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MOD S1 > Lecture 11: Epidemiology of Infectious Diseases > Flashcards

Lecture 11: Epidemiology of Infectious Diseases Flashcards

1
Q

Define flora/microflora.

A

Microorganisms present on the surface of AND within the body.

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2
Q

What is the term to describe flora that has no adverse effects?

A

Commensalism

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3
Q

What is the term to describe flora that benefits the host?

A

Mutualism

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4
Q

Why are flora useful?

A

They can compete with disease-producing microorganisms, thus inhibiting their growth.

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5
Q

What are the 3 ways pathogens cause disease?

A

Direct destruction of host cell
Interference with host cell metabolism
Exposure of host cell to toxins

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6
Q

What is a prion?

A

It is a protein that causes infection. It is just mutated protein particles, but causes incurable and 100% fatal diseases such as Creutzfeld-Jakob Disease, kuru, and bovine spongiform encephalopathy (mad cow disease)

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7
Q

What is the mechanism behind prions?

A

They interact with normal proteins and cause the normal ones to turn into more infected ones. They generally accumulate in nerve cell axons, causing slow but progressive NONinflammatory neuronal degeneration.

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8
Q

What is a virion and capsid?

A

Virion refers to the entire virus particle.
Capsid is a protein coat found on all viruses.

Note:
We can just inject some proteins from a capsid for vaccines instead of the entire virus.

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9
Q

What does not always surround a virion?

A

Lipoprotein envelope

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10
Q

What are obligate intracellular pathogens?

A

They bind to receptors on host cells, entering it and converting the host cell’s metabolism to make more viral nucleic acids and proteins instead.

Eventually, the cell goes haywire and undergoes lysis.

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11
Q

What period do viruses sometimes undergo prior to symptoms? What is a famous virus that works like this?

A

Latency period. HIV is a prime example of a virus with a latency period, in which there are little to no symptoms.

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12
Q

What are the layers of a typical virus?

A

Superficial to deep:
Glycoproteins
Lipoprotein Envelope (optional)
Tegument
Capsid
DNA/RNA core

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13
Q

What are the two types of metabolism for bacteria?

A

Aerobic and anaerobic.

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14
Q

What does it mean to be facultatively anaerobic?

A

They can switch between aerobic and anaerobic.

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15
Q

What is a key difference between virus and bacteria replication?

A

Viruses require hosts. Bacteria can live on their own.

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16
Q

What is a key distinguishing factor between a bacteria and a human cell?

A

Cell walls made of peptidoglycan. Human cells lack this cell wall.

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17
Q

What organelles do bacteria lack compared to human cells?

A

No organized nucleus
Mitochondria
Endoplasmic reticulum

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18
Q

What is a plasmid?

A

A circular strand of DNA that replicates independently of chromosomes.

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19
Q

How do bacteria move around?

A

Flagella

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20
Q

How do bacteria stick to things?

A

Pili

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21
Q

Where do we have a lot of bacteria in our body?

A

GI tract, which is anaerobic.

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22
Q

What 3 things do we generally categorize bacteria by?

A

Shape (cocci, bacili, spirochete, spirilla)
Grouping (diplo, strepto, staphylo)
Staining (G+, G-, acid-fast)

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23
Q

What is the difference between an endotoxin and exotoxin?

A

Endotoxins are the physical remnants of bacteria that can produce an immune response.

Exotoxins are what bacteria make, often as a byproduct of their metabolism.

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24
Q

What is an endospore?

A

A dormant bacteria that has been reduced down to a simpler form. It is way more resistant to everything and requires reactivation later.

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25
Q

What color are G+ bacteria usually?

A

Purple

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26
Q

What color are G- bacteria usually?

A

Pink

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27
Q

What kind of infection is a fungal infection?

A

A mycotic infection.

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28
Q

What are the two types of mycoses?

A

Superficial, limited to surface areas of the body.

Deep, invading deep tissue.

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29
Q

Where do I usually find fungi?

A

Skin and mucous membranes. They can become opportunistic pathogens.

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30
Q

Whats the difference between yeast and mold?

A

Yeast are UNIcellular (you and u)
Mold are multicellular (M and M)

Yeast reproduce via budding and pseudohyphae.

Mold reproduce via hyphae.

They can all form spores which are highly resistant.

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31
Q

What are protozoa?

A

Unicellular, complex organisms with a nucleus and organelles.

They usually have motility and spend part of their life outside of humans.

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32
Q

What diseases do protozoa cause?

A

Malaria
Toxoplasmosis
Trichomoniasis
Giardiasis
Amoebiasis

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33
Q

How are protoza transmitted?

A

Direct host-host contact
Contaminated food/water
Arthropod vectors

Note:
They can also form cysts to aid in transmission.

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34
Q

What are helminths?

A

Wormlike parasites

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35
Q

What is included in helminths?

