Exam 4

Portals of Entry

-Contact: exposure to microbes -Infection: penetrate defenses, enter tissues, and multiply -Disease: the infection damages or disrupts tissues and organs

T-Lymphocytes

-T lymphocytes (cell mediated) -T-helper (recognition) -T-cytotoxic (inactivation) -T-memory (regulation and modification of cell mediated immune response)

MHC Pathway I

-all cells except red blood cells -response from Cytotoxic T-Lymphocytes (CD8+)

Natural Killer Cells v.s T-Cytotoxic Cells

-both kill virally infected cells and cancer cells. -TC cells kill those cells that have the MHC I+specific antigen complex. -NK cells are activated by interferon, cytokines to kill all sick cells, not MHC-specific.

MHC Pathway II

-dendritic cells, mononuclear phagocytes, B-Lymphocytes, some endothelial cells, epithelium of the thalamus -response from Helper T-Lymphocytes (CD4+)

Cell-Mediated Immunity

-does not involve antibodies, involves the activation of phagocytes, natural killer cells (NK), antigen-specific cytotoxic T-lymphocytes and the release of various cytokines in response to an antigen

Chemicals Released by Damaged Cells

-histamine: vasodilation, increased permeability of blood vessels -kinins: vasodilation and increased permeability of blood vessels -prostaglandins: intensify histamine and kinin effect -leukotrienes: increased permeability of blood vessels, aid in phagocytic attachment

B-Cells

-mature in the bone marrow and gain B-cell receptors (BCR's) which are displayed in large number on the cell surface, these membrane-bound protein complexes have antibodies which are specific for antigen detection. -each B cell has a unique antibody that binds with an antigen. -mature B cells migrate from the bone marrow to the lymph nodes or other lymphatic organs, where they begin to encounter pathogens. Activated by: -T-dependent antigens: antigen presented with (self) MHC to TH cell, TH cell produces cytokines that activate the B cell -T-independent antigens: stimulate the B cell to make antibodies

Stages of Phagocytosis

1. Chemotaxis: chemicals attract phagocytes to a particular location. 2. Adherence: opsonization with complement proteins or antibody proteins helps. 3. Ingestion: the phagocyte engulfs the microbe with its plasma membrane, forming a vesicle 4. Fusion: microbe containing vesicle fuses with a lysosome. 5. Killing: lysosome kills the microbe within the vesicle 6. Elimination: waste is dispelled by exocytosis

Public Health

"the science and art of preventing disease, prolonging life and promoting health through the organized efforts and informed choices of society, organizations, public and private, communities and individuals" (1920, C.E.A. Winslow).

Pathogen's Success

1. Maintain a Reservoir: the primary habitat in the natural world from which a pathogen originates Nonliving Reservoir: water or soil Living Reservoir: -Carrier: an individual who inconspicuously shelters a pathogen and spreads it to others without any notice Asymptomatic carriers -Incubation carriers -Convalescent carriers -Chronic carrier -Passive carrier -Animals: Zoonosis: an infection indigenous to animals but naturally transmissible to humans. Human does not contribute to the persistence of the microbe. Can have multi-host involvement Vector: a live animal that transmits an infectious agent from one host to another. Majority are arthropods. Larger animals can also be vectors 2. Leave its reservoir & enter the body of a human host 3. Adhere firmly to the surface of the host's body and thereby colonize it, Adhesins bind to receptors on host cells -Glycocalyx: Streptococcus mutans -Fimbriae: Escherichia coli -M protein: Streptococcus pyogenes Form biofilms 4. Invade the host by entering cells or deeper tissues -Hyaluronidase and Collagenase -Coagulase and Kinase 5. Multiply within the host possibly causing disease The most common forms of bacterial pathogenesis: Exoenzyme production: -Streptokinase: dissolves blood clots. ex. Streptococcus -Hyaluronidase: breaks down hyaluronic acid -Catalase: breaks down hydrogen peroxide. ex. Staphylococcus -Hemolysins: lyse red blood cells. ex. Streptococcus & Staphylococcus -Leukocidins: damage or destroy certain kinds of leukocytes. ex. Streptococcus & Staphylococcus Toxin production -Exotoxins: proteins secreted from the pathogens -Endotoxins: the toxin is part of the pathogen's structure Stimulation of the body's defenses. Disrupt host cell function Produce waste products 6. Evade/Survive the body's elaborate defenses: -Exoenzymes: leukocidins -Capsule: difficult to engulf them, avoid lysogenic activity -Antigenic Variation: some microbes mutate & change their surface antigens so that the immune system does not recognize them. -Surviving phagocytes, Antiphagocytic factors: -Leukocidins: toxic to white blood cells, produced by Streptococcus and Staphylococcus -Extracellular surface layer: makes it difficult for the phagocyte to engulf them Streptococcus pneumonia, Salmonella typhi, Neisseria meningitides, and Cryptococcus neoformans -Some can survive inside phagocytes after ingestion: Legionella sp., Mycobacterium sp., and many rickettsias 7. Leave the host and enter a new reservoir/host.

