Microbiology - Viral Disease Flashcards

1
Q

Ways viruses can be classified

A

Historical classification by host (human,plant, animal)
According to disease or target organ
According to vectors

Molecular biology new permits classification by genetic sequence and biophysical structure

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2
Q

Virus classification (taxonomy)

A
Virus order
Virus family
Subfamily
Type species
Morphology
Genetic material (DNA or RNA)
Envelope
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3
Q

Baltimore classification of viruses

A

Based on method of viral synthesis
Groups viruses into families according to their type of genome
Groups I to VII

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4
Q

Differentiating between bacterial and viral causes of infection

A

Pathognomonic symptoms
Secondary bacterial infection symptoms persist longer than the expected 10 days virus tends to last and fever is usually higher
Diagnostic tests

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5
Q

Purpose of diagnosing viral infection

A

Medical (therapeutic) patient management
Epidemiological (public health)
Intrahospital infection prevention and control
Academic

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6
Q

Molecular techniques used in virology

A

Nucleic-acid based technologies e.g. PCR
Next Generation Sequencing (NGS)
Monoclonal antibodies
Enzyme inmune assays

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7
Q

Point of Care Test

A

Test for key respiratory virus done by the bed side
Tests for influenza A/B and RSV
PCR based

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8
Q

Methods of detecting virus infections

A
Detection of viral antigens 
Detection of nucleic acids (PCR)
Electron microscopy
Virus culture
Histopathology staining
Serology testing
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9
Q

Serology testing

A

Presence of virus-spp antibodies (IgM and IgG)

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10
Q

What is detection of viral pathogens highly dependable on

A

Obtaining an adequate specimen from the appropriate site
Proper timing of specimen collection relative to onset of symptoms
Timely processing of the sample

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11
Q

When does viral shedding begin for most infections

A

Shortly after symptoms occur, peaks rapidly after onset and declines steadily as infection resolves (excluding chronic viral infections e.g. HIV)

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12
Q

Needlestick injury

A

An incident in which the blood of a patient comes into contact w/ the blood of a Health Care Worker

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13
Q

Types of exposure in health care setting associated w/ significant risk from blood or higher risk body fluids

A

Percutaneous injury
Exposure of broken skin - intact skin is a safe protective barrier against BBV transmission
Exposure of mucous membranes incl eyes and mouth

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14
Q

BBV

A

Blood borne viruses e.g. Hepatits B/C and HIV
Viruses which can be present in blood or other body fluids and which have high potential for transmission to another person by direct contact w/ their blood or susceptible fluids

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15
Q

BBV’s organised by how infectious they are

A

Hep B
Hep C
HIV

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16
Q

Transmission rates for susceptible fluids in BBV’s

A

HBV - 30%
HCV - 3%
HIV - 0.3%

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17
Q

Recipient

A

Individual who has been exposed to the possibility of acquiring a BBV as a result of an incident w/ the potential to transmit a BBV

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18
Q

Source

A

Individual who was the source of the blood or body fluid, which made contact w/ the recipient
Usually a patient but may be a HCW as in a bleed back incident

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19
Q

Post Exposure Prophylaxis (PEP)

A

Treatment which may be advised and supplied to the recipient and supplied to the recipient following a risk assessment from a known or high-risk HIV or HBV exposure incident

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20
Q

Main infectious material

A

Blood

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21
Q

Potential infectious material

A
Amniotic fluid
Vaginal secretion
Semen
Human breast milk
Cerebrospinal fluid
Peritoneal fluid
Pleural fluid
Saliva in association w/ dentristy (likely to be contaminated w/ blood even when not visibly so)
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22
Q

Non-infectious bodily fluids

A

Urine
Vomit
Saliva
Faeces

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23
Q

What to do if you pierce/ puncture your skin w/ a used needle

A

Encourage the wound to bleed
Wash the wound using water and plenty of soap
Don’t scrub the wound while you’re washing it or suck it
Dry the wound and cover it w/ a waterproof plaster or dressing

