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Exam #3 Chapters 13-17

by: Alex Bock

Exam #3 Chapters 13-17 BIOL 455

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The answers to objectives listed in the chapters from class PowerPoints. Use these objectives to study for the test.
General Microbiology
Alina M De La Mota-Peynado
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This 20 page Study Guide was uploaded by Alex Bock on Monday November 16, 2015. The Study Guide belongs to BIOL 455 at Kent State University taught by Alina M De La Mota-Peynado in Fall 2015. Since its upload, it has received 20 views. For similar materials see General Microbiology in Biology at Kent State University.


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Date Created: 11/16/15
Exam #3 Ch. 13, 14, 15, 16, 17 Chapter 13 1. What is a virus? Composition and general characteristics.  Virus- From Latin word “poison” A submicroscopic, parasitic, filterable agent consisting of nucleic acid surrounded by a protein coat  Composition-single type of nucleic acid, DNA OR RNA. Protein coat (sometimes enclosed by an envelope of lipids, proteins, and carbohydrates) that surrounds nucleic acid  Characteristics- obligatory intracellular parasites (require living host to multiply), DNA OR RNA, no ribosomes, no ATP generation, use living host cell’s machinery to multiply, synthesize specialized structures (capsid) that can transfer the viral nucleic acid to other cells 2. What are the differences between viruses and other acellular agents, prions, viruses and viroids.  Prions-proteinaceous infectious particles, inherited and transmissible by ingestion, transplant, and surgical instruments o PrPc: normal cellular prion protein, on cell surface o PrPsc: scrapie protein; accumulates in brain cells, forming plaques  Viroids- Made of single stranded, circular RNA. Infectious agents composed only of closed, circular ssRNAs, smallest infectious agents, do not code any proteins, cause diseases in PLANTS 3. Understand host range and what factors determine it.  Range from 20nm-1000nm length  Most viruses infect only specific types of cells in one host (viral specificity), which is determined by specific host attachment sites and cellular factors 4. Describe the physical and chemical structure of both enveloped and non-enveloped viruses. How do they acquire an envelope?  Enveloped- Ex: poxviridae, herpesviridae, hepatnaviridae, togaviridae.- lipid, protein, and carbohydrate coating that covers capsid. Some animal viruses released from host cell by extrusion process that coats the virus with a layer of host cell’s plasma membrane, which becomes the envelope. Sometimes envelope contains nucleic acids from host cell that determine virus proteins. Some have spikes  Non-enveloped-protects nucleic acid from nuclease enzymes in fluids and promotes virus attachment to susceptible host cells. Some viruses escape antibodies because regions of the gene that code for viruses’ surface proteins are susceptible to mutations. 5. How are viruses classified based on their morphology, and how are they taxonomically classified?  Morphology- Helical viruses- hollow, cylindrical capsid, polyhedral viruses- many sided, enveloped, complex- complicated structures  Taxonomy- Genus name ends in –virus, family names end in – viridae, order names end in –ales. Viral species- group of virues sharing the same genetic info and ecological niche (host) o Common names are used for species, subspecies are numbered 6. Know and understand the different techniques to grow bacteriophages and animal viruses. KNOW THIS ONE!  Bacteriophage- Must be grown in living cells, bacteriophages grown in bacteria- form plaques, each plaque corresponds to a single virus; Plaque forming unit (PFU)  Animal viruses- In living animals, injected into egg yolk, growth signaled by death or change in embryo 7. Describe three techniques that can be used to identify viruses.  Cytopathic effects, serological tests- western blotting, reaction of virus w/ anitbiodies, nucleic acids-Restricted Fragment Length Polymorphism (RFLPs) and Polymerase Chain Reaction (PCR) 8. Explain and contrast lytic and lysogenic cycles.  Lytic- phage causes lysis and death of host cell o Attachment-attaches by tail fibers to host cell o Penetration- phage lysosome opens cell wall; tail sheath contracts to force the tail core and DNA into cell o Biosynthesis: production of phage DNA and proteins o Maturation- assembly of phage particles o Release- phage lysosome breaks cell wall  Lysogenic- phage DNA incorporated into host DNA, phage conversion, specialized transduction- specific bacterial genes transferred to another bacterium via a phage, changes genetics of bacteria o Lysogeny- phage remains hidden o Prophage- inserted DNA o Phage conversion- host cell exhibits new properties 9. How does the replication cycle of DNA and RNA-containing animal viruses differ? Know examples of each.  