Intact Skin - physical barrier - difficult to penetrate Keratin - repels water maintains a dry environment Mucosal epithelial cells that are shed take attached microbes with them Mucociliary escalator helps remove microbes What is a crisis of fever? B and T Lymphocytes: where do they form and where do they mature, respectively? First line defenses The role of skin and mucous membranes in innate immunity diapedesis

First line defenses The role of skin and mucous membranes in innate immunity

Lysozyme in tears, saliva, mucous, blood, phagocytes ▪ Peroxidase systems use H2O2 against microbes ▪ Antimicrobial peptides (defensins) form pores in microbial membranes damaging them Where in the human body are adaptive immune responses initiated? What is the effector action of the natural killer cells (NK)? 1Vector-borne pathogens (mechanical and biological functions of vectors, outline the difference) Antimicrobial substances and their respective role, provide examples

Antimicrobial substances and their respective role, provide examples

Propionibacterium degrades lipids to fatty acids inhibiting the growth of pathogens ▪ E. coli can synthesize colicins in intestinal tract (toxic to some bacteria) ▪ Lactobacillus decreases the pH in the vagina Damage may help pathogen to exit and spread ▪ Vibrio cholerae ▪ Bordetella pertussis\ Competitive exclusion of pathogens by the normal microbiota contributes to defense mechanisms of the human body. Name some examples Antimicrobial substances and their respective role, provide examples What is an epitope?

Competitive exclusion of pathogens by the normal microbiota contributes to defense mechanisms of the human body. Name some examples

I. PPRs detect microbial components called MAMPs MAMPs/PAMPS include Cell wall associated compounds (peptidoglycan, teichoic acids, lipopolysaccharides, lipoproteins) ▪ Flagellin subunits or ▪ Microbial nucleic acid Pattern recognition receptors (PRRs) allow for detection of microbial invasion Response to antigens varies depending on the type: Proteins generally elicit a _____ response lipids a _____ response What is the difference between a primary pathogen and an opportunistic pathogen? What is the role of the normal microbiota?

Pattern recognition receptors (PRRs) allow for detection of microbial invasion

TLRs *anchored in membrane of sentinel cells *detect MAMPs a) cytoplasmic membranes [extracellular] b) Lumen of phagosomes NLRs *cytoplasmic proteins *detect MAMPs & DAMPs RIG-like receptors *cytoplasmic proteins What is a crisis of fever? BCRs, TCRs, and MHC molecules Toll-like receptor NOD-like receptors RIG-like receptors Factors that affect the outcome of transmission include:

Toll-like receptor NOD-like receptors RIG-like receptors

INF IS ACTIVATED/EVERYTHIG IS DETECTED FROM THE LONG dsRNA PRODUCED FROM VIRAL REPLICATION 1. Detect Viral RNA promotes antiviral state through INF 2. Interferons cause neighboring cells to express iAVP 3. iAVP activated by infection, leading to apoptosis outcome apoptosis of infected cell Competitive exclusion of pathogens by the normal microbiota contributes to defense mechanisms of the human body. Name some examples Outline the general characteristics of adaptive immunity What are the two basic strategies of adaptive immune response Surveillance of infectious diseases by RIG-like receptors and the interferon response against viruses (steps) what is the outcome of an interferon response?

RIG-like receptors and the interferon response against viruses (steps) what is the outcome of an interferon response?