First Line of Defense

1. Skin and Mucous Membranes: -cells are very close together -sloughing reduces microbe numbers -secretes mucus to trap microbes 2. Movement of Bodily Fluids: -mucus covers most exposed epithelial cells, traps pathogens as well as forms a barrier between pathogens and a cell's surface -bodily fluids can be expelled to remove pathogens (coughing, sneezing, salivating, diarrhea, vomiting) 3. Secretions: Secreting liquid with protective properties: -lysozyme, an enzyme that destroys the bacterial cell wall is present in sweat, tears and saliva -sweat is highly salty, creating a hypertonic environment -stomach acid creates a highly acidic environment -fatty acids in oil secreted by the skin make the skin slightly acidic 4. Normal Flora: microbes already present within us -outcompete pathogens for resources -produce substances that are harmful to pathogens -alter conditions that affect the survival of the pathogens (microbial antagonism) 5: Antimicrobial Peptides and Chemicals: Peptides: -triggered by sugars and protein -some specificity Chemicals: -Fungistatic fatty acid in sebum -low pH (3-5) of skin -lysozyme in perspiration, tears, saliva, and urine -low pH (1.2-3.0) of gastric juice -low pH (3-5) of vaginal secretions

Antigen Presentation

1. pathogen enters body 2. general inflammation response takes place 3. dendritic cells phagocytose the pathogen 4. dendritic cells process pathogen and put antigen on surface of dendritic cell. 5. phagocytosis causes the dendritic cell to make and release interleukin signals.

Natural Killer Cells

A type of white blood cell that can kill tumor cells and virus-infected cells; an important component of innate immunity. Do not need to recognize a specific antigen before action

Types of Infectious Disease

Acute disease: develops rapidly and runs its course quickly (ex. Cold, Flu, food poisoning) Chronic disease: develops more slowly, is usually less severe, and persists for a long period (ex. Hepatitis B & C, tuberculosis, mono) Local infection: confined to a specific area Systemic infection: generalized infection; affects most of the body. Septicemia: pathogens are present in and multiply in the blood Primary infection: initial infection in a previously healthy person. Secondary infection: follows a primary infection (ex. Sinusitis: a bacterial infection following a cold, Pneumocystis: pneumonia in AIDS patients). -Superinfection: secondary infection that results from the destruction of normal microflora and often follows the use of broad-spectrum antibiotics Mixed infection: caused by several species of organisms present at the same time. Communicable: disease spreads from one host to another Noncommunicable: disease not spread from one host to another (ex. Tetanus) Contagious: diseases that spread easily form one host to another (ex. Chicken Pox)

Sterile Sites and Fluids within the Body

All internal tissues and organs: -Heart and circulatory system -Kidneys and bladder -Liver -Lungs -Brain and Spinal Cord -Muscles -Bones -Ovaries and testes -Glands (pancreas, salivary, thyroid) -Sinuses -Middle and inner ear -Internal eye Fluids within an Organ or Tissue: -Blood -Urine in kidneys, ureters, bladder -Cerebrospinal fluid -Saliva prior to enter oral cavity -Semen prior to entering the urethra -Amniotic fluid

