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Micro/Immuno > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

_______ was instrumental in developing the field of virology and expanding the field of biology

A

Bacteriophages

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2
Q

First animal viruses discovered

A

Foot and mouth disease

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3
Q

First human virus discovered

A

Yellow fever virus

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4
Q

Viruses replicate when

A

Provided a host

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5
Q

Viruses are _____ ______ parasites

A

Obligate intracellular

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6
Q

Viruses are not

A

Autopoietic

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7
Q

Viruses are ____in nature

A

Ubiquitous

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8
Q

Theories of Virus origin: Cellular Origin

A

Proposes that viruses were once cellular components but over time they evolved separately

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9
Q

Theories of virus origin: Autopoietic origin

A

Proposes that viruses once entities became dependent on cells for replication

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10
Q

Attributes for virus classification

A 
Virus particle structure
Genome
Replication features
Serology
Stability
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11
Q

Virus particle structure

A

Composition
Shape
Size

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12
Q

Nucleocapsid

A

RNA or DINA in a core that is protected by a protein coat

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13
Q

Virus is defined by the ______ structure

A

Nucleocapsid

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14
Q

3 Nucleocapsid structural symmetry

A

Helical
Pleomorphic
Icosahedral

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15
Q

Nucleocapsid is comprised repeating

A

Protein subunits=capsomerese

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16
Q

Capsomeres

A

Comprised of repeating protein subunits

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17
Q

Virus envelopes

A

Virus modified cellular membranes acquired upon ext from host

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18
Q

Exposure of virus envelope to lipid solvents

A

Renders enveloped viruses noninfectious

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19
Q

Enveloped viruses may

A

Have nucleocapsids with different structures

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20
Q

Smallest virus particle structure size

A

18 nm

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21
Q

Largest virus particle structure size

A

300 no

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22
Q

Viruses Genome : DNA

A

Double stranded

Single Stranded

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23
Q

Virus Genome: RNA

A 
Double stranded
Single Stranded
-Plus sense (+)ssRNA
-Minus sense (-)ssRNA
-Ambisense
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24
Q

Virus Genome: Structure

A

Linear
Circular
Segmented
Diploid

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25
Q

Virus Replication

A 
Attachment
Entry
Transcription
Translation
Replication
Assembly
Release
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26
Q

Virus cellular receptors

A

Signaling molecules-induced cellular response to binding
Cell adhesion
Transport

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27
Q

Viral receptors

A

Usually do not mimic cell receptors normal ligand
Typically are spike like projections on particle surface
May require a co-receptor

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28
Q

Genetic engineering can change

A

Receptor recognition

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29
Q

Integrin RGD sequence

A

Used by Ad, engineered into lambdaphage

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30
Q

Pseudotyping particles

A

Improve retroviral entry, VSV, Ebola, LCMV

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31
Q

Attachment is a major of virus ______

A

Tropism (host range)

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32
Q

Viruses infect

A

essentially all known life forms

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33
Q

Zoonosis

A

Specific host ranges, some can infect humans and animals

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34
Q

Virus infection not shared

A

Across divergent hosts ranges

Plants
Bacteria
Fungi

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35
Q

Smallpox

A

Only humans

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36
Q

Yellow fever

A

Mosquitoes and humans

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37
Q

Host range is a major factor in

A

Eradication

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38
Q

Nonenveloped virus entry

A

Not well understood

Pores:picornavirus
Membrane disruption: adenovirus reovirus

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39
Q

Virus entry

A

Receptor mediated endocytosis

Direct penetration of plasma membrane

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40
Q

Enveloped virus entry

A

Membrane fusion

Best understood fo influenza
Receptor conformational change
-low pH
-Receptor induced

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41
Q

Influenza entry

A

Enveloped

HA protein -attachment and fusion

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42
Q

Virus Uncoating

A

Nuclear replication

Cytoplasmic replication

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43
Q

Nuclear replication

A

Genome and remaining protein coat transported to the nuclear membrane

Delivery of genome to nucleus

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44
Q

Cytoplasmic replication

A

Release of the genome in cytoplasm

Transportation of the genome to intracellular site of replication—man RNA viruses replicate in membrane associated complexes

dsRNA viruses never relates their genomic material from the entering particle

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45
Q

Transcription-Virus replication

A

Production of messenger RNA templates for protein synthesis

DNA viruses usually rely upon cellular RNA polymerase

There are a variety of strategies used to subvert the cells transcription

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46
Q

The genome of +ssRNA virus an serve as

A

mRNA

Production of new transcripts can occur later using a (-)ssRNA template

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47
Q

(-)ssRNA, dsRNA viruses must bring their own

A

Polymerase into the cell

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48
Q

Translation-virus

A

Production of proteins

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49
Q

All viruses need the cells ribosome to produce

A

protein

-no exceptions

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50
Q

Viral protein production can be regulated at the

A

transcript (mRNA) level or translation level

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51
Q

Structural proteins are produced

A

in high quantities

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52
Q

Non-structural proteins are only seen

A

inside the infected cell

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53
Q

Genome replication objective

A

Make additional genome copies

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54
Q

Genome replication : (+)ssRNA

A

Genome serves as template for translation

Polymerase makes (-)ssRNA copy as template for new genomes

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55
Q

Genome replication : (-)ssRNA

A

Virus made particle must include the viral polymerase
Polymerase makes messenger RNA for translation
Genome replication through full length (+)ssRNA intermediate

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56
Q

Genome Replication: dsRNA

A

Virus particle includes viral polymerase
dsRNA induces innate immune response so genome stays inside particle
mRNA synthesized in particle and exported to cytoplasm
mRNA serves as (+) strand in virus genome, (-) strand synthesized during assembly

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57
Q

Genome Replication: ssDNA and dsDNA

A

Must gain access to the nucleus
-poxviruses are an exception virion contains the necessary RNA polymerase and the genome encodes the DNA polymerase for replication

Prepare the cell for DNA replication
-growth phase dNTP production replication machinery

Ensure genome ends are copied

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58
Q

Virus replication assembly

A

Package new genomes into functional particles

Localize strucutral proteins to aid assembly
-cellular viral factories

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59
Q

Genome contains

A

Packaging signals

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60
Q

Assembly mechanisms: Adenovirus

A

Empty protein coats imports genome

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61
Q

Assembly mechanisms: Reovirus

A

RNA packaged during capsid assembly

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62
Q

Assembly mechanisms: Retrovirus

A

Preassembly on a membrane

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63
Q

Lysis

A

Best known for bacteriophage

Viral molecules that rupture cellular membrane

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64
Q

Weak lysis

A

Depends on membrane breakdown after cell death

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65
Q

Budding

A

Enveloped only

Enveloped viruses use cell membranes as the out coat of the virus particle

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66
Q

One step growth cure

A

Infect every cell at same time

Every cell dies at end of infection

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67
Q

Replication phases

A

Eciplise -attachment and uptake

Exponential growth - replication and assembly

Plateau-cell death

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68
Q

Useful to assess

A

Mutations
Cell entry
Process design

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69
Q

Time for one step growth

A

Start of infection to beginning of plateau

Bacteriophage 30 min

Vesicular stomatitis virus 6 hours

Vaccinia 24 hours

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70
Q

Productivity

A

Measure application

VSV 1: 1000
Vaccinia 1: 100

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71
Q

Principal of detection and quantification methods

A

Infectvity
Physical
Genome
Serological

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72
Q

Infection assays: Cytopathic effect

A

Cell rounding
Syncytia formation
Inclusion bodies

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73
Q

Infection assays: Fluorescent focus assay

A

Infect cells
Expose virus antigen
Stain with labeled antibody
Count areas that fluoresce

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74
Q

Infection assays: Plaque assay

A

Cell monolayer
Inoculate with dilute virus
infected cells die leaving a clear area-plaque

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75
Q

Infection assays: Infectious dose

A

Tissue cultures, eggs, animals

Inoculate with different dilutions of virus
Calculate concentration based on number infected

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76
Q

Particle assays: Electron microscopy

A

Direct image of virus particles

Calibrate with latex bead standard

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77
Q

Particle assays: hemagglutinin assay

A

Viruses that bind red blood cells
Mix contestant number of RBCs with various virus dilutions

If virus concentration is sufficient a matrix of RBCS and virus is formed

Matrix does not allow RBCs to pellet

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78
Q

Genome Assays: PCR

A

DNA primary specific to virus

Amplify the gene

Very sensitive

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79
Q

Genome Assay: Southern DNA and Norther RNA blots

A

Isolate DNA or RNA
Seperate by electrophoresis
Used labeled DNA probe to detect

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80
Q

Serological Assays: Virus neutralization

A

Antibody binding to virus can block infection

Virus concentration determined by amount of antibody needed

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81
Q

Serological Assays: Enzyme link immunosorbant assay

A

Antibody recognition of virus

Amplification by enzyme linked to antibody

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82
Q

Serological Assays: Western blot

A

Separate proteins by electrophoresis

Probe proteins by using an antibody

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83
Q

Poxvirdae

A

Small pox
Vaccinia

dsDNA

Enveloped-brick shaped

Cytoplasm replication

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84
Q

Filovirdae

A

Marburg
Ebola

(-)ssRNA

Enveloped-filamentous

Cytoplasm replication

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85
Q

Arenaviridae

A

Kasa
Junin
Matchups
LCMV

Segmented ambisense ssRNA

Enveloped pleomorphic

Cytoplasm

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86
Q

Flaviviridae

A 
Yellow fever
Dengue fever
West Nile
JE
St. Louis E

TBE

(+)ssRNA

Enveloped spherical

Cytoplasm enveloped gained internally

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87
Q

Orthomyxovidrade

A

Influenza

8 segments (-)ssRNA

Enveloped

Nucleus replication

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88
Q

Togaviridae: alphavirus

A 
EEE
WEE
VEE
Is dubs
Semliki Forest
Chikungunya

(+)ssRNA

Enveloped spherical

Cytoplasm enveloped gained by budding

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89
Q

Reoviridae

A

rotavirus, blue tongue, reovirus

segmented dsRNA

Non-enveloped-spherical

Cytoplasm replication

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90
Q

Coronaviridae

A

SARS
(+)ssRNA
enveloped – protein crown

cytoplasm – subgenomic RNA

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91
Q

Retroviridae

A

murine leukemia virus, HIV

(+)ssRNA – two copies per virion

enveloped - spherical

nucleus – reverse transcription

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92
Q

Picornaviridae

A

poliovirus, rhinovirus

(+)ssRNA

non-enveloped - spherical

Cytoplasm replication

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93
Q

Adenoviridae

A

Adenoviridae 5

dsDNA

Adenoviridae

Nucleus replication

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94
Q

Bunyaviridae: Phlebovirus

A

Rift Valley Fever, Crimean Congo

3 segments
ssRNA, ambisense

enveloped - spherical

Cytoplasm replication

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95
Q

Bunyaviridae: Hantavirus

A

Hantavirus

3 segments (-)ssRNA

Enveloped spherical
Cytoplasm replication

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96
Q

Measles Virus virion and genome

A

Paramyxovirus

Genome (-)ssRNA

Virion: enveloped

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97
Q

Measles proteins

A 
L-polymerase
P-phosphoprotein
H-hemagglutinin
F-Fusion
M-Matrix
N-Nucleocapsid
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98
Q

Measles virus replication

A

Replication in the cell

Fusion protein causes syncytia formation

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99
Q

Measles transmission and incubation

A

Inhalation of aerosolized droplet

10-14 days incubation period—primary infection in respiratory epithelial tissues—>primary viremia

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100
Q

Measles symptom onset

A

Coincides with second round of virus replciation.

