U3.immunity 2 PDF - Immunity Overview

Lines of defense against microorganisms The body relies on three major mechanisms of defence against invaders: Innate immunity Immunity 1st line of defence ; Anatomic barriers...

Lines of defense against microorganisms The body relies on three major mechanisms of defence against invaders: Innate immunity Immunity 1st line of defence ; Anatomic barriers Skin and mucous membranes Tears Bacterial flora 2nd line of defence ;Inflammation Cells – mast cells, neutrophils, macrophages. Inflammatory biochemical mediators Plasma Proteins system Complement clotting factors, fibrinolysis systems Adaptive[acquired] immunity. Third line T and B lymphocytes 1 2  Immune response Adaptive immunity is an acquired state of protection, The immune system protects the body from possibly harmful primarily against infectious agents, that differs from foreign substances which know as antigens, and this is know as inflammation by being the immune response. Examples of Antigens are bacteria , viruses, fungi or parasites Slower to develop substances by recognizing and responding to antigens. More Specific The immune response, is the responsibility of two types of lymphocytes. Having Memory so that it can confer permanent or B lymphocytes or B cells long term protection against specific microorganisms.. T lymphocytes or T cells 3 4 Function of lymphocytes; immune response Each has distinct function. B cells Responsible for humoral immunity, so it produces antibodies that enter the Development of lymphocytes blood and react with the antigen, leading to its neutralization, lysis or induce phagocytosis. T lymphocytes Responsible for cell mediated immunity, in which they kill the antigen directly[ virus or cancer cells]. 5 6  Humoral Immunity B cells that produce antibodies that travel through the blood, it attaches to antigen leading to its neutralization, lysis or induce phagocytosis. Antibodies (also known as immunoglobulins, abbreviated Ig) are globulin proteins that are found in blood or other bodily fluids, Antibodies can be classified by chemical structure and biologic activity as IgG IgM IgA IgE IgD 7 8  IgA Cell mediated immunity T lymphocytes, protects the body against viruses and In mucus membrane and breast milk mutant cells[ cancer cells]. IgE ; IgE also plays an essential role in type I hypersensitivity, T cells are composed of two main subtypes called which manifests various allergic diseases, such as allergic CD4 (T helper); stimulate the activities of immune asthma, allergic rhinitis, food allergy, and some types of system against microorganisms e.g bacteria and viruses chronic urticaria and atopic dermatitis. IgE stimulates the CD8 (cytotoxic T cell) ;which attack and kill targets release of mast cell granules, which contain histamine directly ( viruses, and cancer cells). 9 10  Definition Hypersensitivity refers to undesirable reactions produced by the immune system. Hypersensitivities So it is an inappropriate immune response , it may be in the form of “The Immune System Gone Bad” 1. Allergies – Exaggerated immune response against environmental antigens 2. Autoimmunity – immune response misdirected against host’s own cells 11 12 Mechanisms of hypersensitivity Type I hypersensitivity Hypersensitivity reactions can be divided into four types: type I, type II, type III and type IV, based on the The classic allergic reaction mechanisms involved and time taken for the reaction. Is an immediate allergic or anaphylactic type of. So it a Four types: reaction that occur after an antigen reacts with IgE on mast Type I – IgE-mediated allergic reactions cells. { immediate type hypersensitivity} It is the most common allergic reaction ,against Type III – immune-complex-mediated environmental allergens,. reactions[ autoimmunity] 13 14  Type 1 hypersensitivity; allergy Sequences of events in type 1 B hypersensitivity ( allergy) lymphocytes Initial contact with a special allergen[antigen from the Antigen environemnt]. [allergen] So B cells will form IgE antibodies against that allergen. IgE antibodies will be released in the circulation, to be attached to IgE IgE receptors on the mast cells. antibodies Mast cells On rexposure to the same antigen ,the reaction will be initiated On second when IgE antibodies located on the mast cell membrane are bound exposure to the same antigen by the antigen. Mast cell degranulation releases chemicals [histamin and Antigen –antibody prostaglandins]that mediate the signs and symptoms of allergy reaction and if severe will lead to anaphylaxis. Allergy