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Microbiolgy: Chapter 31


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What differentiates the two types of normal flora, transient and resident flora, from each other?
Transient flora are contaminants that are irrelevant to defenses; they are available as colonizers if the resident flora is disrupted, while resident flora are the normal colonists at a specific site; they are diverse and able to reporduce.
Which of these contributes to the defense of the body?
Resident flora contribute to the defense of the body.
What are the benefits (4 types) and detrimental effects of having normal flora?
The benefits of having normal flora are: 1)Protect against pathogens (first line of defense), 2)Occupy habitats and niches to exclude late arrivals, 3)Produce antimicrobials (bacteriocins, lactic acid, hydrogen peroxide), 4)Stimulate immune system (keep it always tuned up), and 5)Alter host's physiology (vitamins, peristalsis rate, cecum size). The detrimental effects of having normal flora include dental cavities, the generation of carcinogens, adn they are a source of opportunistic infections.
What are "germ-free" and "gnotobiotic" animals?
"Germ-free" animals are those that have no associated flora; they can be brought about by aseptic cesarean section (mice) and aslo through disinfecting of eggs (chickens) and are maintained in sterile incubators. "Gnotobiotic" animals are those that have known flora; they are brought about by starting with 'germ-free' animals and adding known flora.
What are the controlling conditions that determine the normal flora of the skin?
The controlling conditions that determines the normal flora of the skin are a low aw & NaCl secretions (dry, salty environment), low pH (4-6)(organic acids), and inhibitory substances (lysozyme, cathelicidins, complex lipids).
What are the controlling conditions that determine the normal flora of the upper respiratory tract?
The controlling conditions that determine the normal flora of the upper respiratory tract are: moist (high aw), many nutrients (Fe bound by lactoferrin), high flow rate (mucous, fluids), complex normal flora, and lysozyme.
What are the controlling conditions that determine the normal flora of the lower respiratory tract?
The controlling conditions that determine the normal flora of the lower respiratory tract are: moist (high aw), mucocilary blanket, alveolar macrophages, lactoferrin, lysozyme, and no normal flora.
What are the controlling conditions that determine the normal flora of the mouth?
The controlling conditions that determine the normal flora of the mouth are: strong flushing activity, desquamation, and lysozyme.
What are the controlling conditions that determine the normal flora of the stomach?
The controlling conditions that determine the normal flora of the stomach are: low pH (2-3).
What are the controlling conditions that determine the normal flora of the small intestine?
The controlling conditions that determine the normal flora of the small intestine are: bile salts, acidic to basic, and flow rate-minimal resident flora in duodenum and jejunum (mostly transients) and established flor in terminal ileum.
What are the controlling conditions that determine the normal flora of the large intestine?
The contorlling conditions that determine the normal flora of the large intestine are: slow movement, highly evolved ecosystem, and aerobic to anaerobic.
What are the controlling conditions that determine the normal flora of the genitourinary tract?
The upper genitourinary tract is sterile. Male: the terminal urethra has skin and some fecal flora. Female: Urethra-transient vagina flora, Vagina and Cervix-complex flora, lactobacilli, and transient fecal and skin flora.
What are pathogens?
Pathogens are microorganisms that cause disease.
What are opportunistic pathogens?
Opportunistic microorganisms/pathogens are microorganisms that are usually free-living or a part of the host's normal microbiota, but which may become pathogenic under certain circumstances, such as when the immune system is compromised.
What are compromised hosts?
Compromised hosts are hosts with lower resistance to infection and disease for any of several reasons (malnutrition, alcoholism, cancer, diabetes, leukemia).
What cells are members of the myeloid and lymphoid lines?
T cells, B cells, and null cells are members of the lymphoid line, while ???
What are the three types of granulocytic cells?
The three types of granulocytic cells are Basophils (mast cells), Eosinophils, and Neutrophils.
What is the role of Basophils?
Basophils are non-phagocytic cells that function by releasing histamine, prostaglandins, serotonin, and leukotrienes (which all influence the tone and diameter of bv's) from their granuls upon appropriate stimulation, which contributes to inflammation.
What is the role of Eosinophils?
Eosinophils attack eukaryotic parasites by releasing cationic proteins and reactive oxygen metabolites into the extracellular fluid to damage the parasite's plasma membranes.
What is the role of Neutrophils?
Neutrophils are highly phagocytic cells whith primary and secondary granules that contain substances that help accomplish intracellular digestion. They rapidly migrate to the site of tissue damage and infection where they are the principal phagocytic and microbicidal cells.
What are the two different types of phagocytes in the body?
Macrophages and Neutrophils are two types of phagocytes in the body.
How do these two different phagocytes compare in their life span, relative abundance in the peripheral blood, and ability to divide and differentiate?
Macrophages are very long-lived, they are somewhat abundant in the peripheral blood, and they can differentiate into other cells. Neutrophils are short-lived (half-life ~ 6-12 hours), they make up 65% of WBC's in peripheral blood, and they cannot go through mitosis or meiosis (differentiate).
What is the RES or MPS?
MPS, Mononuclear phagocytic system (formerly known as RES, reticuloendothelial system) is a system comprised of mononuclear phagocytes, which are derived from moncytes.
What are the different names for cells in the MPS?
Different names for cells in the MPS include: dendritic cells, histiocytes, alveolar macrophages, dust cells, microgleal cells, and Kupfer cells.
How does normal flora contribute to nonspecific defense of the body?
Normal flora acts as competition for transient flora; the normal flora block attachment sites in the body where potentially pathogenic microorganisms would bind; they also take up nutrients and resources, keeping them from invaders.
What are superinfections?
A superinfection is a new bacterial or fungal infection of a patient that is resistant to the drug(s) being used for treatment
What three classes of cells provide a protective barrier for the outside of the body?
What features in the cell confer this defense?
Fluids and chemical secretions of the body protect the body by their flow rate, entrapment, and antimicrobial activity (ex: armpit-oil glands secrete complex lipids which G+ bacteria convert to fatty acids which have strong antimicrobial activity against G- bacteria).
What is the role of noraml flora in the body's interior?
The normal flora protect against pathogens, occupy habitats/niches, produce antimicrobials, stimulate immune system, and alter the host's physiology.
What physical barriers are present to inhibit the spread of organisms within the matrix of the body?
Physical barriers present to inhibit the spread of organisms within the matrix of the body include: collagen, hyaluronic acid, cell junctions, and fibrin (can be mobilized to restrain organsims).
What is the mechanism of action of flow rate of blood?
The increased blood flow bring into the area more antimicrobial factors and leukocytes, as well as the higher concentration of blood enzymes that cleave C3 to activate the ACP (alternative complement pathway).
How can there be specific and non-specific binding as a prelude to endocytosis?
Specific binding: Compliment system dumps C3b onto surface of bacterium & phag. cells bind to these receptors and pull them in.

