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Microbiology Exam 1 > Host-Parasite Relationships Normal (Flora) Microbiota Opportunistic Infections > Flashcards

Host-Parasite Relationships Normal (Flora) Microbiota Opportunistic Infections Flashcards

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1
Q

Normal Flora: Esophagus and Stomach

A

Lactobacilli

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2
Q

Normal Flora: Small Bowel

A

Duodenum: Lactobacilli and Streptococci

Jejunum and Ileum: Enterobacteria and Bacteroides spp.

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3
Q

Normal Flora: Large Bowel

A

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

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4
Q

Normal Flora: Fecal Material

A

Bacteroides, Bifidobacteria, Eubacteria, Coliforms, Strep faecalis

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5
Q

Colonized Sites of the Body

A

Skin, Mucosa, Intestine, Urogenital tract

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6
Q

Normally Sterile Sites of the Body

A

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

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7
Q

Resident Microbiota

A

Long-term members of the body’s normal microbiota

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8
Q

Transient Microbiota

A

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
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9
Q

Staphylococcus epidermidis

A
  • 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
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10
Q

Group A Strep (GAS)- Streptococcus pyogenes

A
  • 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
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11
Q

Strict Pathogens

A

Organisms ALWAYS ASSOCIATED with disease

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

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12
Q

Opportunistic Pathogens

A
  • 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
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13
Q

Are most infections caused by strict or opportunistic pathogens?

A

Opportunistic

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14
Q

Opportunistic Infections (7 examples)

A
  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)
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15
Q

Pathogenicity vs. Virulence

A

Pathogenicity: ability of a microorganism to cause disease

Virulence: measurement of pathogenicity

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16
Q

Virulence Factors

A

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

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17
Q

Carrier

A
  • 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

18
Q

Adhesion

A

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
19
Q

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

A

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

20
Q

Biofilms

A

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

21
Q

How are cells in biofilms different than planktonic cells?

A
  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
22
Q

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

A

Biofilm

23
Q

How do bacteria invade cells?

A

-Hijack host cell machinery

May modulate maturation of the phagosome to promote survival

24
Q

Dissemination

A

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)

25
Q

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

A

Listeria

26
Q

Endotoxin vs Exotoxin

A

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

27
Q

Two examples of Exotoxins

A
  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)
28
Q

Exotoxin: How does the Diphtheria toxin exert its effects?

A

Inhibits protein synthesis leading to cell death

29
Q

Exotoxin: How does the Cholera toxin exert its effects?

A

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

30
Q

Exotoxin: How does C. tetani exert its effects?

A

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

31
Q

Exotoxin: How does C. botulinum exert its effects?

A

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

32
Q

Superantigens

A
  • 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
33
Q

Mechanisms for Evading Host Defense: Encapsulation (Bacteria Capsule)

A
  • Generally, a poor antigen
  • Masks more antigenic epitopes on bacterial surface
  • Prevent binding of antibody or complement
34
Q

Mechanisms for Evading Host Defense: Antigen Mimicry

A
  • 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)
35
Q

Mechanisms for Evading Host Defense: Antigenic Variation/Shift

A
  • 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
36
Q

Mechanisms for Evading Host Defense: Inactivation Antibody

A

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

37
Q

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

A
  • 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

38
Q

Mechanisms for Evading Host Defense: Bacteria Escaping Phagocytic Clearance

A

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

39
Q

Regulation of Virulence Factors in Bacteria: Quorum Sensing

A

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
40
Q

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

A

Peptidoglycan

41
Q

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?

A

Inhibit conjugation

42
Q

Bacteriocins

A

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

Microbiology Exam 1 (11 decks)

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