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Micro > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

what does a vaccine contain

A

dead or weakened or subunits of pathogens that stimulate the immune system

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2
Q

what do vaccines produce

A

Abs or CTL
- exactly like it would if you were exposed to the disease

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3
Q

after getting vaccinated, what do you develop

A

immunity to that disease

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4
Q

B cells need to be activated to become plasma cells to make Abs. Which cells need to be activated for this to occur?
- macrophages
- NK cells
- CD8+ T cells
- CD4+ T cells

A

CD4+ T cells

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5
Q

CD4+ T cells recognize antigen presented on….

A

MHC 2

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6
Q

in order to present on MHC 2, antigens must be processed via….

A

lytic enzymes in the phagolysome

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7
Q

are antigens on MHC 2 exogenous or endogenous

A

exogenous

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8
Q

memory CD4+ T and B cells are generated when…

A
  • APCs engulf antigens and present peptides to CD4+ T cells
  • B cells engulf antigens and become activated when they receive T cell help
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9
Q

memory CD4+ T and B cells are produced efficiently even when

A

the microbe has not infected an APC

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10
Q

true or false, in order to generate CTL, APCs need to be infected by the microbe

A

true

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11
Q

memory CD8+ T cells are generated when…

A

when an APC becomes infected
- digests the antigen into peptides and presents it to CD8+ T cells (which receive T cell help)

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12
Q

memory CD8+ T cells are produced when

A

the microbe infects an APC

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13
Q

what are the two major categories of vaccines

A
  1. attenuated vaccines
  2. inactivated vaccines
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14
Q

what are attenuated vaccines

A

they use a live/active but weakened form of the pathogen
- uses whole bacterial cells or viruses as the antigen

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15
Q

can attenuated vaccines cause diseases

A

no

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16
Q

what are inactivated vaccines

A

they are unable to replicate

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17
Q

which of the following is an advantage to using an inactivated vaccine over a live attenuated vaccine?
- good Ab and cell-mediated responses
- requires fewer boosters and a lower initial dose
- confers longer-lasting immunity
- no risk of causing infectious disease

A

no risk of causing infectious disease

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18
Q

what are considered safer, inactivated vaccines or live attenuated vaccines

A

inactivated vaccines

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19
Q

do inactivated vaccines need boosters

A

yes

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20
Q

inactivated vaccines come with a reduced ____ of the vaccine

A

effectiveness

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21
Q

live attenuated vaccines production is usually done with

A

meticulous quality checks ensuring their safety

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22
Q

for live attenuated vaccines who should be careful with those types of vaccines

A

pregnant women and immunocompromised people

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23
Q

what are the four types of inactivated vaccines

A
  • inactivated or killed whole agent vaccines = use killed whole cells or inactivated whole viruses
  • subunit vaccines = use key protein antigens or antigenic fragments from a pathogen
  • DNA or RNA vaccines = inject pieces of the pathogen’s genetic code
  • vector vaccines = use a chemically weakened virus to transport pieces of the pathogen’s genetic code
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24
Q

what do subunit vaccines often require

A

adjuvant = a chemical that enhances antigenicity by stimulating dendritic cells and macrophages
- boosts immune response

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25
Q

what are three types of subunit vaccines

A
  • toxoids = contain inactivated exotoxin (toxin is modified to no longer have toxicity but still retain antigenic epitopes)
  • polysaccharide vaccines = contain capsular polysaccharides
  • conjugate vaccines = polysaccharides (usually capsule) linked to proteins
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26
Q

would a vaccine that contains bacterial capsule (ie a polysaccharide vaccine - T-independent) elicit a robust response in young children

A

no

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27
Q

are polysaccharides T-independent antigens or T-dependent antigens

A

T-independent antigens

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28
Q

polysaccharides (T-ind antigens) need to be ____ to a protein (T-depend antigens) to enhance their ___ in young children

A

conjugated; antigenicity

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29
Q

do T-independent antigens bind to other T-independent antigens

A

no
- T-independent antigens can only bind to other T-dependent antigens

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30
Q

do conjugate vaccines require T-cell help

A

no

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31
Q

the preparation of conjugates makes T-independent antigens into

A

T-dependent antigens

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32
Q

vaccination confers ___ ___ to the individual vaccinated

A

active immunity

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33
Q

true or false - some people believe that naturally acquired immunity is better than the immunity provided by vaccines

A

true

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34
Q

what are some usual side effects of vaccines

A
  • local soreness at the injection site
  • minor fever
  • malaise
  • feeling tired
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35
Q

what are two rare side effects of vaccines

A
  • febrile seizures = convulsions in young children associated with high fever
  • anaphylaxis = allergic reactions to chemicals other than the antigen which may be present in the preparations
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36
Q

what is microbiota

A

the microorganisms that normally colonize various sites on/within the body without causing disease

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37
Q

what are two different types of microbiota

A
  1. resident microbiota = inhabit sites for extended periods
  2. transient microbiota = inhabit temporarily for days, weeks, or months and then disappear
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38
Q

what does colonization mean

A

the ability of a microbe to stay affixed to a body surface and replicate

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39
Q

where do these microbiota colonize

A

nose, mouth, throat, skin, LI, urethra, and vagina

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40
Q

where in the body is free of microbes (sterile)

A

blood, CSF, and internal organs

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41
Q

part of our first line of defense against infection competitively exclude

A

pathogens

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42
Q

how does our first line of defense exclude pathogens

A
  • covering of binding sites prevents attachment
  • consumption of available nutrients
  • production of compounds toxic to other bacteria
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43
Q

what does microbiota aid in

A
  • digestion
  • vitamin production
  • drug metabolism
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44
Q

how is the microbiota acquired

A
  • humans are initially colonized by microorganisms at birth
  • after, the microbiota may continue to undergo small changes in response to external factors (diet, environment, interactions with other humans, etc.)
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45
Q

by age three, a child’s microbiome looks a lot like

A

an adult’s
- and becomes much more stable

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46
Q

microbiota changes in response to events like

A
  • illness
  • disease
  • antibiotic treatment
  • fever
  • stress
  • injury
  • changes in diet
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47
Q

what is a pathogen

A

any bacterium, virus, fungus, protozoan, or helminth that causes disease

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48
Q

what is pathogenicity

A

the ability of an organism to cause disease

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49
Q

what are types of pathogenicity

A
  • genetic makeup of the pathogen
  • location in/on the host’s body
  • host immune response
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50
Q

what can true (“primary”) pathogens cause

A

they can cause disease in a host regardless of the host’s resident microbiota or immune system

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51
Q

are true pathogens ever part of the normal microbiota

A

no

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52
Q

what do opportunistic pathogens cause

A

disease only under opportunistic conditions, ie situations that compromise the host’s defenses

