Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

INF > MECHANISMS OF BACTERIAL VIRULENCE 2 > Flashcards

MECHANISMS OF BACTERIAL VIRULENCE 2 Flashcards

1
Q

PATHOGENICITY DEFINITION?

A

CAPACITY TO INITIATE DISEASE (QUALITATIVE, ALL OR NONE CONCEPT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

WHAT IS VIRULENCE?

A

CAPACITY TO CAUSE DISEASE AND THE SEVERITY OF THAT DISEASE (QUANTIFIES PATHOGENICITY)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

WHAT IS INFECTIVITY?

A

ABILITY OF A PATHOGEN TO BREAK HOST DEFENSES

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

WHAT ARE VIRULENCE FACTORS?

A

PROTEINS ENCODED BY A BACTERIAL ORGANISM THAT ARE ESSENTIAL FOR ITS PATHOGENICITY (HELP ACHIEVE INFECTION)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

ROLE OF KOCH’S POSTULATES AND WHEN WERE THEY CREATED?

A
  • TO DETERMINE WHETHER A MICROORGANISM CAUSES A DISEASE

- 19 TH CENTURY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

LIST THE KOCH’S POSTULATES?

A

1) THE SUSPECTED CAUSATIVE AGENT MUST BE ABSENT FROM ALL HEALTHY ORGANISMS BUT PRESENT IN ALL DISEASED ONES
2) IT MUST BE ISOLATED FROM THE DISEASED ORGANISM AND GROWN IN PURE CULTURE
3) THE CULTURED AGENT MUST THE SAME DISEASE WHEN INOCULATED INTO A HEALTHY SUSCEPTIBLE ORGANISM
4) THE SAME CAUSATIVE AGENT MUST THEN BE REISOLATED INOCULATED, DISEASED ORGANISM

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

LIMITATIONS OF KOCH’S POSTULATES?

A
  • CAUSATIVE AGENTS ARE SOMETIMES PRESENT IN HEALTHY ORGANISMS BUT NEVER CAUSE A DISEASE, WHICH KOCH OVERLOOKED
  • NOT ALL PATHOGENS CAN BE GROWN IN PURE CULTURE
  • SOME HUMAN DISEASE CAN’T BE RELIABLY REPLICATED IN HUMAN HOSTS, SO THE POSTULATES AREN’T ALWAYS USEFUL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

WHAT ARE THE STEPS TO INFECTION?

A

1) TRANSMISSION (EXPOSURE TO PATHOGENS)
2) ADHERENCE (BINDING TO THE SKIN OR MUCOSA)
3) INVASION (BREAKING THROUGH THE BARRIER)
4) SURVIVAL IN THE HOST (GROWTH ON ORIGINAL AND DISTAL SITES, PRODUCTION OF VIRULENCE FACTORS)
5) TISSUE DAMAGE (TOXICITY AND THE DISEASE)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

WHAT ARE BACTERIAL SECRETION SYSTEMS AND HOW MANY TYPES ARE THERE?

A
  • KEY TO PATHOGENICITY
  • SYSTEMS WITH THE CAPACITY TO SECRETE MOLECULES AND VIRULENCE FACTORS OUT OF THE BACTERIAL CELL TO THE CONTACT HOST CELL
  • TYPES I-IX
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

WHICH BACTERIAL SECRETION SYSTEMS HAVE THE CAPACITY TO TRANSFER PROTEINS DIRECTLY FROM THE CYTOPLASM TO THE OUTSIDE OF THE BACTERIAL CELL (ONE-STEP MECHANISM)? HOW IS SECRETION DONE BY OTHER SYSTEMS?

A

I, III, IV, VI AND VII
OTHER SYSTEMS CAN ONLY SECRETE PROTEINS FROM THE PERIPLASM TO THE OUTSIDE SPACE (TWO-STEP ACTIVITY, PROTEINS ARE FIRST TRANSPORTED OUT OF THE INNER CELL MEMBRANE, THEN DEPOSITED IN THE PERIPLASM AND FINALLY THROUGH THE OUTER CELL MEMBRANE INTO THE HOST CELL)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

WHICH BACTERIAL TRANSPORT SYSTEMS DELIVER PROTEINS DIRECTLY INTO THE CYTOPLASM OF THE HOST CELL, USING SPECIALISED PILI?

A

III, IV, VI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

WHICH SECRETION SYSTEMS ARE PRESENT IN BOTH G+ AND G- BACTERIA?

A

I, II, V, VI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

TYPE VII SECRETION SYSTEM IS SPECIFIC TO WHICH TYPE OF BACTERIA?

A

GRAM POSITIVE BACTERIA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

TYPES III AND VI SECRETION SYSTEMS ARE EXCLUSIVE TO WHICH TYPE OF BACTERIA?

A

GRAM NEGATIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

WHICH TYPE OF SECRETION SYSTEM IS INVOLVED IN FLAGELLA BUILDING?

