Micro Lecture CH15

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  1. Identify the principal portals of entry.
    Pathogens can gain entrance to the human body and other hosts thru several avenues, which are called the the portals of entry

    • Skin
    • Parenteral (injection, bite)
    • Mucous membranes (most common route)
    • –Repiratory tract
    • –Urogenital
    • –Placenta
    • –Gastrointestinal Tract

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    • Many microorganisms can penetrate mucous membranes of the conjunctiva and the resporatory, gastrointestinal and genitourinary tracts.
    • Most microorganisms cannot penetrate intact skin; they enter thair follicles and sweat ducts
    • some microorganisms can gain access to tissues by inoculation thru the skin and mucous membranes in bites, injections and other wounds. This route of penetration is called the parenteral route

    • The preferred portal of entry:
    • many microorganisms can cause infections only when they gain access thru their specific portal of entry
  2. Define LD50 and ID50.
    •Higher number of pathogens increase the likelihood of developing disease.

    • •ID50:(infectious dose 50)
    • Infectious dose for 50% of the test population. Number of microbes that will cause a demonstrable infection in 50% of inoculated test animals.

    • •LD50: (lethal dose 50)
    • Lethal dose (of a toxin) for 50% of the test population.
    • Number of microbes that will kill 50% of inoculated test animals.
  3. Using examples, explain how microbes adhere to
    host cells.
    • Adherance: Attachment between of microbe to host
    • tissue requires. adherance is done by-
    • Adhesions/ligands: Surface molecules on pathogen that bind specifically to host cell surface molecules.

    • Glycocalyx: Streptococcus mutans, a bacterium that plays a key role in tooth decay by attaching to the surface of teeth by its glycocalyx (external sticky stuff)
    • Fimbriae: Escherichia coli**, use fimbriae to adhere only to specific kinds of cells in certain regions of the small intestines(external spikes)
    • M protein: Streptococcus pyogenes, the M protein mediates attachment of the bacterium to epithelial cells of the host and helps the bacterium resist phagocytosis by white blood cells (adheres to mucosal cells of throat)
    • Opa protein: Neisseria gonorrhoeae, use both Opa, an ourter membrane protein, and fimbriae containing adhesins, which in this case permit attachments to cellswith appropropriate receptors in the genitourinary tract, eyes, and pharynx (adheres to genital/urinary cells)
    • Tapered end: Treponema pallidum, uses tapered endas a hook to attach to host cells(used to bind to genital/urinary cells)
  4. Explain how capsules and cell wall components
    contribute to pathogenicity.
    • Capsules
    • •Greatly increases the virulence of many pathogens.

    •Examples: Streptococcus pneumoniae, Klebsiella pneumoniae, Hemophilus influenzae, Bacillus anthracis, and Yersinia pestis.

    Resist host defenses by preventing host cells from recognizing and engulfing (like the trojen horse)

    Cell wall components are M proteins and Opa (on flashcard 3)
  5. phagocytes
    • •Phago: from Greek, meaning eat
    • •Cyte: from Greek, meaning cell

    •Phagocytes are human cells that normally protect us by ingesting foreign objects

    •Some bacteria can survive and reproduce in phagocytes
  6. Enzymes
    Extracellular enzymes (exoenzymes) lyse cells, form or dissolve clots, and dissolve materials in tissue.

    • Coagulase: Coagulate blood
    • Kinases: Digest fibrin clots
    • Hyaluronidase: Hydrolyses hyaluronic acid
    • Collagenase: Hydrolyzes collagen
  7. Define and give an example of antigenic variation.
    some pathogens can alter their surface antigens by a process called antigenic variation

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    • Trypanosoma brucei (a protozoan sleeping sickness)
    • transmitted by the tsetse fly vector
    • when its in the fly, it only has one antigenic varient on their protein coat
    • when the tsetse fly bites humans, 1000's of varients can be found on their protein coat which hides them from us

    • Trypanosomes:
    • •Surface antigens vary with life cycle stage
    • –Insect stages have one antigen/gene
    • –Initial vertebrate infection (single antigen/gene)
    • –Once in the blood,over 1000 varients (multiple genes/multiple antigens)

    • •Antigenic variation involves changing which antigen is
    • expressed (protein), DNA recombination (combination antigens) or DNA gene conversion (new antigen)

    • •Many internal copies, 1000+ antigens
    • –Abundant gene duplication may increase antigenic repertoire
  8. Describe how bacteria use the host cell’s cytoplasm to enter the cell.
    • Penetration into Host Cells
    • •Invasins: Surface proteins that alter actin filaments of host cell cytoskeleton, allowing microbes to enter cells.

