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what are strict "true" pathogens
- must infect a host organism as part or all of their life cycle
- can cause disease in healthy individuals with competent immune systems
- are typically associated with specific diseases (anthrax, syphilis, plague)
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what are opportunistic pathogens
do not require a host for survival but can infect a host in immunocompromized individuals or disrupted healthy microbiomes
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what are three examples of opportunistic bacteria that are part of the healthy microbiome
- staphylococcus spp
- clostridium dificile
- e. coli
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what are some examples of opportunists that are from the environment
- pseudomonas aeruginosa: usually infects burn victims
- vibrio cholerae
- clostridium tetani
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what are virulent bacteria
promotes their own growth within a host at the expense of the host's tissue or organ function, causing disease
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what are virulence factors
molecules and structures of both strict and opportunistic pathogens that allow organisms to infect a host
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what are mobile genetic elements
- virulence factors from bacteria that transfers to another bacteria
- located in pathogencitiy islands and plasmids
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what are avirulent bacteria
- bacteria that are unable to infect a host
- may be caused by mutations
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what is the difference between virulent and avirulent strains of streptococcus pneumoniae
- virulent: smooth, contains a polysaccharide capsule.
- avirulent: rough, no capsule
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what are pathogenicity islands
- mobile genetic elements
- large chromosomal regions containing sets of genes that encode virulence factors. Contains repetitive sequences that allow the entire region to move within a chromosome or between organisms by horizontal gene transfer
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what are plasmids
- a mobile genetic element
- can be transferred between bacteria through conjugation
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what are the environmental factors that influence the movement of pathogenicity islands and plasmids between bacteria
- low pH (stomach acid)
- temperature
- oxidative stress (reaction to immune system cells)
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describe the immune response that bacteria cause
- inflammatory immune response: body recruits immune cells to site of bacterial invasion in response to eradicating invaders
- includes redness, swelling (edema), heat (release of pyrogens or fever agents), pain
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what happens the longer the bacterium remains in the body
- the greater the bacteria proliferates, the greater its ability to spread and its potential to cause tissue damage and disease.
- it also causes a larger host reponse
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how does bacterial load affect disease
- the inoculum size and bacterial strain affect the onset of disease.
- different numbers of bacteria are required to initiate infection depending on the strain
- ex) 200 cells of shigella required to induce shigellosis, 10^8 cells of vibrio cholerae required to cause GI tract infection
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how can host factors affect disease
- changes in host resistance: whether the host is already immunocompromized, nutritional deprivation, obseity, pregnant
- external factors: trauma, medical treatment, overuse of antibiotics
- modification of healthy host microbiome
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how do antibiotics affect drug resistant bacteria
- in a group, some bacteria are already drug resistant
- when antibiotics kill the bacteria causing the illness, it leaves some of the drug resistant bacteria
- the drug resistant bacteria then proliferate and can transfer their resistance to other bacteria, causing more problems
- presence of antibiotics puts selective pressure on bacterial cells to acquire antibiotic resistance
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how do bacteria enter a host to cause infection
- tears in skin
- tumor or ulcer in bowel
- internal wound
- sexual transmission
- bug bite
- inhalation
- trauma
- injestion
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what are the host's natural defenses against bacterial entry
- skin
- mucous membranes
- ciliated epithelium
- secretions containing antibacterial substances
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how do bacterial adhere to host tissue (4)
- adhesins
- pili
- biofilms
- capsules
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what are adhesins
molecules on surface of cells that bind to receptors on host tissue and keep bacteria from being washed away
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what are pili
projections from bacterial cells that often have adhesins on their ends and keep bacteria anchored to host tissues
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what are biofilms
- sticky matrix of polysaccharides, proteins, and nucleic acids that bind bacterial cells together and to surfaces.