Histamine prostaglandins antigen 15 16  Symptoms and Signs of Allergy—Urticaria One common manifestation Released histamine, and prostaglandines, cause of allergy is urticaria Capillary vasodilatation and increased vascular permeability, (hives). Histamine-induced causing redness , edema ,urticaria , and hypotension. vasodilataion and Constricts bronchial smooth muscle causing bronchospasm and increased vascular signs of bronchial asthma. permeability in the skin Conjunctivitis (eyes) and rhinitis (mucous membranes of nose). results in redness and fluid Diarrhea or vomiting exudation that presents as Examples of type I reactions include drug reactions, bee pruritic fluid-filled blisters sting reactions, and asthma. surrounded by redness 17 18 Symptoms and Signs of Allergy— Symptoms and Signs of Allergy— Respiratory System Respiratory System Allergic rhinitis Asthma most commonlly during times of the year when pollen counts are high. Asthma is an allergic Symptoms include nasal disease that affects the congestion, rhinorrhea, lower respiratory tract postnasal drainage, sneezing, itchy nose, watery eyes, with inflammation, headache, and loss of smell and bronchoconstriction, and taste. mucus formation. Asthma swollen, pale nasal mucous membranes, nasal and can be extremely serious pharyngeal erythema, nasal and can even result in polyps, and clear fluid behind the eardrums (serous otitis respiratory failure and media). death 19 20 Severe anaphylaxis and anaphylactic shock Anaphylaxis, the most rapid and severe immediate hypersensitivity Anaphylactic shock reaction, is an explosive reaction that occurs within minutes of Hypotension, edema (esp. of reexposure to the antigen and can lead to cardiovascular shock. larynx), rash, Urticarial rash and itching Angioedema and laryngeal edema; Treatment: [ABCs] Bronchospasm Maintain airway and oxygenation Obstructed breathing Epinephrine, antihistamines, tachycardia, pale cool skin, corticosteroids Hypotension , Fluids convulsions and cyanosis death 21 22 Type III – Immune-complex Type III Hypersensitivity; [autoimmune reactions[ autoimmune] diseases]types In autoimmunity the B lymphocytes attacks the body own cells ( it is not able to differentiate between self Systemic lupus and non-self erythematosus [SLE], different tissues , e.g., serosa (pleura, pericardium, kidneys (e.g., synovium), and glomeruli. Not organ specific glomerulonephritis), IgG and IgM mediate this type of hypersensitivity Blood vessels (e.g., reaction polyarteritis), Joints (e.g., rheumatoid arthritis). 23 24  Systemic lupus eryhtromatosus (SLE) which is a type III hypersensitivity Immune deficiency reaction caused by autoantibody production. It is a member of the group Immunodeficiency (or immune deficiency) is a state of diseases variably called autoimmune ,connective tissue; Common symptoms include in which the immune system's ability to fight Pleural effusion infectious disease is compromised [ weak]or entirely Cardiac problems absent. Renal disease Types Vascuilities [ Raynaud's phenomenon] Secondary immunodeficiency [ Acquired] ;most cases of Arthritis immunodeficiency Hematological abnormalities Primary immunodeficiency; some people are born with e.g. anemia. defects in their immune system. 25 26 ‫تسوية‬ HIV Epidemiology Homosexual men(57%) represent the largest Is a disease of the human immune population with AIDS. This is followed by system caused by the human IV drug users(24%), immunodeficiency virus (HIV), Heterosexual contact(9%), and which infect T helper lymphocytes Combined homosexual with intravenous drug use (CD4 cells). 8%. Women are most likely exposed via heterosexual contact(57%) 27 28  prophylaxis Modes of infections The use of safe sex practices such as condoms and The use of safe parenteral practices such as sterile Sexual transmission via semen and needles/syringes decrease the risk of infection. vaginal and cervical secretions; The universal use of standard precautions decreases the Perinatal transmission from an risk of infection. infected mother to her infant antepartum, intrapartum, and postpartum via breast milk. Parenteral transmission via blood, blood products, and contaminated needles/syringes 29 30 Risk for health care givers Clinical Manifestations Exposure to blood and body fluids of infected Clinical manifestation is divide into two stages individuals through skin, mucous membranes, and Early stage of HIV infection [ asymptomatic] accidental needle sticks is the primary risk factor for Late stage of AID( acquired immune deficiency health care workers. syndrome) After