Host Microbe Interactions Flashcards
Commensalism
One partner benefits and the other remains unharmed. Skin microbes
Parasitism
Microbe benefits while host is harmed
How can bacteria colonize a site of the human body?
Has to be able to resist the antimicrobial effects at that site
Kochs postulates
Criteria needed to determine the cause of infectious diseases
Microorganism must be present in every case of the disease, but not in heathy hosts.
Microorganism must be grown in lure culture from diseased hosts.
The same disease must be produced when a pure culture of the microorganism is introduced into susceptible hosts.
The same microorganism must be recovered from the experimentally infected hosts.
Koch: criteria to establish that bacillus anthracis causes anthrax
Molecular kochs postulates
Virulence factor gene or its product should be found in pathogenic strains of the organism.
Mutating the virulence gene to disrupt its function should reduce the virulence of the pathogen.
Reversion of the mutated virulence gene or replacement with a wild type version should restore virulence to the strain.
Mechanisms of pathogens sis
Production of toxins that are then ingested. (Food borne illness…does not grow on or in the host)
Colonization of mucous membranes of the host, followed by toxin production. (Cholera, bloody diarrhea by ecoli, and diphtheria)
Invasion of host tissues then multiplies in tissues. (Avoid destruction of by macrophages, avoid antibodies) tuberculosis, plague, salmonella.
Invasion of host tissues followed by toxin production. Diarrhea, tetanus
Balanced pathogenicity
Pathogen becomes less virulent and host becomes less susceptible over time
Adherence of pathogens
Use adhesins at the end of pili and capsules to adhere to first line defenses (skin and mucosa).
Receptor is highly specific so bacteria can only attach to certain cells.
More adhesins = broader range of cells that bacteria can attach to.
So pathogens usually have more adhesins
Colonization of pathogens
Siderophores - bind iron to the pathogen. Pathogens need iron to grow. So the defense system can’t prevent the iron binding.
Rapid turnover of pili sheds the IgA antibody and they have antigenic variation (makes it more specific)
Must tolerate toxic products from the normal biota.
Deliverance of effector proteins to host cells
Some gram- pathogens deliver proteins to host cells. These proteins change the cytoskeleton of the host and direct the cell to engulf the bacteria.
Pathogens penetrating the skin
Skin is the most difficult anatomical barrier.
Pathogens rely on skin damaging injury (cut/wound…S.aureus and tetanus)
Pathogens penetrating mucous membranes
Induce Endocytosis in cells by membrane ruffling from effector proteins.
Macrophages engulf material that passes through the m cell and then the pathogen survive and relocate, causing the phagocytes to undergo apoptosis. Then the pathogen attaches to the base of epithelial cells and induce them to engulf the pathogen.
Avoiding the host defenses
Hiding within the cell:
Avoiding destruction by phagocytes: make C5a peptidase that degrades the C5a that attracts phagocytes. Make membrane damaging toxins that destroy the phagocytes.
Avoid recognition and attachment by phagocytes: have capsules, has m protein that binds to C3b and inactivated it. Has Fc receptors that bind to the red flag region (phagocyte doesn’t recognize the fab region)
Surviving within phagocytes: escaping from the phagosome, preventing phagosome-lysosome fusion, surviving within the phagolysosome.
Avoiding killing by compliment system proteins
Gram positive bacteria have a thick peptidoglycan layer that prevents the membrane attack complexes from reaching the membrane.
Called serum resistant.
Avoiding antibodies
IgA protease: cleaves IgA antibody
Antigenic variation: alters the surface of their surface antigens.
Mimicking host molecules: cover themselves with molecules similar to the host molecules