Non-specific (nonopsonic): Recognizes other receptors(lectin, protein-protein, hydrophobic interactions)
What are opsonins?
An opsonin is any molecule that acts as a binding enhancer for the process of phagocytosis. During the process of opsonization, antigens are bound by antibody and/or complement molecules. Phagocytic cells express receptors that bind opsonin molecules. With the antigen coated in these molecules, binding of the antigen to the phagocyte is greatly enhanced. Most phagocytic binding can not occur without opsonization of the antigen.
Endocytosis yeilds a bacterium in what compartment(vacuole)? What is the vacuole called after lysosomal fusion?
Phagosome; phagolysosome
What are defensins?
Small basic proteins that disrupt membranes and kill things like bacteria/fungi/and disrupt envelopes on viresus.
What are ROIs and RNIs and what is the term for the metabolic adjustment leading to them?
The term is Respiratory burst in which the cells shift from EM-PW to Hexose monophosphate shunt PW (like PPP)and produces NADPH. This NADPH formation forms reactive oxygen intermediates(ROIs) and reactive Nitrogen intermediates(RNI)
What is the primary product of the myeloperocidase system? What cells have this system?
Hypochlorous acid formation (with reactive Oxygen in phagosome) (in PMNs) yeilding ClO (halite ion) and water
What is the chronic granulomatous disease?
Caused by Myeloperoxidase defect which makes dense accumulations of macrophages and T-cells (grandulomas). Attept to wall off the infection

