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114 Cards in this Set
- Front
- Back
Constitutive genes
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their products are constantly produced at a fixed rate.
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Promoter
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region of DNA where RNA polymerase initiates transcription.
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Operator
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region of DNA; “stop” or “go” signal for transcription of structural genes.
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Operon
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Operator and promoter sites and the structural genes they control.
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Repression
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inhibits gene expression; decreases synthesis of enzymes.
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Vertical gene transfer
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genes are passed from an organism to its offspring.
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Horizontal gene transfer
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genes passed to other microbes of the same generation.
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What are Three types of Horizontal Gene Transfer:
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1. Transformation.
2. Conjugation. 3. Transduction |
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Transformation
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transfer of genes between bacteria as “naked” “DNA.
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Competence
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recipient cell is in a state that allows it to take up DNA.
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Plasmid
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circular piece of DNA; replicates independently from chromosome.
● Carry genes that are not essential for normal growth of cells. |
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Resistance factors (R factors)
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plasmids that carry toxin, antibiotic resistance, etc. genes.
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Pathology
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study of disease.
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Etiology
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the cause of disease.
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Pathogenesis
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the way a disease develops.
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Infection
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invasion or colonization of body by a pathogen.
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Disease
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occurs when infection results in change of health.
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Normal microbiota
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colonize the body but don’t normally produce disease.
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Transient microbiota
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present for days-weeks and then disappear.
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Microbial antagonism
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normal flora prevents overgrowth of harmful microbes.
► Protect host against colonization by: • Competing for nutrients. • Producing substances harmful to other microbes. • Affect pH and available oxygen. |
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Symbiosis
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relationship between normal microbiota and host.
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Commensalism
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one organism benefits, other is unaffected.
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Mutualism
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benefits both organisms.
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Parasitism
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one organism benefits at the expense of the other.
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Opportunistic Pathogens
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don’t cause disease in their normal habitat.
Cause disease if they: ► Gain access to other body sites. ► Host is weakened. |
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Koch’s Postulates
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used to study the etiology of any infectious disease.
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Symptoms
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subjective changes not apparent to observer (pain, malaise).
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Signs
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objective changes doctor can observe and measure (lesions, fever).
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Syndrome
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specific group of symptoms or signs; always accompany particular disease.
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Communicable disease
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spreads from one host to another.
• Chickenpox, tuberculosis, genital herpes. |
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Contagious disease
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easily spread from one person to another.
• Chickenpox, measles. |
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Non-communicable disease
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not spread from one host to another.
• Tetanus. |
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Sporadic disease
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occurs occasionally (typhoid fever).
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Endemic disease
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constantly present in the population (common cold).
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Epidemic disease
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many people in a given area get the disease in a short period of time (influenza, AIDS).
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Pandemic disease
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worldwide epidemic (influenza).
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Acute disease
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develops rapidly, lasts a short time (influenza).
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Chronic disease
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develops slowly, often less severe, likely to be continual or recurrent (mononucleosis).
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Subacute disease
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between acute and chronic (subacute sclerosing panencephalitis).
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Latent disease
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agent inactive for a time, becomes active, produces symptoms (shingles).
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Immunity of a population determines:
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► The rate at which a disease spreads
► Number of individuals infected. |
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Vaccination
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enough people in a population are protected to prevent rapid spread.
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Herd immunity
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many immune individuals present in a population.
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Local infection
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microbes limited to a small area (boils, abscesses).
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Systemic infection
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microbes and their products spread through body by lymph/blood (measles).
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Focal infection
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local infection spreads to another area where its confined (arise from teeth, tonsils).
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Sepsis
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toxic inflammatory condition from spread of microbes or their toxins from an infected area.
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Septicemia
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blood poisoning; systemic infection from multiplying pathogens in the blood.
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Bacteremia
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bacteria in the blood.
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Toxemia
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toxins in the blood (tetanus).
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Viremia
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viruses in the blood.
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Reservoir
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source of pathogens for infectious disease.
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Transmission
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to susceptible host; direct contact, vehicle, or vector.
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Invasion
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microbe enters host and multiplies.
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Pathogenesis
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microbe injures host.
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Incubation period
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interval between infection and appearance of signs or symptoms.
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Prodromal period
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short period in some diseases; early, mild symptoms.
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Period of illness
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clear signs and symptoms, disease is most severe; immune system or treatment end this period or patient dies.
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Period of decline
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signs and symptoms subside; vulnerable to secondary infection.
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Period of convalescence
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body returns to prediseased state.
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Reservoirs of Infection
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source of disease causing organisms.
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Zoonoses
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disease that occurs in animals, can be transmitted to humans.
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Direct contact transmission
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physical contact, no intermediate object involved.
• Kissing, touching, sexual intercourse. |
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Indirect contact transmission
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transmitted via a nonliving object (fomite).