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53
Q

opportunistic pathogens can be members of

A

normal microbiota or common in the environment

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54
Q

what are some situations that compromise the host’s defenses

A
  • changes in the composition of the normal microbiota (ie taking antibiotics)
  • displacement of normal microbiota to another site in the body
  • weakened immune system
    • immune suppression (chemotherapy, organ
      transplants)
    • immunodeficiency (AIDS)
    • old age or stress or other diseases
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55
Q

what are two examples of opportunistic pathogens

A
  • candida albicans = a yeast found in the vaginal microbiota
  • c. diff = a bacterium that can be part of someone’s transient gut microbiota
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56
Q

what is c. diff resistant to

A

a lot of antibiotics

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57
Q

what does lactobacillus do in the vagina

A

it’s a bacterium in the vagina that suppresses yeast growth

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58
Q

can someone be infected but not have an infectious disease

A

yes

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59
Q

what is an infection

A

a successful colonization and multiplication of microorganisms within a host with or without the manifestation of disease

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60
Q

what is an infectious disease

A

illness caused by damage to host cells by an infectious agent (bacteria, viruses, fungi, and parasites) or its products (exotoxin) resulting in signs and symptoms

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61
Q

what does virulence mean

A

the degree or severity of disease

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62
Q

pathogens differ in their ___ of virulence

A

degree

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63
Q

what are virulence factors

A

proteins and other molecules that contribute to the pathogen’s ability to establish itself in a host or cause host damage

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64
Q

how can virulence be measured

A

by LD50 (lethal dose 50)
- the number of microbes that kills 50% of an experimental group of animal hosts

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65
Q

which LD50 would be more virulent - LD50 = 400 or LD50 = 600

A

LD50 = 400 because that means it will take less work to kill the organisms with the infection

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66
Q

what does infectious dose (ID) mean

A

the minimum number of microbes required to be taken in by the body to cause infection

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67
Q

what does ID50 mean

A

the number of microbes that will cause infection in approx. 50% of an experimental group of hosts

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68
Q

which is LEAST likely to cause an infection according to the data below
- E.Coli ; ID50 = 10-100
- Shigella dysenteriae ; ID50 = 10-200
- salmonella ; ID50 = 1,000
- vibrio cholerae ; ID50 = 1,000,000
- hepatitis A virus ; ID50 = 10-100

A

vibrio cholerae because it would take exposure to 1M host to infect 50% of the population

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69
Q

what are the four stages of pathogensis

A
  1. adhesion = to skin or mucosa
  2. invasion = through epithelium and immune evasion
  3. infection = colonization and growth
  4. tissue damage, disease
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70
Q

between what two stages of pathogenesis do toxins or host immune response occurs

A

between infection and tissue damage - disease

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71
Q

what are the six portals of entry

A
  1. fecal-oral = through mucosal surfaces of GI tract
  2. respiratory = through mucosal surfaces of respiratory tract
  3. transplacental = through the placenta to infect a fetus
  4. skin = through epithelial surfaces
  5. urogenital = through mucosal surfaces of genital and urinary tracts
  6. parenteral = through injection into the bloodstream (ex: insect bites or needle sticks)
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72
Q

what cellular structures help pathogens adhere

A
  • fimbriae adhesions
  • cell wall adhesions
  • glycocalyx (slime and capsular polysaccharides)
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73
Q

how do pathogens invade tissue and evade host immune response

A
  • invasion
    • ability of some pathogens to spread through tissues
    • produce enzymes or toxins which serve as virulence
      factors that allow them to colonize and damage host
      tissues as they spread deeper into the body
  • immune evasion: antigenic variation
    • acquire changes in the genes for surface antigens that
      alter the structure of surface antigens that Abs would
      otherwise recognize
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74
Q

how does replication within a phagocyte benefit the pathogen
- avoid recognition by phagocytes
- avoid recognition by complement
- avoid recognition by Abs
- all of the above

A

all of the above

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75
Q

what are four ways that intracellular bacteria survive within phagocytes

A
  1. by preventing fusion of the lysosome with the phagosome
  2. by escaping from the phagosome before the lysosome fuses
  3. by preventing acidification of the phagosome
  4. by resisting killing by lysosomal chemicals
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76
Q

once a pathogen is in, attached and evade the immune response, what does it do

A

it replicates and grows

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77
Q

true or false - with colonization and growth, new organisms must compete with established organisms for nutrients and space

A

true

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78
Q

what does localized mean

A

when pathogens grow locally at the site of the invasion

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79
Q

what does systemic mean

A

when pathogens may spread throughout the body

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80
Q

cellular damage can be a direct result of ___ or indirect via ___

A
  • pathogen (such as toxin production)
  • immune response
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81
Q

toxins may be transported by ___ or ____

A

blood; lymph

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82
Q

what are the two general types of toxins

A
  1. exotoxins
  2. endotoxins
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83
Q

what are exotoxins

A

proteins produced by pathogenic bacteria (gram positive and gram negative) and secreted

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84
Q

what are endotoxins

A

the lipid A portions of LPS that are part of the outer membrane of the cell wall of gram negative bacteria

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85
Q

when are endotoxins liberated

A

when the bacteria die and the cell wall breaks apart

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86
Q

how do you name exotoxins

A
  • by types of cell affected
  • by associated disease
  • by bacterium producing it
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87
Q

what are the three major modes of exotoxins’ action

A
  1. cytolytic toxins
  2. AB toxins
  3. superantigen toxins
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88
Q

what does cytolytic toxins do

A

they work by disrupting cytoplasmic membrane integrity, causing cell lysis and death
- toxins that lyse RBCs are called hemolysins

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89
Q

what do AB toxins do

A

consist of two subunits, A and B
- B binds to host cell receptor and transfers subunit A (the toxic part) across the cell membrane
- usually inhibits protein synthesis or disrupts ion homeostasis aka intracellular-targeting toxins

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90
Q

what do superantigen toxins do

A

overactivate the immune system by activating non specifically CD4+ T cells which leads to an excessive cytokine release and excessive inflammatory response

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91
Q

where do bacteria get their exotoxin genes

A

horizontal gene transfer
- most genes for exotoxins are carried on plasmids or phages

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92
Q

how does the body fight exotoxins

A

the body makes Abs (antitoxins) -> provide immunity

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93
Q

how are exotoxins inactivated

A

by heat or chemical -> toxoid vaccine to stimulate antibody production

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94
Q

an example of an endotoxin is Lipid A (the toxic part), what happens when LPS gets into the circulation

A

it can trigger a massive inflammatory response

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95
Q

endotoxin - excessive release of cytokines from host is called

A

cytokine storm

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96
Q

what do endotoxin induce

A

inflammatory trauma throughout the entire body
- fever, shock, disseminated intravascular coagulation, and death

