Infection Flashcards

0
Q

Allergy’s

A
  1. Exaggerated response against noninfectious environmental substances
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1
Q

Hypersensitivity Reactions

A
  1. Inappropriate responses by the immune system
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2
Q

AutoImmunity

A
  1. Misdirected response against the body’s own cells
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3
Q

Alloimmunity

A
  1. Misdirected response against beneficial foreign tissues, such as transfusions or transplants
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4
Q

Factors Influencing Infection

-Communicability

A
  1. Ability to spread from one individual to another and cause disease

Ex. Measles and Pertussis spread very easily
-HIV has lower communicability

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5
Q

Factors Influencing Infection

-Immunogenicity

A
  1. Ability of pathogens to induce an immune response
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6
Q

Factors Influencing Infection

-Infectivity

A
  1. Ability of the pathogen to invade and multiply in host
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7
Q

Factors Influencing Infection

-Mechanism of Action

A
  1. Manner in which the microorganism damages tissues
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8
Q

Factors Influencing Infection

-Pathogenicity

A
  1. Ability of an agent to produce disease – depends on all of the above mentioned:
    - communicability
    - immunogenicity
    - infectivity
    - mechanism of action
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9
Q

Factors Influencing Infection

-Portal of Entry

A
  1. Route by which a pathogenic microorganism infects the host
    - Direct Contact
    - Inhalation
    - Ingestion
    - Insect “bites”
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10
Q

Factors Influencing Infection

-Toxigenicity

A
  1. Ability to produce soluble toxins or endotoxins

- factors that greatly influence virulence

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11
Q

Factors Influencing Infection

-Virulence

A
  1. Capacity of pathogen to cause severe disease
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12
Q

Classes of Infectious Microorganisms

A
  1. Bacteria
  2. Viruses
  3. Fungi
  4. Parasites
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13
Q

Pathogens Defense Mechanisms

-All Defenses

A
  1. Prevents Phagocytosis
  2. Changes surface antigens
  3. Hides
  4. Fast proliferation
  5. Produce Toxins
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14
Q

Pathogens Defense Mechanisms

-Changes surface antigens

A
  1. Adds surface antigens or causes major changes to surface antigens (antigenic Drift/Shift)
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15
Q

Antigenic Shift

A
  1. A major change in the genetic makeup of an organism, usually resulting from gene reassortment or occurring when different species share genetic material.

Ex. Influenza Virus Type A is the most common example of an organism that undergoes antigenic shift

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16
Q

Antigenic Drift

A
  1. A minor change in the protein marker or antigen on an organism.
  2. Ex. Influenza virus change from year to year
  3. Vaccinations against the virus have to be adapted annually to combat changes
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17
Q

Pathogens Defense Mechanisms

-Hides

A
  1. The pathogen hides inside the cell
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18
Q

Pathogens Defense Mechanisms

-Fast Proliferation

A
  1. Quickly multiplies to surpass the development of the protective response
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19
Q

Pathogens Defense Mechanisms

-Produce Toxins

A
  1. Produces toxins that destroy neutrophils
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20
Q

Pathogens Defense Mechanisms

-Prevent Phagocytosis

A
  1. Produce thick capsules of protein and carbohydrates to prevent phagocytosis
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21
Q

Pathogen

-Site of Entry

A
  1. Skin and mucous membrane
  2. Alimentary, GU and Respiratory Tracts
  3. Eyes and ears
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22
Q

Pathogen

-Route of Entry

A
  1. Direct Contact
  2. Inhalation
  3. Ingestion
  4. Vector bite
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23
Q

Pathogen

-Mechanism of Infection

A
  1. Adhesion
  2. Enzyme release
  3. Phagocytic escape
  4. Acid resistance
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24
Q

Pathogen for Each Entry Point

-Skin

A
  1. Chickenpox
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25
Q

Pathogen Entry Points

-Lungs

A
  1. Measles

2. TB

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26
Q

Pathogen Entry Points

-GU

A
  1. Gonorrhea
  2. AIDS
  3. Hepatitis B
  4. Yellow Fever
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27
Q

