Unit 5-Immunology+Viruses Flashcards
(219 cards)
1
Q
Eosinophils
A
Eosinophils are a type of disease-fighting white blood cell. This condition most often indicates a parasitic infection, an allergic reaction or cancer.
2
Q
Immune Response Design functions
A
• surveillance surveillance • recognition recognition • attack attack • destruction destruction • proportional response
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Q
Levels of Defense
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First Second Third
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Q
First Line of Defense
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Non-specific Barrier Defenses Body Excretions (Tears, Sweat)
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Q
Second line of defense
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Non-Specific Inflammation Couplement (antimicrobial proteins) Phagocytosis
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Third Line of defense
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Specific And adaptive Antibodies (antimicrobial proteins) Cytotoxic Cells
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Q
Levels of defense Timing
A
Primary (first encounter) Secondary (subsequent encounters)
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Q
Non-Specific Host Defenses
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Intact Skin (Stratum Corneum) Mucous membranes Responses (Typically involve secretions)
9
Q
Mechanical Host Defense responses
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Mechanical • tears • saliva • ciliary action • vomiting • urination • coughing • sneezing
10
Q
Chemical Host Defense Responses
A
lysozyme • sweat/oils • dermcidin • hydrochloric acid
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Lysozyme
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an enzyme that catalyzes the destruction of the cell walls of certain bacteria, occurring notably in tears and egg white
12
Q
Dermcidin
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an antimicrobial peptide secreted by sweat glands that attacks any bacteria on our skin
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Q
Inflammation
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Increased blood flow to the affected area (arterioles constrict) Edema Phagocytosis by immune response cells Fever Completment activated Chemical signaling
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Phagocytosis
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the ingestion of bacteria or other material by phagocytes and amoeboid protozoans.
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Q
Pyrogens
A
a substance, typically produced by a bacterium, that produces fever when introduced or released into the blood.
16
Q
Pluripotent stem cells can turn into what type of cells?
A
Erythrocytes Leukocytes Platelets
17
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Components of blood
A
Platelets Erythrocytes Leukocytes Plasma
18
Q
Two types of Leukocytes
A
Granular (Lobed Nucleus) Agranular (Round Nucleus)
19
Q
Granular Leukocytes can turn into what type of cells?
A
Basophils Neutrophils Eosinophils
20
Q
Basophils
A
Few in #, secrete Histamine, triggering inflammation
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Neutrophils
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A Majority in #, short-lived (A few days), found mostly in tissues and function in phagocytosis
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Eosinophils
A
Few in #, directed against large, multicellular parasites; function in inflammation
23
Q
Agranular Leukocytes can turn into what kind of cells?
A
Monocytes Lymphocytes
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Q
Monocytes
A
Third most common in number, function in phagocytosis
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Lymphocytes
Second most common, secrete antibodies and destroy infected cells.
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Monocytes can turn into what type of cells?
Macrophages
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Macrophage
a large phagocytic cell found in stationary form in the tissues or as a mobile white blood cell, especially at sites of infection.
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Lymphocytes turn into what type of cells?
B-Cell T-Cell
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Antigen
a toxin or other foreign substance that induces an immune response in the body, especially the production of antibodies.
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What cells are antigen-presenting cells
Macrophages
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Humoral response
involves B cells that recognize antigens or pathogens that are circulating in the lymph or blood
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Cell-Mediated Response
an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen
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What type of cells generate Plasma Cells?
B-Lymphocytes
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what type of cells generate Cytotoxic T-Cells?
T-Lymphocytes
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What type of cells generate Antibodies?
Plasma Cells
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Function of Antibodies in the Immune Repsonse Cascade
Signals phagocytic cells and activates complement (Extracellularly located pathogens)
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Function of Cytotoxic T-Cells
Destroy the body's own infected cells (Intracellularly located pathogen)
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secondary immune response in the cascade
Antigen causes memory B or T Cell activation, generating Plasma or Cytotoxic T-cells.
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Antigen recognition and Clonal Selection
Using genetic recombination, the body produces many different cell-surface proteins capable of recognizing many different antigens
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when an antigen appears, it will bind to its B or T Cell w/ the matching receptor. Then what happens?
The cell will be induced to divide to create additional copies of the cell.
