You don't actually have to read this... I just thought it would be funny to post. I'll bet you wish you were a bio major, too! ;)

Medical Microbiology

Chapter 6 - Viral Classification, Structure, and Replication

5. Describe the steps of viral replication. Be sure to differentiate between the events of naked viruses and enveloped viruses that have DNA or RNA genomes (including positive and negative sense RNA). Also explain the replication of retroviruses.

Enveloped - insert proteins into membranes, assembled at membrane.

Chapter 7 - Fungal Classification, Structure, and Replication

1. Describe the basic structure of a fungal cell. Why is it difficult to develop anti-fungal medications?
Eukaryotic. Cell wall is made of chitin and glucan, has ergosterols. V. similar to our cells (80S ribosomes, ER, Golgi, etc.).

2. Describe or define the following: yeasts, pseudohyphae, molds, hyphae, mycelium, dimorphic fungi, mycosis, dermatophytes, and thermal dimorphism.
Yeasts – single cells.
Pseudohypahe – strips of yeast cells together
Molds – multicellular
Hyphae – long “strings” of cells in the fungal structure
Mycelium – many hyphae woven together to create a “mat”
Dimorphic – can switch from yeast to mold and back
Mycosis – fungal infection
Dermatophytes – fungi that cause disease in the skin (cutaneous fungal infection)
Thermal di – switch from yeast to mold caused by change in temperature

3. Briefly describe each of the following types of fungal infections: superficial mycoses, cutaneous mycoses, subcutaneous mycoses, endemic mycoses, and opportunistic mycoses.
Superficial – not harmful, cosmetic only. Very rare
Cutaneous – v. common, infection of skin, nails, hair.
Subcutaneous – deeper tissues
Endemic – thermal dimorph fungi, seen in healthy people (abcesses, ulcers)
Opportunistic – seen in immunocompromised individuals. Normally non-pathogenic.

4. What specific types of infections do the following fungi cause: Candida spp., Cryptococcus neoformans, and Aspergillus spp.?
Opportunisitc.

5. Disease of the Day - "The Terminator" article
Mucormycosis – in the sinus. Feeds on sugar, so elevated risk for diabetics.

Chapter 9 - Commensal and Pathogenic Microbial Flora

1. What is normal flora?
Does not cause disease, often helps us. Takes up space and nutrients (microbial antagonism).

2. Define the following terms: transient colonization, permanent colonization, disease, strict pathogen, and opportunistic pathogen.
Transient – comes and leaves
Permanent – is always there (eg. Staph on skin)
Disease - change from a state of health
Strict pathogen – always causes illness
Opportunistic – may cause disease, depends on location

3. In what ways do pathogens cause damage to host tissues?
Toxins, resource use, damage cells, secrete enzymes like collagenase and hyaluronidase that damage connective tissues.

4. List the normal flora and pathogens discussed in class for each of the following body sites: mouth, oropharynx, nasopharynx; external ear; lower respiratory tract; esophagus; stomach; small intestine; large intestine; anterior urethra; vagina; and skin.
Oropharynx – anaerobes, strep, neisseria,.
Nasopharynx – straep and staph
Ear – staph and pseudomonas
Resp. – strep aureus, pneumonie, klebsiella
Eso – none
Stomach – lactobacillus, h. pylori
Intestine – salmonella, e coli
GI system – lactobacillus, candida, N gonorrhoeae, chylamidia
Skin - pyogenes

Chapter 10 - Sterilization, Disinfection, and Antisepsis

1. Define the following terms: sterilization, disinfection, disinfectant, antisepsis, antiseptic, sanitizer, germicide, bactericide, and bacteriostatic agent.
S- all dead
Dis- mostly dead
Anti- used on living tissue
Sani- dis. Used on food equipment
Germicide – kills bacteria
B-static - inhibits growth of bact.

2. Describe the rate of microbial death when treated with a physical or chemical agent.
Affected by factors such as exposure length, chemical used, individual susceptibility, environment, etc.

