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140 Cards in this Set
- Front
- Back
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For chlamydia, the host cell provides the bacteria with ____
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ATP
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Chlamydia has a cell wall, but it is formed by ____ as opposed to ____.
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Cell wall proteins crosslinked by disulfide bonds
Instead of peptidoglycan |
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Chlamydia are ____, meaning they can only reproduce inside a host
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Obligate intra-cellular parasites
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Chlamydia has 2 forms of cells
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1. Elementary bodies
- Small, made for transmission and infection - Introduced by phagocytosis - rearrange to form next form 2. Reticulate body - Larger, made to reproduce - Cause cell lysis - Reform into EBs within 24-48 hours following binary fission |
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Chlamydia trachomatis
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1. Trachoma = rough eye
2. Repeat infections = entropion, lashes turn inward --> blindness 3. Clean water and azithromycin as treatment/prevention 4. Also causes non-gonococccal urethritis - Pain in urination, discharge, infertility, epididymitis, PID -Treated with doxycycline |
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Chlamydia psittaci
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Parrot fever --> feces dust particles inhaled by humans
Fever, chills, coughs, respiratory illness in general Treated with tetracycline and doxycycline, but not penicillin |
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Elementary bodies in chlamydia
Cell wall, RNA:DNA ratio, toxicity to mice, resistance |
Rigid cell wall
1:1 Toxic to mice Resistant to sonication and trypsin |
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Reticulate bodies in chlamydia
Cell wall, RNA:DNA ratio, toxicity to mice, resistance |
Fragile cell wall
3:1 Not toxic to mice Sensitive to sonication and lysed by trypsin |
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Rickettsia
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Rods, coccoid, nonmotile, gram -
Parasites that grow in erythrocytes, macrophages, vascular endothelial cells Vectors include ticks, fleas, lice |
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Rickettsia parasitize to obtain what?
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Coenzymes, nutrients
They do not use glycolysis, oxidize succinate, and take amino acids for energy? Cytoplasmic membrane exchange --> ADP for host ATP |
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Rickettsia prowazekii
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Louse-born typus
Reproduce in louse gut --> feces scratched into body by humans --> enters blood stream --> vasculitis and death if not treated Treated with tetracycline |
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Rickettsia typhi
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Typhus fever
Rat --> flea --> human |
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Rickettsia rickettsii
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Rocky Mountain Spotted Fever
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What are mycoplasmas?
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Bacteria without cells walls, pleomorphic
Grow only with osmotic protection |
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Mycoplasmas are resistant to...
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Antibiotics targeting cell wall synthesis
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Mycoplasma pneumoniae
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Primary atypical pneumonia (also known as walking pneumona, pleuropneumonia)
Inflammation of pleura (membranes surrounding lungs) |
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Mycoplasma hominis/genitalium
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Non-gonococcal urethritis --> infertility
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Mold and yeast shared features
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Absorb nutritional elements
No chlorophyll Chitin cell walls Form spores Non-motile Tolerate dryness, high osmotic pressure, acid and alkaline environs Saprophytes |
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What is a saprophyte
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Any organism residing on dead/decaying matter and permits recycling
Release hydrolytic enzymes to digest external food |
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Mold features
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Have long branched filaments known as hyphae
Coenocytic - multiple nuclei located within one cell wall No perpendicular cross walls Grow by extension and branching of hyphae Mycelium = mass of hyphae = colony Spores are dormant and can germinate |
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Yeast features
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Unicellular
Single nucleus Bud progeny in most cases |
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Dimorphic fungi features
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Yeast form in body, filamentous form in media
Some cause disease |
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Mycology - Reproduction
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Asexual: Mitosis followed by:
- Transverse cell wall formation to form two equal daughter cells - Budding forming mother cell and bud - Transverse cell wall formation forming spores in hypha or at end of it Sexual: - Homothallic - self-fertilizing on same mycelium - Heterothallic - Crossing between different but compatible mycelia -Haploid gametes fues --> diploid gametes --> meiosis --> haploid spores |
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Zygomycetes
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Coenocytic - Haploid nuclei, hyphae
Rhizoids extend into media to absorb nutrients Stolons - Erect hyphae forming sporangia with black sporangiospores |
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Rhizopus nigricans - Phylum of fungi and feature
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Zygomycete
Common black bread mold |
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Asomycetes
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Septate hyphae --> conidiospores at end of conidiophore
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Aspergillus fumigatus - Phylum of fungi and feature
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Asomycete
Home allergen causing asthma, sinusitis and allergic reactions Opportunistic pathogen (such as in those with HIV) |
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Aspergillus flavus - fungi phylum and feature
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Asomycete
Aflatoxins |