Occurs in LN, tonsils, lungs, GI tract, and spleen—-> secondary viremia

Recover 20 days after infection

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101
Q

Characteristic rash of Measeles

A

Virus and immune response damage to epithelial and endothelial cells

Koop like spots

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102
Q

Measles Complications: Immune suppression

A

Interference with CD46 and signaling lymphocyte activation molecule (SLAM) receptors

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103
Q

Measles Complications: Opportunisitic infections

A

Strep. Pneumoniae

Staph. Aureus

Haemophilus influenzae

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104
Q

Measles Complications

A

Blindness in Vitamin A deficient children

Acute disseminate encphalomyelitis

Subacute sclersoing panencephalitis

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105
Q

Measles Diagnosis

A 
Fever
Cough
Cortazzo
Conjunctivitis
Koplik spots

Lab:
Virus isolation in culture
Serology
ELISA, RT-PCR

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106
Q

Measles Prevention

A

One of the most contagious diseases known

People are infections 2-3 days prior to rash

Humans are only host

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107
Q

Measles Prevention

A

Vaccination

  • Primary option
  • life long immunity
  • Live attenuated vaccine
  • Safe

Provide vitamin A can reduce severity

No antiviral

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108
Q

Respiratory Syncytial Virus Genome and Virion

A

Paramyxovirus

Genome: (-)ssRNA
Virion: enveloped

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109
Q

Respiratory Syncytial Virus Proteins

A 
L-polymerase 
G-glycoproteins 
F-Fusion
M-Matrix
P-phosphoprotein
N-Nucleocapsid
NS1&NS2-replication and immune response
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110
Q

Respiratory Syncytial Virus: replication

A

Replication i n the cell
-similar steps as for measles virus

Infects ciliated cells in respiratory tract epithelium

Fusion protein creates syncytia

Virus buds from cellular surface

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111
Q

Respiratory Syncytial Virus: Infection

A

By inhalation of aerosol, fomites

Virus replication limited to respiratory tract

4-5 incubation

1-3 lower respiratory tract after upper

7-12 days recovery after symptoms onset

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112
Q

Respiratory Syncytial Virus that infects humans….

A

Does not infect other animals—no animal reservoir

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113
Q

Respiratory Syncytial Virus infections does not

A

Yield life long immunity

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114
Q

Respiratory Syncytial Virus infection is limited to

A

Respiratory tract epithelial cells where IgA response is short lived.

Low cytoxicity thought to result in slower immune response

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115
Q

Respiratory Syncytial Virus Risk factors for infection

A

Attending day care

School age siblings

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116
Q

Respiratory Syncytial Virus risk for more sever disease

A

Premature birth

Male

Second hand exposure to tobacco

Lack of breast feeding

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117
Q

Respiratory Syncytial Virus Prevention

A

Ribarvirin administered by inhalation

No Vaccine

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118
Q

Respiratory syncytial virus: passive immunoprophylaxis

A

Palivizaumab-humanized monoclonal antibody

  • Targets F protein
  • Given IM once a month
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119
Q

Varicella Zoster genome and virion

A

Alphaherpesvirus

Genome: dsDNA (large)
Virion: enveloped

Hundreds of proteins

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120
Q

Varicella Zoster: replication in the cell

A

Active cell for replication

Resting cell (neuron)-latent infection (circular genome)

Infects neighboring host cells first

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121
Q

Varicella Zoster: Chickenpox

A

INfection through inhalation of aerosolzied droplets

10-21 incubation period

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122
Q

Varicella Zoster: symptoms

A

Fever, malaise, headache

Rash 1-2 days after onset

Rash progresses 3-6 days

Rash on scalp face trunk

Recover by 2 weeks—cell mediated immunity most important

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123
Q

Varicella Zoster: Latent reactivation

A

Shingles

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124
Q

Chickenpox Prevention: vaccination

A

Primary option
Life long immunity
Live attenuated vaccine

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125
Q

Chickenpox Prevention: Antivirals

A

Acyclovir

  • interferes with genome replication
  • can not elimante latent virus
  • Does not prevent infection of cells
  • Drug resistance is being observed
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126
Q

Poliovirus Genome and virion

A

Genome: (+)ssRNA
Virion: Non Enveloped

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127
Q

Poliorvirus proteins

A

Capsid-VP1, VP2, VP3, VP4

Non-structural-proteases, polymerase, others

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128
Q

Poliovirus replication

A

In cell after ingestion of material containing virus

Virus particle creates pore in cell membrane

Genome serves as mRNA

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129
Q

Poliovirus primary replication

A

In Peters patches of small intestine

-minor viremia

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130
Q

Poliovirus secondary replication

A

Major viremia

Mild disease
Fecal shedding of virus for 6 weeks

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131
Q

Poliovirus: CNS involvement

A

1:200 of infections

Virus replications in gray matter of brain and spinal cord

  • limb paralysis from anterior horn cell damage
  • respiratory paralysis from damage to medulla oblongata
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132
Q

Poliovirus Prevention

A

Vaccination
Salk-killed
Sabin-live attenuated

Humans , no animal reservoir

targeted for eradication

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133
Q

Rotavirus Genome and Virion

A

Genome: dsRNA, 11 segments

Virion: non-enveloped

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134
Q

Rotavirus Proteins

A

VP1-polymerase
VP2-RNA binding
VP3-Transferase
VP4-attachment and fusion

Other structural and non structural proteins

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135
Q

Rotavirus replication

A

In cell

Membrane disruption

Genome never exposed

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136
Q

Rotavirus the disease

A

Infection by ingestion of material contains the virus

2 days incubation -vomiting and fever
2-3 days- diarrhea —3-8 days in duration

Virus shedding for weeks before symptom onset and days after recovery

Severe disease most common in 6 to 24 month old children

Diagnose by antigens in stool

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137
Q

Rotavirus Prevention

A

Infant vaccines available

No antivirals

Hygeine

treatment -oral rehydration

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138
Q

Mumps virus

A

Paramyxovirus

Mumps

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139
Q

Rubella virus

A

Togaviruses

German measles

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140
Q

Parvovirus b19

A

Parvovirus

Fifth disease

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141
Q

Human Herpesvirus-6

A

Betaherpesvirus

Roseola

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142
Q

Virus infection of the liver

A

Hepatitis viruses

Primarily infect and replicate in hepatocytes

Liver damage from virus and host response

Some cause acute infections some cause chronic infections

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143
Q

Hepatitis B Virus: Genome and virion

A

Genome: dsDNA (smallest genome of the human viruses)

Virion: enveloped

Hepadnaviridae

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144
Q

Hepatitis B Virus: Proteins

A 
HBsAG-S-virion assembly
HBsAG-M-?
HBsAG-L-Cell attachment
HBcAG- capsid
POL-reverse transcriptase
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145
Q

Hepatitis B Virus cannot be

A

Grown in cell culture

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146
Q

Hepatitis B Virus genome has a ____ intermediate

A

RNA

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147
Q

Hepatitis B Virus cccDNA is

A

Template for transcription

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148
Q

Hepatitis B Virus requires

A

Liver specific transcription factors

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149
Q

Hepatitis B Virus produces many

A

Empty particles

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150
Q

Hepatitis B Virus: infection

A

Sexual and drug use

30-180 day incubation period

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151
Q

Hepatitis B Virus: symptom onset

A 
General malaise
Anorexia
Vomiting 
Fatigue
Cough
Serum like sickness

Jaundice
Elevated alanine transaminase levels

3-4 months recovery after jaundice

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152
Q

Hepatitis B Virus: chronic disease

A

Sporadic episodes of hepatitis

Cirrhosis of the liver

Increased risk for hepatocullar carcinoma

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153
Q

Hepatitis B Virus: Vaccination

A

First recombinant vaccine approved for use in humans

requires multiple inoculations

Not effective against chronic infection

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154
Q

Hepatitis B Virus: treatment for chronic cases

A

Interferon alpha therapy

Nucleoside analogs: Adefovir, Iamivudine, tenofovir

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155
Q

Hepatitis D Virus

A

Subviral Agent

Rare in human viruses

Only other example is Adeno-associated virus which requires adenovirus infections

Requires active HBV infection

RNA genome encodes a single protein

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156
Q

Hepatitis C Virus: Genome and Virion

A

Genome : (+)ssRNA

Virion: enveloped

Flaviviridae

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157
Q

Hepatitis C Virus: Proteins

A

E1/E2 attachment and entry
C: core
Various non structural

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158
Q

Hepatitis C Virus: replication

A

Genome passed into cytoplasm

Genome template for translation
-missing cap, ribosomes, recognize internal ribosome entry sites

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159
Q

Hepatitis C Virus: symptoms

A

Typically milder signs and symptoms than observers for HBV

Chronicle infection are much more common

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160
Q

Hepatitis C Virus: Extrahepatic disease

A

Mixed cryoglobulineima

Antibody and virus complexes despot in other tissues eliciting an immune response and subsequent tissue damage

