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Exam 3 > Bacterial Pathogenesis and Host Defenses > Flashcards

Bacterial Pathogenesis and Host Defenses Flashcards

1
Q

What is a pathogen?

A

bacteria capable of causing disease

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2
Q

What is virulence?

A

quantitative measure of pathogenicities measured by the number of bacteria required to cause disease

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3
Q

What is LD50?

A

number of bacteria necessary to kill half the host

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4
Q

What is ID50?

A

number of bacteria necessary to cause infection in half the hosts

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5
Q

What are virulence factors?

A

properties of a bacteria which assist in causing disease ex: pili, capsules, toxins, etc.

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6
Q

What are the stages of bacterial pathogenesis?

A
  1. Transmission from an external source into the body
  2. Evasion of initial host defenses
  3. Attachment to mucous membranes
  4. Colonization at attachment site
  5. Sometimes spread and reattachment
  6. Disease symptoms caused by toxins or tissue invasion followed by inflammation
  7. Non specific and specific immune host responses
  8. Progression or resolution of the disease
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7
Q

What are the mechanisms of bacterial disease?

A

TIT
1. Tissue invasion followed by inflammation

  1. Toxins (exotoxins and endotoxins)
  2. Immunopathogenesis eg. Rheumatic fever
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8
Q

How does transmission occur between humans?

A

DNTT

  1. Direct contact cg infections mono
  2. Non-direct contact eg. fecal-oral
  3. Transplacental
  4. Transferred blood products or contaminated needles
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9
Q

How does transmission occur non-human to human?

A

SWAI

  1. Contaminated soils eg. Tetanus
  2. Contaminated water eg. Legionnaires’ disease
  3. Direct from animals eg. Cat Scratch fever
  4. Insect vectors eg. Lyme disease
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10
Q

What are the portals of entry?

A

RiGGS!
Respiratory tract- largest mechanism

GI tract- second

Skin

Genital tract

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11
Q

What are bacterial structures that effect virulence?

A

Structures that allow bacteria to attack!

  1. Pili eg. N. gonorrhea to urinary tract epithelium
  2. Capsules eg. Strep. pneumonia
  3. Glycocalyx eg. Strep. viridans in heart valves
  4. Endotoxin eg. Gram negative bacteria
  5. Biofilms eg. Pseudomonas in cystic fibrosis patients
  6. Bacterial Secretion Systems eg. T3SS in Salmonella typhimurium
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12
Q

What are secreted enzymes that effect virulence?

A

LICC

  1. Collagenase & hyaluronidase eg. Strep. pyogenes cellulitis
  2. Coagulase eg. Helps coat Staph. aureus with fibrin to help PROTECT from phagocytosis
  3. Immunoglobulin A protease eg. Degrades IgA allowing Strep. Pneumonia to adhere to mucous membranes
  4. Leukocidins Destroy neutrophilic leukocytes and macrophages eg. Staphylococci and group A Streptococci
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13
Q

What are other bacterial factors that effect virulence?

A
  1. M protein - antiphagocytic protein produced by Strep. pyogenes found on surface of bacteria, helps bacteria to survive
  2. Protein A - binds to IgG and prevents activation of complement (complement necessary to lyse bact)
  3. Invasins - bacterial molecules which promote bacterial entry or contact with host cells - eg. Heliobacter pylori
  4. Outer membrane proteins - produced by Yersinia species to inhibit phagocytosis and cytokine production (cell signaling)
  5. Pathogenicity Islands (PAIs) – code for groups of virulence factors particularly in Gram negatives (get rid of PAI, bacteria loses ability to cause disease)
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14
Q

What are endotoxins?

A
  1. Lipid A component of Gram negative bacteria
  2. Encoded in chromosome, plasmid or phage
  3. Become toxoids (inactivated) when treated with formaldehyde, and/or heat and used for protective vaccines
  4. A-B subunit structure (A portion has toxic activity and B portion is involved in binding to cells)
  5. Only weakly antigenic; no toxoids made
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15
Q

What are exotoxins? What are the biological effects of exotoxins?

A

Secreted by gram pos and gram neg bacteria, may be genetically encoded chromosome, plasmid or phage

  1. Alter cellular components
  2. Act as super-antigens and cause inapproprite release of cytokines
  3. Inhibit protein synthesis
  4. Increase synthesis of cAMP
  5. Alter nerve impulse transmissions
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16
Q

What are the biological effects of endotoxins?

A
  1. Induce the release of endogenous pyogenes
  2. Increase vascular permeability
  3. Imitate complement and blood coagulation cascades
  4. Cause fever, hypotension, disseminated intracellular coagulation and shock
17
Q

What are the components of innate immunity?

