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Infectious Disease > Infectious Disease Transmission/Host Defenses & Pathophysiology > Flashcards

Infectious Disease Transmission/Host Defenses & Pathophysiology Flashcards

1
Q

Describe Prions:
Structure and function?3
Examples?3

How can our body respond to these?

Transmission?3

A
  1. Protein particles without a genome
  2. Infectious and capable of producing disease
  3. (normal or altered host proteins)

Examples:

  1. Creutzfeldt-Jakob disease,
  2. Kuru and
  3. “mad cow” disease

We dont really have a response to this.

Eating humans
Unclean cervical instruments
Animals

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2
Q

What is a virus?

What is the structure of a virus?2

A

Intracellular pathogen/incapable of replication outside a living cell

  1. Consist of a protein coat (capsid), surrounding either RNA or DNA (never both)
  2. Some viruses have a lipoprotein envelope derived from the parasitized host cell
    (make an envelope from host)
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3
Q

What must viruses have to live?

A

Viruses MUST penetrate a susceptible living cell & use the biosynthetic machinery of the cell to produce viral progeny (Latency)

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4
Q

What is the pathology of an oncogenic virus?

Examples?4

A

Some viruses have the ability to transform normal host cells into malignant cells during the replication cycle

HPV
CMV- hodgkins lymphoma
Herpes
Adenoviruses

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5
Q

Pathology of retro virus?

2

A

reverse transcriptase to turn their RNA into DNA

Transmit DNA into the host

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6
Q

What are the happy viruses?

A

DNA viruses
herpes
adenoviruses

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7
Q

STructure of bacteria?

5

A
  1. Autonomously replicating unicellular organisms—prokaryotes*
  2. Generally contain no organized intracellular organelles
  3. Genome consists of a single chromosome of DNA and RNA
  4. Does have reproductive and metabolic machinery in the cytoplasm of the cell (unlike viruses)
  5. unicellular-prokaryote
  6. no organelles
  7. single DNA or RNA chromosome
  8. does have reproductive and metabolic machinery unlike viruses
  9. Have cytplasmic membrane and cell wall-peptinoglycan (helps us kill them because we dont have it)
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8
Q

How do bacteria reproduce?

A

Most produce asexually be cellular division

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9
Q

What does gram pos stain?

Gram neg stain?

A

Gram-positive—PURPLE

Gram-negative—RED

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10
Q

How are some ways that bacteria reproduce?

3

A

chains (streps)
clusters (staff)
Pairs

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11
Q

What are fungi?

A

Free-living, eukaryotic saprophytes found in every habitat on earth

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12
Q

acid fast assciated with what?

A

TB

acid alcohol

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13
Q

How do fungi reproduce?

A

Reproduction is sexual or asexual (Involves production of spores)

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14
Q

What are the two groups of fungi we talk about?

A

yeasts

Molds

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15
Q

Describe structure of yeasts, reproduction and appearance of colonies?

A

Single-celled organisms
Reproduce by a budding process
Colonies are smooth with a waxy or creamy texture

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16
Q

What do molds produce?

3

A
  1. Produce long, hollow, branching filaments—hyphae
  2. Some produce cross walls which segregate the hyphae others do not
  3. Produce cottony or powdery colonies of mats of hyphae–mycelium
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17
Q

Types of parasites?

4

A

Athropods
Ectoparasites
Protozoa
Helminths

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18
Q

Examples of parasitic arthropod vectors?

3

A

ticks, mosquitoes, biting flies

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19
Q

What makes the arthropod parasitic?2

A

Actual infectious agent is carried by the arthropod

Usually a virus

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20
Q

Mechanism of infection for ectoparasites?

A

Infest external body surfaces and cause localized tissue damage or inflammation secondary to the bit or burrowing action

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21
Q

Some of the most prominant ectoparasites?

4

A

Mites (scabies)
Chiggers -
Lice
Fleas

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22
Q

What is a protozoa?

How do they reproduce?

A

Unicellular animals with complete eukaryotic machinery**

Reproduction may be sexual or asexual

Most are saprophytes but some can cause human disease

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23
Q

Examples of protozoa infectious to humans?

3

A

amebic dysentery, malaria, and giardiasis

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24
Q

What are helminths?

Examples?3

A

Collection of wormlike parasites

Include nematodes (roundworms), cestodes (tapeworms), & trematodes (flukes)

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25
Q

Helminths mechanism of reproduction and infection needs what?

A

Often an intermediate host is required for development & maturation of the offspring and then humans are infected and sexual reproduction occurs in the human host

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26
Q

Hemolinth infections often involve what?