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24
Q

Measles

A

Acute viral illness caused by a Morbillivirus

Important global cause of child mortality

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25
Q

What are measles deaths largely due to

A

Increased susceptibility to secondary bacterial and viral infection due to a prolonged state of immunosuppression

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26
Q

Presentation of measles

A

Prodromal stage
Characteristic rash
Koplik spots may appear on mucous membranes of mouth 1-2 days before rash appears and may stay for further 1-2 days

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27
Q

Prodromal stage of measles

A
Onset of fever
Malaise
Coryza
Conjunctivitis
Cough
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28
Q

Characteristic rash of measles

A

Erythematous and maculopapular

Starts at head and spreads to trunk and limbs over 3-4 days

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29
Q

Koplik spots

A

Small red spots w/ blueish-white centres

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30
Q

Infection of measles

A

Spread by airborne or droplet transmission

Individuals are infectious from beginningof prodromal period to 4 days after rash appears

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31
Q

Incubation period of measles

A

10 days (ranges between 7-18 days) w/ a further 2-4 days before rash appear

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32
Q

Which features are strongly suggestive of measles

A

Rash for at least 3 days
Fever for at least 1 day, and
At least one of the following - cough, coryza or conjunctivitis

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33
Q

Most common complications of measles

A
Otitis media
Pneumonia
Diarrhoea
Convulsions
Encephalitis
Subacute sclerosing pan-encephalitis (SSPES)
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34
Q

Different forms of measles encephalitis

A

Post-infectious encephalitis ~ one week after onset of rash
Measles inclusion body encephalitis
SSPE

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35
Q

Measles inclusion body encephalitis

A

Occurs in immunocompromised patients

Characterised by deterioration of consciousness, seizures and progressive neurological damage

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36
Q

SSPE

A

Rare, fatal, late complication of measles

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37
Q

Influenza

A

Acute viral infection of the respiratory tract w/ freq antigenic changes
Highly infectious
Can cause explosive outbreaks of febrile respiratory illness and death in those w/ chronic disease

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38
Q

Types of influenza

A

A, B, C

A & B are responsible for most clinical illness

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39
Q

Incubation period of influenza

A

1-3 days

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40
Q

Virology of influenza

A

Segmented -ve strand RNA genome
A and B carry 8 diff RNA segments that code for 11 diff proteins
Subtypes only occur for A viruses

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41
Q

Pathogenesis of influenzas

A

Initial site of infection is mucosa in respiratory tract
Human influenza viruses prefer the a2,6-linked sialic acid receptors present in URT & LRT
Infection results in degeneration of respiratory epithelial cells wil loss of ciliated tufts, desquamation oedema, hyperaemia and mononuclear cell infiltrates in lamina propria

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42
Q

Risk of complications from influenza

A

Infection of LRT
Admission to Hosp
Death

43
Q

At risk group for influenza incl patients w/

A
Chronic respiratory system diseases
Cardiovascular system diseases
Endocrine system diseases
Hepatic system diseases
Renal system diseases
Neurological/ neuromuscular conditions
44
Q

Additional risk factors for influenza

A

Any condn compromising respiratory functions eg. BMI>40, age >65
Immunosuppression
Antenatal women

45
Q

Treatment for influenza

A

Neuraminidase inhibitors:
Oseltamivir - 75 mg BDS for 5 days (10 days if immunocompromised)
Zanamivir - inhalation of powder, 10mg BDS for 5 days

46
Q

Influenza vaccines

A

Live attenuated vaccine quadrivalent - children’s
Inactivated influenzas vaccine (quadrivalent: H1N1,H3N2, influenza B two subtypes)
Trivalent adjuvanted inactivated vaccine (age over 65)

47
Q

Human immunodeficiency virus

A

HIV-1 and HIV-2 are enveloped viruses
RNA viruses
Reverse transcribe their genome to form double - stranded DNA which integrates into host genomic DNA

48
Q

Genetic groups of HIV-1

A

M,N,O,P

49
Q

HIV life cycle

A
HIV approaches human CD4 T-lymphocyte
Binding
Fusion
Reverse transcription
Integration
Transcription
Assembly
Budding
Immature virus breaks free of infected cell
Maturation
50
Q

