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I&I WC1 > Emerging infectious diseases - Pathogens > Flashcards

Emerging infectious diseases - Pathogens Flashcards

1
Q

To which group of viruses does Mpox belong?

A

Poxviridae

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2
Q

Which groups of animals can be infected by poxviridae?

A
  1. Vertebrae
  2. Insects
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3
Q

Which two obligate human pathogens can be found in the family of poxviridae?

A
  1. Variola virus (smallpox)
  2. Molluscum contagiosum virus
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4
Q

What are common zoonotic pathogens of the poxviridae? (3)

A
  1. Cowpox
  2. Vaccinia virus
  3. Monkeypox
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5
Q

What are the genomic characteristics of poxviridae?

A

Large and complex linear dsDNA viruses

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6
Q

What is the prototypic shape of poxviridae?

A

Brick-shaped tagument surrounded by an envelope

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7
Q

Where in the cell do poxviridae replicate?

A

Cytoplasm

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8
Q

Which stages of gene transcription are there during poxvirus replication?

A
  1. Early gene transcription
  2. Intermediate gene transcription
  3. Late gene transcription
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9
Q

During particle production of poxviridae, different types of particles are produced. Which? (3)

A
  1. Intracellular mature viruses particles (IMV)
  2. Intracellular enveloped particles (IEV)
  3. Extracellular enveloped particles (EEV)
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10
Q

Immature virions of poxviridae are much [smaller/larger] than mature virus particles

A

Immature virions are larger than the mature particles

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11
Q

When was smallpox declared eradicated by WHO? When did smallpox vaccination stop?

A

Eradication: 1980
Vaccination stopped in 1985

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12
Q

When was Mpox first identified?

A

1958

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13
Q

What is the animal reservoir of Mpox?

A

Unknown, detected in various species

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14
Q

When was the large Mpox outbreak?

A

2022

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15
Q

Were there cases of Mpox in humans before 2022?

A

Yes, but only sporadic

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16
Q

How many clades of Mpox are there? Where are these clades indigenous?

A

Clade I: Congo
Clade II: West-Africa

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17
Q

Which of the Mpox clades is more pathogenic?

A

Clade I

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18
Q

Which clade of Mpox was responsible for the 2022 outbreak?

A

II2b

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19
Q

Mpox is genetically [unstable/stable]. Why?

A

Stable, due to Pol-proofreading

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20
Q

What is the most common cause of death in humans that have been infected by Mpox?

A

Brainstem encephalitis

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21
Q

How is Mpox transmitted from animal to human? (3)

A
  1. Hunting/consumption of infected animals
  2. Bite/scratch from infected animals
  3. Contact with infected secretions/lesions
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22
Q

How is Mpox transmitted from human to human? (3)

A
  1. Respiratory droplets in close contact
  2. Direct contact with lesions
  3. Contaminated objects
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23
Q

Why is Mpox less transmissible than smallpox?

A

Smallpox was very transmissible via aerosols, Mpox less so

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24
Q

What is the incubation period of Mpox?

A

7-21 days

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25
Q

Which phases can be distinguished after Mpox infection?

A
  1. Incubation period
  2. Prodormal phase = fever-like symptoms
  3. Rash phase
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26
Q

How long does the prodromal phase of Mpox last? What are its symptoms? (8)

A

1-4 days, with flu-like symptoms
1. Headache
2. Myalgia
3. Fever
4. Chills
5. Sore throat
6. Malaise
7. Fatigue
8. Lymphadenopathy

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27
Q

How long does the rash phase of Mpox last? What are its symptoms?

A

2-4 weeks, during which a skin rash forms that develops into papules and vesicles

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28
Q

Mpox causes a centrifugal rash. What does this mean?

A

Develops in the extremities, then migrates towards the rump

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29
Q

How can the migration pattern of Mpox be used to distinguish it from chickenpox?

A

Mpox has a centrifugal pattern (extremities to rump), whereas chickenpox is the other way around (rump to extremities)

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30
Q

True or false: chickenpox is a virus belonging to the poxviridae

A

False; chickenpox is not a poxvirus!

