Term
|
Definition
| Lack of resistance to a disease |
|
|
Term
|
Definition
| Ability to ward off (a) disease |
|
|
Term
|
Definition
| defense against any pathogens |
|
|
Term
|
Definition
| immunity or resistance to a specific pathogen (only if innate fails) |
|
|
Term
|
Definition
| Skin; mucous membrane and secretions; normal flora |
|
|
Term
|
Definition
| Phagocytes and other WBCs; inflammation; fever; antimicrobial substances |
|
|
Term
| 3rd line (adaptive) of defense |
|
Definition
| specialised lymphocytes; T and B cells; antibodies |
|
|
Term
|
Definition
| 1st line of defense. Intact, it provides a physical and chemical barrier through its tightly packed cells, shedding mechanisms, and dry, keratin-covered surface. |
|
|
Term
|
Definition
| The dermis is thicker than the epidermis and contains sweat, hair, and macrophages - all of which help deter infections. |
|
|
Term
|
Definition
| These are epithelial cells which secrete mucus. Physical structures in this category include: lacrimal apparatus (tears), nose and ear hairs, vaginal secretions, and cilia of the lower respiratory tract. Peristalsis (movement of food through body) and defecation (removal of food wastes from body) are also a part of this system and help push harmful microbes out of the body. |
|
|
Term
| Lower respiratory structures and cilia cont'd |
|
Definition
| Goblet cells of the lower respiratory tract produce mucus which traps microbes that are breathed in. Ciliated cells have cilia which beat rhythmically to "sweep" globs of contaminated mucus up towards the nasal/oral opening, where it will either be coughed up or swallowed (to be destroyed by acidic gastric pH). |
|
|
Term
| Chemical factors of the 1st line |
|
Definition
| Sebum, lysozyme, gastric juices, vaginal secretions, urine. |
|
|
Term
|
Definition
| Secreted by sebum glands, sebum contains fatty acids which inhibit microbe growth such as S. aureus. Fatty acids inhibit such growth by maintaining an acidic pH. |
|
|
Term
|
Definition
| A chemical found in both urine and tears which attacks peptidoglycan layers in gram+ microbes. Lysozyme breaks apart NAG-NAM bonds in the pg layers and destabilises the cell walls as a result. |
|
|
Term
|
Definition
| Very low (acidic) pH of the stomach and surrounding regions inhibits microbial growth (with some exceptions). |
|
|
Term
|
Definition
| A microbe capable of surviving gastric pH conditions and thriving inside the human GI tract. |
|
|
Term
|
Definition
| Low pH prevents colonisation from harmful microbes. A yeast infection is typically a sign of a pH imbalance. |
|
|
Term
|
Definition
| Low pH, high levels of lysozyme and urea; very sterile. Motion of urine through urethra keeps microbes out, for the most part. |
|
|
Term
|
Definition
| Normal flora prevent microbial infections in 3 major ways. 1) They physically take up space, which makes it hard for invading flora to grow. 2) They take up nutrients that invading flora would have to use as well, thus providing direct competition to any invaders. 3) They typically produce inhibitory compounds that prevent successful colonisation and growth from invaders. |
|
|
Term
|
Definition
| Blood contains plasma (the fluid portion), formed elements ("solids" in plasmid suspension), and 3 cell groups: RBCs, WBCs, and platelets. |
|
|
Term
|
Definition
| NOT INVOLVED IN IMMUNITY. They are concerned primarily with CO2/O2 transport. |
|
|
Term
|
Definition
| Heavily involved in immunity. They come 6 flavours: neutrophils, basophils, eosinophils, monocytes, dendritic cells, and natural killer cells. |
|
|
Term
|
Definition
| NOT INVOLVED IN IMMUNITY. They are involved in blood clotting. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Involved in allergic reactions; they are the ones that produce histamine and thus typical allergic responses (as when cedar season is upon us). |
|
|
Term
|
Definition
| Primarily concerned with killing parasites, such as amoebas and protozoans. |
|
|
Term
|
Definition
| Mature into macrophages, another form of phagocyte. |
|
|
Term
|
Definition
| Phagocytes which link the innate with the adaptive immune system |
|
|
Term
|
Definition
| Cells which target only "marked" macrophages and other phagocytes which have successfully consumed and neutralised a pathogen. Analogy: Pathogens are trash, and macrophages are garbage bins. Natural killer cells are the garbage collectors picking up the trash to take to the incinerator! :D |
