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ACEM Primary Written > Infectious diseases: Pathology - Viral infections > Flashcards

Infectious diseases: Pathology - Viral infections Flashcards

1
Q

What type of virus is rhinovirus?

A

Unencapsulated icosahedral ssRNA

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2
Q

How does rhinovirus induce mucus hypersecretion?

A

Binds to ICAM-1 on epithelial cells of upper respiratory tract and induces mucus secretion via bradykinin release

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3
Q

Describe the structure of influenza and how this relates to its type and subtype

A

8 helices of ssRNA
Bound by nucleoprotein which determines the type of virus (A, B, C)
Enclosed by lipid bilayer containing haemagglutinin (HA) and neuraminidase (NA; determines viral subtype H1 to H3 and N1 or N2)

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4
Q

What kind of protection do host antibodies to influenza haemagglutinin and neuraminidase confer?

A

Antibodies to HA prevent future infection
Antibodies to NA ameliorate future infection

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5
Q

Describe the morphological features of influenza infection

A

Produces mucosal hyperaemia and swelling with predominantly lymphomonocytic and plasmacytic infiltrate, and mucus hypersecretion

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6
Q

What is the difference between type A and type B/C influenza in terms of their virulence?

A

Type A is a major cause of pandemics and epidemics, and undergoes antigenic drift and shift
Type B/C mostly infects children, who develop antibodies that effectively prevent re-infection (because these viral types are not subject to antigenic drift or shift)

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7
Q

Explain the difference between antigenic shift and drift

A

Antigenic drift: mutation of surface HA and NA -> responsible for regional epidemics
Antigenic shift: HA and NA replaced through recombination of RNA segments with animal virus -> responsible for pandemics

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8
Q

What increases risk of bacterial superinfection in influenza? What organisms are typically implicated?

A

In laryngotracheobronchitis and bronchiolitis, mucociliary function is impaired which increases risk of bacterial superinfection (e.g. pneumococcus, Staphylococcus, Haemophilus)

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9
Q

What are the three mechanisms of immune clearance of influenza?

A
  1. Cytotoxic T cells: kill virus-infected cells
  2. Intracellular anti-influenza protein Mx1: induced in macrophages by stimulation with IFN-alpha and IFN-beta
  3. Acquired immunity to HA and NA (but not long-lived in influenza A due to antigenic drift/shift)
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10
Q

What type of virus are herpesviruses?

A

Large encapsulated dsDNA

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11
Q

What is the typical pattern of infection of herpesviruses?

A

Cause acute infection followed by latent infection with periodic reactivation

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12
Q

How many herpesviruses are there? How are they classified?

A

8: 3x alpha-group, 3x beta-group, 2x gamma-group

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13
Q

Three alpha-group herpesviruses and the infective syndromes caused by each

A
  1. HSV-1: cold sores, herpetic whitlow
  2. HSV-2: genital sores
  3. VZV: chickenpox, shingles
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14
Q

Three beta-group herpesviruses and the infective syndromes caused by each

A
  1. CMV: asymptomatic (except in utero or in immunosuppression)
  2. HHV-6: roseola infantum
  3. HHV-7
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15
Q

Two gamma-group herpesviruses and the infective syndromes caused by each

A
  1. EBV: infectious mononucleosis
  2. HHV-8: Kaposi sarcoma
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16
Q

What cells are infected by alpha-group herpesviruses, and in which cells do they become latent?

A

Infect epithelial cells
Produce latent infection in neurons (typically dorsal root sensory ganglia)

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17
Q

What cells are infected by beta-group herpesviruses?

A

Infect variety of cell types

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18
Q

In which cells do gamma-group herpesviruses become latent?

A

Produce latent infection mainly in lymphoid tissue

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19
Q

Five infective syndromes caused by HSV-1

A
  1. Skin/mucosal ulceration (cold sores)
  2. Herpetic whitlow
  3. Corneal epithelial damage and blindness
  4. Encephalitis
  5. Disseminated in immunodeficiency
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20
Q

Two virulence factors of HSV-1

A
  1. Inhibit MHC class I pathways (evade cytotoxic T cells)
  2. Produce Fc receptors to inhibit complement and evade humoral responses
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21
Q

Six infective syndromes caused by VZV

A
  1. Chickenpox
  2. Shingles
  3. Interstitial pneumonia
  4. Encephalitis
  5. Transverse myelitis
  6. Necrotising visceral lesions
22
Q

Where does VZV become latent?

A

Infects neurons and satellite cells around dorsal root ganglia (most commonly in trigeminal ganglia)

23
Q

How can VZV cause facial paralysis?

A

Via infection of geniculate nucleus (Ramsay Hunt syndrome)

24
Q

Where does CMV become latent?