Complement System

At least 26 blood proteins that work together to destroy bacteria and certain viruses, set off a cascade reaction of serum proteins activated by: -Antigens: antibody reaction -Proteins: C3, B, D, P and a pathogen Function of Complement Proteins (COLA): -Chemotaxis: act as chemotactic chemicals to attract phagocytes to the scene. -Opsonization: bind to the surface of the microbe & then interact with receptors on phagocytes to promote phagocytosis. -Lysis: complement proteins, forms membrane attack complexes (MAC) that cause lysis -Activation: activation of an inflammatory response Three different pathways: -Classical pathway: antibodies bind to antigens following invasion. The complex is recognized b some complement proteins which immediately bind and activate a cascade of events -Mannan-Binding Lectin pathway: Mannose binds to Leptin, triggering the activation of serine protease that initiate the complement cascade -Alternative pathway: Pathogen surface spontaneously leads to complement activation Evasion of Compliment: -capsules prevent C activation -surface lipid-carbohydrate complexes prevent formation of membrane attack complex (MAC) -enzymatic digestion of C5a

Types of Active Vaccines

Attenuated: Live, weakened viruses or bacteria, weakened in the lab EX.: -MMR vaccine: mumps, measles, rubella -Varivax vaccine: Varicella zoster virus -Flumist vaccine: influenza virus -Oral Sabin Polio vaccine (OPV): poliovirus Inactivated (killed): Inactivated by heat or chemical agents such as formalin, phenol, or acetone Ex.: -Pertussis portion of DTP series: diphtheria, pertussis, tetanus -Fluzone (injected): influenza virus Polysaccharide Vaccines: contain purified antigenic polysaccharides from bacterial capsules Ex.: -Pneumovax vaccine: pneumococcal (PC) diseases: meningitis, pneumonia, etc. caused by Streptococcus pneumoniae bacteria -Menomune vaccine: Neisseria meningitidis bacteria causes meningococcal meningitis Conjugated vaccines: polysaccharides are combined with proteins to make them more immunogenic, these vaccines are called protein conjugate vaccines Ex.: -Hib vaccine: Haemophilus influenzae type B bacteria cause meningitis; vaccine is composed of capsule polysaccharide + diphtheria toxin protein Toxoids: for diseases caused by exotoxins, vaccines are made of toxoids stimulate the production of antibodies called antitoxins require boosters Ex.: -Tetanus vaccine: Clostridium tetani bacteria cause tetanus -Diphtheria vaccine: Corynebacterium diphtheriae bacteria cause diphtheria Genetically engineered: use of bacteria to produce the protein antigens found in viral capsids and the bacterial cell envelopes Ex.: -Hepatitis B vaccine: Hepatitis B virus causes Hepatitis B disease -Gardasil vaccine: Human Papillomavirus (HPV) causes warts & cervical cancer

Blood Components for Specific Immunity

B-Cells: -mature in bone marrow -primarily responsible for humoral immunity T-Lymphocytes: -mature in thymus -involved in cell mediated immunity

Fever

Benefits: -heat inhibits the growth of some microbes -heat increases the heart rate so that white blood cells are delivered to infection sites more rapidly -heat increases B cell & T cell proliferation (division) -heat speeds up chemical reaction rates -heat decreases the effects of endotoxins. Steps: 1. phagocytes secrete interleukins 2. interleukins travel to the brain 3. hypothalamus secrete prostaglandins which "reset" the thermostat to a higher temperature 4. nerve impulses cause shivering, increased metabolic rate and inhibit sweating and vasoconstriction in order to raise the body temperature to the :new setting"

Inflammation

Body's basic response to injury range from Acute to Chronic. The sequence of events can vary Symptoms: -redness: results from large amount of blood flowing through the area -heat: results from the release of heat energy from chemical reactions -swelling: results from fluid seeping from arterioles -pain/irritation: results from injury of nerve fibers, irritation by toxins produced by microbes, increased pressure due to swelling and/or from prostaglandin release.