|
|
Term
|
Definition
| 4 parts: Lymph (the fluid), lymphatic vessels, lymphoid tissues (e.g., tonsils or pyer's patches; store immune cells), red bone marrow (make RBCs). |
|
|
Term
|
Definition
| From the Greek, "to devour," "cell," and "process"; literally, the process of eukaryotic cells devouring another cell or particle. |
|
|
Term
|
Definition
| A generalised term for any cell which can perform phagocytosis. |
|
|
Term
|
Definition
| Phagocytes have pattern recognition receptors on their surface which are sensitive to unique cell wall molecules of microbes. This allows them to recognise invading cells and engulf them. |
|
|
Term
|
Definition
| Pathogen Associated Molecular Patterns, or the unique cell wall molecules which phagocytes can recognise. These include LPS, flagella, teichoic acids, fmet, and pg (in gram+). |
|
|
Term
|
Definition
| The structure created when a phagocyte engulfs a pathogen. |
|
|
Term
|
Definition
| The structure created when a phagosome fuses with a lysosome. This destroys the bacterial cell. |
|
|
Term
|
Definition
| Cell-signaling protein molecules which are released when phagocytosis begins. These signal the rest of the immune system and begin recruiting more phagocytes to the site of infection. Cytokines can also affect the brain by resetting the body's temperature at the hypothalamus; this produces a fever. Cytokines are also responsible for inflammation, pain, and swelling along infected sites. |
|
|
Term
| Pathogenic methods of phagocytosis avoidance |
|
Definition
| Capsules; toxins that can damage phagocytes; biofilms that make engulfing difficult; survival inside of the macrophage (e.g., Mycobacterium spp.) |
|
|
Term
|
Definition
| A system of over 30 serum proteins which must be activated in a specific order (called a cascade) in order for them to work. They are extremely potent and virtually unstoppable once they are triggered. The complement cascade enhances cytolysis of bacteria, inflammation, and phagocytosis through the process of opsonisation. |
|
|
Term
| Complement protein nomenclature |
|
Definition
| Complement proteins are named "C" + a number, which indicates their place in the cascade (C1, C2, C3...). When they are activated, complement proteins split into 2 parts, a and b. An active complement protein would then be called "C" + # + either b or a. For example, "C3b". |
|
|
Term
| Complement cascade cont'd |
|
Definition
| Once a complement protein has been activated (formed a and b proteins), the C#b will bind to the bacterial cell surface to begin opsonisation. The C#a will bind to mast cells to begin the process of inflammation via histamine production. |
|
|
Term
|
Definition
| The binding of the C#b proteins to bacterial cell surfaces to make them easier for phagocytes to "see." This binding process recruits phagocytes to the site of infection. |
|
|
Term
| Membrane attack complex (MAC) |
|
Definition
| During the end of the complement cascade, some complement proteins will form a ring structure that can bind to bacterial cell surfaces and punch a hole through the cell wall. This lyses the cell and kills it. |
|
|
Term
|
Definition
| Antiviral proteins which interfere with the replication of viruses within eukaryotic cells. Infected cells can tell when they are infected, and they will release interferons, which bind to healthy neighboring cells and protect them from being infected by the virus. |
|
|
Term
|
Definition
| Both humans and bacteria need iron to live. Free-floating iron in the human body is essentially candy to an invading microbe, so your body will release iron binding proteins to bind up all the free-floating iron available and keep it away from the bacteria. |
|
|
Term
|
Definition
| Very small peptides of about 12-50 amino acids. Their synthesis is usually triggered by proteins or sugars on the pathogens' surfaces (PAMPs). Antimicrobial peptides are usually broad spectrum (they affect a lot of different kinds of microbes). They can inhibit cell wall synthesis and break down DNA/RNA of bacteria. No bugs have ever been found to be resistant to these peptides. |
|
|
Term
|
Definition
