

A

PCR
Lateral flow test

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49
Q

Pre-exposure management for Ebola

A

Vaccine available!
Highly effective

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50
Q

Methods of contact tracing for ebola

A
  1. History based contact tracing
  2. gene sequencing based contact tracing.
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51
Q

Rabies virus and epidemiology/transmission

A

Family Rhabdoviridae, genus lyssavirus
Dog, fox, raccoon bat
Similar diseases → european bat lyssavirus, australian bat lyssavirus
Long incubation period → weeks to months (can even be years)
Spreads from bite site to brain, then spreads outward to skin, saliva etc.
Route of inoculation - broken skin, mucous membranes, transplants.

52
Q

Rabies symptoms

A

Encephalopathy (fluctuant)
Confusion, agitation, aggression
Flaccid paralysis
Autonomic stimulation - salivation, frothing
Hydrophobia
Aerophobia
Muscle spasms
30% is paralytic rabies - paralysis, loss of reflexes, fasiculations, sphincter dysfunction

53
Q

Diagnosis for rabies

A

Sample at hair follicle - usually back of neck

54
Q

Management of rabies

A

no cure once symptomatic
Sedatives
Barrier nursing
Vaccinate those exposed
Depending on category can choose vaccine vs vaccine + immunoglobulin. (animal derived)
Wash wound
Dont suture

55
Q

Which diseases increase the risk of HIV transmission

A

Trichomoniasis
HSV2
Schistosoma haematobrium

(diseases causing breaks in urogenital area)

56
Q

What are the stages of the HIV viral cycle

A
  1. Binding: GP120 binds to CD4 receptor on host cell - Co-receptor CCR5 or CXCR4 must also bind to allow entry (depends on the type of HIV as to which one it can bind with)
  2. Fusion - Fusion occurs with the viral envelope and cell membrane
  3. Reverse transcription - Reverse transcriptase enzyme creates DNA from RNA
  4. Integration- The integrase enzyme integrates the viral DNA into host DNA.
  5. Transcription and translation then occurs to create new viral proteins
  6. The new viral proteins leave the host cell by budding, using host cell wall as its envelope
  7. Protease enzyme cleaves the long chain proteins into its active components - HIV is now active to infect another CD4 cell.
57
Q

Cell target for HIV

A

CD4 cell with GP120 receptor and CCR5 co-receptor (or CXCR4)

58
Q

In what ways is viral load and CD4 count used in monitoring

A

viral load - indicates treatment response
CD4 - indicates disease stage

59
Q

what is the HIV ‘set point’

A

Where HIV viral load reaches equilibrium with CD8 –> HIV will eventually escape this set point, but can last years

60
Q

Protective mutations in HIV

A

delta 32 mutation
HLA-B57

61
Q

HIV testing

A

High resource/ inpatient:
CD4 count
HIV viral load

Low resource/ self test:
- 4th Generation p24 antigen ELISA (detects within 14 days)
- Rapid diagnostic tests
- immunochromatography
- immunofiltration (INSTI) - (only useful in HIV1 types M,O)
Oraquick - HIV self test (better in high prevalence than high incidence)
Alere Ag/Ab combo test

62
Q

Recommended HIV drug regime

A

2x NRTI + 3rd agent (INSTI or NNRTI)

63
Q

List of NRTIs and their side effects

A

1st drugs:
TDF - GI symptoms, hypophosphatemia, osteoporosis, renal impairment
TAF - GI symptoms, hypophosphatemia, osteoporosis, renal impairment (all less than TDF)
Zidovudine - Anaemia, nausea, lipodystrophy, muscle pain
Abacavir - HLA-B5701 hypersensitivity, rash, nausea, flu-like symptoms.

2nd drugs:
Lamivudine - Peripheral neuropathy, Hair loss, Insomnia, Lactic acidosis.
Emtricitabine - GI symptoms, Hyperglycaemia, Hypertriglyceridemia, Itch, Skin darkening.

64
Q

List of NNRTIs and their side effects

A

Efavirenz - Rash, Hepatotoxicity, Insomnia, Depression
High drug interactions, CYP2B6 G516T genotype affects plasma concentrations.

Rilpiverine - Rash, Insomnia, headache, depression. Hypertriglyceridemia. Must be taken with food.

65
Q

List of INSTIs and their side effects

A

Dolutegravir - Rash, insomnia, depression, GI effects, weight gain.

Bictegravir -

66
Q

List of PIs and their side effects

A

Lopinavir - GI side effects, headache, pancreatitis, hypertriglyceridemia, hyperglycaemia, arrhythmia.

Atazanavir - GI side effects, headache, jaundice, renal stones, arrhythmia.

67
Q

Definition of virological failure of HIV treatment and management

A

viral load >1000 on 2 separate occasions with good adherence.

