Micro Final Review - Lecture notes CH 15, and 21-26 PDF

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Notes on final exam of BIOL 1353 with Knapp...

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FA 17 1353: EXAM 4 Review (CH 15 & Selected Diseases from CH’s 21-26) Chapter 15 (Microbial Pathogenesis .Concept of: Pathogenicity  Virulence  Virulence factors; infectivity vs. virulence a. Pathogenicity: ability to cause disease; directly relates to # of virulence factors b. Virulence: the degree or extent of pathogenicity c. # of virulence factors directly relates to how infectious it may be d. More virulence factors = how effective it can cause infections e. Virulence factors: anything pathogens have to do to get into body ->virulence genes (gene types that can be passed from cell to cell) i. Adherence ii. Cell invasion iii. Immune Response Inhibitors iv. Colonization v. Toxins b) Disease process: Pathogen enters host  penetrate host defenses  cause damage to host a. Enter hosts i. Adhesion; numbers of infecting microbes b. Penetrate host defenses i. Capsule ii. Enzymes iii. Fimbriae iv. Pili c. Damage host i. Toxins ii. Intracellular pathogens (Ex: lytic cycle of a virus) c) Portals of Infection a. Skin/Mucous membranes/Parenteral route: be able to distinguish between these three types and what characterizes each; preferred portal of entry for a pathogen b. Pathogen enters host: Portals of Entry i. Mucous Membranes: respiratory tract; gastro-intestinal (GI) tract; genitourinary tract ii. Skin: Hair follicles, sweat glands, conjunctiva (eye; pink eye) iii. Parenteral route: deposition of microbes directly under skin or mucous membrane

a)

d) Numbers of invading microbes a. LD50 and ID50 (measures of virulence); be able to interpret data from these b. ID50 (infectious dose 50%)- Infections dose needed to cause disease symptoms in 50% of experimental hosts i. Bacillus antracis –antrax portal entry

c.

1. Portal of entry Skin (cutaneous anthrax) Inhalation (deadliest)

ID50 10-50 endospores 10,000-20,000 endospores

Ingestion (rarest)

250,000-106 endospores

LD50 (lethal dose 50%)- dose of pathogen required to kill 50% of experimental group of animal hosts  Measure of potency i. If an organism takes less dosage but the percent of mortality is faster, than it is more deadly ii. Toxin Botulinum (Botox) Shiga toxin Staphylococcal enterotoxin

iii.

LD50 .03 ng/kg 250 ng/ kg 1350 ng/kg

e) Enter host: a. adherence (adhesins/ligands of pathogen) bind to glycocalyx/fimbriae/pili/M protein (Streptococcus) i. Adherence: pathogens attaching themselves to host tissues at their portal of entry ii. Adhesins or ligands: attachment between pathogen and host accomplished by means of surface molecules 1. Bind specifically to complementary surface receptors on the cells of certain host tissues 2. Adhesins located on : a. Glycocalyx b. Fimbriae c. Pili d. M protein (streptococcus); role more towards avoidance/evasion i. Involved in many types of skin infections ii. Attachment function iii. Antiphagocytic properties 1. Interferes w/ complement activation b.

iv. Biofilm formation: exopolysaccharide formation  form plaque (on teeth); form on catheters, heart valves i. Microbial community contained in an exopolysaccharide matrix; adhere to surfaces 1. Very resistant

f)

g)

h)

Penetration of host defenses a. Capsule: Impairs phagocytosis by host cells b. Cell wall components i. M protein: streptococcus pneumoniae (resists phagocytosis, glycoproteins on surface of Strept. that fight host defenses, inactive complement) ii. Opa protein of Neisseria gonorrhea & others : facilitates entry into cells iii. Cell wall mycolic acids of Mycobacterium tuberculosis (tuberculosis, leprosy, thick cell wall, material penetrates very slowly, intracellular) c. Exoenzymes: coagulases/hyaluronidase/collagenase/proteases; extracellular enzymes; allows deeper penetration into tissues, must get through skin first, penetrate skin through wound, more virulent i. Coagulases: clot blood; isolate bacteria from host (staphylococci) 1. Fibrino(coagulase)Fibrin ii. Hyalurondinase: hydrolyzes hyaluronic acid, polysaccharide bridging cells of connective tissue  allows microbe to spread (streptococcus) iii. Collagenase: Digests collagen; in connective tissue of muscles, organs, tissue iv. Proteases: destroy host proteins; igA protease (Nesseria: entry through mucous membrane) binds to pathogen and prevents it from attaching to host cell 1. Kinasesdestroy blood clots; streptokinase d. viii. Antigenic variation: Alteration of pathogen surface proteins; possess alternate genes (Neisseria) i. Only works with ONE antigen type; immune avoidance ii. Type 1 flagellin protein type 1 antibody attached to type 1 flagellin protein new generation type 2 iii. Can proliferate until body catches up to immune response; during the time type 2 can cause damage e. Invasins (Salmonella)  manipulate cell cytoskeleton; induce membrane ruffling of cell; causes engulfment and subsequent entry of bacterium Host cell damage a. Use host nutrients ‐ scavenge iron (siderophores) i. Iron is a limiting nutrient for pathogens in the body 1. Required for growth of most pathogenic bacteria 2. Iron chelators binds molecules up for itself (chelators bind any molecule up) 3. Siderophores released in order to take away from iron-transport proteins by binding the iron even more tightly a. Once iron-siderophore complex is formed, it is taken up by siderophore receptors on bacterial b. Direct damage by penetrating cells (intracellular pathogens) i. viruseslytic infection c. Production of toxins: transported by blood, lymph i. Inhibit protein synthesis ii. Disrupt membrane function d. Induction of hyerpsensitivity reactions i. Overproduction of cytokines

