z-MicroBio Final – Ch. 21

Mutualism
both host and microbe benefit
Commensalism
microbe causes no damage to host
Pathogenic relationship
microbe causes damage to host
Normal Flora
microorganisms normally found in or on the body that typically do not cause disease
Synergistically
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
Communicable
able to be transmitted between hosts
Disease reservoir
a natural source of disease agent. Reservoirs may include sick patients, asymptomatic carriers, animals, recovered patients, environmental sources, etc
virulence
The measure of degree pathogenicity
opportunistic pathogen
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.
Compromised Host
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
Infection
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 !!
Infestation
Presence of organism; not growing and reproducing; just presence
Disease
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!!!!
Internal tissues Free from Bacteria
brain, blood, cerebrospinal fluid, muscles. Genitourinary Tract-upper [kidney, ureters, & uninary bladder. Stomach (Mycobacteria, Salmonella are resistant.)
Entry of Pathogen
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Adherence
Bacteria or viruses usually initiate infection by adhering specifically to epithelial cells through interactions between macromolecules on surfaces of the pathogen and host.
Tissue Selective
Neisseria gonorrhoeae adheres more strongly to urogenital epithelium (tissue specificity). Opa surface protein binds with host CD66 protein.
Host Selectivity
a microorganism that normally infects humans binds to human epithelial cells better than those of a rat
Capsules
glycocalyx or slime layer (loose network of polymer fibers) may be involved in adherence.
Fimbriae & Pili
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.
Virulence
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
Resistance
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
Virulence Factors: Invasiveness
Hyaluronidase
Coagulase
Fibrinolysin
Lipase
Collagenase
Leukocidins
Streptokinase and Streptodornase
Hyaluronidase
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]
Coagulase
This enzyme catalyzes the conversion of fibrinogen to fibrin with resultant clot formation. Present in pathogenic Staphyloccus.
Fibrinolysin
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.
Lipase
Production of excessive amounts of lipase allow bacteria to penetrate fatty tissue with the consequent formation of abscesses.
Collagenase
This enzyme catalyzes the degradation of collagen, a protein found in tendons, nails and hair.
Leukocidins
cause lysis of white blood cells; Staphyloccus aureus
destroys rbc’s & other tissue cells
Streptokinase and Streptodornase
actually fibrinolytic enzymes (category 3)
lyse rbc’s
Capsules
antiphagocytic
Pilli
attachment to surface receptors on host cells
LD50
(lethal dose50)
The LD50 is the dose of an agent that kills 50%of the animals in a test group
Invasiveness
the ability of an organism to grow in host tissue
Toxicity
the ability of an organism to cause disease by means of a preformed toxin that inhibits host cell function or kills host.
Colonization and Growth
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
Virulence Factors
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Endotoxins vs Exotoxins
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Toxoid
Toxin -> Heat or chemical treatment -> Toxoid -> inject into animal -> Antitoxin
EXOTOXINS: GENERAL TYPES
Cytolytic toxins
A-B toxins
Superantigen toxins
Cytolytic toxins (hemolysins)
damage cell membranes, causing cell lysis & death
A-B toxins
B promotes specific binding of toxin to host cell receptor. A is the toxic part
Superantigen toxins
Stimulate large numbers of immune lymphocytes and causes systemic as well as inflammatory responses
EXOTOXINS: SITE OF ACTION
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)
Diptheria Cytoxin[A-B toxin]
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.
Lysogenic versus Lytic
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Exotoxins – Neurotoxins Botulinum
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
Exotoxins – Neurotoxins Tetanus
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
Exotoxins – Enterotoxins
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
Endotoxins
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.
Portals of Entry
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

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