Chapter Eight - Infection And Defects In Mechanisms Of Defense Flashcards
Communicability
Ability to spread from one individual to others and cause disease
Infectivity
Pathogen ability to invade and multiply in host
-involves attachment, escape of phagocytes, dissemination
Virulence
Severity or harmfu;ness of a disease or poison
Toxigenicity
Ability to produce toxins
-greatly influence pathogens virulence
Portal of entry
Route by which a pathogen infects host
-direct contact, inhalation or ingestion
Prokaryote cell
Nucleoide, pilus, flagellum, cell wall
Eukaryote cell
Nucleus, Golgi apparatus, ER, mitrochondrion, lysosome
Bacteria
Prokaryotes - lack discrete nucleus
-aerobic or anaerobic
-gram positive or negative
Two main factors that make GN more difficult to defeat than GP
outer membrane and porin channels
Porin
Gateway
-very few doors that are well guarded can only enter through porin
Staphylococcus aureus
-life threatening
-major cause of nosocomial infections
-common on normal skin and nasal passages
Virulent abilities of S.aureus
1.produce protein that blocks compliment attack
2. Avoid innate immunity by producing inhibitors that avoid recognition
3. When engulfed, they can resist lysosome by changing chemistry of cell walls
4. Resist actions of antibiotics
Exotoxins
Released from inside of pathogen
-enzymes that damage host cell plasma membranes or inactivate enzymes critical to protein synthesis
Endotoxins
Released from outer capsule
-activate inflammatory response and produce fever
Bacteremia
Presence
Septicaemia
Growth
What toxin activates complement and clotting systems
Endotoxins
Endotoxins =
- Inc capillary permeability
- Large volumes of plasma into surrounding tissue
- Resulting hypotension
If either bacteremia or septicaemia exists that means
Defense mechanisms failure
What is the most common affliction of humans
Viral diseases
Replication of viruses requires
Entry into host cell
Simple structure of virus
DNA and RNA surrounded by capsi and perhaps envelope
Viruses are self limiting (true or false)
True
Viruses transmitted via
-aerosol
-infected blood
-sexual contact
-vector (ticks, mosquitos)
Cytopathic
Causing damage to living cells
Cytopathic inhibit
Host cell DNA or RNA synthesis
Cytopathic release
Lysosomes into host cell, killing cell
Cytopathic: fusion of host cells into
Multicellular giant cell
Cytopathic: alteration of host cells antigen properties =
Uninhibited growth
Cytopathic: utilization of
Host cell resources
Influenza
Highly contagious viral infection of respiratory passages
Antigenic variation
Ability to change viral antigen (spikes) yearly
-antigens utilized to activate adaptive immune response
Ability to change =
Dysfunction adaptive immune response
-B or T cells
SARS-CoV-2 virus’s
Responsible for COVID 19
Fungal infections
-large eukaryotes with, thick rigid cell walls
-resist penicillin
-exist as single called yeasts, multi cellular, molds or both
Fungal reproduction
Simple division or budding
Moulds
Filamentous fungi grow as multinucleate, branching hyphae, forming a mycelium
-ringworm
Yeasts
Yeasts grow as ovoid or spherical, single cells multiply by budding and division
-histoplasma
Mycoses
Diseases caused by funhi
Dermatophytes
Fungi that invade skin, hair or nails
Diseases dermatophytes produce are called
Tineas
Pathogenicity of fungus
Adapt to host environment —> wide temp variations, low oxygen
-suppress immune defences
low white blood cell count promotes
fungal infection
Most common cause of fungal infections
Candida albicans
Candida albicans is found
In normal skin micro biome, GI tract, and vagina of many individuals
Candida albicans is most commonly found in
Cancer patients and transplantations
-higher risk of deep infection and higher mortality rates
Death rate of disseminated candidiasis
30-40%
-immunocompromised, and spreading
Parasitic infections can vary from
Unicellular Protozoa to large worms
How do parasitic infections spread
Spread human to human via vectors
-ticks, mosquitos
Or ingestion of contaminated food or water
Parasitic infection causes