Exotoxins: i.

toxigenicity/toxemia; general features of toxins; antitoxins (toxoids)-provide immunity 1. Toxigenicity: capacity of microorganisms to produce toxins 2. Toxemia: presence of toxins in the blood 3. General features of toxins: exotoxin and endotoxin

ii. Exotoxins are secreted to the surrounding the environment iii. Water soluble proteins (many are enzymes); most are plasmid-based or in phages (lysogenic conversion) iv. Action: destroy specific host cell structures or inhibit metabolic functions; can be very lethal b. A‐B toxins (botulism toxin, tetanus toxin, vibrio enterotoxin, diphtheria toxin) i. Consist of an active enzyme component (A) and a cell binding component (B) 1. (A) gets in, (B) binds to cell ii. Botulism toxin: (Clostridium botulinum ) neurotoxin; prevents nerve impulses to muscles; causes flaccid paralysis; muscles can’t contract (gram+) iii. Tetanus toxin: (clostridium tetani) neurotoxin tetanospasmin; blocks inhibitory nerve impulses to muscles; causes spasmodic contractions; *tetatnus shot= antitoxins (gram+) iv. Vibrio enterotoxin: (vibrio cholorae) cholera toxin; causes cellular secretion of fluids & electrolytes  severe diarrhea & dehydration v. Diphtheria toxin: (Corynebacterium diphytheriae) inhibits protein synthesis; phage carries tox gene c. Superantigens: stimulate intense immune response of T cells, excessive cytokine production; regulate immune response i. Excessive cytokine levels: enter blood stream & induce symptoms; can lead to shock & death ii. Erythrogenic toxin (Streptococcus); Staphylococcal enterotoxin 1. Erythrogenic toxin (Streptococcus pyogenes): damage blood capillaries under skin rash; scarlet fever 2. Staphylococcal enterotoxin (S. aureus) iii. Membrane disrupting toxins (hemolysins/leukocidins) 1. Cause lysis of host cells by disrupting the plasma membrane by a. Forming protein channels in membrane or by disrupting phospholipids i. Leukocidins: kill phagocytic white blood cells ii. Hemolysins: kill red blood cells (streptolysins) d. Endotoxin: Gram‐negative cells – Lipid A of LPS Layerreleased when cells die & lyse i. Endotoxins: toxins composed of lipids that are part of the cell membrane ii. Endotoxic shock: drastic drop in blood pressure 1. TLR will respond to PAMPS (Pathogen Associated Molecular Pattern; can be Lipid A material) a. Gram (-) cells dielipid Ainto macrophage releases cytokines which can release i. Clotting factorscapillaries blocked ii. IL2 (interleuken; acts on hypothalamus) fever iii. Vasoactive factorsfluid lossblood volume drops  blood pressure dropsshock b. Septic infection: shock caused by bacteria and in the blood i. Can affect cells and tissues e. h. Cytopathic effects of Virus‐infected cells (cyticidal & non‐cytocidal effects) i. include syncytium formation and formation of granules, interferon production, antigenic changes on cell surface 1. Evading host defenses grow inside host cells 2. Cytopathic effects: visible effect of viral infection a. Cytocidal effects: results in cell death i. Cytocidal viruses stop host cell biosynthesis & induce cell’s lysosomes to release contents ii. Inclusion bodies/ granules in some infected cells

1.

iii. iv. v. vi.