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97
Q

what are some mechanisms of bacterial pathogenesis

A
  • produce toxins that are ingested
  • colonize and invade host tissues
  • colonize and produce toxins (no invasion)
  • colonize and invade host tissues, produce toxins
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98
Q

what is epidemiology

A

the science that underlies public health

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99
Q

what does epidemiology study

A

how disease originates and spreads throughout a population

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100
Q

what is the goal of epidemiology

A

to prevent outbreaks and contain them when they do occur

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101
Q

what are four patterns of infectious disease occurrence

A
  1. endemic = disease consistently present (often at low level) in a population
  2. sporadic = when occasional cases are reported at irregular intervals
  3. epidemic = occurrence of more cases of disease than expected in a given area over a particular period of time (“outbreak”)
  4. pandemic = an epidemic occurring on several continents and usually affecting an exceptionally high proportion of the global population
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102
Q

what does prevalence mean when measuring disease frequency

A
  • number of existing cases of disease in a population during a defined period of time
  • individuals with outcome of interest, regardless of when diagnosed
  • how much of a population is affected
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103
Q

what does incidence mean when measuring disease frequency

A
  • number of new cases of disease that develop in a population during a defined period of time
  • individuals who change in disease status over a specified period of time
  • how quickly are people becoming infected
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104
Q

what does mortality rate mean

A

incidence of death due to a disease during a particular time period

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105
Q

what does case fatality rate mean

A

mortality rate/incidence rate

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106
Q

are all infectious diseases contagious

A

no

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107
Q

true or false - an infectious disease may or may not be communicable

A

true

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108
Q

what is a communicable disease

A

an infectious disease that is contagious and which can be transmitted from one infected host to another
- reproductive number R0 is a measure of contagiousness

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109
Q

during which period can a host be contagious
- incubation period
- prodromal period
- period of illness
- period of convalescence
- all of the above

A

all of the above
- but depends on the infection

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110
Q

which stage is an infection transmissible

A

transmissible during any of the stages depending on the pathogen

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111
Q

what are the two types of contact transmission

A
  1. direct
    - skin-skin
    - mucous-mucous (sexually transmitted)
    - across placenta
    - through breast milk
  2. indirect
    - droplets = close range (ie respiratory droplets) inhaled by someone close by)
    - fomites = inanimate objects that transmit pathogens (ie doorknobs)
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112
Q

what are three types of vehicle transmission

A
  1. air-borne
    - aerosols
    - droplet nuclei inhaled by those over a long distance
  2. food-borne
  3. water-borne
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113
Q

droplet transmission vs airbone transmission

A
  • droplet transmission = coughs and sneezes can spread droplets of saliva and mucus; droplets fall down within three feet of host (more than 5 microns)
  • airborne transmission = tiny particles, possibly produced by talking, are suspended in the air for longer and travel further; droplet nuclei travel further, >3ft (less than 5 microns)
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114
Q

what is vector transmission

A
  • living organisms that can carry pathogens
  • arthropods: insects (flies, mosquitos) and arachnids (mites, ticks, and spiders)
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115
Q

what is a reservoir

A
  • where microorganisms can live, accumulate, or persist outside of the host of interest
  • serves as a source of infection for other host organisms
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116
Q

what are three types of reservoir

A
  • human reservoir
  • animal reservoir
  • non-living reservoir
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117
Q

how can a human act as a carrier

A

a human acting as a reservoir of a pathogen may or may not be capable of transmitting the pathogen

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118
Q

what is a human reservoir capable of transmitting

A

a pathogen who do not present signs or symptoms of disease is an asymptomatic carrier

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119
Q

what are zoonoses

A

diseases that can be transmitted from animals to humans

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120
Q

true or false - 75% of all emerging infectious disease are zoonotic

A

true

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121
Q

what type of people are at highest risk of zoonotic infections

A

people who are more likely to come into contact with animals or who share air and space with animals

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122
Q

how are zoonotic diseases acquired

A

through various routes

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123
Q

in zoonoses animals are the ___ host

A

definitive

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124
Q

in zoonoses humans are typically __-__ host

A

dead-end

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125
Q

what are three types of durations of the disease

A
  1. acute disease = symptoms develop rapidly (strep throat)
  2. chronic disease = symptoms develop gradually over months, years, or lifetime and are slow to resolve (hepatitis C)
  3. latent disease = the casual pathogen goes dormant for extended periods of time with no active replication
    - no symptoms unless organism reactivates and infection again becomes acute (cold sores due to Herpes)
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126
Q

are latent organisms ever eliminated

A

no

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127
Q

which bacteria are gram positive

A
  • staphylococcus
  • streptococcus
  • bacillus
  • clostridium
  • corynebacterium
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128
Q

which bacteria are atypical

A
  • mycoplasma (no cell wall)
  • mycobacterium (acid-fast cell wall)
  • spirochetes (thin cell wall) includes Treponema and Borrelia
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129
Q

what is the most virulent staphylococcal species

A

s. aureus

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130
Q

what does s. aureus produce

A
  • impetigo
  • TSS
  • SSS
  • food poisoning
  • folliculitis, carbuncle, and furuncle
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131
Q

what kind of virulence does s. epidermidis (CoNS) have

A

low virulence

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132
Q

true or false - s. epidermidis is the normal microbiota of the skin

A

true

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133
Q

what does s. epidermidis cause

A

opportunistic infections

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134
Q

what are some characteristics of s. aureus used in clinical diagnosis to distinguish s. aureus from other species

A
  • coagulase production
  • pigment production (hemolysis)
  • fermentation of mannitol and halotolerance
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135
Q

is s. aureus coag positive or negative

A

positive
- have solid at the bottom

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136
Q

is s. epidermidis coag positive or negative

A

negative
- going to be liquid

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137
Q

different types of hemolysis on blood agar

A
  • B-hemolysis = complete hemolysis (halo)
  • alpha-hemolysis = incomplete hemolysis -> green pigment
  • y-hemolysis = no hemolysis (clear)
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138
Q

what type of hemolysis is s. aureus

A

b-hemolytic
- produces hemolysins called staphylolysins

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139
Q

what type of hemolysis is s. epidermidis

A

y-hemolytic

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140
Q

what does mannitol salt agar inhibit

A

the growth of many organisms EXCEPT staphylococci which is halotolerant (ie facultative halophile)

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141
Q

organisms that ferment mannitol are detected by a change in the

A

pH indicator from red to yellow

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142
Q

what type of media is mannitol-salt agar
- selective
- differential
- general purpose
- enriched
- selective and differential

A

selective and differential

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143
Q

how do we distinguish staphylococcus from streptococcus

A

staphylococci produce catalase

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144
Q

what does catalase break down

A

hydrogen peroxide (H2O2) produced during oxidative metabolism
- bubbles will appear

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145
Q

do streptococci produce catalase

A

no

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146
Q

how is s. aureus resistant to penicillin

A

because it produces beta lactamase (penicillinase) and thus is resistant to penicillins and cephalosporins

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147
Q

do streptococci produce beta lactamase

A

no most strepc don’t, therefore remain sensitive to beta lactam antibiotics

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148
Q

true or false - s. epidermidis are relatively avirulent

A

true

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149
Q

what helps s. epidermidis adhere to devices

A

the production of slime layer because it forms biofilms on the devices (catheters, shunts, prosthetic joints, etc)