3. How do things like heat and disinfectants kill bacteria?
Damage cell membranes, cell proteins.

4. Describe the following methods of controlling microbial growth (be sure to include the most common uses and benefits or limitations of each method): moist heat, autoclaving, boiling water, pasteurization, Ultra High Temperature (UHT) treatment, dry heat, flaming, low temperature, filtering, ionizing radiation, UV radiation, Ethylene Oxide Gas, aldehydes, hydrogen peroxide, halogens, alcohols, chlorhexidine, and triclosan.
Moist heat – v. good. Common. Kills all.
Autoclave 0 type of moist heat
Pasteurization 0 use moist heat to kill some/many of pathogens in food/liquid
UHT – for food, sterilizes milk – no fridge needed.
Dry heat – kills, but not as fast
Low temp – slows growth
Filter – removes pathogens
Ion – x and gamma rays. Kills. Used on equipment
UV – used in rooms
Ethy gas – instruments
Aldehyde – eg. Formaldehyde
H2O2 – oxidizes
Halogens – proteins
Alcohols – membranes
Chlor and tri – in soaps

Chapter 11 - Elements of Host Protective Responses

1. List and describe the 3 layers/walls of defense against pathogens and toxins. What are the elements of each layer?
1st – barriers such as skin, mucus menbranes and secretions (lysozyme, tears, fatty acids, lactic acid, stomach acid)
2nd – innate – non-specific. Complement pathways, imflammatory response, phagocytosis, NK cells.
3rd – Ig-mediated. Specific. Actions of B and T cells.

2. Describe the activities of each of the following chemicals that allow communication between cells: cytokines, interferons, and chemokines.
Cytokines – for immune response
Interferons – anti-viral, from cell to cell, stimulate immune response.
Chemokines – inflammatory response

3. Give the function(s) for each of the following cells: Natural Killer cells, neutrophils (polymorphonuclear cells or PMN's), eosinophils, macrophages, monocytes, dendritic cells, Langerhans cells, microglial cells, Kupffer cells, B-cells, memory B-cells, T-cells (both CD4/helper cells and CD8/cytotoxic cells), memory T-cells, plasma cells, basophils, and mast cells.
NK cells – kill cells with Ig on them and virus infected cells and tumor cells. No MHC use.
Neutrophils – phagocytosis
Eosiniphils – parasite defense, allergis response – (IgE)
Macrophages – phagocytosis, antigen presentation, imflammatory response
Monocytes – phagocytosis, APC
DC – APC
Langerhans – antigen transport to lymph nodes
Microglial – cytokines production, APC
Kupffer – filter particles from blood
B – Ig production, memory.
T – help activate B and TC, Tc kills infected cells
Memory T – type of CD8
Plasma – produce Ig (types G, E, A)
Basophils and MAST– histamine, allergic response, IgE receptors.

4. What does "CD" stand for (as it applies to cells in the immune system)? What is the MHC? What cells have MHC class I molecules? What cells have MHC class II molecules? What do these proteins do?

Cluster of Differentiation
Major Histocompatability Complex
All cells
Antigen-presenting cells (APCs) - macrophages, dendritic cells, B cells (different case - can't activate CD4 cells)
MHC proteins display the antigens on the outside of the cell. Class I and II are receptors for different reactions.

5. Describe the structure and function of the following lymphoid organs: lymph nodes, spleen, mucosa-associated lymphoid tissue (MALT), Peyer's patches, and tonsils.
Nodes – little “balls” that the lymph travels through as it is transported to be put back into the blood. Helps Macrophages meet up with B and T cells to help the immune response connect. Three parts – cortex, parac- , medulla.
Spleen – large organ, like a node. Filters antigens. Removes old blood cells. Red and white pulp.
MALT – lymphoid cells, not highly structured. PP and tonsils are types of MALT.
Tonsils – accumulations of nodes.

Chapter 12 - The Humoral Immune Response

1. Define the following terms: antibody, antigen, epitope, monoclonal antibody, T-independent antigens, and T-dependent antigens.
Antibody - protein made by B cells that has affinity and specificity for antigens of pathogens.
Antigen – particle that our immune system recognizes as non-self
Epitope – specific part of the antigen that the antibody recognizes
Monoclonal antibody – antibodies produced by the same B cell, and which therefore all have the same specificity.
T-independent antigens – antigens that do not require T cell involvement to fight. They have a large and repetitive structure (eg flagella) that B cells can recognize and have several membrane-bound antibodies bind to. This activates the B cell to produce antibodies, though it is not a full response – they only produce IgM and no memory cells are produced. Class switching requires the TH cell activation.
T-independent antigens – antigens that need the help from TH cells to activate the B cells. Both T and B cells need to be stimulated. Usually proteins, and create memory cells.

