L21: Host-Parasite Relationships/Normal Flora/Opportunistic Infections Flashcards
(42 cards)
1
Q
Commensalism vs mutualism vs parasitism?
A
- Commensalism: host neither benefits nor is harmed, microorganism benefits
- Mutualism: host and microorganism benefits
- Parasitism: host is harmed, while microorganism benefits
2
Q
Niche
A
- Shelter or food for bactereium
3
Q
What are bacteriocins?
A
- Toxins that harm pathogenic microorganisms and are produced by bacteria
4
Q
What locations on the body are considered sterile?
A
- Internal organs/tissue
- Cervix
- Middle ear
- Urinary bladder
- Lungs (may be not however)
5
Q
Resident vs transient microbiota?
A
- Resident: long-term members of body’s normal microbiota
- Transient: organisms attempt to colonize, unable d/t competition with other resident microbiota, elimination by immune system, physical or chemical changes
6
Q
Resident microbiota of skin, nose and ears?
A
- Staphylococcus epidermidis (G+)
7
Q
Causative agent of strep throat?
A
- Streptococcus pyogenes – group A strep (GAS) – G+
- Transiently colonize oropharynx in children and young adults without clinical disease
8
Q
Strict vs opportunistic pathogens?
A
- Strict: organism always associated with disease – Eg. Mycobacterium TB, N. gonorrhea, rabies virus
- Opportunistic: tends to be member of normal microbiota, but takes advantage of preexisting conditions such as immune suppression – eg. E.coli, Candida albicans
9
Q
Bacteria associated with opportunistic infections involving IV catheters?
A
- Staph epidermidis, staph aureus
10
Q
Opportunistic infections of wound/surgical sites involve what organisms?
A
- Staph aureus, Klebsiella pneumonia, Pseudomonas aeruginosa
11
Q
Opportunistic infections leading to bacterial endocarditis are caused by what organisms?
A
- Streptococci viridans bacteria
12
Q
UT opportunistic infections result from what bacteria?
A
- E. coli
13
Q
Opportunistic infections leading to colitis result from what bacteria?
A
- C. difficile
14
Q
Opportunistic infections leading to otitis media result from what bacteria?
A
- Strep. Pneumonia, nontypeable H. influenza and Moraxella catarrhalis
15
Q
Pathogenecity vs virulence
A
- Pathogenecity: ability of microorganism to cause disease
- Virulence: measure of pathogenicity d/t factors: toxins etc.
16
Q
Routes of microorganism entry into host
A
- transplacental
- secretions: genital, GI and respiratory
- stool: fecal oral
- skin cuts
- blood
- zoonotic: animal to human
- arthropod
17
Q
Barriers to prevent pathogen entry into humans
A
- ) Mechanical
- ) Enzymatic
- ) Chemical
- ) Immunity
- ) Commensals
- ) Physical
18
Q
What structure do bacteria typically use to gain entry / bind to host?
A
- Typically through adhesins associated with bacterial pili
19
Q
What are biofilms?
A
- Bacteria encased in exopolymeric substance composed of polysaccharides, DNA, proteins etc.
- Most bacterial therefore are stationary/sessile and don’t live planktonically
20
Q
What differences do biofilms confer to bacteria that planktonic bacteria do not experience?
A
1.) Altered metabolism, slowed typically
2.) Increased resistance to antibiotics
3.) Increased genetic exchange
4.) Resistance to disinfection
• biofilms tend to be unique given the infection
21
Q
Endotoxin vs exotoxin in bacteria
A
- Endotoxin refers to lipid A portion of LPS
- Exotoxin = bacterial products that directly harm tissue or lead to destructive biologic activities – eg. Hemolysins, pore forming toxisn, A-B subunit toxins
22
Q
Function of A-B subunit bacterial exotoxins
A
- B=binds
- A=active component of toxin that performs the harmful action
23
Q
C. diphtheria exotoxin function
A
- B binds, A inactivates elongation factor-2 and prevents protein synthesis by ribosome
24
Q
V. cholera exotoxin function
A
- composed of A2B5
- B binds, A1 increases adenylate cyclase activity and increased cAMP concentration causing efflux of sodium, water, chloride, potassium and bicard = diarrhea
25
C. tetani exotoxin function
- Exotoxin = tetanospasmin, which blocks inhibitory transmitter release allowing for continuous stimulation by excitatory transmitter leading to spastic/rigid paralysis
26
C. botulinum exotoxin function
- Toxin blocks release of ACh from vesicles at NMJ causing flaccid paralysis
27
Action of superantigens. Examples
- Bind both TCR and MHC II without antigen presence. Leads to cytokine storm
- Examples: S. aureus TSST, Staphylococcal enterotoxin, S. pyogenes erythogenic toxins
28
What are various mechanisms by bacteria for escaping host defenses?
