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Nester's Microbiology CH. 16: Host-Microbe Interactions
Terms in this set (44)
What is mutualism? Give an example.
an association in which both partners benefit.
In the large intestine, some bacteria synthesize vitamin K and certain B vitamins. These nutrients are then available for the host to absorb. The bacteria residing in the intestine benefit as well, supplied with warmth and a variety of different energy sources.
What is commensalism? Give an example.
an association in which one partner benefits but the other remains unharmed.
Many microbes living on the skin are neither harmful nor helpful to the human host, but they obtain food and other necessities from the host.
What is parasitism? Give an example.
an association in which one organism, the parasite, benefits at the expense of the other.
All pathogens are parasites, but medical microbiologists often reserve the word parasite for eukaryotic pathogens such as certain protozoa and helminths (worms).
the population of microorganisms routinely found growing on the body of healthy individuals
How do babies acquire their normal microbiota at birth?
During the passage through the mother's birth canal, the baby is exposed to lactobacilli and an assortment of other microbes that take up residence in its digestive tract and on its skin.
How do c-section babies get their normal microbiota?
The baby is not exposed to the genital fluids, so microbes from the mother's skin and the environment establish themselves as residents on the newborn instead.
the analysis of the DNA extracted directly from a given environment; this allows scientists to investigate all members of the microbiota, including those that have not yet been grown in culture.
Beneficial roles of the normal microbiota
Protecting against infection: cover binding sites that might otherwise be used for attachment, consuming available nutrients, and producing compounds toxic to other bacteria, stimulates adaptive immune system.
Promoting oral tolerance: our defenses learn to lessen the immune response to the many microbes that routinely inhabit the gut, as well as foods that pass through.
Aiding digestion: human intestinal microbiota allows the body to extract more energy from foods; one reason is that the human genome encodes relatively few enzymes that degrade complex carbohydrates; instead, the body relies on microorganisms to break down most types of dietary fiber.
Producing substances important for human health: bacteria in intestinal tract produce vitamin K and certain B vitamins that can be used by the host; in addition, butyrate, one of the short-chain fatty acids produced as a result fermentation of dietray fibers, is an important energy sorce for the epithelial cells that line the large intestine.
a microbe or virus that causes disease in otherwise healthy individuals; plague, malaria, measles, influenza, diphtheria, tetanus, and TB.
causes disease when the body's innate or adaptive defenses are compromised, or when introduced into an unusual location; can be members of the normal microbiota or they can be common in the environment.
refers to the degree of pathogenicity of an organism; highly virulent is more likely to cause disease.
traits of a microorganism that specifically allow it to cause disease.
time between introduction of a microbe to a susceptible host and the onset signs and symptoms.
Phase of illness
follows the incubation period; person will experience the signs and symptoms of the disease; can be preceded by prodromal phase.
period of early, vague symptoms such as malaise and headache.
stage of recuperation and recovery from the disease; even though there is no indication of infection during the incubation and convalescent periods, many infectious agents can still be spread during these stages.
characterized by symptoms that develop quickly but last only a short time; example is strep throat.
develop slowly and last for months or years; example is TB.
never completely eliminated; the microbe continues to exist in host tissues, often within host cells, without causing any symptoms; if there is a decrease in immunity, the latent infection may reactivate and become symptomatic.
microbe is limited to a small area; example is a boil.
infectious agent is disseminated (spread) throughout the body; an example is Lyme disease;often include a characteristic set of signs and symptoms - such as fever, fatigue, and headache - that result from the systemic immune response to the infecting agent.
bacteria are circulating in the bloodstream.
toxins are circulating in the bloodstream.
viral particles are circulating in the bloodstream.
1. The microorganism must be present in every case of the disease.
2. The organism must be grown in pure culture from diseased hosts.
3. The same disease must be produced when a pure culture of the organism is introduced into susceptible hosts.
4. The organism must be recovered from the experimentally infected hosts.
Molecular Koch's Postulates
1. The virulence factor gene or its product should be found in pathogenic strains of the organism.
2. Mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen.
3. Reversion of the mutated virulence gene or replacement with a wild-type version should restore virulence to the strain.
Adherence: bacteria use adhesins to attach to host cells; these are often located at the tips of pili; adhesins can also be a component of other surface structures such as capsules or various cell wall proteins; the molecule to which an adhesin attaches is called the receptor; adhesin-receptor binding is highly specific, dictating the type of cells to which the bacterium can attach.
Colonization: microorganism must multiply in order to colonize the host; to colonize a mucosal surface, the pathogen must deal with the host's defenses that protect those surfaces.
Delivering effector proteins to host cells: some gram- pathogens deliver proteins directly into host cells using secretion systems.
Type III secretion system: syringe-like structure that injects proteins into eukaryotic cells; injected proteins induce changes such as altering the cell's cytoskeleton structure.
Breaching anatomical barriers
skin is the most difficult anatomical barrier for microbes to penetrate; bacterial pathogens that invade via this route rely on skin-damaging injury.
mucous membranes are the entry points for most pathogens, but the invasive processes are complex and difficult to study, but there are at least 2 mechanisms used for invasion.