| This is the ability of the 3rd line immune cells to differentiate your own body tissues/cells from those of invading pathogens. T and B cells which can recognise "self" (i.e, will attack host tissues) are typically destroyed before they ever leave their production structures. |
|
|
Term
|
Definition
| The ability of the adaptive immune system to remember pathogens you have been previously infected by, and to respond faster and more efficiently to all subsequent infections by that pathogen. |
|
|
Term
| 2 major aspects of the adaptive immune system |
|
Definition
| Humoral (B cells) and cell mediated (T cells) |
|
|
Term
| Where are B cells produced? |
|
Definition
|
|
Term
| Where are T cells produced? |
|
Definition
|
|
Term
|
Definition
| Produced in response to antigen infection or vaccination exposure |
|
|
Term
| Humoral immunity: PASSIVE |
|
Definition
| Received from somewhere else, i.e., from placental transfer or breast milk or through serums (such as antivenom). Passive immunity lasts only as long as the antibodies are present in the body, so this form of immunity tends to be short lived. |
|
|
Term
|
Definition
| A substance that causes an immune response. Can be: protein, polysaccharide, nucleoprotein, lipoprotein. Ag structures and their specific ags include pg (NAG-NAM), capsule (K ags), flagella (flagellin), toxins. Non-microbial ags include transfused blood or tissues and pollen. |
|
|
Term
| Epitope (antigenic determinant) |
|
Definition
| Portion of ag that reacts with an antibody. They can be all over a bacterial surface, for example the cell wall or flagella. |
|
|
Term
|
Definition
| Haptens are small molecules that aren't big enough for antibodies to notice. They must be complexed with something larger in order to elicit an immune response. |
|
|
Term
|
Definition
| Increase immunogenicity in vaccines. |
|
|
Term
|
Definition
| Globular glycoproteins made in response to an ag. They have ag binding sites that are specific to certain ag epitopes. Abs can have more than 1 ag binding sites, but those sites will only respond to one kind of ag and its epitope. Generic abs are Y-shaped with heavy chains of variable binding sites on top and light chains of constant sites on the bottom. |
|
|
Term
| Ab classification by function |
|
Definition
| Antitoxins; antivenoms; neutralising (bind viral surfaces before they can interact with any other cells). |
|
|
Term
|
Definition
|
|
Term
|
Definition
| A pentomer (5 monomers) held together by J chain. This is the largest ab; as a result, it doesn't diffuse well. IgM is most common in the circulatory system. It is the first to appear on the surface of B cells after ag exposure. It prevents the dissemination of pathogens throughout the circulatory system. |
|
|
Term
|
Definition
| 2 heavy chains and 2 light chains. Appears after IgM, and is most common in serum. It is involved in opsonisation and the enhancement of phagocytosis; it may also neutralise toxins and viruses and it binds to the complement system. IgG is also found in passive immunity, where it is passed on to newborns and helps protect them from infection just before and after birth. |
|
|
Term
|
Definition
| 2 "Y" shaped abs bound together by a secretory component and a J chain. IgA is found in secretions like tears, mucus, and colostrum. The latter allows it to protect newborns from GI pathogens. IgA neutralises infection from pathogens via the mucous membranes. |
|
|
Term
|
Definition
| Generic "Y" shaped ab. Found primarily on the surface of B cells. Involved in lymphocyte activation. |
|
|
Term
|
Definition
| Generic "Y" ab. Found in mast cells and basophils. It primarily defends against parasites (e.g., worms), but is also involved in allergic reactions. |
|
|
Term
|
Definition
| Occurs when there is more ag in the blood than ab. Multiple ags bind to 1 ab. This enhances the ability of the phagocytes to find the ag. |
|
|
Term
|
Definition
| Helps complement proteins form the attack system and begins the cascade. |
|
|
Term
| Ab-dependent cell-mediated immunity |
|
Definition
| Ab attach to the target cell and mark it for destruction by macrophage or other phagocyte. |
|
|
Term
|
Definition
| Ab can block adhesion of bacteria and viruses to mucous membranes. |
|
|
Term
| B cell activation (2 types) |
|
Definition
| T-cell independent and T-cell dependent |
|
|
Term
| T-cell dependent activation of B cells |
|
Definition