What are three strategies parasites use to avoid the lethal effects of phagocytosis?
What is meant by antigen presentation?
Antigen presentation is a process in the body's immune system by which macrophages, dendritic cells and leukocytes capture antigens and then carry those antigens to T-cells. Once a T-cell has been attuned to an antigen it will then circulate throughout the bloodstream, seeking out that antigen and destroying it.

The basis of adaptive immunity lies in the capacity of immune cells to distinguish between the body's own cells, and the unwanted invaders. The host’s cells express “self” antigens that identify them as such. These antigens are different from those on the surface of bacteria ("non-self" antigens) or on the surface of virally infected host cells (“missing self”). The adaptive immune system is triggered through a process known as antigen presentation.
What is specific of a M0 release of endogenous pyrogen?
Interleuken 1 causes a release of prostaglandins in the hypothalamus resulting in fever.
What is the febrile response? What organ controls it?
Increase in body temperature, and decrease of Fe availability. Hypothalamus.
What are 3 benefits that the febrile response contributes to the non-specific defenses of the body?
Causes increased immune activity, causes temp above growth optimum of bacteria, strips Fe away from transferon so organisms have a hard time to grow
What kind of a molecule are the interferons?
by and for stroma cells (normal cells that make up tissues)
What is the target of interferon released from a cell? And how does interferon protect a cell against viral infection?
by and for stroma cells (normal cells that make up tissues) with many stimulators including viruses. IFN released by cell. and it goes off and stimulates cells around it which stimulates increase of RNAse activity and decrease invading virus can't use the cells machinary.
What are the 5 cardinal signs of inflammation?
functio laesa=lose of fxn
What underlying process does each of the cardinal signs represent?
Tumor=increased capillary premeability/leakage of fluids & solutes; Dolor=release of prostaglandins/increased nerve firing & pain; Calor & Rubor=arteriolar dilation, increased blood flow.
What roles do the chemical mediators bradykinin and histamine play?
Bradykinin-can bind to endothelium which changes it to have an increased capillary permeabiliy which causes swelling (tumor). Also causes release of prostaglandins-increase nerve firing and pain (dolor).

Can also bind to Mast cells and starts to allow Ca influx in the cell which causes Mast cell to release histamine (increase permeability, increase dolor, etc and cause arteriolar dilatoin which increases blood flow (look redder-rubor), alter the temp localy(calor)and transfers heat closer to core body temp.
What roles do Mast cells, PMNs and M0 playin inflammation?
M0 (macrophages)-infiltration is slower (less degranulation, more cleanup)
PMN-infiltration + degranulation ( release digestive enzymes)- augmentation of response and draw in more!
What chemical signals bind to Mast cells in an inflammatory response to cause their degranilation?
How is the inflammatory response "down regulated"?
Macrophages-cleanup damage, Phagocytsis.