A

MC (MARY CARLSON my mama will protect you…all the time)
1. Macrophages: Phagocytize and digest bacteria

  1. Complement: Assist host immune cells and antibody in lysis of bacteria and virus-infected cells
18
Q

What are the components of acquired immunity?

A
  1. Antibodies-
    a. Cytolytic,
    b. Neutralizing (antibody that reacts with viral attachment protein, covers up attachment protein so no longer can infect)
    c. Opsonins (created for anything that is foreign)
  2. Cytotoxic T Cells- Kill antibody-coated bacteria and virus-infected cells (viral antigens on surface, antibodies react with them, T cells see that and kill cel)

**Aquired–only occur after you have stimulus from one of foreign parasites you’ve experienced

19
Q

What is passive immunity?

A

Administration of preformed antigen-specific antibodies to help protect from disease

ex. Human rabies immune globulin–preformed human rabies antibodies that you give to someone you thing has rabies, then they don’t have to generate antibodies themselves

20
Q

What is active immunity?

A

Administration of specific antigens to stimulate an individual to develop immunity to help protect from a disease

ex. Influenza vaccine–give person virus that is less likely to produce disease, body generates immune response, so when virus comes in it is neutralized/limited

**some diseases have passive and active, some just have passive

21
Q

What are the differences between live and killed viruses?

A
  1. Live are better because they go through natural progression of virus replication in humans
  2. Killed are injected into blood, so you get less of immune response
22
Q

What are the three bacterial strategies to deal with phagocytic cells?

A
  1. Avoiding contact with phagocytes
  2. Inhibition of engulfment
  3. Survival within the phagocyte
23
Q

How does the bacteria avoid contact with the phagocyte?

A
  1. The bacteria can reside in a niche not patrolled by phagocytes.
  2. The bacteria can suppress inflammation and/or chemotaxis.
  3. The bacterium can coat itself with host proteins (more later).
24
Q

How do bacteria inhibit engulfment by phagocytes?

A
  1. Many bacterial capsules are anti-phagocytic.
  2. Some surface polysaccharides (such as those that aid in biofilm structure) are anti-phagocytic.
  3. Some bacteria produce specific anti-phagocytic products.
  4. Capsules can inhibit phagocytosis AND complement activation
25
Q

How do bacteria survive within phagocytes?

A

Intracellular survival is mediated by bacteria in three basic ways:
Escape the phagosome
Shigella, Lysteria
Adapt to the phagosome
Coxiella, Leishmania
Modify the phagosomal compartment
Salmonella, Legionella, Mycobacteria, etc.

26
Q

What are the other methods of avoidance by bacteria?

A

LPS O-antigen
Blocks MAC access - keeps at “arm’s length.”
Complement component peptidases
Destroy complement components. This inactivates the components AND stops complement activation.

27
Q

What is antigenic variation?

A

Use to avoid acquired immune response

  1. Some bacteria spontaneously change the profile of the surface proteins that they express.
  2. Antibodies are formed in response to specific antigens on the bacteria.
  3. Because of a delay in the immune response (antibody formation), the bacteria can stay one step ahead by producing variants of itself.

Ex. Trypanosome Variant-Specific Glycoprotein (VSG) cassettes.

28
Q

What is immunological disguise?

A

Use to avoid acquired immune response
1. Bacteria coat themselves with host proteins
2. Disguised by “self” proteins – camouflage!
3.Examples:
E.g. proteins produced by some bacteria bind Antibodies – BACKWARDS!
E.g. The Treponema pallidum parasite coats itself with host fibronectin.
E.g. S. aureus produces coagulase and clumping factor. This leads to the deposition of host fibrin on the bacterial surface.

29
Q

**How does staphylococcus avoid immune response?

A
  1. Synthesizes protein A
  2. Bacteria looks normal to immune system, disguises itself by having normal cellular proteins bind to it, so that immune system doesn’t see it, then it’s not killed
30
Q

What are the important aspects of pseudamonas?

A
  1. Gram -
  2. Involved in CF pts
  3. Forms biofilm (mixture of bacteria over areas of body)–can occur in place where joints have been replaced
  4. Mechanisms of antibiotic resistance
31
Q

What is quorum sensing? (Salmonella and pseudamonas)

A
  1. Bacteria go in and don’t sythesize all of their virulence factors so they won’t look to foreign to the body
  2. Synthesize autoinducers
  3. Bacteria multiplies–when conc of those molecules increase, bind to surface of cell, and set off rxn to make a HUGE amt of virulence factors, enough to sur
  4. Occurs in biofilms, made up of individual bacteria and things it secretes

Exam 3 (12 decks)

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