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MICI Module 2 > Molecular Testing, Virology, HSV, HIV, HEP > Flashcards

Molecular Testing, Virology, HSV, HIV, HEP Flashcards

1
Q

Desceibe nucleic acid testing

A

Molecular diagnostic
Relatively stable
Ubiquitous in nature (everythjng has it)
Purification processes are virtually identical irrespective of organism

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2
Q

Describe the steps of nucleic acid amplification tests

A

1- nucleic acid extraction
2- amplification
3- detection
4- interpretation of results

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3
Q

How js nucleic acid extracted

A

Lysis- release of nucleic acids (using heat,sonification, chemical or enzymatic
Purification - sequential wash steps eliminate contaminants
Recovery (elution)

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4
Q

What does PCR stand for

A

Polymerase chain reaction

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5
Q

What is PCR

A 
Target site amplification 
Rapidly and exponentially amplify a particular DNA sequence 
Rapid
Sensitive 
Specific
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6
Q

Describe the components of a pcr

A

Need a forward primer and a reverse primer
Template dna
Raw material
Dna polymerase (TAQ, thermostable)

Primers are small sefments of DNA complimentary to strands on template

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7
Q

How does PCR work?

A

Double stranded DNA separated, 94° heat applied, double strand turns to 2 single strands
Attach primers at lower heat (55°/anneal temp)
Anneal temo depends on primer

Get target site amplification, billions of copies from one double strand DNA
Find infection as long as nucleic acid is present

This reaction happens over and over

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8
Q

What is a virus

A

A package of genetic informstion protected by a protein shell for delivery into a host cell to be expressed and replicated

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9
Q

Where did the word virus come from

A

Greek meaninng poison

Initially described by edward jennner

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10
Q

What differentiates viruses from other micro organisms

A 
Nucleic acid (one if either dna or rna)
Lack of nuclear membrane and external cell wall
Very small genomes, limited number of proteins
Do not possess intracellular systems (obligate intracellular parasites) meaning they can not replicate on their own
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11
Q

What are bacteriophages

A

Viruses thst infect bacteria

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12
Q

How are viruses named or classified

A
  • disease they are associated with
  • cytopathology they cause
  • site of isolation
  • places or oeople that discovered them
  • biochemical features
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13
Q

What is viral classification based upon

A 
Size and shape
Enveloped or naked (lipid envelop or no?)
Nucleic acid composition
Genome organization 
antigenic differences
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14
Q

Describe a virus structure

A

Capsomere: protein subunits of the capsid; smallest protein unit

Capsid: capsomeres assemble to form viral capsid - surrounds viral genome

Nucleocapsid: capsid + genomic nucleic acids (dna/rna); genetic material found within

Shape: capsid is usually symmetrical

Surface projections and glycoproteins; bind host receptors/allows entry

Envelope (sometimes)

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15
Q

What are the three different shapes of a virus

A

Icosehedral (cubic) MOST COMMON
Helical (influenza virus)
Complex (pox viruses);dont fit a shape

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16
Q

Describe the envelope

A

Lipid layer surrounding some bacteria; derived from host cell membrane
Does not protect cell more infact naked cells are more protected
Envelope makes it essier to kill bc it is lipid based
Envelope is less stable

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17
Q

Describe non enveloped viruses

A

Stable in environment
Resist desiccation, heat, detergents and acids
Transmitted easily on hands and fomites

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18
Q

Describe enveloped viruses

A 
Labile in environment 
Must stay moist 
Damaged by drying, acid, detergents or heat (ex herpes viruses, hiv, hbv, influenza)
Transmitted in droplets of body fluids 
Doesnt usually infect GI
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19
Q

How are RNA viruses organized

A

Single strand -> positive polarity or negative polarity (MRNA or not)
RNA double stranded -> one piece or segmented

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20
Q

Describe how DNA Virusss are organized

A

Single stranded or double stranded

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21
Q

How are viral infections acquired

A 
Direct personal contact
Airborne 
Parenteral (exposure to blood)
Fomites
Vectors 
Vertical transmission (mum to fetus)
Enteral (food/waterborne)
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22
Q

