Viral and Prion Pathogens Flashcards

(192 cards)

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
Where does HSV-2 establish latency?
Latency in sensory nerve ganglia of the SACRAL ganglia Therefore, when periodic reactivations occur, they occur in the genital area
26
Location of latency of HSV-1 vs HSV-2?
HSV-1: trigeminal nerve sensory ganglia HSV-2: sacral nerve sensory ganglia
27
What syndromes are caused by HSV-2?
1. Vesicles/ulcers to skin or mucous membranes (typically genitals/buttocks) 2. Meningitis 3. Neonatal herpes (life threatening)
28
What does meningitis from HSV-2 typically follow?
An outbreak of genital lesions
29
Define 'viraemia'?
viruses present in the bloodstream
30
How are neonates exposed to HSV-2?
Vertical transmission from mother's genital tract after vaginal birth
31
Typical disease names for Varicella zoster virus?
Primary infection: 'chicken pox' Reactivation: 'herpes zoster' or 'shingles'
32
What is the mode of transmission for Varicella zoster?
Respiratory droplets from person with chicken pox (highly infectious) or Direct contact with vesicle fluid from person with chicken pox or shingles
33
Where is latency for Varicella zoster established?
Dorsal root ganglia of whole CNS (i.e. shingles can reactivate down any of the dermatomes)
34
What are the 2 important syndromes caused by Varicella zoster?
1. Chicken pox | 2. Shingles
35
Typical disease names for Epstein Barr virus?
Glandular fever / infectious mononucleosis
36
What % of UK are infected with Epstein Barr?
90% in the UK are infected by age 25 Of these, 50% infected before age 5yrs
37
Mode of transmission for Epstein Barr?
Virus is shed in saliva and §genital secretions - 'kissing disease'
38
Where is latency for Epstein Barr established?
In B cells
39
What is the primary infection caused by Epstein Barr?
Infectious mononucleosis
40
How does infectious mononucleosis typically present (symptoms)?
- Tonsilitis - Fever - Lymphadenopathy (swollen lymph nodes) - Hepatosplenomegaly
41
How does infectious mononucleosis appear on blood film?
Atypical lymphocytes on blood film --> look like monocytes - 'mononucleosis'
42
What % of clinical infectious mononucleosis is caused by EBV?
80%
43
What does reactivation of EBV lead to?
- If unwell or immunosuppressed (e.g. solid organ or bone marrow transplant) - Associated with malignant B cell lymphoproliferative disorders
44
In the UK what is the prevalence of Cytomegalovirus (CMV)?
% prevalence roughly equals age E.g. 20% of 20 year olds, 30% of 30 year olds ...
45
What are the mode of transmissions for CMV?
- Saliva or genital secretions | - Donated blood, stem cells or solid organs
46
Where does CMV take latency?
Various cells of the immune system: myeloid progenitors, monocytes, dendritic cells
47
What are the 2 important clinical syndromes caused by CMV?
1. Infectious mononucleosis (primary infection) - makes up the other 20% of causes of this disease 2. Congenital CMV infection
48
How is congenital CMV infection acquired?
In infants born to mothers who have infection during pregnancy
49
Presentation of congenital CMV infection?
Retinitis, deafness, microcephaly, hepatosplenomegaly in the neonate
50
Who is most susceptible to reactivation of CMV?
Immunosuppressed patients (e.g. transplant patients, advanced HIV)
51
What can reactivation of CMV lead to?
Reactivation of latent CMV can cause retinitis, colitis, pneumonitis
52
What are the 4 major viruses behind the 'common cold'?
1. Rhinoviruses 2. Coronaviruses 3. Influenza viruses 4. Respiratory syncytial virus
53
What virus is the most common cause of the common cold?
Rhinovirus
54
Mode of transmission of rhinovirus?
Aerosolised respiratory secretions (coughs and sneezes), droplets from nose and eyes
55
Important clinical syndrome caused by rhinovirus?
Common cold
56
Symptoms of common cold?
sneezing, nasal obstruction & discharge, sore throat, cough, headache and fever
57
Mode of transmission of coronaviruses?
Aerosolised respiratory secretions and droplets from nose and eyes
58
Important clinical syndromes caused by coronaviruses?
COVID-19, SARS, MERS, common cold
59
How can coronaviruses be divided?