HIV - Binding

A

HIV binds w/ glycoproteins to CD4 receptor and another co-receptor protein

51
Q

HIV - Fusion

A

Virus fuses w/ host cell and releases RNA

52
Q

HIV - reverse transcription

A

Reverse transcriptase converts single stranded RNA into double stranded HIV DNA

53
Q

HIV - integration

A

HIV DNA enters host nucleus and is integrated into hosts DNA using integrase, creating a provirus

54
Q

HIV - transcription

A

Provirus becomes active and creates copies of HIV genomic material using RNA polymerase

55
Q

HIV - assembly

A

Protease cuts long chain and assembles virus particle containing HIV RNA

56
Q

HIV-budding

A

Newly assembled virus buds and takes a part of cells outer envelope

57
Q

HIV - maturation

A

Protease completes cutting and HIV can go and infect other cells

58
Q

HIV transmission

A

When certain fluids come into contact w/ mucous membranes, damaged issue or is injected into the body

59
Q

Fluids that can transmit HIV

A

Blood
Semen
Vaginal secretions
Breast milk

60
Q

Clinical manifestations of HIV

A
Fever
Pharyngitis
Headache
Myalgia
Arthralgia
Malaise
Non-pruritic, maculopapular rash on face and trunk
Generalised lymphadenopathy
61
Q

HIV lab tests

A

CD4 count - measures state of a person’s immune function

62
Q

HIV virological tests

A

Serological diagnosis - HIV- 1 virus load
Defects amount of virus present - higher viral load increases risk of disease progression and HIV transmission
Monitors effectiveness of ART
Used during acute infections to detect virus
Measured by HIV-1 RNA PCR

63
Q

5 C’s

A
Informed consent
Confidentiality
Counselling pre- and post-testing
Correct test results
Connection (linkage to care, treatment and other HIV services)
64
Q

Management of HIV infection

A

No cure but effective anti retroviral drugs can control virus and prevent transmission

65
Q

Anti-retroviral treatment

A

ARV’s divided into 56 classes, each of which blocks HIV in a diff way
Always 3 or more diff ARV medications for therapy

66
Q

Examples of ARV medications

A

Nucleoside reverse transcriptase inhibitors (NRTI’s)
Non-nucleside reverse transcriptase inhibitors (NNRTI’s)
Protease inhibitors (PI’s)
Integrase inhibitors (INSTI’s)
Fusion inhibitors
Chemokine receptors antagonist (CCRS antagonists)

67
Q

When is AIDS diagnosed

A

When CD4 count is less than 200

68
Q

Systemic and organ-spp manifestations of AIDS

A

Opportunistic infections
Oncological complications
Cardiovascular complication
CNS complications

69
Q

RSV

A

Respiratory Syncytial virus

Major cause of LRT infection in young children and adults

70
Q

Predisposing factors for RSV

A
Prematurity 
Low birth weight 
Congenital cardiopulmonary disease 
Male sex 
Attending day care 
Overcrowding 
Maternal smoking (tobacco exposure)
71
Q

Virology of RSV

A

Pneumovirus

Two genetically distinct subgroups: RSV/A and RSV/B

72
Q

RSV transmission

A

Small inoculum is necessary to infect

Trasnmitted via respiratory secretions

73
Q

Respiratory secretions that transmit RSV

A

Direct contact
Via fomites
By large droplets

74
Q

Entry of RSV

A

Occurs through contact w/ nasal mucosa or eyes

75
Q

Incubation period of RSV

A

Varies from 2-8 days

76
Q

Bronchiolitis pathophysiology

A
Mucus buildup inside bronchial tube 
Inflamed tissue 
Collapsed alveoli 
Alveoli over-inflated w/ trapped air 
Smooth muscle tightening around bronchial tubes 
Necrosis and loss of epithelium
77
Q

What does the antibody response in infants hospitalised following infecting w/ RSV consist of

A

Virus - spp IgM (persists for 10 weeks)

Virus - spp IgG and IgA (produced during 2nd week, peak by 3-4 weeks)

