Immunoglobulin classes Antibody Structure for IgG, IgD and IgE: consist of 4 protein chains -2 identical light chains

and 2 identical heavy chains to form a Y-shaped molecule Structure for IgA and IgM are aggregated of two or five monomeres, respectively, they are joined together IgG - accounts for 80% of all antibodies in serum. Most abundant in serum - In regions of inflammation these monomer antibodies readily across the walls of blood vessels and enter tissue fluids -provides long term resistance to disease as a product of a memory B-cell -Location: blood, lymph, intestine. -function: protect against circulating bacteria and viruses, neutralize bacterial toxins, trigger the complement system and when bound to antigens, enhance the effectiveness of phagocytic cells structure: monomer IgM make up 5-10% of the antibodies in serum -structure: Pentamer. consist of five monomers held together by a polypeptide called J (joining) chain. -largest Ab. The large size of the molecule prevents IgM from moving about as freely as IgG does, therefore remains in blood vessels w/out entering the surrounding tissue -Involve in the response to the ABO blood group antigens on the surface of red blood cells -Location: Blood, lymph, b-cell surfaces -Function: Effective against microorganisms and agglutinating antigens. IgM appears first in response to a primary infection and is relatively short lived makes it uniquely valuable in the diagnosis of disease IgA -make up 5-10% of antibodies in serum; Most abundant in serum -Location: Most common form in mucous membranes and in body secretions such as mucus, saliva, tears and breast milk -2 types: serum IgA and secretory IgA -Structure: Dimer w/ secretory componet. Usually in the form or monomer. Effective form consist of 2 connected monomers that form a dimmer called secretory IgA. -Main function is to prevent the attachment of microbial pathogens to mucosal surfaces. It is important in resistance to intestinal and respiratory pathogens IgD make up 0.2% of total serum antibodies -structure: Monomer -it is a cell surface receptor on the B lymphocytes together with IgM -found in blood, lymph and particularly on the surfaces of B-cells -has no well define function IgE -make up 0.0002% -Structure: Monomer

- Location: IgE molecules bind tightly by their stem regions to receptors on mast cells and basophils, specialize cells that participate in allergic reactions. When an antigen such as pollen cross-links w/ the IgE antibodies attached to a mast cell or basophil, that cell releases histamine and other chemical mediators. These chemical provoke a response such as allergic reaction-hay fever -Funtion: Allergic reations; possibly lysis of parasitic worms Immunity Passive naturally acquired immunity: natural transfer of antibodies from a mother to her infant. Antibodies in a pregnant women cross the placenta to her fetus or through breast feeding. Ex. If the mother is immune to diphtheria, rubella or polio, newborn will temporarily immune to these disease as well Active naturally acquired immunity: develops when a person is exposed to antigens, becomes ill, and then recovers. Once acquired, immunity is lifelong for some diseases such as the measles. Ex: subclinical infections or inapparent infections Passive artificially acquired immunity: involves the injection of antibodies into the body. These antibodies come from an animal or person who is already immune to the disease Active artificially acquired immunity: The result of vaccination Antibody mediated and cell mediated immunity Antibody mediated immunity (Humoral Immunity) B-cells -Red bone marrow stem cells give rise to B-cells with IgM and IgD on their surfaces, which recognize specific epitopes -Humoral response is carried out by antibodies -Produce by lymphocytes B-cells -the process that leads to the production of abs start when B-cells are exposed to free antigens. - T- helper cells are required to help B-cells produce abs by releasing cytokines that causes clonal expansions of the B-cells -Activated B- cell proliferates into a large clone of cells, some which will differentiate into antibody producing plasma cells. Other clones of activated B-cells become long lived memory cells which provide life long immunity to a microbe or vaccine antigen encounter earlier in life Cell mediated immunity ( T-Cells ) -T-cells develop from stem cells in the red bone marrow. The precursors of the T-cells migrate from the bone marrow and reach maturity in the thymus. -mature T-cells migrates from the thymus by way of the blood and lymphatic system to various lymphoid tissue, where they are most likely to encounter antigens. -Directed against intracellular Ags not exposed to circulating Abs (bateria , virus) -Before an inactive T-cell can attach Ags, the T-cell must become sensitize to recognize the Ags -Sensitization involves macrophages wh/ phagocytize and present the partially digested Ag on the macrophages surface to the T-cells -macrophages secrete interleukin-1 and interferons wh/ stimulate T-cell growth and divison -most of the time T-cell is inactive -Once T-cell are sensitize they increase in size and # to produce clone Types of T-cells:

T-helper cells: -activates cells involve in cellular immunity -associated with allergic reactions and parasitic infection -activates B-cell to produce Abs and activates cytotoxic T-cells T-Cytotoxic cells: -killer cell that works against cells w/ foreign intracellular Ags T-regulatory cells: -suppress T-cells against self ABO Blood Group System Plasma antibodies A B AB 0 Anti-B Anti-A Neither anti A nor anti-B antibodies Anti A & Anti B Blood that can be donated A, AB B, AB AB O,A,B,AB Blood that can be rcvd A,O B,O A,B,AB,O O

Autoimmune disease Autoimmune disease: When the action of the immune system is in response to self antigens and causes damage to ones own organs. Occurs when there is a loss of self tolerance, the immune systems ability to discriminate self from nonself. The loss of self tolerance leads to the production of antibodies or a response by sensitized t-cells against a persons own tissue organs. Cytotoxic Autoimmune Reactions Graves disease cause by antibodies called long acting thyroid stimulors. Attach to receptors of thyroid gland cells. Results in enlarge thyroid gland. Signs of the disease are goiter and bulging staring eyes myasthenia gravis-muscles become progressively weaker. Cause by antibodies that coat the acetylcholine receptors at the junctions at which nerve impulses reach the muscle. Muscule controlling diaphragm and rib cage may fail to rcvd the necessary nerve signals, and resp arrest and death results. Immune Complex Autoimmune reactions Sytemic Iupus erythematosus-sytemic autoimmune disease, involve immune complex reactions, that mainly effects women. Damage the immune complexes in the kidney glomeruli Rheumatoid arthritis- immune complexes of IgM, IgG and complement are deposited in the joints. Leads to severe damage to the cartilage and bone of joints Cell-Mediated Autoimmune Reactions Multiple sclerosis-neurological disease in which t-cells and macrophages attack the myelin sheath of nerves. Symptoms are fatigue, weakness and severe paralysis Insulin dependent diabetes mellitus-cause by immunological destruction of insulin secreting cells of pancreas. Psoriasis-characterize by itchy red patches of thicken skin; many develop psoriatic arthritis. Allergy testing

Allergy testing is done through skin testing-involves inoculating small amounts of the suspected antigen just beneath the epidermis of the skin. Sensitivity to the antigen is indicated by rapid inflammatory reaction that produces redness, swelling and itching Desensitization: procedure consist of a series of gradually increasing dosage of the antigen carefully injecting beneath the skin. Obj. is to cause production of IgG rather than IgE antibodies in the hope that the circulating IgG antibodies will act as blocking antibodies to intercept and neutralize the antigens before they can react with cell bound IgE.

Hypersensitivity Type I thru Type IV Hypersensitivity: antigenic response beyond that which is considered normal (allergy) Type I: Anaphylactic -often occurs within 2 to 30 mins after a person sensitized to an antigen is reexposed to that antigen. -Anaphylaxis: reaction caused when certain antigen combine with IgE antibodies that bind to mast cells and basophils to sensitize the host. -The binding if two adjacent IgE antibodies to an antigen causes the targer call to release chemical mediators, such as histamine, leukotriens and prostaglandins, which cause the allergic reaction -Anaphylactic response can be: -systemic reactions, which produce shock and breathing difficulties and are sometimes fatal. May result in circulatory collapse and death -Localized reactions: which include common allergic conditions such as hay fever, asthma, and hives -can be prevented by skin test or desensitization Type II: Cytotoxic -Involve the activation of complement by the combination of IgG or IgM antibodies with an antigenic cell. -Antibodies are directed toward foreign cells or host cells. Complement fixation may result in cell lysis. Macrophages and other cells may also damage the antibody-coated cells -Reaction: Transfusion reactions, in which red blood cells are destroyed as a result of reacting w/ circulating antibodies. Involves blood group systems that include the ABO and Rh antigen Type III: Immune Complex -involves antibodies against soluble antigens circulating in the serum. The antigen-antibody complexes are deposited in organs and cause inflammatory damage -Reaction: Immune complexes-occurs when IgG antibodies and soluble antigen form small complexes that lodge in the basement membrane of cells Glomerulonephritis: an immune complex disease, cause inflammatory damage to the kidney glomeruli. Type IV: Delayed Cell-Mediated -cause by T-cells. Instead of instant reaction after exposed to an antigen, these delayed cell mediated reactions are not apparent for a day or more.