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161
Q

Hepatitis C Virus: treatment

A

No vaccine

Zepatier can treat some genotypes

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162
Q

Hepatitis A Virus

A

Recalls contaminated water
-absorbed through intestine and moves to liver via portal system

15-40 day incubation

Symptoms:
Consistent with hepatitis infection: malaise anorexia vomiting jaundice
More severe in adults than children
Resolves approximately 8 weeks post infection

Prevention
-Vaccine

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163
Q

Hepatitis E Virus

A

Causes Foodborne and waterborne hepatitis

Disease is very similar to that caused by HAV distinguished by serology

Infection can be life threatening for pregnant women

No prevention available
-vaccines are under development

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164
Q

HAV Summary

A

15-40 day incubation

Asymptomatic

No chronic infections

No long term sequelae

Fecal oral, Sexaul, parenteral

(+)ssRNA
Nonenveloped
Picornavirdiae

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165
Q

Hep A Genome virion

A

(+)ssRNA
Nonenveloped
Picornavirdiae

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166
Q

Hep B Genome and Virion

A

Circular dsDNA

Enveloped

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167
Q

Hep C Genome and Virion

A

(+)ssRNA

Enveloped

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168
Q

Hep delta Genome and Virion

A

(-)ssRNA

Enveloped

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169
Q

Hep E Genome and Virion

A

(+)ssRNA

Nonenveloped

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170
Q

HAV route of transmission

A

Fecal
Sexual
Parenteral

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171
Q

HBV transmission

A

sexual
Vertical
Parenteral

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172
Q

HCV transmission

A

Sexual
Vertical
Parenteral

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173
Q

HDV transmission

A

Sexual
Vertical
Parenteral

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174
Q

HEV

A

Fecal oral
Sexual
Parenteral

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175
Q

HBV

A

Asymptomatic often
Chronic yes
Long term sequelae yes

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176
Q

HCV

A

60-120 days
Asymptomatic often
Chronic yes
Long term sequelae yes

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177
Q

HDV

A

60-180 days
Asymptomatic possible
Chronic yes
Long term sequelae exacerbation of HBV

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178
Q

HEV

A

21-42
Asymptomatic often
Chronic no
Long term sequelae no

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179
Q

Eastern equine encephalitis

A

Togaviridae

(+)ssRNA
Enveloped

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180
Q

Venezuelans equine encephalitis

A

Togaviridae

(+)ssRNA
Enveloped

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181
Q

West Nile

A

Flaviviridae

(+)ssRNA
Enveloped

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182
Q

Rabies

A

Rhabdoviridae

(-)ssRNA
Enveloped

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183
Q

Select togaviruses and flaviviruses are transmitted through

A

A vector

Arthropod transmission

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184
Q

Arthropod transmission: common vectors

A 
Mosquitoes
Aides
Culiseta
Culex
Ticks
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185
Q

Arthropod transmission: Reservoirs

A

Birds

Small mammals

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186
Q

Transmission requires _____ in vector

A

Replication

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187
Q

_______ determined by vector and reservoir habitat

A

Geographic location

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188
Q

EEE and VEE virus biology

A

Togaviridae
Togaviridae

(+)ssRNA
Enveloped

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189
Q

EEE and VEE proteins

A

E1 and E2: cell attachment and entry

Capsid protein

Various non structural proteins

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190
Q

EEE and VEE virus is introduced

A

Through he bite of an infected arthropod

Infects cells locally and carried by larger hands cell to LN

Replication and release into blood stream

Infection in other target organs such as CNS

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191
Q

Encephalitis Disease

A

Fever
Headache
Irritability vom
Diarrhea convulsions coma

1/3 of encephalitis cases die from disease 2-10 days after onset

Those who recover can have long term sequelae
-seizures, personality disorders, paralysis

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192
Q

West Nile Virus Disease

A

Incubation 2-14 days
Most asymptotic

20% fever headache fatigue

Neuroinvaise less than 1%

Aseptic meningitis, encephalitis, flaccid paralysis altered mental state tremors

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193
Q

West Nile Prevention and Control

A

No approved vaccine
No treatment
Mosquito control
Repellant

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194
Q

Main transmitters of west Nile

A

Culex sp.

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195
Q

Zika Virus

A

Flavivirus
Envelope;d
RNA genome

Hosts:
Life long infections in mosquitos

Transient infection in primates rodents

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196
Q

Zika Fever

A

Resemble dengue fever
Lasts several days, fever, red eyes, joint pain, rash

Transmitted by mosquitoes possible via sex, blood transfusion vertically

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197
Q

Zika complications

A

Gillian barre syndrome- autoimmune disease attacking autonomic nervous system

New born microcephalic

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198
Q

Rabies Virus

A

Rahabdoviridae

-ssRNA
Enveloped

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199
Q

Rabies Proteins

A 
N-nucleoprotein
P-phosphprotein
M-matrix
G-gylcyoprotein
-attachment and entry
L-polymerase
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200
Q

Rabies has broad

A

Tropism

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201
Q

Rabies replicates

A

In cytoplasm only

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202
Q

Rabies genome order dictates

A

Abundance of transcripts and proteins

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203
Q

Rabies binding of N to

A

RNA triggers genome replications

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204
Q

Rabies frequently produces

A

Defective interfering particles

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205
Q

Rabies reservoir

A

Bats
Skunks
Raccoons

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206
Q

Rabies transmission

A

15% bite

60% if on face or head

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207
Q

Rabies spread

A

Replicates locally until it finds neurons

Moves passively in axoplasm of peripheral nerves to spinal ganglia spinal cord and brain

Spreads back to periphery highly inner gated salivary glands and replicates

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208
Q

Rabies symptoms

A

Pricking or itching where bitten fever headache

Hydrophobia-difficulty swallowing even saliva leads to foaming

Cerebral dysfunction anxiety confusion delirium halucatnoiinms insomnia

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209
Q

Rabies outcome

A

Once symptoms appear disease is nearly always fatal

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210
Q

Rabies prevention and control

A

Vaccine available

Post exposure prophylaxis
-4 doses

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211
Q

Spumaviruses

A

Do not cause human disease

Makes foamy structures inside the cell

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212
Q

Two families of retroviridae

A

Orthoretroviridae

Spumaviridae

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213
Q

Retroviridae genome

A

+ssRNA

Enveloped

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214
Q

Retrovirus Proteins

A

Reverse transcriptase
(RNA—>DNA, DNA—>DNA)

Integrate
Protease

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215
Q

Retroviruses were character by ______ & ———-

A

Nucleocapsid structure

Location in the particle

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216
Q

_____ now used to classify retroviruses as simple or complex

A

Genome contents

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217
Q

Simple retroviruses

A

Only encode the Gag, Pro, Pol and Env genes

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218
Q

Complex retroviruses

A

Encode
Gag
Pol
Env and more genes

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219
Q

Retroviruses Replication Cycle

A 
Attachment
Entry
Reverse Trasncritpion
Integration
Transcription from provirus
Translation
Assembly
Release
Maturation-protease activity
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220
Q

Reverse transcription

A

SsRNA genome to dsDNA

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221
Q

Retroviruse replication integration

A

Virus dsDNA into host making provirus

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222
Q

Reverse Transcription

A

Defining feature of retroviruses

Initiates once nucleocapsid is in cytoplasm

  • need higher levels of NTPs present
  • Low NTP levels prevent reverse transcription

Occurs within a large complex similar to nucleocapsid

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223
Q

Infection cannot progress if___________ does not occur

A

reverse transcription

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224
Q

Reverse transcription is ____ between genome copies

A

Promiscuous

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225
Q

Reverse transcription silent when

A

Copies are identical

Many different recombination when different genomes are in the Virion

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226
Q

Retrovirus must access

A

The nucleus

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227
Q

Retrovirus access the nucleus during

A

Mitosis

Importation can also infect non dividing cells

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228
Q

_____ end processing of dsDNA

A

3’

Attack target DNA, nick created

Host repair

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229
Q

Retrovirus integration of virus DNA is

A

Permanent

No mechanism to remove it

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230
Q

If retrovirus is integrated into the germ-line then ________ is inherited and is called ______

A

Provirus

Endogenous

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231
Q

Retrovirus can also disrupt host genes to cause

A

Cancer or other diseases

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232
Q

Integration of retrovirus identified oncogenes (4)

A

Transcription factors
Secreted Growth factors
Growth factor receptors
Cell signal transduction pathways

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233
Q

Defective retroviruses

A

Many defective viruses are made during replciation

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234
Q

Defective retroviruses are missing at least one of

A

Gag
Pol
Env

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235
Q

Retroviruses require _______ to make progeny

A

Complementary infection

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236
Q

Many retroviruses infections are

A

Benign
Usually not cytopathic
Little impact to cell replication and physiology

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237
Q

Viruses are never

A

Eliminated by the host response

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238
Q

Slow Retroviruses

A

Ex. Leukemia viruses

Effect is like high level mutagenesis

Eventually results in tumorigenesis

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239
Q

Cytopathic Retroviruses

A

Minority of retroviruses carry cytopathic genes

Cause Tissue damage directly

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240
Q

Acute transforming Viruses

A

Induce rapid tumor formation
Carry host genes
Often replication defective because host gene replaces an essential gene

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241
Q

Human T cell Leukemia Virus (HTLV)

A

Four distinct types

Deltaretrovirus

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242
Q

HTLV-1 Transmission: Person to Person

A

Mother-child via breastfeeding
Sharing needles
Blood transfusions
Sexual transmission

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243
Q

HTLV-1 Transmission: Within Host

A

Highly cell associated

Primary mode for spread is contact between infected and naive cells

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244
Q

HTLV-1 Disease

A

Adult T cell Lymphoma/leukemia

Latent period of 30-50 years

Infects memory T cells, antigen activation triggers transcription of provirus. Virus Tax protein and others stimulate cell proliferation. Cells become transformed generating tumors
-with or without protein expression

