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CP reviewer 1 > Viral and Prion Pathogens > Flashcards

Viral and Prion Pathogens Flashcards

1
Q

What do viruses require to survive?

A

Need a host cell to survive

‘Steal’ energy, metabolic intermediates and enzymes from host cells to replicate

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2
Q

What does a virus consist of?

A
  1. Genome (RNA or DNA)
  2. Capsid (protein coat)
  3. Envelope (lipid bilayer)

Some viruses also carry their own enzymes

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3
Q

Do all viruses have an envelope?

A

No

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4
Q

What is adsorption?

A

Interaction between host receptor molecule and virus ligand

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5
Q

What occurs after adsorption?

A

Penetration and uncoating of virus

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6
Q

What does uncoating of virus involve?

A

Nucleic acid is liberated (from phagosome and/or capsid)

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7
Q

What are the 2 ways in which viruses are classified?

A
  1. By the genetic material inside them

2. Do they have an envelope

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8
Q

How are viruses classified by the genetic material inside them?

A
  • DNA or RNA

- Single or double stranded

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9
Q

If the genetic material inside viruses is single stranded, how is this further classified?

A

If single, positive vs negative sense

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10
Q

What is the classification of Herpes viruses?

A

Double-stranded enveloped DNA viruses

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11
Q

How many types of Herpes viruses are known to infect humans?

A

9

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12
Q

Herpes viruses are characterised by their ability to…?

A

Establish latency in the body and REACTIVATE

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13
Q

What are the 9 types of human herpes viruses?

A
  1. Herpes simplex 1
  2. Herpes simplex 2
  3. Varicella zoster
  4. Epstein Barr
  5. Cytomegalovirus
  6. Human herpes virus 6A
  7. Human herpes virus 6B
  8. Human herpes virus 7
  9. Human herpes virus 8
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14
Q

Disease name for herpes simplex 1 (HSV-1)?

A

Cold sores

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15
Q

What % of the population will experience HSV-1 in their lives?

A

80%

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16
Q

How is HSV-1 transmitted?

A

Mainly transmitted by oral-to-oral contact via direct contact with HSV-1 lesions in sores/saliva/surfaces around mouth

HSV-1 can also be transmitted to the genital area through oral-genital contact to cause genital herpes

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17
Q

Where does HSV-1 establish latency?

A

In sensory nerve ganglion of trigeminal nerve of infected individuals

Has periodic reactivations

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18
Q

What is the trigeminal nerve?

A

The 5th cranial nerve

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19
Q

What are the 2 syndromes caused by HSV-1?

A
  1. Vesicles/ulcers to skin or mucous membranes (typically mouth, sometimes genitals)
  2. Encephalitis
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20
Q

What is encephalitis?

A

Inflammation of the brain - often severe or fatal

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21
Q

What is the commonest cause of viral encephalitis worldwide?

A

HSV-1

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22
Q

Typical disease name for herpes simplex 2 (HSV-2)?

A

Genital herpes (‘herpes’)

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23
Q

How is HSV-2 transmitted?

A

Direct contact with vesicle fluid from lesions (active vesicle)

Almost exclusively sexually transmitted

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24
Q

Can the herpes viruses be cured?

A

No - only managed

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25
Q

Where does HSV-2 establish latency?

A

Latency in sensory nerve ganglia of the SACRAL ganglia

Therefore, when periodic reactivations occur, they occur in the genital area

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26
Q

Location of latency of HSV-1 vs HSV-2?

A

HSV-1: trigeminal nerve sensory ganglia

HSV-2: sacral nerve sensory ganglia

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27
Q

What syndromes are caused by HSV-2?

A
  1. Vesicles/ulcers to skin or mucous membranes (typically genitals/buttocks)
  2. Meningitis
  3. Neonatal herpes (life threatening)
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28
Q

What does meningitis from HSV-2 typically follow?

A

An outbreak of genital lesions

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29
Q

Define ‘viraemia’?

A

viruses present in the bloodstream

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30
Q

How are neonates exposed to HSV-2?

A

Vertical transmission from mother’s genital tract after vaginal birth

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31
Q

Typical disease names for Varicella zoster virus?