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Penicillium notatum - fungi phylum and feature
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Asomycete
First penicillin |
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Penicillium roqueforti
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Asomycete
Cheese softening/ripening |
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Claviceps purpurea
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Ergot of rye - plant disease
Ergotism in people - toxin - lysergic acid diethylamide LSD - Gangrene, psychotic delusions, abortion, convulsion, death |
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Basidiomycetes
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Mushrooms
Diploid hyphae growing in soil push through soil Cap forms which forms basidiospores |
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Dermatophytes and subtypes
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Fungi on/in/under skin, hair, nails
a. Superficial: outer surfaces, tropical Soap and water treatment? b. Cutaneous: Within hair/skin/nails Ringworm, athlete's foot c. Subcutaneous: Introduces through skin, such as in puncture wounds Spread along lymph channels |
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Histoplasma capsulatum
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Causes histoplasmosis
Mild respirator infection - recovery in healthy people without them knowing the disease was present Endemic to Ohio River Valley Severe illness with weak immune system |
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COCCIDIODES IMMITIS
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Coccidioidomycosis, or desert fever
Mostly causes mild respiratory issues, some get TB-like symptoms Rarely spreads to brain, bones, meninges, joints |
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Cryptococcus neoformans
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Cryptococcosis
Respiratory tract --> CNS Meningitis |
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Pneumocystis carinii
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Pneumocystis pneumonia
Occurs in immunocompromised |
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Treatment of systemic fungal infections
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Amphotericin B: Disrupts membrane function. Toxic for people
Fluconazole: Prophylactic in AIDS patients that inhibits sterol synthesis --> inhibits normal membrane function |
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Candida albicans - details
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Flourishes in immunocompromised, when antibiotics disrupt normal floral balance and prokaryotic balance
Vaginitis, diaper rash, thrush, discharge Treated with: A. Nystatin - Streptomyces antibiotic that causes damage to membranes and cytoplasmic leakage B. Miconazole - Antibiotic that disrupts sterol synthesis and damages membranes |
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Mutualism of termite and protist
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Termites ingest cellulose --> protist digests cellulose to H2, CO2, and Acetate --> Bacterium in protist converts CO2 and H2 to Acetate and atmospheric N2 to NH3 --> Used by protist and termite
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Commensalism
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One benefits, the other is neither harmed nor benefits
Ex: Non-pathogenic neisseria species and lactobacillus (lactic acid fermentation to sugars) |
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Parasitism
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One benefits, other harmed
Ex: Streptococcus pneumoniae and other pathogens |
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Symbiosis
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Living together. Can be mutualistic, commensal, or parasitic
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What is virulence?
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Degree of intensity of disease, degree of pathogenicity
Ex: Highly virulent - rotavirus Weak - candida albicans |
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Nosocomial infection?
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Infection by health care facility.
Seen in surgical wounds, catheters, immunosuppressed people |
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Normal flora found on skin
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Staphylococcus aureus
Staphylococcus epidermidis Candida albicans |
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Normal flora of eye
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Lysozyme - hydrolyzes peptidoglycan
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Upper resp. tract normal flora
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Pathogen carriers - Streptococcus pyogenes
Neisseria meningitidis Opportunistic pathogens - Pneumocystis carinii |
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Normal flora of mouth/throat
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Pathogen - Streptococcus mutans
Opportunistic pathogen - Candida albicans |
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Flora of intestine
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E. coli, enteric organisms that are gram - rods
E. coli is usually nonpathogenic, but can cause illness, such as with the enterohemorrhagic strains (hemolytic uremic syndrome) This causes hemolytic anemia, renal failure Also find Shigella, Salmonella, Campylobacter, Enterococcus Coliforms : gram - rods, facultative anaerobes, non-spore forming - Klebsiella, Enterobacter, Escherichia Fecal variants also present |
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Flora of urogenital tract
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Commensals, such as lactic acid bacteria
Opportunistic path.s cause : -vaginitis (candida and trichomonas vagnalis) -Cystitis (bladder inflammation) and UTIs Enterococcus faecalis Enterococcus faecium Uropathogenic E. coli |
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Koch's postulates (4)
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1. Same organism present in every case of disease
2. Organism must be isolated from diseased host and grown in pure culture 3. Introducing pure culture to same type of host causes same disease 4. Organism must be isolated from this new host and grown again successfully in pure culture |
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Endemic
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Always present (such as histoplasma capsulatum)
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Epidemic
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Sudden increase in occurrence (such as in cholera)
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Pandemic
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World-wide epidemic
HIV |
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Sporadic outbreak
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Localized outbreak, such as Hanta virus
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What is incidence?