| B cells internalise ag and present it on their surface as a receptor that T cells can recognise and bind to. Once the T cell is bound, clonal expansion begins. |
|
|
Term
|
Definition
| help B cells make cytokines and activate B cells during clonal expansion. |
|
|
Term
| B cells differentiate into 2 different cells |
|
Definition
| Plasma (make ab) and memory cells |
|
|
Term
|
Definition
| They remember prior ag infections and come prepackaged with abs for that specific ag. |
|
|
Term
|
Definition
| The process by which B cells differentiate into plasma or memory cells |
|
|
Term
|
Definition
| Slow. Only about one B cell/ag. The activation of B cells and production of plasma and memory cells takes time, as this infection has never been seen before. |
|
|
Term
| Immune response: secondary |
|
Definition
| Faster. Memory cells kick in first, usually about 5 days after initial infection (as opposed to 10 days for primary response). |
|
|
Term
| T cell-independent activation |
|
Definition
| somewhat weaker, tends to be most effective against polysaccharide pathogens. No memory cells involved; only plasma cells. |
|
|
Term
| Cell mediated immunity (CMI) |
|
Definition
| helps fight intracellular pathogens with the help of T cells. CMI is also responsible for transplant rejection, as this system can recognise self vs non self. Also involved in activating phagocytes and in response to tumor cells. |
|
|
Term
|
Definition
| Help activate B cells by releasing cytokines that help B cells differentiate into plasma and memory cells. Subsequently responsible for: ab production, phagocytosis, and immune system response enhancement. |
|
|
Term
|
Definition
| recognise pathogens previously encountered, involved in the secondary response. |
|
|
Term
|
Definition
| interact with MHC I (found on all cells in body), which can mark pathogens and virally infected cells. Cytotoxic T cells will recognise infected cells displaying ag with MHC I and initiate cell death sequence in those cells. |
|
|
Term
| Problems with immunity: Autoimmunity |
|
Definition
| Immune reaction against self; the immune system sees self as "foreign" and will attack its own tissues. Examples: Multiple sclerosis (targets myelin sheaths of neurons); rheumatoid arthritis (attacks synovial joints and destroys synovial fluid); type II diabetus mellitus (targets pancreatic beta cells and destroys insulin). |
|
|
Term
| Problems with immunity: Ineffectiveness |
|
Definition
| This can be due to infection, for example some pathogens are not killed and go on to live inside macrophages (Mycobacterium spp., Legionella, Listeria). In this case, the body will try to wall off the infected phagocytes and create granulomas - pockets of isolated tissue containing these "rogue" phagocytes. Ineffectiveness can also be caused by biofilm formation, which prevents proper function of phagocytes and causes the immune system to fail to recognise the pathogen(s). |
|
|
Term
| Problems with immunity: Loss of all/part of immune system |
|
Definition
| As through genetic defect or disease. 2 examples: AIDS (acquired immunodeficiency syndrome) and "bubble boy" defects. In the case of the latter, individuals are born with little to no immune system to speak of, and must live in highly sterile bubbles to avoid dying of everythingitis. Most people with this defect do not live much older than 5 years, though one quintessential case lasted 12 years. |
|
|
Term
|
Definition
| AIDS is thought to have transferred from other apes to humans in the 1930s. The first known casualty of AIDS occurred in 1959 in the Congo. AIDS has become widespread largely due to a combination of unsafe sexual behaviour and the rise of modern transportation. In 1981, the first cases of AIDS appeared in the US. These were found in clusters of young gay men who were showing rare cases of pneumocystis and Kaposi's sarcoma - both extremely rare diseases not seen in this group before. In 1983, the virus causing this immune dysfunction was discovered and named: HIV. |
|
|
Term
|
Definition
| HIV destroys t4 lymphocytes (T-helpers). This means: no active B cells, no plasma cells, and no memory cells. The immune system essentially falls apart, leaving the body vulnerable to secondary infections. HIV recognises CD4+ cell markers on T cells and binds to them, obliterating specific immunity and leading to rare diseases like pneumonias, sarcomas, herpes, and TB. It is these secondary infections that kill people, not HIV itself. |