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245
Q

HTLV-1 infected T cells enter

A

The CNS

Activate astrocytes microglial cells

Recruit inflammatory cells cause further tissue damage

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246
Q

HTLV-Assocaiated Myeolopathy (HAM)/(TSP) Tropical paraperisis

A

Shown to be the same

Onset typically 3 years after infection

Starts with bladder control issues

Proposes to lower back pain, leg weakness or stiffness in hips or knees

Men impotent

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247
Q

HAM/TSP treatment

A

Corticosteroids interferon yield temporary relief of symptoms

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248
Q

ATLL treatment

A

Treat the lymphoma with chemotheratpy regardless of HTLV infection

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249
Q

HIV

A

Two many types in humans

Lentivirus

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250
Q

HIV Disease

A

Latent Period for AIDS: 6 months to 25 years

Infection begins virus containing blood or bloody fluid to a mucosal surface or blood

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251
Q

HIV targets

A

memory T-cells (CD4+)

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252
Q

HIV initial acute infection

A

2 weeks after infection

Mucocutaneous ulceration and weight loss more indicative of HIV infection

GALT seeded as a result

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253
Q

HIV Chronic infection established

A

Ongoing virus replciation and T cell depletion

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254
Q

Influenza

A

Orthomyxoviridae

Segmented (-)ssRNA

Enveloped

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255
Q

Adenovirus

A

Adenoviridae

DsDNA

Non-enveloped

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256
Q

Rhinovirus

A

Picornavirus

+ssRNA

Nonenveloped

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257
Q

Three types of influenza virus

A

A, B, C

Type A is most common and associated with greatest concerns

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258
Q

Influenza Proteins

A 
HA-hemagglutinin, cell attachment
NA-Neuraminidase, viral budding and release
M1-Matrix
M2-Ion Channel
PB1,2, PA-Transcription complex
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259
Q

Influenza virus identified by

A

Surface antigens HA and NA

16 HA serotypes
9 NA serotypes

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260
Q

Avian vs Human Influenza Strains

A

HA major determinant and for human to human transmission

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261
Q

Influenza A uses a ____ ___

A

Animal reservoir

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262
Q

Influenza Type A attachment

A

Attachment by HA brings cell and virus membranes into proximity

Conformation change triggered after Cell attachment by pH change in endosome

Causes membrane fusion (B)

Model for all enveloped viruses

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263
Q

Influenza replication

A

Transcription and replication take place in nucleus

Protected genome escapes nucleus and buds from cell surface

NA critical to budding

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264
Q

Current circulating strains of influenza

A

H3N2 H1N1

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265
Q

Highly Pathogenic Avian Influenza

A

HPAI strains have multi basic residences at HA cleavage site allowing replciation throughout the body

Skin lesions
Necrotic and swollen combs
Systemic infection

H5 or H7 strains

266
Q

H5 and H7 strains can mutate to

A

HPAI strains

267
Q

Adenovirus

A

Adenoviridae

dsDNA

Nonenveloped

Proteins
Fiber-cell attachment
Penton base-cell entry
Hexon-capsid

268
Q

Adenovirus entry

A

Entry via coxsackie adenovirus receptor

PH triggered capsid disassembly
Moves to nucleus

269
Q

Adenovirus Gene expression 3 stages

A

Immediate-early:

Early
Later

270
Q

Adenovirus Gene expression: Immediate

A

E1A portion of genome

  • 2 transcriptional regulators
  • necessary to reach early stage
271
Q

Adenovirus Gene expression: Early

A

5 genome sections
E1B E2 E3 E4 and L1

DNA replciation and post transcriptional events

272
Q

Adenovirus Gene Expression: Late

A

Take over of cellular mRNA synthesis

273
Q

Adenovirus genome replication

A

Initiated on either end, indentical end sequences

Replication in 5->3 direction, one strand displaced

Displaced strand circulations to allow template copy to be made

Primed by the protein pTP unusual priming strategy

274
Q

Adenovirus cell regulation

A

DNA replciation occurs during S phase

Not all cells are actively replciation

275
Q

E1A inactives _______ leading to ___ _____ gene expression

A

PRb

S phase

276
Q

E1B inactivates ______ leading to _ __ and preventing ____

A

P53
S phase
Apoptosis

277
Q

Adenovirus E3 gene

A

Produces proteins important to evasion

Blocks MHC class I expression reducing CTL cell killing

Blocks TNF induced apoptosis

Blocks IFN-a IFN-b action keeping protein translation active

278
Q

Rhinovirus

A

Frequent cause of mild upper respiratory infections

Large antigenic diversity

  • over 100 serotypes
  • makes vaccine development impractical

Humans only known reservoir

279
Q

Rhinovirus attaches to

A

Intercellular adhesion molecule 1 (ICAM-1) or the very low density lipoprotein VLDL receptor

280
Q

Ebola

A

Filovirus

Polymorphic particle enveloped

RNA genome

Helical nucleocapsid

281
Q

Herpes Simplex Virus Type 1

A

Aphaherpesviridae

DsDNA

Enveloped

282
Q

Herpes Simplex type 2

A

Alphaherpesviridae

dsDNA

Enveloped

283
Q

Cytomegalovirus

A

Betaherpesviridae

DsDNA

Enveloped

284
Q

Epstein Barr Virus

A

Gammaherpesviridae

dsDNA

Enveloped

285
Q

Human Papillomavirus

A

Papillomaviridae

DsDNA

Nonenveloped

286
Q

Alphaherpesvirus

A

Variable host range
Short reproduction cycle
Rapid spread in culture

Efficient destruction of infected Cells

Capacity to establish latency in sensory ganglia

287
Q

HSV-1 Infection

A

Oral-oral
Oral-genital
Nearly 2/3 adults are seropositive

288
Q

HSV-2 Infection

A

Primarily genital-genital
oral-genital also possible
1/5 adults are infected

289
Q

Alphaherpesvirus infects

A

Epithelial cells in the skin or mucosa

Mucosa are more susceptible

290
Q

Latency of alphaherpesvirus

A

Stationary cells, genome circulizes and stays as an episode in the nucleus

Peripheral ganglia common site of laten infections

Triggers: Sunburn, systemic infection, immune impairment, stress

291
Q

Betaherpesvirus

A

restricted host range
Long reproductive cycle

Slow progression in cell culture

Enlargement of infected cells

292
Q

Gammaherpesvirus

A

Restricted host range

Targets T and B lymphocytes

Lyric infections

Latency in lymphoid tissues

Protypical member: Epstein Barr virus

293
Q

Burkett’s lymphoma

A

Most common childhood cancer in Africa

Tumor in jaw eye socket ovaries

In all cases, tumor cells have monoclonal EBV episode

Role of EBV unsure
-spur B cell growth, mutations or genes transform cells

294
Q

Hodgkins lymphoma

A

EBV associated carcinoma

3 types
NL-modular sclerosing
MC-Mixed cellularity
LD-Lymphocyte Depleted

295
Q

Beta/gammaherpesvirus immune evasion: Intrinsic

A

Blocks cell death inhibits apoptosis

296
Q

Beta/gammaherpesvirus immune evasion: Innate

A

Decreases NK cell activity Inhibit NK receptor activation

297
Q

Beta/gammaherpesvirus immune evasion: Adaptive

A

Decreased antigen presentation

Degrades MHC class I and II

Blocks MHC class II and T-Cell receptor interactions

298
Q

CMV persistence

A

Persist in hematopoietic progenitor cells and macrophages in vitro

Chronic persistent infection, not latency

Controlled by healthy, active immune system

299
Q

EBV persistence

A

Persistence of genome in memory B cells

Virus proteins ensure B cell proliferation and EBV genome replication

300
Q

Human papoillomaviurs proteins

A

L1-cell attachment

L2- Membrane penetration

301
Q

HPV gain access

A

Through abrasion of the skin then establish an infection in the basal layer.

Cell polymerase required for genome replication

Virus production in differentiating cells

Non-lyric virus, released wit dead cell shedding

302
Q

HPV: Oncogenesis

A

E7 blocks retinoblastoma protein-continued cell proliferation

E6 blocks the p53 tumor suppressor pathway

HPV requires actively replicating cells to replicate and produce progeny

303
Q

Antivirals block

A

Specific steps in the virus life

304
Q

Antivirals must be active against

A

Virus replcaitions but not normal celllular function to reduce toxicity

305
Q

Antivirals exploit

A

Structural function and genomic information to identify targets

306
Q

Enfuvirtide-HIV

A

Blocks remolding of gp41, inhibits membrane fusion

Prevents entry

307
Q

Amantadine & Rimantadine-influenza

A

Blocks influenza ion channel preventing nucleocapsid release at the end of the cell entry process

Prevents entry

308
Q

Nucleoside analogs

A

Chain terminators

Prevent genome replcaitions

309
Q

Acyclovir

A

treatment of herpesvirus

Prevent Genome Replication

Most effective against HSV-1 and HSV-2

310
Q

Ganciclovir

A

Effective against CMV more toxic due to interference with cellular kinases

Prevent genome replication

311
Q

Valganciclovir

A

Activity similar to acyclovir, improved oral biovalability

Prevents genome replcaition

312
Q

Foscarnet

A

Herpes virus treatment prevents genome replication

Prevents viral polymerase activity
IV administration
Toxic

313
Q

Nucleoside inhibitors of HIV and HBV

A

Good oral availability

Toxicity is an issue

Resistance often observed

HIV therapy usually includes more than one, including one from a different class

314
Q

Ribavirin

A

Inhibitor of RNA viruses prevent genome replication

Triphosphate form inhibits polymerase

Monophosphate form inhibits inosine monophosphate dehydrogenase lowering GTP in cell

Impairs capping of mRNA

315
Q

Maturation of progeny viruses often requires

A

Cleavage of virus polypeptide

316
Q

Immature progeny are not

A

Infection

317
Q

Ritonavir

A

HIV Treatment blocks cleavage of Gag-pol polypeptide

Boosts activity of other protease inhibitors because it also blocks the action of cellular protease that act on other viral protease inhibitors

318
Q

Antiviral challenges

A

Bioavailability
Specificity
Toxicity

319
Q

Interferons

A

Natural antiviral

Effective against RNA viruses more than DNA

320
Q

Active immunization

A

Administering all or part of a pathogenic agent to induce antibodies or cell mediated immunity

321
Q

Passive Immunization

A

Administration of exogenously produced antibodies

322
Q

Advantages of live attenuated

A

Easy to administer
Produces immunity at site of first infection
Induces antibody and cell mediate immunity
Long lasting