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Antibodies
glycoproteins (Combinations of Amino Acid Chains and sugars) that can be found in the blood serum (Soluble Antibodies) or attached to the surface of certain cells such as B-Lymphocytes
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Antibody Structure
four separate polypeptide chains held together by disulfide bridges. Two are longer/larger (Heavy chains) and are identical to one another. And 2 light chains (Smaller) w their own variable and constant regions
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Antibody Domain structure
Variable domain constant domain Hinge Constant Domain 2 Constant Domain 3
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Paratope
Antigen-Binding Site
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Binding of an antigen occurs
On the Epitope (on the antigen) and the Paratope (On the Antibody)
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What are the 5 types of Antibodies
IgG IgD IgA IgM IgE
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IgG
Single Monomer Triggers/activates complement proteins May enter tissue fluids can cross the placenta to protect the fetus
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What is the most abundant class of Antibody?
IgG (80%)
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IgA comprises what % of antibodies
10-15%
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IgA structure
Dimeric (2 Y-shaped w the usual 2 heavy and light chains)
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IgA
Found in Body secretions (Saliva, tears, perspiration, breast milk) Bind to pathogen/antigen to prevent adhesion to body surfaces
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IgD
Single Monomer Located on the cells of B-Lymphocytes Function as Antigen receptors May bind to basophils/mast cells stimulating inflammation
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IgE
Single Monomer Can interact w Basophils (In bloodstream) and mast cells (In connective tissue) to release histamine and other chemical signals Generates an inflammatory response
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IgM
First to appear in the infection process 10-15% of antibodies 5 Y-Structures joined around a common center (Pentameric) Functions in agglutination and complement function
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Zymogen
an inactive substance that is converted into an enzyme when activated by another enzyme
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Proper immune system functioning depends on
Proportional responses to the offending agents
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Immunodeficiency can lead to
Cancers
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Autoimmunity can lead to
Hypersensitivities (Lupus, RA, Psoriasis)
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Autoimmunity
the system of immune responses of an organism against its own healthy cells and tissues. Any disease that results from such an aberrant immune response is termed an "autoimmune disease".
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Passive Immunity
the short-term immunity that results from the introduction of antibodies from another person or animal.
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Active Immunity
the immunity that results from the production of antibodies by the immune system in response to the presence of an antigen
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Natural (Innate) Immunity
the inborn ability of the body to protect itself against pathogens and is transferred from mother to the baby.
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Artificial Immunity
can be induced by a vaccine, a substance that contains antigen. A vaccine stimulates a primary response against the antigen without causing symptoms of the disease.
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The Antibiotic Discovery Void began when?
around 1990
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Staphylococcus Characteristics
Gram (+) Cocci No flagellae No endospores Capsules Facultative Anaerobe Common in the environment (Soil Microbe), Harbored by humans intermittently Resistant to many physical extremes
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Facultative Anaerobe
an organism that makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation or anaerobic respiration if oxygen is absent
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Obligate Anaerobe
poisoned by oxygen, so they gather at the bottom of the tube where the oxygen concentration is lowest
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What types of Exotoxins to Staphylococcus produce?
Coagulase Hyaluronidase Hemolysins Leukocidins enterotoxins Exfoliative Toxins
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How does Staphylococcus usually enter the body
Typically through hair follicles or wounds (cutaneous)
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Some strains of Staphylococcus aureus may be resistant
MRSA (Multiple Resistant Staphylococcus Aureus) or Penicillinase resistance
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MRSA is resistant to what drugs?
Methicillin Oxacillin Penicillin Amoxicillin
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Staphylococcus infections typically produce what skin lesions?
Furuncles and Carbuncles
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Systemic Staphylococcus infections typically result in
Bacteremia or Sepsis
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Systemic infections from staphylococcus can spread and cause
Osteomyelitis Meningitis Pneumonia
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Staphylococcus is cultured on what type of Agar?
SBA (Sheep's Blood Agar) or MSA (Mannitol Salt Agar)
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Common Staphylococcus Species
S. Aureus S. Capitis S. Epidermidis S. Hominis S. Saprophyticus
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Staphylococcal skin lesions
Carbuncle/Furuncle Imetigo Styes Scalded Skin Syndrome
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Staphylococcal Food poisoning
usually caused by contaminated milks and cheeses Salt Tolerant Heat Resistant Sliced Meat, Pudding, pastries, sandwiches
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Symptoms of Staphylococcal Food Poisoning?
nausea, vomiting, stomach cramps, diarrhea
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Streptococcus characterisics
Gram (+) Cocci No Flagellae No Endospores May posess capsule+ Slime Layers Facultative Anaerobe
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True or False: Streptococci are hearty bacteria which are not very sensitive to the environment?
False: They are susceptible to environmental factors 9Drying, heat, disinfectants)
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What is an important part of classification of Streptococcal bacteria?