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31
Q

What are the proposed pathogenic phases in Mpox? (3)

A
  1. Virus entry, starts replication in draining lymph nodes and causes primary viraemia
  2. Primary viraemia allows more lymphoid organs to be infected -> massive viral replication -> secondary viraemia
  3. Infection of tertiary organs/skin -> clinical manifestations
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32
Q

Why was the clinical presentation of the 2022 Mpox virus atypical? (2)

A
  1. Presented as solitary genital lesions, causing delayed diagnosis due to a differential diagnosis of many STDs
  2. Lesions involving palms & soles
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33
Q

Why does the long incubation/asymptomatic phase of Mpox increase transmission?

A

Individuals can transmit a lot of virus in this period, usually via sexual contacts

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34
Q

What are Mpox risk factors in endemic areas? (4)

A
  1. Living in forested areas
  2. Disease burden in children & females
  3. Human-to-human transmission through close contact
  4. Nosocomial infection of females
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35
Q

What was the major risk factor in the 2022 Mpox outbreak?

A

Unprotected sexual contact, mainly among MSM

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36
Q

What are available preventions & treatments for Mpox? (4)

A
  1. Supportive care during infection
  2. Vaccinia immunoglobulin (crossreactive)
  3. Vaccines (crossreactive from smallpox)
  4. Antivirals effective against orthopoxviruses
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37
Q

In which group was vaccinia immunoglobulin used for treatment of Mpox?

A

Immunocompromised individuals, unable to generate a humoral immune response

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38
Q

How many generations of smallpox vaccines are there?

A

4 (0, 1, 2, 3)

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39
Q

What is considered to be the 0th generation of smallpox vaccines?

A

Variolation

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40
Q

What is variolation?

A

Transfer of a small amount of smallpox/cowpox virus into uninfected individuals

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41
Q

What is the 1st generation of smallpox vaccines?

A

Unattenuated vaccinia virus grown on the skin of live animals, then freeze-dried

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42
Q

What is the 2nd generation of smallpox vacines?

A

Vaccinia virus purified from cell lines

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43
Q

What is the 3rd generation of smallpox vaccines?

A

Modified vaccinia virus, grown in primary chicken fibroblasts

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44
Q

Why are vaccines against smallpox also protective for Mpox?

A

Crossreactivity, with similar antibodies against the two viruses

45
Q

Which antivirals against smallpox are available? What is their target? (3)

A
  1. Tecovirimat: viral protein p37
  2. Cidofovir: DNA polymerase
  3. Brincidofovir: prodrug of cidofovir
46
Q

What is the disadvantage of cidofovir?

A

Nephrotoxicity

47
Q

How can antivirals against smallpox be developed, despite the virus being eradicated? (no human testing possible)

A

FDA animal rule: allowing for the approval of drugs/biologial products based on animal studies only when human efficacy studies are not ethical/feasible

48
Q

Why do compounds approved under the FDA animal rule still need to be tested in humans?

A

To establish their pharmacokinetic properties

49
Q

To which family and genus does poliovirus belong?

A

Family: picornavirales
Genus: enterovirus

50
Q

What is the genetic structure of poliovirus?

A

RNA+ virus

51
Q

How many species of enterovirus are there?

A

~350

52
Q

Which enteroviruses are human pathogens? (4)

A

A, B, C, D

53
Q

Which groups of clinical manifestations of poliovirus can be distinguished? (5)

A
  1. Asymptomatic
  2. Non-paralytic polio
  3. Non-paralytic CNS disease
  4. Paralytic poliomyelitis
  5. Bulbar paralytic poliomyelitis
54
Q

What are symptoms of non-paralytic polio? (7)

A
  1. Fever
  2. Sore throat
  3. Headache
  4. Vomiting
  5. Fatigue
  6. Pain/stiffness in back, neck, arms or legs
  7. Muscle weakness or tenderness
55
Q

What is the most frequent non-paralytic CNS disease caused by poliovirus?

