Final Exam Flashcards
(38 cards)
Range of symbiotic relationship: 2 different species closely interact with each other for much of their lives.
What are the types?
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
What are the sites of extracellular pathogen infection
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
What are the defence mechanisms that limit extracellular pathogen infections
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
What are the mechanisms employed by extracellular pathogens to evade the immune system i.e. changing surface proteins?
- 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
Areas in the cell where intracellular pathogens can survive
- 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
What are the means employed to survive intracellularly
- Hide in host cell vesicle or cytoplasm – enter through phagocytosis
- Live in: o Prevent phagosymal fusion o Phagolysosome o Cytosol o Alter phagosomal mutation
Roles of IFNy
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
Intracellular Pathogen Diseases
- Malaria
- Toxoplasma
- Listeria
- Leishmania
- All viruses
Passive vs active, natural + artificial immunity examples
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
Polyclonal vs Monoclonal Antibodies
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
Whata re the advantages and Risks associated with Vaccines
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
What is herd Immunity
- 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
Hypersensitivity Type 1 Phases
3 phases to it
- 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 - 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.
- Effector stages:
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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
What are the causes and mechanisms of Hypersensitive 2,3, 4
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
Whats the difference between primary and secondary immunodeficiencies
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
The outcome for the 4 groups of SCIDS
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
Immunodeficiency impacting other parts of immune system
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
What is the course of HIV from infection to AIDS
3 Phases:
- 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 - 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 - 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
Whats the difference between prokaryotes vs Eukaryotes?
Just view notes
What are the different shapes of bacteria present?
- Coccus = Spherical
- Rod or Bacillus
- Vibrio- comma
- Spiral
- Stalked
- Branched
- Square
What is the difference in cell walls of gram +’ve and gram -ve bacteria?
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
Draw and explain the microbial Growth curve
view notes repeat
What are the environmental factors affecting bacterial growth?
- 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 - 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) - pH
- Disrupts membranes
- Inhibits enzymes
- Inhibits transport/ uptake systems
- Alters nutrient availability - Oxygen
- Substantial component of atmosphere – 20 %
- Essential for aerobic respiration
- Poison’s for anaerobes
The different types of bacteria and their oxygen preferences?
What is their 02 preference and name?
- Aerobes:
Require O2 for respiration - Microaerophils: Require low levels of O2 (5-10%) – GI Tract
- Facultative Anaerobes: Can grow aerobically or anaerobically
- Obligate anaerobes: Grow only without O2
- Aerotolerant Anaerobes: Do not use O2 but can tolerate it
