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MBBS - Year 1 > Microbiology - Viral Disease > Flashcards

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
What are measles deaths largely due to
Increased susceptibility to secondary bacterial and viral infection due to a prolonged state of immunosuppression
26
Presentation of measles
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
27
Prodromal stage of measles
``` Onset of fever Malaise Coryza Conjunctivitis Cough ```
28
Characteristic rash of measles
Erythematous and maculopapular | Starts at head and spreads to trunk and limbs over 3-4 days
29
Koplik spots
Small red spots w/ blueish-white centres
30
Infection of measles
Spread by airborne or droplet transmission | Individuals are infectious from beginningof prodromal period to 4 days after rash appears
31
Incubation period of measles
10 days (ranges between 7-18 days) w/ a further 2-4 days before rash appear
32
Which features are strongly suggestive of measles
Rash for at least 3 days Fever for at least 1 day, and At least one of the following - cough, coryza or conjunctivitis
33
Most common complications of measles
``` Otitis media Pneumonia Diarrhoea Convulsions Encephalitis Subacute sclerosing pan-encephalitis (SSPES) ```
34
Different forms of measles encephalitis
Post-infectious encephalitis ~ one week after onset of rash Measles inclusion body encephalitis SSPE
35
Measles inclusion body encephalitis
Occurs in immunocompromised patients | Characterised by deterioration of consciousness, seizures and progressive neurological damage
36
SSPE
Rare, fatal, late complication of measles
37
Influenza
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
38
Types of influenza
A, B, C | A & B are responsible for most clinical illness
39
Incubation period of influenza
1-3 days
40
Virology of influenza
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
41
Pathogenesis of influenzas
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
42
Risk of complications from influenza
Infection of LRT Admission to Hosp Death
43
At risk group for influenza incl patients w/
``` Chronic respiratory system diseases Cardiovascular system diseases Endocrine system diseases Hepatic system diseases Renal system diseases Neurological/ neuromuscular conditions ```
44
Additional risk factors for influenza
Any condn compromising respiratory functions eg. BMI>40, age >65 Immunosuppression Antenatal women
45
Treatment for influenza
Neuraminidase inhibitors: Oseltamivir - 75 mg BDS for 5 days (10 days if immunocompromised) Zanamivir - inhalation of powder, 10mg BDS for 5 days
46
Influenza vaccines
Live attenuated vaccine quadrivalent - children's Inactivated influenzas vaccine (quadrivalent: H1N1,H3N2, influenza B two subtypes) Trivalent adjuvanted inactivated vaccine (age over 65)
47
Human immunodeficiency virus
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
Genetic groups of HIV-1
M,N,O,P
49
HIV life cycle
``` HIV approaches human CD4 T-lymphocyte Binding Fusion Reverse transcription Integration Transcription Assembly Budding Immature virus breaks free of infected cell Maturation ```
50
HIV - Binding
HIV binds w/ glycoproteins to CD4 receptor and another co-receptor protein
51
HIV - Fusion
Virus fuses w/ host cell and releases RNA
52
HIV - reverse transcription
Reverse transcriptase converts single stranded RNA into double stranded HIV DNA
53
HIV - integration
HIV DNA enters host nucleus and is integrated into hosts DNA using integrase, creating a provirus
54
HIV - transcription
Provirus becomes active and creates copies of HIV genomic material using RNA polymerase
55
HIV - assembly
Protease cuts long chain and assembles virus particle containing HIV RNA
56
HIV-budding
Newly assembled virus buds and takes a part of cells outer envelope
57
HIV - maturation
Protease completes cutting and HIV can go and infect other cells
58
HIV transmission
When certain fluids come into contact w/ mucous membranes, damaged issue or is injected into the body
59
Fluids that can transmit HIV
Blood Semen Vaginal secretions Breast milk
60
Clinical manifestations of HIV
``` Fever Pharyngitis Headache Myalgia Arthralgia Malaise Non-pruritic, maculopapular rash on face and trunk Generalised lymphadenopathy ```
61
HIV lab tests
CD4 count - measures state of a person's immune function
62
HIV virological tests
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
5 C's
``` Informed consent Confidentiality Counselling pre- and post-testing Correct test results Connection (linkage to care, treatment and other HIV services) ```
64
Management of HIV infection
No cure but effective anti retroviral drugs can control virus and prevent transmission
65
Anti-retroviral treatment