• Tissues, towels, bedding, cups, money. |
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Droplet transmission
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spread in mucus droplets that travel short distances.
• Sneezing, coughing, talking. |
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Vehicle Transmission
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disease transmitted by a medium; food, water, blood, etc.
Waterborne, Airborne, Foodborne |
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Vectors
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Animals/insects that carry pathogens from one host to another.
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Nosocomial (Hospital-Acquired) Infections Result from an interaction of:
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► Microbes in the hospital.
► Compromised hosts. ► Chain of transmission in the hospital. |
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Epidemiology
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study of when and where diseases occur and how they’re transmitted in populations.
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Morbidity
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number of people that contract the disease during a particular period of time.
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Mortality
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number of deaths that occur from those diseases.
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Adhesins (ligand)
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surface molecule on pathogen that binds to receptors on host tissue cells.
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Surface receptors
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molecule on host cell that is specific to host cell tissue; complementary to the adhesin.
► Mostly carbohydrates. |
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Phagocytosis:
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host cell engulfs and destroys microbes.
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Coagulases
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convert fibrinogen in blood plasma to fibrin; fibrin clots blood.
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Kinases
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breaks down fibrin; digest clots.
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Hyaluronidase
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breaks down hyaluronic acid.
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Collagenase
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breaks down collagen.
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Antigen
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foreign substance/molecule.
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Siderophores
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Iron-binding proteins secreted by pathogens.
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IgA proteases
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destroy IgA antibodies made against pathogens.
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Exotoxins
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produced inside and secreted. Gm(+) AND gm(-)
• Signs and symptoms depend on type of exotoxin; no fever results except from superantigens. |
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Endotoxins
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part of gram (-) cell wall. ONLY gram (-) →→ LIPID A
>>Results in Fever<< |
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Three types of exotoxins:
(#1) A-B toxins: |
• Two polypeptide parts (A and B); A is enzyme; B is binding portion.
• Bacteria releases A-B exotoxin. • B part binds to receptor on host cell. • A-B toxin transported into host cell by pinocytosis. • A & B separate. à A inhibits protein synthesis; cell death. à B is released from cell. |
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Three types of exotoxins:
(#2) Membrane-disrupting toxins: |
• Lyse host cells by disrupting plasma membrane.
• Form pores in membrane (S. aureus) or disrupt phospholipids (C. perfringens). • Some are hemolysins: disrupt membrane of red and white blood cells = cell lysis. • Streptococci sp. and staphylococci sp. |
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Three types of exotoxins:
(#3) Superantigens: |
• Bacterial proteins that provoke intense immune response
• Result in: fever, nausea, vomiting, diarrhea, shock and death. • Staphylococcus aureus toxin: toxic shock. |
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Shock
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life-threatening decrease in blood pressure.
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Immunity
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ability to fight off disease caused by microbes and their products.
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Leukocytosis
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increase in total white blood cell count during infection.
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Leukopenia
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decrease in total white blood cell count during infection.
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● Fixed macrophages
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located in certain tissues and organs of the body (liver, lungs, etc.)
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● Wandering macrophages
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roam tissues and go to sites of infection.
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Natural Killer (NK) cells
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kill wide variety of infected body cells and some tumor cells.
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Perforin
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makes channels in membrane and causes fluids to flow into cell = cell lyse (cytolysis).
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Granzymes
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cause target cell suicide (apoptosis).1
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Chemotaxis
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chemical attraction of phagocytes to microbes.
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Adherence
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attachment of phagocyte to microbe.
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Opsonization
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coating of microbes with serum proteins; aids phagocytosis.
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What Are Four signs and symptoms of inflammation?
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► Redness, pain, heat, and swelling.
► Sometimes a fifth: loss of function. |
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Acute inflammation
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cause is removed over short period of time; response is intense.
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Chronic inflammation
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cause is difficult to remove; response is longer, but less intense.
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Edema
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swelling caused by fluid build up.
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Margination:
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phagocytes stick to inner surface of blood vessels.
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Emigration
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collected phagocytes squeeze between cells of blood vessels to injured area.
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Lectins
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proteins that bind to carbohydrates.
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Induction
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turns on transcription of a gene or genes.
Inducer: molecule that turns on transcription. |
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Carriers
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carry and transmit pathogen without showing signs of illness.
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cytokines
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chemical messengers produced by immune cells.
Ex: (IL-1 and TNF-a) |
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Phagosome
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sac surrounding the microbe.
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Phagolysosome
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Fuses with lysosome containing digestive enzymes
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Induction
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turns on transcription of a gene or genes.
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I gene
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regulatory gene; encodes repressor protein.
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Antigenic variation
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alteration of surface antigens by some pathogens.
► Host immune response against pathogen. ► Pathogen alters surface antigens and is unaffected by antibodies. |
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Abscess forms
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localized collection of pus (dead cells, body fluids).
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