Defense Against Infectious Diseases Test Flashcards

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1
Q

Magnification=

A

Measured/ actual size

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2
Q

Identifying Blood Types

A

-Anti-A antibodies bind to A proteins (if causes “clumping” in a blood sample, shows that A proteins ARE PRESENT)
-Anti-B antibodies bind to B proteins (if causes “clumping” in a blood sample, shows that B proteins ARE PRESENT)
-Anti-D antibodies bind to Rh proteins (if causes “clumping” in a blood sample, shows that Rh proteins
ARE PRESENT)
-Note: no clumping = that protein is NOT present

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3
Q

HIV

A

-Surface proteins on HIV are highly specific, as are all viral proteins, and can ONLY interact with SPECIFIC proteins on SPECIFIC cells in the body to infect them.
-The cells that HIV infects are T-lymphocytes (CD4+).
Helper-T cells, remember, activate B cells to produce antibodies to “tag” infections in the body and to create memory B cells to protect a person from secondary infections
-When HIV infects helper-T cells it becomes “latent”/ dormant (symptoms of the disease do not show up for a long period of time after the infection)
-When HIV becomes active, helper-T cells begin to die off, causing B cells to remain inactivated during infection (no antibodies and no memory cells)
-This causes the symptoms of AIDS to develop (final stages of the infection), as a person is no longer able to fight off pathogens the same way they did before. Because of this, secondary infections usually kill individuals with AIDS, as they have no long-term immunity anymore.
-HIV is transmitted through the exchange of bodily fluids (unprotected sex (latex condoms provide barrier to HIV), blood-to-blood contact – needle sharing, breastfeeding, childbirth etc.)
-HIV RNA injected into helper-T cells, copied into DNA (reverse transcriptase), incorporated into helper-T cell DNA.
-Helper-T cells divide, spreading the infection – eventually results in symptoms of AIDS due to lowered numbers of healthy helper-T cells
-Small number of people are immune to HIV infection (they do not have the CD4+ protein receptor on their helper-T cells, so the virus has no way to get in)

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4
Q

Monoclonal Antibodies and Treatments

A

-Used in injections given to patients who have been bitten by rabid or venomous animals
-Used in cancer treatments: Cancer cells produce cancer-cell-specific antigens. Monoclonal antibodies to these antigens can be produced in a lab and attached to toxins or radioisotopes.
-When they are injected into cancer patients, the toxins will target the cancer cells, or the radioisotopes will identify exact locations of cancer cells for pin-point radiation therapy

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5
Q

Monoclonal Antibodies and Pregnancy Tests

A

-Monoclonal antibodies to HCG (human chorionic gonadotropin) are produced in a lab. HCG is ONLY produced by an embryo, so only a pregnant woman will have HCG in her bloodstream (and urine).
-In a pregnancy test, HCG antibodies are attached to a color-changing enzyme and these are placed in a well (or on a test strip etc.).
-IF HCG is present in a woman’s urine, a color change will occur when the HCG antibodies bind with the HCG antigens present in her urine!

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6
Q

Monoclonal Antibodies and Disease Detection

A

ELISA wells are coated with antigens from a specific pathogen and a color-changing enzyme. A sample of the patient’s blood is placed in the wells. If a color change occurs, their body is producing the antibody to that specific antigen – showing that they have the infection (malaria/ HIV etc.)

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7
Q

Monoclonal Antibodies Production

A

-A particular antigen is injected into a lab animal
-A primary immune response is allowed to occur in the animal (polyclonal)
-The animal’s spleen is harvested (blood cells collected)
-Lymphocytes (B cells) are identified/ isolated and removed and grown with cancerous cells (myelomas – divide forever)
-SOME of the B cells (which produce antibodies) and myelomas fuse as they are growing together, creating cells called hybridomas
Individual hybridomas are identified and grown in their own SEPARATE containers
-An ELISA (enzyme-linked immunosorbent assay) test is used to identify which hybridoma cultures are producing the ONE desired antibody
-The cells in these cultures continue to divide (mitosis) and produce a large amount of the ONE (monoclonal) desired antibody (which can be purified and used to treat or diagnose patients)

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8
Q

Monoclonal Antibodies Overview

A

Monoclonal (mono = one, clonal = copy): all of the antibodies that are produced are the exact SAME (typically, this is done in a lab – NOT in the body!)

Understand that monoclonal antibodies are produced by hybridoma cells and that fusion of a tumor cell with an antibody-producing plasma cell creates a hybridoma cell.

Monoclonal antibodies are produced in labs for treatments (such as a rabies shot, antivenom, to treat Covid-19 etc.) or diagnoses (such as a pregnancy test)

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9
Q

Vaccines

A

Understand that vaccines contain antigens that trigger immunity but do not cause the disease (trigger active immunity).