Hemolysis (Alpha, Beta, Gamma)
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Alpha hemolysis
Partial Degredation of RBCs
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Beta Hemolysis
Complete degredation/rupture of RBCs
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Gamma Hemolysis
No Degredation of RBCs
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Streptolysins
SL-O and SL-S Damage cells other than RBCs
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Common Streptococcal species
S. Agalactiae S. Faecalis S. Pneumoniae
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Streptococcus pneumoniae
causative agent of most bacterial pneumonias (encapsulated w Polysaccharide layer for enhanced virulence) can also cause meningitis and otitis media
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Streptococcus Pyogenes
Most pathogenic Humans are reservoir gnetic highly variable
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Streptococcus pyogenes virulence factors
polysaccharides tolerate lysozyme lupotechoic acids on fimbriae M-Proteins Streptolysins (exotoxin) Streptokinase(Penetrate host tissue) c5a Protease (Inactivates neutrophil response)
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Streptococcus Mutans
Plays a significant role in tooth decay creates biofilm on tooth enamel metabolizes various carbohydrates producing lactic acid as a byproduct
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Clostridium
Gram (+) Bacilli No flagellae produce endospores obligate Anaerobe Saprophytic
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Saprophytic
an organism which gets its energy from dead and decaying organic matter
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Disease-Causing Clostridium species in humans
C. Tetani C. botulinum C. Difficile C. Perfringens
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Gas Gangrene
When bacteria or spores enter the wound where the blood supply is interrupted, anaerobic state arises and allows bacteria to multiply and leads to necrosis. Bacterium releases carbon dioxide and hydrogen gas causing the tissue to swell and inflate/ Effective treatment involves Debridement (C. Perfringens)
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Antibiotic-Associated Disease
Clostridium Difficile
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Tetanus
A serious bacterial infection that causes painful muscle spasms and can lead to death.
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Clostridium Tetani
Gram (+) bacillus Obligate Anaerobe Spore-Forming Present in contaminated soil from fecal waste Produces Tetanus Neurotoxin
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Tetanus Neurotoxin (TeNT)
Prevents neurons from releasing certain neurotransmitters that inhibit muscle contraction so muscles remain in a permanently contracted state
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True or False: The binding of TeNT is reversible
False: It is irreversible
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Tetanus structure
Composed of 2 protein chains (heavy and light)
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True or False: The Toxoid vaccination for Tetanus does not give lifelong immunity
True: Booster shots are required every ten years or so
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True or False: The amount of TeNT that can be fatal causes the response ot be immunogenic
False: It is too low to be immunogenic. Exposure to the toxin does not elicit an immune response while still being fatal
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Botulism
clostridium Botulinum Common in soil and water Produces Botulinum toxin under certain growth conditions Endospores will germinate and grow, producing the toxin in certain conditions requires a bacteriophage infection
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How does the botulinum toxin work
Prevents acetyl choline release at neuromuscular Junctions (NMJ), resulting in flaccid paralysis
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Forms of Botulinum toxin
Foodborne, Infant (Colonization of the gut) and wound
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Can the botulinum toxin be destroyed?
Yes, by heating ot the proper temperature for a certain period of time
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Symptoms of a botulinum toxin infection
blurred vision, drooping eyelids, loss of facial expression, paralysis progressing from head and neck to chest and legs
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Is there an effective antitoxin available for botulinum toxin?