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150
Q

when does s. epidermidis become opportunistic infections

A

when introduced into deeper tissues or a normally sterile site

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151
Q

when are opportunistic infections of s. epidermidis usually acquired

A

during a hospital stay

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152
Q

what is the major cause of hospital acquired infections

A

s. epidermidis

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153
Q

what are some examples of infections that were hospital acquired s. epidermidis infections

A
  • subacute endocarditis
  • infections of foreign bodies (ie catheters, shunts, prosthetic joints, etc) and urinary tract infections
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154
Q

is s. aureus very contagious

A

yes

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155
Q

who are the main reservoirs for s. auerus

A

humans

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156
Q

about 30% of healthy adults are ___ __ for s. aureus

A

nasal carriers

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157
Q

what are the three types of transmission of s. aureus

A
  1. direct skin to skin contact
  2. indirect contact via fomites
  3. ingestion of contaminated food
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158
Q

s. aureus has a high tolerance to

A

salt and desiccation (drying conditions)

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159
Q

what are the major virulence factors of s. aureus

A
  • capsule
  • catalase
  • exotoxins: enterotoxin, TSST-1, and exfoliative toxin
  • coagulase
  • staphylolysin
  • leukocidin
  • protein A
  • hyaluronidase
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160
Q

what are virulence factors

A

they can be genetic, biochemical, or structural features that enable an organism to produce disease

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161
Q

pathogenesis may depends on

A

a single or multiple virulence factors

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162
Q

how do strains of s. aureus differ

A

by which virulence factors they produce
- some strains are more virulent because they make more virulence factors

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163
Q

for most disease caused by s. aureus, pathogenesis depends on the combined actions of

A

several virulence factors

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164
Q

what does catalase do

A

neutralizes hydrogen peroxide
- a type of ROS
- counteracts phagocytes’ oxidative killing

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165
Q

what does capsule do

A

inhibits phagocytosis
- composed of polysacchs

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166
Q

which virulence factors are exotoxins that were produced by s. aureus

A
  • staphylolysin
  • enterotoxin
  • toxic shock syndrome toxin 1 (TSST-1)
  • exfoliative toxin
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167
Q

what does stphylolysin do

A

lyses RBCs and WBCs

168
Q

what is an enterotoxin and what does it act as

A

it is a potent GI toxin as well as superantigen activity

169
Q

what does TSST-1 act as

A

a potent superantigen

170
Q

what does exfoliative toxin do

A

an exotoxin that causes desquamation of the skin, weak superantigen activity

171
Q

how do coagulase, protein A, catalase, and capsule contribute to s. aureus virulence?
- destroy human host cells
- allow the bacterium to invade mucosal tissues
- prevent phagocytosis
- act as endotoxin, inducing septic shock
- make the bacteria resistant to antibiotic treatment

A

prevent phagocytosis

172
Q

is hyaluronidase a major virulence factor of s. aureus

A

yes

173
Q

what does hyaluronidase do

A

degrades hyaluronic acid that cements cells together to promote spreading through tissues

174
Q

what diseases cause more frequent and varied types of disease than any other human pathogen

A

s. aureus diseases

175
Q

what are the three toxin-mediated s. aureus diseases

A
  1. staphylococcal food poisoning
  2. scalded skin syndrome
  3. toxic shock syndrome
176
Q

s. aureus is the most common cause of

A

pyogenic skin infections called pyodermas

177
Q

what does pyogenic mean

A

pus producing

178
Q

pyogenic infections are characterized by the formation of an

A

abscess

179
Q

what are four diseases of localized skin infections

A
  1. folliculitis
  2. furuncle
  3. carbuncle
  4. impetigo
180
Q

what is an abscess

A

a localized collection of pus surrounded by fibrin

181
Q

what does pus contain of

A

debris consisting of dead PMNs and epithelial cells, dead and live bacteria and edema fluid

182
Q

what is folliculitis

A

infection of hair follicle
- superficial pustule (pus filled vesicle)
- usually mild, resolves, or progresses to furuncle

183
Q

what is a furuncle

A

aka boil; large painful lesion that extends from hair follicles to surrounding tissues
- abscesses in the skin involving subcutaneous tissue
- resolves or progresses to carbuncle

184
Q

what is a carbuncle

A

multiple interconnected abscesses forming from the aggregration of furuncles
- extends deeper into the tissue
- requires debridement and antibiotics

185
Q

what is the most common type of pyoderma

A

impetigo

186
Q

what does impetigo look like

A
  • small flattened red patches
  • pus filled vesicles
  • rupture and crust over
187
Q

what are the symptoms of impetigo

A

usually little fever or pain
- nearby lymph nodes often enlarge
- itchy and highly contagious

188
Q

impetigo is common among ____ and ___ ___

A

infants and young children

189
Q

impetigo can also be caused by

A

streptococcus pyogenes

190
Q

gastroenteritis is commonly caused by

A

bacteria, viruses, or toxins

191
Q

when is it called food poisoning

A

when gastroenteritis is caused by a toxin and not an infection

192
Q

staphylococcal food poisoning is an example of..
- infection
- intoxication
- infection and intoxication

A

intoxication

193
Q

if its intoxication and not an infection, what is the onset and recovery

A
  • has a rapid onset, usually within 4 hours
  • rapid recovery usually within 24 hours
194
Q

what are the symptoms of staphylococcal food poisoning

A

nausea and vomiting

195
Q

does staphylococcal food poisoning have fever as a symptom

A

no

196
Q

what can staphylococcal enterotoxin cause

A

food intoxication

197
Q

what are some characteristics of staphylococcal enterotoxin

A
  • resistant to low pH (stomach acid)
  • heat stable
  • superantigen activity
198
Q

why do you think the blood cultures failed to isolate any pathogens
- s. aureus is too difficult to grow up in the lab
- s. aureus is too small to detect on a light microscope
- the cell wall of s. aureus does not react with the gram stain and therefore went undetected
- there were no bacteria in the blood samples because replicating bacteria were not causing the systemic disease
- fever is not a typical sign of a bacterial infection so it is probably caused by a virus

A

there were no bacteria in the blood samples because replicating bacteria were not causing the systemic disease

199
Q

when does toxic shock syndrome (TSS) sometimes occur

A

as a complication of other localized or systemic infections such as skin wounds

200
Q

what is TSS caused by

A

TSST-1

201
Q

what is TSST-1

A

an exotoxin that induces fever, vomiting, rash and shock

202
Q

what does TSST-1 act as

A

a potent superantigen

203
Q

TSST-1 causes ___% of all cases

A

75%

204
Q

TSS can also be caused by

A

streptococci

205
Q

what are some symptoms of TSS

A
  • abrupt onset of high fever (102F or above)
  • red erythematous (sunburn-like) rash
  • desquamation
  • hypotension -> multi system organ failure
206
Q

staphylococcal scalded skin syndrome (SSSS) is a ___ infection and a ____ intoxication