What is the virus life cycle

A 
Attachment
Penetration
Uncoating (expose genome)
Transcription (dna/rna)
Translation 
Genome replication
Assembly of genome and protein material
Release and infect other cells
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23
Q

Describe DNA/RNA Transcription

A

Dna can be directly transcribed
Negative RNA has to get MRNA to transcribe
Positive RNA directly transcribes

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24
Q

Describe stages of virus-host interaction

A 
Entry to host
Primary replication 
Spread
Cell and tissue trophism 
Secondary replication 
Cell injury or persistance 
Host immune response (depending on virus)
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25
Q

What are consequences of virus-cell interaction

A

Viral proliferation and cell lysis

Latent infection (non replicating)

Persistent infection (ongoing replication)

Oncogenesis (cellular proliferation)

No apparent disease

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26
Q

How are viral infections disgnosed

A

Clinical features typical of infection

Laboratory diagnosis: serology or amplification, detection of antigens, antibody testing,virus isolation

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27
Q

What are prions

A 
Proteinaceous infectious particles
An infectious agent composed of protein
Does not self replicate, induces existing proteins to take on the rogue form
Very highly resistant 
Caused severe neurological diseases
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28
Q

What are some diseases caused by prions

A

Creutzfeldt-jacobs disease
Kuru

Animal forms: bovine spongiform encephalopathy (mad cow)

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29
Q

What herpesviridae affect humans?

A 
Herpes simplex 1 & 2
Epstein barr 
Varicella zoster 
Cytomegalovirus 
Human herpes virus 6,7,8
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30
Q

Describe herpesviridae

A

Large ICOSAHERDREAL double stranded DNA viruses
Replicate in nucleus of cells
Enveloped w/ numerous glycoprotein spikes
Develop LATENT infections
Initial infection usually asymptomatic

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31
Q

Describe HSV 1/2

A

Infection of oral genital or ocular epithelium
Hsv- 1 more associated with oral and ocular infection
Hsv-2 frequently associated with genitsl infections

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32
Q

Describe herpes simplex virus

A

ENVELOPED ds-DNA virus with ICOSAHEDRAL CAPSID

Genital herpes = most common STI world wide

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33
Q

Describe clinical manifestations of primary infrction HSV type 1

A 
Primary: 
Oral 
Genital 
Ocular 
Peripheral (dentists used to get this)
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34
Q

Describe clinical manifestations of HSV1 recurrent infection

A

Oral,ocular,genital,peripheral
Symptomatic
Asymptomatic shedding

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35
Q

What is herpes labialis

A

Cold sore
May be single or clustered
10-14 days
Treatment only necessary in immunocompromised patients

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36
Q

Describe HSV-2 infection

A

Not synonymous with genital herpes however:
Primarily infections of the genital tract
Neonates can be infected at delivery
Lesions do occur

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37
Q

Describe genital herpes

A

Many recognized first outbreaks may actually be reoccurrence

First episode tends to be more severe and longer in duration

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38
Q

Describe symptoms associated with genital Herpes

A

Fever, malaise, inguinal lymph node inflammation, headache, sometimes neck stiffness

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39
Q

Describe shedding for HSV 2

A

Reoccurrence more common
Asymptomatic shedding 28% of days
Shedding not completely suppressed by acyclovir

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40
Q

Describe shedding in HSV 1

A

Reoccurrence less frequent

Asymptomatic shedding does occur but less frequently

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41
Q

Describe neonatal herpes

A

In utero infection rare (does occur) intra partum (delivery) more likely
Primary infection in mum is highest risk
Asymptomatic shedding accounts for most transmission to infected neonates
Can be fatal if untreated

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42
Q

How is Herpes simplex diagnosed

A

Virus isolation

**PCR (nucleic acid amplification) especially with CSF to check for meningoencephalitis

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43
Q

Why is viral serology not a great diagnostic tool for Herpes simplex virus

A

70% have been exposed to HSV 1 so everyone is going to light up

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44
Q

How is HSV 1 & 2 treated?