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Number of cases of disease within a specified period of time
It is a rate in a given location, shown as numbers of incidence per unit of population (# per 100,000) |
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What is prevalence?
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Number of cases of disease within population at any time or any defined time period
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Diseases caused by exotoxins
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1. Diphtheria from Corynebacterium Diphtheriae
Lysogenic with prophage 2. Botulism from Clostridium botulinum Lysogenic 3. Tetanus from Clostridium tetani Plasmid 4. Gas gangrene from Clostridium perfringens Plasmid 5. Anthrax from Bacillus anthracis Two plasmids |
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Innate Host defense types - 7
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1. Physical barriers
2. Chemical barriers 3. Phagocytosis 4. Inflammation 5. Complement system 6. Opsonization 7. Cytokines |
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Innate Host defense - Physical barriers
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1. Skin
A. Epidermis - outer layer keratin B. Dermis - inner layer 2. Mucous membranes Mucus traps organisms and lysozymes destroy them (Hydrolyzes peptidoglycan) |
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Bacteria that colonize mucous membranes
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Neisseria gonorrhoeae
Mycobacterium tuberculosis Streptococcus pyogenes Treponema pallidum |
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Innate Host defense - Chemical barriers
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Tears, sweat - Lysozymes, flushing
Saliva - digestive enzymes Urinary tract - flushing Interferons: Antiviral proteins;cytokines - Produced by virus-infected cells but act on normal cells to limit virus production -Hydrolyze virus DNA and inhibit virus protein production Host-specific, not virus-specific Cationic peptides: alter plasma membrane permeability |
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Blood components
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1. Blood - fluid + cells
2. Plasma - fluid without cells 3. Serum - fluid remaining after clot forms and traps cells |
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Blood Cells - Principal types of leukocytes
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1. Basophil
2. Neutrophil - most common 3. Eosinophil 4. Monocyte (which become macrophages) 5. Lymphocytes (T and B cells) |
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Hematopoiesis
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Formation of blood cellular components
Hematopoietic stem cells form in bone marrow and differentiate into: A. Myeloid stem cells - Myeloid - develop in bone marrow, spinal cord B. Lymphoid stem cells - lympoid - Form in lymph tissues - thymus, lymph nodes, spleen, bone marrow |
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Myeloid stem cells form into...
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1. Granulocytes - Basophil (allergies), Neutrophil (phagocytosis), Eosinophil (phagocytosis)
2. Megakaryocytes - fragment into thrombocytes = platelets for clotting 3. Agranulocytes - Monocytes that differentiate into macrophages and dendritic cells - ingest and process foreign material for antigen presentation Reticulocytes - RBC |
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Lymphoid stem cells form into...
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Agranulocytes - lymphocytes
A. T cells: Help B cells in humoral immunity and function in cell-mediated immunity B. B cells: Humoral immunity - differentiate into plasma cells and secrete antibodies Natural killer cells |
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Monocytes and their destinies
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Circulate and migrate into tissues, then mature into macrophages and dendritic cells
Have receptors for common components of pathogens --> phagocytize invaders (innate resistance) --> digest and process invaders, display their antigens on surface to contribute to acquired immunity Macrophages are found in all tissues, especially lymph nodes and channels Dendritic cells are found in mucous membranes |
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Innate Host defense types - 7
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1. Physical barriers
2. Chemical barriers 3. Phagocytosis 4. Inflammation 5. Complement system 6. Opsonization 7. Cytokines |
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Innate Host defense - Physical barriers
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1. Skin
A. Epidermis - outer layer keratin B. Dermis - inner layer 2. Mucous membranes Mucus traps organisms and lysozymes destroy them (Hydrolyzes peptidoglycan) |
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Bacteria that colonize mucous membranes
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Neisseria gonorrhoeae
Mycobacterium tuberculosis Streptococcus pyogenes Treponema pallidum |
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Innate Host defense - Chemical barriers
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Tears, sweat - Lysozymes, flushing
Saliva - digestive enzymes Urinary tract - flushing Interferons: Antiviral proteins;cytokines - Produced by virus-infected cells but act on normal cells to limit virus production -Hydrolyze virus DNA and inhibit virus protein production Host-specific, not virus-specific Cationic peptides: alter plasma membrane permeability |
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Blood components
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1. Blood - fluid + cells
2. Plasma - fluid without cells 3. Serum - fluid remaining after clot forms and traps cells |
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Blood Cells - Principal types of leukocytes
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1. Basophil
2. Neutrophil - most common 3. Eosinophil 4. Monocyte (which become macrophages) 5. Lymphocytes (T and B cells) |
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Hematopoiesis
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Formation of blood cellular components
Hematopoietic stem cells form in bone marrow and differentiate into: A. Myeloid stem cells - Myeloid - develop in bone marrow, spinal cord B. Lymphoid stem cells - lympoid - Form in lymph tissues - thymus, lymph nodes, spleen, bone marrow |
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Myeloid stem cells form into...