A

Primary infection: ‘chicken pox’

Reactivation: ‘herpes zoster’ or ‘shingles’

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32
Q

What is the mode of transmission for Varicella zoster?

A

Respiratory droplets from person with chicken pox (highly infectious)

or

Direct contact with vesicle fluid from person with chicken pox or shingles

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33
Q

Where is latency for Varicella zoster established?

A

Dorsal root ganglia of whole CNS (i.e. shingles can reactivate down any of the dermatomes)

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34
Q

What are the 2 important syndromes caused by Varicella zoster?

A
  1. Chicken pox

2. Shingles

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35
Q

Typical disease names for Epstein Barr virus?

A

Glandular fever / infectious mononucleosis

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36
Q

What % of UK are infected with Epstein Barr?

A

90% in the UK are infected by age 25

Of these, 50% infected before age 5yrs

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37
Q

Mode of transmission for Epstein Barr?

A

Virus is shed in saliva and §genital secretions - ‘kissing disease’

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38
Q

Where is latency for Epstein Barr established?

A

In B cells

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39
Q

What is the primary infection caused by Epstein Barr?

A

Infectious mononucleosis

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40
Q

How does infectious mononucleosis typically present (symptoms)?

A
  • Tonsilitis
  • Fever
  • Lymphadenopathy (swollen lymph nodes)
  • Hepatosplenomegaly
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41
Q

How does infectious mononucleosis appear on blood film?

A

Atypical lymphocytes on blood film –> look like monocytes - ‘mononucleosis’

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42
Q

What % of clinical infectious mononucleosis is caused by EBV?

A

80%

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43
Q

What does reactivation of EBV lead to?

A
  • If unwell or immunosuppressed (e.g. solid organ or bone marrow transplant)
  • Associated with malignant B cell lymphoproliferative disorders
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44
Q

In the UK what is the prevalence of Cytomegalovirus (CMV)?

A

% prevalence roughly equals age

E.g. 20% of 20 year olds, 30% of 30 year olds …

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45
Q

What are the mode of transmissions for CMV?

A
  • Saliva or genital secretions

- Donated blood, stem cells or solid organs

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46
Q

Where does CMV take latency?

A

Various cells of the immune system: myeloid progenitors, monocytes, dendritic cells

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47
Q

What are the 2 important clinical syndromes caused by CMV?

A
  1. Infectious mononucleosis (primary infection) - makes up the other 20% of causes of this disease
  2. Congenital CMV infection
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48
Q

How is congenital CMV infection acquired?

A

In infants born to mothers who have infection during pregnancy

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49
Q

Presentation of congenital CMV infection?

A

Retinitis, deafness, microcephaly, hepatosplenomegaly in the neonate

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50
Q

Who is most susceptible to reactivation of CMV?

A

Immunosuppressed patients (e.g. transplant patients, advanced HIV)

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51
Q

What can reactivation of CMV lead to?

A

Reactivation of latent CMV can cause retinitis, colitis, pneumonitis

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52
Q

What are the 4 major viruses behind the ‘common cold’?

A
  1. Rhinoviruses
  2. Coronaviruses
  3. Influenza viruses
  4. Respiratory syncytial virus
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53
Q

What virus is the most common cause of the common cold?

A

Rhinovirus

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54
Q

Mode of transmission of rhinovirus?

A

Aerosolised respiratory secretions (coughs and sneezes), droplets from nose and eyes

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55
Q

Important clinical syndrome caused by rhinovirus?

A

Common cold

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56
Q

Symptoms of common cold?

A

sneezing, nasal obstruction & discharge, sore throat, cough, headache and fever

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57
Q

Mode of transmission of coronaviruses?

A

Aerosolised respiratory secretions and droplets from nose and eyes

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58
Q

Important clinical syndromes caused by coronaviruses?

A

COVID-19, SARS, MERS, common cold

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59
Q

How can coronaviruses be divided?

A

Alpha and beta coronaviruses

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60
Q

Is the current COVID-19 pandemic due to alpha or beta coronaviruses?

A

Beta - SARS-CoV-2

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61
Q

Who can coronaviruses infect?