A

In monocytes

25
Q

Describe the morphological features of disseminated CMV infection

A
  1. Focal necrosis with minimal inflammation in virtually any organ
  2. CMV-infected cells exhibit gigantism with large inclusion surrounded by clear halo (“owl’s eye”)
26
Q

How is CMV transmission dependent on age group?

A
  1. Foetus: transplacental
  2. Neonatal: via birth canal or breastfeeding
  3. Preschool aged children: saliva
  4. Adults: venereal (most common), respiratory, faecal-oral
  5. Iatrogenic: organ transplant, blood transfusion
27
Q

How does CMV infection present?

A

In healthy hosts: asymptomatic
In utero: causes cytomegalic inclusion disease (similar to hydrops foetalis)
In immunocompromise: disseminated infection (pneumonitis, oesophagitis, colitis, hepatitis, renal tubulitis, chorioamnionitis, meningoencephalitis)

28
Q

Seven infective syndromes seen in disseminated CMV infection

A
  1. Pneumonitis
  2. Oesophagitis
  3. Colitis
  4. Hepatitis
  5. Renal tubulitis
  6. Chorioamnionitis
  7. Meningoencephalitis
29
Q

What is the classic genetic derangement seen in Burkitt lymphoma?

A

8:14 translocation of c-myc oncogene

30
Q

Burkitt lymphoma is linked to which virus?

A

EBV

31
Q

What are five features of clinical presentation of infectious mononucleosis?

A
  1. Fever
  2. Generalised lymphadenopathy
  3. Splenomegaly
  4. Sore throat
  5. Appearance of atypical activated T cells (mononucleosis cells)
32
Q

Three possible complications of infectious mononucleosis

A
  1. Hepatitis
  2. Meningoencephalitis
  3. Pneumonitis
33
Q

Three diagnostic criteria for infectious mononucleosis (in order of greatest to least specificity)

A
  1. Lymphocytosis with mononucleosis cells
  2. Positive monospot
  3. Specific EBV antibodies
34
Q

Where does EBV become latent and how?

A

In B cells, due to EBV proteins EBNA and LMP-1

35
Q

What type of virus is measles?

A

ssRNA paramyxovirus

36
Q

Five examples of paramyxoviruses

A
  1. Measles
  2. Mumps
  3. RSV
  4. Parainfluenza
  5. Human metapneumovirus
37
Q

Describe the pathogenesis of measles, including the seven infective syndromes/symptoms it produces

A

Replicates in many cells including lymphoid tissue
Produces viraemia, resulting in dissemination to many tissues
Causes croup, pneumonia, diarrhoea, keratitis, encephalitis, haemorrhagic rash, transient profound immunosuppression

38
Q

Describe the pathogenesis of the measles rash

A

Children develop T-cell mediated immunity -> hypersensitivity to viral antigens produces rash

39
Q

Two rare late complications of measles

A
  1. Subacute sclerosing panencephalitis
  2. Measles inclusion-body encephalitis
40
Q

What are Koplik spots and for which infection are they pathognomonic?

A

Ulcerated mucosal lesions near opening of Stensen ducts, pathognomonic of measles

41
Q

What type of virus is measles?

A

ssRNA paramyxovirus

42
Q

What is the function of the two surface glycoproteins of the mumps virus?

A
  1. HA/NA activity
  2. Cytolytic activity
43
Q

Describe the pathogenesis of mumps virus, including complications

A

Infects salivary glands (including parotid) and may spread to other sites including CNS, testis, ovaries and pancreatitis
Can cause aseptic meningitis, and sterility due to scarring and atrophy post mumps orchitis

44
Q

What type of virus is polio?

A

Spherical nonencapsulated ssRNA enterovirus

45
Q

What are the two types of polio vaccine and how many strains are included in each?

A
  1. Salk (killed) vaccine
  2. Sabin (oral attenuated) vaccine

Both contain three major strains

46
Q

What are three reasons polio has been able to be nearly eliminated through vaccination?

A
  1. Only infects humans (no other reservoirs)
  2. Only briefly shed
  3. Does not undergo antigenic variation
47
Q

How is poliovirus transmitted?

A

Faecal-oral route

48
Q

How does poliovirus present clinically in most cases?

A

Transient viraemia and fever (or asymptomatic)

49
Q

What host surface marker does poliovirus bind to?

A

CD155

50
Q

How does poliovirus cause paralysis and how often does this happen?

A

Invades CNS in 1 in 100 infected
Replicates in motor neurons of spinal cord or brainstem motor neurons (causes muscular or respiratory muscular paralysis respectively)

51
Q

Six infectious syndromes caused by various enteroviruses

A
  1. Childhood diarrhoea
  2. Conjunctivitis: enterovirus
  3. Rashes: coxsackievirus A
  4. Viral meningitis: coxsackievirus, echovirus, non-paralytic poliovirus
  5. Myopericarditis: coxsackievirus B
  6. Polio: poliovirus

ACEM Primary Written (150 decks)

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