    •Examples: Salmonella typhinurium and E. coli.
  9. How bacterial cells damage host cells
    Four mechanisms:

    • –1.Using the host’s nutrients
    • •Siderophores: Take iron from host iron-binding proteins

    –2.Direct damage

    –3. Toxins*

    • –4. Hypersensitivity Reactions (discuss later)*
    • Most bacterial damage is carried out by toxins.
  10. Describe the function of siderophores.
    Take iron from host iron-binding proteins (stealing iron from the host)
  11. Provide an example of direct damage, and compare this to toxin production.
    • Direct Damage:
    • •Some bacteria can induce host cells to engulf them (E. coli, Shigella, Salmonella, and Neisseria gonorrhoeae).-after inside the cell, they steal the nutrients and produce waste products. this kills the host cell
    • •Microbial metabolism and multiplication kills host cells. (bursing the host's cells)
    • •Other microbes enter the cell by excreting enzymes or through their own motility. such penetration can itself damage the host cell

    • Most damage by the bacteria is done by Toxins:
    • Toxin: Substances that contribute to pathogenicity.
    • Toxigenicity: Ability to produce a toxin.
    • Toxemia: Presence of toxin in the host's blood.(the illness)
    • Toxoid: Inactivated toxin used in a vaccine.(used to make vaccines)
    • Antitoxin: Antibodies against a specific toxin.

    • •Two types of toxins:
    • –Exotoxins
    • –Endotoxins

    Some toxins produce fever, cardiovascular disturbances, diarrhea and shock. Toxins can also inhibit protein synthesis, destroy blood cells and blood vessels, and disrupt the nurvous system by causing spasms.
  12. Contrast the nature and effects of exotoxins and endotoxins.
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    • Exotoxin: (called exo because its outside)
    • bacterial source-mostly from gram-pos bacteria
    • relation to microorganism-metabolic product of growing cell
    • chemistry-proteins, usually with two parts (A-B)
    • Pharmacology (effect on body)-Specific for a particular cell structure or function in the host (mainly affects cell functions, nerves, and gastrointestinal tract)
    • heat stability- Unstable; can usually be destroyed at 60-80*C (except staphylococcal enterotoxin)
    • Toxicity (ability to cause disease)- high
    • fever-producing- No
    • Immunology (relation to antibodies)- can be converted to toxiods to immunize against toxin; neutralized by antitoxin
    • Letal dose- small
    • represetative disease- gas gangrene, tetanus, botulism, diphtheria, scarlet fever

    • Endotoxin:
    • bacterial source-Gram-Neg bacteria
    • Relation to microorganism: Present in LPS of outer membrane of cell wall and released with destruction of cell or during cell division
    • chemistry-Lipid portion (lipid A) of LPS outer membrane (lipopolysaccharide.)
    • Pharmacology (effect on body)-General, such as fever, weaknesses, aches, and shock; all produce the same effects
    • heat stability- stable, can withstand autoclaving (121*C for 1 hour)
    • Toxicity (ability to cause disease)- low
    • fever-producing- Yes
    • Immunology (relation to antibodies)- Not easily neutralized by antitoxin; therefore, effective toxiods cannot be made to immunize against toxin
    • Letal dose- considerably larger
    • represetative disease- typhoid fever, UTIs and meningococcal meningitis

  13. Exotoxins
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    • Exotoxins
    • produced inside some bacteria as part of their growth and metabolism and are secreated by the bacterium into the surrounding medium or relased following lysis.
    • Exotoxins are Proteins: Enzymes that carry out specific reactions. (because of the enzymatic nature of most exotoxins, even small amounts are quite harmful because they can act over and over again)
    • -Bacteria that produce extotoxins may be gram-pos or gram neg
    • Soluble in body fluids, rapidly transported throughout body in blood or lymph.
    • –Most genes for toxins are carried on plasmids or transmitted by phages.
    • -Produced inside bacteria and released into host tissue
    • –Responsible for disease symptoms and/or death.

    • Cytotoxins: Kill or damage host cells.
    • Neurotoxins: Interfere with nerve impulses.
    • Enterotoxins: Affect lining of gastrointestinal tract.

    Antibodies called antitoxins provide immunity
  14. Outline the mechanisms of action of A-B toxins, membrane-disrupting toxins, and superantigens.
    • A-B toxins
    • 1. in the first step, the A-B toxin is released from the bacterium
    • 2. the B component attaches to host cell receptor
    • 3. the plasma membrane of the host cell invaginates (folds inward) at the point where the A-B exotoxin and plasma receptor make contact, and the exotoxin enters the cell by endocytosis
    • 4. the A-B exotoxin and receptor are enclosed by a pinched-off portion of the membrane
    • 5. the A-B components of the exotoxin separate. The A component alters the function of the host cell, often by inhibiting protein synthesis. The B component is released from the host cell, and the receptor is inserted into the plasma membrane for reuse.
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    • Membrane-disrupting toxins:
    • cuase lysis of host cells by disrupting their plasma membranes
    • some do this by forming protein channels on the plasma membrane
    • others disrupt the phospholipid portion of the membrane