EXAM 3 STUDY GUIDE QUESTIONS Flashcards

Intact Skin - physical barrier - difficult to penetrate Keratin - repels water maintains a dry environment Mucosal epithelial cells that are shed take attached microbes with them Mucociliary escalator helps remove microbes

Lysozyme in tears, saliva, mucous, blood, phagocytes ▪ Peroxidase systems use H2O2 against microbes ▪ Antimicrobial peptides (defensins) form pores in microbial membranes damaging them

Propionibacterium degrades lipids to fatty acids inhibiting the growth of pathogens ▪ E. coli can synthesize colicins in intestinal tract (toxic to some bacteria) ▪ Lactobacillus decreases the pH in the vagina

Hematopoiesis: the formation and development of blood cells, including those of the body's defenses All blood cells originate from the same cell type called the hematopoietic stem cell in the bone marrow Blood Cells 1) Erythrocytes 2) Platelets 3) WBC/Leukocytes

Granulocytes 1) Neutrophils [55-65%] Function: phagocytize and engulf material Can kill in 3 different ways a. Phagocytosis b) release content of granules (destructive enzymes + antimicrobial substances) c. NETs release DNA to form neutrophil extracellular traits 2. Eosinophils [2-4%] Inflammatory reaction/ immunity to some parasites 3. Basophils [0-1%], mast cells Function: release histamine + other inflammation-inducing chemicals from granules

Mononuclear Phagocyte System (MPS) Monocytes phagocytize and digest engulfed material Macrophages- sentinel cells 1. phagocytize and digest engulfed material 2. put "bits" of the invader on their surfaces to display them to cells of the adaptive immune system Dendritic cells collect antigen from tissues and then bring it to the lymphocytes [T CELLS] that gather in the secondary lymphoid organisms

1) Surface Receptors * transmembrane proteins that specifically bind to ligand * binding -> change in receptor->signal received-> triggers chemotaxis Function: allow cells to sense and respond to external signals 2) Adhesion molecules * when phagocytic cells in blood are needed in tissues endothelial cells that line the blood vessels produce adhesion molecules that bind to the passing phagocytes -> binding slows rapidly moving phagocytes allowing them to leave bloodstream and reach site of infection Function: on surface molecules on cells that allow them to "grab" other cells 3) Cytokines trigger different cellular responses/processes *act at low conc. have local vs systematic effects *can act together or in a sequence Function: can trigger different cellular responses/processes

I. PPRs detect microbial components called MAMPs MAMPs/PAMPS include Cell wall associated compounds (peptidoglycan, teichoic acids, lipopolysaccharides, lipoproteins) ▪ Flagellin subunits or ▪ Microbial nucleic acid

TLRs *anchored in membrane of sentinel cells *detect MAMPs a) cytoplasmic membranes [extracellular] b) Lumen of phagosomes NLRs *cytoplasmic proteins *detect MAMPs & DAMPs RIG-like receptors *cytoplasmic proteins

INF IS ACTIVATED/EVERYTHIG IS DETECTED FROM THE LONG dsRNA PRODUCED FROM VIRAL REPLICATION 1. Detect Viral RNA promotes antiviral state through INF 2. Interferons cause neighboring cells to express iAVP 3. iAVP activated by infection, leading to apoptosis outcome apoptosis of infected cell

1. Inflammatory response C3a and C5A Induce changes that contribute to vascular permeability and attract phagocytes 2. Opsonization C3b binds to microbial cells, functioning as an opsonin 3. Lysis of foreign cells - MACs C5b combines with complement proteins C6-9 to form membrane attack complexes that insert into cell membranes regulated by binding C3b with regulatory proteins

1. Chemotaxis: phagocytes are recruited by chemoattractants (products of microorganisms, phospholipids from injured host cells, chemokines, complement system component C5a) 2.Recognition/Attachment receptors of phagocytes bind mannose of certain bacteria (direct) or bind opsonized material (indirect) 3. Engulfment: pseudopods surround the microbe to engulf it resulting in a phagosome Phagosome maturation/phagolysosome formation: involves fusion of the phagosome with the lysosome ▪ Destruction/digestion: toxic ROS and nitric oxide, pH decreased by proton pumps, lytic enzymes of the lysosome, antimicrobial peptides ▪ Exocytosis: vesicle fuses with plasma membrane and expels undigested material

1. Phagocytosis 2. Release the content of their granules (destructive enzymes + antimicrobial peptides 3. NETs release DNA to form neutrophil extraceceular traps for granules to accumulate and release their content killing them