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1. Granulocytes - Basophil (allergies), Neutrophil (phagocytosis), Eosinophil (phagocytosis)
2. Megakaryocytes - fragment into thrombocytes = platelets for clotting 3. Agranulocytes - Monocytes that differentiate into macrophages and dendritic cells - ingest and process foreign material for antigen presentation Reticulocytes - RBC |
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Lymphoid stem cells form into...
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Agranulocytes - lymphocytes
A. T cells: Help B cells in humoral immunity and function in cell-mediated immunity B. B cells: Humoral immunity - differentiate into plasma cells and secrete antibodies Natural killer cells |
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Monocytes and their destinies
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Circulate and migrate into tissues, then mature into macrophages and dendritic cells
Have receptors for common components of pathogens --> phagocytize invaders (innate resistance) --> digest and process invaders, display their antigens on surface to contribute to acquired immunity Macrophages are found in all tissues, especially lymph nodes and channels Dendritic cells are found in mucous membranes |
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Phagocytosis mechanism
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Neutrophils and macrophages act in acquired and innate immunity
1. Pathogen recognition - phagocyte receptors bind common elements on invaders 2. Intracellular digestion as phagosome and lysosome combine to form phagolysosome with digestive enzymes that hydrolyze and reactive oxygen intermediates 3. Exocytosis: Phagolysosome fuses with membrane and disposes of components. Macrophages and dendritic cells display these components as antigens for acquired immunity |
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Inflammation - Innate
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Non-specific response to tissue injury
Injury --> signals released that activate endothelium of capillaries --> Selectins displayed on endothelium to attract neutrophils --> integrins synthesized by neutrophils that bind to selectins --> diapedesis occurs, which involves neutrophil squeezing into capillary wall into interstitial fluid --> extravasation, migration to injury --> ATTACK! Inflammation is mediated by increased capillary permeability and increased blood flow |
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The complement system - Innate
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Serum proteins (~30), defend against microbes, enhance phagocytosis, bridge innate and acquired immunity
Activated during invasion --> macrophages break down invaders --> product of the degradation active complements An activated complement can: A. Release peptide mediators during inflammation B. Opsonization of pathogens = enhance phagocytosis by neutrophils C. Activation of membrane attack complexes which lyse eukaryotic cells and enhance susceptibility of prokaryotes to lysozyme |
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How does opsonization work in the complement system?
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It enhances phagocytosis by coating invaders with antibodies, the complement itself, or both.
Having both gives the best result as it increases binding the most |
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Cytokines - Innate
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Proteins produced and released by one cell type to regulate activity of another cell type
Regulators of innate resistance and specific immune response A. Interleukins: Produced by one leukocyte type, act on another leukocyte type B. Lymphokines: Produced by one type of lymphocyte, act on another type C. Chemokines: Regulate inflammation D. Erythropoetin: stimulates RBC production E. Interferons: Limit viral infection |
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Acquired immunity - Diversity
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Antibodies recognize trillions of specific structures
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Acquired immunity - Specificity
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Immunity directed at one unique pathogen
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Acquired immunity - Memory
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Responding quickly to re-exposure
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Acquired immunity - Humoral immunity
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Circulating, soluble proteins and antibodies
React to bacteria, some viruses, toxins B lymphocyte deficiency = Agammaglobulinemia and bacterial infections |
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Acquired immunity - Cell-mediated immunity
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Cells which specifically attack host cells
Deals with some viruses, fungi, and tumors T lymphocyte deficiency = DiGeorge Syndrome and viral infections |
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T and B lymphocyte deficiency can cause...
