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Chap 25 - Infection
Microbial Infection and Pathogenesis
| Question | Answer |
|---|---|
| Define infection | a situation in which a microorganism is established and growing in a host, whether or not the host is harmed |
| define pathogen | microbial parasite that causes disease or tissue damage in a host |
| define pathogenicity | the ability of a parasite to inflict damage on the host |
| ___________________ is the enhanced ability of microbes to attach to the host tissue | Adherence |
| for infection, adherence is necessary and (is/is not) sufficient to start disease | if infection, adherence is necessary and IS NOT sufficient to start disease |
| describe how adhesion is done | with receptors. both the tissue and the microbe will have receptors what fit like a lock and key and allows the microbe to bind to the tissue |
| what are adhesins | glycoproteins or lipoproteins that enable the microbe to bind to the host cell |
| a capsule (is/is not) and adherence structure | a capsule IS and adherence structure |
| what is a capsule | a thick coating outside the plasma membrane and cell wall. |
| what are the two important functions of the the capsule serves during pathogenicity | 1) it is sticky and contains the appropriate receptors, 2) can help protect the bacteria from ingestion of white blood cells |
| Fimbriae, Flagella, and Pili (are all/are not) considered to be adherence structures | Fimbriae, Flagella, and Pili ARE ALL considered to be adherence structures |
| define colonization (after infection) | the growth of a microorganism after they have gained access to host tissue |
| when does colonization begin in a human host | AT birth |
| where does colonization usually begin | in the mucous membranes (tightly packed epithelial cells coated in mucus) |
| what is mucus | a thick liquid secretion of glycoproteins |
| ______________ is/are an oral microbial disease | dental cavities |
| what are the two main bacteria that cause dental cavities | Streptococcus sobrinius and Streptococcus mutans |
| dental plaque is caused by | a biofilm excreted by bacteria |
| define invasiveness | ability of a pathogen to gro in a host tissue at densities that inhibit host function |
| ________________________: the presence of bacteria in the blood stream | Bacteremia |
| Septicemia is | a bloodborne systemic infections that may lead to massive inflammation, septic shock, and death |
| what is an infection | any situation when a non-resident flora invades a host and establishes growth in a host |
| what is virluence | the relative ability of a pathogen to cause disease |
| (not a question) pathogens use various strategies to establish virluence | |
| how is virulence established | experimental studies that are at 50% of lethal dose |
| what is 50% lethal dose | the amount of an agent that kills 50% of the test group population (animals) |
| how to tell a highly virulent pathogen from less virulent pathogen | there is little difference in the number of cells required to kill 100 % of the population compared to 50% of the population |
| __________________ is the decrease of loss of virluence. These types of microrganisms are often used for __________________ | attenuation; vaccines |
| vaccines are made out of | attenuated strains of various pathogens |
| _________________________ species encode a large number of virulence factors | Salmonella |
| Salmonella is known to have several genes that specifically direct host invasion and are clustered together on a chromosome. These genes are known as | pathogenicity islands |
| other aspects of pathogenicity islands in Salmonella can contain for other important invasion factors, including | genes that promote more systemic disease and contain resistance plasmids (R plasmids) |
| the pathogen-host interaction is dependent on | both the pathogen and the host |
| what can predispose individuals to develop diseases | certain medical procedures (surgery) and underlying medical conditions |
| nosocomial infections are ______________________ and affect nearly 2 million people yearly | hospital-aquired |
| HIV would be known as a ______________________ and would weaken the immune system enough to predispose an individual for an infection | underlying condition |
| a microorganism that causes a(n) ___________________________ infection, are not known to cause infections in healthy hosts | opportunistic infections |
| invasiveness requires a pathogen to ___________ | breakdown host tissue |
| what is used by the microorganism to breakdown host tissue | enzymes |
| the enzyme Hyaluronidase | breaks down host tissues |
| this enzyme forms blood clots | coagulase |
| this enzyme is a blood thinner (breaks down clots) | streptokinase |
| toxicity is | the ability of an organism to cause disease by means of inhibiting a host cell to function properly or kills the host cell |
| an exotoxin is | a protien that is released from the pathogen as it grows |
| name the three types of exotocins | cytolytic toxin, AB toxins, Superantigen toxin |
| why type of exotoxin is used by Diptheria | AB toxins |
| the term AB toxin stands for | Active (A) and Binding (B) |
| what do AB Toxins do | ultimately they prevent protein formation by blocking the elongation phase of RNA translation |
| how do AB toxins work? | adds an ADP-ribosyl group to an EF-TU |
| name two neurological AB exotoxins | Clostridium tetani (tetanus) and Clostridium botulinum (Botox) |
| describe how the neurological AB exotoxin works in Botox (Clostridium botulinum) | the AB exotoxins blocks the release of Acetylcholine |
| what happens as a results of a Clostridium botulinum | flaccid muscle paralysis |
| how does the neurological AB toxin work in Tetanus (Clostridium tetani) | Tetanus AB Toxins block the release of Glycine from inhibitory neurons. Glycine stops the the release of Acetylcholine |
| what happens as a results of contracting Clostridium tetani (think of the word Tetany) | spastic muscle paralysis (i.e. your muscles are always contracted |
| what are enterotoxins | exotoxins that affect the small intestine |
| what do enterotoxins do | they generally cause massive secretion of fluid into the intestinal lumen, resulting in vomiting and diarrhea |
| cholera toxin is an example of | cholera is an example of an enterotoxin |
| how do cytolytic exotoxins work (think cytoplasmic membrane) | they degrade the cytoplasmic membrane integrity, thereby causing cell lysis and cell death |
| cytolytic exotoxins that cause red blood cell lysis are called | hemolysins |
| Staphylococcal alpha-toxins specifically target | nucleated cells and erythrocytes |
| how do alpha-toxins work | they create a alpha toxin pore, this pore allows an influx of extracellular fluids and an efflux of cytoplasmic components |
| what are superantigens | toxins that cause an overstimulation of the immune system |
| superantigens are generally due to a localized infection, but with systemic effects and have the potential to lead to | shock and death |
| (not a question) the endotoxin is a lipopolysaccharide portion of the cell envelope of a certain gram-negative Bacteria...this becomes a toxin when solubilized | |
| (not a question) endotoxins are generally less toxic than endotoxins | |
| what is the laboratorial function of Limulus amoebocyte lysate | helps detect the presence of an endotoxin |
| the blood of the horseshoe crab is used in the __________________ assay | Limulus amoebocyte lysate |
| common name for Bacilus anthracis | anthrax |
| name the exotoxins that are released by Anthrax | Lethal factor, Edema factor, and Protective antigen |
| what are the functions of the exotoxins in Anthrax | all combine to cause cell death |
| what is the common name for Bordetella pertussis | whooping cough |
| what is the common name for Clostridium perfingens | Gas gangrene or Food poinsoning |
| what is the common name for Corynebacterium diphtheriae | Diptheria |
| how does endotoxins and exotoxins defer in chemistry | exotoxins are mostly proteins that are heat-labile; endotoxins are lipopolysaccharide-lipoprotien complexes mostly gram-negative |
| describe the mode of action for exotoxins and endotoxins | exotoxins have well defined specific actions(cell receptors, enterotoxin, neurotoxin), endotoxins general (fever, diarrhea, etc.) |
| describe the toxicity differences between exotoxins and endotoxins | exotoxins are highly toxic and sometimes fatal; endotoxins are moderately toxins and rarely fatal |
| describe the differences in immune response to exotoxins and endotoxins | exotoxins are highly immmunogenic and stimulate production of neutralizing antibody, endotoxins have poor immunogen |
| explain the difference in the toxiod potential of exotoxins v. endotoxins | heat or chemical treatments may destroy the exotoxin, there is none for the endotoxin |
| what is the potential for fever for the exotoxin v. endotoxin | exotoxins do not really produce fevers, endotoxins induce fevers |
| what is the difference in genetic origin for the exotoxin v. the endotoxin | exotoxins are encoded on extrachromosomal elements or lysogenic bacteriophages; endotoxins are encoded by chomosomes |
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kandriot
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