2. Describe the structure of an antibody. List and give the principle site of action and principle biologic effect for the 5 different classes of antibody (see Table 12-1).
Antibodies are made of four chains help together by disulfide bonds. There are 2 heavy and 2 light chains. The light chains run parallel to the heavy chains, and the molecule as a whole makes a Y shape. The tip of the Y arms is the location of antigen binding, and the other end, the Fc portion, interacts with immune system cells. The light chain is variable through changes in V and J, and the heavy chain, through V, J and D. The 5 classes are IgM (first to the infection site, a pentamer, can be membrane bound to B cells, and v. good at agglutination), IgD (membrane-bound, B cell activation), IgG (most common, can cross placenta, longest life span, secondary response, opsinization), IgE (anaphylactic response, interacts with MAST cells), and IgA (in secretions, a dimer). M and G are used to activate the complement system.

3. Describe how a B-cell is activated to secrete large amounts of antibody (also called clonal expansion). What is a secondary antibody response? How is it generated?
The B cell is activated by interaction with the antigen and activation by a TH cell. This causes differentiation and proliferation – antibody production via plasma cells. 2ary response is when memory cells are activated and diff and prol. again

4. What is complement? Describe how complement is activated (both the alternate and classical pathways). What does activated complement do?
Complement cascade – starts w/ Ig and C1.in classical pathway. Leads to MAC formation and inflammatory response (vaso perm and vaso dil. By C3a and C5a – activate histamine which causes dilation and perm.), and opsinization. Alternate pathway and lectin pathways can also activate it. Regulated by C1 inhibitor and C4 inhibitor.

Chapter 13 - Cellular Immune Responses

1. Describe how Natural Killer (NK) cells function to destroy virus-infected and tumor cells.
CD8 cells interact with cells expressing antigen on MHC I receptors. The CD8 cell must also be co-activated by a CD4 cell by the CD4 cell binding to an MHCII receptor. The CD4 cell releases cytokines to activate the CD8 cell. The activated CD8 cell proliferates and differentiates into patrol cells and some memory cells. The patrol cells are activated when presented with another MHC I receptor with the same antigen. It releases vesicles of perforin and leaves. The perforin moves to the infected cell and inserts itself into the membrane in rings, causing holes in the membrane, leading to cell lysis.

2. Describe antigen presentation to T-cells and their subsequent activation. Be sure to include the activities of the CD4 or CD8 molecules as well as the MHC (HLA) molecules.
TH (CD4) cells are activated by antigen presentation on MHC class II molecules. MHC II is expressed on antigen-presenting cells such as macrophages, dendritic cells, and B cells (though this is a special case). Once activated, the CD4 cells act as helpers to activate B cells and CD8 cells as a co-activator with the antigen. CD8 cells are activated when they interact with antigen presented on MHC I receptors. This is the primary signal. All nucleated cells have MHC I. The second activator signal for the CD89 cell comes from a CD4 cell that has been activated by MHC II. It releases cytokines that activate the TC cell, leading to it’s proliferation and differentiation (patrol cells and memory cells).

Chapter 14 - Immune Responses to Infectious Agents

1. Describe the organization of our defense systems (the 3 layers/walls of defense against pathogens and toxins). Be sure to include each of the following components and their functions: barriers, innate responses, acute inflammation, complement, interferon, fever, and Ag-specific responses.
1st wall – barriers. This includes the skin, mucous membranes, and secretions (lactic acid, fatty acids, tears, mucus, lysosyme, acid). Barriers keep the pathogens from ever getting in to the tissues they would infect.
2nd wall – innate response. Non-specific defense from immune system cells such as macrophages and natural killer cells. The inflammatory response is part of this, and it can be mediated by the complement system and cytokines. Interferon helps defend against viral-infected cells as it helps neighboring cells prevent infection. The fever response raises the body temperature which helps B and T cell proliferation.
3rd wall – specific response. Takes some time to mount (5-7 days). Based on antibody interactions in B cells and activation of CD 8 cells. IgM is the first to the scene, and helps especially with agglutination of the antigens. Igs also neutralize the pathogen and toxins, opsinize the pathogen for phagocytosis, and activate the complement system (leading to MAC formations, inflammatory and fever responses, further opsinization). IgG is the second main type produced in the first exposure, and the main type produced in a secondary exposure to the antigen.