A

localized; systemic

207
Q

SSSS is caused by

A

exfoliative toxin

208
Q

what is an exfoliative toxin

A

an exotoxin that causes desquamation of the skin
- also acts as superantigen, but weaker than TSST-1

209
Q

what are the symptoms of SSSS

A

erythema (redness) followed by desquamation
- no scarring

210
Q

SSSS typically affects

A

neonates and infants

211
Q

what is a potential complication of SSSS

A

a secondary infection is more likely to occur in the of areas where the skin has peeled away

212
Q

how do manage staphylococcal infections

A
  • boils, carbuncles may require minor surgery to drain pus
  • antibiotic treatment often follows debridement (removed of dead/damaged tissue)
  • staphylococci produce penicillinase (a type of beta lactamase)
213
Q

what are MRSA strains resistant to

A

beta lactam antibiotics

214
Q

what are MRSA strains sensitive to

A

vancomycin

215
Q

what are VRSA associated with

A

worse outcomes such as longer hospital and ICU stays and higher mortality rates
- many hospitals now screen patients to limit spread

216
Q

is streptococcus gram positive or negative

A

positive

217
Q

is strepcoc catalase negative or positive

A

negative

218
Q

what is strepcoc sensitive to

A
  • heat
  • drying
  • high salt concentration
  • penicillin (most)
219
Q

what are three classification points of strepcoc

A
  1. species determined by biochemical tests or DNA sequencing
  2. group-specific antigens (Lancefield classification)
  3. hemolytic pattern on blood agar
220
Q

what is the lancefield classification

A

is based on differences in a surface antigen (serotypes) called the cell wall C carbohydrate

221
Q

what is the name of group A of lancefield classification

A

streptococci: S. pyogenes

222
Q

what is the name of group B of lancefield classification

A

streptococci (GBS): S. agalactiae

223
Q

what groups of streptococci have no lancefield group classification

A
  • pneumococci
  • viridans
224
Q

what is lancefield grouping based on

A

serotpye

225
Q

what is a serotype

A

a difference in the antigenic composition of a structure or product

226
Q

how do we identify serotypes

A

use Abs (ie antisera) to detect differences in antigens that are unique to a particular species or a strain within a species

227
Q

which groups identify as beta-hemolytic strep

A
  • S. pyogenes
  • S. agalactiae
228
Q

which groups identify as alpha-hemolytic strep

A

S. pneumonia

229
Q

which group identify as alpha or gamma hemolytic strep

A

viridans group strepcoc
- includes S. mutans (alpha hemolytic)

230
Q

how to differentiate between S. pyogenes from S. agalactiae

A

both are beta hemolytic
- but s. aga is group B and bacitracin resistant
- s. pyo is group A and bacitracin sensitive

231
Q

how is S. pyogenes transmitted

A

via respiratory droplets or direct skin contact

232
Q

S. pyogenes frequently infect

A

skin or nasopharynx

233
Q

what is the reservoir for S. pyogenes

A

humans

234
Q

S. pyogenes cause ___% of streptococcal disease

A

90%

235
Q

what are some diseases S. pyogenes cause

A
  • pyogenic = “pus-producing”
    • streptococcal pharyngitis
    • impetigo
    • cellulitis
  • toxigenic
    • toxic shock syndrome
    • necrotizing fasciitis (also pus producing)
236
Q

both S. pyogenes and s. aureus cause the disease, imeptigo. Which of the following is a characteristic that distinguishes these two genera
- catalase
- gram stain reaction
- hemolysis on blood agar
- cellular morphology

A

catalase
- S. pyogenes is catalase negative
- s. aureus is catalase positive

237
Q

what are some characteristics of s. aureus
- (gram (-) or (+) coccal morphology
- catalase (-) or (+)
- coagulase (-) or (+)
- what type of hemolytic
- strains or serotypes,
- penicillin resistant or sensitive
- how does it grow on media

A
  • gram (+) coccal morphology
  • catalase (+)
  • coagulase (+)
  • beta-hemolytic
  • multiple strains
  • penicillin-resistant
  • halotolerant
238
Q

what are some characteristics of S. pyogenes
- (gram (-) or (+) coccal morphology
- catalase (-) or (+)
- coagulase (-) or (+)
- what type of hemolytic
- strains or serotypes,
- penicillin resistant or sensitive
- how does it grow on media

A
  • gram (+) coccal morphology
  • catalase (-)
  • coagulase (-)
  • beta-hemolytic
  • multiple serotypes (80 M protein types)
  • penicillin-sensitive
  • fastidious, grow on enriched media
239
Q

for virulence factors of S. pyogenes what factors inhibit host immunity

A
  • hyaluronic acid capsule
  • M protein
240
Q

for virulence factors of S. pyogenes what are adhesive/invasive factors

A
  • M protein
  • hyaluronidase
241
Q

what are some exotoxins of S. pyogenes

A
  • cytolytic exotoxins: Streptolysin O and S
  • pyrogenic exotoxins: SpeA and SpeB
242
Q

what are antiphagocytic virulence factors by S. pyogenes

A
  • hyaluronic acid capsule
    • mimics the hyaluronic acid found in human
      connective tissue
    • hides the bacteria from phagocytes
  • M protein
    • important adhesion
    • prevents opsonization by breaking down
      complement, C3b
    • more than 80 antigenic types of M protein
      • Abs to one strain do not stop others
243
Q

once you are infected with a pathogen, you develop immunity. Why is it then that children often get recurrent strep throat infections
- the innate immune system clears the infection before memory develops
- S. pyogenes destroys memory T and B cells
- S. pyogenes bacterial DNA integrates into host DNA to establish latency. Later it can be reactivated to cause disease
- they are becoming infected with different serotypes of S. pyogenes

A

they are becoming infected with different serotypes of S. pyogenes

244
Q

what is streptolysin O

A

lyses leukocytes and erthrocytes

245
Q

what is spe A

A

superantigen that causes helper T cells to release a cytokine storm leading to toxic shock

246
Q

what is spe B

A

protease that destroys tissue, leading to fluid accumulation in the areas of damage

247
Q

the genes of spe A and spe B are encoded by a

A

temperate bacteriophage

248
Q

only ___ S. pyogenes strains can synthesize spe A and spe B

A

lysogenized

249
Q

what does lysogenized mean

A

when a bacteria is infected with a temperate phage

250
Q

what can phages carry

A

genes for exotoxins or other virulence factors

251
Q

what is lysogenic conversion

A

new host phenotype due to expressed genes from a phage

252
Q

for S. pharyngitis (strep throat) - are S. pyogenes inhaled

A

yes

253
Q

in S. pharyngitis where does bacteria replicate

A

in mucosa of the pharynx

254
Q

what are some symptoms of S. pharyngitis

A
  • sudden onset of sore throat with patches of pus on tonsils, in back of throat
  • tonsils may be swollen, red, and tender
  • swallowing is painful
  • fever
255
Q

30% of pharyngitis cases in children are due to __. ___ (most other cases are viral)