A

multiple organ systems

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27
Q

For infectious diseases what should our epidemiology include?
6

A
  1. Incidence—number of new cases
  2. Prevalence—number of active cases at any given time
  3. Source of infection
  4. Port of entry, site of infection
  5. Virulence factors, signs & symptoms, and clinical course
  6. Endemic, epidemic, and pandemic
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28
Q

What are the goals of epidemiologic studies for ID?

2

A
  1. Interruption of spread of infectious diseases

2. Eradication of infectious diseases

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29
Q

Whats a vector?

A

Vector—organism that transmits a pathogen from a reservoir to a host

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30
Q

Forms of penetration for portals of entry of bacteria?

3

A
  1. any disruption in the body’s surface barrier Ex. stevens/johnsons breakdown of skin = massive infections
  2. Can be a result of accident, a wound, or a medical procedure
  3. May be a direct inoculation from a an animal or arthropod bite**
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31
Q

Examples of direct contact treansmission of ID?

2

A

STIs,

vertical transmission results in congenital infection

32
Q

Examples of ingestion transmission for ID?

2

A

E. Coli, salmonella,

33
Q

What kind of pt would be more susceptible to GI ID?

A

reduced achlorhydria

34
Q

How can GI transmitted ID spread to other parts of the body?

A

penetrate the intestinal mucosa and be disseminated via the circulatory system to other organs

35
Q

What kind of pts are at a higher risk for inhalation forms of ID?
3

A

Persons that smoke, have CF, or COPD

36
Q

Definition of a toxin?

A

Substances that alter or destroy the normal function of the host or the host’s cells

37
Q

What are toxins primarily produced by?

A

Primarily produced by bacteria (some fungal & protozoan do too)

38
Q

What are the two main types of toxins?

A

exotoxins and endotoxins

39
Q

When are exotoxins released from the cell?

A

Proteins released from the bacterial cell DURING growth

40
Q

Describe the pathology of exotoxins?

A

Enzymatically inactivate or modify key cellular constituents, leading to cell death or dysfunction

41
Q

Examples of endotoxins?

5

A 
diptheria, 
botulism, 
toxic shock syndrome
cholera, 
antrhax
42
Q

What are bacterial exotoxins that produce vomitting and diarrhea?

A

enterotoxins (E. coli 0157:H7)

43
Q

Describe the structure of endotoxins and where they can be found?

A

Complex molecules composed of lipid & polysaccharides found in the cell wall of gram-negative bacteria

44
Q

When aare endotoxins released?

How are they pathological?

Whats a risk factor for endotoxins?

A

NOT actively released during growth of the bacteria & have no enzymatic activity

They are potent activators of regulatory systems (induce clotting, hypotension, fever)

Can induce endotoxic shock

45
Q

Why do we not want to give antibiotics to a bacteria that produces toxins?

A

antibiotics because then they massively release their toxins

46
Q

Sign of toxic shock syndrome?

A

rash - pinpoint rash on the abdomen

47
Q

What are the variables that affect adhesion to the cell? 3

Give two examples of each

A
  1. Site specific (mucous membranes, skin surfaces)
  2. Cell specific (T lymphocytes, respiratory epithelium)
  3. Nonspecific (moist areas, charged surfaces)
48
Q

Site to which a microorganisms adheres to is called a?

On this site there is a?

A

receptor

LIGAND or ADHESIN

49
Q

After initial attachment, a number of bacterial agents embed into a gelatinous matrix of polysaccharides (slime or mucous)—this serves to?
2

Examples of infections that do this?3

A
  1. Anchor the agent to the host tissue
  2. Protect the agent from the immunologic defenses of the host

influenza, mumps & measles,

50
Q

Ways that infection diseases evade our body’s defense system?
3

A
  1. Polysaccharides (capsules, slime, & mucous layers) discourage engulfment & killing by the phagocytic WBCs
  2. Some organisms secrete toxins that deplete the hosts WBCs
  3. Some pathogens can survive INSIDE the ingestion by the WBC
51
Q

What does S. aureus do to evade our body’s defenses?

A

secretes an enzyme—coagulase that causes blood to clot around the pathogen & protects it from phagoctyic host cells & antibodies

52
Q

What does H. Pylori do to evade our body’s defenses?

A

produces urease (an enzyme) that converts gastric urea into ammonia which neutralizes the acidity of the stomach allowing the pathogen to survive

53
Q

What do H. influenzae & N. gonorrhoeae do to evade our body’s defenses?

A

secrete enzymes that inactivate IgA

54
Q

What are products produced by infectious agents that facilitate penetration of anatomic barriers & host tissue?

A

invasive factors

55
Q

What are most invasive factors?

What can they destroy?5

A

enzymes

  1. cellular membranes
  2. connective tissue
  3. intercellular matrices
  4. structural protein complexes
  5. (Just about something for every defense barrier!)
56
Q

What mediates the tissue damage of infectious diseases?