A

Animals and humans

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62
Q

Who can influenza infect?

A

Infect humans and animals, can spread between species

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63
Q

What are the 3 distinct types of influenza?

A

A, B and C

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64
Q

Which type of influenza mutates regularly?

A

A - the strains vary yearly

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65
Q

What are the 2 important surface proteins on influenza?

A

H and N - these have multiple variants –> this is used in nomenclature

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66
Q

What is H1N1?

A

Swine flu

influenza A virus subtype

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67
Q

What is H3N2?

A

Seasonal flu

influenza A virus subtype

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68
Q

What is the mode of transmission of influenza?

A

Aerosolised respiratory secretions (coughs and sneezes!)

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69
Q

What are the 2 important clinical syndromes cause by influenza (1ary and 2ary)?

A
  1. Primary influenza illness

2. Post-influenza secondary bacterial lung infection

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70
Q

Symptoms of primary influenza illness?

A

fever, myalgia (muscle aches), then headache, cough, sore throat, nasal discharge

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71
Q

What bacteria causes a post-influenza secondary bacterial lung infection?

A

S. pneumoniae, H. influenzae, S. aureus

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72
Q

How can influenza lead to a 2ary bacterial lung infection?

A

Virus damages lung tissue –> more susceptible to bacterial infection

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73
Q

Who is respiratory syncytial virus (RSV) most common in?

A

Commonest in young children: 70% are infected and 30% have had clinical illness in their first year of life

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74
Q

Mode of transmission of RSV?

A

Aerosolisation of respiratory secretions

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75
Q

What is the most important clinical syndrome associated with RSV?

A

Bronchiolitis

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76
Q

Who does bronchiolitis affect?

A

Children under 2

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77
Q

What is bronchiolitis?

A

Inflammation of smallest airways – bronchioles

78
Q

Symptoms of bronchiolitis?

A

Causes cough, wheeze, hypoxia and apnoeas

79
Q

Mode of transmission of HIV?

A

Virus is present in blood, genital secretions, breast milk

Transmitted vertically, sexually, needlestick

80
Q

What cells does HIV target?

A

Helper T lymphocytes (CD4) cells (part of the cell-mediated immune system)

81
Q

What may HIV patients develop in the seroconversion period?

A

2-6 weeks after transmission, may develop acute seroconversion illness (flu-like)

82
Q

What is the seroconversion period?

A

the time period during which a specific antibody develops and becomes detectable in the blood

83
Q

What follows seroconversion in HIV?

A

Chronic asymptomatic infection

84
Q

What happens during the chronic asymptomatic infection of HIV?

A

HIV is infecting CD4 cells which then die

The body then makes more CD4 cells, causing more HIV to be produced

This leads to a steady state between virus and immune system

85
Q

How long does the chronic asymptomatic infection of HIV tend to last?

A

5-15 years (during which the patient is entirely asymptomatic)

86
Q

What happens after the chronic asymptomatic infection of HIV?

What is this called?

What happens to the patient?

A

Virus eventually starts to take over - rise in viral load and fall in CD4 count

AIDS: acquired immunodeficiency syndrome

Patient becomes vulnerable to opportunistic infections due to weakened immune system

87
Q

What are AIDS-defining illnesses?

A

Those classified as being directly associated with advanced HIV infection.

88
Q

Examples of AIDS-defining illnesses?

A

Pneumocystis pneumonia, cryptococcal meningitis, Kaposi’s sarcoma

89
Q

What is important to remember regarding hepatitis?

A

many viruses can induce hepatitis (e.g. liver inflammation) as part of a wider clinical syndrome

90
Q

What are the 5 viruses that primarily affect hepatocytes (hepatotropic viruses)?

A
  1. Hep A
  2. Hep B
  3. Hep C
  4. Hep D
  5. Hep E
91
Q

What is important to note about Hep D?

A

defective virus, can only survive with hepatitis B

92
Q

How is Hep A usually spread?

A

Faeco-oral: virus shed in the faeces of an infected individual

93
Q

How is Hep E usually spread?