A

Acyclovir: primary infections, prophylactic and immune compromised

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45
Q

Describe Epstein Barr Virus

A

Tranmission usually by saliva exchange
Virus has affinity for receptors on the surface of B cells
Viral infection results in local replication and a secondary viremia. There is proliferation of both b cells and T8 dubset of t cells

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46
Q

Describe the epidemiology of EBV infection

A

50% of 5 year olds have been infected
Children usually asymptomatic
Secon wave in teens more symptomatic
By 40 90-95% of adults have antibodies

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47
Q

What are clinical manifestations of EBV

A 
Infectious mononucleosis (MONO):
Illness lasts from 2-8 weeks, fatigue persists
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48
Q

What are symptoms of EBV

A 
Tonsilar enlargement 
Pharyngeal redness 
Cervic adenopathy
Large liver/spleen 
Skin rash esp. after ampicillin
49
Q

How is EBV diagnosed

A

Serology more common
Lymphocytes & monocytes increased
Low neutrophils and low platelets

50
Q

Treatment for EBV?

A

Usually supportive, treatment doesnt do much

51
Q

Describe cytomegalovirus

A

Infections occur more in socioeconomic groups
2 peaks: childhood, adulthood
Most adults (70%) are sero positive
All infections resukt in viral latency

52
Q

How is cytomegalovirus spread

A

Peri anal: intrauterine, cervix @ delivery, from breast milk
Saliva or close contact
Blood transfusion/organ transplant (RARELY)
During sexual inter course

53
Q

Describe CMV infection in older hosts

A

Asymptomatic

Some get mononucleosis like syndrome but heterophile antibody does not develop

54
Q

How is CMV diagnosed

A

Serology (determine immunity), molecular
Nucleicacid amplification
Virus isolation
Light microscopy

55
Q

How is CMV treated/prevented

A

Usually no treatment required

Antiviral (gancyclovir) and immunoglobulin therapy usually used to prevent and treat immune compromised host

56
Q

What is HIV

A

Retrovirus

57
Q

What are characteristics of retroviruses

A

Enveloped positive strand RNA virus, encodes reverse transcriptase (reverse transcribes DNA)
Replicate through a DNA intermediate
DNA copy is integrated into host chromosome to become a cellular gene

58
Q

Describe discovery of retrovirus

A

HIV-1 discovered 1981 by Gallo and Montagnier

HIV-2 discovered in west Africa

59
Q

How is HIV transmitted

A

Blood
Semen
Vaginal fluids

60
Q

What factors increase infectiousness of HIV

A

Primary infection - high viral load
Late stage - high viral load
Genital tract infections - mucosal breech and recruitment of inflammatory cells

61
Q

Describe HIV transmission in mother to baby

A

Mother to baby 1 in 4 (25%) without treatment

4% with treatment

62
Q

Describe replication of HIV

A

CD4 cells primary target
Mushroom shaped gp120 (protein on surface if HIV cell) interacts with CD4 surface molecule expressed on t helper lymphocytes and cells of the macrophage lineage
Reverse transcription after release
Copy of DNA produced
Integrsted into genome (integrase)
Each copy contains approx. 5 errors/mutations

63
Q

How does HIV enter the cell?

A

HIV enters the cell by fusion eith the cellular envelope

64
Q

Describe pathogenisis of HIV

A

HIV infection of CD4 lymphocytes results in cell death
CD4 primarily responsible for immunity
As CD4 cells are lost opportunistic infections and malignancies occur
Other cells survive and can store virus

65
Q

What are CD4 cells

A

One of the most important immune cells

Primarily responsible for cell mediated immunity

66
Q

What clinical syndromes can occur as a result of HIV

A 
AIDS
Toxoplasmosis 
Cryptococcal meningitis
Pneumocystis pneumonia 
Aids related dementia 
Wasting syndrome 
Karposi sarcoma (end stage)
Lymphoma 
Cervical cancer
67
Q