Fibrin-from vasculature makes clots which contains infection
What are PAMPs, PRRs, and TLRs?
Phagocytes have receptors dedicated to PAMPSPathogen Associated Molecular patterns(pattern recognitioin receptors-PRR)
PRR's binding their specific PAMPs elicit responses such as endocytosis and cytokine production (C3b binding,etc). PRR's initiate signal transduction cia Toll-like receptors(TLRs)

TLRs-signal transduction releases cytokine(molecules made by cell that go out and effect other cells) which can determine the nature of the innate and immune responses
Why are PAMPs, PRRs, and TLRs considered a central part of the innate defense? How do they "shape" the innate & immune defenses?
Different PRR can stimulate different TLR which can release different cytokins so therefore can determine the nature of the innate and immune responses just by cloud that is being released.
What is the mechainsm of the antimicrobial activities of transferrin?
Transferrin binds iron to keep it away from invading organism (to prevent growth) and devlivers it to other parts of the body.
What is the mechainsm of the antimicrobial activities of beta-lysins?
Beta-lysins are cationic peptides that are released during clotting and disrupt the plasma membrane.
What is the mechainsm of the antimicrobial activities of the complement system?
In the complement PW, a blood enzyme activates the cleavage of C3 into C3a and C3b; C3b (opsonin) cleaves C5 into C5a (chemotaxin) and C5b; this cleavage leads to a cascade that brings about the binding of C6-C9, which forms the MAC (mem attack complex), which creates a pore in the plasma membrane; this pore allows ions/salt and water into the cell and it lyses osmotically.
How do bacteria overcome the restriction on their growth imposed by transferrin?
Why are Gram + cells more susceptible to beta-lysins than Gram - cells?
Gram+ cells are more susceptible to beta-lysins than G- because they can get through the PG and insert in the plasma membrane (due to negative charge of PG???).
What are the three modes of activation of the complement PW?
The three modes of activation of the complement PW are CCP, classical complement pathway, LCP, lectin complement pathway , and ACP, alternative complement pathway.
What special properties do C3b and C5a have?
C3b,an opsonin, works to bind bacteria and make them more readily phagocytosed. C5a, a chemotaxin, induces a directed, chemotactic migration of neutrophils to the site of complement activation.
Why does the MAC effect Gram - bacteria more then Gram + bacteria?
The MAC (membrane attack complex) effects Gram- more than Gram+ bacteria because G+ bacteria lack an exposed outer membrane and have and have a thick PG that prevents attack on the plasma membrane.
Describe Chemotaxis (margination, diapedesis, and migration).
Chemotaxis is broken down into 3 parts: margination, diapedesis, and migration. In margination inflammation casues selectins (receptors) to be displayed on the enothelium; PMNs respond with integrins which bind to cell adhesion molecules (CAMs) causing sticking. In diapedesis marginated cells make openingsin the endothelium and leave the bv (sealing the opening behind them). In migration, they can now sense the chemotactic gradient and move up it.
Describe ingestion.
In the process of ingestion, the phagocytic cell uses one of two basic molecular mechanisms for binding: opsonin-dependent, opsonin-independent. There are 3 different mechanisms to choose from in the opsonin-independent: lectin, protein-protein, and hydrophobi interactions. Next, after binding, endocytosis occurs: microfilaments extend psuedopods around the tightly bound bacteria to creat a tightly adherent phagosome. Next, the phagosome binds to a lysosome and forms a phagolysosome, in which the hight pH begins to degrade the bacterial membrane and proteins.
Describe killing/bactericidal activity.
In the killing/bactericidal portion of phagocytosis, inside the phagolysosome reactive Oxygen intermediates (ROI)(superoxide radical, hydrogen peroxide, singlet oxygen, and hydroxyl radical), reactive Nitrogen intermediates (RNI), and hypochlorus acid are formed as a result of the respiratory burst that accompanies the increased Oxygen consumption and ATP generation needed for phagocytosis. These have cytocidal effects on the contents of the phagolysosome.
Describe degradation.
During degradation, the following are released into the phagolysosome: Lysosome, phopholipas A2, which cleaves polar headgroups off of phospholipids, ribonuclease and deoxyribonuclease, which digest nucleic acids, and proteases, which digest proteins.
Describe sequel.
During sequel, the macrophage/phagocytic cell can present the antigen (place pieces on its outside for signaling), and also releases endogenous pyrogen that brings about fever in the host.

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