Attachment- viruses attach to cell membrane  Entry- by receptor-mediated endocytosis or fusion  Uncoating- by viral or host enzymes  Biosynthesis- production of nucleic acid and proteins  Maturation- nucleic acid and capsid proteins assemble  Release- or budding (enveloped) or rupture  Biosynthesis of DNA viruses o Replicate DNA in nucleus of host using viral enzymes o Synthesized capsid in cytoplasm using host cell enzymes o Adenoviridae- double stranded DNA, non-enveloped, causes respiratory infections in humans, tumors in animals o Poxviridae- double stranded, enveloped, cause skin lesions, smallpox viruses o Herpesviriade- double stranded, enveloped  HHV-1 and 2- cold sores  HHV 3- chickenpox  HHV-4- mononucleosis  HHV-5 cytomegalovirus  HHV-6 and 7- Roseolovirus  HHV-8- Kaposi’s sarcoma o Papovaviridae- double stranded, non-enveloped, causes warts, can transform cells and cause cancer o Hepadnaviridae- double-stranded, enveloped, Hep B virus, reverse transcriptase to make DNA from RNA  Biosynthesis of RNA o Multiplies in host cell cytoplasm using RNA-dependent RNA polymerase o ssRNA; + (sense) strand, viral RNA serves as mRNA for protein synthesis o ssRNA; - (antisense) strand, viral RNA transcribed to a + strand to serve as mRNA for protein synthesis o dsRNA- double stranded RNA o Picronaviridae, single stranded, + strand, non-enveloped, enterovirus, rhinovirus, Hep. A virus o Togaviridae- single stranded, + strand, enveloped, alphavirus, rubivirus o Rhabidoviridae- single stranded, - strand, one RNA strand, lyssavirus/rabies, animal diseases o Reoviridae- double stranded, non-enveloped, respiratory infections and gastroenteritis 10. What is an oncogene? A transformed cell? What is an oncolytic virus?  Oncogene- transform normal to cancer cell  Transformed cell- acquire properties that are distinct from properties of uninfected cells or from infected cells that don’t form tumors. Harbors a tumor-specific transplant antigen (TSTA) on surface and a T antigen in nucleus  Oncolytic- infect and lyse cancer cells 11. What is the relationship between viruses and cancer?  Types of viruses cause cancer, develop long after viral infection, cancers caused by viruses are not contagious  Sarcoma-cancer of connective tissue  Adenocarcinomas- cancers of glandular epithelial tissue 12. How can we use viruses to treat cancer cells.  Oncolytic viral therapy, several viruses known to selectively infect cancer cells, and now being genetically modified to remove virulence genes and add stimulation to promote white blood cells 13. Contrast latent vs. persistent viral infections.  Latent- remains in asymptomatic host cell for long periods, may reactivate, Ex: cold sores, shingles- remains for long time very quiet inside of body  Persistent- active and slow growing but there all the time, person never gets completely better. Occurs gradually over long period, generally fatal, Ex: measles 14. How are plant viruses classified? Describe their lytic life cycle.  Enter through wounds or via insects, plants protected by cell wall  Double stranded DNA non-enveloped  Single stranded RNA, + strand, non-enveloped  Single stranded RNA, - strand, enveloped  Double stranded RNA, non-enveloped  Lytic life cycle-? 15. What is the socio-economic impact of viruses?  ? Chapter 14 1. Define pathology, etiology, infection, and disease.  Pathology- study of disease  Etiology- the cause of disease  Infection-invasion or colonization of the body by pathogens  Disease-an abnormal state in which the body is not performing normal functions 2. Define normal and transient microbiota.  Normal- help infection, increase digestion, permanently colonize the host and do not cause disease under normal conditions  Transient- temporary-may be present for days, weeks, or months 3. Compare commensalism, mutualism, and parasitism, and give an example of each.  Commensalism- one organism benefits, and other is unaffected (staphylococcus epidermidis that inhabit surface of the skin that live off of secretions, but do not harm the host  Mutualism- both organisms benefit- large intestine bacteria like E. coli that synthesize vitamins which are then absorbed into bloodstream and in exchange the large intestine provides nutrients for bacteria  Parasitism- one organism benefits at expense of other- disease causing bacteria are parasites 4. Contrast normal microbiota and transient microbiota with e microorganisms.  Normal and transient microbiota affect the host cell under one condition whereas opportunistic microorganisms might be harmless in one condition, but very harmful in a different environment. 