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Severe Combined Immunodeficiency Disease
Lethal |
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Acquired immunity - Stem cells remaining in bone marrow become...
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B cells --> plasma cells --> antibodies
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Acquired immunity - Stem cells traveling to thymus become...
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T cells --> TH (Intensify immune response); TC - lyse cells; TS - suppress immune response
Can also form memory T cells that act in memory |
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Soluble antibodies are produced in which?
Humoral or cell-mediated system? |
Humoral
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Cytotoxic cells are produced in which system?
Humoral or cell-mediated? |
Cell-mediated
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What is immune tolerance?
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Removal of lymphocytes developing specificity for self molecules to protect the organism
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Antigen-independent period summary
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Lymphocytes are produced in large number with a specific antigen programmed for it for the rest of its life. Lymphocytes that might attack the self are removed
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Antigen-dependent period summary
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Lymphocytes finally populate lymphatic organs and will respond to antigens they are programmed to attack.
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Antigens cause what type of response in acquired immunity?
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Antibody production and cell-mediated response
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Name what typically counts as an antigen
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Fungal/bacterial surface proteins, capsid and envelope proteins of viruses, pollen, dust, dander, toxins, blood cells that are not of the same type as host
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Antigenic determinants (epitope)
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Smaller structures on antigens (amino acid side chains on protein surface) recognized by antibodies
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Immunoglobulin classes
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1. IgG: Gamma heavy chain, monomeric, 80%, fluids, toxins, opsonin, transplacental (can cross to placenta)
2. IgM: Mu heavy chain, pentameric, membrane bound on B cells, activate complement, fights pathogens before IgG 3. IgA: Alpha heavy chain, monomeric, mucous membranes, protect surface 4. IgD: Delta heavy chain, monomeric, B cell surface, recognizes antigens 5. IgE: Epsilon heavy chain, monomeric, immune disorders (anaphylaxis) |
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Another name for antibody?
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Immunoglobulin
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The humoral system can deal with what types of viruses?
Which bacteria is mentioned? |
Non-enveloped (polio, hep A)
Bordetella pertussis |
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How can a person synthesize 10e13 different antibodies?
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1. Rearrangement of antibody gene segments in precursors to B cells (combinatorial joining and gene splicing)
2. Generating different codons during gene splicing 3. Somatic mutations - antigenic stimulus during B cell production causes mutations in V region |
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Immunoglobulin gene splicing - How are light chains made?
Heavy chains? |
Many V, J, C regions in precursor B cells --> splicing to join one V, J, C
Many V, J, C D regions in precursor --> splicing to have one of each |
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Acquired Immunity - T cells - What is the MHC
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Major histocompatibility complex
Found on APCs, such as macrophages and dendritic cells. These bind epitopes. Can then interact with T cells depending on having CD4+ or CD8+ |
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T cells - What type of MHC do cells with CD4+ immunoglobulin react with?
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MHC II
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CD8+ cells and MHC I = what type of T cells formed?
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Cytotoxic T cells
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T cells - What type of MHC do cells with CD8+ immunoglobulin react with?
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MHC I
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CD4+ cells and MHC II = what type of T cells formed?
Which acquired immune systems are these specific T cells seen in? |
T Helper cells
TH1 in CMI, TH2 in Humoral |
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TH1 CD4+ cells secrete cytokines that aid in what?
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Cytotoxic T cell formation
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Humoral, MHC II, TH2, CD4+ cells = what lymphocytes?
CMI, MHC I, Th1, CD8+ cells = ? |
B cells
Cytotoxic T cells |
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T cells - What is perforin?
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Granzyme pathway --> Cytotoxic proteins stored in granules on CT cells --> Recognition of antigen on host cell causes release of perforin and granzymes --> Cause apoptosis of cell
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What is apoptosis?
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Programmed cell death from within
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Monoclonal antibody?
How produce? |
Serum with only one type of antibody - bind same epitope
Inject a mouse with antigen with many epitopes --> Obtain mouse spleen cells producing antibodies --> fuse these cells with myeloma cells (immortal) --> isolate cells producing desired monoclonal antibody --> purify antibody |
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MHC composed of how many proteins?
Where do we find MHC I? MHC 2? |
2 different proteins (heterodimer)
MHC I = All tissues except RBC MHC II = Macrophages, dendritic cells, T and B cells |
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MHC genes are co-dominant. What does this mean?
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Each person has 2 alleles, one from each parent. They are both expressed fully.