- f(x): protects bacteria from host defenses and antibiotics
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what are capsules
slime layer around the outside of cells that help bacteria stick to host cells and evade immune detection
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what are some adherence factors (7)
- ligand
- adhesin
- lectin
- S-layer
- capsule
- lipopolysaccharide
- lipoteichoic acid
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what is an S-layer
- a proteinaceous layer forming the outermost structure of the cell envelope of some bacteria
- f(x): faciliates adhesion, colonization, and immune evasion
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what are lipopolysaccharides
- on the outermost part of the outer membrane of G (-) bacteria. May faciliate adherence to host tissues
- can be a PAMP as an endotoxin
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what is lipoteichoic acid
- cell wall component of G(+) bacteria that may facilitate adherence to host tissues
- may be recognized by host immune system as a PAMP
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what are teichoic acids
- species specific polymers covalently attached to the cell wall of G(+) bacteria
- lipoteichoic acids (LTAs) are bound to cell membrane
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what are functions of wall teichoic acids and lipoteichoic acids
- directing cell division machinery
- shape molecular surface properties (allows sticking to surfaces)
- mediating biofilm formation
- serving as phage receptors
- mediating interactions with host receptors
- controlling susceptibility and/or resistance to antibiotics
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how do bacteria spread into deeper host tissues
using factors such as invasins that include spreading factors and enzymes to facilitate the spread of bacteria
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what are spreading factors (invasins) by bacteria that affect the physical integrity of tissue matrices and intercellular spaces and their f(x) (3)
- hyaluronidase: degrades hyaluronic acid found in connective tissue
- collagenase: breaks down collagen
- neuramidase: degrades neuraminic acid (coats mucous layer in gut)
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what are the enzymes (invasins) used by bacteria that directly cause host cells to lyse
- phospholipiases: hydrolyze phospholipids in cell membranes
- lecithinase: destroys lecithin in cell membranes
- hemolysins: any enzyme that lyses RBCs
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how do pathogenic bacteria affect tissues?
- bacteria causes tissue destruction by releasing byproducts during growth and metabolism (acids, gas, enzymes, toxins)
- ex) lipases, nucleases (DNAse), proteases, pore forming proteins
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what are examples of bacteria that damage tissues (3)
- clostridium perfringes: opportunistic anaerobic pathogen that destroys tissue releasing enzymes (phospholipase C, collagenase, protease, hyaluronidase) and metabolic byproducts (toxins, acid, gas)
- staphylococci: modify host tissue with hyaluronidase, fibrinolysin, and lipase
- streptococci: produce streptolysins S and O, DNAses, and streptokinases
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what are toxins
- proteins produced by bacteria that interfere with normal host functions
- includes (degradative enzymes that lyses cells, receptor binding proteins that initiate toxic reactions, promotes immune reaction)
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where are toxins encoded on?
- plasmids
- pathogenicity islands
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how do toxins spread in the body
by the circulatory system or body fluids
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what type of symptoms do toxins produce in the body
food poisoning (S. aureus, B.cereus, C. botulinum)
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do toxins require bacterial growth to cause disease?
No
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what are exotoxins
- proteins produced by microbes and released into their surroundings
- produced by both G(-) and G(+)
- ex) cytolytic enzymes
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what do cytolytic enzymes include
- membrane disrupting enzymes (alpha toxin/phospholipase C)
- hemolysins
- pore formin toxins (streptolysin O)
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what are A-B toxins, what does it target, and symptoms
- a type of extoxin that have two subunits (A and B)
- targets ribosomes, transport machinery, intercellular signaling
- symptoms: diarrhea, neuronal loss of function, death
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describe the components of A-B toxin and the function of each component
- A subunit: enters into the cell and performs cytotoxic action
- B subunit: binds to host cell surface receptor
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what are endotoxins
- the lipid A portion of LPS on the outermembrane of G(-) bacteria
- stimulates: fever, vasodilation, edema, inflammation
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what are superantigens
- exotoxins that induce a cytokine storm (large activation of T cells without requiring an antigen) that cause life threatening fever, shock, rash, and autoimmune like response.
- can lead to death
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how do endotoxins illicit an immune response
binds to receptors on antigen presenting cells, stimulating release of acute phase cytokines
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what is sepsis
when G(-) bacteria release high amounts of endotoxins in blood causing shock, hpotension, DIC (blood clots), or death
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what is the most powerful immune stimuli
LPS: an endotoxin, that activates almost every immune mechanism including clotting pathway
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what disease symptoms does LPS induce (7)
- shock
- DIC, thrombosis
- fever
- hypoglycemia
- incrs vascular permeability
- incrs acute phase proteins
- hypotensiondecrs iron
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how do capsules allow bacteria to evade immune system
- capsules are virulence factors
- shield bacteria from immune and phagocytic cells
- mask bacteria as self mimicking human conenctive tissue
- capsule is difficult to grasp for phagocytes
- protect bacteria from destruction within a phagolysosome of a macrophage
- contribute to biofilm formation
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what are the three ways bacteria can escape antibody respondes
- antigenic variation: bacteria modifies their surface proteins to avoid begin detected by antibodies
- antibody inactivation: by proteolytic degradation of antibodies/binding to antibodies to prevent their function
- intracellular growth: when bacteria proliferate inside host cells to avoid being detected by immune cells
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how can bacteria evade phagocytic immune cells (5)
- use enzymes to inhibit or lyse phagocytic cells
- inhibit engulfgment of phagocytes
- prevent lysosome phagosome fusion
- exit the phagosome into the phagocytic cell cytoplasm
- resist bactericidal lysosome compounds
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