What are aids defining illnesses

A

Toxoplasmosis
Cryptococcal menigitis
Pneumocystis pneumonia

68
Q

How is HIV diagnosed

A

Serology (antibodies): WESTERN BLOT
Immunologic studies (CD4 counts)
Viral load testing (pcr quantification of RNA in plasma)
Resistance genotyping

69
Q

Describe western blot

A

Serology test method

Less sensitive more specific

70
Q

What is the biorad geenius

A

Differentiates HIV1 and HIV2
Rapid (~30min)
Removes subjectivity

71
Q

What are the goals of HIV therapy?

A

Durable supression of viral load
Restoration/preservation of immune function (CD4 count)
Improvement of quality of life
Reduction of mortslity
Preservation of future trestment options (simple treatment)

72
Q

How is HIV Treated

A

Anti retrovirals: nucleoside analogs, protease inhibitors fusion inhibitors integrase inhibitors

Usually Highly Active Anti Retroviral Therapy (HAART)

73
Q

What is HAART

A

Highly Active Anti Retroviral Therapy

74
Q

Describe risk of needle stick exposjre

A

Risk depends on stage of patients disease and how much blood

75
Q

Describe post HIV needle stick steps

A

Confirm patient status
Document your status
Begin prophylaxis WITHIN 72 hours!!

76
Q

What is chance of getting HIV from needle stick

A

0.3%

77
Q

What are the 5 types of hepatitis

A 
A: fecal oral transmission 
B: sexual fluids& blood to blood
C: blood to blood
D: travels with B; need B 
E: fecal oral transmission
78
Q

Describe the hep A virus

A

A PICORNAVIRUS; single stranded, naked, icosahedral
Spread almost always by fecal oral spread; either person to person or food contamination
Very common in developing countries
Sporatic usually but can cause outbreaks

79
Q

What is the incubation period for Hep A

A

2-4 weeks

Most cases are asymptomatic therefore jaundice only tip of the iceberg

80
Q

Does Hep A produce a chronic carrier state?

A

Hep A does not produce a chronic carrier state and has no long term sequelae. Meaning you get Hep A then recover

81
Q

How is Hep A diagnosed?

A

Disgnosis is confirmed by demonstrating the appearance of IgM antibodies

82
Q

How is Hep A prevented?

A

Vaccine!! (Twinrex):
Usually for travellers, healthcare workers etc
Immune globulin (antibodies) post infection when you need instant protection

83
Q

Describe Hep B

A

A double stranded HEPADNAVIRUS (DNA virus)

Patients who become carriers may develop a chronic active or persistent hepatitis

84
Q

How is Hep B transmitted?

A

Parenteral, perinatal and sexually

85
Q

How infectious is Hep B?

A

Very infectious!! 30% of needle stick injuries resukt in infection for non immune individuals

86
Q

What is the rule of three?

A

Needle stick risk:
0.3% HIV
3% for Hep C
30% for Hep B

87
Q

How common is Hep B

A

Very common
350,000,000 carriers
1,000,000,000 have serologic evidence of past infection

88
Q

Describe Carrier state for Hep B

A

Chances of developing carrier state depend on age of infection
Younger (neonates) most likely to have carrier state

89
Q

What are some consequences of chronic Hep C

A

No/minimal liver injury
Chronic active Hepatitis
Cirrhosis of liver (failure/hypertension)
Hepato-cellular carcinoma

90
Q

How is Hep B treated and prevented

A

Post exposure prevention for needle stick = HBIG VACCINE
Vaccine: universal for kids
Treatment with lamivudine for chronic hepatitis

91
Q

How is Hep B diagnosed

A

Detection of surface antigen in patients serum (HBsAg)
Detection of antibodies to hep B antigen: evidence of old infection or vaccine immunity
Liver biopsy