-Vaccines are developed by “weakening” a pathogen (heating it, chemical treatments (attenuation)), or selection of a weak strain and injecting it (or its parts) into the body to purposefully trigger a primary immune response (to develop memory B cells without actually having to contract the full blown infection itself)
-The body recognizes the weakened pathogen as “non-self” and begins the process of a primary immune response, which will eventually result in memory B cell formation (long-term immunity)
-Memory cells begin producing antibodies to the pathogen RIGHT away upon subsequent exposures, causing a quicker, more effective response (you may not even have symptoms of the infection!)
-Vaccines do NOT prevent infection by the pathogen, but rather provide the body with its own memory cells to cause a faster, more intense response to the pathogen should it be encountered again

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10
Q

Immunity

A

The ability to resist infection is either innate (genetic – you are born with it) or acquired (you develop it over time)

Acquired immunity is either active or passive, and both active and passive immunity can be conferred to an individual through natural means or artificial means

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10
Q

Active Immunity

A

The immune system is “challenged” by an antigen (naturally or artificially), responds, and produces memory cells, leading to long-term immunity (an individual organism produces its own antibodies)

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11
Q

Passive Immunity Overview

A

One organism receives antibodies from another organism/ source. This confers SHORT-term benefit only (antibodies target antigens and pathogens are destroyed). NO memory cells are produced in the organism who receives the antibodies though (no long-term immunity)

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12
Q

Passive Immunity Examples

A

-Antibodies from mother to fetus (placenta)
-Antibodies from mother to baby (colostrum – first milk production after a baby is born)
-Injections of antibodies (when bitten by snakes, spiders etc.) to prevent massive tissue damage/ death (as a primary immune response in these instances would take too long)

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13
Q

B-Cell Cloning

A

produces TWO types of cells:
1. Antibody-secreting plasma cells: make and secrete antibodies (~2000 secreted into the bloodstream every second) immediately to “target” the (primary) infection for destruction
2. Memory cells: long-lived cells which do not secrete antibodies initially. Instead, they remain in the bloodstream and will secrete antibodies if a subsequent (secondary) infection occurs (providing your body with immunity from the same pathogen should it invade again)

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14
Q

Steps of Antibody Production in the Body

A

-In a PRIMARY INFECTION : Macrophages identify “non-self” antigens and engulf/ ingest pathogens
-Antigens (or pieces of them) from the pathogen remain in the macrophage and are “displayed” on the macrophage cell membrane to WBC’s called helper-T cells (TH cells) which “activates” the TH cells
-Helper-T cells release cytokines to activate specific B cells (lymphocytes – produced in bone marrow – millions of different types) in the body that are able to produce the specific antibody that is needed for that specific pathogen
-Because B cells exist in VERY small numbers in the bloodstream, once they are activated, B cells begin to divide rapidly (mitosis – exact copies) so that there are enough of them to produce the proper antibody in large enough amounts to be effective – this is called B cell cloning

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15
Q

Antibodies Structure and How They Work

A

-Antibodies are “Y-shaped” proteins that are produced by specialized white blood cells (B lymphocytes, aka “B cells”) in your body.
-All antibodies form a constant Y-shaped region (attracts WBC’s) but the two ends of each are UNIQUE to each antibody - these two sites are identical and they are binding sites (bind to the SAME antigen)
-Specific antibodies are produced in response to the detection of specific antigens
-Antibodies are EXTREMELY SPECIFIC – they bind (complementary – like a key in a lock) to SPECIFIC antigens and act as a “tag” on pathogen surfaces
-“Tags” (antibodies) cause pathogens to agglutinate
(stick together) or they trigger white blood cells in the immune system to attack and destroy foreign and/ or infected cells (phagocytosis and lysis) - opsonization

16
Q

Antigen

A

The “non-self” surface proteins of a substance that gets into your body (FOREIGN proteins/ANTIGENS)

Note that ANTIGENS are found on pathogens, but they can also be found on transplanted organs/ blood and even some food molecules

17
Q

Macrophages

A

-WBC’s that are able to change their shape (like amoebas) and move in and out of blood vessels/ tissues in the body “looking” for foreign invaders!
-When a macrophage “meets” a cell, it will determine whether the cell is part of the body (“self”) or foreign (“not-self”) based on the proteins present in the cell’s membrane (cell “ID”)
-Note: Proteins called MHC’s (Major Histocompatability Complexes) in cell membranes identify cells as “self”
FOREIGN proteins (in cell membranes or in protein coats on viruses) are called ANTIGENS
-If a cell is determined to be “not-self” the macrophage will change its shape and engulf it (phagocytosis – a type of endocytosis) and enzymes within the macrophage (in lysosomes - they have LOTS of lysosomes) will chemically digest it – destroying it!
-Macrophages are said to be “nonspecific” because they will engulf and digest ANY cell or substance that is identified as “not-self” – they do not distinguish between different types of pathogens