-Delay is due to the time required for the T-cells and macrophages to migrate to an accumulate near the foreign antigens. -Sensitized T-cells secrete cytokines in response to the appropriate antigen -Cytokines attract and activate macrophages and initiate tissue damage -tuberculin skin test and allergic contact dermatitis ( poison ivy, cosmetic, metal jewelry) are ex of delayed hypersensitivities Blood Elements Blood consist of plasma and formed elements 1. Erythrocytes (red blood cells) Function: Transport of O2 and CO2

2. Leukocytes (white blood cells) -2 types 1.Granulocytes-presence of large granules in their cytoplasm that be seen under microscope after staining. a. neutrophils- stains pale lilac, phagocytic and motile and are active in the initial stage of an infection. Have the ability to leave blood, enter infected tissue and destroy microbe b. Basophils-stains blue purple, release histamine that are important in inflammation and allergic reation c. Eosinophils-stains red/orange, somewhat phagocytic and have the ability to leave blood. Function is to produce toxic proteins against certain parasites 2. Agranulocytes-have granules in cytoplasm, but not visible under microscope a. Monocytes-not actively phagocytic until they leave the blood, enter tissue and mature into macrophages. b. Dendritic cells-deprived from monocytes, abundant in the epidermis of the skin, mucous membrane, thymus and lymph nodes. Function is to destroy microbes by phagocytosis and to initiate adaptive immunity response c. Lymphocytes: -natural killer cells: destroy target cells by cytolysis and apoptosis -T-cells: Cell-mediated immunity -B-cells: Descendants of B-cells, produce antibodies 3. Platelets: blood clotting Inflammation Damage to the bodys tissue triggers a local defensive response called inflammation, another component of the second line of defense. Damage can be caused by microbial infection, physical agents, or chemical agents. 4 cardinal signs of inflammation: 1.redness-due to increase blood flow to the area of injury-vasodilation 2.pain-cause by injury to the local nerves

3. heat-due to increased blood flow and the action of pyrogen (fever producing substance in blood) 4. swelling blood leaks from vessels and you get an accumulation of fluid 5. sometimes a 5th- loss of function Inflammation has the following function: 1. destroy the injurious agent, if possible, and to remove it and its by-products from the body. 2. If destruction is not possible, to limit the effects on the body by confining or walling off the injurious agent and its by products 3. To repair or replace tissue damaged by the injurious agent or its by-product Process of inflammation: 1. vasodilation and increased permeability of blood vessels -Mast cells are tissue cells that trigger an inflammatory reaction. By releasing histamine which is a chemical mediator that dilates blood vessels and increase vascular permeability to plasma proteins - blood vessels dilate in the area of damagem and their permability increases. Dilation of blood vessels, called vasodilation, increase blood flow to the damage area and is responsible for redness and heat associated with inflammation. -the blood clot that forms around the site of activity prevent the microb from spreading to other parts of the body , resulting in pus -Dilation of BVs increase delivery of leukocytes-WBC 2. phagocyte migration and phagocytosis -neutrophils and monocytes stick to endothelium of blood vessels close to the injury know as margination -The WBCs start getting between the endothelial cells and squeeze their way out of the vessels to reach the damage area, this migration period is called diapedesis -The phagocytes then begin to destroy invading microorganisms by phagocytosis. Neutrophils augment phagocytosis while monocytes differentiate into macrophage 3. tissue repair -Tissue replace dead or damage cells. -repair begins during the active phase of inflammation, but cannot be completed until all harmful substances have been removed or neutralize at site of injury.