Cytokines

Chemical messengers secreted by immune cells that have encountered a pathogen to regulate immunity and/or mediate inflammation. Overproduction leads to a "Cytokine Storm" -Interleukins -Interferons -Growth Factors -Tumor necrosis factor -Chemokines

Herd Immunity

Collective immunity through mass immunization confers indirect protection on the nonimmune members. Important force in preventing epidemics

Types of Transmission

Direct Transmission: an infectious agent is transferred from a reservoir to a susceptible host by direct contact or droplet spread. -Direct Contact: occurs through skin-to-skin contact, kissing, and sexual intercourse. Direct contact also refers to contact with soil or vegetation harboring infectious organisms. -Droplet Spread: refers to spray with relatively large, short-range aerosols produced by sneezing, coughing, or even talking. Droplet spread is classified as direct because transmission is by direct spray over a few feet, before the droplets fall to the ground. Indirect Transmissions: transfer of an infectious agent from a reservoir to a host by suspended air particles, inanimate objects (vehicles), or animate intermediaries (vectors). - Airborne Transmission: occurs when infectious agents are carried by dust or droplet nuclei suspended in air. Airborne dust includes material that has settled on surfaces and become resuspended by air currents as well as infectious particles blown from the soil by the wind. Droplet nuclei are dried residue of less than 5 microns in size. In contrast to droplets that fall to the ground within a few feet, droplet nuclei may remain suspended in the air for long periods of time and may be blown over great distances. -Fomites (inanimate objects such as handkerchiefs, bedding, or surgical scalpels) Mechanical Transmission and Vectors: animals such as mosquitoes, fleas, and ticks may carry an infectious agent through purely mechanical means or may support growth or changes in the agent. Examples of mechanical transmission are flies carrying Shigella on their appendages and fleas carrying Yersinia pestis, the causative agent of plague, in their gut

Immunological Dysfunction, Hypersensitivities

Hypersensitivities (Allergies): the immune system responds to a harmless substance as if it were a threat. Allergen: antigens of an allergic response

Stages of Infectious Disease

INCUBATION PERIOD: Time between infection and the appearance of signs and symptoms. PRODROMAL PHASE (prodromos = forerunner): Short period during which nonspecific, often mild, symptoms such as malaise and headache sometimes appear. You feel like you're coming down with something. INVASIVE PHASE: Period during which the individual experiences the typical signs and symptoms of the disease (fever, nausea, rash, cough, etc.). The battle between pathogens and host defenses is at its height during this stage. DECLINE PHASE: Symptoms begin to subside as the host defenses and the effects of treatment if being administered finally overcome the pathogen. CONVALESCENCE PERIOD: Tissues are repaired, healing takes place, and the body regains strength and recovers. Individuals no longer have disease symptoms, but they may still be able to transmit pathogens to others. *pathogen is transmissible during all disease stages!