Yes
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Bacillus Anthraxis
Gram (+) Bacillus Obligate Anaerobe Spore-Forming organism w spores viable for decades
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Exotoxins formed by Bacillus Anthracis
Protective Antigen ( Allows toxins to enter cells) Edema Factor Lethal Factor
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Forms of Anthrax (Based on Exposure route)
Cutaneous Gastrointestinal inhalational
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Cutaneous Anthrax
Spores enter through breaks in the skin, forms popular-vesicular lesions, low mortality if antibiotics are used
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Gastrointestinal Anthrax
spores are ingested, 50% mortality if left untreated
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Inhalational Anthrax
Spores drawn into the lungs. Most dangerous form. near 100% mortality if left untreated
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Borrelia burgdorferi
Spirochete Bacteria (Gram does not apply) Causes Lyme Disease
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Lyme Disease
Caused by Borrelia burgdorferi Zoonotic Disease Transmitted by Ixodes, Ticks (2-3 Days required)
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Lyme Disease Reservoir
Field Mice
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Lyme Disease Symptoms
Fatigue, Chills, Fever, Headache, Muscle/Joint Pain Distinctive rash (Erythema migrans (TARGET)
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Francisella Tularensis
Causes Tulaermia Gram (-) Cocci-Bacillus
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Tularemia
Caused by Francisella tularensis Zoonotic disease highly infectius
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Tularemia Reservoir
Rabbits/hares, Rodents
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Tularemia Vector
Ticks
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Tularemia Symptoms
Fever, Chills, headaches, diarrhea, muscle aches, joint pain
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Tularemia infection routes
Skin (Animal Bites) (Ulceration may occur) Eye (Conjuctiva) Mouth (Contaminated food/water) Lungs (inhaled dust/aerosols, coughing, chest pain and difficulty breathing
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Mycobacterium Tuberculosis
Acid-Fast Bacillus (Mycolic acids in cell wall) Obligate Anaerobe Resistant to drying, disinfectants, and antibiotics
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Tuberculosis
caused by Mycobacterium tuberculosis Slow Growing Long courses of antibiotics for treatment acquired through inhalation and close extended contact
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Fish tank Granuloma
Caused by Mycobacterium Marinum
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Leprosy/Hansen's Disease
caused by Mycobacterium Leprae
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Diptheria
Caused by Corynebacterium diptheriae Spread by aerosol droplets (cough or sneeze)
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Corynebacterium diptheriae
Gram (+) Bacillus Obligate Anaerobe Causes Diptheria No flagella or endospores Found in soil and water Bacteriophage allows it to produce homodimer (exotoxin)
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How does Corynebacterium diptheriae damage the host cells
Interfering with protein synthesis
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Sequelae of Diptheria
Myocarditis and neuropathy
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Untreated Mortality rate of diptheria
50%
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treated Mortality rate of diptheria
10%
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There is no vaccine for Diptheria
FALSE (tDAP)
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Listeria
Gram (+) Bacilli Facultative anaerobe No Spores Produce flagellae @ low temps Grows between 39-100 F Found in soil and water through animal fecal waste
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What bacterium causes Listeria
Listeria Monocytogenes
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What patient population is affected by Listeria?
Children, Pregnant women, and immunocompromised patients (elderly, cancer, immunosuppressed)
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Upon infection, How does listeria spread
Spreads to the bloodstream, causing sepsis or to the central nervous system (causing meningitis - 50% mortality)
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True or False: Listeria can cross the placenta
True: Can lead to brain damage or death of the fetus
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Two pathogenic species of Nisseria in humans
Nisseria Gonorrhoeae Nisseria Meningitidis
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Nisseria
Gram (-) Diplococci Can resist phagocytic neutrophils complement proteins aren't as effective
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Nisseria Meningitidis can produce a capsule, which does what in the body?
Protects it against antimicrobial proteins in the blood serum.
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Meningicoccal disease is most common where?
In group settings, among adolescents and young adults (colleges)
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How much of the population are carriers of Nisseria
10%
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How is Nisseria Meningitidis
Spread by respiratory droplets/ throat secretions/ saliva
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Nisseria Menengitidis symptoms
Inflammation of tissues surrounding the brain and can quickly prove fatal (non-fatal cases can result in life-long brain damage or hearing loss) May cause septicemia (Blood vessels are damaged and hemorrhage)
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Nisseria Meningitidis antibiotic resistance
Antibiotics can be effective if begun early enough. Effective Vaccine is available
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Yersinia Pestis
Plague
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Yersinia Pestis
Gram (-) Cocco-Bacillus Facultative anaerobe Host several virulence plasmids
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Yersinia Pestis Reservoir
Rodents (wild) and rats in urban settings
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Transmitting Vector of Yersinia Pestis
Fleas
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3 forms of Yersinia Pestis (Plague)
bubonic Septicemic Pneuomonic
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Bubonic Plague
Muscle aches, fever, weakness, tissue necrosis, lymphadenopathy (Bubose)
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Septicemic Plague
Fever, vomiting, nausea, abdominal pain, bleeding into tissues
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Pneumonic plague
fever, headache, weakness, chest pain+cough w/ blood, transmitted through respiratory droplets
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Is antibiotic treatment effective in Plage forms?