Immune System Function is to recognize and destroy that which is foreign including invading microbes and their secretion of toxin Consist of 2 components: 1. nonspecific or innate immunity a. acts to prevent microbe from getting into body b. defense are present at birth c. always ready to respond to damage or invasion 2. Specific or adapted: Physical barriers:

-Skin: structure of skin and waterproof protein keratin provide resistance to microbial invasion -dermis-inner thicker protion -epidermis outer layer -can be broken by cuts, insect bits. Allow staphylococci to enter blood -is home for normal microbiota which are antagonistic to pathogens -Mucous membrane: lines the internal body cavity and act as a mechanical barrier to microbes -Cilia in airways propel microbes and mucus into the pharynx where they are swallowed into the stomach -stomach acid destroy microbs -lacrimal apparatus: protects the eye from irritating substances and microbe -saliva washes microbes from teeth and gums -Hairs and cilia -Epiglottis: cover larynx when swallowing and keeps microbes from entering resp tract -Mucus traps many microbes that enter the respiratory and gastrointestinal tracts -urine moves microbes out of the urinary tract and vaginal secretion move microbes our of the vagina Chemical barriers: -Sebum: prevents hair frm drying out and becoming brittle -Contains unsaturated fatty acid which inhibit the growth of pathogenic bacteria. -Perspiration: produce by sweat glands -helps maintain body temp and flush microbes from the skin -lysozyme: enzyme capable of breaking down cell walls of gram positive bacteria and gram negative bacteria. -found in tears, saliva, nasal secretion and perspiration. -gastric juice: produce by glands of the stomach -acidic juice pH 1.2-3.0 is sufficient to destroy bacteria to prevent microbe growth in the stomach - vaginal tract: has a low pH due to the normal microbiota Lactobacillus producing various acids Gamma globulin: contain most of antibodies, often use to transfer passive immunity. Found in IgG. Also called immunoglobulin is a class of blood plasma proteins, most notably including the antibodies that help fight infections and disease. Abnormal amounts of gamma globulin can have adverse effects on health or can be indicative of disease. In medicine, gamma globulin injections are used to treat certain conditions Humoral immunity: -when describing immunity brought about by antibodies -antibodies produce be B-cells -humoral antibodies are effective against pathogens such as virus and bateria that circulates freely where antibodies can contact them Cell mediated immunity: -involves T-cells -response to aspect of pathogenicity- the need to combat intracellular pathogens. Such as a virus within a infected cell that are not expose to circulating antibodies -They are also the way in which immune system recognize cells that are nonself, expecially cancer cells. Diseases Rheumatoid arthritis: autoimmune disease in which immune complexes of IgM, IgG and complement are deposited in the joints