5. List Koch’s postulates  Every case  Pure culture  Pathogen from pure culture must cause same disease when introduced into healthy person  Pathogen isolated from person and be the same organisms originally put into that person 6. Differentiate a communicable from a noncommunicable disease.  Communicable is a disease that is spread from one host to another  Noncommunicable is a disease that is not spread from one host to another 7. Categorize diseases according to frequency of occurrence, and severity.  Occurrence of disease o Incidence: number of people who develop a disease during a particular time period o Prevalence: number of people who develop a disease at a specific time, regardless of when it first appeared (old and new cases) o Sporadic: occurs occasionally o Endemic: constantly present in a population o Epidemic: acquired by many people in a given area in a short time o Pandemic: worldwide epidemic  Severity/duration o Acute: rapidly develop symptoms but disease only lasts short time o Chronic: symptoms develop slowly o Subacute: intermediate between acute and chronic o Latent: causative agent is inactive for a time but then activates and produces symptoms o Herd immunity: immunity in most of the population 8. Define herd immunity.  immunity in most of the population 9. Identify four predisposing factors for disease.  Gender  Climate and weather  Inherited traits  Fatigue  Age  Lifestyle  Nutrition  Chemotherapy 10. Define reservoir of infection.  Sources of infection o Human reservoirs o Animal reservoirs-zoonoses transmitted from animals to humans o Nonliving reservoirs- soil and water 11. Contrast human, animal, and nonliving reservoirs, and give one example of each.  Human reservoirs  Animal reservoirs-zoonoses transmitted from animals to humans  Nonliving reservoirs- soil and water 12. Explain three methods of disease transmission.  Direct contact- requires close association between infected and susceptible host  Indirect- spreads to a host by a nonliving object (fomite)  Droplet- transmission via airborne droplets less than 1 meter 13. Define healthcare-associated infections, and explain their importance.  Nosocomial infection acquired while in hospital because of non sterile instruments  1 in 25 hospital patients  result from- microorganisms in hospital environment, weak immune system of host, chain of transmission 14. Define compromised host.  Depressant immune system- link with nosocomial infections-Ind. Whose resistance to infection is impaired by disease, therapy, or burns 15. List several methods of disease transmission in hospitals, and explain how healthcare-associated infections can be prevented.  Transmitted from patient to nurse, doctor, instrument, and then introduced into host  Hand washing, disinfecting tubs used to bathe patients  Cleaning instruments scrupulously  Using disposable bandages and intubation 16. List several probable reasons for emerging infectious diseases, and name one example for each reason. Why are we so at risk? 1. Diseases can travel 2. Resistance of bacteria  Genetic recombination- E. coli  Evolution of new strains- vibrio cholera  Widespread use of antibiotics and pesticides- antibiotic resistant straints  Changes in weather patterns- hantavirus  Modern transportation- West nile virus  Ecological disaster, war, and expanding human settlement  Animal control measures- lyme disease  Public health failture- diphterhia 17. Define epidemiology, and describe three types of epidemiologic investigations.  Epidemiology- study of where and when diseases occur and how they are transmitted in populations  John Snow mapped occurrence of cholera in London  Ignaz Semmelweis showed hand washing decreased the incidence o peurperal sepsis 18. Identify the function of the CDC. What organization does the work of CDC at global scale?  Centers for Disease Control and Prevention 19. Define the following terms: morbidity, mortality, and notifiable infectious diseases  Morbidity- incidence of a specific notifiable disease  Mortality- deaths from notifiable disease  Notifiable infectious diseases: diseases in which physicians are required to report occurrence Chapter 15 1. Identify the principal portals of entry.  Mucous membranes  Skin  Parenteral route 2. Define ID 50and LD 50  Ex: x=2 y=100. X is more virulent it only takes 2 doses to kill 50%  ID50- infectious dose for 50% of sample pop. Measures virulence of a microbe  LD50- lethal dose for 50% of a sample pop. Measures potency of a toxin 3. Using examples, explain how microbes adhere to host cells.  Adhesins (ligands) on the pathogen bind to receptors on the host cells o Glycocalyx o Fimbriae  Biofilms share nutrients 4. Explain how capsules and cell wall components contribute to pathogenicity.  