Viral infections Flashcards

1
Q

How do the levels of IgG and IgM differ in primary and secondary response to viral infection?

A

=> Primary exposure
IgM rises before IgG

=> Secondary exposure

  • Both rise at same time
  • Greater rise in IgG compared to IgM
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2
Q

What are the general steps of viral replication/infection?

A
  1. Virus binds to receptor on host cell
  2. Endocytosis
  3. Un-coating
  4. Reverse transcriptase action to form viral DNA
  5. Viral DNA enters nucleus
  6. Integration into host DNA
  7. Transcription + Translocation
  8. Viral proteins assembled
  9. Released
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3
Q

What are the principles of anti-viral therapy?

A
  • Viral replication is recognised by Pattern Recognition Receptors (PRRs) on the surface of immune cells
  • These receptors trigger the innate immune response to produce restriction factors such as Type 1 Interferons

=> Antiviral therapy either stimulates these PRRs or boosts the immune response through exogenous Type 1 Interferons

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4
Q

What are the 2 different subtypes of the Herpes Simplex Virus?

A

HSV 1 => oral lesions
HSV 2 => genital herpes

There may be considerable overlap

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5
Q

What is Herpes Labialis?

A
  • Cold sores which tend to be caused by HSV-1
  • Spread via direct contact with the lesion
  • Primary infection is frequently asymptomatic
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6
Q

What is the clinical presentation of Herpes Labialis?

A
  • Pharyngitis
  • Fever
  • Mouth ulceration
  • Lymphadenoapthy
  • Localised painful blisters that resolve in 5-7 days
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7
Q

What is the management of Herpes Labialis?

A

Topical Aciclovir

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8
Q

What is Herpes Genitalis?

A
  • Genital herpes caused by HSV-2
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9
Q

What is the clinical presentation of Herpes Genitalis?

A
  • Painful genital ulceration
  • Fever
  • Lymphadenoapthy
  • Urinary retention
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10
Q

What is the management of Herpes genitalis?

A

PO Aciclovir. Some people with frequent exacerbations may benefit from long term Aciclovir

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11
Q

What is Herpes Simplex Encephalitis?

A
  • Severe life threatening infection of the CNS
  • Typically affects the temporal and frontal lobes of the brain
  • Virus spreads in the body via neurones
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12
Q

What is the clinical presentation of Herpes Simplex Encephalitis?

A
  • Fever, headache, psychiatric symptoms, seizures, vomiting

- Aphasia

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13
Q

What is the pathophysiology of Herpes Simplex Encephalitis?

A
  • HSV-1

- Typically affects medial temporal or inferior frontal lobes

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14
Q

What are the investigations in suspected Herpes Simplex Encephalitis?

A

=> CSF

  • Lymphocytosis
  • Elevated proteins

=> Imaging

  • CT - typically performed first to exclude raised ICP (contraindicates CSF analysis)
  • MRI is better

=> EEG

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15
Q

What is the management of Herpes Simplex Encephalitis?

A

IV Aciclovir

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16
Q

What is chicken pox (varicella) and its investigations?

A
  • Caused by primary infection with Varicella Zoster Virus
  • Spread via respiratory route
  • Latent reactivation results in shingles
  • Infective 4 days before rash till 5 days after rash onset when all lesions crusted over

=> Diagnosis:

  • Clinical diagnosis made
  • If immunocompromised: viral PCR, culture, immunofluorescence
17
Q

What is the management of Varicella infection?

A

PO Aciclovir

This medication is most effective in this order:

  • HSV 1
  • HSV 2
  • VZV

Aciclovir resistant herpes is treated with Foscarnet or Cidofovir

18
Q

What categories of patients should always be treated with antiviral therapy in cases of infection?

A
  • Immunocompromised
  • Pneumonitis
  • Encephalitis
  • Eye disease
19
Q

What is Cytomegalovirus (CMV) and its diagnosis?

A

One of the herpes viruses
- Usually affects foetuses or the immunocompromised

=> Diagnosis:
- Quantitative nucleic acid amplification testing

20
Q

What are the complications of CMV in the immuncompromised?

A
  • CMV mononucleosis
  • CMV encephalitis
  • CMV colitis
  • CMV retinitis
  • CMV pneumonitis
21
Q

What clinical syndromes come und the Human Herpesvirus?

A

=> HSV:

  • Herpes Labialis (HSV-1)
  • Herpes Genitalis (HSV-2)
  • Herpes Encephalitis (HSV-1)
  • Herpes Gingivostomatitis (primary HSV-1 cold sore infection)
  • Herpes Keratoconjunctivitis
  • Herpetic Whitlow

=> Others

  • Varicella Zoster Virus (HHV 3)
  • EBV (HHV 4)
  • CMV (HHV 5)
  • Human Herpesvirus 6
  • Human Herpesvirus 8
22
Q

What is the Epstein Barr Virus (EBV) and its diagnosis?

A
  • Also known as HHV-4
  • Most common cause of infectious mononucleosis (grandular fever)
  • Salivary transmission

=> Diagnosis:

  • Blood film showing lymphocytosis
  • Heterophile antibody tests - 1st line
  • IgM serology
  • Reverse transcriptase viral PCR

=> Hetrophile Antibody test (Monospot) and FBC should be done in 2 weeks to confirm the diagnosis of grandular fever)

23
Q

What are the clinical features of EBV infection?

A

=> Classic triad: sore throat, fever, lymphadenoapthy

  • Splenomegaly
  • Headache
  • Malaise
  • Macular rash (can develop in people who take amoxicilin) and Palatal Petechiae
24
Q

What is the management of CMV and EBV?

A

For EBV, rest, avoid alcohol and simple analgesia for any aches and pains. Avoid all contact sports for 8 weeks to reduce risk of splenic rupture

  • Aciclovir not effective
  • First line treatment - Ganciclovir and Vanganclicovir
  • Second like treatment - Forcarnet or Cidofovir
25
Q

What 2 malignancies is HHV-8 associated with?

A
  • Karposi sarcoma

- Multi-centric Castleman’s disease

26
Q

What is the management of HHV-8 infection?

A
  • Ganciclovir
  • Foscarnet
  • Cidofovir
27
Q

How are the Herpes Simplex Viruses diagnosed?

A
  • Clinical diagnosis

- Confirmation via CSF, viral swab, vesicle scraping

28
Q

What is the Parvovirus B19?

A
  • DNA virus
  • Causes Erythema Infectiosum

=> Clinical presentation:

  • Mild fever
  • Slapped cheek syndrome
  • Can infect unborn fetus in first 20 weeks of pregnancy so maternal IgG and IgM will need to be checked
  • Spread via respiratory route and is not infectious from the onset of the rash, so school exclusion not necessary

=> Other presentations:

  • Aplastic crisis
  • Pancytopenia in immunosuppressed patients