Infection

  • Bacterial/Viral
  • Clinical Manifestations
A
  1. Fever
  2. Body aches
  3. Lymph node enlargement
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28
Q

Infection

  • Fungal
  • Clinical Manifestations
A
  1. Itching
  2. Redness of skin
  3. Thrush
  4. Nail thickening
29
Q

Infection

  • Protozoal/Helminths
  • Clinical Manifestations
A
  1. Itching
  2. Rash
  3. Diarrhea
  4. Fever
30
Q

Bacterial Virulence and Infectivity

-Exotoxins

A
  1. Enzymes release during growth, causing specific responses
  2. Immunogenic (capable of producing immune reponse)
    - Antitoxin production

Ex. Cytotoxins / neurotoxins / pneumotoxins / enterotoxins / hemolysins

31
Q

Bacterial Virulence and Infectivity

-Endotoxins

A
  1. Lipopolysaccharides contained in the cell walls of GRAM NEGATIVE organisms
  2. PYROGENIC effects
  3. Increase capillary permeability further by activating anyphlatoxins
32
Q

Bacterial Virulence and Infectivity

-Bacteremia or Septicemia

A
  1. Presence of bacteria in the blood as a result of a failure of the body’s defense mechanisms
  2. Usually caused by GRAM-NEGATIVE bacteria
33
Q

Bacterial Virulence and Infectivity

-Gram-Negative Bacteria

A
  1. Release toxins into the blood that cause:
    - Widespread Vasodilation
  2. Tumor Necrosis Factor-Alpha (TNF-alpha)
    - Produced by activated macrophages when exposed to endotoxins from GRAM-NEGATIVE bacteria (chachectin)
34
Q

Segmented Neutrophils

A
  1. Mature WBC’s
35
Q

Bands of Neutrophils

A
  1. Immature WBC’s
36
Q

Left Shift

A
  1. Greater % of Immature (bands) than Segments (Mature) = severe prolonged infection
37
Q

Infection

-Diagnostics

A
  1. Increased WBC count shows infection

2. Increased number of immature Leukocytes

38
Q

WBC’s

-Normal Values

A
  1. WBC’s = 5-10
  2. Immature (bands) = 3-6%
  3. Mature (Segments) 50-62%
39
Q

WBC’s

-Shift to the Left

A
  1. WBC’s = 15
  2. Immature (bands) = 10%
  3. Mature (Segments) = 65%
40
Q

Viral Infection & Injury

-Overview

A
  1. Intracellular “parasites”
    - Dependent on host cells
    - No metabolism or incapable of independent reproduction
    - Virion binds to receptors on the plasma membrane
    - Spreads cell to cell
41
Q

Viral Replication Process

A
  1. Virion binds to receptor site
  2. Penetration
  3. Uncoating
  4. Replication
  5. Budding
  6. Release of new infective virions
42
Q

Cellular effects of Viruses

A
  1. Stops DNA, RNA, and Protein Synthesis
  2. Disrupts lysosomal membranes
  3. Fusion of host cells, producing giant cells
  4. Alteration of antigenic identity, causing immune system attack
  5. Transformation of host cells into cancerous cells
  6. Promotion of secondary bacterial infections in tissues damaged by viruses
43
Q

Fungal Infection & Injury

-Overview

A
  1. Large w/ thick cell walls
  2. Eukaryotes
  3. Exist as:
    - Single-celled yeasts
    - Multi-celled molds
    - Both yeasts and molds (dimorphic)
44
Q

Molds

A
  1. Filamentous fungi grow as multinucleate, branching hyphae, forming a mycelium

(Ex. Ringworm)

45
Q

Yeasts

A
  1. Yeasts grow as ovoid or spherical; single cells multiply by budding and division

(Ex. Histoplasma)

46
Q

Fungal Infection & Injury

-Actions

A
  1. Adapt to host environment
    - Wide temperature variations, digest Keratin, low oxygen
  2. Suppress immune defenses
  3. Low WBC’s promote fungal infection
47
Q