Capsules- Impair phagocytosis o Streptococcus pneumoniae- pneumonia o Haemophilus influenzae-pneumonia and meningitis o Bacillus anthracis- anthrax o Yersinia pestis-plague  Cell wall components o M protein resists phagocytosis o Opa protein allows attachment to host cells o Waxy lipid resists digestion 5. Compare the effects of coagulases, kinases, hyaluronidase, and collagenase.  Coagulases- coagulate fibrinogen  Kinases- digest fibrin clots  Hyluronidase- digests polysaccharides that hold cells together  Collagenase- breaks down collagen  IgA proteases- destroy IgA antibodies 6. Define and give an example of antigenic variation.  Pathogens alter their surface antigens; antibodies ineffective  N. gonorrhea has several copies of opa-encoding gene, resulting in cells with different antigens and in cells that express different antigens over time 7. Describe how bacteria use the host cell's cytoskeleton to enter the cell.  Invasins-surface proteins produced by bacteria that rearrange actin filaments of the cytoskeleton- causes membrane ruffling o Use actin to move from one cell to next 8. Describe the function of siderophores  Siderophores are on bacterias side, all others on host side  Iron required for pathogenic bacteria  Siderophores- proteins secreted by pathogens in order to get more iron and that bind iron more tightly than host cells 9. Provide an example of direct damage, and compare this to toxin production.  Direct Damage o Disrupts host cell function o Uses host cell nutrients o Produces waste products o Multiplies in host cells and causes ruptures o Ex: E. coli, shigella, salmonella can induce host epithelial cells to engulf them through phagocytosis, can disrupt host cells as they pass through and damage it  Toxin production o Toxins: poisonous substances produced by microorganisms  Produce fever, shock, cardiovascular problems, diarrhea o Toxigenicity: ability of microorganism to produce a toxin o Toxemia: presence of toxin in host’s blood o Intoxications: presence of toxin without microbial growth  Direct damage microorganisms affect the host cell directly with themselves whereas toxins are products released by the microorganism that infect the host cell indirectly 10. Contrast the nature and effects of exotoxins and endotoxins.  Exotoxins-Produced more by gram positive. Proteins secreted and produced by bacteria; destroy host cells and inhibit metabolic functions o Antitoxins: antibodies against specific exotoxins o Toxoids: inactivated exotoxins used in vaccines  Membrane-disrupting toxins- lyse host cells by disrupting plasma membrane o Leukocidins- kill phagocytic leukocytes o Hemolysins-kill erythrocytes by forming protein channels o Streptolysins- hemolysins produced by streptococci  Superantigens- cause intense immune response due to release of cytokines from host cells (T cells)- symptoms like fever, nausea, vomiting, diarrhea, shock, and death  Genotoxins- damage DNA cause mutations disrupting cell division, and leads to cancer  Endotoxins- Inside the body- Lipid A portion of lipopolysaccharides of gram negative – bad toxin Lipid A that when ruptures can have bad consequences for host, allergic reaction and can kill someone  Release when gram negative die or bacterial multiplication 11. Using examples, describe the roles of plasmids and lysogeny in pathogenicity.  Plasmids might carry genes for toxins, production of antibiotics, and enzymes  Lysogenic conversion- changes characteristics of microbe due to incorporation of a prophage 12. List nine cytopathic effects of viral infections. 1) Stop cell synthesis 2) Cause cell lysosomes to release enzymes 3) Inclusion bodies in cytoplasm- some are viral part granuals- nucleic acids or proteins in process of becoming virions. Others can help identify causative agent 4) Fusing cells to create syncytium- adjacent infected cells fuse to form a very large multinucleate cell 5) Change host cell function 6) Induce antigenic changes on cell surface 7) Induce chromosomal changes- frequently cancer causing (oncogenic) genes might be activated by virus 8) Loss of contact inhibition in cell causes unregulated growth leading to cancer- cells don’t stop growing when they come in close contact with other 9) Producing interferons to protect uninfected cells- host cell DNA codes for these 13. Discuss the causes of symptoms in fungal, protozoan, helminthic, and algal diseases.  