92
Q

Describe Acute Hep B

A

Surface antigen increases and decreases as virus does

Develop antibody to surface antigen & anti HB

93
Q

Describe Chronic Hepatitis B infection

A

Lots of surface antigens and anti HBE antibodies

No antibodies for surfave antigens unless patient is treated then you see SOME

94
Q

If a patient js HBsAG positive

Anti HBsAG negative and ANTI HB core positive what is the likely interpretation of these results

A

They have a chronic infection

95
Q

If a patient js HBsAG negative

Anti HBsAG positive (>10IU) and ANTI HB core negative what is the likely interpretation of these results

A

They have vaccine induced antibodies and are protected

96
Q

If a patient js HBsAG negative

Anti HBsAG positive (>10 IU) and ANTI HB core positive what is the likely interpretation of these results

A

Previous natural infection and are protected from future infection

97
Q

If a patient js HBsAG negative

Anti HBsAG positive (<10IU) and ANTI HB core negative what is the likely interpretation of these results

A

Vaccine induced antibodies but failed vaccine series

98
Q

What does it mean if a patient has less than 10 (>10) International units (IU)

A

They failed their vaccine series

99
Q

What does it mean if a patient is HBsAg positive

A

They have a chronic hep B infection

100
Q

Describe Hep C

A

Small ENVELOPED RNA virus (flavivirus)

Usually parentally transmitted although less infectious than HBV (3% needle prick)

101
Q

How does Hep C usually occur?

A

Usually occurs as sporadic disease in IV drug users, not as common sexual transmission, 75% mild or asymptomatic

102
Q

What js the incubation period for Hep C

A

2-20 weeks

103
Q

What are potential risks of Hep C infection

A

40-60% may get chronic liver disease, much higher than HEPB
20% may develop cirrhosis
Cancer may develop

104
Q

How is Hep C diagnosed

A

Typically qualitative pcr (detects viral RNA)

recombinant immunoblot assay (RIBA)

105
Q

How is Hep C treated and prevented?

A

No vaccine
Good public health measures
New hep C drugs >95% cure; largest breakthrough

Used to use interferon

106
Q

Describe Hep D

A

Rare infection due to incomplete RNA virus that requires presence of Hep B
Found mostly in IVDUS
Concurrent infection may be more severe

107
Q

Describe Hep E

A

A calivivirus (rna)
Almost never seen in north america
Fecal oral spread, lack of chronicity, low fatality rate

108
Q

What is 16s rRNA

A

Essential gene common to all bacteria
Codes for small ribosomal units
Gene evolves at a very low rate so little mutation seen

109
Q

How does 16s gene testing work

A

Perfectly conserved unchanging ateas of gene
Primers bind to conserved areas look for divergence in 16s rRNA

Only works on single bacteria type

110
Q

Describe 16s rRNA gene sequencing

A

Molecular diagnosis
Pcr primers anneal to conserved regions
Any organism present will be amplified
Amplicon will contain several variable regions

111
Q

What are some advantages of 16s rRNA gene sequencing

A

No need for viable organisms
Detection/identification of organisms in “partially” treated patients
Detection of slow growing or non growing organisms

112
Q

What are some disadvantages of 16s rRNA gene sequencing

A

Only useful from normally sterile sites (monomicrobial)
Contamination significant problem
May take a week to obtain identification

113
Q

Why do we use typing systems

A

To determine if a series of isolates obtained from epidemiologic cluster are clonally related

114
Q

What are benefits of typing systems

A 
Ease of interpretation 
Reproducibility 
Ease of performance 
Discriminatory power
Cost
115
Q

What are phenotypic systems

A

Bio typing
Antibiograms
Phage typing
Serotyping

Based on presence of metabolic or biologic activities

116
Q

What are genotypic typing systems

A

Molecular
Substantial generic diversitt within microbial species
Evoluntionary divergence

117
Q

What is pulsed field gel electrophoresis

A

System of electrical currents

118
Q

What is whole genome sequencjng

A

Most pulsed field moved to whole genome sequencing

MICI Module 2 (3 decks)

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