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40 Cards in this Set

  • Front
  • Back
Viroids
All Nucleic Acids
Prions
All proteins
Viruses
Obligated to be parasites, have no organelles need a host to survive and replicate
Fungi
Eukaryotic cells
Prokaryotic
Bacteria, some have lost the ability to grow on their own
Virulence factors
Components of the structure of bacteria which contribute to the ability of the bacteria to cause disease.

FIMBRIA--allow attachment

Toxins which contribute to disease. Some secrete enzymes.

REALLY DEPENDS ON structure and what it it is capable of doing
Bacterial structure
A. No organelles
B. Cell Wall
C. Gram + or -
D. Some antibiotics do not work on G+ wall or vice versa due to inability to get pass the wall
Gram - Bacteria
Lipopolysaccarides, external component that is associate with FEVER, ACTIVATIOn OF LYMPHOCYTES,

CAUSE OF ENDOTOXIN
Gram Stains
Crystal violet stain which gets into cells colors them blue the Gram + will stay blue while the - will be red since the when alcohol is added it is washed out
Pili
Help in colonization, they grip to the enviroment that they land in
Capsules
Genetically produced by bacteria
Immune systems will not be able to digest or remove efficiently
Bacteria consists of the plasmid and other shit that it can pick up to influence activity
Biofilms
ARTIFICIAL IMPLANTATIONS

Colonies form and communicate with eachother and form layers! Cause problems like infection caused by bacteria occurs in vivo
Generational time
Replication occurs at different rates,
Abscess bacteria cannot grow as fast, if you give a static drug it will not be effective due to slow growth rate
Anaerobes
Superoxid Dimutase present and eliminates radical, uses fermentation route,
uses derivative of pyruvate to grow,
slow growening,
make certain fermentation products that tell you what they are
Facilitative Bacteria
Grow Aerobically and anaerobically

Anaerobically is slower than aerobic prefer aerobically.
Conjunction
Mediated by F factor
1. F+ factor moves in from another cell(F+ to F- cell) via a sex pili thingy. Then integrates into other cell's genome.
2. Enters F- cell with some other component first then has HFR come last. THe HFR activates host chromosomoe and integrates.
3. This is the result of biological exchange

TRANSFER OF RESISTANCE
Transformation
Bacteria has lysed DNA floating around

Pick up floating DNA by competence factor add to it's genome, this may make it more virulent or allow it to be resistant to something
Transduction
Bacteria have phages

Phages can kill other bacteria by 2 methods
Lytic: Enter Cell, replicate, lyse cell, don't play a role in virulence, use medically.

Lysogenic-genetic material enters cell, depending on synthesis of repressor gene stops the ability of the host for totall replication. Sets phage genetic material for integration into host chroms.
Can also lyse the cell if integration fails.
Specialized transduction
Transfer of host DNA sements near site of prophage integration contains viral and Host DNA
Generalized Transduction
Randomly packages host DNA in a bacteriophage coate and may transfer any gene

Transducing particle contains only host DNA
Plasmid
Dna Pieces that self replicat. Can carry antibiotic resistance, toxic genes and transposons
Transposons
Movable genetic elements incapable of independent replication. Inserts int chrom.
Integrons
mobile genetic element consist of an integrase gene, resistance genes, and insertion sequence. NO SELF REPLIC.
Pathogenicity islands
Genes code for unique secreation systems, toxins adhesion, etc, contains integrase and transponse genes.
Bacterial Pathogenesis
Transmission
Evasion of 1* host defenses
Adherence to mucase membranes by pili or capsules, adherins mediate adherence. BIOFILMS FORM
Colonization by growth
Disease sympoms caused by toxin production
Host response nospecific and specific
Progression or resolution of disease
Exotoxins
polypeptides relased by cell highly toxic both gram + and -
Endotoxins
lipopolysaccarides, intergal part of gram -,
cause
SMALL AMOUNTS:::
Fever, Vasodialation, Increased Antibody Synthesis, Inflammation

LARGE AMOUNTS:::
SHock, intravascular coagulation
Pyogenic
Pus producing where neutrophils are predominant
Granulomatous
Macrophages and t cell predominate
Survival of Host Defenses
1. Invactivation of antibody
2. Inhibition of complement action (keeps complement from binding to cell
3.Antigenic (phase) variation- alteration of epitopes on major bact. surface molecules avoiding antibodies.
4. Molecular mimicry-Pathogens mimic host factors and allow evasion of adaptive host impun system.
5. Lipopolysac. Modification- changes stop phago. or membrane attack complexes. IE MAC forms to far from the cell when modified to damage cell.
LIVE Vaccines In U.S.
Measles, mumps, Rubella, Varicella, Polio, Yellow Fever, smallpox, influenza, TB, Typhloid
Killed Vaccines in US
Polio, Hep A, flu, polio, rabies, cholera, pertuss, plague, typhoid.
Exotoxin subunits??
A-active does harm to cell
B-Binder binds to cell surface.
5 Class of Antibacterial Attack
Inhibit cell wall synthesis,
Inhibit NA synthesis
Protein synthesis at 30S subunit and 50S
Alteration of cell membrane function to target gram negative bacteria
Innate Immunity
Skin, resporitory epithelia, saliva
Active (Adaptive) Immunity
B Cells respond by making antibodies specific to virus receptors and have the ability to bind to our own cell receptors to keep viruses away from them.

IgM=first antibody that comes up when comes across antigenes

IgG- antibodies stored from past encounters

T-lymophcytes, compliments,
Compliment-
binds to antibody which binds to cell which then puts holes in bacteria cell, this then attracts phagocytes to eat it
Lukocydins
Made to kill macrophages
Super antigens
Super stimulate cells of the body to secrete cytokines which shocks the body
Sialic Acid
Added to endotoxin by lipopolysaccharide to hide it from host defenses in gram negative cells.