-infection, genes, and hormones changes may be linked to this disease -affects joints on both side of the body, numbness, stiffness -requires lifelong treatment, including medicine, physical therapy -complications: damage to lung tissue, increased risk of hardening of the arteries inflammation of blood vessels Chicken pox: pathogen herpesvirus varicella-zoster. A DNA virus that is contagious before rash breaks out. Mild childhood disease -Acquired when the virus enters the respiratory system by droplets of fluid in vesicles. -The infection localize in skin cells after 2 weeks. Skin is vesicular for 3 to 4 days. During that time, vesicles fill with pus, ruptures and form a scab before healing -can cause fatal damage if contracted during pregnancy -attenuated vaccine -complications include encephalitis and Reyes syndrome -after chickenpox, the virus can remain latent in nerve cells and subsequent activate as shingles Smallpox: cause by orthopoxvirus cause by variola pathogen -2 forms: variola major, variola minor. -transmitted by respiratory route, the virus infect many internal organs before they move into bloodstream, infecting the skin and producing more symptoms -signs: high fever, fatique, bachaches -humans are the only reservoir source -infects internal organs before going to bloodstream -Monkey pox resembles smallpox in symptoms and is an orthopoxvirus -smallpox has been eradicated as a result of a vaccination effort by WHO -only host is humans German measles (Rubella): cause by rebella virus -RNA virus -Symptoms: macular rash of small red spots and a light fever -transmitted by the respiratory route, secretions and occasional urine -Serious complications are very rare. Apart from the effects of transplacental infection on the developing fetus, rubella is a relatively trivial infection. -Congenital Rubella Syndrome= deafness, eye cataracts, heart defects Warts: papillomas, generally benign skin growths caused by viruses -Pathogen: papillomas. More than 50 types of papillomavirus are now known to cause diff kind of warts w/ varying appearance -transmitted person to person by contact, sexually -pathogen can cause some skin and cervical cancers and genital warts -treatment is to apply cold liquid nitrogen, dry them w/ an electrical current or burn them with acid, lasers, injection of bleomycin or antitumor drug. -genital warts (human papilloma)-HPV 16 associated w/ cervical cancer Shingles (herpes Zoster): vesicles similar to those of chickenpox occur but are localize in distinctive areas -pathogen: varicella -antiviral drugs acyclovir, valacyclovir and famciclovir are approved for treatmeant. -after primary infection the virus retreats up the peripheral nerves to the dorsal root ganglion where it can remain dormant for decades

-can be reactivated -people who have not had chickenpox can contract them - Infection follows the distribution of the affected cutaneous sensory nerves and is usually limited to one side of the body at a time because nerves are unilateral. Occasionally, nerve infection can result in nerve damage that impairs vision or even causes paralysis Keratitis: is a condition in which the eye's cornea, the front part of the eye, becomes inflamed. The condition is often marked by moderate to intense pain and usually involves impaired eyesight -Herpetic keratitis : cause by herpes simplex type 1 virus that causes cold sores and is latent in the trigeminal nerves. -infects the cornea, often resulting in deep ulcers -drug trifluridine is often the treatement -Acanthamoeba Keratitis: Amoeba has been found in fresh water, tap water, hottub and soil. -contact lenses, wearing them overnight or swimming -inadequate, unsanitary disinfecting procedures -treatment w/ propamidine isethionate eye drops and topical -neomycin -severe damage can lead to corneal transplant or removal of the eye. Roseola: mild childhood disease -child is at high fever for a few days, follow by rash over much of the body last for a few days -pathogen: human herpesviruses 6 (HHV-6) and 7 (HHV-7) both are presented in saliva of most adults Reyes Syndrome is an occasional severe complication of chickenpox, influenza and other viral disease. -is a potentially fatal disease that causes numerous detrimental effects to many organs, especially the brain and liver, as well as causing a lower than usual level of blood sugar (hypoglycemia). - The classic features are liver damage, aspirin use and a viral infection. -The exact cause is unknown, and while it has been associated with aspirin consumption by children with viral illness, it also occurs in the absence of aspirin use. -The disease causes fatty liver with minimal inflammation and severe encephalopathy (with swelling of the brain). The liver may become slightly enlarged and firm, and there is a change in the appearance of the kidneys. -coma death can follow -survivors may have neurological damage -Early diagnosis is vital; while most children recover with supportive therapy, severe brain injury or death are potential complications. Measeles (Rubeola): An RNA virus. Pathogen rubeola. Is a contagious disease that is spread by the respiratory route -treatment: MMR vaccine. -no animal reservoir for measles, but because the virus is so much more infectious than smallpox, herd immunity is difficult to obtain. - infection is cause by contact with infected ppl who come from outside the US -humans are the only reservoir -MMR vaccine for treatment -It is hazardous to infants who are more likely to have serious complications -development begins in the upper resp system. Sypmtoms develop resembles those of a common cold. Rash appears, beginning on the face and spreading to the trunk and extremities -frequently complicated by middle are infections or pneumonia caused by the virus itself or secondary bacterial infection