Tissue damage due to toxin or inflammatory immune response
Plasmodium malaria occurs in RBC
Continual infection of RBC
-anemia in 48-72 hours
-RBC release cytokines = fever chills and vomiting
What cytokines do RBC release in plasmodium malaria
TNF-a and IL-1
Antibiotics
Natural products of fungi, bacteria or other microorganisms that affect growth of specific microorganisms
Antimicrobials (2)
-bactericidal
-bacteriostatic
Bacterial
Agent that kills other microorganisms
Bacteriostatic
Agent that inhibits growhrt of other microorganisms
1944
Penicillin effective at treating infection in British hospital
1946
14% of all S.aureus are penicillin resistant
1950
59% of S.aureus are resistant
1990
89% s.aureus are resistant
What has caused rise in antibiotic resistance
-lack of compliance with therapeutic duration
-overuse of antibiotics
Lack of compliance with therapeutic regimen
Not using antibiotics iotas for prescribed duration
-results in strongest microbes are left alive and repopulation within pathogens are resistant to specific antibiotic
Overuse of antibiotics
Destruction of normal micro biome = opens space for more infectious and resistant pathogens
Vaccines
Biological preparations of weakened or dead pathogens
Adaptive response of vaccine usually requires
Two weeks to activate
Vaccine allows this two week period to be performed against a
Non viral pathogen
When infection by viral pathogen occurs….
Adaptive immunity is already prepared (no two week delay)
Vaccine mixture
DTaP (diphtheria, tetanus, pertussis
HERD immunity requires
85 percent of population to be immunized
Toxoids
Chemically altered pathogen toxin injected into body
-allows body to learn to defeat pathogens toxin
Passive immunotherapy
Performed antibodies (against pathogen) are given to individual
Human immunoglobulin antibodies are obtained from
Pathogen survivor
Passive immunotherapy is becoming focus after rise of
Antibiotic resistance
Primary (congenital) immunodeficiency is caused by
A genetic defect
Secondary (acquired) immunodeficiency is caused by
Another illness
-cancer
Most primary deficiencies result of a
Single gene defect
Mutations are
Sporadic, and not inheritited
-occurs before birth, but symptoms appear early or late in life
Statistics for primary deficiencies in Canada
1 in 200 have condition
70% undiagnosed
Severe combined immunodeficiency
Underdeveloped thymus
-a serene of T cells
-few detectable lymphocytes
DiGeorge syndrome
Thymus and parathyroid gland dysfunction
-inadequate T cell production and management of plasma calcium
Hypogammaglobulinemia
Results from defect in B cell maturation or function
-lower levels of circulating immunoglobulins (antibodies) in blood
Secondary deficiencies are
Acquired deficiencies
-far more common than primary definitives but not as clinically relevant
severe examples of secondary deficiencies
AIDS or cancer
CBC or complete blood count
Total numbers of RBC, WBC and platelets
Differential
Individual numbers and lymphocytes, granulocytes and monocytes
Quantitative determination of immunoglobulins
Determine sub populations of immunoglobulins
Total complement assay
Total number of complements in blood
Stem cell transplantation from
Bone marrow, umbilical cord cells
-most cases improvement is temporary
Mesenchymal stem cell injection
-undifferentiated stem cells found in bone marrow
-undergo differentiation into other cell types
-have potent immunosuppressive properties
Gene therapy
Two girls received first therapeutic replacement of defective genes
-inserted normal genes into genetic material
-caused reconstitution of immune system
-some recipients develop leukaemia
AIDS
-depletes helper T cells that are necessary for activation of both T and B cells
Results of HIV
-dysfunctional adaptive immune system
-inc susceptibility to disease
-AIDS
Epidemiology of AIDS
-Heterosexual acuity is most common transmission route worldwide
-women constitute more than 50% of people infected
-children contract via placenta or breastfeeding
Difficulties with vaccine development of HIV