Granulomas fuse with giant cells, T cells wall off and retain organisms resistant to destruction (TB) prevent their escape but interfere with normal tissue function

Inflammation occurs when tissues are damaged or microbes gain access to normally sterile body sites Symptoms + what causes them 1. Redness/Heat increased vasodilation caused by inflammatory mediators a. Greater blood flow to site of infection helps deliver clotting factors/defense cells 2. Swelling/Pain Increased vascular permeability allows phagocytes to leve bloodstream and reach site of infection [diapedesis] Leakage of fluids causes swelling (edema) and pain associated w/ imfllamation. pressure on nerve ending

Phagocytes that leave the bloodstream through

1. Neutrophils (1st) 2. Monocytes (macrophages) 3. Lymphocytes

Acute -short term inflammatory/ prevalence of neutrophils - macrophages ingest dead cells, debris, tissue is repaired and scar tissue forms Chronic -long term imflammatory process - macrophages, giant cells accumulate and granulomas form

purpose is to contain the site of damage, localize the response, eliminate the invader, restore tissue function

Fever indicator of infection, temp ^ due to pyrogens 1. Constricted blood vessels carry less blood to the skin (chills associated w fever) endogenous pyrogens ,pro-inflammatory cytokines produced by macrophages carried in the bloodstream to the brain -when TLRs detect microbes Exogenous pyrogens microbial products (i.e., LPS) Beneficial effects of fever include ▪ Lower microbial growth rates ▪ Enhanced inflammatory response ▪ Increased phagocytic killing by leukocytes ▪ Improved production of interferons/antibodie

processes that indicate an infection has been overcome 1. perspiring 2. lowering metabolic rate 3. dilating blood vessels in the skin

takes >1 week to build an adaptive response to first exposure to an antigen Characteristized by 1. Molecular specificity precise recognition of the antigen 2. Memory adaptive immunity "remembers" and a faster/more effective response results upon reexposure to the same pathogen 3. Self-Tolerance Targets pathogens or cancerous cells and not "healthy self" Two Basic Strategies 1. Humoral immunity acts against microbes or toxins in the bloodstream and tissues (extracellular antigens) * B lymphocytes 2. Cell-mediated immunity (CMI) deals with viruses or bacteria replicating within host cells * T cells

B lymphocytes (antibody response/humoral immunity) form: bone marrow mature: bone marrow T lymphocyte form: bone marrow mature: thymus they contact the antigen in the lymphatic system

Based on their stage of development and activity, B and T lymphocytes are named as 1. Immature lack fully developed antigen-specific receptors 2. Naive have not yet encountered the antigen 3. Activated able to proliferate and differentiate to plasma cells a. Effector descendents of activated lymphocytes i. Effector B cells: Plasma ii. Effector T cells: Tc cells, Th cells 4. Memory long lived decsendants of activated lymphocytes, can quickly mount a response when the same antigen is encountered again

1. Humoral immunity acts against microbes or toxins in the bloodstream and tissues (extracellular antigens) A. B cells i. BCR: b cell receptor a membrane bound version of the specific antibody the activated B cell (plasma cell) will produce binding antigen -> BCR of a naive B cell signals the cell that it should respond Before the B cell can respond, ▪ It must receive a second signal from a T lymphocyte (TH cell) ▪ Once the B cell receives "confirmation" from a TH cell, it becomes activated ii. Activated B cell proliferates differentiates into plasma cells iii. Plasma cells produce-> antibodies that bind to antigens w/high degree of specificity antibodies bind to surface of cells, viruses, or toxins many are needed to reocgnize and bidn to wide arraw iv. some activated B cells become memory B cells (secondary response) B. T cells 1. Cytotoxic t cells [TC] 2. Helper T cells [TH] Both have TCRs (T-cell receptors) TCRs recognize an antigen presented by other host cell (MHC bound to antigen) recognizes the peptide-MHC complex i. activation of naive T cells involves recognition of the antigen by the TCR [not free fluid antigen] must be present by a MHC molecule ii. Activated T cells proliferate and differentiate into effector T cells a) Tc cells b) Th cells ^^^^ form memory T cells [secondary response}