What are the 2 mechanisms used for invasion of the mucous membranes?
Directed uptake by cells: some pathogens induce non-phagocytic cells to engulf them; the pathogen first attaches to a cell, then triggers the process of endocytosis; gram- bacteria often inject effector proteins that induce engulfment by host cells.
Exploiting antigen-sampling processes: several pathogens use M cells to cross the intestinal barrier; some pathogens invade by means of alveolar macrophages, which engulf material that enters the lungs: actually allows them to avoid a process that could otherwise lead to macrophage activation.
Avoiding host defenses
some pathogens enter host cells, where they hide from complement proteins, phagocytes, and antibodies.
Preventing encounters with phagocytes
some pathogens prevent phagocytosis by avoiding macrophages and neutrophils altogether.
C5a peptidase: this enzyme degrades the complement system component C5a, a chemoattractant that recruits phagocytic cells.
Membrane-damaging toxins: kill phagocytes and other cells, often forming pores in their membranes; the leaky cells swell and then lyse.
Avoiding recognition and attachment
some pathogens avoid being recognized by phagocytes.
Capsules: long been recognized for their ability to prevent phagocytosis: they do this by interfering with opsonization; in some cases, the capsule binds the host's complement regulatory proteins that inactivate C3b; by quickly inactivating C3b, the molecule is no longer an effective opsonin and can't activate the complement system by the alternative pathway.
M protein: component of the cell wall of Streptococcus pyogenes functions in a manner similar to that described for capsules; it binds a complement regulatory protein that inactivates C3b, thereby preventing it from being an effective opsonin and avoiding the alternative pathway of complement system activation.
Fc receptors: proteins bind the Fc regions of antibodies, interfering with their function as opsonins.
Surviving with phagocytes
some bacteria make no attempt to avoid engulfment by phagocytes, instead using t as an opportunity; it allows them to hide from antibodies, control some aspects of the immune response, and be transported to other locations in the body.
Escape from the phagosome: some pathogens escape from the phagosome before it fuses with the lysosomes; bacteria then multiply within the cytoplasm of the phagocyte, protected from other host defenses.
Preventing phagosome-lysosome fusion: bacteria that prevent phagosome-lysosome fusion avoid the otherwise inevitable exposure to the destructive components of lysosomes.
Surviving within the phagolysosome: relatively few microbes can survive the destructive environment within the phagolysosome; once the organism has been ingested by a macrophage, it delays fusion of the phagosome with the lysosome, allowing additional time for the microbe to equip itself for growth within the phagolysosome.
Avoiding killing by complement system proteins
bacteria that avoid killing by the complement proteins are said to be serum resistant; these strains hijack the mechanism that host cells use to prevent their own surfaces from activating the complement system; by binding to the host's complement system, they avoid complement activation by the alternative pathway, thereby postponing MAC formation.
IgA protease: enzyme cleaves IgA, the class of antibody found in mucous and other secretions.
Antigenic variation: some pathogens routinely alter the structure of the surface antigens; allows them to stay ahead of antibody production by altering the very molecules that antibodies would otherwise recognize.
Mimicking host molecules: pathogens sometimes cover themselves with molecules similar to those normally found in the host; this molecular mimcry takes advantage of the fact that the immune system typically doesn't attack against "self" molecules.
proteins that have very specific damaging effects; often major cause of damage to an infected host.
either secreted by the bacterium or leak into the surrounding fluid following lysis of the bacterial cell; can act locally, or they may be carried in the bloodstream throughout the body, causing systemic effects.
consist of 2 parts: the A subunit is the toxic (active) protion and the B subunit binds to a specific surface molecule on cells.
cytotoxins that disrupt eukaryotic cytoplasmic membranes, causing the cell to lyse; many lyse red blood cells, causing hemolysis that can be observed when the organsisms are grown on blood agar.
damage membranes by inserting themselves into the phospholipid bilayer, forming channels that allow fluids to enter the cell
Streptolysin O: compound responsible for characteristic B-hemolysis of Streptococcus pyogenes grown anaerobically on blood agar.
hydrolyze phospholipids in the cytoplasmic membrane.
exotoxins that stimulate too many Th cells, causing a massive release of cytokines; leads to fever, nausea, vomiting, and diarrhea; effects can be life-threatening.
override the normal specificity of antigen recognition by a T helper cell; do this by binding simultaneously to the outer portion of the major histocompatibility class II molecule on antigen-presenting cells and the T-cell receptor.
destroys material that binds together the layers of skin, causing the outer layer to peel.
lipopolysaccharide, the molecule that makes up the outer layer of the outer membrane of the gram- cell wall; heat-stable
Damaging effects of the immune response
inflammatory response itself can destroy tissue because phagocytic cells recruited to the area release some of the enzymes and toxic products they contain.
Immune complexes: when antibodies bind to antigens, the complexes can settle in the kidneys and joints, where they activate the complement system, causing destructive inflammation.
Cross-reactive antibodies: certain antibodies produced in response to an infection bind to the body's own tissues, promoting an autoimmune response.
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