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28 Cards in this Set

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WHAT IS ANOTHER NAME FOR PATHOGENICITY
VIRULENCE
WHAT ARE THE (2) METHODS USED TO MEASURE VIRULENCE
INFECTIVE DOSE 50 (ID50)

LETHAL DOSE 50 ( LD50)
DEFINE INFECTIVE DOSE 50
THE # OF PATHOGENS REQUIRED TO CAUSE A STATE OF INFECTION ( PATHOGEN IS ESTABLISHED AND GROWING) IN 50% OF AN EXPERIMENTAL POPULATION
DEFINE INFECTIVE DOSE 50
THE # OF PATHOGENS REQUIRED TO CAUSE A STATE OF INFECTION ( PATHOGEN IS ESTABLISHED AND GROWING) IN 50% OF AN EXPERIMENTAL POPULATION
DEFINE LETHAL DOSE 50
THE # OF PATHOGENS REQUIRED TO KILL 50% OF AN EXPERIMENTAL POPULATION
WHAT ARE THE THREE WAYS A PATHOGEN BECOMES MORE VIRULENT
INFECTIVITY

INVASIVENESS

PATHOGENIC POTENTIAL
DEFINE INFECTIVITY

HOW IS INFECTIVITY IMPROVED
ABILITY OF THE PATHOGEN TO ESTABLISH AN INITIAL SITE OF INFECTION

INFECTIVITY IS IMPROVED BY GLYCOCALYX, PILI, FIMBRIAE, ADHESINS----COMPOUNDS THAT ALLOW THE PATHOGEN TO BIND TO THE SURFACE ODF A HOST CELL
DEFINE INVASIVENESS

HOW IS INVASIVENESS IMPROVED
THE ABILITY TO SPREAD BEYOND THE INITIAL SITE OF INFECTION

INVASIVNESS IS IMPROVED BY THE PRODUCTION OF ENZYMES SUCH AS GELITINASE, COLLAGENASE, THAT DEGRADE HOST TISSUES
WHEN DISCUSSING INVASIVENESS...WHAT DO STAPHYLOKENASE/STREPTOKINASE DO
THEY INHIBIT BLOOD CLOTTING
WHEN DISCUSSING INVASIVENESS,,,DESCRIBE MOTILITY
FLAGELLA, CILIA, PSEUDOPODIA
OUR BODIES HAVE 100 TRILLION MICROORGANISMS ON/IN OUR BODIES...BUT THEY'RE NOT ALL PATHOGENS...SO....WE NEED TO LOOK AT_____________
PATHOGENIC POTENTIAL
DEFINE PATHOGENIC POTENTIAL
THE ABILITY TO CAUSE DAMAGE/MALFUNCTION IN HOST TISSUES
WHAT ARE THE TWO WAYS TO CAUSE "DAMAGE"/ MALFUNCTION IN HOST TISSUES ( PATHOGENIC POTENTIAL)
DIRECT DAMAGE

INTOXICATION
DEFINE DIRECT DAMAGE

WHAT MUST BE PRESENT FOR DAMAGE TO OCCUR

DAMAGE IS LIMITED TO ______________________
DAMAGE CAUSED BY THE GROWTH OF THE PATHOGEN

THE PATHOGEN MUST BE PRESENT FOR DAMAGE TO OCCUR

DAMAGE IS LIMITED TO THE LOCATION OF PATHOGEN GROWTH
GIVE AN EXAMPLE OF DIRECT DAMAGE
ENTEROAGGREGATIVE E-COLI IN THE LARGE INTESTINE ( SEE FIGURE IN NOTES)
DEFINE INTOXICATION ( ONE OF TWO PATHOGENIC POTENTIALS/DAMAGE)

IS THE PATHOGEN PRESENT

WHERE IS THE DAMAGE
THE DAMAGE CAUSED BY THE RELEASE OF TOXINS FROM THE PATHOGEN

THE PATHOGEN MAY NOT BE PRESENT

DAMAGE IS NOT LIMITED TO THE LOCATION OF THE PATHOGEN ( BETTER SPREAD)
DESCRIBE EXOTOXINS
EXOTOXINS ARE ALWAYS PROTEIN WITH ENZYMATIC ABILITY
HOW ARE EXOTOXINS MADE
THE TOXINS ARE ACTIVELY MADE AND SECRETED BY THE PATHOGEN
ONCE EXOTOXINS ARE SECRETED,,,WHAT HAPPENS
ONCE SECRETED, EXOTOXINS USUALLY HAVE A TISSUE-SPECIFIC TARGET ( ie NEUROTOXIN)
ONCE AN EXOTOXIN REACHES THE TARGET TISSUE, WHAT HAPPENS
ONCE AN EXOTOXIN REACHES THE TARGET TISSUE, IT USUALLY ENTERS THE CELLS AND CAUSES DAMAGE FROM INSIDE
WHAT KINDS OF S/S DO EXOTOXINS CAUSE
EXOTOXINS CAUSE PATHOGEN SPECIFIC S/S
WHEN EXOTOXINS CAUSE "DAMAGE" INSIDE OF THE CELL....WHAT HAPPENS
DAMAGE INSIDE OF THE CELL INHIBITS PROTEIN SYNTHESIS BY CLEAVING PART OF THE RIBOSOME
DEFINE ADP-RIBOSYLATION
THE EXOTOXIN CAUSES ADP-RIBOSE TO BE ATTATCHED TO CERTAIN PROTEINS IN THE HOST CELL ( INACTIVATES PROTEINS) EXAMPLE OF THE BOOT ON THE CAR
EXO TOXINS INHIBIT INTRACELLULAR MOVEMENT IN THE HOST CELL ( MICROTUBULES)
NOTE
WHAT DOES BOTOX DO
BLOCKS THE RELEASE OF NEUROTRANSMITTERS THAT STIMULATE MUSCLE CONTRACTION=PARALYSIS
WHAT DOES TETANOSPASMIN ( AN EXO TOXIN) DO
BLOCKS THE RELEASE OF NEUROTRANSMITTERS THAT INHIBIT MUSCLE CONTRACTION = UNCONTROLLED CONTRACTION "LOCK JAW"
DEFINE ENDOTOXINS

WHERE DO ENDO TOXINS ORIGINATE

WHEN ARE ENDOTOXINS RELEASED

DO ENDO TOXINS HAVE SPECIFIC TARGETS

DO ENDOTOXINS HAVE PATHOGEN SPECIFIC S/S
USUALLY NOT PROTEIN, NO ENZYMATIC FUNCTION

\THEY ORIGINATE FROM A CELL STRUCTURE LIKE A CELL WALL

ENDOTOXINS ARE RELEASED ONLY DURING REPLICATION OR LYSIS

ENDO TOXINS DON'T HAVE SPECIFIC TARGETS. INSTEAD..THEY CIRCULATE IN BLOOD, LYMPH, AND THE SPACE BTWN CELLS

ENDOTOXINS DON'T HAVE PATHOGEN SPECIFIC S/S
WHAT ARE THE MORE GENERAL EFFECTS OF ENDO TOXINS BASED ON
THE MORE GENERAL EFFECTS ARE BASED ON [ ] . AT LOW [ ] FEVER CHILLS, WEAKNESS, ACHES, INFLAMATION

AT HIGH [ ] CAUSES BLOOD CLOTS , BLOOD CLOTS LOWER BLOOD PRESSURE WHICH CAUSES SEPTIC SHOCK AND DEATH