i. BCR: b cell receptor a membrane bound version of the specific antibody the activated B cell (plasma cell) will produce binding antigen -> BCR of a naive B cell signals the cell that it should respond the binding of a BCR of a naive B cell ro an antigen will signal the cell to respond. Before the B cell can respond ii. it must receive a 2nd signal from the TH cell as confirmation to be activated

Activated B cells proliferate and differentiate into plasma cells Plasma cells produce antibodies that bind to antigens w/ a high degree of specificity some activated cells become memory B cells

no must be present by a MHC molecule. does not recognize anitgen that is free in fluids

presenting antigenic peptides to T cells TCRs recognize an antigen presented by other host cell (MHC bound to antigen) recognizes the peptide-MHC complex

1) dendritic cell must present antigen to T cell along with stimulatory molecules [MHC] 2) Activated cytotoxic cells [Tc cells] will encounter an infected "self" cell will induce apoptosis of the infected cell 3. Activated helper cells (TH cell) will produce specific cytokines that activate B cells and macrophages

[TC CELLS] "self" cell undergoes apoptosis 1. nucleated cells of the body present peptides on MHC class I 2. Binding by TC cells indicate reocgnition 3. Apoptosis

recognize host cells lacking MHC class I molecules (viruses can interfere with antigen presentation) and induce the infected cells to undergo apoptosis Fc receptor -> IgG ADCC APOPTOSIS

If TH cells recognzies peptides presented on MHC class II, activate macrophage Activated macrophage ^ killing power increase in size, metabolism, prod of nitric oxide can fuse to form giant cells and T cells to form granulomas

antibody generator any molecule that specifically binds to an antibody, B/T cell receptors Antigens that elicit an immune response are called Immunogenic 2 categories T dependent antigens - B cell requires TH cells to be activated T-independent antigens - activate B cells w/o TH cells e.g LPS Microbial Antigens 1. components of the cell walls, 2. capsule 3. flagella or toxins 4, proteins and glycoproteins of viruses fungi or protozoa

requires the confirmation signal by the effector T helper cells it must receive a 2nd signal from the TH cell as confirmation to be activated

Activated B cells proliferate and differentiate into plasma cells Plasma cells produce antibodies that bind to antigens w/ a high degree of specificity normally secrete Igm -TH cells can induce some activated B cells to becomes plasma cells that sceret other antibody classes Bcells in lymph - IgG B cells in MALT - iGA some activated cells become memory B cells Activated B cells undergo... affinity maturation (fine-tuning)

lymphatic vessels contain lymph [tissue fluid carrying antigens that travels through lymph nodes and re-enters the circulatory system primary lymphoid organs Bone Marrow Thymus secondary lymphoid organs where adaptive immune responses can be initiated tonsil lymph nodes SALT (skin associated lymphoid tissue) spleen appendix MALT (mucosa associated) [m cells transfer samples of intestinal contents to lymphocytes in the Peyer's patches [PEYERS PATCH] Dendritic cells can also sample material in the intestine to present it to lymphocytes

Lymphoid organs

strong; protein weak;lipid

Epitope region of antigen/antigenic determinants [macromolecules] or three dimensional shapes "sticks out" in a molecule precisely/reversibly through many non-covalent bonds