A

Faeco-oral: virus shed in the faeces of an infected individual

94
Q

How is Hep B usually spread?

A

Blood borne

95
Q

How is Hep C usually spread?

A

Blood borne

96
Q

Clinical presentation of Hep A and Hep E?

A

Nausea, myalgia, fevers, jaundice, right upper quadrant pain

97
Q

Why are Hep A and E more prominent in the developing world?

A

Contaminated water

98
Q

Prevalence of Hep A in Europe?

A

prevalence of antibody in adults (therefore indicating previous exposure) varies from 10-50%

99
Q

Difference in symptomatic populations for Hep A?

A
  • Infection in children is usually asymptomatic, esp. under 5yrs old
  • 50% infected adults are symptomatic
100
Q

Who is Hep A more associated with?

A

lower socio-economic groups, returning tourists and men who have sex with men (MSM)

101
Q

Prevalence of Hep E in Western Europe and North America?

A

In Western Europe & North America, clusters of cases are associated with pigs / undercooked pork

102
Q

Symptomatic populations for Hep E?

A

95% of cases are asymptomatic

103
Q

What is fulminant hepatitis?

A

When your liver begins to fail very quickly within days or weeks.

This sudden liver failure can happen in people who previously had stable liver disease or never had liver problems.

104
Q

Who is most at risk from Hep E?

A

Pregnant women - around 25% infected will develop fulminant hepatitis (with high mortality rate)

105
Q

Modes of transmission for Hep B?

A

Vertical (most common)

Sexual

Parenteral

106
Q

What is parenteral transmission?

A

the process of acquiring an infectious agent into one’s body through something other than the gastrointestinal (or enteral) route e.g. subcutaneous, IV and intramuscular injections.

107
Q

Acute clinical hepatitis may occur after transmission of Hep B.

But, what % of children and adults are asymptomatic?

A

90% children and 50% young adults are asymptomatic

108
Q

What happens after the period of acute clinical hepatitis after infection by Hep B?

A

Hepatitis B is then cleared by body, or persists and becomes chronic

109
Q

Who is more at risk of Hep B progressing to chronic?

A

Risk of chronicity is inversely related to age at infection:

90% perinatally acquired infection progress to chronic
vs. <5% adult-acquired infections

110
Q

What can chronic hepatitis lead to?

A

chronic hepatitis –> cirrhosis –> hepatocellular carcinoma

111
Q

Prevalence of Hep C in developed countries?

Who is more prone to Hep C in UK?

A

Prevalence in developed countries is low, ~0.5-2%

In the UK, 50% of PWIDs have evidence of hepatitis C

112
Q

What % of PWIDs in UK have have evidence of hepatitis C?

A

50%

113
Q

Mode of transmission of Hep C?

A

Sharing needles, needlestick injuries, transfusion of contaminated products

Vertical & sexual transmission (less common)

114
Q

What % of those infected with Hep C will develop acute clinical hepatitis?

A

25%

115
Q

What % of those with Hep C will clear the virus? What % will become chronically infected?

A

15% will then clear the virus

85% will become chronically infected

116
Q

Over time, what can chronic hepatitis lead to?

A

chronic hepatitis –> cirrhosis –> hepatocellular carcinoma (HCC)

117
Q

What do Norovirus and Rotavirus both cause?

A

Gastroenteritis (diarrhoea and vomiting/ D&V)

118
Q

What gives rotavirus its name?

A

Virus looks like a wheel on electron microscopy – so called ‘rota’

119
Q

Prevalence of norovirus?

A

90% of adults have been infected at some time.

Immunity is short-lived (<1yr) so reoccurrence is likely

120
Q

Who is norovirus typically associated with?

A

Closed communities / with point-source outbreaks, e.g. cruise ships, hospitals, military

121
Q

Mode of transmission of norovirus?

A

Ingestion / inhalation of aerosolised vomit particles

122
Q

Typical presentation of norovirus?

A

Vomiting is dominant feature

123
Q

Prevalence of rotavirus?

A

Virus of childhood: 80-100% infected in 1st 3 years of life (pre-vaccine availability).

Seasonal, peaks in winter

Major cause of infant mortality in developing world

124
Q

Mode of transmission of rotavirus?