Classes of Antibodies

Ig μ (Mu): -largest of all the antibody molecules -accounts for about 5-10% of the immunoglobulin pool -located in the blood, lymph, and on B cell surfaces these are the first antibodies to be produced in the first few -agglutinate microbes; first Ab produced in response to infection -days of a primary immune response to an infecting organism -effective against microbes and agglutinating antigens -fix complement -half-life = 5 days Ig G (Gamma): -smallest immunoglobulin of blood, cerebrospinal fluid, and peritoneal fluid -makes up 80% of the total immunoglobulins -the only class of immunoglobulin that crosses the placenta conferring fetus the mother's immunity on the -fix complement -enhance phagocytosis; neutralize toxins and viruses; protect fetus and newborn -half-life = 23 days Ig E (Epsilon): -difficult to find constituting about .002% of immunoglobulins -mediators of allergic reactions -generally responsible for an individual's immunity to invading parasites (allergic reactions and lysis of parasitic worms) -on mast cells, on basophils, and in blood -half-life = 2 days Ig A (Alpha): -represents 10 to 15% of the total circulatory immunoglobulin pool -predominates in body secretions -plays an important role in protection against respiratory, urinary tract and bowel infections Mucosal protection -significant presence in colostrum and breast milk indicates that it can be transferred across the gut mucosa in the neonate and plays an important role in protecting the neonate from infection. -half-life = 6 days Ig D (Delta): -primarily a cell membrane immunoglobulin found on the surface of B lymphocytes -accounts for less than 1% of the total immunoglobulin pool known to initiate immune response on the B-cell surface is expressed on B cells as an antigen receptor -found in small amounts in the tissues that line the belly or chest -0.2% of serum antibodies -found in blood, in lymph, and on B cells -on B cells, Half-life = 3 days

Three Phases of Initial Immune Response

Innate Immunity (immediately, 0-4 hours): -infection -recognition by nonspecific effectors -removal of infectious agent Early Induced Response (early, 4-96 hours): -infection -recognition of microbial-associated molecular patterns -inflammation and recruitment/activation of effector cells -removal of infectious agent Adaptive Immune Response (late, over 96 hours): -infection -transport of antigen by lymphoid organs -recognition by B and T Cells -clonal expansion and differentiation to effector cells -removal of infectious agent

Interferons

Involved against viruses in immune regulation and intercommunication. Virus infected cell create then secretes interferons, these bind to the cells next to them so the cells can secrete antiviral proteins so they are not infected. Three major types: -IFN-α and IFN-β: cause cells to produce antiviral proteins that inhibit viral replication -IFN-γ: causes neutrophils and macrophages to phagocytize bacteria

Transient Flora

Microbes that can sometimes be cultured from body surfaces, but aren't permanent residents. Hospital workers gather large transient flora populations, these can lead to infections later on

Normal Flora (microbiota)

Microbes that use the human body as their permanent habitat. Bacteria produce nutrients for host and in exchange, the host provides nutrients/protection Sites: -skin -upper respiratory tract -GI tract -outer opening of urethra -external genitalia -vagina -external ear canal -external eye Microbial antagonism : natural flora protects the host by competing with and edging out many pathogens.

Types of Host-Pathogen Interactions

Mutualism the way two organisms of different species biologically interact in a relationship in which each individual derives a benefit ex. Bovines and bacteria within their intestines Commensalism is a class of relationship between two organisms where one organism benefits without affecting the other Parasitism is a non-mutual relationship between organisms of different species where one organism, the parasite, benefits at the expense of the other, the host. Infection: multiplication of a microbe in a host

Acquired Immunity

Natural Immunity: acquired through normal life means, not medically induced -active: developed in response to a microbe -passive: receiving immunity from another person (breast feeding) Artificial Immunity: produced purposefully through medical procedure -active: developed in response to a microbe (immunizations) -passive: receiving temporary immunity from another means (an IV)

Disease Vocabulary

Pathology: study of disease. Etiology: study of the cause of the disease (the microbe that causes the disease) Pathogenesis: the manner in which a disease develops Pathogenic microbe: microbe that has the capacity to produce disease. Virulence: refers to the degree of pathogenicity Pathogenicity: property for causing disease, depends on: -ability to invade a host -ability to multiply in the host -ability to avoid being damaged by host's defenses

Antibodies

Proteins produced by B cells that specifically bind an antigen, the antigen binding site region is "variable" region (Fab) and the rest is "constant" region (Fc). Also known as an immunoglobulin Functions: -Neutralization: the binding of Ab with Ag blocks/neutralizes the damaging effect of some bacterial toxins and prevents attachment of some viruses to body cells. -Immobilization: If Ab forms against cilia or flagella of motile bacteria, the Ab-Ag complex may cause the bacteria to lose their motility, limiting their spread into nearby tissues. -Agglutination: the Ab-Ag reaction may cross-link pathogens to one another, causing agglutination (clumping together) enhancing phagocytosis. -Activation: complement proteins can 1. be chemotactic to wbc's 2. cause lysis of microbe 3. act as opsonins 4. activate the inflammatory response. -Opsonization: antibodies enhance phagocytosis by coating the microbe