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MHC I proteins act as ___ in people with different MHC I amino acid sequence
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Antigens
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How does tissue rejection occur?
What drug is used in tissue rejection cases? How is this more complicated when the graft attacks the host? |
Foreign MHC antigens recognized by T Helper and Tc cells that attack graft
Or foreign MHC antigens stimulate T helper cells to release cytokines that stimulate macrophage attack Or graft immune cells attack host body (bone marrow transplants) Cyclosporin. Must treat donor marrow in such cases with cyclosporin |
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Acquisition of immunity - Active acquisition
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1. Infection and recovery with antibodies and CTL production
2. Artificial - vaccination |
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Acquisition of immunity - Passive acquisition
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1. Natural - fetus receives antibodies from mother
2. Injection of antiserum, which contains known antibodies or pooled normal sera |
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Vaccines - Bacterial
How treat Bordetella Pertussis? Mycobacterium tubcerculosis? |
1. Killed vaccine
2. BCG strain (attenuated) - immunogenic but not pathogenic |
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Vaccines - viral
How treat polio? Rabies? Small pox? |
1. Salk vaccine (killed), Sabin vaccine (attenuated)
2. Killed/attenuated 3. Vaccinia virus - mild infection |
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Vaccines - toxins
How treat generally? Name one vaccine that does this? |
Use chemically altered toxin that stimulates immunity, no longer toxic
Tetanus |
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What are subunit vaccines?
Name the mentioned disease in this case. |
Proteins of a virus that are not pathogenic and stimulate immunity
Hep B |
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Type 1 immune disorder
Mechanism |
Anaphylaxis, allergy
IgE binds to receptors of basophils, eosinophils, mast cells --> produces histamine --> IgE binding sensitizes cells to antigen that caused IgE production --> second exposure causes antigen to bind to IgE + mast cell --> degranulation (release of histamine) --> allergic reaction symptoms |
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Localized allergic reaction - triggers?
Location of affect? |
Dust, pollen, dander, house mites, etc.
Upper resp. tract Lower resp. tract = asthma Digestive system = hives, gastroenteritis |
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Systemic allergic rxn - triggers?
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Drugs, venom, food allergies
All throughout body effect |
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Type 2 immune disorder
Mechanism |
Cytotoxic reactions
Antigen-antibody interaction damages own host cells. IgM and IgG react on host cells Seen in mismatched blood donation |
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RBC types - antigens present
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A = A
B = B AB = A and B O = none |
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RBC types - Antibodies in blood
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A = Anti B
B = Anti A AB = None O = Anti A and Anti B |
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RBC types - Alleles present
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A = Ia Ia or Ia i
B = Ib Ib or Ib i AB = Ia Ib O = i i |
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Typing of blood mechanism
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Add unknown blood type sample with a known antibody
U + Anti A --> clumping = A U + Anti B --> clumping = B U + Anti A and B --> clumping = AB U + Anti A and B --> no clumping = O |
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Why is Type O blood considered universal for donation?
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Although it contains Anti A and Anti B antibodies, they are diluted in recipient blood
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Why are Type AB considered universal recipients?
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Have no antibodies against blood cells of any type
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Cytotoxic immune disorder - Erythroblastosis fetalis
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Rh+ antigens on some RBC.
85% individs are Rh+ (Rh+ is dominant) Rh- = No Rh+ antigen and no anti Rh antibody |
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Erythroblastosis fetalis mech.
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First pregnancy with Rh+ fetus --> RBCs of baby stimulate mother's production of Anti Rh antibodies
Second pregnancy --> Rh+ baby affected by antibodies --> hemoglobin degrade to bilirubin (toxic) |
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Type 3 Immune Disorder - Immune complexes damage host
Details and areas affected |
Too small AG-AB complexes escape phagocytosis --> lodge into tissues and cause inflammation --> phagocytes can't engulf these complexes and release digestive enzymes --> further damage
Arthritis Lupus (skin) Acute post-Streptococcal glomerulonephritis (kidneys) |
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Type 4 Immune Disorder - Delayed CMI rxn
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First exposure - antigens stimulate immune response
2nd = Th and CTLs attack cells, cytokines attract more leukocytes, further damage So basically an immune response is present on first exposure, then 2 days or so later a secondary reaction occurs |
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Type 4 Immune Disorder - Tuberculin
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Tuberculin skin test (M. tuberculosis protein and antigen)
Not infected + tuberculin injection = no response Infection --> CMI response --> tuberculin injctn --> skin inflammation = evidence of infection |
