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CHI 305: Immunology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Range of symbiotic relationship: 2 different species closely interact with each other for much of their lives.
What are the types?

A

2 different species closely interact with each other for much of their lives

  • Commensalism: Symbiont benefits, no harm or benefit to host E.g. Remoras + pilot fish
  • Mutualism: Both host + symbiont benefit – obligatory relationship
  • Parasitism: Symbiont benefits at the expense of host e.g. parasite – tapeworm
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2
Q

What are the sites of extracellular pathogen infection

A

Respiratory (e.g. bordetalla Pertussis)
Gastrointestinal (Helicobacter pylori)
Tissue + bone (Staphylococcus aureus = boils, necrotic infection, osteomyelitis)
Blood (Strep )
Eyes
Cavities – pleural, cranial, peritoneum, bronchial
Skin

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3
Q

What are the defence mechanisms that limit extracellular pathogen infections

A

Innate Immune: Phagocytosis (macrophages and neutrophils); complement; antibacterials (peptides + lysosomes)

Adaptive Immunity: Humoral (opsonising, neutralising immunoglobulin); B cell + T helper cells

Gram +ve Bacteria:

  • Thick peptidoglycan wall = resistant to lysis by complement
  • Defence = opsonisation + phagocytosis = antibodies + other opsins

Gram –ve Bacteria:

  • Cell wall contains lipopolysaccharide – an endotoxin
  • Polysaccharide portion is antigenic
  • Can be lysed by complement system + opsonisation
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4
Q

What are the mechanisms employed by extracellular pathogens to evade the immune system i.e. changing surface proteins?

A
  • Inhibition of phagocyte chemotaxis
    o e.g. pertussis toxin
  • Inhibition of phagocytosis
    o Produce slippery coat (casule)
    o Inhibition of FC portion of antibody means cannot activate macrophages
  • Lethal Toxins
    o Lyse phagocyte or induce apoptosis
  • Antigen variation
    o Small number of pathogens in infection with altered glycoproteins
    o Immune response is not directed to population that has altered proteins :. remain untouched
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5
Q

Areas in the cell where intracellular pathogens can survive

A
  • Cytoplasm/ vesicles (after alteration)
  • Can live in phagosome but still prevent phagosome- lysosome fusion (e.g. TB)
  • Live in fused phagolysome but can avoid enzymes (leishmania)
  • Escape from phagosome
  • Live in cytosol like Listeria
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6
Q

What are the means employed to survive intracellularly

A
  • Hide in host cell vesicle or cytoplasm – enter through phagocytosis
-	Live in:
o	Prevent phagosymal fusion
o	Phagolysosome 
o	Cytosol 
o	Alter phagosomal mutation
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7
Q

Roles of IFNy

A

IFN-gamma is produced mainly by T-cells and natural killer cells activated by antigens,

  • activates macrophages
  • inhibits viral replication directly
  • feed forward- so increases the activity of more Killer T cells and natural killer cells.
  • Activates macrophage – fusing phagosome + lysosome
  • Increases MCHI + II expression
  • Increase costumulatory molecule expression
  • Activates T cells
  • Increase NK cell activity
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8
Q

Intracellular Pathogen Diseases

A
  • Malaria
  • Toxoplasma
  • Listeria
  • Leishmania
  • All viruses
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9
Q

Passive vs active, natural + artificial immunity examples

A

Active Immunity: Provide long lasting immunogenic protection, assist children throughout childhood disease e.g. vaccinations

Passive Immunity: Transient protection against particular infections e.g. rabies
few notes for pictures

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10
Q

Polyclonal vs Monoclonal Antibodies

A

Polyclonal

  • Antibodies extracted from a host
  • Desired antibodies are small fraction of total

Monoclonal

  • Uses hybridoma technology
  • One specificity and one isotype
  • I.e. IgG specific from rabies virus
  • Most have been developed or treatment of cancer
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11
Q