A

Meningitis

56
Q

What symptomatology does paralytic poliomyelitis cause?

A

Acute flaccid paralysis

57
Q

What is bulbar paralytic poliomyelitis?

A

Acute flaccid paralysis with involvement of the brain stem

58
Q

There [is/is not] a treatment for polio available

A

No treatment available; only supportive therapy

59
Q

What increases the chance of severe symptomatology in polio infection?

A

Higher age

60
Q

What are the clinical outcomes after paralytic poliomyelitis (%)?

A

~10% = complete recovery
~80% = permanent paralysis
~10% = fatal (higher in case of bulbar involvement)

61
Q

What is post-polio syndrome?

A

A syndrome that occurs 15-60 years after initial polio infection, in 20-75% of polio survivors

62
Q

What are the sypmtoms of post-polio syndrome? (5)

A
  1. Muscle atrophy and weakness
  2. Pain
  3. New disabilities
  4. Fatigue
  5. Sleeping problems
63
Q

Which two vaccines for polio are available?

A
  1. Salk-inactivated polio vaccine
  2. Sabin live-attenuated vaccine
64
Q

What are the advantages of the Salk polio vaccine? (2)

A
  1. Almost 100% seroconversion, prevents severe disease
  2. No severe side effects
65
Q

What are the disadvantages of the Salk polio vaccine? (4)

A
  1. Requires a cold chain
  2. Expensive
  3. Needles required
  4. Low intestinal immunity -> only reduced viral shedding
66
Q

What are the advantages of the Sabin polio vaccine? (5)

A
  1. Cheap
  2. Provides intestinal immunity
  3. Passive immmunisation of unvaccinated persons by shedding vaccine virus
  4. No cold chain required
  5. Oral drops -> easy to administer
67
Q

What are the disadvantages of the Sabin polio vaccine? (3)

A
  1. Can acquire virulence mutation
  2. Can cause vaccine-associated paralytic poliomyelitis (VDVP)
  3. Can lead to circulation of VDVP virus
68
Q

What is the global polio eradication initiative?

A

An effort to complete the eradication and containment of all wildtype and vaccine-related polioviruses

69
Q

How much has the global incidence of polio declined since the global polio eradication initiative started?

A

99%

70
Q

Which types of polio have been eradicated?

A

WPV2, WPV3

71
Q

Where does the WPV1 polio type still circulate?

A

Pakistan & Afghanistan

72
Q

Why are there still outbreaks of poliovirus from time to time outside of areas in which the wildtype virus circulates?

A

Vaccine-associated paralytic poliomyelitis due to use of the Sabin vaccine

73
Q

Why has the triple oral polio vaccine been changed into a bivalent vaccine?

A

WVP2 has been eradicated since 2015 -> no longer a need to vaccinate

74
Q

Why is removal of WVP2 from the polio vaccine advantageous?

A

WVP2 caused the majority of VDVP-cases

75
Q

Why does eradication of poliovirus not mean eradication of all acute flaccid paralysis?

A

There are more viruses/pathogens that can cause acute flaccid paralysis, such as neutrotropic enteroviruses

76
Q

How does enterovirus D68 present itself?

A

Severe respiratory illness, followed by acute flaccid paralysis 4-5 days after respiratory disease in some patients

77
Q

How long after respiratory disease does enterovirus D68 cause acute flaccid paralysis?

A

4-5 days

78
Q

When is the number of enterovirus D68-caused acute flaccid paralysis highest?

A

Along with the seasonal pattern of enterovirus D68, on a biannual cycle

79
Q

What are the main complications of enterovirus D68 infection? (2)

A
  1. Predominantly severe respiratory disease
  2. CNS diseases such as acute flaccid paralysis, cranial nerve dysfunction & encephalomyelitis
80
Q

In which group does enterovirus D68 (mainly) cause severe respiratory symptoms? Which group is even more severely affected?

