z-MicroBio Final – Ch. 21 – Flashcards
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| Mutualism |
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| both host and microbe benefit |
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| Commensalism |
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| microbe causes no damage to host |
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| Pathogenic relationship |
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| microbe causes damage to host |
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| Normal Flora |
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| microorganisms normally found in or on the body that typically do not cause disease |
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| Synergistically |
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| capable of working together; two microorganisms are synergistic if they are able to produce a host response greater than the sum of the effects they produce when acting alone |
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| Communicable |
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| able to be transmitted between hosts |
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| Disease reservoir |
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| a natural source of disease agent. Reservoirs may include sick patients, asymptomatic carriers, animals, recovered patients, environmental sources, etc |
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| virulence |
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| The measure of degree pathogenicity |
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| opportunistic pathogen |
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| if host defense mechanisms are weakened, it becomes an opportunistic pathogen. Examples: AIDS patient: Pneum. carnei Woman whose normal flora are killed by antibiotics frequently gets this Candida yeast infection. Aspergillis niger eye infection in immunocompromisedhost. |
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| Compromised Host |
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| Compromised Host has lowered resistance to infection and ultimately disease. Malnutrition, Alcoholism Trauma from surgury or an injury Cancer or leukemia Diabetes Immunosupression due to drugs, viruses like HIV, genetic deficiencies Altered normal flora due to antibiotics |
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| Infection |
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| refers to any situation in which a microorganism is established and growing in or on a host, regardless of whether or not the host is harmed !! |
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| Infestation |
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| Presence of organism; not growing and reproducing; just presence |
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| Disease |
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| damage or injury to the host that impairs host function. Infection is not synonymous with disease!!!!! Normal flora can sometimes cause disease if the host resistance is compromised!!!! |
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| Internal tissues Free from Bacteria |
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| brain, blood, cerebrospinal fluid, muscles. Genitourinary Tract-upper [kidney, ureters, & uninary bladder. Stomach (Mycobacteria, Salmonella are resistant.) |
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| Entry of Pathogen |
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| [image] |
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| Adherence |
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| Bacteria or viruses usually initiate infection by adhering specifically to epithelial cells through interactions between macromolecules on surfaces of the pathogen and host. |
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| Tissue Selective |
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| Neisseria gonorrhoeae adheres more strongly to urogenital epithelium (tissue specificity). Opa surface protein binds with host CD66 protein. |
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| Host Selectivity |
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| a microorganism that normally infects humans binds to human epithelial cells better than those of a rat |
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| Capsules |
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| glycocalyx or slime layer (loose network of polymer fibers) may be involved in adherence. |
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| Fimbriae & Pili |
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| are bacterial surface proteins structures that also function in attachment (bind host cell glycoproteins).Enterotoxic strains of E. coli express fimbrial proteins called CFA (Colonization factor antigens) that adhere specifically to cells in small intestine. Produce enterotoxins. |
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| Virulence |
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| Invasiveness: grow in large numbers and may spread throughout host body Toxigenicity: toxins that inhibit host cell function or kill host cells. Two types: Exotoxins & Endotoxins |
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| Resistance |
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| Acquired or Induced Immunity(Resistance) Humoral Immunity: mediated by antibodies Cellular Immunity: mediated by cells (T cells) Natural Resistance or Innate Immunity Cells: macrophages Mechanical Barriers: skin & mucous membranes Chemical Factors: interferon, fatty acids on skin Microbial Factors: Normal flora competition |
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| Virulence Factors: Invasiveness |
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| Hyaluronidase Coagulase Fibrinolysin Lipase Collagenase Leukocidins Streptokinase and Streptodornase |
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| Hyaluronidase |
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| This is also called the spreading factor because it catalyzes the breakdown of hyaluronic acid, the substance that cements the human cells together. This allows the bacterial cells to spread through tissue causing a condition known as cellulitis.[Staphyloccus, Streptococcus & Clostridia] |
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| Coagulase |
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| This enzyme catalyzes the conversion of fibrinogen to fibrin with resultant clot formation. Present in pathogenic Staphyloccus. |
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| Fibrinolysin |
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| This catalyzes the conversion of plasminogen to the fibrinolytic enzyme plasmin. Thus it acts opposite of coagulase. In Staphylococcus aureus, the gene for fibrinolysin is on a bacteriophage and is expressed during lysogeny. |
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| Lipase |
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| Production of excessive amounts of lipase allow bacteria to penetrate fatty tissue with the consequent formation of abscesses. |