A

S. pyogenes

256
Q

what is absent in S. pharyngitis in children

A

absence of cough and nasal discharge

257
Q

what is present in S. pharyngitis in children

A

presence of pus on tonsils

258
Q

S. pharyngitis is most common in _ - __ year old children

A

5-10

259
Q

how does impetigo enter

A

through the skin that is already irritated or raw

260
Q

what does impetigo look like

A

small, flattened, red patches that develop into pustules that eventually rupture and crust over with a honey colored crust

261
Q

is impetigo highly contagious

A

yes

262
Q

impetigo is caused S. pygoenes, which other pathogen is it caused by

A

S. aureus

263
Q

true or false - cellulitis spreads to the deeper demis and subcutaneous tissues

A

true

264
Q

what are some symptoms of cellulitis

A
  • fever
  • chills
  • leukocytosis
265
Q

what does cellulitis present as

A

red puffy patches with ill-defined edges

266
Q

what ages does cellulitis usually occur in

A

middle-aged and elderly

267
Q

necrotizing fasciitis also means

A

flesh eating disease

268
Q

what is necrotizing fasciitis caused by

A

highly virulent strains that produce spe A and spe B as well as other enzymes such as streptolysin O

269
Q

what does necrotizing fasciitis infect

A

a wound that can be very minor

270
Q

the enzymes and toxins in necrotizing fasciitis allow the bacteria to

A

invade and destroy muscle, fat, and organ fascia

271
Q

true or false - necrotizing fasciitis has a strong inflammatory response

A

true

272
Q

what does necrotizing fasciitis cause the skin to do

A

to swell, which stretches and discolors the skin

273
Q

is the pain level consistent with the severity of the original injury in necrotizing fasciitis

A

no

274
Q

what will happen is necrotizing fasciitis goes without treatment

A
  • streptococcal toxic shock
  • multi-organ failure
  • death
275
Q

what kind of disease is strep toxic-shock syndrome (TSS)

A

toxigenic disease

276
Q

what is strep TSS caused by

A

strep pyrogenic exotoxin (spe A and B) and additional virulence factors

277
Q

what does pyrogenic mean

A

exotoxins that generate a fever

278
Q

true or false - strep TSS is less common but more deadly than staph TSS (caused by s. aureus)

A

true

279
Q

what are some symptoms of strep TSS

A
  • high fever
  • diffuse sunburn-like rash
  • hypotension
  • shock
  • multi-organ failure
  • but may also include necrotizing fasciitis
280
Q

strains of strep pyogenes that cause toxic shock syndrome must be infected by a phage
- true or false

A

true

281
Q

what shape is s. pneumoniae

A

lancet (blade) - shaped diplococci

282
Q

what type of hemolytic is s. pneumoniae

A

alpha-hemolytic

283
Q

is s. pneumoniae capsule antiphagocytic

A

yes

284
Q

the makeup of the polysacch s. pneumoniae capsule differs from ___ to ___

A

strain to strain

285
Q

more than 90 different serotypes of S. pneumoniae have been identified based on

A

capsule structure
- all of which are capable of causing infections

286
Q

what type of test does s. pneumoniae capsule use

A

quellung test

287
Q

what is a quellung test

A

a biochemical reaction in which Abs bind to a bacterial capsule

288
Q

what does a positive quellung test reaction cause

A

the capsule to become opaque and swell and enlarge

289
Q

what is quelleung test used to serotype

A

s. pneumoniae

290
Q

is s. pneumoniae quellung (+) or (-)

A

positive

291
Q

what is s. pneumoniae reservoir

A

human carriers

292
Q

where are s. pneumoniae located

A

transient part of the normal microbiota of the nasopharynges (20-60% kids are nasal carriers)

293
Q

how are s. pneumoniae transmitted

A

via contact with respiratory droplets

294
Q

s. pneumoniae disease causes disease typically in

A

very young and very old people

295
Q

true or false - s. pneumoniae disease can cause otitis media (ear infection) and pneumonia

A

true

296
Q

s. pneumoniae disease is the number one cause of ___ ___ in infants and young children

A

otitis media (ear infection)

297
Q

s. pneumoniae disease is the number one cause of community-acquired ____ ___ in older adults

A

bacterial pneumonia
- also in immunocompromised, including smokers, diabetics, and alcoholics

298
Q

what is the biggest risk factor of getting a bacterial ear infection

A

viral infections of the upper respiratory tract (URT), ie colds

299
Q

otitis media by s. pneumoniae - viral URT infections create ___

A

exudate
- washes bacteria from the nasopharyngeal microbiota into the middle ear by Eustachian tube

300
Q

what are some symptoms of otitis media

A
  • inflammation
  • swelling
  • fluid, pus collect behind eardrum
    • cause pressure where eardrum may burst
301
Q

for pneumococcal pneumonia, humans are the carriers and the risk of pneumonia rises when

A

mucociliary escalator is damaged/non functional

302
Q

is there microbiota in the lungs

A

no
- that means that bacteria can rarely reach the lung

303
Q

pneumonia pathogenesis predisposing factors include

A
  • ciliated epithelium damaged by viruses, smoking, and chemicals
  • bacteria enter LRT and infect alveoli
  • inflammation = fluid accumulation
304
Q

what is the development of pneumonia

A
  • growth of strepcocci on damaged ciliated epithelium
  • growth in alveoli, which stimulates increased fluid accumulation
305
Q

what are some signs and symptoms of pneumonia

A
  • cough, fever, congestion, chest pain, rust-tinged sputum
  • breathing becomes shallow and rapid
  • skin becomes dusky due to poor oxygenation
  • night sweats
306
Q

how to diagnose pneumonia

A
  • cheat radiograph confirm infiltrates (some kind of fluid)
  • gram stain of the patients sputum (diplococci is gram (+))
307
Q

what. are two vaccines against pneumococcal capsule

A
  1. for children 2mo - 5yo -> pneumococcal conjugate vaccine (PCV13)
    • 13 valent = protection against 13 serotypes
      (strains)
  2. for adults 65yos or older -> pneumococcal polysaccharide vaccine (PPV)
    • 23 valent
308
Q

is pneumococci enters the bloodstream what does it lead to

A

meningitis or sepsis

309
Q

what is sepsis

A

an infection-induced systemic inflammatory response syndrome

310
Q

what does sepsis cause

A
  • vasodilation
  • increased WBCs
  • leakage of fluid from capillary beds
  • remote from site of infection
311
Q

what is the most common cause of sepsis

A

bacteremia (bacteria in the blood)

312
Q

when does sepsis occur

A

when a pathogen that has entered the bloodstream overwhelms our innate immune response and replicates at high numbers

313
Q

what are the steps in sepsis

A
  1. infection of the bloodstream
  2. excessive inflammation
  3. cytokine release (“cytokine storm”)
  4. complement is also activated, further amplifies
  5. additional phagocytes recruited, further amplifies
  6. cell/tissue damage
314
Q

what does “shock” mean in septic shock

A

general term used to describe cardiovascular collapse
- meaning the heart fails and there is not enough blood pressure to perfuse the tissues