2. Define/describe the following: diapedesis, chemotactic factors, exogenous pyrogens, and endogenous pyrogens.
Diapedesis – immune cells moving through the capillary, especially once the inflammatory response has been initiated (heat, redness, oedema, pain) via increased vasopermeability and vasodilation.
Chemotactic factors are parts of the complement system and that attract macrophages and neutrophils to the site of the infection.
Exogenous pyrogens are fever-inducers that come from a pathogen that is infected the body (eg.toxins, LPS).
Endogenous pathogens are fever-inducers that come from within your body (cytokines).

3. What do the following terms mean in relation to the Ag-specific responses: specificity and memory?
Specificity means that each antibody will interact with only one antigen (or, more specifically, one epitope on that antigen. It will not interact with other antigens. Memory refers to the differentiation and proliferation of memory cells. These cells remain in the body for years after initial exposure to the antigen and are activated upon a second exposure. They are able to proliferate immediately, decreasing the time for the second immune response.

4. What types of Ag are B-cells effective against? What types of Ag are Cytotoxic T-cells effective against?
B cells are effective against pathogens that remain outside the cells such as bacteria, toxins, and multicellular parasites. CD8 cells are effective against intracellular parasites such a viruses and some bacteria. They are also useful against some non-infectious diseases such as cancer.

5. Describe the activation of B-cells and T-cells (in the depth covered in class). What role do helper T-cells play?
B cells are activated when the membrane-bound IgD or IgM on the B cell comes in contact with the antigen. This is the first activation signal. The B cell takes in the antigen and presents it using MHC II. A CD4 cell comes and binds to the MHC II receptor coupled with the antigen and completes the activation of the B cell. Once activated, the B cell proliferates and differentiates, producing plasma cells (antibody factories, can produce 2-3000 antibodies per second, but live for only 24 hours) and memory cells (stay in the body for years, ready to mount another defense against the pathogen).
TH cells are activated when the bind to MHC II receptors with antigen presented on APC cells. After activation, they help with activation of B and TC cells.
TC cells are activated when they bind to an MHC I complex (first signal). A TH cell then comes and, once activated by MHC II presentation, releases cytokines to activate the TC cell (2nd signal). The TC cell then proliferates and differentiates into patrol cells and memory cells.

6. How do B-cells respond to protein Ag? How does that differ from carbohydrate Ag?
Proteins give a stronger response than carbohydrates.

7. List and describe the functions for Ab.
Agglutination – contains the pathogens. Easier to phagocytose.
Neutralization of pathogens and toxins
Opsinization – phagocytosis
Complement activation- C1 binds to Ig.

8. Describe the differences in the primary and secondary responses to an Ag.
1ary – first exposure. Slower response. Has to activate all cells. IgM high.Makes memory cells.
2ary – subsequent exposures. Fast response. Cells already useful. Much greater level of Ig produces. More IgG than IgM. Uses memory cells.

9. What does an immunization do? What are vaccines made of?
Gives the immune system a 1st exposure w/o causing illness. Several types – attenuated whole (full cell, weakened chemically), inactive (dead), conjugated (w/ adjuvant to increase immune response), toxoid (inactive toxin used to create Igs against toxin – esp. for Clostridium spp.), recombinant – part of the cell)eg. Just the antigens) are made in the lab using yeast w/ the gene inserted. Good for bacts. that do not culture well).

10. What are allergies? How do they occur?
Abnormal immune response to a non-pathogenic antigen. Uses IgE and MAST cells to release histamine in response to the antigen. Response too great. Leads to dilation and perm, which can be systemic (bad – anaphylactic shock – decrease in BP). Histamine also causes runny nose and sneezing. Athsma – hist. released in the lungs. Can be decreased w/ allergy shots – use the antigen to teach the body to respond w. IgG and IgA instead.

11. What is autoimmunity?
Immune cells interpret self cells and non-self cells. Immune response is initiated for self-tissues. Normal proteins are seen as not normal.

12. Describe why transplanted tissues and organs are commonly rejected by the host.
The transplant tissues have proteins on them that are not “self”, so they immune cells attack them.