Alpha and beta coronaviruses
60
Is the current COVID-19 pandemic due to alpha or beta coronaviruses?
Beta - SARS-CoV-2
61
Who can coronaviruses infect?
Animals and humans
62
Who can influenza infect?
Infect humans and animals, can spread between species
63
What are the 3 distinct types of influenza?
A, B and C
64
Which type of influenza mutates regularly?
A - the strains vary yearly
65
What are the 2 important surface proteins on influenza?
H and N - these have multiple variants --> this is used in nomenclature
66
What is H1N1?
Swine flu influenza A virus subtype
67
What is H3N2?
Seasonal flu influenza A virus subtype
68
What is the mode of transmission of influenza?
Aerosolised respiratory secretions (coughs and sneezes!)
69
What are the 2 important clinical syndromes cause by influenza (1ary and 2ary)?
1. Primary influenza illness | 2. Post-influenza secondary bacterial lung infection
70
Symptoms of primary influenza illness?
fever, myalgia (muscle aches), then headache, cough, sore throat, nasal discharge
71
What bacteria causes a post-influenza secondary bacterial lung infection?
S. pneumoniae, H. influenzae, S. aureus
72
How can influenza lead to a 2ary bacterial lung infection?
Virus damages lung tissue --> more susceptible to bacterial infection
73
Who is respiratory syncytial virus (RSV) most common in?
Commonest in young children: 70% are infected and 30% have had clinical illness in their first year of life
74
Mode of transmission of RSV?
Aerosolisation of respiratory secretions
75
What is the most important clinical syndrome associated with RSV?
Bronchiolitis
76
Who does bronchiolitis affect?
Children under 2
77
What is bronchiolitis?
Inflammation of smallest airways – bronchioles
78
Symptoms of bronchiolitis?
Causes cough, wheeze, hypoxia and apnoeas
79
Mode of transmission of HIV?
Virus is present in blood, genital secretions, breast milk Transmitted vertically, sexually, needlestick
80
What cells does HIV target?
Helper T lymphocytes (CD4) cells (part of the cell-mediated immune system)
81
What may HIV patients develop in the seroconversion period?
2-6 weeks after transmission, may develop acute seroconversion illness (flu-like)
82
What is the seroconversion period?
the time period during which a specific antibody develops and becomes detectable in the blood
83
What follows seroconversion in HIV?
Chronic asymptomatic infection
84
What happens during the chronic asymptomatic infection of HIV?
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
How long does the chronic asymptomatic infection of HIV tend to last?
5-15 years (during which the patient is entirely asymptomatic)
86
What happens after the chronic asymptomatic infection of HIV? What is this called? What happens to the patient?
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
What are AIDS-defining illnesses?
Those classified as being directly associated with advanced HIV infection.
88
Examples of AIDS-defining illnesses?
Pneumocystis pneumonia, cryptococcal meningitis, Kaposi's sarcoma
89
What is important to remember regarding hepatitis?
many viruses can induce hepatitis (e.g. liver inflammation) as part of a wider clinical syndrome
90
What are the 5 viruses that primarily affect hepatocytes (hepatotropic viruses)?
1. Hep A 2. Hep B 3. Hep C 4. Hep D 5. Hep E
91
What is important to note about Hep D?
defective virus, can only survive with hepatitis B
92
How is Hep A usually spread?
Faeco-oral: virus shed in the faeces of an infected individual
93
How is Hep E usually spread?
Faeco-oral: virus shed in the faeces of an infected individual
94
How is Hep B usually spread?
Blood borne
95
How is Hep C usually spread?
Blood borne
96
Clinical presentation of Hep A and Hep E?
Nausea, myalgia, fevers, jaundice, right upper quadrant pain
97
Why are Hep A and E more prominent in the developing world?
Contaminated water
98
Prevalence of Hep A in Europe?
prevalence of antibody in adults (therefore indicating previous exposure) varies from 10-50%
99
Difference in symptomatic populations for Hep A?
* Infection in children is usually asymptomatic, esp. under 5yrs old * 50% infected adults are symptomatic
100
Who is Hep A more associated with?
lower socio-economic groups, returning tourists and men who have sex with men (MSM)
101
Prevalence of Hep E in Western Europe and North America?
In Western Europe & North America, clusters of cases are associated with pigs / undercooked pork
102
Symptomatic populations for Hep E?