Yes, if it is started early enough
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Nucleocapsid
Nucleic acid and Capsid in a virus
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Capsid
Protein shell in a virus
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Naked Virus
Injects its nucleic acid from the outside of the host cell
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Encapsulated/enveloped virus
is engulfed into the cell in order to inject its nucleic acid
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Pleomorphic Viron
Has the ability to change its shape based on its environmental selective pressures
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Capsomere
a subunit of the capsid, an outer covering of protein that protects the genetic material of a virus. Capsomeres self-assemble to form the capsid
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Complex Virus
Contains additional virulence factors and protein filaments: fibrillar outer matrix, lip polysaccharides as well as the tail fibers, pins, collar and sheath of bacteriophages
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ssRNA
+ -
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ssRNA Virus
+ -
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Adsorption
host range determined by the ability of glycoproteins on host cell membrane receptors to bind to virion
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Penetration
through endocytosis or cell membrane fusion
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Uncoating
removal of envelope and capsid
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Synthesis
replication and translation of viral nucleic acid
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Assembly
viral proteins associate to create new capsids
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Release
cell lysis for non-enveloped, complex virions and budding or exocytosis for enveloped virions
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Steps of a Viral infection
Adsorption Penetration Uncoating Synthesis Assembly Release
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Cytopathic Changes in a host cell
Giant/Multinucleate Cells/Syncytial Clumping Cell Inclusions Genetic (Oncogenic Changes)
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Oncogenic changes
cells are transformed and are unable to regulate their own division
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Cell Inclusions
partially formed, crystalline capsids
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Origin of the Human Immunodeficiency Virus (HIV)
It is thought to have mutated from SIV (a retrovirus of the genus Lentivirus (species Simian immunodeficiency virus) that causes a disease in monkeys similar to AIDS and that is closely related to HIV-2 of humans — called also simian immunodeficiency virus ) and arose in the 1980s in San Francisco, CA
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Prion
A Misshapen infectious protein that promotes others to mutate
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Viruses can live and reproduce on their own outside the cell (T/F)
False: They are obligate intracellular parasites and are metabolically inert outside the cell.
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Simple Viruses
Nucleocapsid Only
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Complex virus
Nucleocapsid+ spikes, tails, pins, or fibrillar matirices
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What bodily fluids have high numbers of the HIV viron present?
Semen, Blood, Vaginal secretions, breast milk
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What bodily fluids have low numbers of the HIV Viron present?
Swear, Urine, tears, Saliva
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Rabies Virus structure
Enveloped, Single-Stranded, Non-Segmented RNA Virus
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How does the Rabies virus move through the body?
moves from peripheral nervous system to central nervous system and then migrates to salivary glands
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Initial symptoms of Rabies infection
fever, nausea, vomiting, headache and fatigue
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Manifestations of Rabies infection
“furious” (muscle spasm, seizures, pain swallowing) and “dumb” (disorientation and paralysis) with either one eventually leading to coma and death
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Treatments for Rabies
thorough wound cleaning, administered antibodies and a (intramuscular) vaccine (injection series)
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Opsonization (Antibody Function)
enhance macrophage attachment and phagocytosis
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agglutination (Antibody Function)
whole cells) / precipitation (soluble antigens -clumping of particles
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Complement Fixation (Antibody Function)
initiated by IgG and IgM that recruit complement proteins to form a membrane attack complex resulting in bacterial cell lysis
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Neutralization (Antibody Function)
prevent antigen from normal binding
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Four Primary ways Antibodies Function
Neutralization
agglutination
Complement Fixation
Opsonization
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Describe the Infection/Lesion/Disease
Anthrax
197
Identify the type of organisms present on the Bacterial Cell
Bacteriophage
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Identify the Lesion/Infection/Disease
Botulism
199
Identify the Disease present in this patient
Colostrim Difficile (C. Diff)
200
Identify the Infection/Lesion/Disease
Diptheria
201
Identify the Infection/Lesion/Disease
Fish tank Granuloma
202
Identify the Lesion/Infection/disease
Gas Gangrene
203
Identify the Infection/Lesion/Disease
Hansen's Disease/Leprosy
204
Identify the Infection/Lesion/Disease
HIV
205
Identify the Infection/Lesion/Disease
Listeria
206
Identify the Infection/Lesion/Disease
Lyme disease
207
Identify the Infection/Lesion/Disease
Lyme Disease
208
Identify the Infection/Lesion/Disease
Measles
209
Identify the Cell type
Multinucleate/Syncitial
210
Identify the Infection/Lesion/Disease
Necrotizing Fasciitis
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Identify the cell structure present (arrows)
Negri Bodies
212
Identify the Cell Type
Nisseria (Diplococci)
213
Identify the Infection/Lesion/Disease
Plague (Black Plague)
214
Identify the Infection/Lesion/Disease
Rabies
215
Identify the Infection/Lesion/Disease
Rheumatic fever
216
Identify the Infection/Lesion/Disease
Tetanus
217
Identify the Infection/Lesion/Disease
Tuberculosis
218
Identify the Infection/Lesion/Disease
Tuberculosis
219
Identify the Infection/Lesion/Disease
Tullaremia