323
Q

Disadvantages of live attenuated

A

May revert during replciation

Not safe for immunodeficiency person

324
Q

Advantages of killed vaccines

A

Safe for immunocompromised persons

Cannot revert

325
Q

Disadvantage of killed viruses

A

Usually injected

Does not induce cell mediated immunity

Protection is shorter

326
Q

Three important immune cell types in vaccination

A

B Cells
CD8+ T cells
CD4+ T Cells

327
Q

Vaccines utilizing B cells only

A

Pneumonococcal

HIB

328
Q

Vaccines utilizing B cell and T cell immunity including secretory IgA

A

Influenza
Polio
Oral Typhoid

329
Q

Innate Immunity Cells

A 
Epithelial barriers
Phagocytes 
Dendritic cells
NK cells
Plasma proteins
330
Q

Viruses must reproduce within cells because

A

They cannot generate energy or synthesis proteins on their own

331
Q

Viruses are

A

Obligate intracellular parasites

332
Q

Protozoa

A

Microscopic single called eukaryotes

333
Q

Helminths

A

Macroscopic multicellular worms of various length, possessing differentiated tissues and complex organ systems

334
Q

Intermediate host

A

A host used by a parasite in the course of its life cycle and can multiply asexually bunt no sexually

335
Q

Definitive host

A

Where sexual reproduction of a parasite takes place

336
Q

Three groups of protozoan

A

Sarcodina
Mastigophora
Apicomplexa

337
Q

Protozoan nucleus

A

A true membrane bound nucleus

338
Q

Protozoan cytoplasm

A

Divided into inner endoplasm and thin outer ectoplasm

339
Q

Endomplasm protozoan

A

Granular contains nutrients

340
Q

Protozoan ectoplasm

A

Organized into specialized organelle of locomotion

  • pseudopods
  • flagella
341
Q

Most Protozoa are hetertroiphic

A

Assimilate organic nutrients engulfing soluble or particular matter

  • pinocytosis
  • phagocytosis
342
Q

Amoeba-Entamoeba histolytica

A

Microscopic

Causes amebic dysentery

50 million people

343
Q

Entameoba hystolytica principal host

A

Humans are principal host and reservoirs

Transmitted by fecal-oral route directly or indirectly though water

Highly infectious

344
Q

Entameoba hystolitica: Cysts

A

Environmental form-resistant to heat, low pH and chlorine levels in municipal water supplies

345
Q

Entameoba hystolitica: Trophozites

A

Dwell in lumen or wall of colon

346
Q

Entameoba hystolitica cysts mature vs immature

A

Immature cysts have single nucleus

Mature cysts have quadrincuclues

Chromatid bodies are present in immature and get absorbed as cyst matures

347
Q

Entameoba hystolitica trophozoites

A

Are microaerophilic
Multiply rapidly in aneraobic environment of gut

Feed on bacteria and tissue cells

Amitonchodriate-no mitochondria

348
Q

Entameoba hystolitica cysts turn to trophozites where

A

Distal small instestine which then invade intestinal mucosa

349
Q

Amebic Dysentery

A

Most infections are asymptomatic

Invasive Disease causes abdominal pain diarrhea bloody diarrhea and flatulence

350
Q

Fulminating amebic dysentery

A

abrupt onset high fever, severe abdominal cramps, liver pain, and profuse diarrhea
• 5% with symptoms have liver abscesses that can spread to pericardiu

351
Q

Extraintestinal Disease

A

Can result in liver abscesses lung and brain involvement

352
Q

Naegleria fowleri causes

A

Primary amebic meningoencephalitis

353
Q

Naegleria fowleri enters through the

A

Nose, penetrate nasal mucosa, migrates to the brain via olfactory nears

354
Q

Acanthamoeba causes

A

Keratitis (corneal ulceration) or Granulomatous embers encephalitis

355
Q

Keratitis

A

Chronic progression ulcerative lesion of the eye may result in blindness

Contact lens wearers at risk

356
Q

Only _____ flagellates induce disease

A

4

357
Q

Trichomonas Vaginalis exists only as

A

One morphological state —trophozoite

358
Q

Trichomonas Vaginalis lacks

A

A mitochondria

359
Q

Trichomonas Vaginalis causes

A

Trichomoniasis-very common sexually transmitted disease

Spread by direct skin to skin contact

360
Q

Giardia Lamblia infects

A

Humans and many mammals

361
Q

Giardia Lamblia exists as

A

A dormonatn microbial cysts in contaminated water

362
Q

Giardia Lamblia spread by

A

Fecal to oral route mainly through drinking water

363
Q

Giardia Lamblia flagellated parasite colonize and reproduce

A

In the small intestines causing giardiasis

-not in blood or other GI

364
Q

Giardiasis

A

1-3 weeks after infection

Diarrhea
Gas
Floating stool

365
Q

Leishmania spp. Type of parasite

A

Obligate intracellular flagellate parasite of mammals

366
Q

Leishmania is transmitted by

A

Phlebotomine sandflies

367
Q

Leishmania reservoirs

A

Rodents

Dogs

368
Q

Leishmania organims 2 forms

A

Amastiogite

Promastigote

369
Q

Amastigote

A

Mononuclear phagocytes and bloodstream

-intracellular nonmotile form

370
Q

Promastigote

A

Alimentary tract of sandflies

Extracellular and motile form

371
Q

Leishmania pathogenesis

A

Sandflies feed—ingest amastigotes from host—Promastigotes injected into next host—also inject peptides that inactivate macrophages—alters classical complement pathway-promastigote s get phagocytosis—amastigotes form within phagolysozome

372
Q

3 diseases caused by leishmaniasis

A

Cutaneous leishmaniasis

Mucocutaneous leishmaniasis

Visceral leishamanisais

373
Q

Localized cutaneous leishmaniasis

A

CD4+T cells of TH1 type secrete inf-gamma in response to antigens

Macrophages produce nitric oxide to kill intracellular amastigotes

374
Q

Visceral Leishmaniaisis

A

Pathogen causes dramatic inhibition of Th1 response-disseminate through bloodstream to visceral organs

TH2 response and antibodies associated with visceral disease

375
Q

Chagas’ disease caused by

A

Trypanosomiasis cruzi

376
Q

Chagas’ disease spread by

A

Redivide insect kissing bug

377
Q

T. Cruzi is in

A

Reduviid feces the poop after they feed

378
Q

2 Phases of Chagas Disease

A

Acute Phase- a week after bite
Fever fatigue headache rash

Chronic Phase-decades later

379
Q

Trypanosoma Brunei

A

Transmitted by tsetse fly

African sleeping sickness

380
Q

Sporozoa-Apicomplexa

A

Obligate intracellular parasite

Apical complex structre

This group included

Plasmodium
Toxoplasma
Cryptosporidium
Babesia

381
Q

Oocyst

A

Sexual forms

382
Q

Merozoite

A

Asexual form that can infect host cells

383
Q

Plasmodium causes

A

Malaria

384
Q

Plasmodium transmitted by

A

Anopheles mosquitoes

Causes periodic fever and anemia when erythrocytes burst

385
Q

Plasmodium reproductive stages

A

Sexual-mosquitoes

Asexual -humans

386
Q

Plasmodium life cycle

A

Almost the same for all 5 species

Sporozoite in saliva gets injected by female mosquito into human

Moves to liver

Infects hepatocytes

Merozoites are released from hepatocytes infect erythrocytes

Inside erythrocytes-trophozoites form then schizont

Erythrocytes ruptures releasing merozoites which invade new erythrocytes

387
Q

Plasmodium falciparum

A

Causes falciparum malaria which is the worst type to have

Cerebral malaria

388
Q

Plasmodium vivax

A

Most frequent and widely distributed causing of recurring malaria

Less virulent

Splenomegaly

389
Q

Malaria reason for fever

A

IL-1 and TNF produced by macrophages that ingest cell debris

390
Q

Malaria anemia

A

Phagocytosis of infect earthy types and parasite induced cell rupture leads to reals of toxic products

391
Q

Toxoplasma gondii

A

Toxoplasmosis

Cats are the only definitive host

Both sexual and asexual cycles take place in GI of felines

Oocytes in feces ingested by humans

Still births

392
Q

Toxoplasmosis steps

A

Oocyst are excreted in cats feces

Oocyst ingested

Most people are asymptomatic
Cervical nodes most often affected

393
Q

Nematodes

A

Worms with bodies that are round in cross section

394
Q

2 categories of nematodes

A

Intestinal nematode

Tissue nematodes

395
Q

Large round worms

A

Largest and most common intestinal helminth

396
Q

Hookworms

A

One the most common intestinal nematodes worldwide

397
Q

Pinworms

A

Common in children in US

398
Q

Whipworms

A

Common soil transmitted in southern US

399
Q

Strongyloides stercoralis

A

Similar to hookworm

Greater risk for life threatening infections

400
Q

Ascaris lumbriucoides

A

Large round worm

Causes ascariais

401
Q

Ascaris Infection: Life Cycle

A

Contracted through ingestion of eggs excreted in feces

Eggs hatch in intestines

larvae burrow through gut wall migrate to lungs via blood

Break into alveolar walls-travel up the throat where they get coughed up and swallowed

Upon reaching small insetting develop into adult worms and have a free constant supply of food

Takes 3 months

402
Q

Large round worm infection symptoms

A

Shortness of breath

Abdominal swelling

Diarrhea
Slow growth
Learning problems in children

403
Q

Anyclostoma and NEcator

A

Hookworms

Toothlike structures that allow attachment to small bowel

-suck blood

404
Q

Hookworms life cycle

A

Eggs deposited in soil hatch into Rhabditiform larvae then molt into filariform larvae (infectious form)

Contact with human
-penetrate skin carried through blood vessels to hear then lungs

Travel to alveoli to throat

Coughed then swallowed

Larvae then reach small intestine’