Fungi- toxic metabolic products, allergic response, inhibit protein synthesis, proteases modify host cell membranes, capsules prevent phagocytosis  Ergot- hallucinations  Aflatoxin- carcinogenic toxin produced by aspergillus  Mycotoxin- produced by mushrooms and are neurotoxic o Phalloidin and amanitin  Protozoa- waste products cause symptoms  Avoid host defenses by: o Digesting cells and tissue fluids o Growing in phagocytes o Antigenic variation  Helminths- use host tissue for growth, large masses causing cell damage, waste products that cause symptoms  Algae- some produce neurotoxin called saxotoxin o Paralytic shellfish poisoning 14. Differentiate portal of entry and portal of exit.  Portals of entry- muscous membranes, skin, parenteral route (not by swallowing, but like an injection)  Portals of Exit- respiratory tract (cough or sneeze), gastrointestinal (feces, saliva), genitourinary (urine and secretions from pewee and vageena), skin, blood (needles, syringes, animal bites) Chapter 16 1. 2 things for successful pathogens- Get into host, and survive immune responses 2. Immunity- ability of host to resist infection or disease 3. Susceptibility- lack of immunity 4. Immune system- cells, tissues, and organs 1. Function-recognize anything that is non-self/foreign and neutralize them 5. Differentiate innate and adaptive immunity.  Innate- really fast response, same type of response no matter what’s attacking, acts as first line of defense, born with it, reactions to destroy invading cells, lacks immunology memory  Adaptive- production of antibodies proteins, response to particular agents called antigens, has “memory”, more effective the more exposed to agent, slower response because have to generate antibodies specific to your body 6. Define Toll-like receptors.  TLRs on host cells attach to pathogen-associated molecular patterns (PAMPs). Induces release of molecular components to regulate duration and intensity of immune response 7. Describe the role of the skin and mucous membranes in innate immunity. Physical barriers Ciliary escalator- transports microbes trapped in mucus away from lungs Earwax- prevents microbes entering Urine- cleans urethra via flow Vaginal secretions- out of vaginal tract Peristalsis, defecation, vomiting, diarrhea Skin o when attack the skin you have direct factors like nutrition, fever, age, genetics o Indirect- o Dermis-inner portion of connective tissue o Epidermis- outer portion of tight epithelial cells containing keratin, protective protein o Shedding skin is important to protection against microorganisms, dry skin prevents colonization from pathogens  Mucous membranes o Muscus- also lysozyme, an enzyme that will interfere with cell wall of bacteria and demantle it  Have lysozymes in our tears also o Have cilia that increase movement to secrete things o Epithelial layer that lines gastrointestinal, respiratory, and gastrourinary tracts covered in mucous to prevent colonization o Mucus: viscous glycoproteins that trap microbes and prevent tracts from drying out o Lacrimal apparatus: if get anything in your eye drains tears; washes eyes also preventing colonization 8. Differentiate physical from chemical factors, and list five examples of each.  Sebum- forms protective film and lowers pH (3-5)  Lysozyme- perspiration, tears, saliva, and urine destroys bacterial cell walls  Low pH (1.2-3) of gastric juice destroys most bacteria and toxins  Low pH (3-5) of vaginal secretions inhibit microbes 9. Describe the role of normal microbiota in innate immunity.  Compete with pathogens via microbial antagonism o Produce substances harmful to pathogens o Alter conditions that affect survival  Commensalism- one benefits other (host) is unharmed  Probiotics- live microbial cultures administered to exert a beneficial effect o Diet high in probiotics and look at results and affects of this diet 10. Classify leukocytes, and describe the roles of granulocytes and monocytes.  SECOND LINE OF DEFENSE  Leukocytes- white blood cells  Granulocytes- neophils (phagocytic, toxic against parasites and helminthes), Basophils (production of histamine, work in allergic response), Neutrophils (attack first), leukocytes with granules in cytoplasm and visible under a light microscope  Monocytes- Agranular, stain and look under microscope no granules o Macrophages- phagocytic o Dendritic o Lymphocytes- T and B cells, and natural killer cells 11. Describe the eight different types of WBCs, and name a function for each type.  Leukocytes are WBC  Granulocytes o Neutrophils- attack first, leave blood, enter infected tissue, destroy foreign microbes o Basophils- production of histamine, allergic response o Eosinophils -phagocytic, toxic against parasites and helminthes  Agranulocytes o Monocytes- most actively phagocytic until leaving blood, enter tissues, and mature into macrophages o Dendritic cells- maybe derived from same precursor as monocytes, in epidermis of skin, mucous membranes, thymus, and lymph nodes. Destroy microbes by phagocytosis and initiate adaptive immunity responses o Lymphocytes- natural killer cells, ability to kill wide variety of infected body cells and certain tumor cells, release toxins  B cells-adaptive role in immunity  T cells-adaptive role in immunity 12. Differentiate the lymphatic and blood circulatory systems.  