Are usually viral parts (nucleic acids, proteins) to be assembled; can be diagnostic Infected cells may fuse to form multinucleate syncytium Oncogenic viruses transform cells into cancerous cells Some virus-infected cells form interferons, protects noninfected cells Viral infection induces antigenic changes on cell surface – rid body of infected cell 1. Tc Cells, NK cells (handles virus infected cells)

i. Portals of exit: Secretions, excretions, discharges, tissue that is shed i. Related to the part of the body that was infected ii. Generally, microbe uses the same portal for entry & exit 1. Mucous membranes 2. Skin 3. Parenteral route iii. Most common: respiratory tract & GI tract Chapter 21‐26 (Selected Diseases): g. a. Chapter 21: Microbial Diseases of the Skin i. i. Staphylococcus: S. aureus; Gram-positive cocci in grape-like clusters; S. aureus virulence factors (toxins, hyaluronidase, coagulase); opportunistic pathogens 1. S.epidermidis (coagulase negative); nosocomial pathogen; possess slime layer a. Can penetrate skin via catheter insertion 2. S.aureus (coagulase positive); possesses a number of virulence factors a. Toxins: anti phagocyte b. Resists opsonization c. Neutralizes AMPS of host d. Lysozyme resistant e. Antibiotic resistant (MRSA, VRSA) 3. Staphylococcal skin infections: boils, carbuncles, impetigo, scalded-skin syndrome; toxic shock syndrome a. Acute diseases i. Furuncle (Boils): abscess; pus surrounded by inflamed tissue ii. Carbuncle: inflammation of tissue under the skin iii. Impetigo: crusting (nonbullous) sores, spread by autoinoculation iv. Sty: folliculitis of an eyelash b. Non‐acute disease i. Scalded‐skin syndrome: Form of impetigo (bullous) due to toxins; causes separation of skin layers 1. Hyaluronidase, collagenase: enzymes that allow for penetration in the tissue ii. Toxic shock syndrome: ii. ii. Streptococcus: Gram-positive cocci in chains: characterize pathogen types by appearance on blood agar - alpha, beta, gamma (what do these mean?) iii. 1. 1. alpha-, beta-, and gamma-hemolytic strep: what are they, what diseases do they cause? a. Alpha‐hemolysis: Partial hemolysis (greenish color); Streptococcus Pneumoniae  Pneumonia meningitis i. A‐hemolysis also forms viridans: S. Mutans 1. Dental caries 2. Plaque f.

iv.

3. Biofilms 4. Endocarditis b. Beta‐hemolysis: complete hemolysis (complete clear zone around growth); Group A Streptococci; Streptococcus pyogenes Strep throat, scarlet fever, necrotizing fasciitis c. Gamma‐hemolysis: NO hemolysis; Enterococcus species i. Gastrointestinal upsets (GI tract issues) 2. Streptococcal skin infections: S. pyogenes virulence factors (capsule, streptolysin/streptokinase/M protein), Necrotizing fasciitis, secondary immunological responses sequelae (antibodies cross react) a. S.pyogenes virulence factors: i. M Protein: Prevents complement activation; kills neutrophils, faciliatates adherence ii. “Heavy” capsule –made of hyaluronic acid (non antigenic) 1. Non antigenic because it is a component of our own tissues iii. Produces streptokinase, hyaluronidase, streptolysin, exotoxin A (superantigen) iii. Viral: Herpesvirus‐varicella zoster chickenpox  shingles (latent disease)

CH 22: Microbial Diseases of the Nervous System i)

i. Bacterial Meningitis; meningococcal meningitis (Neisseria meningitidis); virulence factors (capsule, pili, phase variation, endotoxin); diagnosis; Gram-negative diplococci a. Neisseria meningitis: 40% of people are healthy nasopharyngeal carriers b. Begins as throat infection, rash leading to bacteremia  meningitis; fatal after onset of fever j) Tough for pathogens to pass blood brain barrier a. Initial symptoms of fever, headache, and stiff neck  followed by nausea and vomiting  may progress to convulsions and coma b. Diagnosis by gram stain and latex agglutination of CSF c. Healthy CSF free of bactiera k) i ii. Listeria monocytogenes: foodborne a. Ingestion of contaminated food  milk, dairy foods, processed meats (deli meats, hot dogs), smoked seafood, raw vegetables b. Characterized by flu-like symptoms & GI symptoms i. For most: asymptomatic or a mild illness ii. Serious form: septicemiameningitis, meningoencephalitis; >25 % mortality c. Illness primarily among pregnant women, infants, elderly, immunocompromised persons d. Etiologic agent listeria monocytogenes i. Small, Gram-positive rods ii. Widely distributed in soil/ water iii. In mammals, birds, fish, insects e. Pathogenesis/ virulence factors i. Adherence: D-galactose on surface binds host cell receptor ii. Produce invasins: allows for penetration of host cells induces phagocytosis 1. Infect epithelial cells of GI; multiples intra- and extra-cellularly 2. Host defense  primarily T cells (Tc), interferon iii. Polymerization of host cell actin  form “actin rockets”; propels cells into, within, and between host cells iv. Produce 1. Hemolysins 2. Phospholipase C 3. Protease

4.

l)

Growth at low temperature 5. Contaminated foodgutlymph nodes blood stream: spleen and liver; brain and placenta

v. Non-invasive/invasive listerosis vi. Pregnant women: cross placenta; can lead to still born, aborted, or acutely ill infant vii. Prevention: effective sanitation of food contract surfaces; refrigerate foods...