|
|
Term
| Problems with immunity: excessive immune response |
|
Definition
| Allergies, caused by immune response to allergens. |
|
|
Term
|
Definition
| Immediate or anaphylactic hypersensitivity, better known to us as seasonal allergies. These work fast; withing 15-30 minutes after exposure, allergic response symptoms materialise. Type I makes IgE abs which bind to mast cells. Mast cells produce histamines, which induce anaphylaxis -- or the immune response known to all sufferers of hayfever, cedar fever, etc. |
|
|
Term
|
Definition
| Ab-dependent cytotoxic hypersensitivity. Abs combine with cell death by complement activation or phagocytosis. This can be seen in Rh factor allergies. For example, when an Rh+ father impregnates an Rh- mother, the mother's immune system will form Rh factor antibodies while she is pregnant. This will not harm her first child, but subsequent children will be attacked as if they are pathogens by the mother's immune system. |
|
|
Term
|
Definition
| immune-complex hypersensitivity. Small particulate ab-ag complexes can overstimulate the immune system, causing the immune system to destroy the tissues surrounding these complexes. This can form blood clots in the skin. |
|
|
Term
|
Definition
| Delayed or cell mediated. Response begins 24-72 hours after exposure. Examples: poison ivy, TB skin test. |
|
|
Term
|
Definition
| His process of identifying anthrax led to the formation of Koch's Postulates. |
|
|
Term
|
Definition
| 1) The organism or pathogen should be present in all cases of the disease but should NOT appear in healthy individuals. 2) Pathogen can be isolated from host and grown in pure culture. 3) Once pathogen is isolated in pure culture, it can be used to infect a healthy host, who will then express the disease caused by that pathogen. 4) the pathogen can be reisolated from the newly infected host, isolated in pure culture, and found to be the same pathogen as isolated in step 1-2. |
|
|
Term
|
Definition
| The ability of an organism to cause disease. |
|
|
Term
|
Definition
| The "weapons" a pathogen uses to inflict disease on its host(s). These can include capsules and/or toxins. |
|
|
Term
|
Definition
| The number of organisms you must be exposed to in order to be infected. In some organisms, such as Shigella, this is a low number (~100). In others, this number is very high. |
|
|
Term
|
Definition
| Short but severe. Example: Strep throat |
|
|
Term
|
Definition
| Prolonged infection. Example: TB |
|
|
Term
|
Definition
| Sudden and very intense. Example: Meningitis |
|
|
Term
|
Definition
| related to one area of the body. Example: Strep |
|
|
Term
|
Definition
|
|
Term
|
Definition
| the invading pathogen is first on the scene and causes the symptoms associated with its particular infection. example: flu |
|
|
Term
|
Definition
| occurs following a primary infection; caused by opportunistic pathogens. |
|
|
Term
|
Definition
|
|
Term
|
Definition
| bacteria growing in the blood |
|
|
Term
|
Definition
|
|
Term
|
Definition
| Areas where pathogens can enter the body. Example: skin (esp if broken), mucous membranes. |
|
|
Term
|
Definition
| the ability of pathogens to penetrate and stick to host cells/tissues. pathogens use adhesins or ligands that bind to specific host cell receptors. |
|
|
Term
|
Definition
| the ability of a pathogen to enter the host tissue. This is an ideal process for a pathogen, as it is harder for the immune system to "see" a pathogen inside of host tissues and the tissues contain a lot of pathogen "food." Penetration can be active (as when the pathogen secretes enzymes to help it get inside specific tissues) or passive (as when a pathogen trips and falls into a wound, burn, or other break in the skin). |
|
|
Term
| Avoidance behaviours and structures of pathogens |
|
Definition
| Capsule formation; modification of cell surfaces; growth inside of immune cells. |
|
|
Term
| Pathogenic damage to tissues |
|
Definition
| caused primarily by pathogen toxins and collateral damage from immune system response (inflammation) |
|
|
Term
|
Definition
| the ability of microbes in communities to count their own numbers. this permits them to change their biochemical and behavioural makeup, communicate with one another using chemical signals, and to perform behaviours that were impossible for just 1 microbe. |
