Immunology sec D ADDU

1. Lecture Day 2

2. PneumocystisCarinii Pneumonia Most common opportunistic infection,80% ommonly found in the lungs of healthy people, but being a source of opportunistic infection it can cause a lung infection in people with a weakened immune system P. carinii, Pneumocystisjirovecii is a fungus and invades within pulmonary alveoli and forms consolidation in parenchyma the disease attacks the interstitial, fibrous tissue of the lungs, with marked thickening of the alveolar septa and alveoli and leading to significant hypoxia

3. Sx: nonproductive cough fever, chills, SOB, dyspnea, weight loss and night sweats Tx: trimethoprim-sulfamethomexazole, pentamidine and steroids

5. Mycobacterium Avium Complex Also, M. intracellulare, , M. scrofulaceum are acid fast bacilli cause respiratory tract infection and increase mortality rates Sx:include fever, fatigue, and weight loss Tx: Clarithromycin/Azithromycin, Anti-tuberculosis medication

7. Wasting Syndrome Profound, involuntary weight loss exceeding 10% of baseline body weight and chronic diarrhea for more than 30 days, intermittent fever May be due to hypermetabolic state, anorexia, diarrhea, malnutrition, GI malabsorption, low food intake Treatment: Symptomatic,diet, control of diarrhea

9. Kaposi’s sarcoma Most common HIV-related malignancy Involves endothelial layers of blood and lymphatic vessels First noted by Dr. Moritz Kaposi in 1872, a tumor caused by Human herpesvirus 8 Sx: may range from localized cutaneous symptoms to disseminated disease which may appear brownish pink to deep purple Treatment: palliative, HAART

11. Cryptococcus Neoformans Fungal infection that causes meningitis, and symptoms of fever, headache,malaise and stiff neck Tx: Amphotericin B, fluconazole

12. Post exposure prophylaxis a course of antiretroviral drugs which is thought to reduce the risk of seroconversion after events with high risk of exposure to HIV To be most effective, treatment should begin within an hour of possible infection, and no longer than 72 hours post-exposure. Prophylactic treatment for HIV typically lasts four weeks

13. Needle stick Injuries and aids CDC guidelines generally recommend a PEP protocol with 3 or more antiviral drugs, when it is known that the donor was HIV positive PEP drugs for prevention of HIV infection are given for 4 weeks and may include nucleoside reverse transcriptase inhibitors (NRTIs), nucleotide reverse transcriptase inhibitors (NtRTIs), nonnucleoside reverse transcriptase inhibitors (NNRTIs), protease inhibitors (PIs), and a single fusion inhibitor. Regardless whether PEP is instituted, follow-up of exposed individuals includes counseling and HIV testing by enzyme immunoassay to monitor for a possible seroconversion for at least 6 months after exposure. Such tests are done at baseline, 6 weeks, 12 weeks, and 6 months, and/or longer.

14. TREATMENT There is currently no publicly available vaccine for HIV or cure for HIV or AIDS "highly active antiretroviral therapy“(HAART) Drugs that inhibit the reverse transcriptase prevent it from copying the RNA into DNA Drugs called protease inhibitors prevent the viral protease from trimming down the large proteins made late during infection

15. HYPERSENSITIVITY

16. Allergy- an inappropriate response of the immune system to normally harmless substances Atopy- refers to allergic reactions by the actions of IgE antibodies and a genetic predisposition to allergic conditions. Mast cells- also called basophils, are trigerred by IgEs to release chemical mediators to produce allergic reactions T cells- secrete substances called lymphokines that encourage cell growth, activation, destroys target cells, and stimulate macrophages

17. Antigens are divided into 2 groups: Complete protein antigens-stimulate complete humoral response eg. Animal dander, pollen, horse serum Low molecular weight substances- eg. haptens

18. CHEMICAL MEDIATORS

19. Primary mediators found in mast cells Histamine- causes erythema, localized edema, pruritus, contraction of bronchial muscle,dilation of small venules and constriction of large ones.

20. Prostaglandins- are composed of unsaturated fatty acids, produce smooth muscle contraction, vasodilation and increased capillary permeability.

21. 2. Secondary mediators a. Leukotrienes- released by mast cells that initiate inflammatory response, cause smooth muscle contraction,bronchial constriction and mucus secretion on the pathways. b. Bradykinin- polypeptide that causes increase vascular permeability, vasodilation, hypotension, and smooth muscle contraction and stimulates nerve cell fibers c. Serotonin- released during platelet aggregation causing contraction of bronchial smooth muscle

22. HYPERSENSITIVITY Is a reflection of excessive or aberrant immune response It does not usually occur with first exposure to an allergen, but with re-exposure after sensitization in a predisposed individual

23. TYPES of hypersensitivities Type I/ Anaphylactic Characterized by edema in tissues , larynx and hypotension It is immediate and mediated by IgE antibodies Example:asthma, urticaria,allergic rhinitis,

25. Type II/ Cytotoxic Occurs when the system mistakenly identifies a normal constituent of the body as foreign Involves binding of IgG and IgM antibodies resulting to destruction of cells Example: myasthenia gravis, idiopathic thrombocytopenic purpura, hemolytic anemia

26. Type III/Immune Complex Involves immune complexes formed when antigens bind to antibodies Example: Systemic Lupus Erythematosus, Rheumatoid arthritis

27. Type IV/Delayed type Also called cellular hypersensitivity, occurs 24-72 hours after exposure to an allergen Example: contact dermatitis, mantoux test, transplant rejection

28. ALLERGIC DISORDERS

29. Allergic Rhinitis Also called hay fever, pollinosis Sensitization begins with exposure and on re-exposure the nasal mucosa reacts followed by edema formation and leukocyte infiltration Sx: nasal congestion, watery nasal discharge, sneezing,nasal itching Mgt: Avoid allergens, antihistamine, adrenergics, mast cell stabilizers, corticosteroids

31. Contact Dermatitis Or dermatitis venenata, a type IV hypersensitivity Acute or chronic skin inflammation that results from direct skin contact with chemicals or allergens 80% are due to excessive exposure to irritants Sx: itching, burning, erythema, vesicles, edema, followed by weeping crusting , drying and peeling of the skin

33. Atopic Dermatitis A type I hypersensitivity, affects mostly children Sx: pruritus and hyperirritability of the skin Chronic with remission and exacerbation Mgt: wearing cotton fabrics, using mild detergent, avoiding allergens, moisturizer,

35. Food Allergy IgE mediated hypersensitivity Most common: seafood, legumes, nuts, egg, milk and chocolate SX: urticaria, wheezing, cough, laryngeal edema, swelling of lips, tongue, abdominal pain, cramps, vomiting, diarrhea Mgt: elimination of allergen, H1 and H2 blockers, antihistamine, corticosteroids

36. Serum sickness A type III hypersensitivity, traditionally results from administration of antisera of animal sources Sx: usually begin 6-10 days after administration includes: inflammation of injection site, lymphadenopathy, tender joints, peripheral neuritis, vasculitis Mgt: Antihistamines and corticosteroids

37. Latex Allergy Reaction to natural rubber proteins derived from the rubber tree (Heveabrasiliensis) found in Africa and Southeast Asia. Implicated with rhinitis, conjunctivitis and contact dermatitis Prevention:nonpowdered, low-protein latex and nonlatex gloves.