significant accidental exposure to HIV-infected blood or body fluids, it is recommended that health care workers take postexposure antiretroviral medication before 72 hours has elapsed after exposure. The administration of two reverse transcriptase inhibitors should be initiated 31 32  Early Disease Primary infection with HIV is characterized by a flu-like illness , including fever, chills, headaches, nausea ,vomiting, fatigue, weakness, arthralgia, and sore throat. The symptoms often goes unrecognized as HIV infection. In subsequent weeks, months, and years, the immune system is able to combat the HIV infection so Billions of T helper cells are infected, destroyed, and replaced by the bone marrow each day so that the individual is most often asymptomatic ,this is known as clinical “latency” (no symptoms of infection). 33 34  During this time, the individual infect others. Seroconversion During this early period ,the CD4 [ T helper Means the detection of antibodies against HIV in the serum of the patient , so the serum of the patient is lymphocytes]count is greater than 400/mm3. converted from being negative to positive. Normal Values - In a healthy adult, a normal CD4 This occurs between 3 weeks and 6 months after count can vary a great deal but is typically 600 to exposure. 1200 cells /mm3 35 36 Seroconversion Late stage ( AIDs progressive disease) Window period After years of combating the HIV infection, the ability of the host to replace infected and killed T helper cells begins to decline, and the numbers of active viruses in the blood stream begin to rise. As the number of functional T helper cells declines, the immune No antibodies in patient serum [3w to 6 m] response becomes increasingly compromised and the clinical manifestations of HIV infection such as opportunistic infections and malignancies begin to appear. This signals the progression of Time of HIV infection to AIDS. infection Appearance of antibodies ‫ا(لتهابات ا(نتهازية‬ Time of Seroconversion 37 38  ‫ميزة‬%‫السمة ا‬ In addition, malignancies may Progressive Disease manifestations[late stage]. develop such as The hallmark of AIDS is a decrease in CD4 Kaposi sarcoma (caused by coinfection cells [ < 200/mm3, including T-helper with a herpesvirus) and lymphocytes and macrophages. lymphomas. Serious opportunistic infections with organisms such as Other complications of HIV infection Fungal infections (e.g., candida infection and include thrush). Wasting syndrome and Pneumocystis jerovici (previously called Pneumocystis carinii), AIDS-related dementia. Mycobacterium tuberculosis, Toxoplasmosis gondii, and Epstein –Bar virus cytomegalovir 39 40 Focus point Diagnosis of HIV Seroconversion takes 3 w- 6 m after infection[ window ELISA [Enzyme-linked immunosorbent assay] period]. Measuring antibodies to HIV Early stage [period of latency ] the patient is asymptomatic Remains the most commonly used screening and diagnostic test for HIV [ not expensive, simple and rapid]. Progressive state is characterized by There are two main problems with this test: Opportunistic infection { fungal , Pneumocystis jerovici,TB} "False positives"—meaning that the test falsely detects Malignancies {Kabosi sarcoma, and lymphoma} antibodies in the blood even when infection is not present. i.e. The hallmark of AIDS is a decrease in CD4 cells [ < 200/ antibodies in no infection. mm3] "False negatives"—meaning that antibodies are not detected even though HIV infection is present i.e. no antibodies in infection. 41 42  Seroconversion Window period[incubation period] False negatives are more difficult to prevent. False Period of false negative negatives may occur because individuals may not become seropositive for the antibodies for several weeks or months after primary infection, leaving a “window No antibodies in patient period” during which the person may be infectious to serum [3w to 6 m] others but still be HIV antibody negative. The point at which antibodies can be detected in an HIV-infected individual is called seroconversion. Time of infection Appearance of antibodies Time of Seroconversion 43 44  Polymerase chain reaction (PCR). The criteria for diagnosis of AIDS, as defined by The presence of HIV in the blood can be detected very the Centres for Disease Control and Prevention, are: early in the course of infection by measuring viral Documented HIV infection proteins using a technique called a polymerase chain ELIZA test (antibodies) or reaction (PCR). PCR ( viral protein) Unfortunately, this test is expensive and complicated CD4 (T helper) count of