95% of cases are asymptomatic
103
What is fulminant hepatitis?
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
Who is most at risk from Hep E?
Pregnant women - around 25% infected will develop fulminant hepatitis (with high mortality rate)
105
Modes of transmission for Hep B?
Vertical (most common) Sexual Parenteral
106
What is parenteral transmission?
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
Acute clinical hepatitis may occur after transmission of Hep B. But, what % of children and adults are asymptomatic?
90% children and 50% young adults are asymptomatic
108
What happens after the period of acute clinical hepatitis after infection by Hep B?
Hepatitis B is then cleared by body, or persists and becomes chronic
109
Who is more at risk of Hep B progressing to chronic?
Risk of chronicity is inversely related to age at infection: 90% perinatally acquired infection progress to chronic vs. <5% adult-acquired infections
110
What can chronic hepatitis lead to?
chronic hepatitis --> cirrhosis --> hepatocellular carcinoma
111
Prevalence of Hep C in developed countries? Who is more prone to Hep C in UK?
Prevalence in developed countries is low, ~0.5-2% In the UK, 50% of PWIDs have evidence of hepatitis C
112
What % of PWIDs in UK have have evidence of hepatitis C?
50%
113
Mode of transmission of Hep C?
Sharing needles, needlestick injuries, transfusion of contaminated products Vertical & sexual transmission (less common)
114
What % of those infected with Hep C will develop acute clinical hepatitis?
25%
115
What % of those with Hep C will clear the virus? What % will become chronically infected?
15% will then clear the virus 85% will become chronically infected
116
Over time, what can chronic hepatitis lead to?
chronic hepatitis --> cirrhosis --> hepatocellular carcinoma (HCC)
117
What do Norovirus and Rotavirus both cause?
Gastroenteritis (diarrhoea and vomiting/ D&V)
118
What gives rotavirus its name?
Virus looks like a wheel on electron microscopy – so called ‘rota’
119
Prevalence of norovirus?
90% of adults have been infected at some time. Immunity is short-lived (<1yr) so reoccurrence is likely
120
Who is norovirus typically associated with?
Closed communities / with point-source outbreaks, e.g. cruise ships, hospitals, military
121
Mode of transmission of norovirus?
Ingestion / inhalation of aerosolised vomit particles
122
Typical presentation of norovirus?
Vomiting is dominant feature
123
Prevalence of rotavirus?
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
Mode of transmission of rotavirus?
Faeco-oral - contaminated food / water, and aerosolised faeces / vomit
125
Typical presentation of rota?
Fever, vomiting and watery diarrhoea
126
How many serotypes of enteroviruses exist? How were most identified?
>70 serotypes exist, most were identified in stool samples during polio research
127
What is: poliovirus, echoviruses and Coxsackie A and B all examples of?
Enteroviruses
128
When do enteroviruses tend to peak in UK?
Peak in summer / autumn in UK
129
Are enteroviruses more common in adults or children?
75% cases occur in those under 15yrs old
130
What % of enteroviruses cases in children are symptomatic?
Only around 10%
131
Mode of transmission of enteroviruses?
Enteric route: faeco-oral, contaminated food/water.
132
Where do enteroviruses replicate?
Gut - but do NOT cause GI symptoms
133
Where do enteroviruses pass after the gut?
From gut --> lymph nodes --> blood (and sometimes to CNS)
134
What are 4 important clinical syndromes associated with enterovirsues?
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
What is the most common cause of viral meningitis in UK?
Enteroviruses (>50%)
136
When do cases of mumps tend to peak?
Cases peak in temperate climates in winter
137
Mode of transmission of mumps?
- Virus shed in saliva and respiratory secretions - Respiratory droplet transmission (Very infectious)
138
Important clinical syndromes that mumps can cause?
1. Acute parotitis (unilateral or bilateral) 2. Orchitis / oophoritis 3. Meningitis
139
What is acute parotitis?
Swelling of one or both of the salivary glands
140
What is orchitis?
an inflammation of one or both testicles
141
What is oophoritis?
an inflammation of the ovaries
142
What % of males with mumps does orchitis affect?
20-30%
143
When does orchitis develop after infection with mumps?
Typically develops 4-5 days after parotitis
144
What % of mumps cases can develop meningitis?
Up to 15%
145
What can meningitis caused by mumps lead to?