WBC’s and Fungal Infection

A
  1. Low WBC’s promote fungal infection
48
Q

Fungal Infection & Injury

-Mycoses

A
  1. Disease caused by fungi
    - superficial
    - deep
    - opportunistic
49
Q

Fungal Infection & Injury

-Dermatophytes

A
  1. Fungi that invade the skin, hair, or nails are known as dermatophytes
    - Disease they produce are called tineas (ringworm
    - Tinea capitis, tinea pedis, and tinea cruris
  2. INTENSE ITCHING
50
Q

Infection Treatment

-Vaccines (GOALS)

A
  1. GOAL: induce long-lasting protective immune responses that will not results in disease in healthy recipient
51
Q

Infection Treatment

-Vaccines -(Types)

A
  1. Attenuated organism
  2. Killed organisms
  3. Recombinant viral protein
  4. Bacterial antigens
  5. Toxins
52
Q

Infection Treatment

-Antimicrobials

A
  1. Inhibit synthesis of cell wall
  2. Damage cytoplasmic membrane
  3. Alter metabolism of nucleic acid
  4. Inhibit protein synthesis
  5. Modify energy metabolism
53
Q

Antibiotic Therapy

-Penicillin

A
  1. For GRAM-POSITIVE cocci
54
Q

Antibiotic Therapy

-Aminoglycoside

A
  1. For GRAM-NEGATIVE aerobes
55
Q

Antibiotic Therapy

-Metronidazole

A
  1. For ANAEROBES
56
Q

Antibiotic-Resistant Microorganisms

-MRSA

A
  1. Methacillin-resistant Staphylococcus aureus
57
Q

Antibiotic-Resistant Microorganisms

-VRE

A
  1. Vancomycin-resistant enterococcus
58
Q

Antibiotic-Resistant Microorganisms

-PRSP

A
  1. Penicillin-resistant Streptococcus pneumococci
59
Q

Antibiotic-Resistant Microorganisms

-CDAD

A
  1. Clostridium difficile-associated diarrhea
60
Q

Resistant Bacteria

-Traits

A
  1. Produce Enzymes that:
    - Inactivate the antimicrobial
    - Alter cell metabolism
    - alter cell permeability
61
Q

Prokaryotic Cells

A
  1. Prokaryotic cells do not have nuclei, which are partitioned by an intracellular membrane
  2. DNA forms one main coil in the cell cytoplasm

Ex. Bacteria

62
Q

RNA Viruses

A
  1. Replicated their genetic material in the cytoplasm of the infected cell
  2. EXCEPTIONS: influenza and retroviruses
63
Q

DNA Viruses

A
  1. Require the DNA to enter the nucleus and use the cell’s DNA polymerases to replicate
  2. EXCEPTION: poxviruses
64
Q

Poxviruses

-replication

A
  1. provide their own DNA polymerase and replicate their DNA in the cytoplasm of the infected cell
65
Q

Retrovirus

-Replication

A
  1. Convert their RNA genetic information to DNA using an enzyme contained in the virion, REVERSE TRANSCRIPTASE
66
Q

Toxoids

A

Purified toxins that have been chemically detoxified without loss of immunogenicity

67
Q

Attenuated Viruses

-Vaccines

A
  1. Contain live viruses that are weakened
  2. Attenuated viruses can establish life-threatening infections in individuals whose immune system are congenitally deficient or suppresed
68
Q

Bacteremia

A
  1. Bacteria in the blood
69
Q

Systemic Signs and symptoms of Septicemia

A
  1. Fever
  2. Massive vasodilation
    - causes decrease in BP

Warm to touch / flush / BP low / tachycardic /

70
Q

Classic S/S of a Pt going Septic?

A
  1. Caused by Gram-negative toxins
  2. Massive vasodilation
  3. Warm / flush / hypotensive / tachycardic / Confusion due to decreased oxygen to brain