Suck blood

405
Q

Trichinella spiralis

A

Trichinosis

Contracted from eating undercooked pork with encysted larvae

Matured adult worms penetrate intestinal mucosae causing nausea

Larva invasion of striated muscle begins 1 week later

406
Q

trichonosis symptoms

A

Fever muscle pain

Eyelid swelling
Myocardial involvement and heart failure

407
Q

Cestodes

A

Long ribbon like worms

Tapeworm

Beef tape worm

Pork tapeworm

Fish tapeworm

408
Q

Beef tape worm

A

human is definitive host, cow intermediate host- cysts form in cow muscle

409
Q

Pork tape worm

A

both pork and humans are intermediate hosts (may acquire cysts)

410
Q

Fish tapeworm

A

Humans and fish eating mammals are definitive host- Crustacean and fish intermediate host

411
Q

Taeniasis

A

Tapeworm infection

After ingestion by animal, eggs hatch and oncospheres penetrates intestinal wall and circulate to muscles where they become cysticerci

Humans ingest cysticerci from undercooked meat

Adult tapeworm develops in humans small intestine over several months

412
Q

Beef Tapeworm infection

A

Contracted by eating meat contains larval form-infection is in gut lumen of humans

413
Q

Porktapeworm infection

A

Eggs can infect both pigs and humans

Humans are an intermediate unlike beef

Cysts from in muscles or in the brain

414
Q

Cysticercosis of brain

A

Pork tapeworm

Can develop in
Subcutaneous tissues
Muscles
Heart
Lungs
Liver
Eye
Brain
415
Q

Fungi make up

A

Their own kingdom

Fungi are eukaryotes

416
Q

Fungi are mostly

A

Strict aerobes

A few are facultative anaerobes

417
Q

Fungi cause disease by

A

Inducing an inflammatory response or through direct invasion or destruction of tissues

418
Q

Fungal cell membrane consists of

A

Ergosterol

419
Q

Fungi cell walls are unique

A

Different from cell walls of plants and bacteria

NO peptidogluycan, LPS, Glycerol or teichoic acid

Fungal wall contains chitin, mannan and glucan

420
Q

Fungi 3 medically important categories

A

Yeast
Molds
Dimorphic fung

421
Q

Yeast is a ______ fungi

A

Unicellular

Single cells-asexual reproduction

422
Q

Molds are ______ fungi

A

Multicellular

Both secula and asexual repodoctuion possible

423
Q

Dimorphic fungi can exist as

A

Both mold and yeast

424
Q

Molds reproduce two ways: Asexually

A

By conidia that form on the tips of growing hypahe

425
Q

Molds reproduce two ways: sexually

A

Through development of spores

426
Q

Hypahe of molds

A

Vary depending on species

Septa may contain pores and incomplete walls-allow moment of nutrients organelles and nuclei between adjacent cells

427
Q

Fungal asexual reproduction

A

Asexual form is call anamorph and forms stricter called conidia

Involves mitosis division of haploid nucleus . No genetic recombination

428
Q

Fungal sexual reproduction

A

Sexual from is called Teleomorph and forms specialized structures called spores, also called ascospores, zygospores, absidpores depending on struction

-haploid nuclei of donor and receipting cells fuse to form a diploid nucleus which divides by classic meiosis. Genetic recombination can occur

429
Q

Fungi dimorphism is

A

Reversible and is linked to virulence

430
Q

Thermally dimorphic

A

Temperature determines whether mold or yeast

431
Q

3 ways to encounter fungi

A

Incidental contact in environment

Normal human flora

Contact with infected individual

432
Q

Most fungal infections are

A

Mild and self limiting

433
Q

Primary barriers against fungal infections

A

Intact skin and mucosal surfaces are primary barriers

Dedication epithelial cell turnover fatty accidents and low pH of skin

434
Q

_______ compete with fungi and inhibit growth

A

Bacterial normal flora

435
Q

_______ Immunity is required to elimante fungal infections

A

T cell mediated

CD4+TH1/TH17 cell mediated immune response

436
Q

Primary mechanisms for contains fungal infections

A

Phagocytosis and killing by neutrophils

Some fungi are too large so secrete enzyme and reactive oxygen species that can digest or kill large fungi

437
Q

Immunity to fungal infections is mediate by

A

T cells

438
Q

CD4+ T cells Recogonize

A

Presented antigens in MHC complex on APC (dendritic Cell) through an interaction with their TCR

This stimulates the resale’s of cytokines which activate neutrophils and macrophages

439
Q

Azoles

A

Itraconazole

Interfere with ergosterol synthesis

Fungistatic

440
Q

Polyenes

A

Amphotericin B

Bind to cell wall ergosterol and forms channels

441
Q

Polyenes must be administered

A

Intravenously as a colloidal suspension

442
Q

Azoles target either

A

Yeast of mold forms of fungi

Better tolerated than amphotericin B

target enzymes that converts lanosterol to ergosterol resulting in defective membranes

Toxic to liver

Resistance can occur and arythmias

443
Q

Superficial and Cutaneous Mycoses

A

Limited to epidermis and skin structure

Dermatophytes

Malassezia

444
Q

Dermatohphyte Skin Infections

A

Most common fungal infections in humans

Infect keratizned tissues

445
Q

Dermatophytes clinical diseases called

A

Tineas

(ringworm athletes foot jock itch)

Microsporum
Trichophyton
Epidermophtyon

446
Q

Dermatophytes Entry

A

Skin trauma is required

447
Q

Dermatohphyte Hyphae grows

A

Outward in centrifugal pattern

Systemic infections very rare

448
Q

Tina Capitis

A

Hyphae invade hair shaft

Hair can Brea at the root and fungus can plug hair follicle causing bald patches

449
Q

Tina Unguium

A

Nail plate invasion leads to hyperkeratosis and discoloration-dislodges and distort nail

450
Q

Seborrheic dermatitis

A

Patches with greasy scales in facial hair and scalp -dandruff

451
Q

Tina versicolor

A

Hypopigmented or hyperpigmented patches on chest or neck with scaling

452
Q

Subcutaneous mucosal usually enter skin via

A

Thorns or splinters

453
Q

Sporothrix schenckii-subcutaneous mycoses

A

Thermally dimorphic fungus

Sporotrichosis-rose pickers Disease

Disseminated only in immunocompromised patients

454
Q

Sporothrix Schenckii infection starts as

A

A painless applies developing a few weeks to a few months after inoculation. Papuans slowly enlarge and eventually ulcerate leaving open sores. Infection follows lymphatics**

455
Q

Chromoblastomycosis

A

Scaly wart like lesions usually on feet or leg

Amputataion required

456
Q

Mycetoma

A

Caused by different species of environmental fungi, chronic infection with sinus tract nodules and discharged visible grains

457
Q

Opportunistic fungal pathogens

A

Not considered tru pathogens

Only cause disease when host defense are decreased

458
Q

Candida Albicans

A

Most frequent opportunistic fungal pathogen

Colonies grow rapidly

459
Q

Candida Albicans reproduce by

A

Forming buds or blastocondidia

Some form hyphae or pseudo in vivo

Polymorphic fungus-not true dimorphism

460
Q

Candida shift from

A

Yeast to hyphae associated with invasion

461
Q

Candida hyphae

A

From strong attachment to epithelial cells

Hyphae secrete proteinases and phospholipase that digest epitheal I cells-facilitate invasions

Also forms biofilms on prosthetic surfaces

462
Q

Candidiasis

A

INfection only when normal flora is disrupted

Broad spectrum antibiotics biggest culprit

Decreased T cell function

463
Q

Mucosal Candidiasis

A

Mucosal (Thrush) thick white plaques on orophaygneal and vaginal mucosa

464
Q

Cutaneous candidiasis

A

Warm moist areas of skin

Diaper rash

465
Q

Urinary tract infections

A

Candidiasis

Ascending infections

466
Q

Disseminated Candidiasis

A

Life threatening

When gains access to bloodstream

Enters through skin lesion, GI disruption, prosthetic devices, intravenous cat here’s , UT

Once in blood stream-micro abscesses in multiple organs

Disseminated candidiasis symptoms are similar to bacterial infections-however they often involve the eyes and can lead to blindness

467
Q

_______ involved in defense against candida infection

A

Both humoral and cell mediated immunity

468
Q

Osponziing IgG antibodies

A

Against yeast carbohydrate mannan-activate classical complement pathway

469
Q

T cell mediated immunity: candida

A

Keep candida in check on mucosal surfaces (neutrophils)-main host defense against invasion through muscles

470
Q

Th1 mediated immunity candida

A

IL2 INFy TNFa correlate with enhanced resistance to candida infection

471
Q

Th2 candida

A

IL4 IL6 IL10 associated with chronic disease

472
Q

Aspergillosis

A

Filamentous fungi

Ubiquitous in soil

INhaltion of spores

473
Q

Aspergillosis reproduce by

A

Forming candidiasis and area conidiophores (sexual)

474
Q

Aspergillosis Entry

A

Candidiasis are inhaled

Germinate into hyphae

Macrophages unable to kill hyphal form

Neutrophils line up along hyphae and secrete reactive oxygen intermediates that kill the fungus

475
Q

Aspergillosis pneumonia

A

Most common patients with emphysema and bropnchiectsia are at risk

476
Q

Disseminated aspergillosis

A

Disseminated through bloodstream can occur and affect any organ system

477
Q

Allergi respiratory disease aspergillosis

A

Occurs in people with allergies build up of mucous allows fungus to grown

478
Q

Aspergillosis

A

Results in patients with prior lung infections with scarring and cavities

Fungal spores germinate in cavities and fungal hypahe grow into balls

479
Q

Zygomycetes

A

Colonize oral mucosa paranasal sinuses and pharyngeal mucosa

Associated with diabetic ketoacidosis

480
Q

Pneumocystis

A

Colonizer of human airway

481
Q

Cryptococcosis

A

Environmental yeast

Polysaccharide capsule

482
Q

Cryptococcus virulence factors

A

Capsule
Lactase engulfment
Phospholipase s
Urease

483
Q

Cryptococcus capsule

A

Made of GXM glucuronaxulmannan

484
Q

Lactase enzyme

A

Produces antioxidant melanin pigments

485
Q

Cryptococcus

A

Are inhaled into alveoli producing lung infection

In the lungs they produce polysaccharide capsule
-t cell mediated immunity crucial