Make switch within class - Tenofovir/ABC to Zidovudine or other way
Continue Lamivudine or Emtricitabine (forces virus to maintain a certain resistance gene which has a big impact on fitness)
Change 3rd drug from NNRTI to dolutegravir or dolutegravir to PI.

(keep lamivudine/emtricitabine as it increases viral fitness cost)

68
Q

When does U=U not apply?

A

breast feeding

69
Q

What HIV regimen should be used in Hep B co-infection

A

Tenofovir regimen

70
Q

When should ART be delayed

A

CNS TB or cryptococcal meningitis

71
Q

Which ART drug class has the highest barrier to resistance

A

Protease inhibitors

72
Q

Important interactions with HIV drugs

A

Tacrolimus (CYP3A4 interactions)
Dolutegravir and metformin
Rilpiverine and PPI’s
Protease inhibitors and TB drugs

73
Q

What is the biggest cause of HIV drug resistance?

A

Non-compliance

74
Q

What happens to HIV virus once drugs that it has formed resistance to are removed

A

Reverts to wild-type virus for improved fitness - but archives resistance genes so will recur faster if re-exposed.

75
Q

HIV drugs with low RAM barriers and high RAM barriers (RAM = resistance associated mutation)

A

Low RAMs = Lamivudine, Emtricitabine, Efavirenz

High RAMs = PIs, Dolutegravir

76
Q

When should a HIV drug not be used based on population data?

A

If that population has >10% resistance to a specific drug

77
Q

When should first viral load be checked after commencement of ART?

A

6 months - this is how long ART takes to have full effect (may take up to 9 months.

78
Q

Methods of HIV resistance testing

A
  1. Genotype testing
    - pol gene
    - integrase gene (for INSTI)

Note - there are many quasi species that develop in an infection - Sanger sequencing can only detect a resistance mutation if it is present in >20% of quasi species.

2, Phenotype testing
- serial dilutions with ART

79
Q

Method of naming gene mutations

A

original peptide - position number - new peptide

80
Q

Why should ART be switched early if resistance is noted?

A

Because resistance genes accumulate over time - with higher accumulation you risk class resistance developing.

81
Q

How does HIV get to the lymph nodes + infect more CD4 cells.

A

picked up in periphery by dendritic cell (also has CCR5) and taken to LN.
Infected cells die via pyroptosis which attracts more inflammatory cells to the site.

82
Q

Why does immunity drop in HIV prior to CD4 count?

A

Due to early effect on mucosal CD4 cells not picked up on serum samples

83
Q

Difference in TB presentation in HIV+ patients

A

Less likely to form granulomas
More likely to see widespread necrosis

84
Q

What are the 2 types of IRIS

A

Unmasking - signs and symptoms of a disease develop after ART.
Paradoxical - OI is improving with treatment - ART is commenced and there is then a clinical deterioration in that disease.

85
Q

Management of newly diagnosed HIV without signs of TB

A

6 months isoniazid prophylaxis

86
Q

Best HIV drug (3rd) to use alongside TB drugs

A

Efavirenz (NNRTI)

87
Q

Prophylaxis for HIV based on CD4 counts

A

<250
Coccidioidomycosis (in endemic areas only) with fluconazole.

<200
- PJP with Bactrim

<150
- Histoplasmosis (in endemic areas only) with itraconazole

<100
Toxoplasmosis with Bactrim
Cryptococcus - screen and treat

<50
MAC - no treatment required if starting ART

88
Q

Pathogens causing CNS disease in HIV

A

TB
Toxoplasmosis
Cryptococcus
CMV
HSV

Malaria
JEV
JC virus (causes PML)
Chagas

89
Q

Causes of stroke in HIV

A

HIV associated vasculopathy
Vasculitis
aneurysm formation
accelerated atherosclerosis
opportunistic infections
neoplasia
endocarditis septic emboli
Mycotic anurysm
IHD
HIV associated cardiac dysfunction
coagulopathy/hyperviscosity

90
Q

HIV effect in paediatrics

A

impaired brain growth/atrophy
developmental decline
motor language tone dysfunction

91
Q

Stages of HAND (HIV associated neurocognitive disorder)

A

For hand must have deficits in 2 cognitive domains

  1. Asymptomatic neurocognitive impairment (ANI)
    - mild deficit in 2+ domains but no functional impairment
  2. Mild neurocognitive impairment (MNI)
    - mild/mod deficit in 2+ domains with mild functional impairment
  3. HIV associated dementia
    - severe deficit in 2+ domains with severe functional impairment
92
Q

HIV drug with best CNS penetration

A

Zidovudine
Dolutegravir
Nevirapine

93
Q

Management of babies born to HIV+ mothers

A

Need 6 months Isoniazid prophylaxis
Testing at 6 weeks, 9 months, 18 months.