Diagnostic Immunology

Sensitivity: probability that the test is reactive if the specimen is a true positive Specificity: probability that a positive test will not be reactive if a specimen is a true negative Immunologic-based tests: Guinea pigs with TB are injected with Mycobacterium tuberculosis: site became red and slightly swollen

Noticed and Unnoticed Disease

Sign: any objective evidence of disease as noted by an observer Symptom: the subjective evidence of disease as sensed by the patient Syndrome: when a disease can be identified or defined by a certain complex of signs and symptoms Asymptomatic: subclinical/inapparent infections

Humoral Immunity

Steps: 1. B-Cell activation: -B cell encounters an antigen -antigen is bound to the receptor and taken inside the B cell by endocytosis -antigen is processed and presented on the B cell's surface again by MHC-II proteins. 2. B-Cell proliferation: -B-Cell waits for a helper T cell (TH) to bind to the complex. -binding activates the TH cell, which then releases cytokines that induce B cells to divide rapidly, making thousands of identical clones of the B cell. These daughter cells either become plasma cells or memory cells. The memory B cells remain inactive here; later when these memory B cells encounter the same antigen due to reinfection, they divide and form plasma cells. On the other hand, the plasma cells produce a large number of antibodies which are released free into the circulatory system. 3. Antibody-antigen reaction -antibodies will encounter antigens and bind with them, this will either interfere with the chemical interaction between host and foreign cells, or they may form bridges between their antigenic sites hindering their proper functioning, or their presence will attract macrophages or killer cells to attack and phagocytose them.

Monoclonal Antibodies

an antibody produced by a single clone of cells or cell line and consisting of identical antibody molecules. 1. a mouse is injected with a specific antigen to induce the production of antibodies 2. the spleen of the mouse is removed and homogenized in a suspension 3. the spleen cells are then mixed with myeloma cells that are capable of continuous growth in the hope that they will fuse to create hybrid cells that will continuously multiply while producing antibodies 4. the mixture of cells is placed in a medium where only the hybrid cells will grow 5. hybrid cells proliferate into clones calles hybridomas, which are then screened for the desired antibody 6. selected hybridomas are then cultured to produce large quantities of monoclonal antibodies to isolate antibodies for treating and diagnosing disease

Antigen Presenting Cells

cell that displays foreign antigens complexed with major histocompatibility complexes (MHC's) on their surfaces. T-cells may recognize these complexes using their T-cell receptors (TCRs). -dendritic cells: phagocyte invader and presents bits of invader to other cells in the immune system, acting as messengers between the innate and adaptive immunity. -B-Cells -macrophages

Leukocytes

cells that survey tissues for microbes and injured/dead cells to ingest and eliminate these materials. Extract immunogenic information (antigens) from foreign matter Granulocytes: white blood cells in the innate immune system characterized by the presence of granules in their cytoplasm. -Neutrophils: circulate around the body in the bloodstream, the first cells to migrate to the site of the infection to begin killing the invading microbes. -Eosinophils: attack and destroy large eukaryotic pathogens , also aid in inflammation and allergic reactions -Basophils: parallel eosinophils, release histamine during allergic reactions. Agranulocytes: no granules present, large nucleus -Monocytes: can mature into macrophages or dendritic cells -Lymphocytes: made in the bone marrow and found in the blood and lymph tissue, part of specific line of defense

Immunization

deliberately introducing an antigen into the body that can provoke an immune response & the production of memory cells. -First injection elicits a primary immune response -Second injection (booster) elicits a secondary immune response (bigger & more memory cells)

Nosocomial Infections

diseases that are acquired or develop during a hospital stay. 2-4 million cases a year, the importance of medical asepsis