486
Q

Cryptococcus most often presents as

A

Meningitis

487
Q

Endemic mycoses

A

Dmorphic Fungi that infect heathy people

Histoplasmosis

Blastomycosis

Coccidioidomycosis

488
Q

Histoplasmosis

A

Dimorphic soil fungus

In lungs transforms into yeast

489
Q

Blastomycosis

A

Disease occurs when inhaled into the lungs

Skin lesions also common occur dissematined spread by blood

Granulomas can develop

490
Q

Coccidioidomycosis

A

Dimorphic not temperature dependent

491
Q

Coccidioidomycosis: Arthroconidia

A

Highly infection mold form inhaled into alveoli

Phagocytosis

492
Q

Coccidioidomycosis: Spherules

A

In lungs transform into spherules filled with endosomes

Resist phagocytosis

493
Q

Coccidioidomycosis life cycle

A

Desert climates

Hyphae differentiate into arthrocondia which break loose and get suspended in the air

Inhaled into lungs

In humans differentiation produces cleavage planes and eventually huge spherules

The spherules rupture releasing endosomes which can then repeat the in vivo cycle

494
Q

Coccidioidomycosis cell mediated immunity

A

CD4 T cell is need to control infection and activate macrophages

495
Q

Coccidioidomycosis can disseminate

A

Can spread to other organs

Chronic meningitis possible

496
Q

Active Immunity

A

The development of antibodies in response to antigenic stimulation

497
Q

Passive immunity

A

Transferred protection through preformed antibodies produced by another individual

498
Q

Active immunization

A

Vaccination

  • longer duration of protection
  • Delayed onset
499
Q

Passive immunization

A

Preformed antibodies

  • immediate onset
  • shorter duration of protection
500
Q

Disadvantages of passive immunization

A

No long term protraction
Serum sickness
Risk of infection
Graft vs host disease

501
Q

Natural passive immunity

A

Placental trasnfer of IgG

Colostral transfer of IgA

502
Q

Artificial passive immunity

A

Antibodies or immunoglobulins

Immune cells

503
Q

Vaccination

A

A process of induction of immunty to a pathogen by deliberate injection of a weakened modified or related form of the pathogen which is no longer pathogenic

504
Q

Principal behind the smallpox vaccine

A

Cowpox and smallpox shave some surface antigens

Immunization with cowpox induces antibodies against cowpox surface antigens

Cowpox antidisestablishmentarianism bind to and neutralize smallpox virus

505
Q

Immunologic adjuvants

A

Substances when mixed with an immunogenicity enhances the immune response

506
Q

Immunologic adjuvants examples

A

Prolongs antigen persistence

Enhances costimulatory signals
Induces germinal center formation
Stimulate lymphocyte proliferation

507
Q

Enhanced co stimulators signals

A

Increases expresssion of MHC and B7 molecules

Secretion of cytokines

  • > increased antigen presenting ability
  • > maximal activation of TH cells
508
Q

Animal adjuvants

A

CFA
Oil in water mullion

Complete Freunds

509
Q

Human Adjuvants

A

Alum (alumninum hydroxide )

510
Q

Live Attenuated Vaccines

A

Contain a version of the living microbe that has been weakened in the lab so it cant cause disease

  • closet thing to a natural infection
  • lifelong immunity
511
Q

Live attenuated vaccines induce

A

Robust immune responses

CD4 CD8 strong cellular responses
Strong antibody response long lived memory B cells

512
Q

Live attenuated Disadvantages

A

Possibility of reversion to a virulent form

Must be refrigerated

Contraindications in very young
Very old
HIV patients

513
Q

Attenuated Advantages

A

Easy to create
Small number of genes
Easier to control their characteristics

514
Q

Viruses are attenuated in cells in

A

Which they do not reproduce well in.

Hostile environment takes the fight out of viruses
-they evolve to adapt to the new environment

They become weaker with respect to their natural host

515
Q

Why are bacteria difficult to attenuate

A

Bacteria have thousands of genes and thus are much harder to control
-recombinant DNA technology to remove several key genes in various bacteria is one approach

516
Q

Attenuated vaccine examples

A

Measles
Mumps
Chickenpox

Influenza vaccines
-A/H1ni
A/H3N2
And inactivated vaccine

517
Q

Influenza vaccine

A

A flu virus contains 8 gene segments

Combine desired HA and NA genes from flu strain 1 with flu strain 2 grow in an egg

518
Q

How are viruses inactivated to create inactivated vaccines

A

Chemicals
Heat
Radiation

519
Q

Inactivated vaccines are ____ and ____ than live vaccines

A

Stable
Safer

Microbes cant mutate back to their disease causing state

Don’t need refrigerated
Can be freeze dried

520
Q

Inactive vaccines stimulate

A

A weaker immune system response than live vaccines

-usually take several doses

521
Q

Killed Advantages

A 
Safe
Stable
No refrigeration
Nontranmissible
Cannot multiply or rever
522
Q

Killed disadvantages

A 
Multiple doses
Unnatural route
High Ag concetration needed
Variable efficacy
Weak CMI responses
Inadequate killing
523
Q

Subunit Vaccines

A

Instead of the entire microbe, subunit vaccines include only the antigens that best stimulate the immune system

-immunodominat epitope

524
Q

Chances to adverse reaction in subunit vaccines

A

Lower
No live microbes
Less microbial particles

525
Q

Subunit vaccines from 2 ways

A

Microbe broken down

Antigen molecules manufactured using recombinant DNA

526
Q

Toxoid Vaccines

A

Used when a bacterial toxin is the main cause of illness

527
Q

Toxins can be inactivated by treating them with

A

Formalin

  • solution of formaldehyde and sterilized water
  • detoxed toxins are called toxoids are safe for use in vaccines
528
Q

Toxoid vaccine example

A

Diptheria

Tetanus

529
Q

Conjugate Vaccines

A

Encapsulated bacteria may be more difficult for the immune system to detect

-polysaccharide coating evade immune detection

530
Q

A conjugate vaccine links

A

Antigens or toxins from a microbe to the outer polysaccharides
-helps the immature immune system react to polysaccharide coating and defend against the disease causing bacterium

531
Q

Conjugate vaccine example

A

Haemophilus influenza type B

532
Q

Herd immunity

A

The more people that are vaccinated the fewer susceptible individuals will be exposed and the less likely person to person transmission will occur

533
Q

Some components of the innate immune response are common to all pathogens

A

Phagocytosis and killing of microbes

Antigen presentation

Cytokines production to induce inflammation and reactive endothelium

534
Q

NK cells produce

A

Cytokines

535
Q

Both innate and adaptive immunity work to

A

Protect against infection and eradicate infection

536
Q

IgG

A

Virus

537
Q

IgA

A

Mucosal virus

538
Q

PAMPS go to what receptors

A

Toll like receptors

539
Q

Chemokines

A

Make chemical gradient specialized cytokines that tell cells where to go

540
Q

Type I interferons

A

Interferon alpha

Interfereon beta

541
Q

The most potent stimulus for IFNs are

A

Viral nucleus acids

detected by pattern recognition receptors

542
Q

Type I IFN does what

A

Inhibits viral replication and inhibits viral protein synthesis

543
Q

How does the immune system deal with intracellular pathogens

A

Kill the infected host cell

Cytoxic cell
NK cell

544
Q

NK cell

A

Kill cancer cells

Viral infected cells

Lymphocyte but not MHC

Not capable of generating memory

545
Q

NK cells kill target cells by 2 mechanisms

A

The death receptor

Granule dependent pathways-contact dependent perpherin

546
Q

What is immunologic memory

A

Specific to B and T lymphocytes

Acquired after initial exposure to Ag

547
Q

All T cells recognize Ag via

A

T cell receptor

548
Q

Before TCR can recognize Ag it must be

A

Processed by APC
-Ag broken down into shor fragments

Presented by APC

  • MHC I
  • MHC II
549
Q

B cells do not require

A

Ag to be processed/presented

B cells via membrane bound Ig can recognize Ag in its native form

550
Q

MHC I

A

On inside cell

Endogenous Ag
-critical to viruses

Not on erythrocytes

551
Q

MHC II

A

Always on
-professional APCs

Exogenous Ag

Typically present Ag to helper T cells

552
Q

Helper T cells function

A

Cytokines Secretion

553
Q

Acationg of macrophages

A

Th cells make IFN gamma

554
Q

Actaiviton and enchanted Ab production by B cells

A

Th cells make IL4

555
Q

Activation and enchanted killing of TC cells

A

Th cells make IFN-gamma

556
Q

What do TC cells do

A

Killing of infected of tumor transformed cells

  • perforn
  • Granzymes

-Cytokine Secetefrion
-IFN GAMMA
-Tumor necrosis factor
TNF alpha

557
Q

Central tolerance

A

Occurs in generative lymphoid oranges involving immature self reactive lymphocytes recognizing self antigen

558
Q

Peripheral Tolerance

A

In peripheral sites involving mature self reactive lymphocytes encountering self antigen

559
Q

Immunological tolerance is NOT

A

Simply a failure to recognize an antigen

560
Q

Immunological tolerance IS

A

An active response to a particular epitope and is just as specific as an immune response

561
Q

Tolerance can be ______ or _______

A

Natural

Induced

562
Q

Immunological Tolerance

A

A state unresponsive for a particular antigen

  • LEARNED very specific and induce prior to exposure to antigen
  • INclude tolerances to non self
563
Q

Self Tolerance

A

Physiological state in which the immune system does not react destructive against self tissue

564
Q

Self tolerance my be induced in _____

A

Immature self reactive lymphocyte in generative lymphoid oranges

Or in mature lymphocyte in peripheral sites

565
Q

Response to self antigen

A

Anergy

Deletion

Change in specificity

566
Q

Reactivity is prevented by processes that occur during

A

Development rath than being genetically pre-programmed

567
Q

CD4/8- start in bone marrow and fetal liver travel to

A

Thymus

568
Q

Lymphocytes that do not bind MHC through their TCR

A

Are destined to die by apoptosis

569
Q

Positive selection and lineage commitment occur in

A

Cortical region of the thymus

570
Q

Negative selection occurs

A

In the medullary region of the thymus

571
Q

Positive selection uses what avidity

A

Low avidity

572
Q

Negative selection uses what avidity

A

High avidity

573
Q

During maturation in the thymus most immature T cells that recognize antigens with high adviity are