    • Superantigens:
    • provoke a very intense immune response
    • thru a series of interactions with various cells of the immune system, superantigens nonspecifically stimulate the proliferation of immune cells called T cells. (types of WBCs that act against foreign organisms and tissues and regulate the activation and proliferation of other cells of the immune system
    • In response to superantigens, T cells are stimulated to release enormous amounts of chemicals called cytokines (small protein molecules produced by various body cells, esp T cells)
    • the excessively high levels of cytokines released by T cells enter the blood stream and give rise to a number of symptoms including fever, nausea, vomiting, diarrhea and sometimes shock and even death
  15. Endotoxins
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    –Part of outer membrane surrounding gram-negative bacteria.

    • Endotoxin is lipid portion of lipopolysaccharides
    • (LPS), called lipid A.

    –Effect exerted when gram-negative cells die and cell walls undergo lysis, liberating endotoxin.

    • –All produce the same signs and symptoms:
    • •Chills, fever, weakness, general aches, blood clotting and tissue death, shock, and even death. Can also induce miscarriage.

    •Fever:Pyrogenic response is caused by endotoxins.

    • Does not respond well to the lipids:
    • Endotoxins do not promote the formation of effective antibodies.

    • –Organisms that produce endotoxins include:
    • • Salmonella typhi
    • •Proteus spp.
    • •Pseudomonas spp.
    • •Neisseria spp.

    –Medical equipment that has been sterilized may still contain endotoxins.

    •Limulus amoebocyte assay (LAL) is a test used to detect tiny amounts of endotoxin.

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    • Events leading to fever:
    • 1.Gram-negative bacteria are digested by phagocytes.
    • 2.LPS is released by digestion in vacuoles (because when the lysosomes of the macrophage broke it down, it released the LPS from the bacteria's cell walls), causing macrophages to release interleukin-1 (IL-1).
    • 3.IL-1is carried via blood to hypothalamus, which controls body temperature.
    • 4.IL-1 induces hypothalamus to release prostaglandins, which reset the body’s thermostat to higher temperature.
  16. Using examples, describe the role of plasmids and lysogeny in pathogenicity.
    • Plasmids: Small, circular pieces of DNA that are not connected to chromosome and are capable of independent replication.
    • R (resistance) factors contain antibiotic resistance genes.
    • –Other plasmids contain genes for toxins and pathogenic factors: tetanus toxin, staphylococcal enterotoxin, E. coli enterotoxin (heat-labile), adhesins, and coagulase.

    • Bacteriophages and Transduction:
    • Can incorporate genetic material into chromosomal DNA and remain latent (lysogeny).
    • Bacterial cell can change characteristics (lysogenic conversion) and produce certain toxins or pathogenic factors:
    • –Diphtheria toxin
    • –Capsules in S. pneumoniae
    • –Botulinum neurotoxin
    • –Staphylococcal enterotoxin
    • –Cholera toxin

    • Lysogeny- when some bacteriophages (viruses that infect bacteria) can incorporate their DNA into the bacterial chromosome, becoming a prophage and thus remaining latent (do not cause lysis of bacterium).
    • So cells containing a prophage are said to be lysogenic.
    • Once outcome of lysogeny is that the host bacterial cell and its progeny may exhibit new properties encoded by the bacteriophage DNA (lysogenc conversion)
    • As a result of lysogenic conversion, the bacterial cell is immune to infection by the same type of phage
  17. List nine cytopathic effects of viral infections.
    Viral infection may result in one or several of the following cytocidal (kill cells) or noncytocidal effects in infected cells:

    1. Inhibit macromolecular synthesis (DNA, RNA, protein). Some viruses irreversibly stop mitosis (herpes simplex virus).

    2. Release of lysosomal enzymes, resulting in cell death.(punching holes in your lysosomes)

    3. Inclusion bodies: make granules in cytoplasm or nuclei of infected cells. May contain viral parts.

    4. Syncytium: Fusion of several adjacent cells to form a single giant cell (cytoplasmic mass).

    5. Metabolic changes in host without visibly damaging infected cells. May increase hormone or protein production by infected cells, which in turn affects other cells.