Tinea-Capitis, pedis, Cruris -dermatophytes-Fungi that colonize the hair, nail and outer layer of the epidermis Tinea capitis: ringworm of the scalp, common around school children and cal result in bald patches. -infection expands circularly -transmitted by contact with fomites. Dogs and cats are also frequently infected w/ fungi that cause ringworm in children tinea cruris: ringworm of the groin or jock itch tinea pedis: ringworm of the feet or athletes foot -3 genera of fungi are involve in cutaneous mycosis: Trichophyton-infect hair, skin or nails; Microsporum-usually hair or skin; Epidermophyton-affects only the skin or nail -treatment of infection include miconazole and clotrimazole. Pathogens: Herpes Virus HSV -also known as Human herpes virus 1 and 2 (HHV-1 and -2), are two members of the herpes virus family, Herpesviridae, that infect humans. -Both HSV-1 (which produces most cold sores) and HSV-2 (which produces most genital herpes) are ubiquitous and contagious. They can be spread when an infected person is producing and shedding the virus. -Symptoms of herpes simplex virus infection include watery blisters in the skin or mucous membranes of the mouth, lips or genitals. Lesions heal with a scab characteristic of herpetic disease. -development of cold sores, fever blisters, canker sores Papillomavirus -HPVs establish productive infections only in keratinocytes of the skin or mucous membranes. -More than 30 to 40 types of HPV are typically transmitted through sexual contact and infect the anogenital region. -Some sexually transmitted HPV types may cause genital warts. Persistent infection with "high-risk" HPV types different from the ones that cause skin warts may progress to precancerous lesions and invasive cancer.[2] HPV infection is a cause of nearly all cases of cervical cancer. However, most infections with these types do not cause disease. Acanthamoeba -genus of amoebae, one of the most common protozoa in soil, and also frequently found in fresh water and other habitats. - it is nearly always associated with contact lens use, as Acanthamoeba can survive in the space between the lens and the eye. For this reason, contact lenses must be properly disinfected before wearing, and should be removed when swimming or surfing.

Lab:::::::::::::::::::::::::::::::::::::::::: Oxidase test: use to detect cytochrome; use by oxygen aerobically respiring bacteria positive= purple ring within 60 seconds Catalease test: see if bacteria has catalease enzyme, breaks down hydrogen peroxide positive= see bubbles after drops

SIMS (sulfide indole motility): starts off as yellow tube, selects for: H2S (blackening) Indole (red layer) motility: (turbidity)

I How it looks before inocu. How it looks w/ positive reaction Reagent added E. Coli E. Aerogenes C. Friundi Clear Red layer on top Kovaks + -

M Clear yellow Turns all red Methyl red + +

SIMs results C-Kosers clear Turns turbid

C-Simmons

Clear yellow Turns all red

Green agar Clear yellow slant Persian blue H2S (blackening) Indole (red layer on top) motility: (turbidity) none + + + + + + +

Alpha none Naphthol + + +

IMVC results for the 3 Gram- bacterias Tip: E. Coli is complete opposite of E. Aerogenes, and C. Friundi alternates : I(-)M(+)V(-)2C(+) Primary stains and counter stains Gram Primary stain Crystal violent Counter stain Safranin

Acid Fast Carbo Fusion Methylene blue

Spore Malachite green safranin

Selective and differential media Blood agar Color of uninoculated red

media

Eosin Methylene red G- bacteria lactose fermenting Lactose +: dark color; metallic sheen colonies Lactose -: colorless colonies E. coli: dark w/ metallic sheen E. arogenes: dark purpule

MacConkey yellow G- bacteria Fermenter lactose +: pink-red colonies -: colorless colonies

Mannitol Salts Red Halophiles; Fermenting of mannitol Turns media to yellow color

Selects for Differentiates by

G- bacteria hemolysis
Alpha: green zones around colonies Beta: clear zones around colonies Gamma: no zones

(what you see visually)

Geneus of positive reaction

E. coli: apha E. arogens: apha S. aureus: beta

E. coli, E. arogenes

S. aureus

Durham tube fermentation- starts off as red color Positive fermentation= turns media to yellow positive gas reaction= see bubble floating on tube