Whata re the advantages and Risks associated with Vaccines

A

Advantages

  • Can be very effective at eradicating disease when administered effectively
  • Immunize enough individuals + achieve herd immunity – communication of disease is interrupted, helps entire population (even those not vaccinated)
  • Potential carriers avoid infection + therefore avoid spread of disease

Risks

  • Vaccines from live viruses made less virulent – have potential to cause disease e.g. rare cases of polo from vaccine
  • Precaution in immunocompromised individual or those undergoing immunosuppressive therapy
  • Fear of this led → inactivated (killed) vaccine virus
  • Effective vaccine use where disease is so infrequent vaccine complications outnumber disease outbreak
  • Diphtheria Pertussis+ tetanus vaccine – heat killed pertussis has caused serious side effects such as encephalopathy in infant
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12
Q

What is herd Immunity

A
  • Immunization to enough individuals – achieve herd immunity
  • Communication of disease interrupted
  • Helps entire pop- even those not vaccinated – potential carriers avoid infection + :. Avoid spread of disease
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13
Q

Hypersensitivity Type 1 Phases

3 phases to it

A
  1. Sensitisation phase:
    - IgE allergic reactions
    - antigen enters body
    - CD4 and Th2 cells specific to that antigen stimulate Bcell production of IgE antibodies.
    - IgE binds to mast cells + basophills = sensitized
    - if exposed to same allergen
  2. Activation phase:
    -IgE on sensitised cells cause degranulation of mast cells and basophillls causing them to release histamine and other inflammatory mediators. Enters tissue and causes
    GIT:
    -increased fluid secretions from cells and glands
    -more peristalsis
    -vomiting and diorrhea
Lung:
-Bronchiole constriction 
-increased mucus production 
-coughing, wheezing, phlegm produced 
Blood vessels:
-increased blood flow, permeability therefore increased fluid in tissue and an inflammatory response.
  1. Effector stages:
    ?
    The slow reacting substances of anaphylaxis
    -serotonin- present in mast cells, causes constriction of smooth muscle
    -chemotactic factors= attract eosinophils, neutrophils, basophil, macrophages, platelets + lymphocytes
    -heparin = inhibits coagulation
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14
Q

What are the causes and mechanisms of Hypersensitive 2,3, 4

A

Hypersensitive II
- Cytotoxic or Cytolytic reactions involving antibodies
- 3 types where targeted cell is damaged or destroy by:
o Complement mediated reaction
o ABDCM cytotoxicity
o AB mediated cellular dysfunction
- Reaction stimulated by binding of ab directly → agon cell surface
- Uses FC receptors on many immune cells to link cell AB coated target = release of perforins on target cell (lysis)
- Transfusion of ABO incompatible blood = in complement mediated cytotoxic reactions
- Mediated by IgG + IgM

Hypersensitive III
- Immune complex reactions
- Stimulated antibody + antigen immune complexes
- Can be localised or systemic
- Can be from bacteria or intradermal or intrapulmonary antigens
- E.g. SLE :
o Local + systemic manifestation of immune complex occurs
o Central to type III is complement fixation, activation of complement cascade + release of active component of complement cascade
o Damages glomerular basement membrane

Hypersensitive IV
- Delayed type hypersensitivity
- Cell Mediated
o More delayed than other reaction
o Activation, proliferation + mobilization of antigen specific T cells
o Damage due to inappropriate larger levels of cytokines (+ chemokines) by T cells = recruitment due to chemokines responsible for delecterious outcome
- Characteristics
o Clinical=Contact hypersensitivity; tuberculin type; granulomatous
o Pathophysiology = activation of ag specific TH1 + TH17 cells, recruitment + activation of ag non-specific inflammatory leukocytes
- Exposure activates + expands TH1 + TH17 cell population (sensitization)
- Sensitisation occurs over 1-2 weeks
- Effort Phase takes 18-48 hrs

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15
Q

Whats the difference between primary and secondary immunodeficiencies

A

Primary Immunodeficiency:
- Deficiency is the cause of the disease
- Hereditary or acquired
- Can have deficiency of:
o Antibody (50%) humoral and cell mediated (20%)
o Phagocytic (18%), cell mediated alone (10%), complement (2%)

Secondary Immunodeficiency:
- Deficiency is the result of disease e.g. aids

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16
Q

The outcome for the 4 groups of SCIDS

A

The outcomes for the four groups of SCIDS defect of cell mediation and antibody production.