A

Deleted

574
Q

Self reactive CD4+ T cells that see self antigens in thymus

A

Are not deleted but instead differentiate into regulatory T cells

575
Q

Choice between lymphocyte activation and tolerance is determined by

A

The properties of the antigens

State of maturation of the antigen specific lymphocytes

Types of stimuli received when these lymphocytes encounter self antigens

576
Q

Central Tolerance in B cells

A

Occurs in Immature B cells in the bone marrow

577
Q

Potentially autoreactive cells can

A

Be eliminated or inactivated by contact with self Ag

578
Q

________ and _______ of the self Ag detriments the fate of B cells

A

Nature

Concentration

579
Q

Multivatlent Ag

A

Induce B cell death

580
Q

High concentrations of Ag

A

Induce B cell death

581
Q

Lower concentrations of small soluble self Ag induce

A

Functional anergy

Results in decreased membrane Ig

Blocked signal transduction by membrane bound Ig

582
Q

Peripheral tolerance

A

is the mechanism by which mature T cells that recognize self antigens in peripheral tissues become incapable of responding to these antigens

583
Q

Colonial Deletion/apoptosis

A

Actual elimination from the cellular repertoire by activation induced cell death

584
Q

Colonial anergy

A

Mature cell is present but is functionally inactivated

585
Q

Suppression

A

Inhibitor of cellular activity through interaction with other cells

Tregs (CD4+/CD25+ T cells, TGF beta or IL10 secreting reg T cells)

586
Q

Ignorance

A

Co-existence of self reactive clones and antigen; cells do not respond to antigen

587
Q

Factors determine which mechanisms are operative

A

Concentration of self antilnge in lymphoid organs

Affinity of antigen receptor for antigen

Nature of antigen

Concentration and availability of co-stimulators molecules

588
Q

Without helper T cells

A

Won’t get a full B cell response

589
Q

B cell clonal expansion

A

Antibody secretion
Isotype switching
Affinity maturation
Memory B cell

590
Q

How to T cells affect the outcome of B cell activation in the periphery

A

2 signal hypothesis

591
Q

Signal one

A

Generated though the Ag receptor

592
Q

Signal two

A

Mediated by CD40 and CD40L

B cell anergy results if one the signals is missing

593
Q

IL4

IL13

A

+

IFN-gamma =-

594
Q

Anergic cells shopw a block in TCR induced signal tranduction

A

Lack of costimulation by B7 and B72

Costimulation by inhibitory receptors

595
Q

CTLA-4 competes with _____ for b71 and b72

A

Cd28

596
Q

CTLA4 keeps ______ in check

A

T cells

597
Q

Knockout mice lacking CTLA4 develop

A

Uncontrolled lymphocyte activation

Massively enlarged lymph nodes and spleen

Fatal multiorgan lymphocytic infiltrates

598
Q

Self reactive cells may be deleted from repertoire

A

Activation in the absence of IL2 can lead to death

Persistent Ag

Activation induced cell death

599
Q

Capsase 8/9

A

Apoptosis

600
Q

Caspase 9

A

Passive cell death

601
Q

Caspase 8

A

Induced cell death

602
Q

How does ignorance happen

A

Antigen is expressed in a privileged site/sequestered

T cells cannot get to the antigen across an endothelial barrier

Perhaps the antigen is not expressed in the context of MHC molecules

603
Q

Oral administration of Ag favors

A

Tolerance induction

604
Q

A state of immune _______ follows oral administration of an antigen

A

Hyporepsoiveness

605
Q

T cells

A

Cell mediated response

Recognize processed antigen in the context of MHC to irradiate infection

-effector functions include cytokine productin adn release of cytotoxin factors

606
Q

B cells

A

Humoral responses

Recognize free antigen via Ig receptor to irradiate infection

-effector functions include antibody mediated destruction of antigen

607
Q

Autoimmune disease occurs when

A

The immune system becomes dysregulated and attacks the very organis it was designed to protect

608
Q

Autoimmunity results when

A

Central and peripheral tolerance is broken

609
Q

Factors that can predispose an individual to various auto immune diseases

A

MHC association

Familial concordance

Gender

Climate

Chemical angers

Infections agents

Immune dysregulation

610
Q

What initiates an autoimmune response

A

Incomplete deletion of self reactive cells

Aberrant stimulation of normally anergic self reactive cells

Altered regulation of anergic self reactive cells

611
Q

Systemic Autoimmune Diseases

A

Immune cells target multiple organ systems and tissues

Thought to be due to aberrant regulation of many clones of lymphocytes

612
Q

Organ specific autoimmune disease

A

Immune cells target specific organs or tissue

Thought to be due to failure of self tolerance in only a few clones of cells which react to a limited number of antigens

613
Q

MS

A

Immune systems targets central nervous system via myelin specific T cells

614
Q

Systemic Lupus erythematosous

A

A systemic disorder in which a variety of autoantibodies (DNA, nucleoproteins, platelets, lymphocytes) can cause multisystem damage

615
Q

Systemic AI diseases

A

Lupus

RA

616
Q

Organ Specific AI

A

Insulin dependent diabetes mellitus

Multiple sclerosis

617
Q

SLE increased risk associated with

A

HLA DR2 and HLA DR3

Female

618
Q

SLE symptoms

A 
Fatigue 
Fever
Alopecia
Mucosal Ulceration
Butterfly rash
Joint and muscle pain
619
Q

SLE Pathogenesis

A

Immune complex disease Type III

Large amounts of autoantibodies produced a giants self antigens

  • DNA
  • Nucleoproteins
  • Platelets
  • Lymphocytes
620
Q

MS

A

HLA DR2

Impaired vision 
Ataxia
Spasticity
Bladder dysfunction
Weakness
Sensitivity to temperature
Cognitive impairment
621
Q

MS pathogenesis

A

T cell mediated autoimmune diseae in which T cells are specific for components for eh myelin sheath

Also evidence of macrophage and microglial cell involvement in myelin degradation

Damage to/loss of myelin impairs nerve conduction

622
Q

Allergy

A

Deleterious effects of hypersensitivity to environmental antigens

623
Q

Autoimmunity

A

Disturbance in immunologic tolerance of self antigens with damages to self tissue

624
Q

Alloimmunity

A

Immune reaction to tissues of another individual

625
Q

Type I hypersensitivity

A

IgE mediated

626
Q

Type II hypersensitivity

A

Tissue specific reactions

627
Q

Type III hypersensitivity

A

Immune complex mediated

628
Q

Type IV hypersensitivity

A

Cell mediated

629
Q

Alloimmunity is when the immune system reacts with

A

Antigens on tissue of other genetically dissimilar membranes of the same species

  • transplant rejection
  • Transient neonatal
630
Q

Transient neonatal alloimmunity

A

Fetus expresses parental antigens not found in the mother

631
Q

MHC molecules have a

A

Broad specificyt for peptides

632
Q

Peptides associated with MHC have a

A

Slow on and slow off rate

633
Q

MHC molecules do not discriminate

A

From self and foreign peptides

634
Q

The MHC haplotype

A

Of an individual determines which peptides bind and how peptides bind

635
Q

HLA

A

Human leukocyte antigen

636
Q

MHC genes are

A

Highly polymorphic

Hundred of alleles in human with 10^13 combination

637
Q

How are MHC alleles expressed

A

Concomitantly

The set of MHC alleles on an individual chromosome is termed the MHC haplotype

638
Q

MHC haplotype can influence

A

How an individual responds to certain pathogens

Susceptibility to certain diseases

Transplant success

639
Q

Graft Rejection according to time

A

Hyperactive

Acute

Chronic

640
Q

Hyperacute rejection

A

Immediate a rare

Preexisting antibody to The antigens of the graft

641
Q

Acute rejection

A

Cell mediate response against unmatched HLA antigens

Paraenchamhyl cell damage

642
Q

Chronic Rejectgion

A

Months or years

Inflammatory damage to endothelial cells of vessels due to a weak cell mediated reactions against minor HLA antigens

643
Q

Graft Versus Host

A

Immunocompromised individuals are at risk for GVH

T cells in the graft are mature and capable of cell mediated destruction tissues within the recipient

Not a problem if patient is immunocompetent

644
Q

AB blood type

A

Universal recipient

No antibodies

A and B antigen

645
Q

O blood type

A

Universal donor
Anti-a anti-b antibodies

No antigens

646
Q

ABO Blood system

A

A and B are codominat

Individuals have naturally occurring antibodies to the A and B antigens they lack

647
Q

blood antibodies are usually of the

A

IgM class

648
Q

A blood group

A

Anti-B antibodies

A antigen

649
Q

Primary immunodeficiency

A

Congenital

Genetic defects that result in an increased susceptibility to infection

650
Q

Secondary immunodeficiency

A

Acquired

Develop as a consequence of

Malnutrition
Disseminated cancer
Treatment with immunosuppressive drugs
INfection of cells of the immune system

651
Q

Primary immunodeficiency may affect

A

One or more components of the immune system including T, B lymphocytes and Natruarla kIller cells as well as phagocytic cells and complement proteins

652
Q

Immunodeficiency may result from defects in

A

Leukocyte maturation or activation or from defects in effector mechanism of innate and adaptive immunity

653
Q

The types of recurring infections can

A

Predict the type of immunodeficiency

654
Q

Deficient humoral immunity usually results in

A

Increased susceptibility to infection by pyogenic bacteria

655
Q

XLA

A

All antibody isotype are very low

Circulating B cells absent
Pre B cells reduced in numbers in bone marrow

Tiny tonsils and lymph nodes

Thymus and T cell dependent areas are normal

656
Q

XLA defect association with the loss of

A

Burton Tyrosine Kinase

657
Q

X linked immunodeficiency with hyper IgM

A

Characterized by very low serum IgG IgA and IgE

A high concentriaont of polyclonal IgM

Pyogenic infections

Lymphoid hyperplasia

658
Q

Hyper IgM B cells are not

A

Signaled by T cell to go through isotype switching and only produce IgM

659
Q

Deficient Cell-mediated immunity usually results in

A

Increased susceptibility to viruses and other intracellular pathogens

660
Q

Severe Combined Immunodeficieny Diseae

A

Rare fatal syndrome profound deficient of T and B cell function

Bubble boy

Have B cells but don’t produce immunoglobulin

Micro/Immuno (3 decks)

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