Lymph, lymphatic vessels, lymphoid tissues, red bone marrow o Tonsils, spleen, intestines, lymph node, thymus,  Blood circulatory- 13. Define phagocyte and phagocytosis. Describe the process of phagocytosis, and include the stages of adherence and ingestion.  Phagocytosis- cell that eats cells o Fixed macrophages- residents in tissues and organs o Free(wandering) 14. Identify six mechanisms of avoiding destruction by phagocytosis.  Chemotaxis-signal sent by pathogen and attracted to signal  Adherence- attach to surface of microorganism in order to engulf it, does it with coding organism with proteins that allow for ingestion  Ingestion- opsonization- coated with serum of proteins making it easier to ingest  Digestion- degraded inside phagocyte and then excreted LOOK UP OTHER 2 IN BOOK 15. List the stages of inflammation. Describe the roles of vasodilation, kinins, prostaglandins, and leukotrienes in inflammation.  Vasodilation is dilation or enlargement of blood vessels o Responsible for redness and heat associated with inflammation  Kinins- substance that causes vasodilation and increased permeability, once activated play a role in chemotaxis by attracting phagocytic granuoles, mostly neutrophils to injured area  Prostaglandins- substances released by damaged cells, intensify effects of histamine and kinins and help phagocytes move through capillary walls  Leukotrienes- produced by mast cells causing increased permeability of blood vessels and help attach phagocytes to pathogens  Purpose of inflammation is to destroy injurious agent or limits its effects on the body, repairs and replaces tissue damaged by the injurious agent  Process- Tissue damage, bacteria enter, vasodilation happens with more blood flow, and more permeability so you can have cells get to that site to get rid of organism 16. Describe phagocyte migration.  Margination- sticking of phagocytes to blood vessels in response to cytokines at site of inflammation 17. Describe the cause and effects of fever.  Fever- abnormally high temp, hypothalamus normally set at 37C, cytokines cause hypothalamus to release prostaglandins that reset the hypothalamus to a higher temp, body constricts blood vessels, and shivering occurs raising temp, as body temp fall (crisis), vasodilation and sweating occurs 18. TABLE TITLED OUTCOMES OF COMPLEMENT ACTIVATION List the major components of the complement system, describe three pathways of activating complement, and describe three consequences of complement activation.  Compliments innate immune response, have it your whole life  Serum proteins produced by the liver that assists the immune system in destroying microbes o Act in a cascade in a process called complement activation  Proteins are designated with upper case “C” and numbered in order of discovery o Cleaved fragments of these proteins are indicated with lowercase “a” and “b”  Pathway- All involve activation of c3  classical- NEED antigen antibody interaction to be activated, activating c1 then activates c2 and c4, which leads to activation of c3  alternative- DON’T need antibody antigen interaction, have lipid carbohydrate complex that bind directly to c3 and cause it to split into C3a and C3b  Lectin pathway- macrophages ingest microbe they release citokines that activate lectin, have mannosebinding lectin which induces activation of c2 and c4 and then ends up as c3.  KNOW HOW THEY GET ACTIVATED, AND THEY ALL END IN C3  Consequences- cytolysis- causes pores and cell to lyse, opsonization- covering pathogen with protein complex that attract phagocyte and allows to bind to it so it can engulf and get rid of it, inflammation- mast cell releases histamines which causes influx of red blood cells and leukocytes to area leading to inflammation  Regulate compliment- once pathways are started need to shut them down otherwise own cells will be damaged o One way- break down proteins of compliments by host cell so inflammation response goes away  Lack of compliment which assists in innate response so if you don’t have complement you’re more likely to get infection  Evading- production of capsules 19. Define interferons. Compare and contrast the actions of IFN-α and IFN-β with IFN-.  Interferon- Cytokines produced by cells, have antiviral activity. Are host specific, not virus specific o IFN-a ALPHA and B BETA produced in response to viral infections; cause neighboring cells to produce Antiviral protein (AVPs) that inhibit viral replication o IFN y GAMMA- causes neutrophils and macrophages to kill bacteria 20. Describe the role of iron-binding proteins in innate immunity.  