A

Faeco-oral - contaminated food / water, and aerosolised faeces / vomit

125
Q

Typical presentation of rota?

A

Fever, vomiting and watery diarrhoea

126
Q

How many serotypes of enteroviruses exist?

How were most identified?

A

> 70 serotypes exist, most were identified in stool samples during polio research

127
Q

What is: poliovirus, echoviruses and Coxsackie A and B all examples of?

A

Enteroviruses

128
Q

When do enteroviruses tend to peak in UK?

A

Peak in summer / autumn in UK

129
Q

Are enteroviruses more common in adults or children?

A

75% cases occur in those under 15yrs old

130
Q

What % of enteroviruses cases in children are symptomatic?

A

Only around 10%

131
Q

Mode of transmission of enteroviruses?

A

Enteric route: faeco-oral, contaminated food/water.

132
Q

Where do enteroviruses replicate?

A

Gut - but do NOT cause GI symptoms

133
Q

Where do enteroviruses pass after the gut?

A

From gut –> lymph nodes –> blood (and sometimes to CNS)

134
Q

What are 4 important clinical syndromes associated with enterovirsues?

A
  1. Fever-rash syndromes in children, incl. hand foot and mouth
  2. Meningitis
  3. Severe disseminated disease in neonate
  4. Poliomyelitis (cases still in Pakistan / Afghanistan)
135
Q

What is the most common cause of viral meningitis in UK?

A

Enteroviruses (>50%)

136
Q

When do cases of mumps tend to peak?

A

Cases peak in temperate climates in winter

137
Q

Mode of transmission of mumps?

A
  • Virus shed in saliva and respiratory secretions
  • Respiratory droplet transmission
    (Very infectious)
138
Q

Important clinical syndromes that mumps can cause?

A
  1. Acute parotitis (unilateral or bilateral)
  2. Orchitis / oophoritis
  3. Meningitis
139
Q

What is acute parotitis?

A

Swelling of one or both of the salivary glands

140
Q

What is orchitis?

A

an inflammation of one or both testicles

141
Q

What is oophoritis?

A

an inflammation of the ovaries

142
Q

What % of males with mumps does orchitis affect?

A

20-30%

143
Q

When does orchitis develop after infection with mumps?

A

Typically develops 4-5 days after parotitis

144
Q

What % of mumps cases can develop meningitis?

A

Up to 15%

145
Q

What can meningitis caused by mumps lead to?

A

Can lead to meningoencephalitis and sensorineural deafness

146
Q

Why is mumps now a rare cause of viral meningitis?

A

MMR vaccine

147
Q

Why is there now a lower prevalence of measles in the UK?

A

MMR vaccine

148
Q

Mode of transmission of measles?

A

Respiratory droplet transmission

149
Q

How infectious is measles?

A

Highly infectious – environment still infectious after 2 hours

150
Q

Symptoms of measles?

A

Fever, coryza, cough, conjunctivitis (3 C’s), Koplik’s spots on inside of cheek

Then maculopapular rash

151
Q

What clinical syndrome can occur post measles?

A

Acute post infectious measles encephalitis (1:1000)

High mortality rate

152
Q

When does acute post infectious measles encephalitis tend to appear?

A

Occurs 7-10 days after acute infection

153
Q

Measles can also lead to Subacute sclerosing pan-encephalitis SSPE. What is the prevalence of this?

A

1:1000000

154
Q

When does SSPE tend to occur?

A

7-10 years after natural measles infection

155
Q

What is SSPE?

A

Progressive, degenerative and fatal disease of the CNS

156
Q

What is rubella also referred to as?

A

German measles

157
Q

Why is rubella now rare in UK?

A

MMR vaccine

158
Q

Mode of transmission of rubella?

A

Droplet transmission from respiratory route

159
Q

What 2 important clinical syndromes can rubella cause?

A
  1. Primary rubella

2. Congenital rubella

160
Q

Symptoms of primary rubella?

A

Mild illness, fever and maculopapular rash

161
Q

If an adult gets primary rubella, how can this present?