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| Collagenase |
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| This enzyme catalyzes the degradation of collagen, a protein found in tendons, nails and hair. |
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| Leukocidins |
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| cause lysis of white blood cells; Staphyloccus aureus destroys rbc’s & other tissue cells |
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| Streptokinase and Streptodornase |
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| actually fibrinolytic enzymes (category 3) lyse rbc’s |
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| Capsules |
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| antiphagocytic |
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| Pilli |
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| attachment to surface receptors on host cells |
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| LD50 |
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| (lethal dose50) The LD50 is the dose of an agent that kills 50%of the animals in a test group |
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| Invasiveness |
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| the ability of an organism to grow in host tissue |
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| Toxicity |
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| the ability of an organism to cause disease by means of a preformed toxin that inhibits host cell function or kills host. |
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| Colonization and Growth |
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| When a pathogen gains access to tissues, it may multiply; a pathogen must grow within host tissues to produce disease. After adherence to epithelial, microbe may penetrate through small breaks or lesions or even an intact mucosal surface, esp if normal flora is altered. Disease results when anatomical and/or physiological damage occurs |
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| Virulence Factors |
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| Endotoxins vs Exotoxins |
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| Toxoid |
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| Toxin -> Heat or chemical treatment -> Toxoid -> inject into animal -> Antitoxin |
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| EXOTOXINS: GENERAL TYPES |
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| Cytolytic toxins A-B toxins Superantigen toxins |
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| Cytolytic toxins (hemolysins) |
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| damage cell membranes, causing cell lysis & death |
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| A-B toxins |
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| B promotes specific binding of toxin to host cell receptor. A is the toxic part |
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| Superantigen toxins |
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| Stimulate large numbers of immune lymphocytes and causes systemic as well as inflammatory responses |
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| EXOTOXINS: SITE OF ACTION |
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| Cytotoxins: inhibit a cell function or cause cell death Neurotoxins: inhibit nerve transmission Examples: tetanus and botulinum toxin Enterotoxins: alter permeability of intestinal epithelium Examples: Cholera and Staph aureus food poisoning enterotoxin (also superantigen) |
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| Diptheria Cytoxin[A-B toxin] |
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| Diptheria toxin in an A-B toxin that inhibits a cell function: protein synthesis B promotes binding of toxin to cell membrane When it binds to cell membrane, it is cleaved and A is internalized. A catalyzes ADP-ribosylation of EF-2 and it no longer aids the transfer of amino acids to growing polypeptide chain. Only a single toxin molecule is needed to kill a cell. Diptheria toxin is formed only by strains of Corynebacterium diptheriae cells that are lysogenized by phage beta. |
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| Lysogenic versus Lytic |
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| Exotoxins - NeurotoxinsBotulinum |
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| Botulinum toxin: 7 distinct toxins-2 of which are encoded for by genes on lysogenic bacteriophages Toxin binds to presynaptic terminal membranes at nerve-muscle junction, blocking the release of acetylcholine required for transmission of nerve impulse to muscle. Muscle contraction inhibited & have flaccid paralysis 1 mg kills 1 million guinea pigs |
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| Exotoxins - NeurotoxinsTetanus |
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| Tetanus toxin: 2 polypeptides, fixed to nerve synapsis, blocks release of glycine, a factor that induces muscle relaxation Relaxation signal is blocked & paired muscles both contract Spastic paralysis, twitching paralysis |
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| Exotoxins - Enterotoxins |
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| Enterotoxins alters permeability of intestinal epithelium; causes massive secretion of fluid into the intestinal lumen causing diarrhea Staphylococcus aureus - vomiting, diarrhea Vibrio cholera - Cholera toxin: 3 polypeptides (A1, A2, B) B toxin involved in binding to ganglioside GM1 in epithelial cytoplasmic membrane A1 activates adenylate cyclase to produce cAMP which brings about secretion of chloride and bicarbonate ions from mucosal cells in intestinal lumen which causes water secretion into lumen |
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| Endotoxins |
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| Gram-negative bacteria produce lipopolysaccharides as part of the outer layer of their cell envelope These are called endotoxins because they are generally cell-bound but are released in large amounts when the cells are lysed Stimulates host cells to release proteins called endogenous pyrogens causing fever Other symptoms: diarrhea, rapid decrease in lymphocyte, leukocyte, and platelet numbers, generalized inflammation, death Not as toxic as exotoxins. Ex: LD50 for mice is 200-400 g for endotoxin but LD50 for botulinum toxin is about 25 picograms (pg), about 10 million times less. 250o C for 30 minutes for inactivation Major problem if contamination of medical devices LPS affects macrophages, monocytes, and neutrophils by binding to a receptor on these cells & tranfer to a CD 14. LPS-CD14 then complexes with a Toll-like receptor to initiate a response that releases cytokines & tumor necrosis factor alpha. |
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| Portals of Entry |
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| Food and Water Bourne:Staphylococci, Vibrio cholera, Clostridium botulinum Exhalation Droplets: coughing & sneezing Direct Contact: mononucleosis, syphillis, herpes, HIV[Retrovirus] Animal Bite or Scratches:rabies, cat scratch fever Vectors: Rocky Mt. spotted fever, bubonic plague |