18
Q

Blood Clotting Overview

A

-Blood clotting – seals damaged blood vessels (to prevent blood loss and prevent pathogens from entering the bloodstream)
-In the blood (in addition to leukocytes, erythrocytes, hormones etc.), there are plasma proteins (prothrombin and fibrinogen – always present, but in inactive forms) and platelets (fragments of blood cells)

19
Q

Steps of Blood Clot Formation

A

-Damaged blood vessel releases chemicals that stimulate platelets to adhere (“stick”) to the damaged area
-As blood circulates, more platelets are brought to the damaged area and they “stick” to each other and form a primary “plug”
The damaged tissue and platelets secrete proteins called “clotting factors” that convert prothrombin (inactive) in the blood into thrombin (active)
-Thrombin (an enzyme) catalyzes the RAPID conversion of fibrinogen (soluble) into fibrin (insoluble)
-Fibrin (a fibrous protein) forms a mesh-like network/ structure around the “plug” to stabilize it, and to catch more “debris” in the blood to solidify the clot (preventing further blood loss and preventing entry of pathogens)

20
Q

How are mucous membranes effective against pathogens?

A

-External surfaces NOT covered by skin are protected by mucous membranes
-Tissue cells that produce mucous membranes line the trachea, nasal passages, gastrointestinal tract, urethra, and vaginal tract (females)
Cells in these tissues produce and secrete mucous, a “sticky” substance which traps invading microbes (limiting/ preventing them from infecting your body’s cells)
Note: Some mucous cells also produce the enzyme lysozyme, which damages/ breaks down pathogens (also found in tears)
-Some mucous membranes (those in the respiratory tract) also possess structures called cilia (small hair-like extensions)
-Cilia act like “fans,” pushing the mucous-trapped microbes out of these areas of your body (to be expelled – sneezing/ coughing, or to be chemically destroyed – beginning with lysozyme from the mucous cells, and then they are swallowed into the stomach which destroys MOST microbes in its acidic environment)
-Your body’s OWN microflora (natural microbes) also inhabit many of these tracts, destroying or out-competing many invading microbes that make it past the mucous and/ or cilia.

21
Q

How is the skin effective in protecting against disease?

A

-Tough, Dry, made up of two layers:
dermis (underneath layer; living tissue/ cells/ capillaries)
epidermis (“epi” = on/ over/ on top of; layer of cells on top of the dermis; ~15 – 20 layers of dead cells)
-As cells from the dermis die, they fill with keratin and migrate upward into the epidermis. There, they are “shed” after ~2 weeks, carrying with them any microbes lying on the outermost surface of our skin – providing an effective barrier against pathogen entry into our bodies, as pathogens generally only enter LIVING tissue
-Skin also contains sweat glands (which can produce substances that are toxic to some microbes/ lower pH), sebaceous (oil) glands (which can produce substances that limit/ prevent bacterial growth), and ceruminous (wax) glands (which produce wax that traps bacteria and inhibits their growth/ lower pH)
-Our skin’s OWN microflora (natural microbes) also help to prevent infection, as they often destroy/ out-compete invading pathogens
-Note: the skin is an effective barrier as long as we don’t have any cuts/ scrapes/ abrasions etc. that expose our living tissues – blood, dermal cells etc. – to external pathogens!

22
Q

Skin and mucous membranes are the…

A

primary defense against pathogens that can cause infectious disease

23
Q

What are antibiotics?

A

Compounds that kill or inhibit growth by TARGETING/ BLOCKING metabolic reactions (or enzymes within them) in prokaryotic cells (DNA replication, RNA polymerase, cell wall production, protein synthesis/ 70S ribosomes)

24
Q

How do antibiotics work?

A

-Prokaryotic (bacterial) cells have DIFFERENT enzymes/ metabolic pathways/ structures than our cells (which are eukaryotic)
-Antibiotics disrupt bacterial cells’ ability to make new DNA, to make mRNA, to make proteins, and/ or to make new cell walls (preventing them from growing and dividing), thus, killing them (our cells are not affected because we are eukaryotes, so even though our cells carry out most of these processes too, the pathways/ enzymes our cells use are different!)

25
Q

Why don’t antibiotics work on viruses?

A

-Antibiotics target prokaryotic cell structures and pathways only – viruses are NOT prokaryotic (they aren’t even cells) so these drugs are ineffective on them – they have nothing to target!
-Viruses do NOT have their own metabolic pathways (they use ours, so we cannot target them without targeting our own cells)
-Viruses are protected by the host cell structure (they “hide” within our own cells, so we cannot target them without targeting our own cells)

26
Q

Define pathogen

A

A pathogen is a “disease-causing agent” (microorganisms/ cellular = bacteria, protists, fungi, parasites; acellular = viruses, prions) that disrupts the normal physiology of an organism