Host-Parasite Relationships Normal (Flora) Microbiota Opportunistic Infections

Question 1

Normal Flora: Esophagus and Stomach

Answer 1

Lactobacilli

Question 2

Normal Flora: Small Bowel

Answer 2

Duodenum: Lactobacilli and Streptococci

Jejunum and Ileum: Enterobacteria and Bacteroides spp.

Question 3

Normal Flora: Large Bowel

Answer 3

Bacteroides, Fusobacterium, Strep faecalis, E coli, Enterobacteria, Klebseilla, Eubacteria, Bifidobacteria, Lactoballus, Staph aureus, Clostridium, Streptococci, Pseudomonas, Salmonella

Question 4

Normal Flora: Fecal Material

Answer 4

Bacteroides, Bifidobacteria, Eubacteria, Coliforms, Strep faecalis

Question 5

Colonized Sites of the Body

Answer 5

Skin, Mucosa, Intestine, Urogenital tract

Question 6

Normally Sterile Sites of the Body

Answer 6

Internal organs and tissue, Cervix, Middle ear, Urinary bladder

Question 7

Resident Microbiota

Answer 7

Long-term members of the body’s normal microbiota

Question 8

Transient Microbiota

Answer 8

Organisms that attempt to colonize the body but are unable to remain due to:

• Competition from resident microbiota
• Elimination by the body’s immune system
• Physical or chemical changes within the body that discourage growth

Question 9

Staphylococcus epidermidis

Answer 9

• Resident (normal) Microbiota*
• Found on skin, nose, ears
• Gram (+) cocci, in CLUSTERS
• Infections associated with PROSTHETIC DEVICES and INTRAVENOUS CATHETERS
• Common contaminant of blood cultures

Question 10

Group A Strep (GAS)- Streptococcus pyogenes

Answer 10

• Transient Microbiota*
• Gram(+) cocci, in CHAINS
• Transiently colonize oropharynx of children and young adults in absence of clinical disease
• Causative agent of STREP THROAT
• Transmitted via AEROSOL or SALIVA

Question 11

Strict Pathogens

Answer 11

Organisms ALWAYS ASSOCIATED with disease

e.g. Mycobacterium tuberculosis, Neisseria gonorrhoeae, rabies virus

Question 12

Opportunistic Pathogens

Answer 12

• Tend to be members of the NORMAL MICROBIOTA
• Take advantage of preexisting conditions, such as immunosuppression to grow and cause disease
  e. g. E. coli, Candida albicans

Question 13

Are most infections caused by strict or opportunistic pathogens?

Answer 13

Opportunistic

Question 14

Opportunistic Infections (7 examples)

Answer 14

1. Contamination of intravenous catheters
2. Wound/Surgical site infections
3. Bacterial Endocarditis (can get it by flossing)
4. Aspiration pneumonia (inhaling fluids)
5. UTI
6. Pseudomembrane colitis (C. difficile; common after broad spectrum antibiotic use)
7. Otitis media (bacteria present in the nasopharynx migrate into the inner ear)

Question 15

Pathogenicity vs. Virulence

Answer 15

Pathogenicity: ability of a microorganism to cause disease

Virulence: measurement of pathogenicity

Question 16

Virulence Factors

Answer 16

Factors (e.g. toxins or proteins) produced by an organism that enable it to infect, cause disease, and/or kill a host

Question 17

Carrier

Answer 17

• ASYMPTOMATIC individual who is host to a pathogen
• Has the POTENTIAL TO TRANSMIT the pathogen to others
  e. g. GAS, Salmonella Typhi

Carriers may be transient or (semi) permanent

Question 18

Adhesion

Answer 18

Binding of the bacterial adhesin to the host cell surface (receptor)

• Commonly associated with BACTERIAL PILI (fimbrae)
• Specific adhesin and receptor combos often define TROPISM

Question 19

Are most bacteria planktonic (free-moving) or sessile (stationary)?

Answer 19

Sessile; they adhere to surfaces or other bacteria as part of a BIOFILM

Question 20

Biofilms

Answer 20

Bacteria encased in a EXOPOLYMERIC SUBSTANCE (e.g. polysaccharide, DNA, etc.) of their own making

Found throughout nature on moist/wet surfaces, baths/showers, and teeth

***Majority of bacteria on body are living as biofilms

Question 21

How are cells in biofilms different than planktonic cells?

Answer 21

1. Altered, generally SLOWED, metabolism
2. Increased resistance to abx (slowed metabolism = decreased diffusion of abx)
3. Increased genetic exchange –> increased likelihood of abx resistance transfer
4. Resistant to disinfection = decreased diffusion, increased organic matter

Question 22

Most chronic bacterial infections (some acute) have a ____ component

Answer 22

Biofilm

Question 23

How do bacteria invade cells?

