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87 Cards in this Set
- Front
- Back
Organisms live together, both benefit (Ecoli in GI tract)
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Mutualism
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one organism benefits, the other is not particularly benefited or harmed; to eat at the same table. (Most GI tract microbes; we provide a warm wet place to live with food, we don’t get all that much in return.)
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Commensalism
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one organism benefits at the other’s expense (Disease-causing bacteria; to them, we’re dinner.)
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Parasitism
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presence of microbes (where they don’t belong).
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Contamination
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multiplication of parasitic organisms in/on host.
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Infection
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used to describe infection of larger organisms, e.g. lice.
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Infestation
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malfunction in or damage to the host.
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Disease
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Disease is a condition of the ____?
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Host
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a parasite capable of causing disease
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Pathogen
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ability of pathogen to cause disease
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Pathogenicity
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relative ability to cause disease.
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Virulence
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attenuation means?
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Weakened
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microbes normally found on the body.
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Normal microbiota
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always found on human tissues.
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Resident microbiota
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come and go, can include potential pathogens.
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Transient microbiota
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Where do microbes live?
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GI tract (crowded), respiratory tract, skin, genito-urinary tract, fluids
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causes disease
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pathogen
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can cause disease under the right circumstance
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opportunistic pathogen
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decomposes dead stuff
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Saprotroph
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What determines whether we get sick? (Not always clear cut)
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Inf Dis = N x V / HF
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Types of diseases:
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Inherited diseases: caused by a faulty gene.
Congenital: due to damage during development. Degenerative diseases, due to age or lifestyle Nutritional, endocrine, mental, immunological, neoplastic (cancer), idiopathic; same caveat. Iatrogenic: caused by doctor. Nosocomial infections: occur in hospital. Infectious disease: caused by infectious agents like: Bacteria, viruses, fungi, etc. |
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can be spread from one person to another
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communicable
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highly communicable, can easily be spread from one person to another.
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Contagious
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are not spread from one host to another.
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Non-communicable
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How bacteria can cause disease:
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Invasive (usualy through tissues)
Toxigenic (produce and release toxins which dissolve in blood stream) Host processes (inflamation over responding, causing damage. |
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How viruses can cause disease:
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Viruses multiply inside host cells, using cell resources, often killing cells.
Viruses stimulate the immune system to fight back; infected cells are killed. Viruses alter cell cycle regulation to promote their own replication; may lead to cancer. Fungi, Protists, and worms Produce enzymes that damage host cells Multiply in host cells and kill them Cause allergic reactions or inflammation |
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Steps in an infectious disease:
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Entry and attachment
Deal with host defense Damage Escape |
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Things that bacteria have that improve their abilities to cause disease:
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Virulence Factors-Fimbriae, capsules, enzymes, toxins
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A protective mechanism, but can cause local damage.
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Inflamation
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What are Endotoxins and Toxic Shock Syndrome toxins?
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Super antigents (Cause massive over response of WBS
Followed by decreased responsiveness) |
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The study of disease is called?
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Epidemiology
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the study of the causes of disease
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Etiology
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What is signs and symptoms?
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Signs are observable/measurable
Symptoms are experienced by patient |
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collection of signs and symptoms
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Syndrome
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# of new cases during a time period
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Incidence
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ongoing cases at any one time
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Prevalence
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Death and sickness per total population over a given period of time.
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Mortality and morbidity rate:
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The first epidemiological study. Cholera was found to be spreading by water. London in 1854
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John Snow was credited
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Refers to how long the disease lasts..(Acute, subacute, chronic)?
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Acute is short lived, subacute longer,chronic longest
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Refers to how long the disease lasts....(Local, focal, systemic)?
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A local infection is in one specific place, systemic means throughout the body. Focal: started somewhere
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Refers to how long the disease lasts....(Primary, secondary, superinfection)?
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Primary: the first or main infection
Secondary: a second infection once weakened by a first one. Super infection usually blamed on antibiotic Rx |
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bacteria in the blood
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Bacteremia
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a disease condition, microbes actively growing in, infecting blood.
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Septicemia
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viruses in the blood, common in systemic infections
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Viremia
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infection comes from outside the host. Examples: common cold, STD.
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Exogenous
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host is original source of infection. Examples: boils on skin spread by fingers from Staph sinus infection; E. coli urinary tract infection.
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Endogenous
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Weakened immune system, poor lung clearance from bed rest, surgical wounds, bedsores, etc.
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Compromised host
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Where do germs live?
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Humans, animals, non living (soil and water)
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Entry portals for infections:
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Glands, follicles that open to outside
Larger openings: respiratory system, digestive system, genito-urinary tract Cuts, bites, burns, surgical incisions Crossing the placenta, infecting the fetus |
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Exit portals for infections:
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Coughing sneezing speaking: from mouth
Excretory systems: GI tract, in feces; in urine From sex: vaginal fluid, semen From blood: insect bites, shared needles |
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Types of transmission for microbes:
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Contact-
Direct contact: touching, kissing, sex, endogenous spread (one part of you to another) Vehicles- water, food, airborne Vectors-Typically arthropods (insects, ticks) |
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Koch’s Postulates:
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1.Microbe must be found in every instance of the disease.