-HIV genetically and antigenically variable
-individuals with HIV have high levels of antibodies but don’t appear to be protective
-therefore, even if vaccine creates antibodies they might not function effectively
Antiretroviral therapy
Treatment and prevention of HIV
-retroviral means virus with RNA not DNA
Treatment of HIV is not
Curative but death is reduced significantly
Hypersensitivity
Altered immunological response to an antigen that results in disease or damage to host
Allergy
Harmful effects of hypersensitivity to environmental antigens
-pollen, bee stings
Autoimmunity
Disturbance in immunological tolerance of self antigens
-immune system doesn’t recognize bodies own antigens
-clinical disorders are called autoimmune diseases
Alloimmunity
Immune reaction to tissues of another individual
-transfusions, transplants or fetus during pregnancy
Type I
IgE mediated
-hay fever
Type II
Tissue specific reactions
-hemolysis in medication allergies
type III
Immune complex mediated
-gluten allergy
Type IV
Cell mediated
-poison ivy
Most hypersensitive reactions include more than one
Type
Immediate hypersensitivity reactions
Reaction that occurs within minutes or hours
Anaphylaxis
Most rapid and severe immediate reaction
-within minutes
Symptoms of anaphylaxis
-pruritis (severe itching)
-erythema (red patches on skin)
-vomiting, diarrhea, breathing difficulties
Delayed hypersensitivity reactions
Reaction occurs after several hours and are at maximal several days alter
What is the most common hypersensitive reactions
Type I
Type I is mediated by
Mast cells and IgE
-primarily histamine
Type I: against environmental antigens :
Therefore = allergic
Type I: initial exposure to allergen =
IgE binding to mast cell receptors = person now considered sensitized
Type I: subsequent exposure to allergen =
Mast cells relapse of cytokines = hypersensitive reaction
Type I: tissues with high
Mast cells are msot commonly affected
-skin, GI tract, pulmonary tract
Atopic
Individuals predisposed to developing allergies
-one parent has allergies = 40% offspring will
-both parents have allergies = as high as 80%
Initial exposure to allergen =
IgE binding to mast cell receptors = person now considered sensitized
Re exposure to allergen =
Mast cells release of cytokines = hypersensitive reaction
Type II : tissue specific
-cytotoxic hypersensitivity
-immune reactions against a specific cell or tissue
Cytotoxic hypersensitivity
Antibody mediated destruction of healthy host cells
Type II: tissues specific antigens
Because they attach only on plasma membranes of certain cells
Example of type II
Platelets have antigens found on no other cell in body
Type II has five mechanisms
A,B,C,D,E
-each mechanisms begins with antibody binding to tissue specific antigens
Type II: A
Cell is destroyed by antibodies and complements
(A) Antibody binding to cell =
Activation of complement system = formation of membrane attack complex = disintegration or rupture of cell wall
Type II: B
Cell destruction through phagocytosis by macrophages
(B) antibody binding to cell =
Macrophage recognition of a cell to be phagocytize
Type II: C
Tissue damage caused by toxic products produced by neutrophils
-soluble antigens from infectious agents or hosts own cells binds to cell surface
-neutrophils are attracted and release their granules into healthy cells = damage cells
Type II: D
Antibody dependant cell mediated cytotoxicity
-binding of igG antibodies to antigens
-attracts NKC that release toxic sutbances that destroy cell
Type II: E
Target cell malfunction
-Graves’ disease, targets thyroid
(E) mechanism doesn’t destroy cell but
Causes cell to malfunction
-antibody prevents cells interaction with normal molecule
Type III
Antigen antibody immune complexes are formed in circulation and later deposited in vessel walls or extra vascular tissues
Type IV hypersensitivity : cell mediated
Does not involve antibody
-is mediated by T cells
Examples of IV hypersensitivity
-graft rejection
-allergic reactions from poison ivy or metals = T cell activation = macrophage activation = tissue damage