Answer 23

-Hijack host cell machinery

May modulate maturation of the phagosome to promote survival

Question 24

Dissemination

Answer 24

Some bacteria can produce toxins that cause pathology in other parts of the body (e.g. toxin produced in the intestines finds its way to the kidneys)

Question 25

Example of a bacterium that adheres, enters, and disseminates:

Answer 25

Listeria

Question 26

Endotoxin vs Exotoxin

Answer 26

Endotoxin: lipid A portion of LPS (a component of the outer leaflet of the outer membrane of gram negative bacteria) Exotoxin: bacterial product that directly harms tissue or leads to destructive biologic activities

Question 27

Two examples of Exotoxins

Answer 27

1. Cytolytic enzymes (hemolysins, pore forming toxins) 2. Receptor binding proteins that initiate toxic reactions (e.g. A-B subunit toxins (AB toxins); A = active (carries out mechanism) and B = binding (binds target and facilitates entry of the A portion)

Question 28

Exotoxin: How does the Diphtheria toxin exert its effects?

Answer 28

Inhibits protein synthesis leading to cell death

Question 29

Exotoxin: How does the Cholera toxin exert its effects?

Answer 29

Hyperactivation; leads to increased release of solutes in the intestines and subsequent diarrhea

Question 30

Exotoxin: How does C. tetani exert its effects?

Answer 30

Blocks inhibitory transmitter release in nerve-muscle transmission leading to continuous stimulation by excitatory transmitters and PARALYSIS

Question 31

Exotoxin: How does C. botulinum exert its effects?

Answer 31

Blocks release of ACH from vesicles in nerve-muscle transmission, leading to flaccid paralysis (i.e. muscle will never contract)

Question 32

Superantigens

Answer 32

- Binds both T-cell receptor and MHCII without a requiring antigen - "Cytokine storm" due to activation of large numbers of T-cells --> life-threatening autoimmune-like responses * **This is generally IRREVERSIBLE*** e. g. S. aureus TSST, Staph enterotoxin, S. pyogenes erythogenic toxins

Question 33

Mechanisms for Evading Host Defense: Encapsulation (Bacteria Capsule)

Answer 33

- Generally, a poor antigen - Masks more antigenic epitopes on bacterial surface - Prevent binding of antibody or complement

Question 34

Mechanisms for Evading Host Defense: Antigen Mimicry

Answer 34

- Bacteria produce compounds that the host sees as self e. g. S. pyogenes capsule (hyaluronic acid) and S. aureus protein A (binds Fc protein of antibody, thus coating bacteria in host protein)

Question 35

Mechanisms for Evading Host Defense: Antigenic Variation/Shift

Answer 35

- Bacteria change antigenic make up of proteins on their cell surface, creating a "moving target" for the immune system e. g. Neisseria gonorrhoeae type IV pili (many silent copies of the pilin gene in the genome

Question 36

Mechanisms for Evading Host Defense: Inactivation Antibody

Answer 36

Secretion of proteases that degrade specific antibody isotypes (e.g. IgA protease)

Question 37

Mechanisms for Evading Host Defense: Resistance to complement-mediated killing

Answer 37

- Limiting access to the membrane (capsule, long O-antien on LPS (on gram negative bacteria)) - Degradation of components of complement ***Complement either cannot bind or mac attack complex cannot penetrate lipid membrane

Question 38

Mechanisms for Evading Host Defense: Bacteria Escaping Phagocytic Clearance

Answer 38

-inhibit opsonization, inhibit chemotaxis, kill phagocyte, inhibit lysosomal fusion, escape from lysosome, resistant antibacterial lysosomal action

Question 39

Regulation of Virulence Factors in Bacteria: Quorum Sensing

Answer 39

A way for bacteria to sense the size of their population - When concentration is HIGH (Critical mass) they turn on virulence factors and cause disease * **Allows bacteria to act as a GROUP, rather than individuals

Question 40

Which of the following is not classically considered a virulence factor: Pili, Capsule, Exotoxin, Peptidoglycan, Lipopolysaccharide?

Answer 40

Peptidoglycan

Question 41

Which of the following is not a mechanism that bacteria use to avoid phagocytic clearance: Inhibit opsonization, Escape from phagosome, Inhibit chemotaxis, Inhibit lysosomal fusion, Inhibit conjugation?

Answer 41

Inhibit conjugation

Question 42

Bacteriocins

Answer 42

Toxins produced by the normal microbiota (flora) that harm pathogenic microorganisms