A

TYPE III

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

WHAT IS A RESERVOIR?

A

THE NATURAL SITE OF A PATHOGEN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

WHAT IS MODE OF TRANSMISSION?

A

THE MECHANISM BY WHICH THE HOST PICKS UP THE PATHOGEN (E.G. DIRECT OR INDIRECT CONTACT, DROPLET, AIRBORNE..)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

MOST COMMON ROUTES OF ENTRY FOR A PATHOGEN?

A
  • RESPIRATORY
  • GI
  • MUCUS MEMBRANE
  • SKIN
19
Q

WHAT IS INITIAL BACTERIAL ATTACHMENT MOST OFTEN MEDIATED BY?

A

PROTEIN APPENDAGES SUCH AS FIMBRIAE/PILI (SHORT FIBRES, ENABLE BACTERIA TO STICK) AND FLAGELLA (LONGER, USED FOR MOTILITY)

20
Q

WHAT ARE EXOPOLYSACCHARIDES?

A
  • STRUCTURES THAT HELP MEDIATE BACTERIAL ADHESION
  • CONSIST OF MONOSACCHARIDES AND ARE SECRETED BY BACTERIA INTO THEIR ENVIRONMENT
  • HYDROPHOBIC STRUCTURES THAT CAN DISPLACE WATER BETWEEN THE BACTERIUM AND THE HOST CELL SURFACE PROMOTING CLOSER CONTACT
21
Q

DESCRIBE THE ‘ZIPPER MECHANISM’ OF BACTERIAL INVASION?

A
  • BACTERIA EXPRESS PROTEINS THAT BIND WITH HIGH AFFINITY TO HOST CELL ADHESION RECEPTORS (E.G. INTEGRINS, CADHERINS)
  • TRIGGERS HOST CELLS INTO ATTEMPTING TO BIND TO ANOTHER CELL, FORM CELL JUNCTIONS AND SPREAD OVER THE BACTERIUM
  • THE SMALL SIZE OF THE BACTERIAL CELL RELATIVE TO HOST CELL RESULTS IN THE ENGULFING OF THE BACTERIUM
22
Q

DESCRIBE THE ‘TRIGGER MECHANISM’ OF BACTERIAL INVASION?

A
  • BACTERIA EXPRESS PROTEINS KNOWN AS EFFECTORS
  • INJECTED DIRECTLY INTO THE HOST CELL CYTOPLASM USING TYPE III SECRETION SYSTEM
  • ACTIVATE SIGNALLING PATHWAYS LEADING TO CYTOSKELETAL REARRANGEMENTS AND THE FORMATION OF MEMBRANE RUFFLES
  • RUFFLES EXTEND AROUND THE BACTERIA AND FUSE AROUND IT
  • E.G. SALMONELLA AND SHIGELLA
23
Q

DESCRIBE THE BACTERIAL SURVIVAL IN THE HOST?

A
  • VACUOLES (WHERE BACTERIA ARE ONCE ENGULFED) ARE HOSTILE ENVIRONMENTS (LOW PH, NUTRIENT DEPRIVED, TARGETED BY HOST DEFENCES)
  • THEY NEED TO ESCAPE INTO THE CELL CYTOPLASM WHERE THEY MULTIPLY RAPIDLY BEFORE SPREADING TO ADJACENT CELLS
  • BACTERIA SCAVENGE SPECIFIC HOST DERIVED NUTRIENTS LIKE AMINO ACIDS AND IRON (VIA SPECIFIC UPTAKE SYSTEMS)
  • BACTERIA NEED TO HIDE FROM AUTOPHAGY
  • BACTERIA NEED TO AVOID LYSOSOME KILLING
24
Q

WHAT ARE SIDEROPHORES?

A

SPECIFIC BACTERIAL SYSTEMS FOR UPTAKE OF HOST IRON

25
Q

WHAT IS AUTOPHAGY?

A

PROCESS/MECHANISM THROUGH WHICH HARMFUL CYTOPLASMIC MATERIAL IS TARGETED FOR LYSOSOMAL DEGRADATION

26
Q

HOW DOES M. TUBERCULOSIS AVOID LYSOSOMAL KILLING?

A

BY PREVENTING LYSOSOMAL FUSION; RELEASES EFFECTORS THAT MODIFY A LYSOSOME MEMBRANE SIGNALLING LIPID; PtdINS(3)P

27
Q

EXAMPLE OF BACTERIA THAT LOCALISES THE VACUOLE TO NUTRIENT RICH AREAS OF THE HOST CELL?

A

SALMONELLA

28
Q

HOW DOES LEGIONELLA PNEUMOPHILA ESCAPE LYSOSOMAL KILLING?

