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CH 16 Host Microbe Interactions
Terms in this set (55)
a host with a weakness or defect in immune system defenses
intimate relationship between microorganisms and human body. "living together"
both partners benefit.
one partner benefits but other is unharmed
the parasite benefits at the expense of the other partner
microorganisms routinely found on the body of a healthy individual. help in defending the body from pathogens
microbes establish themselves and grow on body surface (normal microbiota)
if the microbe has parasitic relationship with the host. (pathogens). does not always lead to infection
symptoms do not appear or are mild enough to be unoticed
infection that causes disease, a noticeable impairment in body function
Symptoms of disease
effects of disease experienced by patient. ex: nausea, pain
Signs of disease
objective evidence. ex: rash, pus or swelling
the initial infection
an additional infection that occurs as a result of the primary infection
aka pathogen. a microbe or virus that causes disease in otherwise healthy individuals. Ex: plague, malaria, measles, influenza, TB
pathogen that only causes disease when body's defenses are compromised or when introduced to an unusual location. could be normal microbiota or common in environment.
degree of pathogenicity of an organism. highly virulent = more likely to cause disease
traits of a microorganism that specifically allow it to cause disease
Communicable disease (contagious)
diseases that spread from one host to another
the number of microbes necessary to establish an infection. partially reflected on the ease of the spread of disease
indicates number of microbial cells administered that results in disease in 50% of test population. Experimentally determined.
time between introduction of microbe to a host and the onset of illness. could be a few days or two weeks. depends on growth rate of pathogen, host's condition and number of infectious cells encountered. infectious agents can still be spread
follows incubation period. person experiences signs and symptoms of disease. possibly experience vague symptoms known as prodromal phase
follows illness. stage of recuperation and recovery from disease. can still spread infectious agents
spread pathogens but no signs or symptoms of the disease
symptoms develop quickly but only last a short time. ex: strep throat
slowly develop and last for months or years. ex: TB
never completely eliminated from body. microbes always present in body tissues but do not cause symptoms. if immunity decreases, disease may be reactivated. Ex: chickenpox as a kid could result as shingles later in life
microbe is limited to small area. Ex: boil caused by S. aureus
infectious agent is spread throughout the body. ex: measles.
1. bacteremia: bacteria in circulating blood stream. does NOT imply disease
2. toxemia: toxins circulating in blood stream.
3. viremia: viral particles circulating in blood stream
4.septicemia (sepsis): acute, life threatening illness caused by growing infectious agents/products in blood stream
criteria Robert Koch used to establish Bacillus anthracis causes anthrax. provides foundation that a given microbe causes a specific infectious disease
1. microorganism must be present in every case of the disease
2. organism must be grown in pure culture from diseased hosts
3. same disease must be produced when a pure culture of organism is introduced to susceptible hosts
4. organism must be recovered from the experimentally infected hosts
used by bacteria to attach to host cells. often at tips of pili. could also be capsules or cell wall proteins
the molecule an adhesin attaches to. typically glycoproteins or glycolipids.
Adhesin-receptor binding is very specific and therefore dictates which types of cells bacterium can attach to
Colonization for infection
pathogen must multiply to colonize in host. most cases grow in biofilms. some pathogens produce their own iron-binding molecules (siderophores); remember lactoferrin and transferrin bind to iron, limiting growth of microbes.
Invasion of skin
bacteria rely on injuries or cuts to penetrate skin. ex: S. aureus enters cut, Yersinia pestis injected by fleas
Directed Uptake by Cells
One mechanism for pathogens to penetrate mucous membranes. Pathogens induce non-phagocytic cells to engulf them by first attaching to cell then triggering process for endocytosis.
G- bacteria (Salmonella) inject effector proteins using type III secretion (injectisome). cause cell cytoplasm to rearrange resulting in membrane ruffling. Ruffles enclose bacteria bringing them into cell
Exploiting antigen sampling processes
mechanism used for pathogens to penetrate mucous membranes. Use MALT samples. M cells are used to cross intestinal barrier. ex: Shigellad
used to penetrate mucous membranes. ex: Mycobacterium tuberculosis
bacteria that use mechanisms to avoid killing by complement proteins
Avoiding Host Defenses
1. Hiding w/in host cell: pathogens hide from complement proteins, phagocytes and antibodies
2. avoiding killing by complement system proteins
3.avoiding destruction by phagocytes (3 mechanisms)
4. avoiding antibodies
Preventing Encounters with Phagocytes
one mech. to avoid destruction by phagocytes.
C5a peptidase: enzyme degrades complement component C5a which recruits phagocytic cells
membrane damaging toxins: kill phagocytes by forming pores in their membranes
Avoiding recognition and attachment
another mech. to avoid destruction by phagocytes
Capsules: prevent phagocytosis by interfering w/ opsonization. inactivates C3b
M protein: binds to complement regulatory protein that inactivates C3b
Fc receptors: block Fc region on antibodies and cannot be recognized for phagocytosis
Surviving w/in Phagocytes
one mech. to avoid destruction by phagocytes.
Escape from phagosome: bacteria multiply w/in cytoplasm of phagocyte and are therefore protected
Preventing phagosome-lysosome fusion: avoid exposure to the destructive components of lysosomes
Surviving w/in phagolysosome: very few microbes can do this.
IgA protease: cleaves IgA antibodies found in mucus and other secretions
Antigenic variation: pathogens alter structure of surface antigens.
Mimicking host molecules: pathogens cover themselves w/ molecules similar to those found in host. immune system does not typically attack "self" molecules
proteins that have very specific damaging effects.
inactivated toxins. used for vaccines
suspension of neutralizing antibodies. used to treat toxin-mediated disease
damage nervous system
cause intestinal disturbance (vomiting)
damage variety of different cell types by interfering w/ cell mechanisms or by lysing cells
have two parts: A subunit is the toxin (active) and B subunit binds to specific molecules on cells. A (usually enzyme) responsible for effects of toxin and B dictates type of cell affeced
Membrane damaging toxins
cytoxins that disrupt plasma membranes causing cell to lyse.
override specificity of hlper T cell response causing toxic effects due to massive release of cytokines by Th cells
lipopolysaccharide (LPS), makes outer membrane of G+ cell wall.
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