3

A

COMBINED EFFECTS of

  1. invasive factors,
  2. toxins, &
  3. antimicrobial/inflammatory substances released by host cells
57
Q

What makes it more likely that a bacterial species will become antibiotic resistant?
2

A

The more a bacterial species which was

  1. initially sensitive to a particular antibiotic is
  2. inappropriately over exposed to the antibiotic

the more likely it will become resistant

58
Q

Ideally you would isolate the specific organism causing an infection and determine what antibiotics it is sensitive to & treat accordingly

In reality this is seldom the case and treatment is often empirical determined by:
4

A
  1. The body site where the infection is
  2. The most likely pathogens that infects that body site
  3. The setting where the infection occurred
  4. Known community resistances
59
Q

How are Penicillins/Cephalosporins inactivated?

3

A
  1. Inactivation of the drug by beta-lactamases (enzymes)
  2. Decreased penetration to the target site (gram-negative bacteria)
  3. Alterations of the binding site (penicillin-binding-proteins—PBPs)
60
Q

How do beta-lactamases (enzymes) make the drug inactive?2

How would we over come this resistance?

A
  1. DNA by plasmid insertion
  2. Direct chromosomal DNA mutations

Overcoming resistance—add a beta-lactam inhibitor (clavulanic acid)

61
Q

How sulfonomides inactivated by microbes?

How do we overcome this resistance?

A
  1. Overproduction of PABA (para-aminobenzoic acid)
  2. Surplus of folic acid
  3. Structural changes in enzymes so there is less affinity for the sulfonamide substrate

To overcome resistance used in combination w/ other agents (trimethoprim)

62
Q

Three general ways that bacterium can become antibiotic resistant?

A

transformation (resistant gene)
conjugation (plasmid form)
tranduction (virus delivers resistance)

63
Q

What ways can microbes become resistant to Fluoroquinolones?
2

How does this alter the ability of the drug?

What factor leads to a longer likelihood of resistance?

A
  1. Chromosomal mutations—such as active efflux of the drug or protection of DNA gyrase [altered target mechanism]
  2. Sometimes plasmids carry the DNA for resistance

Alterations in their ability to permeate the bacterial cell wall

Longer duration of use

64
Q

In what ways can microbes become resistant to macrolides?

What does this lead to ?

A
  1. Alterations in the macrolide binding site on the ribosomal subunit
  2. Altered transport of the macrolide
65
Q

Whats the throat quadrad for ID?

A

exudate,
red beefy tonsils,
petechia on roof of mouth and strawberry tongue

66
Q

Streptococcus pyogenes, or Group A beta hemolytic streptococcus (GAS) is what kind of bacteria and what are our first and second line therapies?
2 1st
2 2nd

A

Gram positive

Penicillin
Amoxicillin

Erythromycin
First generation Cephalosporins (reccommended with penecillin allergy

67
Q

Types of brain opportunistic infections?

2

A

Toxoplasmosis

Crytococcal menigitis

68
Q

Types of oppotunistic eye infections?

A

Cytomegalovirus (CMV)

-owl eyes

69
Q

Types of mouth and throat opportunistic infections?

A

Candida (yeast)

70
Q

Types of lung opportunistic infections?3

A

PCP pneumocytic pneumonia
TB
Histoplasmosis

71
Q

Types of gut opportunistic infections?

3

A

cytomegalovirus (CMV)
Mycobacterium Avium complex (MAC)
C. Diff

72
Q

Types of skin opportunistic infections?

2

A

Herpes simplex and shingles

73
Q

Types of genital opportunistic infections?

3

A

genital herpes
HPV
vaginal candida (yeast)

74
Q

Functions of the inflammatory response?

A
  1. Provides the body with the ability to sustain injury
  2. The ability to resist attack by microorganisms
  3. Ultimately with the immune response allow most of the time for tissue repair and healing
75
Q

What are the two stages of the inflammatory response and describe each?

2 steps for each

A
  1. Vascular stage:
    - -Serves to “wall” off the infected area localizing the spread of infection
    - -Exudation of fluid dilutes the offending agent
  2. Cellular stage:
    - -Certain WBCs are drawn to the area of inflammation and intracellularly kill the pathogen
    - -Inflammatory mediators increase capillary permeability and draw WBCs to the area
76
Q

Whats the last stage of the inflammatory response?

A

tissue repair

more of an overlap with the inflammatory response

77
Q

What is tissue repair attempting to accomplish?

What two forms can it take?

A

Represents the attempt to maintain normal body structure & function

  1. Regeneration where the injured cells are replaced with cells of the same type
  2. The form where the injured cells are replaced by connective tissue which leaves a scar

Infectious Disease (29 decks)

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