A

Arthralgia / arthritis occurs in 30% adults

162
Q

What is arthralgia?

A

Pain in a joint

163
Q

When is risk of foetal malformation from congenital rubella highest?

A

if women is infected in first 12 weeks of pregnancy

164
Q

What are the classic triad of symptoms of congenital rubella?

A
  1. Bilateral cataracts
  2. Sensorineural deafness
  3. Cardiac defects
165
Q

What is Parvovirus B19 also referred to as?

A

‘Slapped cheek syndrome’ or ‘Fifth disease’

166
Q

What time of year does Parvovirus B19 peak?

A

Spring time

167
Q

Prevalence of Parvovirus B19?

A

50% infected by 15yrs, 90% by 90yrs

168
Q

Mode of transmission of Parvovirus B19?

A

Respiratory droplet transmission

169
Q

What cells does Parvovirus B19 typically infect and kill?

What does this cause?

A

Erythrocyte progenitor cells – causing transient anaemia

170
Q

What 2 important clinical syndromes can Parvovirus B19 cause?

A
  1. Erythema infectiosum

2. Transient aplastic crisis

171
Q

Symptoms of erythema infectiosum?

A

Fever, coryza, fiery red rash to cheeks (‘slapped cheek syndrome’, ‘lacy’ rash to body

172
Q

Who does transient aplastic crisis occur in?

Why is this?

A

Patients with pre-existing conditions which causes high erythrocyte turnover e.g. sickle cell anaemia / thalassaemia

Due to this high erythrocyte turnover, they cannot cope with transient anaemia caused by Parvovirus B19

173
Q

If a pregnant woman is infected with Parvovirus B19 , how dangerous is this?

A

7-10% foetal loss if maternal parvovirus infection in first 20 weeks

2-3% develop hydrops fetalis

174
Q

Cause of hydrops fetalis?

A

severe foetal anaemia –> heart failure –> oedema, ascites

175
Q

What is a prion?

A

NOT a virus

Small infectious particle containing protein, no nucleic acid

176
Q

Where do prion proteins exist naturally?

A

In cells

177
Q

How can prions lead to disease?

A

Gene mutation leads to changes in folding pattern of protein

178
Q

What can abnormal folding of the prion lead to?

A
  1. prion becomes resistant to degradation by protease enzyme due to abnormal folding
  2. prion accumulates abnormally in cell
  3. this promotes other proteins to abnormally fold –> disease
179
Q

How are abnormal prions acquired?

A
  1. Inherited (genetic defects)

2. Transmitted via consumption or direct exposure (e.g. medical instruments)

180
Q

What 4 key properties do prion diseases share?

A
  1. manifest in the CNS
  2. produce spongiform change in brain tissue
  3. have long incubation times (up to 30 yrs)
  4. are progressive and fatal
181
Q

What is an important prion disease?

A

New variant CJD (nvCJD)

182
Q

What is CJD short fot?

A

Creutzfeld-Jakob disease

183
Q

How common is sporadic CJD?

A

Very rare: 1 in a million

184
Q

What is sporadic CJD caused by?

A

Gene mutation

185
Q

Symptoms of CJD?

A

Progressive ataxia, depression, dementia then death

186
Q

Sporadic vs new variant CJD?

A

Sporadic CJD (sCJD) is the most common form and represents about 85% of all CJD cases.

Variant CJD has been linked to bovine spongiform encephalopathy, (BSE)

187
Q

What is nvCJD directly linked to?

A

BSE (bovine spongiform encephalopathy)

188
Q

What are nvCJD cases associated with?

A

associated with consumption of contaminated beef (of affected cows)

189
Q

Difference between bronchiolitis and bronchitis?

A

Bronchitis: involves inflammation of the airways that lead to the windpipe

Bronchiolitis: involves the inflammation of the small airways that branch off the bronchi; bronchioles. Affects children under 2.

190
Q

Which hepatitis viruses can lead to chronic liver disease?

A

B, C and D can cause acute and chronic infections.

191
Q

What can chronic hepatitis lead to?

A

Cirrhosis –> hepatocellular carcinoma (HCC)

CP reviewer 1 (59 decks)

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