|
|
Term
|
Definition
| The organism in which quorum sensing was first discovered and described. This aquatic microbe lives naturally in the ocean, but will enter into and congregate in the light organ of bobtail squid. When Vibrio has reached a specific number of organisms (density of 10^10-10^11 CFU/ml), they will produce light via bioluminescence. This is beneficial to the squid, which uses the bioluminscence to hide its shadow at night and evade predators. In exchange for its light, Vibrio is given an ideal growth environment in the light organ and all the nutrients it could ever require. |
|
|
Term
| How does quorum sensing work? |
|
Definition
| Bacteria produce an autoinducer at a constitutive rate. When the cells reach a certain density, the autoinducer content of the environment is high. This allows the autoinducer to permeate the cell membrane and bind to specific transcriptional regulators which will turn on quorum-dependent genes (e.g., the ability to produce light). |
|
|
Term
| Factors controlled by quorum sensing |
|
Definition
| Light production; virulence factor production; biofilm formation. |
|
|
Term
|
Definition
| Surface associated bacterial communities enclosed in a polymeric matrix (slime) which contains carbohydrates, DNA, and proteins. Biofilms can grow on many different kinds of surfaces -- teeth, skin, and catheters are all "surfaces." the CDC estimates that 60-80% of all bacterial infections are caused by biofilms. |
|
|
Term
| Why are biofilms so important? |
|
Definition
| Besides their role in human health, biofilms make bacteria behave fundamentally differently from how they might behave in the lab or on their own. These biofilms are also highly resistant to immune responses and antibiotics. |
|
|
Term
|
Definition
| Free-living bacteria find a viable substrate and adhere to it. This step of adhesion is the only reversible step in the biofilm process. Once they begin to aggregate on this substrate, they begin to lose their flagella and stop producing flagellin. They begin to make sticky surface proteins to hold each other together and form the polymeric matrix. Eventually, the bacteria grow into towers of doom known as a biofilm. At this point, quorum sensing can begin, and bacteria which can do so may begin to produce virulence factors. |
|
|
Term
| Food/beverage microbiology: applications |
|
Definition
| Food, chemical solvents, alcohol, antibiotics, vitamins (we get these from our GI flora), polymers, enzymes (cellulase), bioremediation (e.g., oil spill cleanup), bioleaching (e.g., acid mine cleanup), probiotics. |
|
|
Term
|
Definition
| One inoculum is used to create a lot of bacteria growing in a massive clump of substrate, usually to form some end product (e.g., enzyme). When the product has been made, it is removed from the substrate and the culture is cleared and removed so a new culture can be created and the process begins again (I.e., in batches). |
|
|
Term
|
Definition
| One inoculum is kept indefinitely, with media being fed into the culture on one side and the desired end product removed on the other side. |
|
|
Term
|
Definition
| the most common microbe in both alcohol fermentation and baking. Strains of S. cerevisiae are developed based primarily on their ability to tolerate alcohol levels (high alcohol density can kill microbes, and most microbes survive only at around 8-9% alcohol because they are lightweights), the speed at which they ferment, the purity of their fermentation (e.g., producing ethanol [friend] versus methanol [NOT FRIEND]), and their ability to flocculate (separate from the fluid, either by settling to the bottom or rising to the top). |
|
|
Term
|
Definition
| The process by which S. cerevisiae turns boring old glucose into delicious alcohol. During the process of glycolysis, glucose is turned into a number of things with very complicated names and, ultimately, pyruvate. Depending on O2 levels in the environment, pyruvate will either be turned into a product for the Krebs cycle or into ethanol. |
|
|
Term
|
Definition
| the process by which pyruvate in an anaerobic environment turns into ethanol alcohol. Microbial cells do not grow in this process, but ethanol is still produced. |
|
|