Second Line of Defense

non-specific processes to kill the pathogen before it begins multiplying: -Complement System -Phagocytosis -Natural Killer Cells -Interferons -Fevers -Inflammation

Primary Immune Response

occurs when an antigen comes in contact to the immune system for the first time. During this time the immune system has to learn to recognize antigen and how to make antibody against it and eventually produce memory lymphocytes. 1. following the first exposure to a foreign antigen. a lag phase occurs in which no antibody is produced, but activated B cells are differentiating into plasma cells. The lag phase can be as short as 2-3 days, but often is longer, sometimes as long as weeks or months. 2. the amount of antibody produced is usually relatively low. 3. antibody level declines to the point where it may be undetectable. 4. the first antibody produced is mainly IgM (although small amounts of IgG are usually also produced).

Secondary Immune Response

occurs when the second time (and following times) the person is exposed to the same antigen. At this point immunological memory has been established and the immune system can start making antibodies immediately. 1. an accelerated 2° or anamnestic immune response (IR) occurs. This lag phase is usually very short (e.g. 3 or 4 days) due to the presence of memory cells. 2. the amount of antibody produced rises to a high level. 3. antibody level tends to remain high for longer. 4. the main type of antibody produced is IgG (although small amounts of IgM are sometimes produced).

Major Histocompatibility Complex (MHC)

proteins on outside of body cells called MHC proteins. These proteins mark that cell as "self" (not foreign) -Class I: non immune nucleated cells -Class II: macrophage, dendritic, B cells (APCs)

Etiologic Agent

the causative agent

Serological Tests

the determination of the presence of specific antigens or antibodies in blood serum, serological tests are available to identify a variety of antigens and antibodies in serum -Monitor the spread of infection within a population -Establish diagnosis of disease Types: Precipitation: the aggregation of soluble molecules Agglutination: the clumping of insoluble particle, occurs due to the cross-linking of antibodies with particulate antigens. Reactions can be easy to see and interpret with the unaided eye Hemagglutination: agglutination of RBCs -direct: no beads are present -indirect: the antibodies bind to latex beads Neutralization: inactivates toxin or virus Fluorescent antibody technique: antibodies linked to fluorescent dye Complement fixation: RBCs are indicator ELISA: peroxidase enzyme is the indicator

Epidemiology

the study of the frequency and distribution of disease and other health-related factors in defined human populations. Trying to find the source of the disease so as to prevent its spread. Interested in surveillance, collecting, analyzing, and reporting data on the rates of occurrence, mortality, morbidity, and transmission of infections -Epidemic: a pattern of disease transmission that affects many members of a population within a short time -Pandemic: an epidemic that spreads worldwide; Six diseases alone account for 90% of deaths from infectious diseases worldwide: Influenza: In the US alone: 97,920,000 cases per year (approximately 25 percent of the population), leading to an average of 20,000 to 40,000 deaths per year. HIV/AIDS: estimated 39.5 million people living with AIDS worldwide; estimated 2.9 million deaths in 2006. Tuberculosis: 3 million die. Malaria: 1.5 to 3 million, mostly children die. Measles: still kills 900,00 people each year. Diarrheal illnesses -Endemic: disease exhibits steady frequency over a long time period in a particular area; numbers generally stay too low to constitute a public health concern -Sporadic: diseases occurring only occasionally in a population Types of Studies: -Descriptive:collection and analysis of data -Analytical: comparison of a diseased group and a healthy group -Experimental: controlled experiments Statistics: -Prevalence: the total number of existing cases with respect to the entire population (fraction of a population having a specific disease at a given time) Prevalence = (total number of cases in population / total number of persons in population) x 100 = % -Incidence: the number of new cases over a certain time period (fraction of a population that contracts a disease during a specific time) Incidence = number of new cases / total number of susceptible persons -Mortality rate: the total number of deaths in a population due to a certain disease -Morbidity rate: the number of persons afflicted with infectious diseases