1050 Unit 5 Flashcards
-describe symbiotic relationship
–hosts and microbes live together long term
–indigenous microbiota (must be careful not to stimulate immune response)
–3 types: communalistic, mutualistic, and parasitic
how does indigenous microbiota exist?
–through co-evolution, co-adaption and co-dependency between bacteria and host
Describe communalistic relationship
–no benefit or harm to either organism
–communalistic bacteria = describing bacteria recovered from culture that do not have pathogen present
Describe mutualistic relationship
–both host and microbes benefit
Describe parasitic relationship
–microbes cause harm to the host
describe infectivity
–organisms ability to establish an infection
–horizontal transmission (person to person spread)
–“contagious”
describe pathogenicity
–ability of an organism to cause disease
–qualitative trait of an organism determined by genetic makeup
describe virulence
–extent of pathology caused by an organism when it infects a host
–quantitative trait refers to extent of damage
what is avirulent?
–bacteria strain not capable of causing disease
what are 3 functions of virulence factor?
1) may increase an organisms ability to establish itself on/in the host
2) invade or damage host cells
3) evade the host immune response
what are the structural features of bacteria that contribute to increased virulence
–endotoxin
–pili
–flagella
–capsule
–exotoxins
how do endotoxins contribute to increased virulence
–lipid A portion of LPS in gram-negative cell walls
–powerful stimulator of cytokine release
how do pili contribute to increased virulence?
–adherence to host cells
–resistance to phagocytosis
how do flagella contribute to increased virulence?
–adherence to host cells
–motility
how do capsules contribute to increased virulence?
–blocks phagocytosis
–antibody attachment
–usually polysaccharides
how do exotoxins contribute to increase virulence>?
–potent, toxic proteins released from living bacteria
–neutrophils, cytotoxins, and enterotoxins
what type of cell is a bacteria cell?
–prokaryote cell
what is peptidoglycan?
–primary component of cell shape and rigidity of bacteria
what are two variations of a bacterial cell wall?
–gram-negative
–gram-positive
describe gram-negative cell wall
–contains LPS (polysaccharide layers)
–LPS has 3 layers
—->outer core polysaccharides
—->inner core polysaccharides
—->lipid A1
what is fimbrae?
–composed of proteins
–involved in specific attachment to prokaryotic surface ligands. “common pili”
what is afimbrial?
–caused by attachment by presence of surface molecules
–non-pili-dependent
describe bacteria defenses in innate immunity
–intact skin and mucosal surfaces (barriers to entry)
–antimicrobial defense peptides
–complement proteins, cytokines, acute-phase reactants
–recognition of PAMPs by PRRs such as TLRs
–defensins
–contributes heavily to bodies ability to overcome bacterial infection
what are defensins?
–soluble peptides
–have 3 classes: Alpha, beta and theta
–theta not found in humans
describe alpha denfensins
–produced by neutrophil, certain macrophages and paneth cells of the small intestine
–disrupt microbial membrane
describe beta defensins
–produced by neutrophils, epithelial cells lining various organs
–increase resistance of epithelial cells to colonization
describe bacterial defenses in adaptive immunity
–antibody production –> bind of C, opsonization, neutralization of bacterial toxins
–cell-mediated immunity–> CD4 T cells produce cytokines that induce inflammation, cytotoxic T lymphocytes attack host cells that contain intracellular bacteria
what are bacterial evasion mechanisms?
1) inhibiting chemotaxis
2) blocking adherence of phagocytes to bacterial cells
3) blocking digestion
4) inhibiting complement C3b binding
5) cleavage IgA
what is primary effect that occurs when phagocyte adherence is blocked?
–release of lysosome contents into cytoplasm of phagocytic cell, killing WBC.
Describe endotoxins
–lipid A
– found in LPS of cell walls of gram negative bacteria
–activates complement cascade –> leads to formation of anaphylaxis C3a and C5a
–immunogenic but does not result in production of protective antibodies
describe exotoxins
–protein molecules that are released from living bacteria (mostly gram positive)
–most potent molecule to harm living life
–may be classified as neurotoxins, cytotoxins, or enterotoxins
–have subunits that bind to receptors
–extremely immunogenic
–induce production of protective antibodies`
what are the 5 laboratory means of detecting causative agent or bacterial infection?
1)culture of the causative agents
2)microscopic examination
3)detection of bacterial agents
4)molecular detection of bacterial DNA or RNA
5)serological testing
describe “culture of causative agent” of bacterial defenses
–grows on broth or solid media
–major means of diagnosis, but may take time or may not be possible
–enriched media usage
–limitations
—->several bacterial pathogens have not been made for clinical use
—->recovery may take to long for some bacteria
—->some may present as dangerous to technologist
describe “microscopic examination” of bacterial defenses
–gram stains or special stains (fluorescent)
—->purple means gram positive is present
—->pink means gram negative is present
–direct fluorescent antibody assay (DFA)–>not used much anymore because not sensitive and not readily available
describe “detection of bacterial antigens” of bacterial defenses
–rapid testing by ELISA, LFA or LA
–LFA and LA are advantageous because relative ease, low cost, and raid turnaround time
describe “molecular detection of bacterial DNA or RNA” of bacterial defenses
–can obtain results in few hours with real-time PCR ( most widely known)
–compact hybridization and gene amplification assays (easy to use)
–Nucleic acid-based assays are more sensitive but have limitations:
—->very few FDA approved assays on market for several infectious agent
—->laboratories usually do not approve costs on these