Transfer and store iron o Transferrin- in blood and tissue fluids o Lactoferrin- milk, saliva, mucus o Ferritin- liver, spleen, red bone marrow o Hemoglobin- red blood cells 21. Describe the role of antimicrobial peptides in innate immunity.  Short peptides produced in response to protein and sugar molecules on microbes o Inhibit cell wall synthesis o Form pores in plasma membrane o Broad spectrum activity Chapter 17 1. Compare and contrast adaptive and innate immunity.  Adaptive- defenses that target a SPECIFIC pathogen, acquired by infection or vaccination, primary response-first time, secondary- more effective due to memory  Innate- NOT specific, are not acquired by infection or vaccination 2. Differentiate humoral from cellular immunity.  Humoral- produces antibodies that combat foreign molecules known as antigens  B cells are lymphocytes created and mature in red bone marrow o Recognize antigen and make antibodies  Fights invaders outside cells, bacteria and toxins  Cellular- Cell mediated immunity- produces T lymphocytes o Recognize antigenic peptides processed by phagocytic cells, mature in thymus  Attacks antigens found inside cells, viruses; some fungi and parasites  T-cell receptors- on T cell surface contact antigens, causing the T cells to secrete cytokines instead of antibodies 3. What are the functions of cytokines, interleukins, chemokines, interferons, TNF, and hematopoietic cytokines?  Cytokines- chemical messengers produced in response to stimulus o Interleukins- cytokines b/w leukocytes o Chemokines- induce migration of leukocytes o Interferons (IFNs)- interfere with viral infections of host cells o Tumor necrosis factor- involved in inflammation of autoimmune disease o Hematopoietic- control stem cells that develop into red and white blood cells 4. Define antigen, epitope, and hapten.  Antigen- substances that cause the production of antibodies, components of foreign particles or invading microbes o Interact with: o Epiptopes-antigen determinant  Haptens- antigens too small to provoke immune responses; attach to carrier molecules 5. Explain antibody function, and describe the structural and chemical characteristics of antibodies.  Antibody function- made in response to an antigen and can recognize and bind to antigen, they are globulin proteins called immunoglobins (Ig)  Structural- Valence is antigen binding sites on an antibody  Four protein chains form a Y shape o Two identical light and heavy chains joined by disulfide links  Variable regions at end of arms; bind epitopes  Constant- stem, indentical for a particular Ig class (IgG, IgM, IgA, IgD, IgE) 6. Name one function for each of the five classes of antibodies.  IgG- protects fetus and newborn  IgM- First antibodies produced in response to initial infection  IgA-Localized protection on mucosal surfaces  IgD- Serum functions unknown, presence on B cells functions in initiation of immune response  IgE- Allergic reactions 7. Compare and contrast T-dependent and T-independent antigens.  T-dependent antigen- antigen that requires a T H cell to produce antibodies o Done by white blood cells, if T cells intermediate process they tell the process to hurry up  T-independent- stimulate B cell without help of T cells o Doesn’t depend on T helper cells to communicate with it  Provoke a weak immune response, producing IgM sometimes  No memory cells generated 8. Differentiate plasma cell from memory cell.  Plasma cell- a cell that an activated B cell differentiates into; plasma cells manufacture specific antibodies  Memory cell- produced in response to the initial exposure are activated by the secondary exposure 9. Describe clonal selection.  Differentiates activated B cells into o Antibody producing plasma cells, and memory cells 10. Describe how a human can produce different antibodies. 11. Describe four outcomes of an antigen–antibody reaction.  Serology- study of these reactions  Agglutination- antibodies cause antigens to clump together making them more easily ingested by phagocytes o Antibodies produced and based on how many viable fragments they have are able to bind to antigens. Pulls bad cells together.  Opsonization- the antigen, a bacterium, is coated with antibodies/complement proteins that enhance its ingestion and lysis by phagocytic cells o Antibodies cover bacteria and also signal for phagocytic cells to come to location and bind to antibodies then eat everything  Antibody dependent cell mediated cytotoxicity o T cell eosinophil recognizing antibody signal and produces proteins called perforin to lyse the cell  Neutralization- IgG antibodies inactivate microbes by blocking attachment to host cell and neutralize toxins in a similar manner o Happens with small particles like viruses and toxins, but also bacteria. If bacteria covered by antibodies it is less likely to cause damage to our cells or release toxins.  