A

Children, with asthma being an exacerbating factor

81
Q

In which respect does the replication of enterovirus D68 differ from other enteroviruses?

A

It replicates in the respiratory tract -> behaves more like a rhinovirus

82
Q

What are characteristics of enterovirus D68 that do not allow it to replicate in the intestine? (2)

A
  1. Acid sensitivity
  2. Replication optimal at 33 °C (other enteroviruses @37 °C)
83
Q

Which part of the respiratory tract is infected by mild infections of enterovirus D68? Which cell types?

A

URT -> infection of respiratory epithelial cells

84
Q

When does enterovirus D68 cause severe respiratory symptoms?

A

When it infects the LRT, causing pneumonia and severe asthma exacerbations

85
Q

How does enterovirus D68 disemminate systemically?

A

Infection of lymphoid tissues, after which viraemia occurs

86
Q

How does enterovirus D68 enter the CNS to cause pathology?

A

Mechanism largely unknown

86
Q

What are CNS complications of enterovirus D68 infection? (5)

A
  1. Acute flaccid myelitis = most common
  2. Cranial nerve dysfunction
  3. Encephalitis
  4. Aseptic meningitis
  5. Meningo-encephalitis
87
Q

What are the proposed routes of CNS infection by enterovirus D68? (4)

A
  1. Cranial nerves
  2. Viraemia
  3. Infection of endothelium of blood-brain barrier
  4. Trojan horse -> infection of leukocytes that travel into the CNS
88
Q

How does poliovirus enter the CNS?

A

Infection of skeletal muscles, after which the virus can infect motor neurons through the motor end plate

89
Q

How can acute flaccid myelitis due to enterovirus D68 infection be prevented?

A

Antibodies against EV-D68 -> vaccination or monoclonals

90
Q

When was MERS-coronavirus identified?

A

2012

91
Q

Why does the incidence of MERS follow a characteristic peak pattern?

A

Every peak is due to a seperate zoonotic event, after which the infection dies down

92
Q

Why are there no vaccines needed to stop MERS outbreaks?

A

Quarantine & isolation very effective

93
Q

What are MERS-vaccines currently used for?

A

Vaccination of dromedaries to prevent zoonosis

94
Q

True or false: there is no human MERS-vaccine available

A

False; a vaccine has been available since 2018

95
Q

Which aspects are needed for MERS outbreak control? (3)

A
  1. Identification & characterisation of pathogen
  2. Development of diagnostics
  3. Identify & isolate infected individuals & place contacts in quarantine
96
Q

From which viruses does MERS originate?

A

Bat CoVs

97
Q

What is the animal reservoir of MERS coronaviruses?

A

Dromedary camels

98
Q

What is the entry receptor for MERS?

A

DPP4

99
Q

Where is the DPP4 receptor (used by MERS to enter cells) located in dromedary camels vs. in humans?

A

Dromedary camels: URT
Humans: LRT -> causes pneumonia

100
Q

When was SARS-CoV first detected?

A

2003

101
Q

How many days post-infection do respiratory symptoms start to deteroriate in SARS?

A

~9 days

102
Q

What happens to the viral load as SARS respiratory symptoms worsen?

A

Viral load decreases

103
Q

What causes fatalities of SARS-CoV infections?

A

ARDS

104
Q

In how many % of SARS-CoV infected individuals does ARDS occur?

A

15%

105
Q

How is SARS-CoV transmitted?

A

Direct or indirect contact
Possibly droplets

106
Q

Which receptor do SARS-viruses use to enter cells?

A

ACE2

107
Q

Why were no vaccines needed to contain SARS? (2)

A
  1. Virus-excretion in SARS-patients peaked after LRT symptoms -> patients easy to recognize, diagnose & quarantine
  2. Few asymptomatic cases
108
Q

Why did SARS-CoV-2 infect many more individuals than the original SARS-virus? (2)

A
  1. Virus release peaks before symptoms
  2. Many asymptomatic individuals

I&I WC1 (20 decks)

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