Structure a) Y shaped protein i) Two identical arms bind the antigen yielding specificity ii) Stem functions as a "red flag" that tags the antigen for elimination ▪ Made of two copies each of a heavy and light chain ▪ Amino acids fold into characteristic conserved or variable domains (constant and variable regions) ▪ Disulfide bonds join heavy and light chains, and the two halves Five major classes of antibodies ▪ IgM - 1st produced binding to antigen -> activation of complement system (classical pathway) ▪ IgG - most abundant, facilitates phagocytosis, activation of complement system (classical pathway), anibody dependent cytotocixitiy ▪ IgA - mucosal immunity, prevents atachement ▪ IgD - development and maturation of antibody response ▪ IgE- binds Fc to mast cells & basophills Actions of Antibodies Opsonization Neutralization Complement System Activation Immobilization & Prevention Cross-linking Antibody-Dependent Cellular Cytotoxicity

To be activated, the B cell must display the antigen on proteins [MHC class II molecules], which enable inspection by TH cells (antigen presentation) 1) B-cell binds to antigen 2) B cell internalizes antigen 3) B cell degrades antigen into peptide fragments 4) Peptide fragments are presented on MHC class II molecules 5a) TH cell regonizes antigen fragment and activates B cell w cytokins 5b) if Th cell does not recognize the peptide, the B cell becomes anergic (unresponsive to future exposure to antigen) ▪ This results in tolerance to that antige examples of T-independent antigens include 1. components of the cell walls, 2. capsule 3. flagella or toxins 4, proteins and glycoproteins of viruses fungi or protozoa

antibody production

affinity maturation (fine-tuning) ▪ Resulting in B cells that bind antigen with higher efficiency ▪ Most likely to proliferate

Primary 10-14 days for sig antibody accumulation/ may develop signs and symptoms Initial Encounter: First exposure to a specific antigen. B Cell Activation: Naive B cells encounter the antigen, become activated, and differentiate into plasma cells, which produce primarily IgM antibodies. ** initial exposure to vaccine antigen induces primary immune response (activation of naive B cells, prod of antibodies IgM, formation of memory cells Secondary memory B cells; subsequent exposure to same antigen yields a faster and more effective response due to 1) Receptors being fine-tuned via affinity maturation 2)quickly becomes plasma cells producing IgG/IgA [class switching] ** subsequent exposure to the same antigen (boosters or natural exposure), memory B cells quickly recognize and respond to the antigen. This leads to a secondary immune response characterized by rapid antibody production, predominantly IgG and IgA, with increased affinity and effectiveness.

1. Identical 2. Surface proteins/Cluster of Differentiation markers Cytotoxic T-cells CD8 T-CELLS Helper T-cells CD4 T-CELLS [RECEPTOR OF HIB]

Can activate B cells without TH cells ▪ Relatively few antigens are T-independent - molecules w evenely spaced epitopes (polysaccharide capsules) bind to clusters of B cell receptors activating B cell

Haemophilus influenzae tybe b

MHC class I molecules

nucleated cells of the human body ▪ Infected host cells present peptides of intracellular pathogens on MHC class I molecules ▪ TC cells respond to endogenous antigens

APCs (B cells/Macrophages) Present peptides from extracellular pathogens ▪ TH cells respond to exogenous antigens

immature dendritic cells reside in skin , mucosa 1. Gather Materials via phagocytosis/pinocytosis - send tenatcle-like extensions between epithelial cells of mucosal barriers and sample material in respiratory tract and lumen of intestine (PRRs) 2. Travel to Secondary Lymphoid organs, mature and produce co-stimulatory organisms 3. Present antigens on MHC mol I & II to naive T cells

NEGATIVE SELECTION OF SELF-REACTIVE B CELLS - if B cell binds to "se;f" molecules, undergo apoptosis to remove most B cells which is critical in preventing the immune system from attacking the healthy body cells + SELECTION OF T CELLS T cells must recognize MHC or elimated if unable - SELECTION OF T CELLS T cells also elimated if recognize "self peptides" 95% of developing T cells undergo apoptosis in thymus

1. Skin 2. Oral Cavity 3. Large IT 4. Genitourinary Resident microbiota inhabit sites for extended periods Transient microbiota inhabit temporarily Composition is dynamic affected by hormonal changes/activities of host (diet)