Susceptible to all microbial infections

T-B+ Subgroup:

  • X-linked SCID – 40-50% SCIDS
  • Lacking NK cells
  • Mutations on x chromosome effecting genes or y chain having receptors for IL-2,-4,-7, -9,-15

T+B- Subgroup:
- Adenosine deawinase deficiency (house keeping gene)
o 20% SCID patient = lacking gene
o = failure of B + T cell development
- Purine Nucleoside Phosphorylase Deficiency
o Mutation in purine pathway
o Build-up of toxic products damages neurologic system + T cells
o Damages all lymphoid tissues
- Recombinase Deficiency + Radiosensitivity SCID
o Recombination activating genes
o Code for enzymes that rearrange IgG genes in pre B Cells + TCR genes in pre T cell
- Omenn Syndrome
o Autoimmune
o Massive skin + GIT infiltration by T cells + eosinophils
o Produce TH2 types cytokines → Hyper IgE syndrome

T+B+ Subgroup:
- Bare Lymphocyte syndrome
o Failure to express human leukocyte antigen
o Missing MCH I, II or both

T-B+ Subgroup
- X-linked: Lymphopenia and lack of NK cells

17
Q

Immunodeficiency impacting other parts of immune system

A

IgA deficiency

  • Causes = unknown
  • Can be transient due to adverse drug reaction
  • Often linked with common variable immunodeficiency disease
  • Treated with antibiotics
  • Major antibiotic in external secretion- saliva, mucous, tears, swear, gastric fluid
  • Does not bind complement
  • Antiviral
18
Q

What is the course of HIV from infection to AIDS

A

3 Phases:

  1. Acute Phase:
    - Can be asymptomatic
    - May show with flu like symptoms: fever, soar throat + general malaise
    - Drop in CD4 cells
    - Dendritic Cells and Macrophages spreads the virus to lymph tissue
  2. Chronic Latent Phase:
    - Can last up to 15 yrs
    - Asymptomatic mostly:
    o Viral replication continues (low level)
    o Lymphadenopathy
    - Macrophages + DC are viral reservoirs + present virus on surface – continuous presentation of virus to T + B cells
    - As CD4 decreases- slowly become symptomatic
  3. Crisis Phase:
    - First recognised by presence of unusual infections + malignancies
    - AIDS is defined by any of the infections + less than 14% of the T Cells
    - Activation of virally infected T cells by antigen causes greater T cell death = exacerbates immunodeficiency
    - Malignancies:
    o Kaposi Sarcoma: associate with aggressive lymphoma; human herpies virus is detectable in Kaposi sarcoma
    o B Cell Lymphomas: mostly diffuse large B cell lymphoma
19
Q

Whats the difference between prokaryotes vs Eukaryotes?

A

Just view notes

20
Q

What are the different shapes of bacteria present?

A
  • Coccus = Spherical
  • Rod or Bacillus
  • Vibrio- comma
  • Spiral
  • Stalked
  • Branched
  • Square
21
Q

What is the difference in cell walls of gram +’ve and gram -ve bacteria?

A

Gram +ve
Peptidoglycan- cell wall -inner membrane - cytoplasm

Gram -ve
lipopolysaccharide - outer membrane- cell wall- inner membrane - cytoplasm

Gram +ve:
-	Peptidoglyean (outside)
-	Plasma membrane
Gram –ve:
-	Outer membrane – Lipopolysaccharide + proteins 	Periplasic space
-	Peptidoglycan
-	Plasma membrane
22
Q

Draw and explain the microbial Growth curve

A

view notes repeat

23
Q

What are the environmental factors affecting bacterial growth?