Activation of complement system- Inflammation will cause microbes in inflamed area to become coated with certain proteins, which leads to attachment to microbe of an antibody- complement complex, which lyses the microbe and attracts phagocytes and other defensive immune system cell to area o Complement is innate immunity. Complements are series of proteins with numbers, C3 ex. Then it pokes holes in the cell and lysis the cell. o Causes inflammation 12. Differentiate T helper, T cytotoxic, and T regulatory cells. TABLE 17.2 PG 485  T helper (TH)-work with B cells in production of antibodies mainly through cytokine signaling. o Recognize an antigen on surface of a macrophage and activate the macrophage making it more effective in phagocytosis and antigen presentation. o Different types of cytokines released TH 1, TH 17, etc., memory cells. o Make neutrophils, basophil, and eosinophil that increase inflammation and also makes macrophages  T cytotoxic cells (CTLp)- can differentiate into an effector cell called a cytotoxic T lymphocyte (CTL) o Not capable of attacking any target cell as they emerge from thymus but quickly obtain this capability. o A cell infected by a virus that is presented in MHC complex, but is a viral particle in itself. T helper releasing cytokines it will kill the virus cell o Can recognize cancer cells because they don’t produce the same MHC complex  T regulatory cells- 5-10% of cell population, subset of TH cells that are distinguished by carrying an additional CD25 molecule, function to combat autoimmunity by suppressing T cells that escape deletion without knowing how to avoid reacting against the body’s self defense. Protect immune system from bacteria in the intestines required for digestion o Makes sure how many T and B cells will be produced. If too many are produced you will have auto immune disease. 13. Define apoptosis.  Programmed cell death, determine whether cell death is natural, in which there is no harm and cell is removed. If death is due to trauma or disease body’s defense and repair mechanisms are utilized. If a cell cannot clear a pathogen in any other way, it clears by dying- or APOPTOSIS  Signal released by cytotoxic cell tells host cell to kill itself because it’s infected 14. Define antigen-presenting cell.  APC- macrophage, dendritic cell, or B cell that engulfs an antigen and presents fragments to T cells 15. Describe the function of natural killer cells.  Large granular leukocytes that attack and destroy target cells, participates in antibody-dependent cell mediated cytotoxicity  Don’t need to be stimulated by an antigen  If signals between normal and killer cell is recognized. But, if killer comes and tries to recognize host cell it releases peroforin and granzymes that will kill the cell 16. Describe the role of antibodies and natural killer cells in antibody-dependent cell-mediated cytotoxicity.  Cell mediated immune system can stimulate natural killer cells to kill targeted cells. An organism like protozoa that is too large to be phagocytized can be attacked by immune system cells- this is antibody-dependent cell mediated cytotoxicity  17. Distinguish a primary from a secondary immune response.  Primary- first time immune system combats a particular foreign substance o On graph, x axis is time in days, y axis is counting of how many antibodies there. o Day 0 when you first encounter something, your innate defense comes to rescue, adaptive defense builds up and produces IgM first because it has 10 binding sites, and then there is a major production of IgG and body fights infection and you get better. Store this in your memory  Second exposure- first produces IgG and produces a large amount and it’s produced much faster than the first exposure  Secondary- later interactions with same foreign substance, faster and more effective due to memory 18. Major histocompatibility complex on surface of cells that signal to all white blood cells I belong to this body and don’t fight me. Can also be the proteins that present the antigens, bad guys 19. Contrast the four types of adaptive immunity.  Naturally acquired active immunity- resulting from infection  Naturally acquired passive immunity-transplacental or via colostrum, breastfeeding the first time has large amount of antibodies that are good for baby  Artificially acquired active immunity-injection of vaccination  Artificially acquired passive immunity-injection of antibodies- made from another source or another animal/person 


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