    6. Interferons: viral infection induces cells to produce interferons, but the host's cell's DNA actually codes for the interferon. This protects neighboring uninfected cells from viral infection

    7. Antigenic changes on cell surface, causing destruction of infected cells by immune system. (putting tags on other cells making your immune system attack you)

    8. Chromosomal changes: Breakage and incorporation of oncogenes.

    9. Transformation: Abnormal cells that have lost contact inhibition.(which forms lumps)
  18. Discuss the causes of symptoms in fungal, protozoan, helminthic, and algal diseases.
    • Fungal:
    • •Fungal waste products may cause symptoms.
    • •Chronic infections provoke an allergic response.
    • Tichothecene toxins inhibit protein synthesis.
    • –Fusarium
    • •Proteases (chops up the innards of your cells)
    • Candida, Trichophyton
    • Capsule prevents phagocytosis
    • –Cryptococcus
    • Ergot toxin (produced by fungus, gets mixed into grains; hallucenagenic toxin)
    • –Claviceps
    • •Aflatoxin (in peanut butter)
    • –Aspergillus (inhaled/ingested)
    • •Mycotoxins
    • –Neurotoxins: Phalloidin, amanitin (ingested)
    • -Amanita

    • Protozoan
    • Just their presence can cause disease
    • •Protozoan waste products may cause symptoms.
    • •Avoid host defenses by
    • –Growing in phagocytes
    • Antigenic variation (change their outside protein coats to hide from immune system)

    • Helminthic:
    • •Use host tissue.
    • •Presence of parasite interferes with host function.
    • •Parasite's metabolic waste can cause symptoms.

    • Algal: (protist kingdom)
    • •Paralytic shellfish poisoning
    • –Dinoflagellates (red tide)
    • •Domoic acid intoxication
    • –Diatoms
  19. Compare and contrast portal of entry and portal of exit.
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    • Portals of Exit
    • Respiratory tract
    • Coughing and sneezing
    • Gastrointestinal tract
    • Feces and saliva
    • Genitourinary tract
    • Urine and vaginal secretions
    • Skin
    • Blood
    • Biting arthropods and needles or syringes
  20. Virulence
    degree of pathogenicity
  21. Pathogenicity
    the ability of a pathogen to produce a disease by overcoming the defenses of the host
  22. The most frequently used portal of entry for pathogens is the

    A) Skin.

    B) Mucous membranes of the respiratory tract.

    C) Mucous membranes of the gastrointestinal tract.

    D) Parenteral route.
  23. The ID50 is a

    A) Measure of pathogenicity.

    B) Dose that will cause an infection in some of the test

    C) Dose that will kill 50% of the test population.

    D) Dose that will cause an infection in 50% of the test
  24. Which of the following does not contribute to a
    pathogen's invasiveness?

    A) Toxins

    B) Hyaluronidase

    C) Adhesins

    D) Capsule
  25. Endotoxins are

    A) Associated with gram-positive bacteria.

    B) Specific in their method of action.

    C) None of the answers.

    D) Excreted from the cell.
  26. Septic shock due to gram-positive bacteria is caused by

    A) Lipid A.

    B) A-B toxins.

    C) Superantigens.

    D) Membrane-disrupting toxins.
  27. A needlestick is an example of which portal of entry?

    A) Skin

    B) Parenteral route

    C) Mucous membranes

    D) None of the answers
  28. Gram-negative fever results from the following events.
    What is the second step?

    A) Phagocytes ingest gram-negative bacteria.

    B) LPS is released from gram-negative bacteria.

    C) Body temperature is reset in the hypothalamus.

    D) IL-1 is released.
  29. Which of the following organisms causes the most severe disease?

    A) E. coli O157:H7 ID50=20

    B) Shigella ID50=10

    C) Treponema pallidum ID50=57

    D) Can't tell
  30. All of the following can occur during bacterial infection.
    Which would prevent all the others?

    A) destruction of adhesins

    B) vaccination against fimbriae

    C) inhibition of phagocytic digestion

    D) phagocytosis
  31. Which of the following statements is true?

    A) The primary goal of a pathogen is to kill its host.

    B) Evolution selects for the most virulent pathogens.

    C) A successful pathogen doesn't kill its host before it is transmitted.

    D) A successful pathogen never kills its host
  32. An encapsulated bacterium can be virulent because the capsule

    A) destroys host tissues

    B) is an endotoxin

    C) interferes with physiological processes

    D) resists phagocytosis
  33. The earliest smallpox vaccines were infected tissue
    rubbed in the skin of a healthy person. The recipient usually developed a mild case of smallpox, recovered and was immune thereafter. The most likely reason
    this vaccine did not kill more people is

    A) Skin is the wrong portal of entry for smallpox.

    B) The virus cannot be passed from skin to skin contact.

    C) The vaccine consisted of a mild form of the virus.

    D) The virus mutated.
  34. The degree of pathogenicity of a microbe is called its
  35. Adhesins (ligands) are commonly made of
  36. Bacteria get iron from the host using
  37. Many genes for antibiotic resistance, toxins and
    capsules are carried on ______________.
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Micro Lecture CH15
2011-06-29 20:48:37
Micro Lecture CH15 Test

Micro Lecture CH15
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