78
Q

Clinical symptoms of bronchiolitis

A
Expiratory wheezing 
Cough and coryza
Air trapping 
Nasal flaring 
Subcostal retractions 
Cyanosis
Fever only in 50% of infants requiring admission
79
Q

Clinical manifestations of RSV in infants

A
Bronchiolitis 
Pneumonia 
Croup 
Exacerbation of asthma
URT infection 
Otitis media
80
Q

Clinical manifestations of RSV in older children and adults

A
URT infection 
Croup 
Laryngitis 
Bronchitis 
Exacerbation of asthma 
Pneumonia (in elderly)
Exacerbation of chronic obstructive pulmonary disease
81
Q

Diagnosis of RSV

A

Clinical (age, season, clinical manifestations)
Lab diagnosis
Nucleic acid detection (Rt-PCR)
Antibody (acute and convalescent sera in adults)

82
Q

Lab diagnosis for RSV

A

Nasopharyngeal aspirate
Nasal swabs
Endotracheal aspirate/ BAAL from those intubated

83
Q

Passive immunoprophylaxis for RSV

A

Humanised monoclonal antibody spp for antigenic epitope A and the F protein of RSV

84
Q

Who is passive immunoprophylaxis recommended to

A

Bronchopulmonary dysplasia
Congenital Heart Disease
Severe combined Heart Disease

85
Q

+ve polarity of viruses

A

Genomic RNA can serve directly as mRNA

86
Q

-ve polarity of viruses

A

Genomic sequence is complementary to the mRNA

87
Q

Group I - Baltimore classification

A

Double stranded DNA
mRNA is transcribed directly from the DNA template
Example - Herpes simplex

88
Q

Group II - Baltimore classification

A

Single stranded DNA
DNA is converted to double stranded form before RNA is transcribed
Examples - parvovirus

89
Q

Group III - Baltimore classification

A

Double stranded RNA
mRNA is transcribed from the RNA genome
Examples - rotavirus

90
Q

Group IV - Baltimore classification

A

Single stranded RNA (+)
Genome functions as RNA
Examples - common cold (picornavirus)

91
Q

Group V - Baltimore classification

A

Single stranded RNA (-)

mRNA is transcribed from the RNA genome

92
Q

Group VI - Baltimore classification

A

Single stranded RNA viruses w/ reverse transcriptase
Reverse transcriptase makes DNA and is then incorporated into host genome to transcribe RNA
Example - HIV

93
Q

Group VII - Baltimore classification

A

Double stranded DNA viruses w/ reverse transcriptase
Viral DNA replicated through RNA intermediate, RNA serves directly as mRNA or as a template for RNA
Example - Hep B

94
Q

Where is the genetic material found in viruses

A

Contained within an coat or capsid, made up of a number of individual protein molecules known as capsomeres

95
Q

Nucleocapsid

A

Combined structure of capsid surrounding the nucleic acid

Usually comprises virion

96
Q

Virion

A

Entire virus particle

97
Q

Nucleocapsid surrounded by outer envelope/ membrane

A

Generally consists of a lipid bilayer originating from the host cell membrane, into which viral proteins and glycoproteins are inserted

98
Q

Host specificity

A

Pathogen usually only infects a restricted range of host species

99
Q

What does the process of attachment of a virus to a host cell depend on

A

General intermolecular forces, then on more specific interactions between the molecules on the surface of the virus (nucleocapsid in unenveloped viruses and virus membrane in enveloped viruses) and the molecules of the host cell membrane

100
Q

What happens when a virus has attached to a host cell membranes

A

The virus particle is carried into the cytoplasm across the plasma membrane

101
Q

Uncoating

A

Occurs after virus has entered plasma membrane

Enzymes from the virus or host degrade the capsid releasing the genomic material into the host cell cytoplasm

102
Q

Eclipse

A

Stage where virus is no longer infective

103
Q

How is viral mRNA translated

A

Using host ribosomes to synthesise viral proteins

The viral mRNA can displace host mRNA from ribosomes so that viral products are synthesised preferentially.

104
Q

Which viruses don’t have an envelope

A

Those released during lysis of the infected cell