A
  1. Water
    - Required for cell metabolism
    - Determined by amounts and types of solutes dissolved in water (inorganic = NaCl, K, Mg vs organic = sugars, amino acids etc)
    - Increase concentration of solutes = decrease availability
  2. Temperature
    - Bacterial temperature = to immediate environment
    - No insulation or internal regulation of temperature
    - Too hot = death; too cold = don’t grow
    - Intermediate temperatures affect rate of growth
    - Heat kills bacteria by:
    o Coagulation + denaturation of proteins
    o Degradation of nucleic acids
    o Disruption + melting of cell membranes
    - Mesophils – can grow 15-45 degrees (humans)
  3. pH
    - Disrupts membranes
    - Inhibits enzymes
    - Inhibits transport/ uptake systems
    - Alters nutrient availability
  4. Oxygen
    - Substantial component of atmosphere – 20 %
    - Essential for aerobic respiration
    - Poison’s for anaerobes
24
Q

The different types of bacteria and their oxygen preferences?
What is their 02 preference and name?

A
  1. Aerobes:
    Require O2 for respiration
  2. Microaerophils: Require low levels of O2 (5-10%) – GI Tract
  3. Facultative Anaerobes: Can grow aerobically or anaerobically
  4. Obligate anaerobes: Grow only without O2
  5. Aerotolerant Anaerobes: Do not use O2 but can tolerate it
25
Q

Temperature and bacteria.

Whats their preferred temp range and name?

A
  1. Psychrophiles:
    ~-5 → 20
  2. Psychrotrophs:
    ~0 → 35
  3. Mesophiles:
    ~15 → 45
  4. Thermophiles:
    ~45 → 80
  5. Hyperthermophiles:
    ~70 → 105
26
Q

What is the function of normal Flora?

A
  • Synthesis + excretes vitamins
  • Prevents colonisation by pathogens
  • Antagonises other bacteria
  • Stimulates the development of gut mucosal tissues
  • Stimulates the production of cross- reactive antibodies
27
Q

What are the processes of Pathogen Infection?

A
  1. Enter Host
    - Penetrate the skin or mucous membranes
    - Ingestion with food
    - Inhalation in aerosols
    - Sexually transmitted
    - Transmission on an object
  2. Adhere to Cell Surface
    - Adhesins = Proteins or glycoproteins found on attachment pili + capsules
    - Attaches pathogen to receptors membranes of certain cells or tissues
  3. Colonise Cell Surface
    - Colonisation is the growth of bacteria on host tissues
  4. Invade Tissues
    - Bacteria invade host tissues using aggressins
    - Aggressins have proteolytic or lipolytic activity to aid in invading tissues and intercellular spaces
  5. Evade Host Defences
    - Some pathogenic bacteria are able to resist the bactericidal components of host tissues
  6. Produces Toxins and other harmful products
    - Bacterial toxins are soluble substances that alter the normal metabolism of host cells and damages the host
28
Q

The difference between Endotoxin and Exotoxins

A

Endotoxins: Protein toxins (secreted by organism)

Exotoxins: Lipopolysaccharide toxins (part of an organism)

Exotoxins:

  • Soluble proteins secreted by living bacteria
  • Produce by gram +ve/-ve bacteria
  • Causes damage to host by destroying cells or disrupting normal cellular metabolism

Types:
o Neurotoxins: Interfere with neurotransmission e.g. tetanus
o Enterotoxins: Effect intestinal cells, may cause diarrhoea e.g. cholera
o Cytotoxins: Attack cells in general e.g. lipases and nucleases
Endotoxins
- Toxin kept within bacterial cell
- Release after destruction of bacterial wall
- Toxic to environment and create immune response
- E.g. lipopolysaccharides

29
Q

What is the Sulphonamides and Trimethoprim Synergistic Effect?

A

Both drugs are:
- Structural analogues of p-aminobenzoic acid + :. Inhibitors of folic acid pathway
Folic acid is required for nuclear acid and protein synthesis
Because structural analogues of PABA :. Achieve synergic tic effect by acting on 2 close steps of folic acid pathway

30
Q

Antibiotic resistant bacteria happens when?