If baby is positive:
Cotrimoxazole prophylaxis from 4 weeks - 18 months

ART:
Neonate - Zidovidine + Lamivudine + Raltegravir
Child - Abacavir + Lamivudine + Dolutegravir

94
Q

Should breastfeeding be recommended in HIV positive mothers

A

high income - no, bottle feed to reduce risk

LMIC - yes. as risk of water contamination is greater

95
Q

Causes of diarrhoea in HIV

A
  1. Seroconversion illness
  2. Infections
  3. ART side effects
  4. HIV enteropathy
96
Q

Treatment of infective diarrhoea in HIV

A

Depending on suspected cause:

  1. Bactrim
  2. Metronidazole
  3. Albendazole
97
Q

Treatment of HSV in pregnancy

A

Aciclovir 400mg

If acquired in 3rd trimester - suppress until delivery
If before the 3rd trimester - suppress from 32 weeks.

98
Q

Hepatitis A virus type and incubation

A

single strand RNA virus
2-4 weeks

99
Q

Hepatitis A transmission

A

faecal-oral route

100
Q

Highest risk areas for symptomatic Hep A

A

transition areas - in endemic areas infection occurs in children who have less severe symptoms.

101
Q

Hep A symptoms

A

hepatitis and jaundice

rare - myocarditis, GBS, AKI

102
Q

Hep A diagnostics

A

Serology
Hep A RNA detection in stool

103
Q

Prevention and management of Hep A

A

Self limiting –> supportive care only

Hep A vaccine - 2 doses 6 months apart - gives 10 years protection.
When to use:
- travel vaccine
- population vaccine in transition areas
- post exposure

104
Q

Hep B virus type

A

double stranded circular DNA virus

105
Q

How does Hep B enter cell

A

NTCP receptor

106
Q

How does Hep B increase risk of malignancy

A

integrates into p53 preferentially (a tumor suppressor gene) → increases malignancy risk.

107
Q

How does Hep B evade the immune system?

A

Overloads the immune system by releasing large volumes of non-functional virus (surface antigen only) → creates eventual down-regulation of the immune system.

108
Q

Hep B vaccination schedule

A

4 doses: 24hrs, 6,10,14 weeks

109
Q

Management of Hep B in pregnancy

A

If viral load >200,000 - give tenofovir
+ give baby Hep B immunoglobulin at birth

110
Q

What are the stages if Hep B infection, and in which stages should treatment be given?

A

Immune tolerance - dont treat
Immune clearance - treat - elevated LFTs
Immune control - dont treat
Immune escape - treat - elevated LFTs

111
Q

Hep B treatment

A

Tenofovir or entecavir

112
Q

Hep D virus type

A

small RNA virus
dependant on Hep B for replication

113
Q

Hep D investigations

A

ELISA
Hep D RNA PCR

114
Q

Hep D treatment

A

Interferon alpha

115
Q

Hep C virus type

A

single strand RNA virus

116
Q

Who to treat with Hep C

A

Everyone! It is curable. No persistance

117
Q

Hep C treatment

A

Need to use drug combinations for treatment due to high risk of resistance

NS3B, NS4A, NS5A, NS5B
(often sofosbuvir combinations)

118
Q

Issues with Hepatitis and HIV co-infection

A

HIV increases the rate of hepatitis hepatic fibrosis
Increased risk of ART causing hepatotoxicity
HIV leads to decreased CD4 cells in gut mucosa leading to increased bacterial translocation - increases work for liver and causes fibrosis.

119
Q

Hep E virus type

A

single strand RNA

120
Q

Hep E incubation transmission and clinical relevance

A

Incubation- 4 weeks, self limiting after 4 weeks
water outbreaks, faecal oral route.
90% of cases are asymptomatic
rare extra hepatic manifestations
increases risk of still births

121
Q

Hep E treatment

A

Ribavirin
+/- Interferon alpha

122
Q

mechanism of Covid-19 lung disease

A

In Covid there is diffuse alveolar damage with severe endothelial injury and microthrombi
= immune mediated thrombotic microangiopathy

123
Q

Covid-19 management

A

B - breathing - give O2 if sats low
A - antivirals (mild - paxlovid, molnuperavir mod/sev- remdesivir)
S - steroids
I - IL6 - Tocilizumab
C - clotting - clexane

124
Q

Monkey pox virus type and clades

A

Variola virus

Clade 1 (Africa) and Clade 2 (USA)
Clade 2b is current outbreak

125
Q

Monkeypox transmission

A

direct, sexual, respiratory (close range), transplacental, fomites

126
Q

Symptoms of Monkey pox

A

Papules or macular rash
Starts on trunk or point of inoculation - includes palms and soles
Mucosal lesions
Clade 1 (Africa) - all lesions at same stage, many lesions
Clade 2 (USA)- lesions at different stages, fewer lesions
Clade 2b - polymorphic rash, few lesions, sometimes anogenital only, lymphadenopathy in 50%

127
Q

Reservoir of infection in Monkey pox

A

Likely to be rodents
(humans and primates are hosts)

DTMH (9 decks)

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