Defense Against Infectious Disease Test Flashcards
Define pathogen.
A pathogen is a “disease-causing agent” (microorganisms/ cellular = bacteria, protists, fungi, parasites; acellular = viruses, prions) that disrupts the normal physiology of an organism
Different pathogens enter the body in different ways, and there are many different ways our bodies protect and defend us from these foreign invaders!
Know what antibiotics are, where they come from/ where we get them, and be able to explain why they are effective against bacteria (prokaryotes) but NOT viruses/ NOT us (eukaryotes). Include bacterial/ prokaryotic structures and functions versus eukaryotic structures/ functions in your response too.
What are antibiotics?
- 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)
How do antibiotics work?
- 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!)
Where they come from/where we get them:
- Antibiotics were first discovered in 1928 (and have been widely used since)
- Broad spectrum (effective against many bacteria) or narrow spectrum (effective against SPECIFIC bacteria)
- HELP? CHECK WORKSHEETS
Why don’t antibiotics work on viruses?
- 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)
Explain how skin and mucous membranes are effective (non-specific) barriers against pathogens.
Understand that the skin and mucous membranes form a primary defense (first line of defense) against pathogens that cause infectious disease.
Skin:
- 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!
Mucous:
- External surfaces NOT covered by skin are protected by mucous membranes - Note: there are only a FEW external surfaces that are NOT covered by skin
- 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.
- Note that our own microflora (naturally occurring bacterial cells) outnumber our own human body cells by about 10 to 1! WHOA!
Describe the steps of blood clotting (IN ORDER) and the roles of NAMED proteins involved in this process.
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)
Steps of clot formation (the “coagulation cascade”):
- 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)
Explain the role of wandering macrophages (phagocytic leukocytes) in defending against pathogens (non-specific).
- 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
Distinguish between an antigen and an antibody (aka “immunoglobulin”).
Antigen: 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
Antibody: “Y-shaped” proteins that are produced by specialized plasma/ 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
Describe HOW antibodies work/ defend your body against pathogens (and know that they are produced by plasma cells - which are produced by B lymphocyte cells during clonal selection/ B cell cloning).
- Antibodies are “Y-shaped” proteins that are produced by specialized plasma/ 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 - Note: Your body has MILLIONS of different B-cells (capable of producing MILLIONS of different antibodies)!
Explain the steps of antibody production in the body (beginning with macrophages/ phagocytic leukocytes, and including the lymphocytes helper T cells, B cells, plasma cells, and memory cells).
- In a PRIMARY INFECTION (first exposure to a pathogen): Macrophages identify “non-self” antigens and engulf/ ingest pathogens
- Antigens (or pieces of them) from the pathogen remain in the macrophage and are “displayed” or “presented” on the macrophage cell membrane to WBC’s called helper-T cells (TH cells) - this “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/ clonal selection
- B cell cloning 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)
Distinguish between innate and acquired immunity, as well as passive and active immunity, and natural and artificial immunity.
Immunity (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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Active immunity: 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)
Passive immunity: 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)
Examples of passive immunity:
- 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)
Define vaccine (aka immunization), describe how vaccines are made, and outline how they work to provide immunity to your body.
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
Explain the differences in antibody concentration in the blood (as seen in a graph) following a vaccine or a primary infection and then following a subsequent infection/ exposure to the same pathogen/ antigen.
LOOK AT NOTES - Defense Against Infectious Disease Part 2 slide 9: https://docs.google.com/presentation/d/19780MU0a7MEC5VYkqWY4BK0BLExIF2wujO0jjPYhDe4/edit#slide=id.p14
Know what monoclonal antibodies are, describe how they are made in a lab (including how hybridoma cells are produced), and what they are used for (in diagnoses and treatments).
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)
To produce monoclonal antibodies:
- 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)
Detection/ Diagnosis of Disease
- 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.)
Pregnancy Tests
- 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!
Treatments for Patients
- 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
Know what HIV is, how it is transmitted, and how it affects the immune system.
- Human immunodeficiency virus (HIV) is the pathogen that eventually causes the set of symptoms collectively called acquired immune deficiency syndrome (AIDS). Note: HIV is a retrovirus (uses reverse transcriptase to make DNA from viral RNA - creepy)!
- 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
- A 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 – that’s how specific viruses are!)
Distinguish HIV and AIDS.
Human immunodeficiency virus (HIV) is the pathogen that eventually causes the set of symptoms collectively called Acquired Immune Deficiency Syndrome (AIDS)
- 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.
Identify blood types (based on images of antibody test results - showing “clumping” and “no clumping”) and identify which blood types a patient could receive based on antibody testing results.
LOOK AT NOTES - Defense Against Infectious Disease Part 2 slide 12: https://docs.google.com/presentation/d/19780MU0a7MEC5VYkqWY4BK0BLExIF2wujO0jjPYhDe4/edit#slide=id.g10a24faf91c_0_7
Antibodies are also used to determine blood type
- 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