A

BY DIRECTLY CONNECTING ITS VACUOLE TO THE ENDOPLASMIC RETICULUM, MANAGING TO AVOID FUSION WITH LYSOSOMES (DONE PRIMARILY BY TARGETING HOST CELL GTPases)

29
Q

HOW DOES CHLAMYDIA AVOID LYSOSOMAL KILLING?

A

BY CONNECTING VACUOLES CONTAINING CHLAMYDIA WITH THE GOLGI BODY

30
Q

WHAT ARE OBLIGATE PATHOGENS + AND EXAMPLE?

A

ORGANISMS THAT REQUIRE A HOST TO FULFILL THEIR LIFE CYCLE, MOSTLY ANAEROBIC (E.G. CHLAMYDIA)

31
Q

WHAT ARE FACULTATIVE INTRACELLULAR PATHOGENS? (+EXAMPLE)

A

ORGANISMS FOR WHICH THE HOST IS ONLY ONE OF THE NICHES THEY CAN EXPLOIT TO REPRODUCE, E.G. SALMONELLA

32
Q

WHAT ARE EXTRACELLULAR PATHOGENS? (+ EXAMPLES)

A

THRIVE INDEPENDENTLY OF A HOST (S. AUREUS, E. COLI)

33
Q

WHAT IS THE PRIMARY CAUSE OF TISSUE DAMAGE DURING BACTERIAL INFECTION?

A

TOXINS

34
Q

2 MAIN TYPES OF BACTERIAL TOXINS?

A

EXOTOXINS AND ENDOTOXINS

35
Q

CAN TOXINS CAUSE DISEASE INDEPENDENT OF BACTERIUM?

A

YES

36
Q

EXOTOXINS VS ENDOTOXINS, WHICH ARE SECRETED BY G+/G- BACTERIA?

A

EXOTOXINS SECRETED BY BOTH G+ AND G-

ENDOTOXINS SECRETED BY ONLY G-

37
Q

PROPERTIES OF BACTERIAL EXOTOXINS?

A
  • HEAT LABILE
  • IMMUNOGENIC (ABLE TO PRODUCE AN IMMUNE RESPONSE)
  • CAN BE ENZYMATIC (MAKING THEM POTENT)
38
Q

TYPES OF EXOTOXINS? (EXAMPLES)

A
  • SUPERANTIGENS (ACT DIRECTLY ON T CELLS, E.G. PYROGENIC, I.E. ‘CAUSING FEVER’)
  • NEUROTOXIN
  • ENTEROTOXIN
  • CYTOTOXIN
  • PORE FORMING TOXIN (INSERTS PORES INTO HOST CELL MEMBRANE)
39
Q

DESCRIBE THE STRUCTURE OF AB EXOTOXINS?

A

SUBUNTIT A: ENZYMATIC ACTIVITY (A- ACTIVE COMPONENT)
SUBUNIT B: BINDING TO SPECIFIC RECEPTOR AND TRANSFERRING ACROSS THE HOST CELL MEMBRANE (B- BINDING COMPONENT)
- ENZYMATIC PART NOT ACTIVE UNTIL THE MATURATION OF TOXIN

40
Q

EXAMPLES OF AB EXOTOXINS?

A

SHIGA-LIKE TOXINS, DIPTHERIA EXOTOXIN, CHOLERA EXOTOXIN, ENTEROTOXINS, PERTUSSIS EXOTOXIN, ANTHRAX TOXINS..

41
Q

DIFFERENCES BETWEEN A+B, A-B AND A/B TOXINS?

A

A+B SYNTHESIZED AND SECRETED SEPARATELY
A-B SYNTHESIZED SEPARATELY BUT ASSOCIATED DURING SECRETION
A/B SYNTHESIZED TOGETHER BUT INACTIVE UNTIL CLEAVED

42
Q

WHAT ARE ENDOTOXINS?

A

TOXIC COMPONENTS OF BACTERIAL CELL ENVELOPE LIPOPOLYSACCHARIDE (LPS) (LIPID A OF LPS)

43
Q

PROPERTIES OF BACTERIAL ENDOTOXINS?

A
  • NOT PROTEINS
  • HEAT STABLE
  • WEAKLY ANTIGENIC (NO VACCINE)
  • NON-ENZYMATIC (NEED HIGHER DOSES)
  • ASSOCIATED WITH ENDOTOXIC SHOCK
44
Q

WHERE IS LIPOPOLYSACCHARIDE (LPS) RELEASED FROM? WHAT IS IT DEGRADED TO AFTER BEING RELEASED?

A
  • FROM THE BACTERIAL MEMBRANE
  • DEGRADED INTO: O-ANTIGEN & CORE PART (NON IMMUNOGENIC) AND TO LIPID A (HIGHLY PRO-INFLAMMATORY, ACTIVATES CASCADE AND PRODUCTION OF CYTOKINES, CAN HAVE MILD TO SEVERE EFFECTS)

INF (40 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions