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22 Cards in this Set
- Front
- Back
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Pathogens
Pathogenicity Virulence Opportunistic pathogen |
1) Microbial parasites
2) The ability of a parasite toinflict damage on the host 3) Measure of pathogenicity 4) Causesdisease only in the absence of normal host resistance |
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Colonization
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The growth of a microorganism after it has gained access to host tissues, begins as mammals are exposed to microorganisms in the birth process. |
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Skin microflora
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Composition is influenced by:
- Environmental factors (e.g.,weather) - Host factors (e.g., age, personalhygiene |
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Oral Cavity microflora
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Salivacontains antimicrobial enzymes ( Lyzosymes, Lactoperoxidase
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Defense against pathogens
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- Antibiotics
- Probiotics – live culture of intestinal bacteria - Ciliatedepithelial cells act as defense by removing particles - Saliva
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Helicobacter pylori and stomach ulcers
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Themost common (>50% of human population) human gut bacteria. It can colonizethe gut walls and can result in chronic gastritis, gastric ulcers, and stomachcancer.
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What makes the large intestine such a great fermentation vessel?
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- Largeintestine most heavily colonized part of the GI
- Colonis an excellent invivo fermentationvessel |
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Benefits of microbes in GI tract
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They carry out a variety of metabolic reactions that produce several important compounds.
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Common microbes/pathogens in upper/lower respiratory tracts
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Arestricted group of organisms colonizes the upper respiratorytract. Examples:
- staphylococci, streptococci, diphtheroid bacilli, and gram-negative cocci - Some potential pathogens (e.g. staphylococcusaureus and streptococcuspneumonia) Thelower respiratory tract lacks microflora in healthy individuals |
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Pneumonia
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Bacteriaand virus can cause infection inlower respiratory tractsand lungs (pneumonia)
Pneumonia cause >4,000,000 deaths yearly |
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Urinary tract infections (UTI)
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- E.coli, P.mirabilis and Staphylococcus saprophyticus frequently cause urinary tractinfections (UTI)
- Viral and fungal infections canalso cause UTI - 10% of females develop UTI yearly |
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Relationship between Lactobacillus acidophilus and estrogen leves
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- Lactobacillusacidophilus, aresident organism in the vagina, ferments the glycogen, producing lactic acid
- Lactic acid maintains a localacidic environment - L.acidophilus is not present before puberty and after menopause (glycogen-estrogen relationship) |
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Measurement of Virulence
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Virulence can be estimated fromexperimental studies of the LD50(lethal dose50). The amount of an agent that kills50% of the animals in a test group
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Attenuation
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The decrease or loss of virulence of a pathogen. Strains are useful for the production of viral vaccines (measles, rabies, rubella, etc.)
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Adherence and types
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- Bacteriaand viruses that initiate infection often adhere specifically to epithelialcells through interactions between molecules on the surfaces of the pathogenand the host cell
Bacterialadherence can be facilitated by: -Extracellular macromolecules thatare not covalently attached to the bacterial cell surface (glycocalyx) -Examples: slime layer, capsule function in attachment, but also for protection against host defense - Opa (opacity associated protein) in Neisseriagonorrhoeae – attach to epithelial cells - Hemagglutinin helps influenza virus attach tolung epithelial cells - Fimbriae and pili |
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invasion (bacteremia/septicemia)
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Invasion: The ability of a pathogen to enter into the host cell tissue, spread and cause infection
Bacteremia is the presence of bacteria in the blood stream, from where they can travel to diff. parts of the body. Septicemia is the spread of a pathogen through the blood and lymph systems which result in blood borne systemic infections |
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Dental plaque and biofilm
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Extensive bacterial growth can result in a thick oral biofilm called dental plaque. Dental plaque is thus a mixed-culture biofilm composed of several different genera and their accumulated products
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Virulence factors (enzymes, adherence molecules, toxins)
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Virulencefactorsaremolecules produced by a pathogens that enhanceinvasiveness:
•Enzymes that enhance virulence by breaking down oraltering host tissue to provide access to nutrients (e.g. collagenase) •Enzymes that protect the pathogen by interfering withnormal host defense mechanisms(e.g coagulase) |
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Exotoxins
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Proteins released from the pathogen
Exotoxins can be divided into threecategories (based on different mechanisms): •Cytotoxins: Work by degrading cytoplasmicmembrane integrity, causing cell lysis and dead. Toxins that lyse red blood cells •AB toxins: Consist of two subunits, A and B. Work by binding to host cellreceptor (B subunit) and transferring damaging agent (A subunit) across thecell membrane •Superantigen toxins |
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Endotoxin
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•The lipopolysaccharide (LPS) portion of the cell envelope of mostgram-negative Bacteria, which is a toxin when solubilized •Not secreted, released when thecell lyse •Generally less toxic thanexotoxins, but large doses can cause hemorrhagic shock and tissue necrosis |
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Innate resistance to Infection
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Hostshave innate resistance to most pathogens •Natural host resistance
•Tissue specificity •Physical and chemical barriers |
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Risk Factors for Infection
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Compromisedhost
•One or more resistance mechanismsare inactive •The probability of infection isincreased •Age is an important factor •Very young and very old individualsare more susceptible •Stress can predispose a healthyindividual to disease •Diet plays a role in hostsusceptibility to infection •Certain genetic conditions cancompromise a host |