A

Nematodes (roundworms)
Cestodes (tapeworms)
Trematodes (flukes)

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36
Q

How are helminths transmitted?

A

Ingestion of fertilized eggs
Penetration of skin by larvae
Arthropod vectors

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37
Q

Where are helminths most commonly found?

A

Developing countries

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38
Q

What are the ectoparasites?

A

Things that infest external body surfaces.

Mites (scabies), chiggers, lice, flea

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39
Q

How are ectoparasites transmitted?

A

Contact with arthropods or larvae/egg forms.

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40
Q

What kind of bacteria is rickettsiae?

A

G-, obligate intracellular pathogen.

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41
Q

What is unique about rickettsiae?

A

Infects arthropod vectors, but does NOT cause any disease in them

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42
Q

What kind of bacteria is mycoplasma?

A

G-, very tiny bacteria.

43
Q

What is unique about mycoplasma vs other bacteria?

A

Size. It is less than 1/3 a normal bacteria’s size.

DNA genome. It is half of a normal bacteria.

Capable of independent replication.

44
Q

How does chylamydiae reproduce?

A

Binary fission.

45
Q

How is chylamydiae transmitted?

A

Direct host-host contact.

46
Q

Out of all the pathogens, which ones have an organized nucleus?

A

Protozoans
Molds
Yeast
Helminths

47
Q

What is the largest pathogen?

A

Helminths.

48
Q

What is the smallest pathogen?

A

Prions

49
Q

What is an endogenous vs an exogenous reservoir?

A

An endogenous reservoir involves opportunistic infections, aka infections from organisms normally in/on our body but we don’t sick from unless immunocompromised.

An exogenous reservoir would be the external environment, like infected food/animals.

50
Q

What is a nosocomial infection?

A

Acquired in a hospital setting.

51
Q

What are the criteria for an infection to be considered nosocomial?

A

Must not be symptomatic prior to arrival.
Generally, it occurs 2 days post admit and/or within 3 days post-discharge.
ICU pts are highest risk.

52
Q

What is a community-acquired infection?

A

It is an infection acquired outside of a hospital or healthcare setting.

53
Q

What increased aspects of infections do immunocompromised hosts have?

A

Increased susceptibility
Increased severity and duration
Increased rates of opportunistic infections.

54
Q

What is a portal of exit?

A

It is how the pathogen leaves the reservoir, so for endogenous reservoirs, it would be via secretions.

55
Q

What are the 4 ways infections are spread? (Think hospital precautions)

A

Direct contact, aka physical contact
Droplet
Airborne
Vector

56
Q

What is the difference between droplet and airborne transmission?

A

Droplet is referring to literal drops, which are bigger and spread only within 3 feet of the person (usually).

Airborne means the particles get aerosolized. This means they are smaller and stay in the air longer, spreading farther.

57
Q

What are the two types of vectors?

A

Biological: required for life cycle of pathogen
Mechanical: not essential to life cycle of pathogen.

58
Q

What are the 5 portals of entry for infections?

A

Penetration
Direct contact
Vertical transmission
Inhalation
Ingestion

59
Q

What is vertical transmission?

A

Mother to fetus

60
Q

What can cause increased risk of inhalation of pathogens?

A

Defective pulmonary function
Mucociliary clearance

61
Q

What can cause increased risk of ingestion of pathogens?

A

Reduced gastric acid

62
Q

How do infections generally spread in the body?

A

Locally (nearby tissues)
Dissemination (circulatory/hematologically)

63
Q

What are risk factors?

A

Things that increase your likelihood of contracting a disease OR having worse outcomes.

64
Q

What are the risk factors?

A

Immunosuppressive medications
Immunocompromised status
Impaired inflammatory response
Poor nutrition
Very young or very elderly
Severe stress
Coinfection or superinfection

65
Q

Define disease.

A

Deviation from and/or interruption of normal structure and/or function of one or more cells, tissues, organs, or organ systems within the body.

66
Q

Define infection.

A

Pathogen enters host and begins multiplying.

Note:
Does not have to be clinically evident yet.

67
Q

Define infection.

A

Pathogen enters host and begins multiplying.

Note:
Does not have to be clinically evident yet.

68
Q

Define pathogenicity.

A

Ability of organism to cause disease.

69
Q

What are the 3 aspects that describe an organism’s infection ability?

A

Virulence (ability to cause severe disease, aka potency)
Infectivity (likelihood of infecting host after exposure)
Toxigenicity (likelihood of producing harmful toxins)

70
Q

What are the 3 aspects that are related to an organism and our immune response?

A

Immunogenicity (likelihood of producing an immune response)

Antigenicity (likelihood of binding with immune system receptors)

Antigenic variability (likelihood of altering antigens)

71
Q

What are the two kinds of antigenic variability?

A

Antigenic drift: natural mutation over time of viral antigens.

Antigenic shift: two or more viruses combining to create a new set of antigens.