1. ) Encapsulation: poor antigen, masks epitopes on bacterial wall, prevents binding of antibody or complement
2. ) Antigenic mimicry: S. pyogenes produces hyaluronic acid found in humans, S. aureus protein A binds Fc portion of antibody and coats bacteria in host protein
3. ) Antigenic variation/shift: moving target as antigenic makeup of proteins on bacteria change – eg. N. gonorrhoeae type IV pili
4. ) Inactivation antibody: secretion of proteases that degrade specific antibody isotypes eg. IgA protease
5. ) Resistance to complement killing: Long O-antigen on LPS means MAC cannot penetrate far enough or components of complement are degraded
6. ) Escaping phagocytic clearance: inhibit opsonization, inhibit chemotaxis, kill phagocyte, inhibit lysosomal fusion, escape from lysosome, resistance to antibacterial action of lysosomal products
29
What is quorum sensing?
- Way for bacteria to sense the size of their population and regulate their gene expression based on this. Bacteria can act as group rather than as individuals when mounting response to host
30
```
Which of the following is not classically considered a virulence factor?
A. Pili
B. Capsule
C. Exotoxin
D. Peptidoglycan
E. LPS
```
- D
31
```
Which of the following is NOT a mechanism that bacteria use to avoid phagocytic clearance?
A. inhibition of opsonization
B. escape from phagosome
C. inhibit chemotaxis
D. inhibit lysosomal fusion
E. inhibit conjugation
```
- E
32
Which of the following is not correct regarding the normal human microbiota?
- Streptococcus mutants in mouth
- Staphylococcus epidermidis on skin
- H. influenza in nasopharynx
- E. coli in large intestine
- Lactobacilli in uterus
- Answer: lactobacilli in uterus
33
Otitis media typically is the result of:
A. Competition with normal middle ear microbiota from a strict pathogen
B. Acquisition of a new virulence factor by a member of normal middle ear microbiota
C. Colonization of middle ear by member of nasopharynx microbiota
D. Colonization of middle ear by a member of GI tract microbiota
- C
34
Normal skin (groin, perineum and feet as well) microbiota
- Staph epidermidis, staph aureus, diphtheroids, streptococci, Pseudomonas aeruginosa, Candida torulopsis, pityrosporum
35
Normal throat microbiota
- Strep viridans, strep pyogenes, strep pneumonia, Neisseria spp., staphylococcus epidermidis, H. influenza
36
Normal teeth microbiota
- Strep mutans, bacteriodes, fusobacterium, streptococci, actinomyces
37
Normal nose microbiota
- Staph aureus, staph epidermidis, diphtheroids, streptococci
38
Normal mouth microbiota
- Strep. Mitis and other streptococci, trichomonas tenax, candida
39
Normal urethra and vagina microbiota
- Staphylococcus epidermidis, diphtheroids, streptococci, gram neg rods
40
Normal microbiota in stomach and small intestine
- Stomach: lactobacilli
| - Small intestine: lactobacilli, streptococci, enterobacteria, bacteroides spp.
41
Normal microbiota in large intestine
- Bacteroides spp, fusobacterium spp, strep faecalis, E. coli, enterobacteria, Klebsiella spp., eubacteria, bifidobacteria, lactobacillus, staph aureus, Clostridium spp, streptococci, Pseudomonas, salmonella
42
Normal microbiota in fecal material
- bacteroides spp, bifidobacteria, eubacteria, coliforms, strep faecalis
