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Exam 5 Study Guide

by: Courtney Erickson

Exam 5 Study Guide Bio 313

Marketplace > Ball State University > Biology > Bio 313 > Exam 5 Study Guide
Courtney Erickson
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Here's my study guide for exam 5. This exam covers chapters 23, 24, 25, and 28, which includes Epidemiology, Immune Responses, and Human-Microbial Interactions. Hope this helps you!
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This 10 page Study Guide was uploaded by Courtney Erickson on Sunday December 13, 2015. The Study Guide belongs to Bio 313 at Ball State University taught by Metzler in Summer 2015. Since its upload, it has received 39 views. For similar materials see Microbiology in Biology at Ball State University.


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Date Created: 12/13/15
EXAM 5 Study Guide Chapter 23: Microbial Interactions with Humans Human Microbiome Humans are microbially sterile in utero, and begin colonization at birth. Skin is colonized: Includes Actinobacteria, Firmicutes, Proteobacteria, Bacteroidetes, and others. Environment varies in nutrients, chemical content, and moisture. Oral Cavity is colonized: Includes Firmicutes, Bacteroidetes, Proteobacteria, Actinobacteria, Spirochetes, and others. Environment is very moist, with low nutrients. Saliva also contains lysozymes and lactoperoxidase. GI tract is the most colonized area: Esophagus bacteria include Prevotella, Streptococcus, and Veillonella. Stomach bacteria include Helicobacter, Proteobacteria, Bacteroidetes, Actinobacteria, and Fuscobacteria. Small Intestine bacteria mainly includes Enterococci and Lactobacilli. Large Intestine bacteria includes Bacteroidetes, Bifidobacterium, Clostridium, Enterobacteria, Enterococcus, Escherichia, Eubacterium, Klebsiella, Lactobacillus, Methanobrevibacter, Peptococcus, Peptostreptococcus, Proteus, Ruminococcus, Staphylococcus, and Streptococcus. Respiratory tract is colonized: Streptococcus, Staphylococcus, Corynebacterium, Neisseria, Haemophilus. Urogenital tract is colonized: Mostly includes Escherichia, Klebsiella, Proteus, Neisseria, Lactobacillus, Corynebacterium, Staphylococcus, Candida, Prevotella, Clostridium, Peptostreptococcus, Ureaplasma, Mycoplasma, Mycobacterium, and Streptococcus. Pathogenesis Pathogenesis​ = ability to cause disease Virulence​= measure of pathogenicity Infection = growth of microorganisms that aren’t normally present Pathogen ​= microbe that lives in the host and can cause disease Disease​= tissue damage that impairs host function Opportunistic Pathogen​ = causes disease in the absence of host resistance Attenuation​ = when a pathogen is weakened (decreased virulence) Microbial Pathogenesis: 1.) Exposure 2.) Adherence pathogen must​ attach before it can cause disease adherence factors include: Capsule/Slime Layer, Lipoteichoic Acids, Adherence Proteins, and Fimbriae/Pilli 3.) Invasion invasion can be localized or systemic 4.) Infection 5.) Disease Pathogens invade, then multiply. Virulence Factors Include Exotoxins, Endotoxins, and Enzymes that enhance invasiveness. Enzymes include Hyaluronidase, Collagenase, Streptokinase, and Coagulase. Hyaluronidase​ destroys hyaluronic acid, which increases pathogen invasiveness. Collagenase​destroys collagen, which also increases pathogen invasiveness. Streptokinase​dissolves blood clots to increase pathogen invasiveness. Coagulase​ promotes blood clotting so that the pathogen can be protected from the immune system. Exotoxins are released as a pathogen grows. Includes cytotoxins, AB toxins, Superantigens, and Enterotoxins. Endotoxins are toxins that aren’t actively released by cells; they’re released after cell death. Chapter 24: Immunity and Host Defense Host Defense Host Defense includes: ● Physical and Chemical Barriers ● Tissue specificity of pathogens ● Normal Microflora Physical and Chemical Barriers Physical Barriers: Skin, flushing of the urinary tract, cilia in upper respiratory tract, tight junctions at epithelial cells. Chemical Barriers: Lysozymes (enzymes in body fluids that dissolve cell walls), and Stomach Acidity. Risk Factors for Disease Risk factors for disease include ● Host Characteristics ● Environmental and Social factors ● Exposure to Pathogen Immune System Innate Immunity is the body’s built in ability to recognize and destroy pathogens. Adaptive Immunity is the body’s acquired ability to deal with pathogens. Antigens are pathogen molecules that the adaptive response is directed at. Cells of the Immune System Granulocytes and Monocytes are cells that do phagocytosis and antigen presentation. Plasma Cells are responsible for antibody production T Cells are responsible for cell mediated immunity. Innate Immunity is the non-specific recognition of a pathogen. This involves PAMPs and PRRs: PAMPs = Pathogen-Associated Molecular Patterns, and PRRs are Pattern Recognition Receptors. Adaptive Immunity is pathogen specific. Key features of adaptive immunity include lymphocytes (B and T cells), tolerance to self-antigens, memory, inducibility, and clonality. T Cells ● Develop in red bone marrow, mature in thymus ● Circulate in lymph/blood systems ● Important in humoral and cell-mediated immunity ● Include Cytotoxic T Cells (c​ and Helper T Cellsh​T​ ○ Tc cells (aka Killer Cells) directly kill other cells with foreign peptides ○ Th cells secrete chemicals that aid cell-mediated response and promote antibody production. B Cells ● Develop entirely in red bone marrow ● Specialized lymphocytes with antibodies on their surface ● Function in humoral immunity; make antibodies. Antibody Functions a) Neutralization: antibodies bind pathogen, prevent it from binding to host b) Opsonization: surface covered with antibodies, causes phagocytosis c) Oxidation: produces H​2​ 2 ​ O​3​which are both toxic and cause cell death d) Agglutination: clumping, prevents toxin from acting e) Antibody-Dependent Cellular Cytotoxicity (ADCC): activates Natural Killer cells Inflammation Inflammation = a general, nonspecific response to pathognens and tissue damage Types of Inflammation: ● Acute Inflammation ● Chronic Inflammation ● Local Inflammation ● Systemic Inflammation Inflammation Symptoms include: ● Redness ● Heat ● Swelling ● Pain Blood Vessel Changes during Inflammation: Dilation: Larger blood vessels allow more blood flow & blood components at site. This is stimulated by histamines and bradykinin. Causes redness and heat (and decreases blood pressure) Permeability: Leaky vessels allow fluids and cells to enter tissues Stimulated by bradykinin, prostaglandins and leukotrienes. Causes swelling and pain. Acquired Immunity Natural Active: development of a natural infection that initiates immune response Natural Passive: antibodies transferred from mother to infant Artificial Active: vaccination Artificial Passive: venom is neutralized by antibodies in a snake’s antivenom Active → Memory; Long-term Protection Passive → Short-term Protection (lasts until antibody proteins degrade); No Memory Active, Artificial Immunization (vaccination) is the best & most cost effective method of disease prevention. Can be used for disease prevention and treatment. Types of Vaccines: ● Attenuated (live) - active pathogens with reduced virulence ● Inactivated (killed) - virus incapable of replication ● Toxoid - a modified exotoxin ● Combined - multiple vaccines in one dose ● Recombinant - pathogenic DNA Immune Disease Immune Diseases are inappropriate immune responses that cause host cell damage. Includes: Hypersensitivity, Autoimmunity, and Immunodeficiencies. Hypersensitivity ​can be immediate or delayed: Immediate​ = Allergies ((Type I Sensitivity) Sensitization = first exposure to allergen. (no symptoms) Subsequent exposures trigger degranulation (causes symptoms) Allergy symptoms include headache, constricted bronchioles, excess mucus formation, rash, sneezing, itchy eyes, etc. Delayed​(Type IV Sensitivity) Delayed response after exposure to allergen; can take hours to days Is a cell-mediated response Autoimmunity​ occurs when the immune system responds to self-antigens. Involves autoantibodies and Killer T Cells. Potential Causes include: - Genetic & Hormonal Links - Failure of clonal deletion - Receptor gene mutation - Inappropriate MHCII expression - Molecular mimicry - Autoimmune regulator defects - Viral infection Autoimmunity can be systemic or organ-specific. Immunodeficiencies​ are when the immune system is incapable of producing a response. Caused by defects in the immune system Victims suffer from recurrent infections, usually with opportunistic microbes Includes Primary Immunodeficiencies and Secondary Immunodeficiencies. Primary: Genetic-based. Develops in infants and young children. Secondary: Acquired from natural causes or immunosuppression. Develops later. Chapter 25: Immune Mechanisms Phagocytes Purpose of phagocytic cells: - to survey tissues for foreign matter or injured/dead cells - to engulf and eliminate these materials - to find antigens to stimulate specific immune responses Phagocytes include Dendritic cells, Neutrophils, Monocytes, and Macrophages. Phagocytic killing involves degradative enzymes and respiratory burst. Respiratory burst is the increase in oxygen uptake and consumption by activated phagocytes. This oxygen is then turned into toxic oxygen compounds, such as hydrogen peroxide, that can be used to kill pathogens. Pathogen Recognition by Phagocytes: involves PRRs (Pathogen Recognition Receptors) each PRR recognizes a specific PAMP (Pathogen-Associated Molecular Pattern) leads to phagocyte activation and inflammatory response Antigens Antigens are substances that react with antibodies/TCRs. Properties of Antigens: ● have epitopes ● tolerance to self-antigens ● bigger is better ● complexity is favored (this is why antigens are commonly proteins) ● aggregation is beneficial (preferred over soluble) Antigen interactions with B Cells: ● B cells interact with soluble antigens ● B cells interact with conformational epitopes ● B cells are less particular about antigen interactions Antigen interactions with T Cells: ● T cells interact with processed antigens ● These antigens are presented by MHC proteins ● T cells interact with linear epitopes (usually individual peptides; must be broken down for T cells) ● Antigen must be presented to T cell in order for it to see the antigen. MHC​ - Major Histocompatibility Complex MHC Class I ● found on all nucleated cells ● present intracellular antigens to CD8 coreceptor on Cytotoxic T Cells ● most important in viral infections, intracellular bacterial infections, and cancer MHC Class II ● found on APCs (Antigen Presenting Cells) ● present extracellular antigens to CD4 coreceptors on Helper T Cells ● most important in bacterial infections (extracellular stuff) T Cells: Cytotoxic T Cells: ● Tc cells directly kill cells displaying foreign antigens ● Contact between Tc cells and target cells activates Tc cell ● Cytotoxic pathways release granules, which contain perforins and granzymes ● These cause apoptosis of target cell Natural Killer Cells: ● NK cells are cytotoxic lymphocytes ● Destroy cancer cells and cells infected with pathogens ● Target cells don’t express MHC Class I Helper T Cells: ● Th cells amplify the inflammatory response ● Secrete cytokines Chapter 28: Epidemiology Epidemiology​ - the study of occurrence, distribution, and determinants of health and disease in a population. Chronic Infection = long term infection Acute Infection = rapid and dramatic disease onset Endemic = infections constantly present, but in low numbers Epidemic = unusually high number of people infected Pandemic = a widespread (often worldwide) epidemic Incidence = number of new cases Prevalence = total number of disease cases (new and existing) Morbidity = incidence of disease in a population Mortality = incidence of death in a population Disease Progression: 1.) Infection -organism invades, colonizes, and grows in the host 2.) Incubation Period -time between infection and appearance of symptoms 3.) Acute Period -height of disease symptoms 4.) Decline Period -disease signs and symptoms subside 5.) Convalescent Period - patient recovers/regains strength; is normal Disease Transmission: Direct - includes sneezing, coughing, physical contact, and fluid exchange Indirect - includes vectors, fomites, and vehicles Epidemic Sources: Common-source epidemic (ex. Cholera is spread by contaminated water) Host-to-Host epidemic (ex. Respiratory disease or STDS) Vector-borne disease (ex. Malaria is transmitted by mosquitos) Disease Reservoirs These are sites where pathogens are maintained as a source of infection - Living hosts include animals, humans, and insects - Nonliving hosts include soil, water, and food Basic Reproductive number - R​ 0 R0​shows the number of expected secondary transmissions if a disease has an Rof 1, then each infected person is expected to pass the 0​ disease on to one susceptible person, etc. Public Health and Epidemiology In order to control disease, epidemiologists use these methods: ● Control of Vehicles ● Control of Reservoirs ● Immunization ● Isolation ​(separation of healthy and infected people) ● Quarantine ( ​separation of healthy people who may have been exposed) ● Surveillance ​(observation of diseases as they occur) ● Pathogen Eradication  


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