Note:
Example of antigenic drift is the flu virus every year.

Example of antigenic shift is H1N1, which combined different flu strains from pigs, birds, etc.

72
Q

Define coinfection vs superinfection.

A

Coinfection means the presence of 2+ pathogens at the same time.

Superinfection means a secondary infection arising when the first one is already present.

73
Q

What is meant by colonization?

A

Multiplication of pathogenic organisms in the host, which will compete with the normal flora.

74
Q

What is an infectious dose?

A

Minimum number of microbes required for a pathogen to cause an infection.

75
Q

What are the 4 ways pathogens can avoid host defenses?

A

Intracellular pathogens (hiding in a cell)
Capsules (outer shield)
Mimicry of host (camouflage)
Antigenic variation (Unrecognizable)

76
Q

What are the 4 ways pathogens interfere with host immune processes?

A

Production of membrane-damaging toxins to destroy leukocytes.

Interference with complement activation

Production of proteases to destroy immune molecules

Inhibition of host immune response.

77
Q

What can pathogens produce to fight a host?

A

Toxins
Enzymes

78
Q

What enzymes do pathogens make to promote their spread/survival?

A

Coagulase: forms fibrin clot to surround and protect microbe

Hyaluronidase: breaks down connective tissue

Fibrinase: breaks down clots that limit the spread of the pathogen.

Catalase: neutralizes bactericidal effects of hydrogen peroxide so they can survive phagocytosis.

79
Q

What are the stages of infection?

A

Incubation

Prodrome

Acute

Declining

Convalescence

Resolution

80
Q

What are the 3 types of infections in terms of staging?

A

Subclinical (no apparent symptoms)
Insidious (lengthy prodromal)
Fulminant (Abrupt onset, little to no prodrome)

81
Q

What is found in pus?

A

Dead leukocytes (usually neutrophils), dead cells, and fluid

82
Q

What describes bacteria that can cause pus formation?

A

Purulent, suppurative, pyogenic

83
Q

Define pustule vs abscess

A

Pustules are superficial collections of pus within or just below epidermis.

Abscess is collection of pus in an enclosed space.

84
Q

What kind of things can cause granulomatous inflammation?

A

Foreign bodies like splinters, sutures, silica, and asbestos.

Pathogens: mycobacterium tuberculosis, syphilis, and deep fungal infections.

85
Q

What are the two macrophages designed to tackle granulomatous inflammation?

A

Giant cells (multinucleated, coalesced macrophages)
Epithelioid cells

86
Q

What kind of tissue eventually surrounds a granulomatous inflammation site?

A

Fibrous tissue.

87
Q

What kind of pathogen usually causes cytopathic-cytoproliferative reactions?

A

Viruses and sometimes intracellular nonvirals.

88
Q

Define cytopathic-cytoproliferative reaction.

A

Damage to a host cell in the ABSENCE of adequate host inflammatory response.

89
Q

What can happen in a cytopathic-cytoproliferative reaction?

A

Cells fuse (measles)
Cells become discohesive (herpes)
Cells proliferate and make weird lesions (poxvirus, HPV)
Cells make viral inclusion bodies

90
Q

What kind of virus makes an owl’s eye?

A

CMV, cytomegalovirus

It is an intranuclear inclusion with a halo.

91
Q

What kind of virus makes negri bodies?

A

Rabies

Eosinophilic cytoplasmic inclusion.

92
Q

What kind of virus makes a ground-glass cytoplasm in hepatocytes?

A

Hep B

93
Q

What do we call extensive necrosis?

A

Gangrene

94
Q

What is necrosis without infection called?

A

Aseptic necrosis

95
Q

How do we remove dead tissue?

A

Debridement

96
Q

What are the 5 types of tissue necrosis?

A

Coagulative
Liquefactive
Caseous
Fat
Fibrinoid

97
Q

When does coagulative tissue necrosis usually happen?

A

Hypoxic environments-
proteins from dead cells are denatured and form a firm gel like substance
maintains tissue architecture

98
Q

When do I usually see liquefactive necrosis?

A

Bacterial/fungal infections, brain infarcts
dead cells are liquified (pus)

99
Q

What is caseous necrosis described as?

A

Cheesy.
Looks white and friable

100
Q

When do I usually see caseous necrosis?

A

Mycobacteria, fungi, and foreign bodies

101
Q

When do I usually see fat necrosis?

A

Breast and pancreas are the most common locations
lipases destroy fatty tissues
may see calcium deposits

102
Q

When do I usually see fibrinoid necrosis?

A

Immune complexes(antigen and antibody) deposited in vessel walls.

damage to vascular structures by immune processes

103
Q

What does chronic inflammation generally lead to?

A

Fibrous scarring = loss of function of cells
Damage to cells = increased risk of DNA damage and cell mutation = increased risk of tumors, cancers.

MOD S1 (18 decks)

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