A
  • Resistance developed when misuse – sub lethal dose, incorrect antibiotic/ method, stopping treatment too soon
  • Information for resistance acquired by mutation or exchange of DNA between bacteria
31
Q

What are the best methods for destroying micro-organisms

A

Moist head:
- I.e. autoclave
- Best for sterilization on glassware, equipment
Heat Labile Materials
- Best sterilized by UV radiation (260nm)
- Or radiation (gamma ray from cobalt 60)

32
Q

What does autoclaving invoke?

A
  • Used to sterilize media, solution, equipment, glassware
  • 121 degrees, 150 pka for 15 minutes
  • High pressure saturated steam
33
Q 
Disease or Eukaryotes?
Malaria 
Cryptpsporidiosis
Giardia 
Sleeping sickness
A 
Malaria:
-	Caused by Plasmodium 
-	Carried by mosquitos 
-	Death toll = 1 million per year
-	Signs and symptoms:
o	Malaise
o	Sore muscles
o	Fever – rupture of schizont 
o	Liver impairment and kidney failure
Cryptosporidiosis:
-	Parasitic disease caused by cryptosporidium 
-	Spreads through fecal-oral route 
-	Major problem for those with poor immunity (HIV infected, immunosuppressed) 
-	Symptoms:
o	Abdominal pain
o	Massive volume of water diarrhoea 
o	Fatigue
o	Nausea
o	Weight loss 
Giardia 
-	Protozoan Parasite 
o	Waterborne also soil + food
o	Passed by faecal oral route 
o	Passed by beavers 
-	Reproduces in intestines 
Sleeping Sickness
-	I.e. Trypanosomiasis 
-	Trypanosoma brucei gambiense (95%) 
-	Carried by T setse fly 
-	Most at risk in tsetse fly areas (agriculture)
-	Loss of agriculture
34
Q

DNA hybridization?
Whats it for?
whats the process?

A
  • Identity + forensics
  • Genetic testing
  • Cancer diagnosis/ prognosis
  • Infections disease testing
  • Drug response testing
    Process:
    1. Target DNA:
  • T-DNA is denatured and separated into two strands
  • Single strands attached to membrane
  • Attached by backbone with nitrogenous based exposed
    2. Probe:
  • Probe is single stranded DNA or RNA molecule that seeks for SNA sequences
  • Always labelled with reporter group – radioactive atom or enzyme
  • Probe is left on target DNA + reacts if match is made
  1. Detection System
    - Reporter provides detection system
    - No detecting = gene or DNA segment not present
  2. Format
    - Dot blot – sample placed on nitrocellulose + procedure performed
    - Southern blotting- Gel- electrophoresis of target DNA prion to assays
35
Q

Polymerase Chain Reaction?

process?

A
  • Denaturation:
    o Heat DNA strand – 94 degrees
    o Double stranded DNA separate to become 2 single stranded DNA strands
-	Annealing :
o	By hybridization 
o	Strands cooled – 60 degrees 
o	2 primers bind to their target site 
-	Extension (DNA synthesis)
o	DNA heated to 72 degrees
o	DNA polymerase builds complimentary strand for each strand of DNA
o	DNA nucleotides used for building
36
Q

Restriction Enzymes

A
  • Enzymes that restrict access to bacteria by invading DNA
  • Binds at palindromic segments – reads from 5’-3’ on both strands
  • Cuts to produce blunt or sticky ends
  • Uses segmented DNA to be fused to another DNA using ligase
37
Q

Found effect- Genetics

A
  • When population is founded by a small number of individuals
  • Small number of individuals carry only small fraction of total genetic variation of the parental population
  • = given allele, gene, chromosome or part of chromosome found in members of pop can be traced back to one ancestral individual
  • Loss of genetic diversity
  • Occurs when a small group of individuals from a genetically diverse pop migrates away and forms a new colony
  • Small gene pool = genetic diversity reduced compared to parent population
38
Q

bacterial Plasmid- whats its role in genetic cloning?

A

?

CHI 305: Immunology (9 decks)

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