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

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

Flashcards in Host-Parasite Relationships Normal (Flora) Microbiota Opportunistic Infections Deck (42):
1

Normal Flora: Esophagus and Stomach

Lactobacilli

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Normal Flora: Small Bowel

Duodenum: Lactobacilli and Streptococci

Jejunum and Ileum: Enterobacteria and Bacteroides spp.

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Normal Flora: Large Bowel

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

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Normal Flora: Fecal Material

Bacteroides, Bifidobacteria, Eubacteria, Coliforms, Strep faecalis

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Colonized Sites of the Body

Skin, Mucosa, Intestine, Urogenital tract

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Normally Sterile Sites of the Body

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

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Resident Microbiota

Long-term members of the body's normal microbiota

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Transient Microbiota

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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Staphylococcus epidermidis

***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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Group A Strep (GAS)- Streptococcus pyogenes

***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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Strict Pathogens

Organisms ALWAYS ASSOCIATED with disease
e.g. Mycobacterium tuberculosis, Neisseria gonorrhoeae, rabies virus

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Opportunistic Pathogens

-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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Are most infections caused by strict or opportunistic pathogens?

Opportunistic

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Opportunistic Infections (7 examples)

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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Pathogenicity vs. Virulence

Pathogenicity: ability of a microorganism to cause disease

Virulence: measurement of pathogenicity

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Virulence Factors

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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Carrier

-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***

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Adhesion

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

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

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

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Biofilms

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

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How are cells in biofilms different than planktonic cells?

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

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

Biofilm

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How do bacteria invade cells?

-Hijack host cell machinery

May modulate maturation of the phagosome to promote survival

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Dissemination

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)

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

Listeria

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Endotoxin vs Exotoxin

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

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Two examples of Exotoxins

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)

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Exotoxin: How does the Diphtheria toxin exert its effects?

Inhibits protein synthesis leading to cell death

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Exotoxin: How does the Cholera toxin exert its effects?

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

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Exotoxin: How does C. tetani exert its effects?

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

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Exotoxin: How does C. botulinum exert its effects?

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

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Superantigens

-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

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Mechanisms for Evading Host Defense: Encapsulation (Bacteria Capsule)

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

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Mechanisms for Evading Host Defense: Antigen Mimicry

-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)

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Mechanisms for Evading Host Defense: Antigenic Variation/Shift

-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

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Mechanisms for Evading Host Defense: Inactivation Antibody

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

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

-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

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Mechanisms for Evading Host Defense: Bacteria Escaping Phagocytic Clearance

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

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Regulation of Virulence Factors in Bacteria: Quorum Sensing

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

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

Peptidoglycan

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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?

Inhibit conjugation

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Bacteriocins

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