Lecture 21 Define nosocomial infections and explain their importance. Nosocomial infections: infection acquired during a hospital stay about5-15% of patients acquire them Define compromised host: patients with compromised immune systems List several methods of disease transmission in hospitals. Direct contact Fomites Explain how nosocomial infections can be prevented. Barriers and cleanliness Isolation and quarantine Aseptic technique Surveillance and infection control List several reasons for emerging infectious diseases, and name one example for each reason. Changing sexual mores HIV/AIDS Mass food production Campy, E Coli More exposure to animals Lyme Disease Increased antibiotic use VRSASUMMARY Nosocomial infections, current situation and history Transmission in the hospital Prevention and control Emerging infectious diseases Major factors contribute to emerging InfectionsLecture 22, 23 Identify the principal portals of entry. Mucous Membranes ex) common cold, pneumonia, TB flu, measles Skin ex) conjunctivitis Parenteral Route: deposited directly into tissue, ex) Hep. B Define LD50 and ID50. Infectious dose for 50% of a population ID50 LD50- lethal does for 50% of a pop Contrast the nature and effects of exotoxins and endotoxins. Endotoxins: in the lipid portion of (LPS) of gram negative bacteria Ex) Salmonella typhimurium; U T I, typhoid fever, menengitis Released during cell division or destruction Fever, weakness, shock Stable (to heat) , low toxicity Not easily neutralized Exotoxins: metabolic product of growing bacteria Made of proteins Specific for each cell Unstable (to heat), high toxicity Can be neutralized Small lethal dose Ex) tetanus, botulism, diphtheria, scarlet fever, gas gangrene Understand virulence factors, toxin, toxoid, and antitoxin. Toxin- substance that contributes to pathogency Toxoid- inactivated toxin (often used in vaccines, exotoxin) Virulence factors Antitoxin- antibodies against a specific toxin Outline the mechanism of action of A-B toxins, membrane-disrupting toxins, and superantigens. A-B Toxins- (most exotoxins) released from cell, B attaches to host, enters by cell-mediated endocytosis, A portion alters function of host cell (protein synthesis), B is released from host cell, receptor inserted into plasma membrane for reuse Membrane-disrupting toxins- cause lysis of host cells by disrupting plasma membrane Superantigens- provoke a very intense autoimmune response due to release of cytokines from host cell Explain=how microbes adhere to host cells and=how capsules and cell wall components contribute to pathogenicity. Adherence- attachment of pathogens to host tissue Adhesins or ligands bind specifically to receptors Describe pathogenicity islands and the roles of plasmids and lysogeny in pathogenicity. DNA sequence in genome Plasmids and phage Lecture 24 Differentiate between innate and adaptive immunity. Innate- defenses present at birth, does not involve specific recognition Adaptive- based on a specific response once microbe has breached theinnate immunity Describe=physical and chemical factors=in innate immunity and some=examples. FIRST LINE: intact skin, mucous membranes/ secretions, normal microbiotaSECOND LINE: phagocytes, inflammation, fever, antimicrobial substances THIRD LINE: ADAPTIVE: specialized lymphocytes: T and B cells, antibodies Describe the role of normal microbiota in innate immunity. Define phagocyte and phagocytosis. Phagocyte: perform phagocytosis Phagocytosis: ingestion of a microorganism or other substances by a cell , also involved in cleaning debris Chemotaxis, adherence, ingestion, digestion List the stages and functions of inflammation. Triggers- acute phase proteins are activated Vasodilation- dilation of blood vessel triggered by histimne, kinin prostaglandins and leukotrienes Phagocyte migrations and phagocytosis Tissue repair Describe the cause and effects of fever. Fever caused by hypothalamus releasing prostaglandins (reset body temp) in response to cytokines released by phagocytes in response to endotoxins When temp returns to normal: crisis Describe three pathways of activating complement. Classical- antibodies bind to antigens (microbes) activate C1-> activates C2 and C4 Alternative- doesn’t involve antibodies, direct contact between compliment proteins and pathogen Lectin- macrophages ingest bacteria, release cytokines and liver produces lectins (proteins that bind to carbohydrates) Describe three consequences (functions) of complement activation. Opsonization- enhancement of phagocytosis by coating with C3b Inflammation- increase blood vessel permeability and chemotactic attraction of phagocytes: C3a and C5a Cytolysis- microbe bursts due to inflow of extracellular fluid thru transmembrane channel formed by membrane attack complex C5b and C6-9 Understand the actions of interferons.- bind to cell receptor and trigger gene expression Interferons- antiviral proteins; interfere with viral replication Alpha- luekocytes Beta- fibroplasts Gamma- Th1 and NK cells Lecture 25 Differentiate between innate and adaptive immunity.Adaptive: specific antibody and lymphocyte response Differentiate between humoral and cellular immunity. Humoral: antibodies produced by B-cells Recognize antigens by antibodies on surfaces, mature in bone marrow, Cell-mediated: involves T-cells Recognize antigens by TCRs on surface, T-cells matures in thymus Define antigen, epitope, hapten, antibody, immunoglobulin (Ig). Antigen: substace that causes body to produce specific antibodies Epitope: region on antigens recognized by antibody Hapten: too small to stimulate antibody formation alone, must combine with a carrier molecule Antibody: proteins made in response to an antigen that specifically recognize antigens Immunoglobin: antibodies Explain the function of antibodies, and describe their structural and chemicalcharacteristics. Typical: 4 protein chains, 2 light and 2 heavy joined by disulfide links Name five classes of antibodies (Igs) and know their differences.== IgG- 80% of serum, monomer, in lymph, blood, intestine, longest life, enhances phagocytosis, neutralizes toxins and viruses,
View Full Document
Unlocking...