2.Obtain microbe in pure culture 3.Produce disease in susceptible host 4.Re-isolate original microbe |
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Stages of Disease:
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Incubation
Prodromal Illness(acute/invasive) Decline Convalescent |
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Frequency of disease terms:
Endemic, Epidemic, Pandemic, Sporadic |
Endemic: continually present in low numbers
Epidemic: higher than normal occurrence Pandemic: epidemic spreads worldwide Sporadic: cases show up only occasionally |
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The more immune individuals, the harder it is for the disease to be spread among many people; the cycle of transmission is broken.
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Herd Immunity
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potentially harmful diseases which must be reported to the CDC or other Health Unit by physicians
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Notifiable disease
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Non-specific Host Defenses
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-Physical barriers
-Cellular defense -Processes: phagocytosis inflammation -Chemical defenses |
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Non-specific Host Defenses -Physical barrier-skin
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Skin-Layered tissue, puncture resistant.
High in keratin, water repellant. Secretions maintain low pH. Outer layers slough off, reducing microbial load. Self-repairing. |
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Non-specific Host Defenses -Physical barrier- mucus
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Mucus traps microbes
-Action of cilia: propel mucus & microbes toward GI tract or to where they can be coughed out. |
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Non-specific Host Defenses: Cellular Barrier: Blood
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60% Plasma
Water and salts (electrolytes) Proteins: albumin, immunoglobulins, fibrinogen, complement, etc. 40% “Formed Elements” (cells mostly) RBCs (erythrocytes, red cells) carry oxygen WBCs (leukocytes, white cells) fight infection Platelets involved in clotting, release prostaglandins. |
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White Blood Cells: Lymphocytes, Monocytes, Granulocytes
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Lymphocytes: 20-50% of total,
T and B cells, deal with specific immunity Monocytes: 2-8% of total, “grow up” to become macrophages, “big eaters” Granulocytes Neutrophils: 50-70%, numerous short-lived phagocytes Eosinophils: 1-5%, stain red, attack parasites Basophils: 0.1%, stain blue, release histamine Granulocytes named according to microscopic appearance, presence of granules, type of stain, etc. |
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Features inactive proteins becoming activated.
Platelets respond to physical roughness |
Blood clotting
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plasma without the clotting factors
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Serum
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Large and mean, clean up debris as well as microbes.
Important link between non-specific immunity and specific immunity |
Macrophages
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patrol bloodstream, stepping into tissues when “called”
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Wandering macrophages
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reside in specific organs, get fancy names like Kupffer cells, histiocytes, microglia, “dust cells”, depending on home.
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Fixed macrophage
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a process by which cells engulf and destroy microbial invaders, debris, foreign material.
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Phagocytosis (Cell-eating)
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the major phagocytic cells in the body:
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Neutrophils (PMNs) and macrophages
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phagocytes respond to (move toward) various chemicals (cytokines) released by host cells and by microbes.
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Chemotaxis
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cell binds to material/microbe.
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Attachment
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Phagocytosis steps in the process:
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Chemotaxis, attachment, engulfment, digestion
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Phagocytosis 2- target brought into cell by endocytosis. Now in cytoplasm in a vesicle.
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Engulfment
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Phagocytosis 2- vesicle (phagosome) containing microbe fuses with lysosome.
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Digestion
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Some microbes have found a way to interfere and save itself by:
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Anti-phagocytic coatings
Capsules, M-protein; aren’t grabbed and engulfed Prevent phagosome-lysosome fusion Prevention of destruction in phago-lysosome Hide from phagocytes by entering “non-professional” phagocytes. Kill phagocytic cells |
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Attach to parasites (protozoa, worms) larger than they are, release enzymes that attack pest.
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Eosinophils
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Non-specific lymphocytes (different from T and B cells) which attack virus-infected cells and kill them.
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Natural killer cells
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Series of vessels and nodes
Drains off excess body fluids from tissues, returns fluids to cardiovascular system Lymph nodes filter out microbes Nodes filled with macrophages and lymphocytes Fluid flows thru slowly, maximizes contact |
Parallel circulatory system
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Largely all explained by increased blood flow and vessel permeability in area of injury; host response to tissue injury.
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Inflammation
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: a substance that causes fever
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Pyrogen
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Fatty acids in sebum on skin, low pH and are toxic
Lysozyme in tears, saliva, other fluids |
Chemical defenses: Secretions
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not being susceptible to disease
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Immunity
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Types of immunity:
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Innate: you have it from birth
Acquired: after exposure, your body remembers specific invader. |
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An atigen is:
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Large, foreign, molecularly complex
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A molecule that is too small to be an antigen without piggy-backing onto another is a ____
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hapten
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The specific part of an antigen recognized by an antibody or receptor is called an _____
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epitope
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refers to body fluids
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Humoral
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refers to the direct involvement of cells to attack an infection
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cell mediated
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