Mutualism both partners benefit ▪ In large intestine, bacteria produce vitamins/host provides a suitable environment Commensalism one partner benefits, other (host) is unharmed ▪ Microbes living on skin are neither harmful nor helpful ▪ Parasitism one organism benefits at the expense of other (host) ▪ All pathogens are parasites

Competitive exclusion against pathogens ▪ Covering binding sites to prevents attachment ▪ Consumption of available nutrients/synthesis of toxic compounds The normal microbiota ' ▪ Stimulate adaptive immunity ▪ Promote oral tolerance (microbes in the gut) ▪ Aid digestion ▪ Produce vitamins important for human health ▪ Killing or suppressing the normal microbiota can lead to disease

can cause disease if an immunocompromised condition exists or gain access to other body sites [e.g Malnutrition, cancer, AIDS or other disease, surgery, wounds, genetic defects, alcohol or drug abuse, immunosuppressive therapy]

Competitive exclusion against pathogens ▪ Covering binding sites to prevents attachment ▪ Consumption of available nutrients/synthesis of toxic compounds

can cause disease if an immunocompromised condition exists or gain access to other body sites [e.g Malnutrition, cancer, AIDS or other disease, surgery, wounds, genetic defects, alcohol or drug abuse, immunosuppressive therapy]

(an infection that results in disease) Colonization of the host indicates a microbe establishing itself

Primary pathogen microbe or virus that causes disease in otherwise healthy individual e.g ▪ Plague, malaria, measles, influenza, diphtheria, tetanus ▪ Opportunistic pathogen causes disease when body's innate or adaptive defenses are compromised or when introduced into different body sites ▪ Microbes common in the environment (Pseudomonas/burn patients) ▪ Members of normal microbiota (E.coli/UTIs)

Number of microbes required to establish an infection ▪ Shigellosis: ~10-100 cells ▪ Salmonellosis: ~ 10^6 ingested cells of Salmonella enterica serotype Enteritidis Infectious dose expressed as ID50 Number of microbial cells that results in disease in 50% of the test population

Damage from a primary infection can predispose an individual to a secondary infection

(diseases spread from one host to another Reflects the infectious dose

Virulence refers to degree of pathogenicity 'Virulence factors enable a microbe to cause disease by damaging the host (i.e., toxins)

Incubation period: time between infection and onset Few days-common cold, months-rabies years-Hansen's disease ▪ It depends on number of infectious cells/virions, growth rate of the pathogen, host's condition Illness: signs and symptoms of the disease ▪ May be preceded by a prodromal phase (general symptoms) ▪ Convalescence: recovery from disease

signs: objective symptoms: subjective

A. Acute Infection short term bc/pathogen is eliminated by host defenses Incubation Period > Illness> Convalescence B. Chronic infections: develop slowly, last for months or years (TB) Incubation Period > Illness> C. Latent infections: never completely eliminated, microbe exists in host tissues/cells Incubation Period > illness > Convalescence -> Latency -> Recurrence ▪ Chicken pox (acute illness) results from varicella-zoster virus, which takes refuge in sensory nerves and it can later produce viral particles resulting in shingles (recurrence)

Localized infection - pathogen limited to a small area of the body Systemic infection, pathogen or products (toxins) disseminated throughout the body ▪ Bacteremia, toxemia, viremia (bacteria, toxins, or viruses circulating in blood) ▪ Septicemia or sepsis is a life-threatening systemic inflammatory response to infectious microbes in the bloodstream

Germ Theory of Disease demonstrates Bacillus anthracis causes anthrax Linked Mycobacterium tuberuculosis to TB Kochs Postulates set of criteria used to establish a causal relationship between a microorganism and a specific disease. 1. The microorganism must be present in every case of the disease not health host 2. The microorganism must be isolated from the diseased host and grown in pure culture. [exception: treponema pallidum cannot be grown in culture media 3. Same disease must be produced when a pure culture of the microbe is introduced into susceptible hosts [exception: infected individuals do not always have symptoms] 4. Same organism must be recovered from experimentally infected hosts