315
Q

what is septic shock

A

sepsis plus persistent hypotension despite adequate fluid resuscitation

316
Q

s. agalactiae can also mean

A

group B strep (GBS)

317
Q

GBS is the most common cause of

A
  • neonatal sepsis
  • neonatal meningitis
318
Q

GBS is the second most common cause (after E. Coli) of

A

neonatal pneumonia

319
Q

s. agalactiae is the transient part of the

A

normal vaginal microbiota
- in 25% of all healthy adult women

320
Q

true or false - s. agalactiae cannot be transferred to infant during delivery

A

false
- it can

321
Q

how is s. agalactiae virulence determined

A

by its ability to avoid phagocytosis (mediated by capsule)

322
Q

to screen a pregnant women for GBS, at how many weeks would the screen occur

A

at 35-37 weeks by a vaginal and rectal swab

323
Q

if the pregnant women was GBS+ what would happen next

A

would administer intrapartum antibiotics via IV to prevent transmission to neonate

324
Q

s. mutan is a member of ___ group strepcocci

A

viridans

325
Q

what type of hemolytic is s. mutans

A

alpha hemolytic

326
Q

are s. mutans encapsulated or non-encapsulated

A

non-encapsulated so quellung (-)

327
Q

what mirobiota is s. mutans a part of

A

normal oral microbiota

328
Q

what kind of environments do s. mutans thrive in

A

acidic ones

329
Q

what is s. mutans involved in

A

pathogenesis of dental caries (ie cavities)
- s. mutans begins the formation of biofilm on teeth
- bacteria ferment dietary carbs producing lactic acid
- lactic acid eats away a tooth enamel

330
Q

what can provide pathogens an entry into the skin

A

cuts, punctures, burns, abrasions, and insect or tick bites that can break the barrier and provide entry for pathogens

331
Q

skin infections can also occur when microorganisms enter the body from another site, like ___ or __ system, and then carried by the bloodstream to the skin

A

respiratory; GI

332
Q

which host pathogens cause the majority of bacterial skin infections

A

staph aureus and strep pyogenes (group A)

333
Q

what bacterial infections do s. aureus and s. pyogenes cause

A

impetigo, folliculitis, carbuncles, furuncles, cellulitis, and scalded skin syndrome (SSS)

334
Q

what skin infections do s. aureus and s. pygoenes cause

A
  • lyme disease = circulatory disease that produces a skin rash
  • gas gangrene = wound infection
  • tetanus = wound infection
335
Q

what are some viral diseases that produce skin rashes

A
  • varicella (chicken pox)
  • zoster (shingles)
  • measles
  • rubella
336
Q

what is one fungal disease (mycoses)

A

tineas

337
Q

what is the most common vector-borne disease in the U.S.

A

lyme disease

338
Q

how is lyme disease transmitted

A

via a bite from an infected black-legged lxodes tick

339
Q

what causes lyme disease and what are its characteristics

A

borrelia burgdorferi
- gram negative spirochete and motile

340
Q

true or false - spirochetes have an outer membrane containing LPS

A

true

341
Q

what are some characteristics of spirochetes

A
  • possess endoflagella
  • moves in corkscrew fashion through its environment
    • might enable pathogenic spirochetes to burrow
      through hosts’ tissues
342
Q

what type of disease is lyme disease and what is its animal reservoir

A

it is a zoonotic disease
- white footed mouse is the main reservoir

343
Q

true or false - borrelia burgdorferi (that causes lyme disease) is maintained in mice out in nature

A

true
- that is why they are the main reservoir

344
Q

when it comes to lyme disease, what occurs in acquisition

A

unfed larva to fed larva in 3-5 days

345
Q

when it comes to lyme disease, what occurs in transmission

A

unfed nymph to fed nymph in 3-5 days

346
Q

when a nymph or adult tick infects a human, what is the human considered

A

accidental host ?

347
Q

what are the three stages of lyme disease

A
  1. multiply, migrate outward in circular fashion; LPS causes inflammatory reaction in skin
  2. enter bloodstream, disseminate
  3. immune system responds and causes damage to host tissue
348
Q

what is stage 1 (erythema migrans) of lyme disease

A
  • about 7 days after a tick bite
  • bull’s eye rash called erythema migrans
  • flu-like symptoms
349
Q

describe stage 2 (injury to nervous and cardiac system) of lyme disase

A
  • 2-8 weeks after the tick bite
  • nervous system is affected
    • dizzy spells, fainting, difficulty concentrating
    • paralysis of face, Bell palsy
350
Q

describe stage 3 (immune response damages host tissue) in lyme disease

A
  • about six months after tick bite
  • arthritis with severe joint pain and swelling, particularly in the knees
  • sometimes meningitis or encephalon
  • most likely immune-mediated
351
Q

what is the treatment for lyme disase

A
  • antibiotics effectively treat first stage of lyme disease
  • treatment of later stages are difficult
352
Q

how is lyme disease prevented

A
  • prevention is best achieved by avoiding ticks
  • no available vaccine for humans
353
Q

what are dermatophytes and what they do they include

A
  • are a group of skin-invading molds
  • include members of genera Epidermophyton, microsporum, and trichophyton
354
Q

what can dermatophyes invade

A

keratinized layers of skin, hair, and nails
- produce keratinase, which breaks down keratin, using it as a nutrient source

355
Q

how are skin diseases caused by fungi (mycoses) transmitted

A

fomites or direct contact

356
Q

what do dermatophytes cause

A

tineas
- ringworm
- athlete’s foot
- toenail fungus

357
Q

what is ringworm

A
  • tinea corporis
    • scaly skin in the center surrounded by a raised red
      margin that occur on smooth skin
      common in young children
  • tinea capitis
    • severe cases affect scalp and hair-bearing region causing patchy areas of hair loss
358
Q

what is athlete’s foot

A
  • tinea pedis
  • more common in adults than in children
  • scaly itchy rash between toes
359
Q

what is nail fungus - onychomycosis

A
  • tinea unguium
  • very common but more common among the elderly
  • about 10% of the general population
  • chronic infection of the nails
  • infected nails of the hands and feet become thickened, yellow, and brittle
360
Q

true or false - normal microbiota or microorganisms from air, fingers, or object contaminate wounds

A

true

361
Q

infection from a wound contamination can result in

A
  • an abscesses by s. aureus
  • wounds with extensive tissue damage and damaged blood supply create anaerobic conditions allow growth of obligate anaerobes such as clostridium tetani
362
Q

what are some characteristics of clostridial species
(spp)

A
  • endospore-former
  • gram positive rods
  • obligate anaerobe
363
Q

what are four major clostridial pathogens

A
  • c. perfringens = gas ganagrene
  • c. tetani = tetanus
  • c. botulinum = botulism
  • c. difficile = antibiotic-associated pseudomembranous colitis
364
Q

obligate anaerobe spores can survive in exposure to

A

air

365
Q

C tetani spores enter the body and germinate in

A

damaged/necrotic tissue

366
Q

tetanospasmin is a type of

A

A-B exotoxin

367
Q

the tetanus toxin is taken up by inhibitory neurons where it

A

prevents release of inhibitory NTs (GABA)