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
Examples of ARV medications
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
When is AIDS diagnosed
When CD4 count is less than 200
68
Systemic and organ-spp manifestations of AIDS
Opportunistic infections Oncological complications Cardiovascular complication CNS complications
69
RSV
Respiratory Syncytial virus | Major cause of LRT infection in young children and adults
70
Predisposing factors for RSV
``` Prematurity Low birth weight Congenital cardiopulmonary disease Male sex Attending day care Overcrowding Maternal smoking (tobacco exposure) ```
71
Virology of RSV
Pneumovirus | Two genetically distinct subgroups: RSV/A and RSV/B
72
RSV transmission
Small inoculum is necessary to infect | Trasnmitted via respiratory secretions
73
Respiratory secretions that transmit RSV
Direct contact Via fomites By large droplets
74
Entry of RSV
Occurs through contact w/ nasal mucosa or eyes
75
Incubation period of RSV
Varies from 2-8 days
76
Bronchiolitis pathophysiology
``` 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
What does the antibody response in infants hospitalised following infecting w/ RSV consist of
Virus - spp IgM (persists for 10 weeks) | Virus - spp IgG and IgA (produced during 2nd week, peak by 3-4 weeks)
78
Clinical symptoms of bronchiolitis
``` Expiratory wheezing Cough and coryza Air trapping Nasal flaring Subcostal retractions Cyanosis Fever only in 50% of infants requiring admission ```
79
Clinical manifestations of RSV in infants
``` Bronchiolitis Pneumonia Croup Exacerbation of asthma URT infection Otitis media ```
80
Clinical manifestations of RSV in older children and adults
``` URT infection Croup Laryngitis Bronchitis Exacerbation of asthma Pneumonia (in elderly) Exacerbation of chronic obstructive pulmonary disease ```
81
Diagnosis of RSV
Clinical (age, season, clinical manifestations) Lab diagnosis Nucleic acid detection (Rt-PCR) Antibody (acute and convalescent sera in adults)
82
Lab diagnosis for RSV
Nasopharyngeal aspirate Nasal swabs Endotracheal aspirate/ BAAL from those intubated
83
Passive immunoprophylaxis for RSV
Humanised monoclonal antibody spp for antigenic epitope A and the F protein of RSV
84
Who is passive immunoprophylaxis recommended to
Bronchopulmonary dysplasia Congenital Heart Disease Severe combined Heart Disease
85
+ve polarity of viruses
Genomic RNA can serve directly as mRNA
86
-ve polarity of viruses
Genomic sequence is complementary to the mRNA
87
Group I - Baltimore classification
Double stranded DNA mRNA is transcribed directly from the DNA template Example - Herpes simplex
88
Group II - Baltimore classification
Single stranded DNA DNA is converted to double stranded form before RNA is transcribed Examples - parvovirus
89
Group III - Baltimore classification
Double stranded RNA mRNA is transcribed from the RNA genome Examples - rotavirus
90
Group IV - Baltimore classification
Single stranded RNA (+) Genome functions as RNA Examples - common cold (picornavirus)
91
Group V - Baltimore classification
Single stranded RNA (-) | mRNA is transcribed from the RNA genome
92
Group VI - Baltimore classification
Single stranded RNA viruses w/ reverse transcriptase Reverse transcriptase makes DNA and is then incorporated into host genome to transcribe RNA Example - HIV
93
Group VII - Baltimore classification
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
Where is the genetic material found in viruses
Contained within an coat or capsid, made up of a number of individual protein molecules known as capsomeres
95
Nucleocapsid
Combined structure of capsid surrounding the nucleic acid | Usually comprises virion
96
Virion
Entire virus particle
97
Nucleocapsid surrounded by outer envelope/ membrane
Generally consists of a lipid bilayer originating from the host cell membrane, into which viral proteins and glycoproteins are inserted
98
Host specificity
Pathogen usually only infects a restricted range of host species
99
What does the process of attachment of a virus to a host cell depend on
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
What happens when a virus has attached to a host cell membranes
The virus particle is carried into the cytoplasm across the plasma membrane
101
Uncoating
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
Eclipse
Stage where virus is no longer infective
103
How is viral mRNA translated
Using host ribosomes to synthesise viral proteins | The viral mRNA can displace host mRNA from ribosomes so that viral products are synthesised preferentially.
104
Which viruses don't have an envelope
Those released during lysis of the infected cell

MBBS - Year 1 (93 decks)

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