▪ Production of toxins that are then ingested ▪ Colonization of mucous membranes followed by toxin production ▪ Invasion of host tissues, avoiding or taking advantage of host defenses ▪ Invasion of host tissue, avoiding or taking advantage of host defenses followed by toxin production

▪ Adhere or attach and multiply (colonization) a) Adhesins (pili, capsules or cell wall) enable attachment to host cell receptors [e.g N. gonorrhoeae attaches receptors that protect host cells from damage by the complement system] b) Multiplication involves ability to deal with host depensive mechanisms ▪ Deal with host defense mechanisms Avoidance of secretory IgA ▪ IgA proteases ▪ Rapid pili turnover ▪ Antigenic variations ▪ Compete with the normal microbiota

Skin cuts, wounds, arthropods (fleas) Mucous Membranes pathogen induces host cell to induce via 1. endocytosis 2. Effector proteins can induce changes in host cells such as rearrangement of the cytoskeleton/uptake of bacterial cells [Salmonella enterica, injects these results in membrane ruffling] 3. M Cells of MALT pathogens use M cells to cross intestinal barrier into peyers patch e.g Shigella 1. Shigella survives peyers patch engulfment 2. Attach to bse on epithelial cells 3. causes host actin to polymerize

▪ Hiding within host cells ▪ Avoiding destruction by phagocytes [e.g N. gonorrhoeae hijacks host, binds to complement regulatory protein to avoid activation of membrane attack complex] [e.g Streptococcus pyogenes produces C5a peptidase/streptolysin O. M protein binds to C3b] a) Preventing chemotaxis b) Interfering with recognition and attachment c)Escaping the phagosome d) Preventing fusion of phagosome/lysosome [Salmonella blocks fusion] Avoiding killing by complement system proteins ▪ Binding to the regulatory protein (inactivating C3b) Avoiding antibodies ▪ IgA proteases, antigenic variation, camouflage, FC receptors

▪ Viruses can infect neighboring cells or spread via bloodstream or lymphatic systems to other tissues of the host ▪ Viruses must avoid host defenses by... ▪ Interferons [ shutting down gene expression of host genes or interfering with activation of antiviral proteins] ▪ Apoptosis [Prevent or delay apoptosis by controlling the regulatory protein p53 (Papillomavirus)] [block MHC class I presentation] herpes [fake MHC class I molecules] ▪ Antibodies : neutralize extracellular virsues a) syncytia (HIV) moving directly from one cell to its immediate neighbors b) rapidly changing surface antigens c) using antibodies to enter macrophages opsonized virsues then infect them

Direct toxins produce Exotoxins ▪ A-B toxins 1. neurotoxins: boutlism, tetanus 2. enterotoxins: E.Coli, vibrio cholerae 3. cytotoxins: anthrax, diptheria, shigella a) subunit : toxic part b) B subunit: binds to host cell, dictates cell type to be infected [e.g Corynebacterium diptheriae releases exotoxin in throat that inhibits protein synthesis "pseudomembrane LOCAL or in blood stream SYSTEMIC ▪ Membrane-damaging toxins cytotoxins disrupt host cell membrane - cell lysis [e.g Hemolysins: 1. Streptolysin O (pore-forming) B-hemolysis by S. pyogenes. 2. Phospholipases hydrolize phospholipids of host plasma membran Clostridium perfringens (Gas Gangrene) ▪ Superantigens simultaneously bind MHC class II/ TCRs of helper T cells -> interpret binding as antigen recognition and become activaated stimulates ^ TH cells cytokine storm. [e.g entertoxin by s. aureus / food borned intoxication] Indirect Endotoxins produced only in gram (-) bacteria released when bacteria lyse Sepsis, sepsis shock heat stable Innate response