368
Q

what is tetany (aka spastic paralysis)

A

when the muscles undergo sustained contractions because the excitatory neurons are now unopposed by inhibitory neurons

369
Q

death from tetany usually results from

A

respiratory failure

370
Q

what is the treatment for tetany

A
  • muscle relaxants
  • human tetanus immune globulin (TIG) injection
    • Abs bind to free toxin molecules, provide passive
      immunity
  • clean the wound
  • antibiotics
371
Q

how to prevent tetany

A

DTaP vaccine

372
Q

what does DTaP vaccine protect against

A

diphtheria, tetanus, and pertussis

373
Q

what does DTaP vaccine contain, does it need boosters, if so how often

A
  • contains toxoid (inactivated tetanospasmin)
  • requires boosters (Td or Tdap) every 10 years
374
Q

true or false - tetanus is the only non-contagious disease we routinely vaccinate against

A

true

375
Q

what are some characteristics of clostridium perfringens

A
  • soil bacterium
  • spore former
  • gram positive rods
  • obligate anaerobe
376
Q

how do spores enter in c. perfringens

A

via severe and open wounds
- the organism requires damaged tissue with disrupted blood supply (ie anaerobic conditions) to germinate

377
Q

what are some signs and symptoms of c. myonecrosis

A
  • severe pain
  • thin bloody or brownish exudate leaks from wound
  • gas bubbles in tissue
  • overlying skin stretched tight and mottled with black
  • victim remains alert until late in illness, then becomes delirious and goes into coma
378
Q

what are some c. perfringens virulence factors

A
  • alpha toxin destroys PMNs, RBCs, and muscle tissue -> causing myonecrosis (death of muscle)
379
Q

what is the treatment of gas gangrene

A
  • prompt debridement of diseased tissue and amputation of all devitalized tissue
  • antibiotics and antitoxin although less effective
  • hyperbaric oxygen therapy
380
Q

what virus is measles caused by

A

rubeola virus
- an enveloped virus

381
Q

measles epidemiology

A
  • humans are the reservoir
  • usually affects young children
  • transmission: respiratory droplet nuclei (airborne - vertical transmission)
382
Q

what is the most contagious of the vaccine-preventable diseases

A

measles
- contagious from 4 days before and 4 days after rash onset

383
Q

measles sign and symptoms

A
  • high fever
  • cough, coryza (nasal inflammation), conjunctivitis (swollen, red eyes)
  • koplik spots (white spots in the inner cheek)
384
Q

describe the measles rash

A
  • virus spreads through the bloodstream and causes a characteristic rash
  • maculopapular rash begins at face, then trunk and extremities
385
Q

what are some complications of measles

A
  • viral pneumonia
  • encephalitis
  • often secondary infections lead to ear infections and bacterial pneumonia
386
Q

what does measles prevention - MMR vaccine

A
  • prevents measles, mumps, and rubella
  • MMR vaccine is a live attenuated vaccine
  • 2 dose vaccine is 97% effective
387
Q

what virus causes rubella

A

the rubella virus
- enveloped virus

388
Q

what is rubella’s epidemiology

A
  • humans are the reservoir
  • transmission: airborne respiratory droplet nuclei and vertical transmission (mother to baby)
  • groups at risk:
    • occurs most often in school-aged children;
      mild
    • most severe in neonates -> congenital rubella
      syndrome
389
Q

what are rubella’s signs and symptoms in children

A
  • widespread faint, shorter-lived red macular rash
  • not associated with koplik spots
  • lymphadenopathy (swollen, inflamed lymph nodes)
390
Q

true or false rubella is an example of a teratogen? define teratogen

A

true
- teratogen = something that disrupts normal development of the embryo

391
Q

what are the most common infections associated with congenital anomalies

A

TORCHeS
- Toxoplasmosis
- “Other” infections (HIV, syphilis, VZV)
- Rubella
- CMV
- Herpes simplex virus

392
Q

what is congenital rubella syndrome

A
  • rubella virus crosses the placenta in first trimester, high risk for
    • stillborn
    • spontaneous abortion (aka miscarriage)
    • congenital rubella syndrome birth defects:
      deafness, heart defects, brain damage
393
Q

varicella (chickenpox) is caused by

A

varicella zoster virus (VZV)
- enveloped virus
- belongs to herperviridae family

394
Q

all herpes viruses have

A
  • double-stranded DNA genomes
  • enveloped
395
Q

true or false - all herpesviruses establish latency

A

true

396
Q

what are latent infections

A

remain inactive inside infected cells as episomes (circular viral genome molecules outside of the host chromosome)
- reactivation causes recurrence of the disease

397
Q

latency is maintained by

A

T cell-mediated immunity

398
Q

what type of agents are not effective against latent viruses

A

antiviral agents

399
Q

are herpe infections curable

A

no

400
Q

what is in the herpesviridae family

A
  • herpes simplex virus 1 and 2
  • varicella-zoster virus (VZV)
  • epstein barr virus
  • cytomegalovirus (CMV)
401
Q

define primary infection

A

first experience with the virus

402
Q

define latent infection

A

persistence of the virus in a non-replicating state

403
Q

reactivated/recurrent infection

A

virus coming out of latency and renewal of viral replication

404
Q

define symptomatic infection

A

with clinical signs and symptoms

405
Q

define asymptomatic infection

A

viral shedding without symptoms

406
Q

with varicella-zoster virus (VZV) what is the primary acute infection

A

chickenpox (aka herpes varicella)

407
Q

with VZV what is the recurrent infection

A

shingles (aka herpes zoster)

408
Q

with varicella (chickenpox) the rash begins as

A

red papules and then progress to vesicles

409
Q

scratching and rupturing the vesicles in varicella, can lead to serious secondary infection by

A

s. pyogenes or s. aureus

410
Q

how is varicella transmitted

A
  • respiratory droplet nuclei (ie airborne)
  • direct skin contact
  • vertical transmission (VZV is a teratogen)
  • highly contagious
411
Q

what group is at most risk for chickenpox

A

most severe in babies; congenital varicella syndrome -> birth defects; ~20-30% will die

412
Q

VZV is latent in the ganglia and when reactivated what does it become

A

shingles

413
Q

how does shingles differ from varicella

A
  • rash pattern (along dermatome)
  • pain level
  • duration (can last up to 1 month)
414
Q

a person with shingles lesions is contagious and can transmit the virus to a nonimmune contact. the newly infected individual would develop…
- shingles
- pneumonia
- chickenpox
- measles
- rubella

A

chickenpox

415
Q

describe the varicella vaccine

A
  • live attenuated vaccine
  • often combined with MMR
416
Q

describe shingles vaccine

A
  • recombinant subunit vaccine
  • advised for adults over the age of 50

Micro (8 decks)

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