Can lead to meningoencephalitis and sensorineural deafness
146
Why is mumps now a rare cause of viral meningitis?
MMR vaccine
147
Why is there now a lower prevalence of measles in the UK?
MMR vaccine
148
Mode of transmission of measles?
Respiratory droplet transmission
149
How infectious is measles?
Highly infectious – environment still infectious after 2 hours
150
Symptoms of measles?
Fever, coryza, cough, conjunctivitis (3 C's), Koplik’s spots on inside of cheek Then maculopapular rash
151
What clinical syndrome can occur post measles?
Acute post infectious measles encephalitis (1:1000) High mortality rate
152
When does acute post infectious measles encephalitis tend to appear?
Occurs 7-10 days after acute infection
153
Measles can also lead to Subacute sclerosing pan-encephalitis SSPE. What is the prevalence of this?
1:1000000
154
When does SSPE tend to occur?
7-10 years after natural measles infection
155
What is SSPE?
Progressive, degenerative and fatal disease of the CNS
156
What is rubella also referred to as?
German measles
157
Why is rubella now rare in UK?
MMR vaccine
158
Mode of transmission of rubella?
Droplet transmission from respiratory route
159
What 2 important clinical syndromes can rubella cause?
1. Primary rubella | 2. Congenital rubella
160
Symptoms of primary rubella?
Mild illness, fever and maculopapular rash
161
If an adult gets primary rubella, how can this present?
Arthralgia / arthritis occurs in 30% adults
162
What is arthralgia?
Pain in a joint
163
When is risk of foetal malformation from congenital rubella highest?
if women is infected in first 12 weeks of pregnancy
164
What are the classic triad of symptoms of congenital rubella?
1. Bilateral cataracts 2. Sensorineural deafness 3. Cardiac defects
165
What is Parvovirus B19 also referred to as?
‘Slapped cheek syndrome’ or ‘Fifth disease’
166
What time of year does Parvovirus B19 peak?
Spring time
167
Prevalence of Parvovirus B19?
50% infected by 15yrs, 90% by 90yrs
168
Mode of transmission of Parvovirus B19?
Respiratory droplet transmission
169
What cells does Parvovirus B19 typically infect and kill? What does this cause?
Erythrocyte progenitor cells – causing transient anaemia
170
What 2 important clinical syndromes can Parvovirus B19 cause?
1. Erythema infectiosum | 2. Transient aplastic crisis
171
Symptoms of erythema infectiosum?
Fever, coryza, fiery red rash to cheeks ('slapped cheek syndrome', ‘lacy’ rash to body
172
Who does transient aplastic crisis occur in? Why is this?
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
If a pregnant woman is infected with Parvovirus B19 , how dangerous is this?
7-10% foetal loss if maternal parvovirus infection in first 20 weeks 2-3% develop hydrops fetalis
174
Cause of hydrops fetalis?
severe foetal anaemia --> heart failure --> oedema, ascites
175
What is a prion?
NOT a virus Small infectious particle containing protein, no nucleic acid
176
Where do prion proteins exist naturally?
In cells
177
How can prions lead to disease?
Gene mutation leads to changes in folding pattern of protein
178
What can abnormal folding of the prion lead to?
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
How are abnormal prions acquired?
1. Inherited (genetic defects) | 2. Transmitted via consumption or direct exposure (e.g. medical instruments)
180
What 4 key properties do prion diseases share?
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
What is an important prion disease?
New variant CJD (nvCJD)
182
What is CJD short fot?
Creutzfeld-Jakob disease
183
How common is sporadic CJD?
Very rare: 1 in a million
184
What is sporadic CJD caused by?
Gene mutation
185
Symptoms of CJD?
Progressive ataxia, depression, dementia then death
186
Sporadic vs new variant CJD?
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
What is nvCJD directly linked to?
BSE (bovine spongiform encephalopathy)
188
What are nvCJD cases associated with?
associated with consumption of contaminated beef (of affected cows) with BSE
189
Difference between bronchiolitis and bronchitis?
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
Which hepatitis viruses can lead to chronic liver disease?
B, C and D can cause acute and chronic infections.
191
What can chronic hepatitis lead to?
Cirrhosis --> hepatocellular carcinoma (HCC)
192
Which viral disease can cause transient anaemia?
Parvovirus B19