▪ Innate immune response Damage associated with inflammation Adaptive immune response ▪ Immune complexes: antigen-antibody complexes can settle in kidneys and joints, and activate complement system leading to inflamation ▪ Cross-reactive antibodies may bind to body's own tissues and promote autoimmune response [e.g Acute rheumatic fever]

▪ Vibrio cholerae induces watery diarrhea, up to 20 liters in one day, can contaminate water supplies leading to outbreaks ▪ Bordetella pertussis triggers severe bursts of coughing, pathogens released into air

Communicable/Contagious transmitted from one host to another non-communicable infectious diseases do not spread from host to host [e.g Legionella penumiphila, Tetani, Lyme disease

Incidence number of new cases in a specific time period in a given population Cases/100,000 people Prevalence total number of cases at any time or for a specific period in a given popoulation cases/100,000 Morbidity incidence of disease in a defined population e.g Influenza, infected individual may transmit disease to several others Attack rate % of people who become ill in a population after exposure to infectious agent Case-fatality rate (selected examples) % of population that dies from a specific disease 1. Plague 2.Ebola 3. AIDS

Outbreak: group of cases that occur in a short period of time/population Sporadic disease: occurs occasionally in a population Endemic diseases: constantly present in a population (common cold) ▪ Epidemic: involves an unusually large number of cases ▪ Pandemic: epidemic that spreads worldwide (Flu, AIDS, Covids)

most commonly arthropods mechanical flies can pick up E. Coli, Shigella or Salmonella biological arthropods harbor pathogen internally, can play an important role of reproductive cycle of pathogen

steps of the spread of infectious disease 1. Reservoir of infectious antigen animals [zoonoses; eg anthrax, rabies, plague, SARS CoV2] humans [systematic vs asymptomatic] environment [endospores] 2. Portal of Exit pathogen must leave its reservoir and enter a host a) secretions b) excretions; 1) respiratory tract mucus droplets 2)intestinal tracts feces 3)Genital pathogens semen or vag secretion 4)Skin shed on skin cells 3. Transmission 1) vertical : women to fetus, infant or breastfeeding 2)horizontal: DIRECT handshake, sex droplet INDIRECT A) airborne, aeroles B) Vehicle Borne fomites food-borne bathogens /water borne pathogens ingestion of contaminated food and wateer vectors (anthropods)

WHO/UN, Public Health Departments and CDC,

1) Virulence factors factors that enable pathogen to adher to or penetrate host cells, overcome immyne defenses, damage host a)infectious dose small dose; asympomatic large; serious disease c)incubation period long IP = extensive spread 2) Host Factors Herd immunity (70-90%) General health Developing world age gender culture practices

Anthrax Boutilism Cholera Legionaries

Emerging new or newly recognized diseases {e.g MERS, SARS, mad cow dieases, ebola, avian Reemerging diseases increasing incidence malaria TB measles

Microbial evolution: virulence factors/resistance Changes in human society: day care centers Advances in technology: contact lenses Population expansion: increased contact with reservoirs (Lyme disease) Development: dams (habitat for host snail) extend range of schistosomiasis ▪ Mass production, distribution, importation of food: foodborne illnesses easily spread ▪ War ..: disruption of infrastructure/eradication efforts ▪ Climate changes: warmer temperatures favor reproduction of arthropods

Healthcare-associated infections (HAIs) acquired while receiving treatment in hospital e.g Candida C diff Enterobacteria Types of nosocomial infections UTI Blood stream infec surgical site infections Pneumonia e.g

1. Healthcare environment Pseudomonas (gram -) thrive in sinks, toilets 2. Healthcare workers 3. PT microbiota: invasice procedures + compromised immune system a) other patients

DIRECT health care workers INDIRECT Fomite: medical devices Airborne transmission: HEPA filters can help

EXAM 3 STUDY GUIDE QUESTIONS

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